Test Details

Patient: SANDRA ALARCON

Test Created September 22, 2025 8:36 pm

Last modified: September 22, 2025 8:36 pm

Current Weight: 275

Current Lifestyle: sedentary

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Blood Test Results Report - SANDRA ALARCON – 09-22-2025 20:36pm

Test(s)	Current	Previous Report	Standard	R	%
Glucose Glucose GLUCOSE Glucose is an important fuel for the body, which affects all tissues, organs, and systems. Glucose also affects the acid/alkaline balance in the body. Breakdown of glucose or starch starts in the mouth via ptyalin, then in the stomach via HCL, and then by pancreatic amylase, lactase and other enzymes. Glucose is then absorbed in the small intestines and is then stored as glycogen in the liver. The liver is the primary site of glucose production. The liver converts lactic acid to glycogen and back to glucose via epinephrine. The liver converts fats and proteins via gluconeogenesis into glucose or glycogen. The head of the pancreas controls chromium, which controls insulin levels and assists in the enzyme action of fats via bile salts. The tail of the pancreas controls zinc, which maintains and sustains levels of insulin. Blood sugar depends on: 1. The liver which stores and releases glycogen 2. The pancreas, which produces insulin that transfers sugar from the blood to the extracellular fluid 3. The adrenal glands, which produced glucocorticoids that, cause the liver to release glycogen into the blood as glucose 4. The sex organs, which deliver the extracellular glucose to the cell 5. The thyroid, which affects the storage of glycogen in the liver 6. The thymus and spleen, which affect the levels of iron and copper in the liver which, determine the liver's ability to handle glucose As you can see there are many organs, or combinations of these organs and glands, which affect glucose levels in the body. Therefore, glucose in itself cannot specifically determine where the problem may lie. Other indicators are necessary to pinpoint the problem.	83	-	65 - 115	-7	-28
Uric Acid Uric Acid URIC ACID Uric acid is the principal end product of purine, nucleic acid, and nucleoprotein metabolism. Uric acid is transported by the blood from the liver to the kidney’s which filter out and secretes about 70% and the remainder excreted via the GI tract. From a pathological view, uric acid is elevated when there is cell breakdown as in leukemia and catabolism of nucleic acids as in gout, or removal via the kidneys is decreased due to renal failure. From a physiologic view, we look at every level of protein combustion where there remain two by-products which are a Mucous (oily residue) and Uric acid (carbon ash) In order for protein to be fully combusted, it must first be influenced in the duodenum by trypsin, chymotrypsin, carboxypolypeptidase, and bile emulsification. Trypsin and chymotrypsin cleave proteins into peptides and carboxypolypeptidase split the peptides into amino acids. The pancreas synthesizes trypsinogen, chymotrypsinogen, and procarboxypolypeptidase, which are enzymatically inactive. When they are released into the duodenum they are all activated by enterokinase. Which now readies the proteins for assimilation in the liver. Therefore, if the proteins are not prepared properly the two end products, uric acid, and mucous, will be out of balance. URIC ACID IS HIGH WHEN General considerations: ¬ Decrease fatty proteins and rich foods ¬ Decrease alcohol and simple sugars ¬ Increase water intake	13.3	-	2.2 - 7.7	8.35	303.64
Bun Bun BLOOD UREA NITROGEN Blood urea nitrogen is formed entirely by liver deamination from protein metabolism. BUN is a byproduct due to the release of nitrogen bonds (and measures the nitrogen portion of urea) from protein substances in the liver. From a pathological perspective, an increased blood urea nitrogen would indicate renal disease, tissue necrosis, increased adrenal gland activity, and rapid protein catabolism. From a physiologic perspective, the purpose of nitrogen is to carry a substance through an aerobic media preventing oxidation, and eventually back into an anaerobic environment. Once in the liver the thyroid through the use of iodine, releases the nitrogen bond, releasing the nitrogen from the protein, allowing the protein to combust into hormones, enzymes and antibodies. The adrenals and anterior pituitary play a vital role in the combustion of this protein. The urea is now sent to the kidneys and is converted into urine. Urea is produced when amino acids, which are not used for protein synthesis, are broken down via hepatic metabolism. These amino acids are de-aminated producing ammonia, which is converted to urea immediately since ammonia levels become toxic. When this metabolic conversion is affected due to faulty metabolism or liver disease ammonia is not converted causing excessive levels of ammonia with possible hepatic encephalopathy. Renal malfunction/failure may also cause a high BUN due to its affect on the removal of urea causing uremia. Uremic wastes usually impair platelet function, and patients may show an increased tendency towards bleeding. BUN IS HIGH WHEN General considerations: ¬ High protein diets can cause increased BUN ¬ Increase water intake if no edema	108	-	5 - 26	92.5	880.95
Creatinine Creatinine CREATININE Creatinine ash is a basic byproduct in the breakdown of muscle creatine phosphate resulting from energy metabolism. From a pathological perspective the kidneys primarily remove creatinine and when there are elevated levels it indicates reduced kidney function. Thus creatine levels give an approximate for the GFR. From a physiological perspective, creatine is a by-product of actin metabolism after being exposed to acetylcholine combustion. The actin fiber joins two stable protein blocks (myosin), which combusts to produce muscle contraction, primarily for activity and secondarily for tonicity. During a muscle contraction, an action potential travels along a motor nerve to a muscle fiber. Acetylcholine is released at the motor endplate, causing multiple acetylcholine lined gated protein channels to open. This causes sodium ions to flow to the interior of the muscle, which initiates an action potential of that muscle. This then leads to depolarization releasing large amounts of calcium into the myofibrils. This initiates a contractive force between the actin and myosin filaments via ATP causing them to slide together, which is the contractile process. After a fraction of a second, calcium is pumped back into the sarcoplasmic reticulum, until the next muscle contraction. The actin fiber is then oxidized (H displaced) via acetylcholine, leaving an oily waxy residue known as creatinine. GABA (Glutamic amino benzoic acid), which is part of the actin fiber, helps it burn better. Creatine becomes creatinine with the release of ATP. Low creatinine levels would indicate muscle loss and weakness.	3.1	-	0.6 - 1.5	2.05	455.56
Sodium Sodium ELECTROLYTES The blood electrolytes include sodium, potassium, chloride, and the bicarbonate (HCO3) ion. Sodium, potassium, and chloride enter the body via ingestion of food. Carbon dioxide, on the other hand, originates within the body via the metabolic process of carbohydrates, fats, and proteins. Normally the excretion of sodium, potassium, and water is equal to their intake. The kidneys secrete 80-90 percent of all electrolytes. Excessive carbon dioxide stimulates the respiratory centers in the brainstem to increase respiration. Therefore, the kidneys and the lungs control sodium, chloride, potassium, water, and carbon dioxide thus exerting control over the acid/alkaline balance in the body. There are also many other organs, and glands involved in this process, such as the posterior pituitary, adrenals, bowel, and uterus/prostate. The purpose of electrolytes is to set up a shifting mechanism in the cell membrane via oxidation, allowing increased or decreased permeability to that membrane site. Sodium, which is found in high concentration outside the cell, has the ability to gather up substances (foods) and bring them to active membrane sites. Chloride is found in the cell membrane and acts as a “doorman” allowing or disallowing exchanges between the intracellular and extracellular fluids. Potassium, which is found in high concentrations within cells, oxidizes chloride, and allows sodium, with the food to cross the cell membrane and enter the cell. Sodium, potassium, chloride, calcium, and hydrogen are all transported via active transport. SODIUM Sodium is the most abundant cation (90%) and is the major base in the body. Sodium is either implanted into the food via saliva or is found in the food and has the following functions: 1. Sodium is an alkaline mineral that helps maintain alkaline activity. Therefore, it helps in acid-alkaline balance, which affect intracellular/extracellular fluid exchange, osmotic pressure, via the sodium/potassium pump and does this in conjunction with antidiuretic hormone and aldosterone. 2. Sodium gathers, and aggregates (polarizes) all substances necessary to be exchanged by semi-permeable membranes. Sodium pumps proteins and sugars into the cell membranes. 3. Sodium also affects the renal tubules for the activity of discharging toxins. It literally aggregates toxins and holds them in suspension. 4. Sodium is controlled by the adrenal cortex and as mentioned above is extremely alkaline and therefore, can cause migration of substances towards its polarity, as well as causing these migrated substances to achieve permeability in an acid antioxidant type media known as a fatty membrane. Sodium is the substance necessary to polarize foods into storage according to that permeable membranes needs. 5. Sodium is also necessary for the transmission of neurological impulses by creating action potentials across neurological membranes. 6. Sodium concentration in and out of cells remains constant due to renal blood flow, carbonic anhydrase enzyme activity, aldosterone, and other steroids controlled by the anterior pituitary, rennin enzyme secretion, hypothalamus, and posterior pituitary control of ADH and vasopressin secretion	139	-	135 - 147	-2	-33.33
Potassium Potassium ELECTROLYTES The blood electrolytes include sodium, potassium, chloride, and the bicarbonate (HCO3) ion. Sodium, potassium, and chloride enter the body via ingestion of food. Carbon dioxide, on the other hand, originates within the body via the metabolic process of carbohydrates, fats, and proteins. Normally the excretion of sodium, potassium, and water is equal to their intake. The kidneys secrete 80-90 percent of all electrolytes. Excessive carbon dioxide stimulates the respiratory centers in the brainstem to increase respiration. Therefore, the kidneys and the lungs control sodium, chloride, potassium, water, and carbon dioxide thus exerting control over the acid/alkaline balance in the body. There are also many other organs, and glands involved in this process, such as the posterior pituitary, adrenals, bowel, and uterus/prostate. The purpose of electrolytes is to set up a shifting mechanism in the cell membrane via oxidation, allowing increased or decreased permeability to that membrane site. Sodium, which is found in high concentration outside the cell, has the ability to gather up substances (foods), and bring them to active membrane sites. Chloride is found in the cell membrane and acts as a “doorman” allowing or disallowing exchanges between the intracellular and extracellular fluids. Potassium, which is found in high concentrations within cells, oxidizes chloride, and allows sodium, with the food to cross the cell membrane and enter the cell. Sodium, potassium, chloride, calcium, and hydrogen are all transported via active transport. POTASSIUM Potassium is intracellular, lining the inside of all cell membranes and affecting intracellular fluids, osmotic pressure, buffering viscosity (potassium bicarbonate is the primary intracellular inorganic buffer). When there is a decrease in potassium bicarbonate you have acid cells, which excites the respiratory centers so the patient hyperventilates. Metabolic acidosis or diabetic ketoacidosis drives potassium out of the cells, affecting electrolyte balance, water retention and carbon dioxide transport in red blood cells. Potassium is responsible via the posterior pituitary for oxidizing secondary hydrogen chloride (affecting adrenal function), allowing the sodium-aggregated substances to cross the cell membrane by affecting the membranes permeability. Potassium is the only substance, which allows oxygen into unoxygenated tissue. About 90% of the body’s potassium supply is intracellular with only a small percent in the serum. 80% of that is found in the muscles (used for muscular contraction) and in the bones. Potassium levels are regulated by the Na/K ATPase pump which requires magnesium for proper function. Potassium is necessary for proper function of mineralocorticoids, (aldosterone and deoxycorticosterone) thus maintaining sodium concentration and alkaline reserve. Therefore, potassium is of great value to the posterior pituitary (ADH/oxytocin), the pineal, and the adrenal cortex via aldosterone secretion. Potassium along with sodium regulate renal acid-base balance, by substituting hydrogen ions for sodium and potassium in the renal tubules. Potassium also facilitates oxygen to the myocardium and oxidizes the S.A. node of the heart. The heart has the highest potassium concentration in the body. Potassium along with calcium and magnesium controls the rate and force of contraction in heart muscle. It is the primary oxidizer of the body capable of expressing all cellular needs. Potassium also regulates neurological impulses via osmotic pressure gradients throughout the nervous system. Potassium directs carbohydrate digestion by polarizing minerals associated with carbohydrate digestion, from the time the carbohydrate enters the body until the cell utilizes it. Potassium also makes proteins soluble and regulates protein synthesis. 80-90 percent of potassium in the cells is excreted by the kidneys (resulting in the loss of 40-50 mEq/L per day even during fasting) with the remainder excreted by the stool and through sweating POTASSIUM IS LOW WHEN General considerations: ¬ Increase water intake ¬ Increase magnesium intake ¬ Decrease calcium intake ¬ Increase potassium intake ¬ Decrease carbohydrate intake	4	-	3.5 - 5.5	-0.5	-50
Chloride Chloride ELECTROLYTES The blood electrolytes include sodium, potassium, chloride, and the bicarbonate (HCO3) ion. Sodium, potassium, and chloride enter the body via ingestion of food. Carbon dioxide, on the other hand, originates within the body via the metabolic process of carbohydrates, fats, and proteins. Normally the excretion of sodium, potassium, and water is equal to their intake. The kidneys secrete 80-90 percent of all electrolytes. Excessive carbon dioxide stimulates the respiratory centers in the brainstem to increase respiration. Therefore, the kidneys and the lungs control sodium, chloride, potassium, water, and carbon dioxide thus exerting control over the acid/alkaline balance in the body. There are also many other organs, and glands involved in this process, such as the posterior pituitary, adrenals, bowel, and uterus/prostate. The purpose of electrolytes is to set up a shifting mechanism in the cell membrane via oxidation, allowing increased or decreased permeability to that membrane site. Sodium, which is found in high concentration outside the cell, has the ability to gather up substances (foods) and bring them to active membrane sites. Chloride is found in the cell membrane and acts as a “doorman” allowing or disallowing exchanges between the intracellular and extracellular fluids. Potassium, which is found in high concentrations within cells, oxidizes chloride, and allows sodium, with the food to cross the cell membrane and enter the cell. Sodium, potassium, chloride, calcium, and hydrogen are all transported via active transport. CHLORIDE Chloride a blood electrolyte, and is the major anion and exists in the extracellular spaces as part of the sodium chloride or HCl molecules. Chloride is used for assessing pH, and electrolyte balance. From a physiologic perspective, the primary purpose of chloride is to regulate the quantity of carbohydrates and proteins entering into the cells, by inhibiting the exchange of mineral controlled substances across the cell membrane and responds to the oxidative power of potassium. Chloride the major anion is predominantly found in the extracellular spaces as part of sodium chloride or in the stomach as hydrochloric acid. Chloride maintains cellular integrity by its influence on acid-base and water balance as well as osmotic pressure. Chloride has a reciprocal power with other anions by decreasing or increasing when there are too many or not enough anions. Aldosterone has a direct effect of reabsorption of sodium and an indirect effect on the increased absorption of chloride. Chlorides are lost via the GI tract through vomiting or diarrhea and thru the kidneys during times of diuresis. Chloride also responds to the antioxidant media (cell membrane) by mobilizing, and collecting sodium/food aggregates on a selectively permeable basis. This reaction is under the influence of the adrenal medulla/epinephrine/norepinephrine thereby maintaining energy stores. Chloride also assists in the production of HCl via the chief cells in the stomach. In the bowel, chloride is important in preventing the passage of water out of the body. Therefore, chloride literally blocks the flow of water/gas exchange across a cell membrane. This is extremely important in the intestines and bladder. Chloride plays a vital role during the conduction of a neurological impulse where sodium lines up on the outside of a cell membrane, and potassium on the inside of the cell membrane, during the resting stage or polarized state. In a normal nerve fiber, the permeability of the membrane to potassium is about 100 times that of sodium. The sodium-potassium pump moves three sodium ions to the exterior of the cell, for every two potassium ions that are moved to the interior of the cell, creating a net positive charge to the outside of the cell membrane for each revolution of the sodium-potassium pump. This creates a positively charged external membrane and a negatively charged internal membrane, which sets up a membrane electrical potential. As a neurological impulse is transmitted down the nerve, (which is the excitation phase of an impulse), sodium crosses the cell membrane, and enters into the cell, while potassium moves to the external portion of the membrane. This then creates the depolarization of the cell membrane, thereby creating a negative charge on the outside, and a positive charge on the inside. The transmission of each impulse along the nerve fiber reduces infinitesimally as the concentration differences of sodium and potassium between the inside and outside of the cell membrane change slightly. In so doing allows the nerve fiber to transmit between 100, 000 to 50, 000, 000 impulses before the concentration differences are rundown. As the neurological impulse passes, the sodium-potassium ATPase pump re-establishes the sodium-potassium ratio back to normal (repolarization). The pumping activity is dramatically increased approximately eightfold to restore the membrane back to the polarized state. The chloride shift to the inside of the cell membrane during the final stages makes the inside of the cell, even more, negative, which further helps repolarize the cell. Chloride generally increases and decreases with plasma or serum sodium levels. CHLORIDE IS HIGH WHEN General considerations: ¬ Drink plenty of water ¬ Decrease sodium levels ¬ Increase fat-soluble vitamins D, E, K, and A	100	-	96 - 109	-2.5	-38.46
CO2 CO2 CARBON DIOXIDE Carbon dioxide is created as a byproduct when potassium forces water into fat. So carbon dioxide is the acid gas factor, which binds fats and selenium creating the intelligent metabolic activity between the water and fat. 80-90 percent of the carbon dioxide found in plasma is bound to protein and is represented as bicarbonate ions (HCO3-) which first exists in the extracellular spaces as CO2 then as H2CO3 and finally is buffered by the plasma and erythrocytes into sodium bicarbonate NaHCO3) and is regulated by the kidneys. The other 10 to 20 percent is dissolved CO2 gas (removed by the lungs), which is bound to protein as CO3 (2), and carbonic acid (H2CO3). The total CO2 comes from dissolved CO2, H2CO3, HCO3- and carbaminohemoglobin (CO2HHb). This occurs in the following way, carbon dioxide in the blood reacts with water in the red blood cells to form carbonic acid. In the blood cells, there is an enzyme called carbonic anhydrase that catalyzes the water and carbon dioxide 5,000 fold, creating a rapid exchange into carbonic acid. This allows tremendous amounts of carbon dioxide reacting with the water in the red blood cells, even before the blood leaves the tissue capillaries. So a red blood cell creates carbonic acid from water and carbon dioxide. In another small fraction of a second, the carbonic acid formed in the red blood cell now disassociates into hydrogen and bicarbonate ions. The hydrogen ions combine with hemoglobin, as the bicarbonate ions diffuse out into the plasma while chloride ions diffuse into the red blood cells taking the place of the bicarbonate ions. This is made possible by the presence of a bicarbonate/chloride carrier protein in the red blood cell membrane, which acts as a shuttle for these two ions. Thus, the chloride content of venous red blood cells is greater than that of arterial cells. This is known as the chloride shift. In addition, carbon dioxide can react directly with hemoglobin to form the compound carbaminohemoglobin. This carbaminohemoglobin creates the reversible reaction releasing carbon dioxide into the alveoli of the lungs. Carbon dioxide then is the venous capillary exchange product after diffusion takes place. The active pressure intake of oxygen relies upon this diffusion. This active process realizes the ability of forced metabolism and is the ash byproduct. Carbon dioxide is vital to pH balance and is controlled by the respiratory, renal, and posterior pituitary adrenal axis. Therefore, any of these glands or organs or combinations thereof can affect carbon dioxide levels. CARBON DIOXIDE IS HIGH WHEN General considerations: ¬ Water loss- increase water intake ¬ Protein loss- increase protein intake ¬ Hypomagnesemia or hypokalemia causes increased CO2- increase potassium and magnesium CARBON DIOXIDE IS LOW WHEN ¬ Water loss- increase water intake ¬ Hypermagnesemia or hyperkalemia causes decreased CO2- decrease potassium and magnesium support	25	-	20 - 32	-1	-16.67
Calcium Calcium CALCIUM Calcium is the largest most nonpolar, alkaline and most abundant of all minerals with 99% of all calcium found in the bones and teeth. Calcium exists in the ionized state 55 percent of the time and 45 percent of the time in the non-diffusible state, bound to either albumin, prealbumin or thyroglobulin. Therefore, if there is a decrease in serum albumin then there will be a decrease in serum calcium. Calcium has many functions: ¬ Provides the mobilizing factor in trauma, infections and stress for tissue repair, along with vitamins A, C, manganese, phosphorus, and fatty acids. ¬ Causes vasoconstriction, while potassium, sodium, magnesium, hydrogen ions, and carbon dioxide cause vasodilatation. ¬ Is necessary for bone formation along with phosphorus, collagen, hydroxyapatite (gives bone its hardness) and bone salts of magnesium, sodium, potassium, carbonate, uranium, plutonium, and strontium. ¬ Calcium is used to create action potentials across smooth and striated muscles leading to contraction. ¬ Calcium is used as an intracellular communicator via calcium ion gated channels. ¬ Calcium collects and gather up lipoproteins, and move them across the intestinal membrane. Attaches to oils, fats, fatty acids and waxes. Calcium is absorbed in the upper portion of the small intestines (duodeneum), and the amount absorbed depends on the "acidity" of the intestinal content, via phosphorylation and protein content. When the ratio of calcium to magnesium (which is found in the intestinal membrane as well as cell membranes) is greater than 2-1, fat is drawn through the intestinal and cell membranes. Calcium also requires vitamin D. and HCl for optimal metabolism. The glands involved with calcium are: 1. The stomach via the release of HCL, which affects the preparation and absorption of calcium. 2. The parathyroids- via parathormone control of calcium ion concentration by controlling intestinal absorption, excretion via the kidneys and the release of calcium from the bones. 3. The liver/gallbladder- via bile emulsification of lipoproteins, preparing them for intestinal absorption. 4. The spleen- which stores and ages fats or lipoproteins. 5. The parotids- due to their ability to program foodstuffs. 6. The thyroid glands-via "calcitonin", promoting deposition of calcium in the bones, while decreasing calcium concentration in the extra-cellular fluids and the blood. 7. The anterior pituitary via its control of magnesium regulating calcium uptake, which regulates protein transport thru the cell membranes. 8. The pancreas- via its ability to oxidize fatty acids Therefore, any of the above glands or organs or combinations thereof has a great impact on calcium levels. CALCIUM IS HIGH WHEN General considerations ¬ Your patient should drink plenty of water ¬ Make sure they are not hypervitaminosis on Vitamins A or D ¬ Very high protein diets may increase calcium levels ¬ Magnesium and phosphates may also increase calcium levels ¬ Using sea salt can help to reduce calcium levels. CALCIUM IS LOW WHEN General considerations: ¬ Increase Vitamin A and D intake ¬ Increase albumin and protein intake ¬ Increase magnesium intake ¬ Increase phosphorus	9.5	-	8.5 - 10.8	-0.15	-13.04
Phosphorus Phosphorus PHOSPHORUS 85% of the total phosphorus exists as phosphates or esters in the body and is found chiefly in the skeleton and is combined with calcium. 14% of the phosphorus is found in intracellular tissues and 1 % is found in the extracellular fluid. Therefore phosphorus levels are a poor indicator of levels of phosphates in the body. Phosphorus runs inversely to calcium levels in the body at a calcium to phosphorus ratio of 10 to 4. Therefore, calcium can be a great indicator for phosphorus as well. As calcium levels increase in the serum, phosphorus levels decrease, and when calcium levels decrease phosphorus levels increase. In fact, causes of high calcium also cause low phosphorus. The controlling factor of phosphorus is parathormone (PTH), which is also the calcium-controlling factor. Phosphorus helps calcium through the cell membrane by increasing the permeability of the cell membrane via oxygen displacement. 1. Phosphorus is responsible for growth and development by way of: ✓ bonding ✓ polymer function ✓ hydration ✓ chemical transport, and ✓ buffering 2. Phosphorus is also responsible for bone formation 3. Phosphorus and metabolism of glucose Phosphorus is also required for the metabolism of glucose via phosphorylation. Phosphorylation is when a phosphate radical promoted by glucokinase in the liver, or hexokinase in other cells captures the glucose and once inside the cells keeps it there. The exception to this occurs in the liver, the kidneys, and the intestinal epithelial cells. Ingestion of carbohydrates causes phosphorus to enter RBC’s with glucose causing a reduction of serum phosphorus levels and lipids. Phosphorus also works in the stomach to stabilize sugars and activate starches by the twofold process of phosphorylation. Phosphorylation and its counterpart, dephosphorylation, turn many protein enzymes on and off, thereby altering their function and activity. By altering pepsin/HCL levels phosphorus can: a. Stabilize simple sugars-simple sugars are easily oxidized (combusted) before they reach the liver, resulting in low sugar levels. Pepsin stabilizes these simple sugars, so they can be transferred to the liver for storage. b. Activation of starches- HCl is necessary to breakdown oily carbohydrates (grains), which are difficult to oxidize (combust). Thus making them readily available for oxidation. The above two mechanisms establish an HCl-pepsin balance in the stomach for proper pH digestion. The presence of both HCl and pepsin in the stomach are critical for preparing carbohydrates, as well as proteins for further digestion in the small intestines. 4. The regulation and maintenance of the acid-base balance in the body by maintaining glandular acidity. 5. The storage and transfer of energy from one part of the body to the other. 6. Used in the Production of phospholipids (90 % produced by the liver): lecithin, A cephalin, and sphingomyelin Phospholipids are necessary for: Proper brain function (sphingomyelins) Phospholipids are a major constituent of lipoproteins which can affect function, formation and transport of these lipoproteins causing serious cholesterol abnormalities Production of cell membranes Thromboplastin production produced from A cephalin 7. Intracellular phosphorus is used for: Energy transport formation of ATP from ADP and creatine phosphate via oxidative phosphorylation. Major constituent of plasma membranes (phospholipids) Major constituent of DNA and RNA (nucleic acids) Calcium transport and osmotic fluid pressure General nutritional considerations when phosphorus is high: 1. Patient should increase water intake 2. Reduce fat intake 3. Reduce Vitamin D intake if overdosing 4. An isotonic saline solution (sea salt) will decrease phosphorus levels 5. Also, decrease phosphorus in the diet and add calcium carbonate to your diet General considerations when phosphorous is low: 1. Vitamin D deficiency 2. Calcium deficiency 3. Magnesium deficiency 4. Patient needs a high protein diet	6.2	-	2.5 - 4.5	2.7	270
Magnesium Magnesium MAGNESIUM Serum magnesium constitutes only a small fraction of the total body stores and may not predict magnesium status correctly. From a physiologic perspective, magnesium directs protein digestion, by polarizing minerals associated with protein digestion, from the entrance of protein into the body to its final deposition in the cell. Approximately 40-60 % of the magnesium is found in the skeleton for bone formation, 20% is found in the muscle, 30% is found in the intracellular cytoplasm, with only 1 % of the magnesium found in the serum. Magnesium affects membrane permeability, nerve impulses, muscle contraction, intracellular fluid regulation, activation of enzyme systems, where magnesium acts as a metallic cofactor in over 300 enzymatic reactions. Regulates protein synthesis, carbohydrate metabolism, nucleic acid synthesis, and blood viscosity. Magnesium along with sodium, potassium and calcium regulate neuromuscular irritability and the mechanism for clotting. Less then 2% of calcium, magnesium and phosphates are found in the plasma and extracellular fluid and are controlled in narrow limits. Albumin accounts for 70% of the bound calcium. Magnesium also binds to albumin and since it has a lower specificity for the receptors it creates more free magnesium in the plasma. Magnesium and calcium are very much linked in their body functions and a deficiency in either one will have an adverse affect on the other. Especially since calcium needs magnesium to be absorbed thru the intestinal membrane as well as needing magnesium for calcium metabolism. For example, a magnesium deficiency will cause calcium to migrate out of the bone and into soft tissues such as the aorta and kidneys. 95% of all magnesium that is filtered thru the glomerulus is reabsorbed by the tubules where parathormone enhances tubular reabsorption of magnesium. When there is a deficiency of magnesium you will see a decrease in urine stores before serum stores. Please note that even when magnesium is in a 20% depleted state, magnesium levels in the serum will appear normal. Calcium, magnesium and phosphates continuously enter the plasma via the kidney, the intestinal brush borders, and the ruffled border from the bones. Steady states of calcium, magnesium, and phosphorus approximate urine loss against intestinal absorption and skeletal mineral apposition against mineral absorption. Magnesium in the cells is complexed to phosphates, citrates and anions such as ATP, AMP and ADP (such as MgATP2-) Magnesium also plays a key role in the hormonal regulation of insulin, estrogen and thyroid hormones. Magnesium also stimulates secretions from the parathyroids and adrenal cortex (corticosteroids). Magnesium is also affected just the way calcium is to parathormone (enhances distal tubular reabsorption of magnesium) and to a lesser degree calcitonin. In fact, calcium, magnesium, and phosphates are depressed in vitamin D deficiencies and increased with vitamin D excess. Magnesium is used in the treatment of elevated cholesterol and triglycerides, muscular contraction, hypertension (A causal relation between decreased Mg2+ content of cardiac muscle/coronary arteries and nonocclusive sudden-death ischemic heart disease has been proposed) and premenstrual syndrome. Magnesium is indicated in collagen and connective tissue diseases, inflammatory disorders, migraines, general endocrine function and neurological and psychosomatic disorders.	1.7	-	1.6 - 2.6	-0.4	-80
Total Protein Total Protein TOTAL PROTEIN Total proteins are divided into two fractions: albumin, and globulin (alpha, beta, and gamma). Please note that total protein also includes fibrinogen. Therefore total protein is made up of albumin, globulin and fibrinogen, all produced in the liver. These are the plasma proteins necessary to produce enzymes, antibodies, clotting factors, kinin precursors, and transport substances for hormones, vitamins, minerals, fats, etc. For example, plasma proteins combine with cholesterol forming lipoproteins such as VLDL, LDL’s, HDL’s etc. The lipoproteins then combine with minerals via enzyme metabolism to form and renew sex hormones such as testosterone, estrogen, progesterone etc. Other deaminated proteins produced in the liver, combusts at the mitochondrial level to form cell structures. These are your tissue building proteins known as nucleoproteins, DNA and RNA (your proteins of mitosis and meiosis). Since there are many glands involved in protein digestion, it is very difficult to make a determination from total protein alone. Glands and organs involved with protein control are as follows: The anterior pituitary, which controls all glands of protein digestion, such as the adrenals, thyroid, pancreatic head, sex organs, and spleen That parotid glands which tag lipoproteins with copper The parathyroids via the calcium/magnesium mobilization of lipoproteins The thyroid which denitrifies protein in the liver The pancreas by trypsin and chymotrypsin which, prepares the protein for assimilation into the bloodstream The sex organs that prepare protein for final deposition into the cells * Any combination of the above TOTAL PROTEIN IS LOW WHEN General considerations: o Increase protein intake o Increase B acid vitamins	7.5	-	6 - 8.5	0.25	20
Albumin Albumin ALBUMIN In pathological levels albumin is used to evaluate: 1. Liver and renal disease 2. Blood osmotic pressure 3. Chronic disease states, which most patients have 4. Dehydration 5. Albumin decreases in acute inflammatory infectious processes From a physiological standpoint, albumin is produced in the liver and is a primary byproduct of sterols and waxes. Its function is used to build and repair tissue. Albumin is responsible for 80 percent of the colloidal osmotic pressure between body tissues and blood cells. 75% of this control occurs inside the cells since most of the protein is intracellular. When you have a decrease in albumin, the osmotic pressure becomes disturbed resulting in fluid transfer and edema. Since albumin influences water movement, it will also influence nutrient and mineral movement. Albumin creates the permeability of the membrane to the osmolarity of the membrane. Therefore, substances can pass from a lesser concentration to a greater concentration. The flow is from the arterial capillaries to extracellular fluid, then from the extracellular fluid to the intracellular fluid, then from the intracellular fluid to the mitochondria. Then back via the same pathway in reverse via osmotic absorption into the veins. Albumin is also a part of a complex buffer system, which accounts for 75% of things that need to be buffered to maintain acid-alkaline balance in the body. The most powerful buffer system out of the four including, the bicarbonate system (HCO3-), the phosphate buffer system, and the liver (nitrogen/urea), the proteins of the cells and plasma, rein supreme. The protein buffer system works by controlling blood Hydrogen (H+) ion homeostasis. Both intracellular and extracellular proteins have negative charges and can serve as buffers for alterations in hydrogen ion concentration. However, because most proteins are inside cells, this primarily is an intracellular buffer system. Hemoglobin (Hb) a globular protein is an excellent intracellular buffer because of it's ability to bind with Hydrogen ions forming a weak acid and carbon dioxide (CO2) bond. After oxygen is released in the peripheral tissues, hemoglobin binds with CO2 and H+ ions. As the blood reaches the lungs these actions reverse themselves. Hemoglobin binds with oxygen, releasing the CO2 and H+ ions. The H+ ions then combine with bicarbonate (HCO3) ions to form carbonic acid (H2CO3). The H2CO3 breaks down to form water (H2O) and carbon dioxide (CO2), which are excreted via expiration through the lungs. Increases in albumin cause arteries to sclerose and a decrease in albumin causes veins to sclerose. Albumin is also a transporter of minerals and accounts for 70% of the bound calcium. Magnesium also binds to albumin and since it has a lower specificity for the receptors it creates more free magnesium in the plasma. Calcium, magnesium, and phosphates continuously enter the plasma via the kidneys, the intestinal brush borders and the ruffled border of the bone. Albumin is also responsible for transporting copper, zinc, and nickel. By controlling the transport of these minerals, albumin is the carrier of choice. The following glands are associated with albumin: 1. The parotids 2. The head of the pancreas 3. The endo-reticular portion of the liver 4. Kidneys Therefore, the function or malfunction of anyone of those glands/organs or combinations thereof can lead to imbalances in albumin levels.	4.2	-	3.5 - 5.5	-0.3	-30
Globulin Total Globulin Total GLOBULIN Organs that are responsible for globulin production are the liver, thyroid, spleen and the rest the immune system. There are four types of globulins alpha 1,2, beta and Gamma. There a few groups of gamma globulins with one group being the immunoglobulins (IgA, IgG. IgM), which produce our antibodies. The thymus produces α and β globulins know as thymoglobulin using Vitamin T and copper for its production. The thyroid produces thyroglobulins that form thyroxin and triiodothyronine via vitamin K and iodine. The spleen produces spleenoglobulins that require vitamin E and iron for its production. Globulin also acts as a polarized colloidal substance necessary for specific glandular hormonal function by acting as a transport mechanism for many hormones such as sex hormone binding globulin. Globulin also assists in: Toxin neutralization by binding soluble antigens in the blood and intracellular spaces Red blood cell production Antibody formation Protection of the gastrointestinal mucosa And is also necessary via the intrinsic factor for digestion and absorption. Globular proteins can be affected via: Nutrition- lack of protein Liver Thyroid Spleen Thymus	3.3	-	2.2 - 4.1	0.15	15.79
A/G Ratio A/G Ratio A/G RATIO The A/G ratio is the ratio of albumin to globulin, and along with fibrinogen (produced by the liver) literally measures the thickness or “collagen factor” of the blood. The A/G ratio then is also a representation of the fibrinogen content in the blood and regulates the amount of protein being utilized at any time in the body. The liver forms prothrombin, which requires vitamin K. for its production. Prothrombin is a plasma protein, which is changed into thrombin via prothrombin activator and calcium. Thrombin, transposes fibrinogen into fibrin, continually causing clotting throughout the body along with blood platelets. Fibrinogen, therefore, provides the clotting thickness (collagen factor) in the blood. These polarized protein fibrous strands are necessary to maintain blood viscosity, which regulates the amount of capillary exchange from the artery to the extracellular fluid. Collagen a protein strand (albuminoid) and proteoglycan filaments also regulate exchange by causing a very slow diffusion of molecules via kinetic motion moving substances through the extracellular fluid either to the cell membrane or back into the circulatory or lymphatic systems. Collagen is also the main structural protein in connective tissue and found in the extracellular spaces. Collagen and proteoglycan filaments are used in the interstitium to provide tensile strength and for healing. As the main component of connective tissue, it makes up from 25% to 35% of the whole-body protein content. Collagen is formed in the sternum and iliac crest. A/G RATIO IS INCREASED WHEN Anything that would decrease globulin would increase the A/G ratio and anything that would increase albumin would also increase the A/G ratio so also look at all the possibilities under low globulin or high albumin THE A/G RATIO IS DECREASED WHEN Anything that would increase globulin would decrease the A/G ratio and anything that would decrease albumin would decrease the A/G ratio so also look at all the possibilities under high globulin or low albumin	10.5	-	0.9 - 2	9.05	1645.45
Bilirubin, Total Bilirubin, Total TOTAL BILIRUBIN Bilirubin comes from the breakdown of hemoglobin and is the byproduct of hemolysis. Bilirubin is produced by the RE portion of the liver and is excreted with the bile. Pathologically elevations in total bilirubin occur when there is a massive amount of destruction of RBC’s, or the liver is congested and unable to excrete bilirubin. From a physiologic perspective, the components of bile are inositol, choline, lecithin, cholesterol, and bilirubin/biliverdin. Cholesterol, which is produced by the liver, is converted into bile salts via the influence of the adrenal glands. The bile salts are converted into cholic acid or chenodeoxycholic acid equally. Approximately 60 percent of all cholesterol is converted into these two acids. These acids then combine with glycine and taurine to form glyco and tauro conjugated bile acids. The salts of these acids are secreted in the bile. These salts do two things: 1. They act like "soap" creating saponification and emulsification of fat. This decreases the surface tension of the fat allowing agitation to break the fat up into smaller sizes. 2. Bile salts help absorb fatty acids, monoglycerides, cholesterol, and other lipids, by forming minute complexes called micelles. Micelles are highly soluble, highly charged, and easily absorbed, increasing absorption by 40 percent. The liver secretes about 600-1,200 milliliters of bile per day. The purpose of bile is to: 1. Digest, emulsify and absorb fats. 2. To excrete waste products, such as excessive cholesterol, and bilirubin, which is the end product of hemoglobin degradation. Bilirubin is the predominant pigment of bile, and is formed from hemoglobin, and destroyed red blood cells. The red blood cells are destroyed by the reticulo-endothelial system (liver and spleen), including the kupfer cells of the liver. If the spleen/liver are hyperactive, the bile production is increased. This allows the passive function of bile production to elevate. As the spleen, liver, and bone marrow destroy hemoglobin it passes into the bloodstream with a protein creating a colloidal state. This creates hemolytic jaundice when there is excessive destruction or impaired production of red blood cells, leading to excessive amounts of prehepatic bilirubin. The liver cells are unable to withdraw the bilirubin from the blood as fast as it is formed. Therefore consequently there is an increase in prehepatic bilirubin (indirect form). Remember total bilirubin = the direct and indirect forms. The direct is elevated in biliary obstruction, which is conjugated and reacted on by the liver. The indirect form is elevated in liver failure, which is unconjugated and not reacted on by the liver. Since the liver, spleen, adrenals and diet play a role in total bilirubin production from a physiologic perspective we must evaluate those glands as well.	0.4	-	0.3 - 1.2	-0.35	-77.78
Alkaline Phosphatase Alkaline Phosphatase ALKALINE PHOSPHATASE Bone osteoblasts, liver cells, and the placenta all produce high levels of alkaline phosphatase, with some activity in the kidneys and intestines. Alkaline phosphatase is called alkaline because it aids in maintaining and works best in an alkaline pH of 9-10. From a pathological perspective, alkaline phosphatase levels rise in liver disease due to impaired excretion of this enzyme from obstruction in the biliary tract, and bone disease via increased osteoclastic activity due to bone breakdown as in cancer. From a physiological perspective alkaline phosphatase is responsible for the balancing of water, and mineral metabolism controlled by the glands below. This exchange of water and mineral metabolism occurs at the cell membranes of ligaments, tendons and disc structures. The balance is created by, setting the minerals involved with electrolyte balance into motion. These minerals, along with proper neurological control, cause the shifting of food thru the membranes. The glands responsible for this balance are as follows: • The adrenal cortex via mineralocorticoids causes excretion of sodium and potassium by the kidney. • The adrenal medulla via epinephrine and norepinephrine increase metabolism, and cellular exchange via the chloride shift at the level of the membrane. • The posterior pituitary via antidiuretic hormone and its effect on potassium (oxidizer) and the water content within the cell. • Prostate/uterus via selenium acts as an oxidative mineral to insure proper membrane exchange in conjunction with the above. Alkaline phosphatase is a member of a family of zinc metalloprotein enzymes whose purpose is to split off a terminal phosphate group from an organic phosphate ester. Enzyme activity is localized in the brush border of the proximal convoluted tubules of the kidney, intestinal mucosal epithelial cells, hepatic sinusoidal membranes, vascular endothelial cells and osteoblasts of bone as mentioned above. It is the introduction of an alkaline media for bone growth. When there is an increased alkaline phosphatase you have too much acidity. In “bone pathology” there is usually a hyper-acidic state, since the foundation of a cell, is nucleic acid. The nucleic acid is composed of phosphoric acid. Phosphoric acid is a component of alkaline phosphatase, therefore, the adrenals regulate the acid/alkaline balance for energy, and growth. Alkaline phosphatase controls the alkaline substance, which controls energy, and the acid substance, which controls growth. Over the years, the laboratory low range has been steadily decreasing from 60, down to 40 now down to the mid 20's. Since this test does measure metabolic output of the adrenals, going to low is not the answer. I recommend that the low range is 70.	86	-	70 - 165	-31.5	-66.32
LDH LDH LACTIC ACID DEHYDROGENASE Lactic acid dehydrogenase is found chiefly in the heart, skeletal muscles, kidneys, and liver, as well as all cells. In pathological states, elevated levels indicate damage to the above areas and is used to determine myocardial and pulmonary infarction. In physiological states, LDH catalyzes the conversion of pyruvate ( the final step in glycolysis) to lactate and back, as it converts NADH to NAD+ and back. A dehydrogenase is an enzyme that transfers a hydride from one molecule to another. When sugar and water (fatty acid metabolism) are exchanged across a muscle cell interface, a by-product called lactic acid is produced. When lactic acid combines with the carbon dioxide of the venous blood you have a hydrogen displacement. Lactic acid now becomes lactic acid dehydrogenase. Lactic acid dehydrogenase, therefore, is a glycolytic enzyme that functions as a catalyst in carbohydrate metabolism to produce energy. The pancreas via insulin and the posterior pituitary via ADH are responsible for this sugar and water exchange across the muscle cell interface. Lactic acid dehydrogenase indicates the active exchange of sugar across the membrane (muscle cell interface) utilizing chloride, zinc, and selenium. The utilization of these minerals creates glycolysis. LDH then from a physiological perspective determines pancreatic function regulating the amount of glucose into muscle. It is also important to note that sugar metabolism is very complex and does involve a series of other organs. Ranges for LDH are between 0-220; again it is rather obvious that LDH is a by-product of sugar metabolism and a 0 figure could not be construed as a low normal range. I feel that the range should start at 80. You will find many patients with a low LDH having problems with decreased function causing heart, skeletal muscle (weakness, loss of strength, muscle wasting), kidney and liver dysfunction, and eventual wasting away of these organs.	194	-	80 - 220	44	62.86
AST (SGOT) AST (SGOT) SERUM GLUTAMIC OXALACETIC TRANSAMINASE (SGOT) (AST) SGOT is highly concentrated in organs and glands of high metabolic activity and in descending order: heart, liver, skeletal muscle, brain, kidneys, pancreas, spleen and lungs. In pathological states, when you have high levels it means that cell damage has occurred in one or more of these areas and there is a release of this enzyme in circulation, elevating in 12 hours and remaining there for 5 days. In physiologic states, we know it is a tissue enzyme present in tissues of high metabolic activity, and concerned with the transfer of nitrogen between aspartic acid, and alpha-keto-glutamic acid, resulting in the synthesis of glutamic acid, alpha keto acid and oxalacetic acid. SGOT, therefore, is the catalyst that creates amino acid metabolism during glycolysis, for the production of energy. Since there are high concentrations of SGOT in skeletal muscle/heart, and the brain, it gives you an idea of the metabolic output of each system. The sex organs via the output of testosterone, estrogen, progesterone (which are formed on the gonadal epithelium by binding cholesterol to protein) are used to maintain muscle mass and strength. Therefore having a dramatic effect on muscle and nerve metabolism. Since amino acid metabolism also affects muscle mass, muscle strength, and the energy to fuel the muscular system, it is apparent that SGOT is the indicator of choice. Not to mention the energy necessary to run the central nervous system which utilizes 60 percent of the available energy necessary to run your body. Please note that most lab ranges start at 0 and since this is a measurement of the metabolic activity of the above organs 0 would mean death. The low range for SGOT should be 15. You will find physiological conditions where there are low levels of SGOT (15-20). This is due to the exhaustion of the above organs. Low levels indicated heart, skeletal muscle and diminished brain function/damage. These patients are usually physically weak/exhausted whether they exercise or not, lack mental clarity, cannot think straight and have brain fatigue/fog. They also have sex hormonal problems and require HRT or erectile dysfunction treatment. Many of these patients have a weak flabby heart, setting the stage for many types of conditions down the road. Low levels may also mean decreased liver function affecting, protein synthesis, detoxification, sluggish metabolism, cholesterol production to name a few of the 500 know liver functions.	37	-	15 - 50	4.5	25.71
ALT (SGPT) ALT (SGPT) SERUM GLUTAMIC PYRUVIC TRANSAMINASE (SGPT) (ALT) SGPT is primarily a liver function test. It has a maximum concentration in the liver (fatty membranes) sinusoids. Low concentrations of SGPT are also found in the kidneys, heart, and skeletal muscle. In pathological states, elevations indicate liver disease. ALT is found in serum and in various bodily tissues but is most commonly associated with the liver. It catalyzes the transfer of an amino group from alanine to alpha-ketoglutarate, and the products of this reversible transamination reaction being pyruvate and glutamate. glutamate + pyruvate ⇌ alpha-ketoglutarate + alanine Alanine transaminase delivers skeletal muscle carbon and nitrogen in the form of alanine to the liver. In skeletal muscle, pyruvate is transaminated to alanine, thus affording an additional route of nitrogen transport from muscle to liver. In the liver, alanine transaminase transfers the ammonia to A-KG and regenerates pyruvate. The pyruvate can then be diverted into gluconeogenesis. This process is referred to as the glucose-alanine cycle. The glucose-alanine cycle is used primarily as a mechanism for skeletal muscle to eliminate nitrogen as the muscles replenish their energy supply. Within the liver, alanine is converted back to pyruvate and is then a source of carbon atoms for gluconeogenesis. The newly formed glucose can then enter the bloodstream for delivery back to the muscle. The amino group transported from the muscle to the liver, in the form of alanine, is converted to urea in the urea cycle and then excreted. In physiological states SGPT is a primary kreb cycle expressant and as a result causes the release of catabolic fats. SGPT occurs in serum as a consequence of substances being released by the fatty membranes of the liver sinusoids, and lymphatic ducts. The liver sinusoids store food, and the lymphatic ducts house toxins. Picture a layer of fat that holds foods or toxins in the cell. Now as that layer of fat is being burned off, foods and toxins are being released in a controlled manner. This allows foods or toxins to be directed to their next destination. Please note that most lab ranges for this test start at 0, which in actuality is false since this is a measurement of liver function, and 0 would mean that the liver was not functioning at all. A low range then should be around 15. Therefore, from a physiological perspective, a low SGPT between 15-20 would indicate a sluggish liver causing many metabolic disturbances. Typically these people have no energy, get sick a lot, cannot tolerate food well and have a slow metabolism.	38	-	15 - 50	5.5	31.43
GGT GGT GAMMA GLUTAMYL TRANSPEPTIDASE (GGT) Is a biliary enzyme useful in the diagnosis of obstructive jaundice, intrahepatic cholestasis and pancreatitis. GGT is more responsive to biliary obstruction than are aspartate aminotransferase (AST) (SGOT) and alanine aminotransferase (ALT) (SGPT). 1. GGT is increased in hepatoma and carcinoma of the pancreas and useful in the diagnosis of metastatic carcinoma of the liver. Increasing levels in carcinoma patients relate to tumor progression and a dubious outcome. 1. CEA, alkaline phosphatase and GGT together are useful markers for hepatic metastasis from the breast and colon. 2. May be useful in the diagnosis of chronic alcoholic liver disease. Follow-up blood chemistries of serum GGT, AST and ALT levels can distinguish recovering alcoholics who resume drinking from those who do not. 3. Increase in body mass correlates with increased GGT levels. 4. GGT along with MCV is a useful test for alcoholism. 5. GGT is the test of choice for pregnant females who may have cholestasis. 6. GGT levels are elevated in cirrhosis and hepatitis. 7. The transaminases, AST and ALT rise higher in acute viral hepatitis; then GGT. 8. Increased in systemic lupus erythematosus GGT IS HIGH WHEN General considerations: If patient has been on a very low-fat diet for long periods of time then increase fat intake	35	-	20 - 70	-10	-40
Ferritin Ferritin A ferritin test can help a doctor determine if a person has enough iron in their body. Low ferritin levels can indicate that the body doesn't have enough iron, while high levels can indicate too much iron. FERRITIN Men 20-250 ng/mL 20-250 ug/L Women 10-120 ng/mL 10-120 ug/L Children 7-140 ng/mL 7-140 ug/L Newborns 25-200 ng/mL 25-200 ug/L	117.4	-	7.3 - 270.7	-21.6	-16.4
Total Iron Total Iron Total Iron Binding Capacity (TBIC)—measures the amount of transferrin, which is a blood protein that transports iron from the digestive system to cells that will be utilizing the iron. Your body produces transferrin in relationship to the body’s need for iron. When iron stores are low, transferrin levels will increase and when transferrin levels are low, too much iron is present. Usually, about one third of the transferrin is being used to transport iron at any one time. Because of this, your blood serum has considerable extra iron-binding capacity, which is called the Unsaturated Iron Biding Capacity (UIBC). The TIBC then equals UIBC plus serum iron measurement. Some laboratories may measure UIBC, some measure TIBC and others measure transferrin. TIBC is increased in iron- deficiency, acute hepatitis, during pregnancy or when oral contraceptives are used. TIBC is decreased in hypoproteinemia from many causes, cirrhosis of the liver, nephrosis and thalassemia or from a number of inflammatory states. TOTAL IRON IRON Men 65-175ug/dL 11.6-31.3 umol/L Women 50-170ug/dL 9.0 -30.4 umol/L Children 50-120ug/dL 9.0-21.5 umol/L Newborns 100-250 ug/dL 17.9-44.8 umol/L	77	-	35 - 175	-28	-40
Cholesterol, Total Cholesterol, Total SERUM LIPIDS Serum lipids serve as a primary source of energy along with glucose. The functions are many, such as the production of cell membranes, precursors to hormones, and bile acids. Lipids are first broken down in the duodenum, along with bile, which emulsifies the fats, and prepares them for absorption into the lymphatic system. Pancreatic lipase hydrolyzes cholesterol, and triglycerides into fatty acids, and glycerol. The fatty acids and glycerol are then reconverted back into triglycerides by the intestinal cells and then discharged into the lymphatic or portal blood system, which is then sent to the liver. Cholesterol is also absorbed in both the free and esterified forms into the lymphatics. Cholesterol is also synthesized in the reticular cells and histiocytes throughout the body but mainly formed in the liver. Under the influence of iodine via the thyroid, carbohydrates, amino acids, and other fats are converted to cholesterol via multiple molecules of acetyl coenzyme A creating a sterol nucleus. Triglycerides are also assembled in the liver from glycerol and fatty acids. The liver is the main organ regulating blood lipids. So the liver can degrade fatty acids for energy, synthesize triglycerides from carbohydrates and proteins. The liver can then hydrolyzes the triglycerides back into three fatty acids, and glycerol then degrades the fatty acids into acetyl coenzyme A via beta-oxidation. Then acetyl coenzyme A is then oxidized to release ATP. The liver also synthesizes phospholipids, lecithin, cephalins (that produce thromboplastin), and sphingomyelin (produces the myelin sheath) are formed in the liver and transported via lipoproteins. An increase in triglycerides or choline/inositol increases phospholipid production. Phospholipids are also important in the production of cell membranes. CHOLESTEROL Cholesterol is a byproduct of protein metabolism. Bonding oily fat (fat-soluble vitamins) to nitrogen via oxidation forms cholesterol. This process utilizes vitamins, D, E, K, A, and T. These are your fat-soluble vitamins that are bound to the nitrogen portion of foods. The basic purpose of fat-soluble vitamins is to lubricate membranes. The vitamin (oil) prevents oxygen from reaching the membrane, which may inhibit its function. Fat-soluble vitamins also provide the substance necessary to make hormones, enzymes, and antibodies. For example, Vitamin D. lubricates all gross membranes that are exposed to air, such as your skin, respiratory passages, and the digestive membranes. This is your antioxidant lubricator Vitamin A. lubricates secondary membranes that are exposed to the blood, such as the liver, kidney, lungs and spleen. Vitamin A. is called your hydrogen lubricator. Vitamin K. lubricates cell membranes that are exposed to water. Vitamin F. fatty acids are used to make enzymes. Vitamin E. is used to make hormones. Vitamin T. which, is sesame seed oil, is used to make antibodies Lecithin prevents oil and fat from going rancid. So the purpose of fat-soluble vitamins is to oxidize and combust with protein to form cholesterol, which then transposes it into a lubricator, a hormone, antibody, or enzyme. Low-density lipoproteins are rich in cholesterol and carry some triglycerides and are used to produce sex hormones. High-density lipoproteins are rich in triglycerides and carry some fat. Please note that at any one time, the body can dictate the percentage of low-density lipoproteins vs. high-density lipoproteins. It's obvious that an imbalance can create multiple diseases in the body. Please note that these lipoproteins also engulf toxins and then are stored in tissue cells. At a later time, the body gradually detoxifies these deposits unless the amount is overwhelming. Similar to glucose, cholesterol is affected by many organs and glands and in itself is not a reliable indicator as to what is going on in the body. Over the years, the labs went from a normal cholesterol reading of 300, down to 250, then down to 200, and now down to 150. If they continue this nonsense they will create a whole new list of diseases. I recommend that your cholesterol levels be between 175-275mg/dL.	129	-	175 - 275	-96	-192
Triglycerides Triglycerides SERUM LIPIDS Serum lipids serve as a primary source of energy along with glucose. The functions are many, such as the production of cell membranes, precursors to hormones, and bile acids. Lipids are first broken down in the duodenum, along with bile, which emulsifies the fats, and prepares them for absorption into the lymphatic system. Pancreatic lipase hydrolyzes cholesterol, and triglycerides into fatty acids, and glycerol. The fatty acids and glycerol are then reconverted back into triglycerides by the intestinal cells and then discharged into the lymphatic or portal blood system, which is then sent to the liver. Cholesterol is also absorbed in both the free and esterified forms into the lymphatics. Cholesterol is also synthesized in the reticular cells and histiocytes throughout the body but mainly formed in the liver. Under the influence of iodine via the thyroid, carbohydrates, amino acids, and other fats are converted to cholesterol via multiple molecules of acetyl coenzyme A creating a sterol nucleus. Triglycerides are also assembled in the liver from glycerol and fatty acids. The liver is the main organ regulating blood lipids. So the liver can degrade fatty acids for energy, synthesize triglycerides from carbohydrates and proteins. The liver can then hydrolyzes the triglycerides back into three fatty acids, and glycerol then degrades the fatty acids into acetyl coenzyme A via beta-oxidation. Then acetyl coenzyme A is then oxidized to release ATP. The liver also synthesizes phospholipids, lecithin, cephalins (that produce thromboplastin), and sphingomyelin (produces the myelin sheath) are formed in the liver and transported via lipoproteins. An increase in triglycerides or choline/inositol increases phospholipid production. Phospholipids are also important in the production of cell membranes. TRIGLYCERIDES Triglycerides compromise 95% of fat stored in adipose tissue and stored as glycerol, fatty acids, and monoglycerides. The liver reconvert's these back to triglycerides. 80% of your triglycerides make up VLDL, and 15% form LDL’S. From a pathological viewpoint, this test evaluates atherosclerosis and measures the bodies ability to utilize fat. From the physiologic perspective, triglycerides are nothing more than three fatty acids, and esters of glycerol. Fatty acids are composed of sugar and alcohol. Triglycerides travel with cholesterol (LDL/HDL) to combust cholesterol at the appropriate time.Triglycerides are needed for calculation of LDLC (low-density lipoprotein cholesterol) concentration. Triglycerides are the matches or “the spark” that ignites and combusts the cholesterol. Triglycerides are implanted in the cell membrane of all neurological and glandular tissue. Triglycerides create the energy for a neurological impulse to occur. When the neurological impulse occurs triglycerides actually “explode” causing the active exchange of electrolytes. Primary glands involved in triglyceride metabolism are the posterior pituitary, the hypophyseal stalk, adrenals, and the head of the pancreas.Therefore, any condition affecting these organs can affect triglyceride levels. High levels are a greater risk for a heart attack then a high cholesterol. Low triglyceride levels from the physiologic perspective cause low energy. Triglycerides Normally Range From 0-199. It Is Rather Obvious That 0 Triglycerides Could Not Be Achieved Physiologically. My Ranges Are From 75-200 mg/dL	179	-	75 - 200	41.5	66.4
TSH TSH T-4, T-3, T3 uptake and TSH Thyroid-stimulating hormone (TSH) from the anterior pituitary, stimulates the production of thyroxin, and triiodothyronine, therefore, having a dramatic effect on the T4/T3 test results. Thyrotrophs makeup 5% of the anterior pituitary and produce between 100-400mU/day of TSH. Circadian peaks with the onset of sleep are between 9 pm-5am and a minimum between 4-7pm. TSH is regulated by an open feedback loop via thyroxin whereby thyroxin passes into the CSF of the lateral ventricles and is taken up by the epithelial cells of the choroid plexus, which when thyroxin levels are low, stimulates TRH-secreting neurons in the hypothalamus. TSH does the following: 1. Stimulates phospholipid metabolism 2. Stimulates purine and pyrimidine precursors and their incorporation into nucleic acids. T-4 and 3 indicate the denitrification power of iodine via thyroxin with T3 being much more powerful than T4. All food contains active biological nutrients that are bound with nitrogen. When this food reaches the liver, the iodine is used to cleave the nitrogen from the nutrient. Therefore, thyroxin and T3 are important in fat and protein digestion, absorption, and growth and endocrine function. This catabolic activity begins once aerobic bound substances become totally anaerobic and lose the need for nitrogen bonding. Nitrogen is cleaved by T3 or T4 in the liver for example as in glycogen storage. Other substances are needed by specific cells and are transported via total binding globulin to the cells where at that point, the nitrogen bonds are cleaved. Less than 1% of T3 is unbound. A high T-3 uptake indicates a hypothyroid, where a low T-3 uptake indicates a hyperthyroid.	0.026	-	0.5 - 5.5	-2.974	-118.96
Thyroxine (T4) Thyroxine (T4) T-4, T-3, T3 uptake and TSH Thyroid-stimulating hormone (TSH) from the anterior pituitary, stimulates the production of thyroxin, and triiodothyronine, therefore, having a dramatic effect on the T4/T3 test results. Thyrotrophs makeup 5% of the anterior pituitary and produce between 100-400mU/day of TSH. Circadian peaks with the onset of sleep are between 9 pm-5am and a minimum between 4-7pm. TSH is regulated by an open feedback loop via thyroxin whereby thyroxin passes into the CSF of the lateral ventricles and is taken up by the epithelial cells of the choroid plexus, which when thyroxin levels are low, stimulates TRH-secreting neurons in the hypothalamus. TSH does the following: 1. Stimulates phospholipid metabolism 2. Stimulates purine and pyrimidine precursors and their incorporation into nucleic acids. T-4 and 3 indicate the denitrification power of iodine via thyroxin with T3 being much more powerful than T4. All food contains active biological nutrients that are bound with nitrogen. When this food reaches the liver, the iodine is used to cleave the nitrogen from the nutrient. Therefore, thyroxin and T3 are important in fat and protein digestion, absorption, and growth and endocrine function. This catabolic activity begins once aerobic bound substances become totally anaerobic and lose the need for nitrogen bonding. Nitrogen is cleaved by T3 or T4 in the liver for example as in glycogen storage. Other substances are needed by specific cells and are transported via total binding globulin to the cells where at that point, the nitrogen bonds are cleaved. Less than 1% of T3 is unbound. A high T-3 uptake indicates a hypothyroid, where a low T-3 uptake indicates a hyperthyroid.	11.4	-	4.5 - 12	3.15	84
T3 Total T3 Total T-4, T-3, T3 uptake and TSH Thyroid-stimulating hormone (TSH) from the anterior pituitary, stimulates the production of thyroxin, and triiodothyronine, therefore, having a dramatic effect on the T4/T3 test results. Thyrotrophs makeup 5% of the anterior pituitary and produce between 100-400mU/day of TSH. Circadian peaks with the onset of sleep are between 9 pm-5am and a minimum between 4-7pm. TSH is regulated by an open feedback loop via thyroxin whereby thyroxin passes into the CSF of the lateral ventricles and is taken up by the epithelial cells of the choroid plexus, which when thyroxin levels are low, stimulates TRH-secreting neurons in the hypothalamus. TSH does the following: 1. Stimulates phospholipid metabolism 2. Stimulates purine and pyrimidine precursors and their incorporation into nucleic acids. T-4 and 3 indicate the denitrification power of iodine via thyroxin with T3 being much more powerful than T4. All food contains active biological nutrients that are bound with nitrogen. When this food reaches the liver, the iodine is used to cleave the nitrogen from the nutrient. Therefore, thyroxin and T3 are important in fat and protein digestion, absorption, and growth and endocrine function. This catabolic activity begins once aerobic bound substances become totally anaerobic and lose the need for nitrogen bonding. Nitrogen is cleaved by T3 or T4 in the liver for example as in glycogen storage. Other substances are needed by specific cells and are transported via total binding globulin to the cells where at that point, the nitrogen bonds are cleaved. Less than 1% of T3 is unbound. A high T-3 uptake indicates a hypothyroid, where a low T-3 uptake indicates a hyperthyroid.	114	-	80 - 200	-26	-43.33
T3 Free T3 Free A free T3 test, or free triiodothyronine test, measures the amount of free triiodothyronine in your blood. Triiodothyronine (T3) is a hormone produced by the thyroid gland that helps regulate metabolism and energy levels. A normal free T3 level is typically between 2.5–4.0 ng/dL, but reference values may vary by lab. A higher-than-normal level of T3 may indicate an overactive thyroid, while a lower-than-normal level may indicate an underactive thyroid.	3.3	-	2.3 - 4.2	0.05	5.26
T4 Free T4 Free Free T4 is the amount of thyroxine (T4) in the blood that is not attached to proteins. T4 is a hormone produced by the thyroid gland that helps control metabolism and growth. A free T4 test measures the amount of free T4 in your blood.	1.7	-	0.89 - 1.76	0.375	86.21
Urine pH Urine pH URINE PH A high urine pH may be due to: Kidney failure Urinary tract infections Vomiting A low urine pH may be due to: Diarrhea Too much acid in the body fluids such as metabolic acidosis and diabetic ketoacidosis Starvation	5	-	5 - 8	-1.5	-100
Bun/Creatin Ratio Bun/Creatin Ratio BUN/CREATININE RATIO BUN plus creatinine are residue byproducts of protein and muscle metabolism respectively. They are kept in continual balance by the water content of your body. The kidneys flush out the excessive BUN/creatinine concentration when it gets too high. The kidneys are under the influence of the posterior pituitary via antidiuretic hormone, which regulates the amount of water leaving the body. Therefore, the posterior pituitary through potassium regulates water balance. The posterior pituitary then regulates the amount of water in any one place of the body. So, therefore, it can either increase or decrease the water content in the blood, thus altering pH. The posterior pituitary besides balancing water also regulates sugar and mineral concentration. BUN/CREATININE IS HIGH WHEN General considerations: ¬ Decrease high protein intake ¬ Or increase water intake ¬ BUN/CREATININE is high when you have a high BUN or a low CREATININE or both BUN/CREATININE IS DECREASED WHEN General considerations: ¬ Increase protein intake ¬ Or decrease water intake ¬ BUN/CREATININE is low when either you have a low BUN or a high CREATININE or both	34.84	-	6 - 25	19.34	203.58

HORMONES

Test(s)

Current

Standard

GFR(Stage 4)

15 - 29

-6

-85.71

GFR(INSULIN)

60.8

14 - 24.9

5.45

19.45

41.35

758.72

GFR(CRP)

2.6

2.5 - 5

1.25

3.75

-1.15

-92

GFR(HOMOCYSTEINE)

39.5

5.2 - 17

5.9

11.1

28.4

481.36

GFR(VITAMIN D,25-OH, TOTAL)

78 - 40

-19

-28

147.37

CORTISOL(Cortisol (Morning 7-9 am):)

9.1

7.3 - 22.5

7.6

14.9

-5.8

-76.32

TOTAL TESTOSTERONE(Free Testosterone)

0.3

0 - 22.5

11.25

-10.95

-97.33

DHEA-SULFATE(DHEA-SULFATE)

79.3

25.9 - 460.2

217.15

243.05

-163.75

-75.41

Hemoglobin A1C

7.1

5.4 - 6.4

0.5

5.9

1.2

240

FSH(FSH (Male))

40.6

1.4 - 18.1

8.35

9.75

30.85

369.46

LH(LH (Male))

16.3

1.5 - 9.3

3.9

5.4

10.9

279.49

PROGESTERONE(PROGESTERONE (Male))

0.23

0.28 - 1.22

0.47

0.75

-0.52

-110.64

ESTRADIOL (E2)(ESTRADIOL (E2) (Male))

24.9

11.8 - 39.9

14.05

25.85

-0.95

-6.76

Cortisol (Morning 7-9 am):

9.1

6.2 - 19.4

6.6

12.8

-3.7

-56.06

DHEA-SULFATE(DHEA-SULFATE)

79.3

37 - 460.2

211.6

248.6

-169.3

-80.01

SEX HORMONE BIND GLOBULIN(SEX HORMONE BIND GLOBULIN (Male))

22 - 113

45.5

67.5

-34.5

-75.82

Total Testosterone

280 - 1100

410

690

-672

-163.9

Free Testosterone

0.3

3.9 - 22.5

9.3

13.2

-12.9

-138.71

CBC/Differentials

Test	Result	Path. Low	Path. High	R1	Low + R1	High - R1	CRC Result	CRC Result Desc
Basophils Basophils BASOPHILS Both basophils and mast cells liberate heparin into the blood, thus preventing clotting. They also release histamine, bradykinin and serotonin, which cause elevation of these cells during allergic reactions on anaerobic membranes, and decreased during toxic reactions and infections. Basophils are phagocytic in nature. Tissue basophils aka mast cells are similar to the basophils found in the blood. Basophils are also used to study chronic inflammation. ABSOLUTE COUNT 15-50/ mm3 DIFFERENTIAL 0-1% OF TOTAL WBC's	0.2	0	8	2.67	2.67	5.33	LOW	Toxic/Infection
Eosinophils (EOS) Eosinophils (EOS) EOSINOPHILS EOSINOPHILS are weak phagocytes and exhibit chemotaxis and are elevated during allergic reactions, parasitic infections on aerobic membranes and decreased during toxic reactions and infections. They are active in the later stages of inflammation and are capable of phagocytosis and ingest antigen-antibody complexes. They respond to allergic and parasitic infections and contain about 1/3 of the bodies histamine ABSOLUTE COUNT 0-700 mm3 DIFFERENTIAL makes up 0-3% of total WBC's .	1.7	0.1	7	2.3	2.4	4.7	LOW	Toxic/Infection
Hematocrit Hematocrit HEMATOCRIT (HCT) PACKED CELL VOLUME (PCV) HEMATOCRIT (Hct) is the measurement of the solid portion (cells) of the blood which is affected by the number or mass of the cells. Hct is increased in: 1. Erythrocytosis 2. Polycythemia vera 3. Shock 4. Thymus malfunction Hct is decreased in: 1. Anemias 2. Anemia, which is caused via cell destruction, blood loss or a dietary vitamin B12/iron deficiency. 3. Hodgkin's disease and other lymphomas 4. Myeloproliferative diseases such as multiple myeloma and leukemia 5. Hemorrhage 6. Lupus erythematosus 7. Adrenal insufficiency such as Addison's disease 8. Rheumatoid arthritis 9. Chronic infection 10. Endocarditis 11. Spleen insufficiency	34.9	42	56	4.67	46.67	51.33	LOW	Spleen
Hemoglobin Hemoglobin HEMOGLOBIN (Hb) HEMOGLOBIN is the chemical that transports O2 and CO2 and is formed by amino acids creating globulin, and a heme portion, which consists of iron atoms and a red pigment called porphyrin. Each gram of hemoglobin can carry 1.34 milliliters of oxygen in 100Ml's of blood. Hb also acts as a buffer in the extracellular fluid. For example, when O2 content in tissues is low and CO2 and H+ ions are high (causing a low pH), oxygen dissociates from Hb faster. The unoxygenated Hb then binds to the H+ ions thereby raising the pH. As CO2 diffuses into the RBC it is converted into bicarbonate via carbonic anhydrase. As the protons bond to the Hb the bicarbonate ions leave the cell and for ever one that leaves a chloride ion enters the RBC. The efficiency of this buffer system rely's on properly functioning lungs for the elimination of CO2 and bicarbonate ions. Increased Hb is found in: 1. Polycythemia vera 2. Congestive heart failure 3. Chronic obstructive pulmonary disease 4. Hemorrhages and burns 5. Thymus malfunctions Decreased Hb is found in: 1. Anemia 2. Iron deficiency, thalassemia, pernicious anemia, and hemoglobinopathy's 3. Liver disease and hypothyroidism 4. Hemorrhage 5. Hemolytic anemia caused by infectious agents, drugs, and transfusions 6. Systemic diseases such as Hodgkin's, leukemia, lymphoma, SLE, sarcoidosis and renal cortical necrosis 7. Spleen conditions	10.3	13.5	18	1.5	15	16.5	LOW	Spleen
Lymphs Lymphs LYMPHOCYTES LYMPHOCYTES are small mononuclear cells without specific granules: They are motile and migrate to areas of inflammation. These cells contain immunoglobulins and play a role in immunological reactions. B-lymphocytes mature in the bone marrow and T-lymphocytes mature in the thymus. B-cells maintain an antigen-antibody response to a specific antigen and have memory. T-cells are coined the “master immune cells” and consist of CD4+ helper T cells, killer cells, cytotoxic cells, and CD8+ suppressor cells. Plasma cells, which are, fully differentiated B cells are not normally found in the plasma. ABSOLUTE COUNT 1,500-4000 cells/mm3 DIFFERENTIAL 25-40% OF THE TOTAL WBC's Lymphocytes (Lymphocytosis >4,000cell/mm3) are increased in: 1. Lymphatic leukemia 2. Infectious lymphocytosis 3. Infectious mononucleosis 4. Upper respiratory viral infections 5. Cytomegalovirus 6. Measles 7. Mumps, 8. Chicken pox 9. HIV 10. Infectious hepatitis 11. Some bacterial diseases TB, pertussis 12. Crohn's disease (ulcerative colitis) 13. Hypoadrenalism 14. Thyrotoxicosis Lymphocytes (leukocytopenia <1000 cells/mm3) are decreased in: 1. Chemotherapy 2. Aplastic anemia 3. Congestive heart failure 4. ACTH or cortisone 5. Hodgkin's disease 6. HIV 7. Severe debilitating illnesses 8. Advanced TB 9. Toxic conditions 10. Allergic reactions	22.1	23	46	7.67	30.67	38.33	LOW	Infection
MCH MCH MCV MCH RED BLOOD CELL INDICES MCV- MEAN CORPUSCULAR VOLUME-refers to the size of the RBC and is classified as normal (normocytic), <82um3 (microcytic) and >100um3 (macrocytic). MCV= HCT(%) x 10 RBC (10 to the 12/L) Microcytic anemias (MCV 50-82) caused by: Disorders of iron metabolism such as iron deficiency from malabsorption, dietary inadequacy, increased iron loss or iron requirements due to chronic disease Disorders of porphyrin and heme synthesis such as sideroblastic anemias and globin synthesis (thalassemias and hemoglobinopathies). Normocytic normochromic anemias (MCV 82-98 fL) Marrow hypoplasia such as aplastic anemia Marrow infiltration by malignant cells Decreased erythropoietin production from endocrine, renal, liver disease and malnutrition. Macrocytic anemias (MCV 100-150 fL) are caused by: B12 (cobalamin) deficiency due to: A lack of animal products (vegetarians) Impaired absorption of intrinsic factor leading to pernicious anemia due to a destruction of gastric mucosa, ileitis, sprue and celiac disease. Infiltrative intestinal diseases such as lymphoma. Increased requirements such as pregnancy, hyperthyroidism, pancreatic disease and neoplasms. Enzyme deficiencies (cobalamin binding protein) Parasites Folate deficiency due to: Decreased intake due to lack of vegetables or from alcoholism Impaired absorption due to steatorrhea, sprue, celiac disease and intrinsic intestinal disease Increased requirements from pregnancy, hypothyroidism, hematopoiesis, neoplastic disease, exfoliative skin diseases. Enzyme deficiencies. MCH- MEAN CORPUSCULAR HEMOGLOBIN is the measurement of the average weight of Hb per RBC MCH = Hb(g/dL) x 10 (pg/cell RBC (10 to the 12th/L An increase in MCH is associated with infections, macrocytic anemia, and newborns A decrease is associated with toxic reactions, microcytic anemia, hyperlipidemia, high WBC counts >50,000 mm3 and high heparin can falsely elevate MCH levels. MCHC- MEAN CORPUSCULAR HEMOGLOBIN CONCENTRATION measures the average concentration of Hb in the RBC’s where the MCHC cannot be more than 37 g/dL per RBC MCHC (g/dL)=Hb (g/dl) x 100 Hct (%) An increased MCHC is found in: Newborns and infants A decrease in MCHC is found in: Iron deficiency Microcytic anemias Chronic blood loss Some thalassemias	31.3	29	34	1.67	30.67	32.33	OK	OK
MCV MCV MCV MCH RED BLOOD CELL INDICES MCV- MEAN CORPUSCULAR VOLUME-refers to the size of the RBC and is classified as normal (normocytic), <82um3 (microcytic) and >100um3 (macrocytic). MCV= HCT(%) x 10 RBC (10 to the 12/L) Microcytic anemias (MCV 50-82) caused by: Disorders of iron metabolism such as iron deficiency from malabsorption, dietary inadequacy, increased iron loss or iron requirements due to chronic disease Disorders of porphyrin and heme synthesis such as sideroblastic anemias and globin synthesis (thalassemias and hemoglobinopathies). Normocytic normochromic anemias (MCV 82-98 fL) Marrow hypoplasia such as aplastic anemia Marrow infiltration by malignant cells Decreased erythropoietin production from endocrine, renal, liver disease and malnutrition. Macrocytic anemias (MCV 100-150 fL) are caused by: B12 (cobalamin) deficiency due to: A lack of animal products (vegetarians) Impaired absorption of intrinsic factor leading to pernicious anemia due to a destruction of gastric mucosa, ileitis, sprue and celiac disease. Infiltrative intestinal diseases such as lymphoma. Increased requirements such as pregnancy, hyperthyroidism, pancreatic disease and neoplasms. Enzyme deficiencies (cobalamin binding protein) Parasites Folate deficiency due to: Decreased intake due to lack of vegetables or from alcoholism Impaired absorption due to steatorrhea, sprue, celiac disease and intrinsic intestinal disease Increased requirements from pregnancy, hypothyroidism, hematopoiesis, neoplastic disease, exfoliative skin diseases. Enzyme deficiencies. MCH- MEAN CORPUSCULAR HEMOGLOBIN is the measurement of the average weight of Hb per RBC MCH = Hb(g/dL) x 10 (pg/cell RBC (10 to the 12^th/L An increase in MCH is associated with infections, macrocytic anemia, and newborns A decrease is associated with toxic reactions, microcytic anemia, hyperlipidemia, high WBC counts >50,000 mm3 and high heparin can falsely elevate MCH levels. MCHC- MEAN CORPUSCULAR HEMOGLOBIN CONCENTRATION measures the average concentration of Hb in the RBCâs where the MCHC cannot be more than 37 g/dL per RBC MCHC (g/dL)=Hb (g/dl) x 100 Hct (%) An increased MCHC is found in: Newborns and infants A decrease in MCHC is found in: Iron deficiency Microcytic anemias Chronic blood loss Some thalassemias	106	91	102	3.67	94.67	98.33	HIGH	Infection
Monocytes Monocytes MONOCYTES MONOCYTES are agranulocytes, are the largest cells and the second line of defense against infection. Histiocytes are large macrophagic phagocytes, which are also classified as monocytes and each can be changed into the other. These cells remove injured and dead cells, microorganisms and other insoluble products from the circulating blood. Monocytes contain interferon (antiviral agent) and escape from the upper and lower respiratory, gastrointestinal and genitourinary systems performing scavenger hunts THE MONOCYTE, MACROPHAGE, AND THE RETICULAR ENDOTHELIAL SYSTEM It takes up to eight hours for a monocyte to become a macrophage. The combination of monocytes, mobile, and fixed tissue macrophages, the spleen, lymph nodes, and the liver are collectively called the “reticular endothelial system. Tissue macrophages are found in the skin, lymph nodes, lung alveoli, liver (Kupfer cells and sinusoids), central nervous system (microglial cells), connective tissue (histiocytes), and synovium as type A and type C cells. The main purpose of macrophages is phagocytosis. Tissue macrophages are considered the first line of defense, followed by neutrophils being the second line of defense, the third being mononuclear cells, and the fourth being granulocytes and monocytes. The spleen and bone marrow trap blood-born bacteria, debris and old red blood cells via filtration through the red pulp by phagocytosis. ABSOLUTE COUNT 100-500/mm3 DIFFERENTIAL 3-7% OF TOTAL WBC's Monocytes (monocytosis >500 cell/mm3 are increased in: 1. Bacterial infections 2. TB 3. Syphilis 4. Carcinoma of the stomach, breast and ovary 5. Hodgkin;s disease 6. Myeloproliferative diseases 7. Chronic ulcerative colitis 8. Collagen diseases and sarcoidosis 9. Surgical trauma 10. Lipid storage diseases (Gaucher's disease) 11. Severe infections 12. Lupus erythematosus 13. Hemolytic anemias 14. Breakdown of non-diseased tissue Monocytes are decreased (monocytopenia 100 cells/mm3) in: 1. Prednisone treatment 2. HIV 3. Aplastic anemia 4. Overwhelming infection 5. toxic reactions	11.1	7.7	13	1.77	9.47	11.23	OK	OK
Platelets Platelets PLATELET COUNT; MEAN PLATELET VOLUME (MPV) PLATELETS (thrombocytes) are the smallest elements circulating in the blood. Platelets are round or oval, flattened, nonnucleated, disc-shaped structures that are formed via fragmentation of RBC's. Platelets are necessary for clot formation, vascular integrity and vasoconstriction. Platelets are also responsible for adhesion and aggregation activity when forming platelet plugs for small breaks in artery walls. Thrombocytes are produced in the bone marrow with a life-span of 7 days. Two-thirds of all platelets are found in the circulating blood with one-third found in the spleen. MEAN PLATELET VOLUME indicates uniformity of size of platelet population and is used to differentially diagnosis thrombocytopenia PLATELET COUNT ADULTS: 140-400 x 10(3)/mm3 or 140-400 x 10 (9)/L CHILDREN: 150-450 x 10(3)/mm3 or 140-450 x 10 (9)/L MEAN PLATELET VOLUME ADULTS: 7.4-10.4 um3 or fL CHILDREN: 7.4-10.4 um3 or fL Platelets are increased in: 1. Allergic reactions 2. Thrombocytopenia 3. Chronic myelogenous and granulocytic leukemia, myeloproliferative diseases 4. Polycythemia vera 5. Splenectomy 6. Iron deficiency anemia 7. Asphyxiation 8. Rheumatoid arthritis and other collagen diseases, SLE 9. Rapid blood regeneration caused by blood loss and hemolytic anemia 10. Acute infections 11. Hodgkin’s disease, lymphomas, and malignancies 12. Chronic pancreatitis, tuberculosis, inflammatory bowel disease 13. Renal failure Platelets are decreased in: 1. Toxic reactions 2. Idiopathic thrombocytopenia purpura, neonatal purpura 3. Pernicious, aplastic and hemolytic anemias 4. Viral, bacterial and rickettsial infections 5. Thrombopoietin deficiency 6. Toxemia of pregnancy 7. Hypersplenism 8. Renal Insufficiency 9. Alcohol toxicity 10. HIV 11. During chemotherapy and radiation 12. Lesions of the bone marrow (leukemia, carcinoma) Increased MPV is found in: 1. Idiopathic thrombocytopenia 2. Massive hemorrhage 3. Splenectomy 4. Myeloproliferative 5. Vasculitis 6. Megaloblastic anemia	252	251	400	49.67	300.67	350.33	LOW	Toxic/Infection
Polys (Neutrophils) Polys (Neutrophils) SEGMENTED NEUTROPHILS/POLYS/GRANULOCYTES SEGMENTED NEUTROPHILS Are the most numerous and most important WBC's since they form the first line of defense via phagocytosis against infection and microbial invasion. Immature neutrophils are called stab or band cells. Neutrophils also release enzymes called endogenous pyrogens, which can also cause tissue damage. ABSOLUTE COUNT 3,000-7,000 mm3 DIFFERENTIAL 50% OT THE TOTAL WBC's Increased neutrophils (neutrophilia >8,000 mm3) is found in: 1. Bacterial, viral, fungal, spirochete and parasitic infections 2. Inflammatory diseases such as rheumatoid arthritis, pancreatitis, gout 3. Tissue necrosis from burns, tumors 4. Diabetes mellitus 5. Uremia 6. Hepatic necrosis 7. Malignant neoplasms 8. Myeloproliferative diseases such as polycythemia vera, myeloid leukemia 9. Lead, mercury, digitalis, snake venoms Decreased neutrophils (neutropenia <1,800 mm3) are found in: 1. Inherited stem cell disorders 2. Acute bacterial infections 3. Viral infections (mono, hepatitis, measles 4. Rickettsial and parasitical infections 5. Drugs 6. Hematopoietic diseases Many of your anemias 7. During inflammation (first 24-48 hours) 8. Allergic 9. Toxic reactions ****Agranulocytosis is a marked neutropenia and leukopenia, which leaves the person open to life-threatening infections.	64.9	66	74	2.67	68.67	71.33	LOW	Inflammation
Red Blood Cell (RBC) Count Red Blood Cell (RBC) Count RED BLOOD CELLS RED BLOOD CELLS (RBC's), hematocrit and hemoglobin follow suit and what causes increases or decreases in one will have the same effect on the other two RBC count (erythrocyte count) (measured in microliters or cubic millimeters of blood) RBC's via hemoglobin carries oxygen from the lungs to the cells and CO2 from the cells to the lungs. RBC's are biconcave thereby increasing the surface area of oxygen to Hb. RBC's can also change shape allowing RBC's to pass into small capillaries. About 5 liters of blood is found in the human body (3 liters of plasma and 2 liters of cells). Blood plasma is derived from the intestinal and lymphatic fluids. THE FUNCTION, PRODUCTION, AND DISTRIBUTION OF THE BLOOD CELLS RED BLOOD CELLS Red blood cells, granulocytes, and platelets are exclusively produced in the bone marrow after birth. B-lymphocytes are produced by the marrow and lymphoid organs whereas T-cells are produced by the thymus. From years five to twenty, your long bones produce most of the red blood cells. After the age of 20, the majority of red blood cell production comes from membranous bones such as your vertebra, sternum, ribs, and ilia. As we age, red blood cell production becomes less productive at these sites. It is imperative for the Doctor of Chiropractic to know that he/she can stimulate red or white blood cell production by correcting spinal distortions that effect bone marrow productivity. The genesis of a red blood cell is as follows: In the bone marrow, there are cells called pluripotential hemopoietic stem cells (PHSC) which act as the template to form all other blood cells. These PHSC differentiate into the various types of blood cells based on physiologic considerations from oxygen content in the blood to infectious diseases, which stimulate white blood cell production, as well as allergic and toxic reactions, which determines the fate of a PHSC. So, PHSC can become erythrocytes, granulocytes (neutrophils eosinophils, basophils/mast cells), monocytes, macrophages, megakaryocytes, platelets, T, and B-lymphocytes. For example, as mentioned above tissue oxygenation is the primary factor in regulating red blood cell production. Hemopoietic stem cells are activated by erythropoietin a glycoprotein with a molecular weight of 34,000 {80-90% of it is produced by the kidneys and 10% by the liver}. During times of stress epinephrin/norepinephrine, and prostaglandin production {via the adrenal medulla} and platelets also stimulate erythropoietin. Therefore, if tissue oxygenation is decreased due to anemia, low blood volume, poor circulation, heart/pulmonary disease etc. the adrenals can help produce erythropoietin as well. RED BLOOD CELL MATURATION The stages of red blood cell maturation are: STAGE 1 PROERYTHROBLAST STAGE 2 BASOPHILIC ERYTHROBLAST STAGE 3. POLYCHROMATOPHIL ERYTHROBLAST STAGE 4. ORTHOCHROMATIC ERYTHROBLAST STAGE 5. RETICULOCYTE-ERYTHROCYTE. Please note that red blood cells require B12 (cyanocobalamin) and folic acid. These vitamins regulate the synthesis of DNA (in all cells as well). If not present, the formation of thymidine triphosphate may be hindered. When this interference occurs blood cells become large, have a flimsy membrane, irregular shape, and have a reduced life span. As you may be aware, the parietal cells secrete a glycoprotein called intrinsic factor that attaches to B12, thus allowing it to be absorbed by the gut and stored in the liver to be released when there is a need for red blood cell production. So gastric conditions can create red blood cell maturation conditions causing irregular/abnormal cells noted in many of your blood cell dyscrasia's such as microcytic, hypochromic, megaloblastic, sickle cell, and Mediterranean anemia's. Here you have abnormal cell shapes, such as poikilocytosis and anisocytosis, which is excessive variation in size of RBC's. RBC's are increased (erythrocytosis) in: 1. Primarily by myeloproliferative diseases such as polycythemia vera and erythremia erythrocytosis (increased bone marrow production) 2. Secondarily by the renal, pulmonary and cardiovascular disease that are secondary to tobacco/carboxyhemoglobin. 3. Alveolar hypoventilation 4. High altitude 5. Hemoglobinopathy 6. Decreased plasma volume via diarrhea/vomiting and water deprivation 7. Toxic reactions A decrease in RBC's occurs in: 1. Anemia, which is caused via cell destruction, blood loss or a dietary vitamin B12/iron deficiency. 2. Hodgkins disease and other lymphomas 3. Myeloproliferative diseases such as multiple myeloma and leukemia 4. Hemorrhage 5. Lupus erythematosus 6. Addison.s disease 7. Rheumatoid arthritis 8. Chronic infection 9. Endocarditis 10. Hemolysis	3.29	4.6	6	0.47	5.07	5.53	LOW	Infection
White Blood Cell (WBC) Count White Blood Cell (WBC) Count WHITE BLOOD CELLS White blood cells (WBC's) are the mobile units of the body's immune system. They move at will all over the body. Where our country may take weeks to months to deploy troops, our body does it in seconds. Your white blood cells are produced both in the bone marrow and in the lymphatic system. WBC's are divided into two groups: Granulocytes: Have distinct granules present in the cytoplasm and multilobed nuclei and are also called polymorphonuclear leukocytes. They consist of your neutrophils, basophils, and eosinophils. Non-granulocytes contain no granules and are your monocytes and lymphocytes. The endocrine system along with site inflammation/infection is responsible for regulation of production, storage and release of leukocytes into the blood stream as well as their destruction or disintegration. The average WBC lives for 13-20 days and is destroyed by the lymphatic system and eliminated from the body thru fecal matter. The WBC's that are produced in your bone marrow originate from cells called myelocytes. A myelocyte will mature into a promyelocyte and either form a megakaryocyte or monocyte. 1. Magakaryocytes split to form granulocytes that will produce your neutrophils (polymorphonuclear cells), eosinophils, and basophils/mast cells and your monocytes 2. Monocytes grow to become tissue macrophages and live for years. These cells utilize a number of weapons in their arsenal such as: ¬ Phagocytosis, whereby some of these cells, such as neutrophils and macrophages encapsulate and use proteolytic enzymes to digest bacteria, virus etc. ¬ Diapedesis, whereby neutrophils and monocytes squeeze through blood vessel pores and move about the body ¬ Ameboid movement for neutrophils and macrophages, and ¬ Chemotaxis a weapon whereby chemicals from bacteria cause neutrophils and macrophages to be attracted to them. ¬ Leukocytes also produce, transport and distribute antibodies as part of the immune response. It is mostly the monocytes and neutrophils that destroy bacteria and virus. Basophils and mast cells, on the other hand, liberate heparin, an anti-coagulant, into the blood. Basophils and mast cells also release histamine, bradykinnin, and serotonin. Therefore, they are involved with allergic reactions and speed up the removal of fat particles after a meal. The lifespan of a granulocyte is 4-5 days. The WBC's that are produced by the lymph tissue are called lymphocytes and plasma cells. These cells are also produced in the spleen, thymus, tonsils, and bone marrow. Lymphocytes keep circulating between the lymph, blood, and intercellular spaces via diapedesis. WBC'S cells/mm3 ADULTS 4,500-10,000 BLACK ADULTS 3,200-10,000 CHILDREN 2MONTHS 6 YEARS 5,000-19,000 6-18 YEARS OF AGE 4,800-10,800 WBC'S are increased in (leukocytosis >11,000/mm3: 1.Neutrophilic leukocytosis or neutrophilia Lymphocytic leukocytosis or lymphocytosis Monocytic leukocytosis or monocytosis Basophilic leukocytosis or basophilia Eosinophilic leukocytosis or eosinophilia Acute infections Measles, pertussis Trauma or injury Malignant neoplasms Toxins, uremia, eclampsia Acute hemolysis Polycythemia vera Tissue necrosis Over exposure to sunlight Exercise Pain Stress Pain Cold WBC's are decreased (leukopenia <4,000/mm3 1. Viral infections 2. Toxic reactions 3. Hyperspleenism 4. Bone marrow depression 5. Antibiotics 6. Barbiturates 7. Antihistamines 8. Anticonvulsants 9. Heavey metal intoxication 10. Diuretics 11. Cardiovascular drugs 12. Bone marrow disorders 13. Leukemia 14. Pernicious anemia 15. Aplastic anemia 16. Marrow occupying lesions such as tumors	8.4	4.4	11.4	2.33	6.73	9.07	OK	OK

Gland Results

Results by Cardio / Urinary / Resp

Gland	Result
Kidneys Kidneys THE KIDNEYS The function of the kidneys is to filter 170,000 mL of blood daily and produce about 1200 mL of urine daily. At the same time, the kidneys are used to filter out all excessive ions such as sodium, chloride, and potassium, while maintaining glucose, amino acids, water and other substances that are essential for body metabolism. The kidneys also remove the following waste products: creatinine, BUN, and uric acid. The two kidneys together contain about two million nephrons and each nephron is capable of forming urine by itself. Blood enters the kidneys thru the renal artery, enters the glomeruli through the afferent arteriole, and leaves through the efferent arteriole. The efferent arteriole is smaller in diameter than the afferent arteriole, therefore creating a hydrostatic (back) pressure forming the glomerular filtrate. (The glomeruli is a network of up to 50 parallel and anastomosing capillaries covered by epithelium cells and encased in Bowman’s capsule.) The pressure of the blood into the glomeruli causes fluid to filter into Bowman’s capsule. This is known as the glomerular filtrate, which then travels to the proximal/ distal tubules in the kidney cortex. As the filtrate passes along the tubules, the capillary blood and the epithelial tubular cells add more solutes. Interposed between the proximal and distal tubules is the loop of Henley, which has a thin descending limb, and a thin and a thick (impermeable to H20, but actively absorbs solutes causing filtrate to become hypotonic) ascending limb. It then travels through the distal tubules, through the corticoid-collecting duct, into the medullar-collecting duct, where things are absorbed or secreted. As the glomerular filtrate flows through the tubules, especially the cortical, medullary and papillary collecting ducts, over 99% of the water (via AVP) and varying amounts of its solutes are reabsorbed. The basic function of the nephron is to clean the blood plasma of unwanted substances, particularly the end products of metabolism (organic substances) such as urea (accounts for ½ of the total dissolved solids in urine), creatinine, uric acid, urate, BUN and inorganic dissolved solids (the highest being chloride followed by sodium and potassium.) The kidney does this through two mechanisms: filtration and secretion. Antidiuretic hormone (AVP) retains water but removes solutes. AVP binds to V2 receptor sites on renal epithelial cells of the basso lateral membrane activating protein kinase and adenylate cyclase to catalyze cAMP from ATP. The cAMP is now phosphorylated, mediating the effects of renal transport. AVP also increases transepithelial conductance and basso lateral membrane conductance of the CL ion channels. AVP also increases co transport units on other cell membranes for NA, K, and CL. Aldosterone controls potassium excretion and sodium reabsorption. Parathyroid hormone causes absorption of calcium and loss of phosphorus. The daily loss of fluid through urine is 1400 mL, 350 mL through the skin and respiratory tract, and 100 mL through sweat and feces. The rennin-angiotensin system is stimulated by decreased blood flow through the kidneys. The purpose of which is to increase blood pressure. Rennin is a small protein enzyme released by the kidney and is stored as pro rennin. When the blood pressure drops, pro rennin is converted into rennin. Rennin also works as an enzyme on another plasma globular protein called rennin substrate 1 and 2 or angiotensin (a powerful vasoconstrictor). Angiotensin 2 is the most powerful constrictor and is also found in the epithelium of the lungs. Angiotension decreases water and mineral loss through the kidneys while stimulating the adrenals. Aldosterone is strongly influenced by this rennin-angiotensin system (90% more than ACTH) causing strong reabsorption of sodium into the distal tubules to balance extracellular potassium ions. The following tests indicates kidney malfunction: 1. SODIUM-Sodium is an alkaline mineral that helps maintain alkaline activity. It helps in acid-alkaline balance, which affects intracellular/extracellular fluid exchange, and osmotic pressure, via the sodium/potassium pump. It does this in conjunction with antidiuretic hormone and aldosterone. Sodium gathers and aggregates (polarizes) all substances necessary to be exchanged by semi-permeable membranes. Sodium also affects the renal tubules for the activity of discharging toxins. It literally aggregates toxins and holds them in suspension. 2. POTASSIUM-Potassium lines the inside of all cell membranes and is responsible, via the posterior pituitary, for oxidizing secondary hydrogen chloride and allowing sodium-aggregated substances to cross the cell membrane. It is the only substance that allows oxygen into unoxygenated tissue. Potassium is necessary for proper function of mineral corticoids, (aldosterone and deoxycorticosterone) thus maintaining sodium concentration and alkaline reserve. Therefore, potassium is of great value to the posterior pituitary (ADH/oxytocin), the pineal and the adrenal cortex, via aldosterone secretion. In turn, the kidneys are greatly affected.	375.6%
Heart Heart HEART Keeping it simple, the heart is a muscle that never rests. It works 24/7. From an ionic standpoint, calcium and potassium ions (calcium pump) are responsible for creating the action potential of heart cells. Potassium causes the heart to relax, and decreases the heart rate, whereas calcium has the exact opposite effect. So, any endocrine imbalance causing problems with calcium or potassium has an adverse affect on the heart. On the other hand, neurotransmitters from the autonomic nervous system and the adrenals such as acetylcholine and epinephrine inhibit and excite the heart. Stimulation of the vagus nerve (parasympathetic division) releases acetylcholine, which decreases the rhythm of the SA node and decreases the junction fiber rhythm of the AV node, due to the acetylcholine effect of increasing cell membrane permeability to potassium. For example, the heart rate of a healthy individual can go as high as 250 beats per minute via sympathetic stimulation, and can almost stop due to parasympathetic stimulation. Epinephrine, on the other hand, has the exact opposite effect on the heart. Other hormones such as vasopressin, angiotensin, oxytocin, norepinephrine, serotonin and histamine also affect all types of muscles. Each type of smooth muscle has hormonal gated excitatory or inhibitory receptors for that respective hormone. Other factors, such as lack of oxygen, and increased carbon dioxide and hydrogen, effect baroreceptors inhibiting vasoconstrictor centers in the medulla and exciting the vagus nuclei cause muscles to relax (decreased contraction) or vasodilate. Perhaps one of the most far-reaching effects on the heart is due to sugar metabolism (glucose and triglycerides.) They give the heart muscle the fuel and the spark it needs to run. Without the proper amounts of fuel, you car and heart cannot make the journey. Sugar metabolism is controlled through many glands such as the pancreas, liver, and adrenals. Let us by no means leave out protein. Listen, every time you exercise a muscle, it breaks down, and without proper protein intake, and you will not build that muscle back up again. Your heart is no different; there are many flabby heart patients due to reduced protein intake. I saved the best for last-fat. You will soon find out how important fat is in your diet, and is much more of a friend then you know. The following blood tests are used to determine a heart conditions: 1. CALCIUM-besides bonding to lipoprotein, calcium also bonds to the oily portion of fatty acids. This is necessary for fatty acids to pass through the intestinal wall. If there is poor oxidation of fatty acids, there will be a specific amount of calcium needed to bond to the fatty acids, thereby decreasing the calcium levels in the blood and decreasing heart muscle function. Calcium ions with ATP also activate the “contractile” process in both smooth and skeletal muscle. 2. POTASSIUM-has prime importance in controlling membrane permeability by displacing the chloride ion as well as epinephrine for the next stage, which permits calcium to cross the cell membrane. This causes the heart muscle to decrease in tone. It is the only substance that allows oxygen into unoxygenated tissue. 3. LACTIC ACID DEHYDROGENASE (LDH)-is a glycolytic enzyme that functions as a catalyst in carbohydrate metabolism, aiding the pyruvic and lactic acid interchange. LDH is a byproduct of muscle metabolism. When sugar and water (fatty acid metabolism) are exchanged across a muscle cell interface, the byproduct left is called lactic acid. Lactic acid is also a byproduct of fatty acid metabolism via the alkalizing and oxidizing affects of the pancreatic head. When lactic acid combines with the venous blood (carbon dioxide), there is hydrogen displacement. The lactic acid then bonds to a double hydrogen forming lactic acid dehydrogenase. LDH is then a byproduct of carbohydrate and fatty acid metabolism. The organs and glands that that are most responsible for sugar and water interchange across the muscle cell interface are the pancreas and posterior pituitary (via antidiuretic hormone.) LDH is found chiefly in the heart, kidneys, liver, skeletal muscles, as well as all tissues. LDH is a normal component of the cerebral spinal fluid. 4. TRIGLYCERIDES-High triglycerides indicate a weak heart. This is because triglycerides create the spark necessary for combustion to produce energy, in this case, muscular contraction. 5. CHOLESTEROL-HDLs clinging to arterial walls	169.5%
Arteries Arteries	50%
Bladder Bladder	38%
Urethera Urethera	38%
Lung Lung THE LUNGS The mechanics of pulmonary ventilation are performed by the diaphragm, which increases the superior-inferior length of the lungs and the expansion of the rib cage, increasing the circumference of the lungs. The major muscles that increase the size of the rib cage by raising the rib cage are the intercostals, and secondarily by the sternocleidomastoideus, scalene, and anterior serratus muscles. The muscles that depress and pull the ribs downward and aid in exhalation are the rectus abdominal and the internal intercostals. The lungs are suspended from the mediastinum via the hilus and literally float in the thoracic cavity and use pleural fluid to act as a lubricator for movement. This creates a pleural pressure between the lung and chest wall causing at rest a -5-cm of water pressure (sucking pressure.) On inhalation, this negative pressure builds to -7.5-cm of water pressure, and then it reverses on exhalation. The alveolar pressure in the lungs is equal to the atmospheric pressure (0 centimeters of water pressure) with your glottis open. The alveoli require very little negative pressure (-1 centimeter of water pressure to bring in ½ liter of air into the lungs.) The trans pulmonary pressure is the pressure between the alveoli and the pleural pressure, which measures the elastic ability of the lungs. The epithelial lining from the nose to the bronchioles contains cilia, sub mucosa and goblet cells that release mucous as the cilia remove mucous at a speed of 1 centimeter per minute. The cilia sweep toward the pharynx in the nose, as the cilia in the bronchioles, sweep up toward the pharynx, either to spit up or ingest the mucus. The turbinates in the nostrils also expedite the movement of mucous. BLOOD FLOW IN THE LUNGS The pulmonary arteries bring blood from the right ventricle of the heart that is actually unoxygenated venous blood. These arteries have very thin walls and large lumens, giving great flexibility and blood supply to the lungs. The pulmonary veins resemble the arteries, but are shorter, and bring oxygenated blood back to the left atrium. The bronchial arteries bring oxygenated blood to the lungs themselves, and the bronchial veins bring the blood back to the left atrium instead of the right, making the output of the left ventricle greater than that of the right. The lymphatics extend into the lungs, connective tissue, the spaces and the terminal bronchioles, and drain back into the right thoracic duct. Capillary exchange dynamics: • Pulmonary capillary pressure is low, 7-millimeters hg, as compared to the 17-millimeters hg in peripheral tissues. • The interstitial fluid pressure is slightly more negative than peripheral tissue. • The pulmonary capillaries leak protein, which increase colloidal osmotic pressure to 17-millimeters hg instead of the 7-millimeters hg in peripheral tissues. • The alveolar walls are extremely thin and weak, and can rupture due to any negative pressure causing fluid to build up in the alveoli. This all creates a negative net diffusion of fluid out of the capillaries into the interstitial fluid and back into the circulatory system, keeping the alveoli dry. The interstitial fluid also creates pleural fluid via the mesenchymal membrane of the pleura, which it exudes and uses to line the potential space between the visceral and parietal pleura. The pleural fluid is then collected via the lymphatic vessels in the pleural cavity, then sucked away via a negative pressure in the lymphatic system. This negative pressure is what keeps the lungs inflated. THE RESPIRATORY UNIT The respiratory unit is composed of the bronchiole, alveolar duct, atria, and alveoli. The alveoli walls are thin and literally contain a sheet of capillaries on them. This membranous system is known as the respiratory membrane, and is composed of the following layers: 1. A layer of fluid that reduces the surface surfactant of the alveolar fluid 2. Alveoli epithelium 3. An epithelial basement membrane 4. A thin interstitial space between the epithelium and the capillary membrane 5. A capillary basement membrane that sometimes fuses with the basement membrane of the alveoli 6. A capillary endothelial membrane The surface area of this membrane is said to be 50-100 sq. meters, with the amount of blood present in the lungs at any one time to be between 60-140mls, making the exchange a breeze. THE TRANSPORT OF OXYGEN AND CO2 Oxygen and carbon dioxide diffuse in and out of the lungs. For example, the oxygen content in the alveoli is higher than that of the blood, 104 millimeters hg to 40 millimeters hg. Therefore, oxygen crosses into the capillaries. Diffusion capacity can be increased 3 fold through exercise, due to increased capillary participation, and the blood remaining in the capillaries longer for full oxygenation. Please note that during strenuous exercise your oxygen demands can increase 20 times normal. When this oxygenated blood reaches the peripheral interstitial tissues, the oxygen is at 94-millimeters hg and the interstitial tissue is 40-millimeters hg. Therefore, oxygen enters the peripheral interstitial spaces. Since the oxygen in cells is between 4-40 millimeters hg, oxygen enters the cells rapidly. Carbon dioxide goes in the opposite direction equal exactly to the number of oxygen molecules coming in. The only difference is that carbon dioxide diffuses 20 times faster. The following tests are used to determine a lung condition: 1. SODIUM-Sodium is alkaline and causes swelling of membranes, which reduce exchange across a cell membrane. It can also affect tissue exchange of oxygen. 2. CARBON DIOXIDE-80-90% of the carbon dioxide found in plasma is bound to protein and is represented as bicarbonate ions (HCO3-.) The other 10 to 20% is bound to protein as CO3 (2) and carbonic acid (H2CO3.) This occurs as follows: Carbon dioxide in the blood reacts with water in the red blood cells to form carbonic acid. There is an enzyme in the blood cells called carbonic anhydrase, which catalyzes water and carbon dioxide 5,000 fold, creating a rapid exchange into carbonic acid. This allows tremendous amounts of carbon dioxide to react with the water in the red blood cells, even before the blood leaves the tissue capillaries. So, a red blood cell creates carbonic acid from water and carbon dioxide. In another small fraction of a second, the carbonic acid formed in the red blood cell disassociates into hydrogen and bicarbonate ions. The hydrogen ions combine with hemoglobin as the bicarbonate ions diffuse out into the plasma while chloride ions diffuse into the red blood cells taking the place of the bicarbonate ions. This is made possible by the presence of a bicarbonate/chloride carrier protein in the red blood cell membrane, which acts as a shuttle for these two ions. Thus, the chloride content of venous red blood cells is greater than that of arterial cells. This is known as the chloride shift. In addition, carbon dioxide can react directly with hemoglobin to form the compound carbaminohemoglobin. This carbaminohemoglobin creates the reversible reaction releasing carbon dioxide into the alveoli of the lungs. Carbon dioxide, then, is the venous capillary exchange product after diffusion takes place. The active pressure intake of oxygen relies upon this diffusion. This active process realizes the ability of forced metabolism and is the ash by-product. Carbon dioxide is vital to pH balance and is controlled by the respiratory, renal and adrenal axis. When there is an accumulation of carbon dioxide in the blood, it causes acid blood.	24.5%
Veins Veins	16%

Show Expanded

#		Arteries	Bladder	Heart	Kidneys	Lung	Urethera	Veins
Glucose Glucose GLUCOSE Glucose is an important fuel for the body, which affects all tissues, organs, and systems. Glucose also affects the acid/alkaline balance in the body. Breakdown of glucose or starch starts in the mouth via ptyalin, then in the stomach via HCL, and then by pancreatic amylase, lactase and other enzymes. Glucose is then absorbed in the small intestines and is then stored as glycogen in the liver. The liver is the primary site of glucose production. The liver converts lactic acid to glycogen and back to glucose via epinephrine. The liver converts fats and proteins via gluconeogenesis into glucose or glycogen. The head of the pancreas controls chromium, which controls insulin levels and assists in the enzyme action of fats via bile salts. The tail of the pancreas controls zinc, which maintains and sustains levels of insulin. Blood sugar depends on: 1. The liver which stores and releases glycogen 2. The pancreas, which produces insulin that transfers sugar from the blood to the extracellular fluid 3. The adrenal glands, which produced glucocorticoids that, cause the liver to release glycogen into the blood as glucose 4. The sex organs, which deliver the extracellular glucose to the cell 5. The thyroid, which affects the storage of glycogen in the liver 6. The thymus and spleen, which affect the levels of iron and copper in the liver which, determine the liver's ability to handle glucose As you can see there are many organs, or combinations of these organs and glands, which affect glucose levels in the body. Therefore, glucose in itself cannot specifically determine where the problem may lie. Other indicators are necessary to pinpoint the problem.	-28
Uric Acid Uric Acid URIC ACID Uric acid is the principal end product of purine, nucleic acid, and nucleoprotein metabolism. Uric acid is transported by the blood from the liver to the kidney’s which filter out and secretes about 70% and the remainder excreted via the GI tract. From a pathological view, uric acid is elevated when there is cell breakdown as in leukemia and catabolism of nucleic acids as in gout, or removal via the kidneys is decreased due to renal failure. From a physiologic view, we look at every level of protein combustion where there remain two by-products which are a Mucous (oily residue) and Uric acid (carbon ash) In order for protein to be fully combusted, it must first be influenced in the duodenum by trypsin, chymotrypsin, carboxypolypeptidase, and bile emulsification. Trypsin and chymotrypsin cleave proteins into peptides and carboxypolypeptidase split the peptides into amino acids. The pancreas synthesizes trypsinogen, chymotrypsinogen, and procarboxypolypeptidase, which are enzymatically inactive. When they are released into the duodenum they are all activated by enterokinase. Which now readies the proteins for assimilation in the liver. Therefore, if the proteins are not prepared properly the two end products, uric acid, and mucous, will be out of balance. URIC ACID IS HIGH WHEN General considerations: ¬ Decrease fatty proteins and rich foods ¬ Decrease alcohol and simple sugars ¬ Increase water intake	303.64
Bun Bun BLOOD UREA NITROGEN Blood urea nitrogen is formed entirely by liver deamination from protein metabolism. BUN is a byproduct due to the release of nitrogen bonds (and measures the nitrogen portion of urea) from protein substances in the liver. From a pathological perspective, an increased blood urea nitrogen would indicate renal disease, tissue necrosis, increased adrenal gland activity, and rapid protein catabolism. From a physiologic perspective, the purpose of nitrogen is to carry a substance through an aerobic media preventing oxidation, and eventually back into an anaerobic environment. Once in the liver the thyroid through the use of iodine, releases the nitrogen bond, releasing the nitrogen from the protein, allowing the protein to combust into hormones, enzymes and antibodies. The adrenals and anterior pituitary play a vital role in the combustion of this protein. The urea is now sent to the kidneys and is converted into urine. Urea is produced when amino acids, which are not used for protein synthesis, are broken down via hepatic metabolism. These amino acids are de-aminated producing ammonia, which is converted to urea immediately since ammonia levels become toxic. When this metabolic conversion is affected due to faulty metabolism or liver disease ammonia is not converted causing excessive levels of ammonia with possible hepatic encephalopathy. Renal malfunction/failure may also cause a high BUN due to its affect on the removal of urea causing uremia. Uremic wastes usually impair platelet function, and patients may show an increased tendency towards bleeding. BUN IS HIGH WHEN General considerations: ¬ High protein diets can cause increased BUN ¬ Increase water intake if no edema	880.95				10
Creatinine Creatinine CREATININE Creatinine ash is a basic byproduct in the breakdown of muscle creatine phosphate resulting from energy metabolism. From a pathological perspective the kidneys primarily remove creatinine and when there are elevated levels it indicates reduced kidney function. Thus creatine levels give an approximate for the GFR. From a physiological perspective, creatine is a by-product of actin metabolism after being exposed to acetylcholine combustion. The actin fiber joins two stable protein blocks (myosin), which combusts to produce muscle contraction, primarily for activity and secondarily for tonicity. During a muscle contraction, an action potential travels along a motor nerve to a muscle fiber. Acetylcholine is released at the motor endplate, causing multiple acetylcholine lined gated protein channels to open. This causes sodium ions to flow to the interior of the muscle, which initiates an action potential of that muscle. This then leads to depolarization releasing large amounts of calcium into the myofibrils. This initiates a contractive force between the actin and myosin filaments via ATP causing them to slide together, which is the contractile process. After a fraction of a second, calcium is pumped back into the sarcoplasmic reticulum, until the next muscle contraction. The actin fiber is then oxidized (H displaced) via acetylcholine, leaving an oily waxy residue known as creatinine. GABA (Glutamic amino benzoic acid), which is part of the actin fiber, helps it burn better. Creatine becomes creatinine with the release of ATP. Low creatinine levels would indicate muscle loss and weakness.	455.56
Sodium Sodium ELECTROLYTES The blood electrolytes include sodium, potassium, chloride, and the bicarbonate (HCO3) ion. Sodium, potassium, and chloride enter the body via ingestion of food. Carbon dioxide, on the other hand, originates within the body via the metabolic process of carbohydrates, fats, and proteins. Normally the excretion of sodium, potassium, and water is equal to their intake. The kidneys secrete 80-90 percent of all electrolytes. Excessive carbon dioxide stimulates the respiratory centers in the brainstem to increase respiration. Therefore, the kidneys and the lungs control sodium, chloride, potassium, water, and carbon dioxide thus exerting control over the acid/alkaline balance in the body. There are also many other organs, and glands involved in this process, such as the posterior pituitary, adrenals, bowel, and uterus/prostate. The purpose of electrolytes is to set up a shifting mechanism in the cell membrane via oxidation, allowing increased or decreased permeability to that membrane site. Sodium, which is found in high concentration outside the cell, has the ability to gather up substances (foods) and bring them to active membrane sites. Chloride is found in the cell membrane and acts as a “doorman” allowing or disallowing exchanges between the intracellular and extracellular fluids. Potassium, which is found in high concentrations within cells, oxidizes chloride, and allows sodium, with the food to cross the cell membrane and enter the cell. Sodium, potassium, chloride, calcium, and hydrogen are all transported via active transport. SODIUM Sodium is the most abundant cation (90%) and is the major base in the body. Sodium is either implanted into the food via saliva or is found in the food and has the following functions: 1. Sodium is an alkaline mineral that helps maintain alkaline activity. Therefore, it helps in acid-alkaline balance, which affect intracellular/extracellular fluid exchange, osmotic pressure, via the sodium/potassium pump and does this in conjunction with antidiuretic hormone and aldosterone. 2. Sodium gathers, and aggregates (polarizes) all substances necessary to be exchanged by semi-permeable membranes. Sodium pumps proteins and sugars into the cell membranes. 3. Sodium also affects the renal tubules for the activity of discharging toxins. It literally aggregates toxins and holds them in suspension. 4. Sodium is controlled by the adrenal cortex and as mentioned above is extremely alkaline and therefore, can cause migration of substances towards its polarity, as well as causing these migrated substances to achieve permeability in an acid antioxidant type media known as a fatty membrane. Sodium is the substance necessary to polarize foods into storage according to that permeable membranes needs. 5. Sodium is also necessary for the transmission of neurological impulses by creating action potentials across neurological membranes. 6. Sodium concentration in and out of cells remains constant due to renal blood flow, carbonic anhydrase enzyme activity, aldosterone, and other steroids controlled by the anterior pituitary, rennin enzyme secretion, hypothalamus, and posterior pituitary control of ADH and vasopressin secretion	-33.33				10	5
Potassium Potassium ELECTROLYTES The blood electrolytes include sodium, potassium, chloride, and the bicarbonate (HCO3) ion. Sodium, potassium, and chloride enter the body via ingestion of food. Carbon dioxide, on the other hand, originates within the body via the metabolic process of carbohydrates, fats, and proteins. Normally the excretion of sodium, potassium, and water is equal to their intake. The kidneys secrete 80-90 percent of all electrolytes. Excessive carbon dioxide stimulates the respiratory centers in the brainstem to increase respiration. Therefore, the kidneys and the lungs control sodium, chloride, potassium, water, and carbon dioxide thus exerting control over the acid/alkaline balance in the body. There are also many other organs, and glands involved in this process, such as the posterior pituitary, adrenals, bowel, and uterus/prostate. The purpose of electrolytes is to set up a shifting mechanism in the cell membrane via oxidation, allowing increased or decreased permeability to that membrane site. Sodium, which is found in high concentration outside the cell, has the ability to gather up substances (foods), and bring them to active membrane sites. Chloride is found in the cell membrane and acts as a “doorman” allowing or disallowing exchanges between the intracellular and extracellular fluids. Potassium, which is found in high concentrations within cells, oxidizes chloride, and allows sodium, with the food to cross the cell membrane and enter the cell. Sodium, potassium, chloride, calcium, and hydrogen are all transported via active transport. POTASSIUM Potassium is intracellular, lining the inside of all cell membranes and affecting intracellular fluids, osmotic pressure, buffering viscosity (potassium bicarbonate is the primary intracellular inorganic buffer). When there is a decrease in potassium bicarbonate you have acid cells, which excites the respiratory centers so the patient hyperventilates. Metabolic acidosis or diabetic ketoacidosis drives potassium out of the cells, affecting electrolyte balance, water retention and carbon dioxide transport in red blood cells. Potassium is responsible via the posterior pituitary for oxidizing secondary hydrogen chloride (affecting adrenal function), allowing the sodium-aggregated substances to cross the cell membrane by affecting the membranes permeability. Potassium is the only substance, which allows oxygen into unoxygenated tissue. About 90% of the body’s potassium supply is intracellular with only a small percent in the serum. 80% of that is found in the muscles (used for muscular contraction) and in the bones. Potassium levels are regulated by the Na/K ATPase pump which requires magnesium for proper function. Potassium is necessary for proper function of mineralocorticoids, (aldosterone and deoxycorticosterone) thus maintaining sodium concentration and alkaline reserve. Therefore, potassium is of great value to the posterior pituitary (ADH/oxytocin), the pineal, and the adrenal cortex via aldosterone secretion. Potassium along with sodium regulate renal acid-base balance, by substituting hydrogen ions for sodium and potassium in the renal tubules. Potassium also facilitates oxygen to the myocardium and oxidizes the S.A. node of the heart. The heart has the highest potassium concentration in the body. Potassium along with calcium and magnesium controls the rate and force of contraction in heart muscle. It is the primary oxidizer of the body capable of expressing all cellular needs. Potassium also regulates neurological impulses via osmotic pressure gradients throughout the nervous system. Potassium directs carbohydrate digestion by polarizing minerals associated with carbohydrate digestion, from the time the carbohydrate enters the body until the cell utilizes it. Potassium also makes proteins soluble and regulates protein synthesis. 80-90 percent of potassium in the cells is excreted by the kidneys (resulting in the loss of 40-50 mEq/L per day even during fasting) with the remainder excreted by the stool and through sweating POTASSIUM IS LOW WHEN General considerations: ¬ Increase water intake ¬ Increase magnesium intake ¬ Decrease calcium intake ¬ Increase potassium intake ¬ Decrease carbohydrate intake	-50	5		5	5
Chloride Chloride ELECTROLYTES The blood electrolytes include sodium, potassium, chloride, and the bicarbonate (HCO3) ion. Sodium, potassium, and chloride enter the body via ingestion of food. Carbon dioxide, on the other hand, originates within the body via the metabolic process of carbohydrates, fats, and proteins. Normally the excretion of sodium, potassium, and water is equal to their intake. The kidneys secrete 80-90 percent of all electrolytes. Excessive carbon dioxide stimulates the respiratory centers in the brainstem to increase respiration. Therefore, the kidneys and the lungs control sodium, chloride, potassium, water, and carbon dioxide thus exerting control over the acid/alkaline balance in the body. There are also many other organs, and glands involved in this process, such as the posterior pituitary, adrenals, bowel, and uterus/prostate. The purpose of electrolytes is to set up a shifting mechanism in the cell membrane via oxidation, allowing increased or decreased permeability to that membrane site. Sodium, which is found in high concentration outside the cell, has the ability to gather up substances (foods) and bring them to active membrane sites. Chloride is found in the cell membrane and acts as a “doorman” allowing or disallowing exchanges between the intracellular and extracellular fluids. Potassium, which is found in high concentrations within cells, oxidizes chloride, and allows sodium, with the food to cross the cell membrane and enter the cell. Sodium, potassium, chloride, calcium, and hydrogen are all transported via active transport. CHLORIDE Chloride a blood electrolyte, and is the major anion and exists in the extracellular spaces as part of the sodium chloride or HCl molecules. Chloride is used for assessing pH, and electrolyte balance. From a physiologic perspective, the primary purpose of chloride is to regulate the quantity of carbohydrates and proteins entering into the cells, by inhibiting the exchange of mineral controlled substances across the cell membrane and responds to the oxidative power of potassium. Chloride the major anion is predominantly found in the extracellular spaces as part of sodium chloride or in the stomach as hydrochloric acid. Chloride maintains cellular integrity by its influence on acid-base and water balance as well as osmotic pressure. Chloride has a reciprocal power with other anions by decreasing or increasing when there are too many or not enough anions. Aldosterone has a direct effect of reabsorption of sodium and an indirect effect on the increased absorption of chloride. Chlorides are lost via the GI tract through vomiting or diarrhea and thru the kidneys during times of diuresis. Chloride also responds to the antioxidant media (cell membrane) by mobilizing, and collecting sodium/food aggregates on a selectively permeable basis. This reaction is under the influence of the adrenal medulla/epinephrine/norepinephrine thereby maintaining energy stores. Chloride also assists in the production of HCl via the chief cells in the stomach. In the bowel, chloride is important in preventing the passage of water out of the body. Therefore, chloride literally blocks the flow of water/gas exchange across a cell membrane. This is extremely important in the intestines and bladder. Chloride plays a vital role during the conduction of a neurological impulse where sodium lines up on the outside of a cell membrane, and potassium on the inside of the cell membrane, during the resting stage or polarized state. In a normal nerve fiber, the permeability of the membrane to potassium is about 100 times that of sodium. The sodium-potassium pump moves three sodium ions to the exterior of the cell, for every two potassium ions that are moved to the interior of the cell, creating a net positive charge to the outside of the cell membrane for each revolution of the sodium-potassium pump. This creates a positively charged external membrane and a negatively charged internal membrane, which sets up a membrane electrical potential. As a neurological impulse is transmitted down the nerve, (which is the excitation phase of an impulse), sodium crosses the cell membrane, and enters into the cell, while potassium moves to the external portion of the membrane. This then creates the depolarization of the cell membrane, thereby creating a negative charge on the outside, and a positive charge on the inside. The transmission of each impulse along the nerve fiber reduces infinitesimally as the concentration differences of sodium and potassium between the inside and outside of the cell membrane change slightly. In so doing allows the nerve fiber to transmit between 100, 000 to 50, 000, 000 impulses before the concentration differences are rundown. As the neurological impulse passes, the sodium-potassium ATPase pump re-establishes the sodium-potassium ratio back to normal (repolarization). The pumping activity is dramatically increased approximately eightfold to restore the membrane back to the polarized state. The chloride shift to the inside of the cell membrane during the final stages makes the inside of the cell, even more, negative, which further helps repolarize the cell. Chloride generally increases and decreases with plasma or serum sodium levels. CHLORIDE IS HIGH WHEN General considerations: ¬ Drink plenty of water ¬ Decrease sodium levels ¬ Increase fat-soluble vitamins D, E, K, and A	-38.46		5				5
CO2 CO2 CARBON DIOXIDE Carbon dioxide is created as a byproduct when potassium forces water into fat. So carbon dioxide is the acid gas factor, which binds fats and selenium creating the intelligent metabolic activity between the water and fat. 80-90 percent of the carbon dioxide found in plasma is bound to protein and is represented as bicarbonate ions (HCO3-) which first exists in the extracellular spaces as CO2 then as H2CO3 and finally is buffered by the plasma and erythrocytes into sodium bicarbonate NaHCO3) and is regulated by the kidneys. The other 10 to 20 percent is dissolved CO2 gas (removed by the lungs), which is bound to protein as CO3 (2), and carbonic acid (H2CO3). The total CO2 comes from dissolved CO2, H2CO3, HCO3- and carbaminohemoglobin (CO2HHb). This occurs in the following way, carbon dioxide in the blood reacts with water in the red blood cells to form carbonic acid. In the blood cells, there is an enzyme called carbonic anhydrase that catalyzes the water and carbon dioxide 5,000 fold, creating a rapid exchange into carbonic acid. This allows tremendous amounts of carbon dioxide reacting with the water in the red blood cells, even before the blood leaves the tissue capillaries. So a red blood cell creates carbonic acid from water and carbon dioxide. In another small fraction of a second, the carbonic acid formed in the red blood cell now disassociates into hydrogen and bicarbonate ions. The hydrogen ions combine with hemoglobin, as the bicarbonate ions diffuse out into the plasma while chloride ions diffuse into the red blood cells taking the place of the bicarbonate ions. This is made possible by the presence of a bicarbonate/chloride carrier protein in the red blood cell membrane, which acts as a shuttle for these two ions. Thus, the chloride content of venous red blood cells is greater than that of arterial cells. This is known as the chloride shift. In addition, carbon dioxide can react directly with hemoglobin to form the compound carbaminohemoglobin. This carbaminohemoglobin creates the reversible reaction releasing carbon dioxide into the alveoli of the lungs. Carbon dioxide then is the venous capillary exchange product after diffusion takes place. The active pressure intake of oxygen relies upon this diffusion. This active process realizes the ability of forced metabolism and is the ash byproduct. Carbon dioxide is vital to pH balance and is controlled by the respiratory, renal, and posterior pituitary adrenal axis. Therefore, any of these glands or organs or combinations thereof can affect carbon dioxide levels. CARBON DIOXIDE IS HIGH WHEN General considerations: ¬ Water loss- increase water intake ¬ Protein loss- increase protein intake ¬ Hypomagnesemia or hypokalemia causes increased CO2- increase potassium and magnesium CARBON DIOXIDE IS LOW WHEN ¬ Water loss- increase water intake ¬ Hypermagnesemia or hyperkalemia causes decreased CO2- decrease potassium and magnesium support	-16.67					5		5
Calcium Calcium CALCIUM Calcium is the largest most nonpolar, alkaline and most abundant of all minerals with 99% of all calcium found in the bones and teeth. Calcium exists in the ionized state 55 percent of the time and 45 percent of the time in the non-diffusible state, bound to either albumin, prealbumin or thyroglobulin. Therefore, if there is a decrease in serum albumin then there will be a decrease in serum calcium. Calcium has many functions: ¬ Provides the mobilizing factor in trauma, infections and stress for tissue repair, along with vitamins A, C, manganese, phosphorus, and fatty acids. ¬ Causes vasoconstriction, while potassium, sodium, magnesium, hydrogen ions, and carbon dioxide cause vasodilatation. ¬ Is necessary for bone formation along with phosphorus, collagen, hydroxyapatite (gives bone its hardness) and bone salts of magnesium, sodium, potassium, carbonate, uranium, plutonium, and strontium. ¬ Calcium is used to create action potentials across smooth and striated muscles leading to contraction. ¬ Calcium is used as an intracellular communicator via calcium ion gated channels. ¬ Calcium collects and gather up lipoproteins, and move them across the intestinal membrane. Attaches to oils, fats, fatty acids and waxes. Calcium is absorbed in the upper portion of the small intestines (duodeneum), and the amount absorbed depends on the "acidity" of the intestinal content, via phosphorylation and protein content. When the ratio of calcium to magnesium (which is found in the intestinal membrane as well as cell membranes) is greater than 2-1, fat is drawn through the intestinal and cell membranes. Calcium also requires vitamin D. and HCl for optimal metabolism. The glands involved with calcium are: 1. The stomach via the release of HCL, which affects the preparation and absorption of calcium. 2. The parathyroids- via parathormone control of calcium ion concentration by controlling intestinal absorption, excretion via the kidneys and the release of calcium from the bones. 3. The liver/gallbladder- via bile emulsification of lipoproteins, preparing them for intestinal absorption. 4. The spleen- which stores and ages fats or lipoproteins. 5. The parotids- due to their ability to program foodstuffs. 6. The thyroid glands-via "calcitonin", promoting deposition of calcium in the bones, while decreasing calcium concentration in the extra-cellular fluids and the blood. 7. The anterior pituitary via its control of magnesium regulating calcium uptake, which regulates protein transport thru the cell membranes. 8. The pancreas- via its ability to oxidize fatty acids Therefore, any of the above glands or organs or combinations thereof has a great impact on calcium levels. CALCIUM IS HIGH WHEN General considerations ¬ Your patient should drink plenty of water ¬ Make sure they are not hypervitaminosis on Vitamins A or D ¬ Very high protein diets may increase calcium levels ¬ Magnesium and phosphates may also increase calcium levels ¬ Using sea salt can help to reduce calcium levels. CALCIUM IS LOW WHEN General considerations: ¬ Increase Vitamin A and D intake ¬ Increase albumin and protein intake ¬ Increase magnesium intake ¬ Increase phosphorus	-13.04			5
Phosphorus Phosphorus PHOSPHORUS 85% of the total phosphorus exists as phosphates or esters in the body and is found chiefly in the skeleton and is combined with calcium. 14% of the phosphorus is found in intracellular tissues and 1 % is found in the extracellular fluid. Therefore phosphorus levels are a poor indicator of levels of phosphates in the body. Phosphorus runs inversely to calcium levels in the body at a calcium to phosphorus ratio of 10 to 4. Therefore, calcium can be a great indicator for phosphorus as well. As calcium levels increase in the serum, phosphorus levels decrease, and when calcium levels decrease phosphorus levels increase. In fact, causes of high calcium also cause low phosphorus. The controlling factor of phosphorus is parathormone (PTH), which is also the calcium-controlling factor. Phosphorus helps calcium through the cell membrane by increasing the permeability of the cell membrane via oxygen displacement. 1. Phosphorus is responsible for growth and development by way of: ✓ bonding ✓ polymer function ✓ hydration ✓ chemical transport, and ✓ buffering 2. Phosphorus is also responsible for bone formation 3. Phosphorus and metabolism of glucose Phosphorus is also required for the metabolism of glucose via phosphorylation. Phosphorylation is when a phosphate radical promoted by glucokinase in the liver, or hexokinase in other cells captures the glucose and once inside the cells keeps it there. The exception to this occurs in the liver, the kidneys, and the intestinal epithelial cells. Ingestion of carbohydrates causes phosphorus to enter RBC’s with glucose causing a reduction of serum phosphorus levels and lipids. Phosphorus also works in the stomach to stabilize sugars and activate starches by the twofold process of phosphorylation. Phosphorylation and its counterpart, dephosphorylation, turn many protein enzymes on and off, thereby altering their function and activity. By altering pepsin/HCL levels phosphorus can: a. Stabilize simple sugars-simple sugars are easily oxidized (combusted) before they reach the liver, resulting in low sugar levels. Pepsin stabilizes these simple sugars, so they can be transferred to the liver for storage. b. Activation of starches- HCl is necessary to breakdown oily carbohydrates (grains), which are difficult to oxidize (combust). Thus making them readily available for oxidation. The above two mechanisms establish an HCl-pepsin balance in the stomach for proper pH digestion. The presence of both HCl and pepsin in the stomach are critical for preparing carbohydrates, as well as proteins for further digestion in the small intestines. 4. The regulation and maintenance of the acid-base balance in the body by maintaining glandular acidity. 5. The storage and transfer of energy from one part of the body to the other. 6. Used in the Production of phospholipids (90 % produced by the liver): lecithin, A cephalin, and sphingomyelin Phospholipids are necessary for: Proper brain function (sphingomyelins) Phospholipids are a major constituent of lipoproteins which can affect function, formation and transport of these lipoproteins causing serious cholesterol abnormalities Production of cell membranes Thromboplastin production produced from A cephalin 7. Intracellular phosphorus is used for: Energy transport formation of ATP from ADP and creatine phosphate via oxidative phosphorylation. Major constituent of plasma membranes (phospholipids) Major constituent of DNA and RNA (nucleic acids) Calcium transport and osmotic fluid pressure General nutritional considerations when phosphorus is high: 1. Patient should increase water intake 2. Reduce fat intake 3. Reduce Vitamin D intake if overdosing 4. An isotonic saline solution (sea salt) will decrease phosphorus levels 5. Also, decrease phosphorus in the diet and add calcium carbonate to your diet General considerations when phosphorous is low: 1. Vitamin D deficiency 2. Calcium deficiency 3. Magnesium deficiency 4. Patient needs a high protein diet	270
Magnesium Magnesium MAGNESIUM Serum magnesium constitutes only a small fraction of the total body stores and may not predict magnesium status correctly. From a physiologic perspective, magnesium directs protein digestion, by polarizing minerals associated with protein digestion, from the entrance of protein into the body to its final deposition in the cell. Approximately 40-60 % of the magnesium is found in the skeleton for bone formation, 20% is found in the muscle, 30% is found in the intracellular cytoplasm, with only 1 % of the magnesium found in the serum. Magnesium affects membrane permeability, nerve impulses, muscle contraction, intracellular fluid regulation, activation of enzyme systems, where magnesium acts as a metallic cofactor in over 300 enzymatic reactions. Regulates protein synthesis, carbohydrate metabolism, nucleic acid synthesis, and blood viscosity. Magnesium along with sodium, potassium and calcium regulate neuromuscular irritability and the mechanism for clotting. Less then 2% of calcium, magnesium and phosphates are found in the plasma and extracellular fluid and are controlled in narrow limits. Albumin accounts for 70% of the bound calcium. Magnesium also binds to albumin and since it has a lower specificity for the receptors it creates more free magnesium in the plasma. Magnesium and calcium are very much linked in their body functions and a deficiency in either one will have an adverse affect on the other. Especially since calcium needs magnesium to be absorbed thru the intestinal membrane as well as needing magnesium for calcium metabolism. For example, a magnesium deficiency will cause calcium to migrate out of the bone and into soft tissues such as the aorta and kidneys. 95% of all magnesium that is filtered thru the glomerulus is reabsorbed by the tubules where parathormone enhances tubular reabsorption of magnesium. When there is a deficiency of magnesium you will see a decrease in urine stores before serum stores. Please note that even when magnesium is in a 20% depleted state, magnesium levels in the serum will appear normal. Calcium, magnesium and phosphates continuously enter the plasma via the kidney, the intestinal brush borders, and the ruffled border from the bones. Steady states of calcium, magnesium, and phosphorus approximate urine loss against intestinal absorption and skeletal mineral apposition against mineral absorption. Magnesium in the cells is complexed to phosphates, citrates and anions such as ATP, AMP and ADP (such as MgATP2-) Magnesium also plays a key role in the hormonal regulation of insulin, estrogen and thyroid hormones. Magnesium also stimulates secretions from the parathyroids and adrenal cortex (corticosteroids). Magnesium is also affected just the way calcium is to parathormone (enhances distal tubular reabsorption of magnesium) and to a lesser degree calcitonin. In fact, calcium, magnesium, and phosphates are depressed in vitamin D deficiencies and increased with vitamin D excess. Magnesium is used in the treatment of elevated cholesterol and triglycerides, muscular contraction, hypertension (A causal relation between decreased Mg2+ content of cardiac muscle/coronary arteries and nonocclusive sudden-death ischemic heart disease has been proposed) and premenstrual syndrome. Magnesium is indicated in collagen and connective tissue diseases, inflammatory disorders, migraines, general endocrine function and neurological and psychosomatic disorders.	-80
Total Protein Total Protein TOTAL PROTEIN Total proteins are divided into two fractions: albumin, and globulin (alpha, beta, and gamma). Please note that total protein also includes fibrinogen. Therefore total protein is made up of albumin, globulin and fibrinogen, all produced in the liver. These are the plasma proteins necessary to produce enzymes, antibodies, clotting factors, kinin precursors, and transport substances for hormones, vitamins, minerals, fats, etc. For example, plasma proteins combine with cholesterol forming lipoproteins such as VLDL, LDL’s, HDL’s etc. The lipoproteins then combine with minerals via enzyme metabolism to form and renew sex hormones such as testosterone, estrogen, progesterone etc. Other deaminated proteins produced in the liver, combusts at the mitochondrial level to form cell structures. These are your tissue building proteins known as nucleoproteins, DNA and RNA (your proteins of mitosis and meiosis). Since there are many glands involved in protein digestion, it is very difficult to make a determination from total protein alone. Glands and organs involved with protein control are as follows: The anterior pituitary, which controls all glands of protein digestion, such as the adrenals, thyroid, pancreatic head, sex organs, and spleen That parotid glands which tag lipoproteins with copper The parathyroids via the calcium/magnesium mobilization of lipoproteins The thyroid which denitrifies protein in the liver The pancreas by trypsin and chymotrypsin which, prepares the protein for assimilation into the bloodstream The sex organs that prepare protein for final deposition into the cells * Any combination of the above TOTAL PROTEIN IS LOW WHEN General considerations: o Increase protein intake o Increase B acid vitamins	20
Albumin Albumin ALBUMIN In pathological levels albumin is used to evaluate: 1. Liver and renal disease 2. Blood osmotic pressure 3. Chronic disease states, which most patients have 4. Dehydration 5. Albumin decreases in acute inflammatory infectious processes From a physiological standpoint, albumin is produced in the liver and is a primary byproduct of sterols and waxes. Its function is used to build and repair tissue. Albumin is responsible for 80 percent of the colloidal osmotic pressure between body tissues and blood cells. 75% of this control occurs inside the cells since most of the protein is intracellular. When you have a decrease in albumin, the osmotic pressure becomes disturbed resulting in fluid transfer and edema. Since albumin influences water movement, it will also influence nutrient and mineral movement. Albumin creates the permeability of the membrane to the osmolarity of the membrane. Therefore, substances can pass from a lesser concentration to a greater concentration. The flow is from the arterial capillaries to extracellular fluid, then from the extracellular fluid to the intracellular fluid, then from the intracellular fluid to the mitochondria. Then back via the same pathway in reverse via osmotic absorption into the veins. Albumin is also a part of a complex buffer system, which accounts for 75% of things that need to be buffered to maintain acid-alkaline balance in the body. The most powerful buffer system out of the four including, the bicarbonate system (HCO3-), the phosphate buffer system, and the liver (nitrogen/urea), the proteins of the cells and plasma, rein supreme. The protein buffer system works by controlling blood Hydrogen (H+) ion homeostasis. Both intracellular and extracellular proteins have negative charges and can serve as buffers for alterations in hydrogen ion concentration. However, because most proteins are inside cells, this primarily is an intracellular buffer system. Hemoglobin (Hb) a globular protein is an excellent intracellular buffer because of it's ability to bind with Hydrogen ions forming a weak acid and carbon dioxide (CO2) bond. After oxygen is released in the peripheral tissues, hemoglobin binds with CO2 and H+ ions. As the blood reaches the lungs these actions reverse themselves. Hemoglobin binds with oxygen, releasing the CO2 and H+ ions. The H+ ions then combine with bicarbonate (HCO3) ions to form carbonic acid (H2CO3). The H2CO3 breaks down to form water (H2O) and carbon dioxide (CO2), which are excreted via expiration through the lungs. Increases in albumin cause arteries to sclerose and a decrease in albumin causes veins to sclerose. Albumin is also a transporter of minerals and accounts for 70% of the bound calcium. Magnesium also binds to albumin and since it has a lower specificity for the receptors it creates more free magnesium in the plasma. Calcium, magnesium, and phosphates continuously enter the plasma via the kidneys, the intestinal brush borders and the ruffled border of the bone. Albumin is also responsible for transporting copper, zinc, and nickel. By controlling the transport of these minerals, albumin is the carrier of choice. The following glands are associated with albumin: 1. The parotids 2. The head of the pancreas 3. The endo-reticular portion of the liver 4. Kidneys Therefore, the function or malfunction of anyone of those glands/organs or combinations thereof can lead to imbalances in albumin levels.	-30
Globulin Total Globulin Total GLOBULIN Organs that are responsible for globulin production are the liver, thyroid, spleen and the rest the immune system. There are four types of globulins alpha 1,2, beta and Gamma. There a few groups of gamma globulins with one group being the immunoglobulins (IgA, IgG. IgM), which produce our antibodies. The thymus produces α and β globulins know as thymoglobulin using Vitamin T and copper for its production. The thyroid produces thyroglobulins that form thyroxin and triiodothyronine via vitamin K and iodine. The spleen produces spleenoglobulins that require vitamin E and iron for its production. Globulin also acts as a polarized colloidal substance necessary for specific glandular hormonal function by acting as a transport mechanism for many hormones such as sex hormone binding globulin. Globulin also assists in: Toxin neutralization by binding soluble antigens in the blood and intracellular spaces Red blood cell production Antibody formation Protection of the gastrointestinal mucosa And is also necessary via the intrinsic factor for digestion and absorption. Globular proteins can be affected via: Nutrition- lack of protein Liver Thyroid Spleen Thymus	15.79
A/G Ratio A/G Ratio A/G RATIO The A/G ratio is the ratio of albumin to globulin, and along with fibrinogen (produced by the liver) literally measures the thickness or “collagen factor” of the blood. The A/G ratio then is also a representation of the fibrinogen content in the blood and regulates the amount of protein being utilized at any time in the body. The liver forms prothrombin, which requires vitamin K. for its production. Prothrombin is a plasma protein, which is changed into thrombin via prothrombin activator and calcium. Thrombin, transposes fibrinogen into fibrin, continually causing clotting throughout the body along with blood platelets. Fibrinogen, therefore, provides the clotting thickness (collagen factor) in the blood. These polarized protein fibrous strands are necessary to maintain blood viscosity, which regulates the amount of capillary exchange from the artery to the extracellular fluid. Collagen a protein strand (albuminoid) and proteoglycan filaments also regulate exchange by causing a very slow diffusion of molecules via kinetic motion moving substances through the extracellular fluid either to the cell membrane or back into the circulatory or lymphatic systems. Collagen is also the main structural protein in connective tissue and found in the extracellular spaces. Collagen and proteoglycan filaments are used in the interstitium to provide tensile strength and for healing. As the main component of connective tissue, it makes up from 25% to 35% of the whole-body protein content. Collagen is formed in the sternum and iliac crest. A/G RATIO IS INCREASED WHEN Anything that would decrease globulin would increase the A/G ratio and anything that would increase albumin would also increase the A/G ratio so also look at all the possibilities under low globulin or high albumin THE A/G RATIO IS DECREASED WHEN Anything that would increase globulin would decrease the A/G ratio and anything that would decrease albumin would decrease the A/G ratio so also look at all the possibilities under high globulin or low albumin	1645.45
Bilirubin, Total Bilirubin, Total TOTAL BILIRUBIN Bilirubin comes from the breakdown of hemoglobin and is the byproduct of hemolysis. Bilirubin is produced by the RE portion of the liver and is excreted with the bile. Pathologically elevations in total bilirubin occur when there is a massive amount of destruction of RBC’s, or the liver is congested and unable to excrete bilirubin. From a physiologic perspective, the components of bile are inositol, choline, lecithin, cholesterol, and bilirubin/biliverdin. Cholesterol, which is produced by the liver, is converted into bile salts via the influence of the adrenal glands. The bile salts are converted into cholic acid or chenodeoxycholic acid equally. Approximately 60 percent of all cholesterol is converted into these two acids. These acids then combine with glycine and taurine to form glyco and tauro conjugated bile acids. The salts of these acids are secreted in the bile. These salts do two things: 1. They act like "soap" creating saponification and emulsification of fat. This decreases the surface tension of the fat allowing agitation to break the fat up into smaller sizes. 2. Bile salts help absorb fatty acids, monoglycerides, cholesterol, and other lipids, by forming minute complexes called micelles. Micelles are highly soluble, highly charged, and easily absorbed, increasing absorption by 40 percent. The liver secretes about 600-1,200 milliliters of bile per day. The purpose of bile is to: 1. Digest, emulsify and absorb fats. 2. To excrete waste products, such as excessive cholesterol, and bilirubin, which is the end product of hemoglobin degradation. Bilirubin is the predominant pigment of bile, and is formed from hemoglobin, and destroyed red blood cells. The red blood cells are destroyed by the reticulo-endothelial system (liver and spleen), including the kupfer cells of the liver. If the spleen/liver are hyperactive, the bile production is increased. This allows the passive function of bile production to elevate. As the spleen, liver, and bone marrow destroy hemoglobin it passes into the bloodstream with a protein creating a colloidal state. This creates hemolytic jaundice when there is excessive destruction or impaired production of red blood cells, leading to excessive amounts of prehepatic bilirubin. The liver cells are unable to withdraw the bilirubin from the blood as fast as it is formed. Therefore consequently there is an increase in prehepatic bilirubin (indirect form). Remember total bilirubin = the direct and indirect forms. The direct is elevated in biliary obstruction, which is conjugated and reacted on by the liver. The indirect form is elevated in liver failure, which is unconjugated and not reacted on by the liver. Since the liver, spleen, adrenals and diet play a role in total bilirubin production from a physiologic perspective we must evaluate those glands as well.	-77.78
Alkaline Phosphatase Alkaline Phosphatase ALKALINE PHOSPHATASE Bone osteoblasts, liver cells, and the placenta all produce high levels of alkaline phosphatase, with some activity in the kidneys and intestines. Alkaline phosphatase is called alkaline because it aids in maintaining and works best in an alkaline pH of 9-10. From a pathological perspective, alkaline phosphatase levels rise in liver disease due to impaired excretion of this enzyme from obstruction in the biliary tract, and bone disease via increased osteoclastic activity due to bone breakdown as in cancer. From a physiological perspective alkaline phosphatase is responsible for the balancing of water, and mineral metabolism controlled by the glands below. This exchange of water and mineral metabolism occurs at the cell membranes of ligaments, tendons and disc structures. The balance is created by, setting the minerals involved with electrolyte balance into motion. These minerals, along with proper neurological control, cause the shifting of food thru the membranes. The glands responsible for this balance are as follows: • The adrenal cortex via mineralocorticoids causes excretion of sodium and potassium by the kidney. • The adrenal medulla via epinephrine and norepinephrine increase metabolism, and cellular exchange via the chloride shift at the level of the membrane. • The posterior pituitary via antidiuretic hormone and its effect on potassium (oxidizer) and the water content within the cell. • Prostate/uterus via selenium acts as an oxidative mineral to insure proper membrane exchange in conjunction with the above. Alkaline phosphatase is a member of a family of zinc metalloprotein enzymes whose purpose is to split off a terminal phosphate group from an organic phosphate ester. Enzyme activity is localized in the brush border of the proximal convoluted tubules of the kidney, intestinal mucosal epithelial cells, hepatic sinusoidal membranes, vascular endothelial cells and osteoblasts of bone as mentioned above. It is the introduction of an alkaline media for bone growth. When there is an increased alkaline phosphatase you have too much acidity. In “bone pathology” there is usually a hyper-acidic state, since the foundation of a cell, is nucleic acid. The nucleic acid is composed of phosphoric acid. Phosphoric acid is a component of alkaline phosphatase, therefore, the adrenals regulate the acid/alkaline balance for energy, and growth. Alkaline phosphatase controls the alkaline substance, which controls energy, and the acid substance, which controls growth. Over the years, the laboratory low range has been steadily decreasing from 60, down to 40 now down to the mid 20's. Since this test does measure metabolic output of the adrenals, going to low is not the answer. I recommend that the low range is 70.	-66.32
LDH LDH LACTIC ACID DEHYDROGENASE Lactic acid dehydrogenase is found chiefly in the heart, skeletal muscles, kidneys, and liver, as well as all cells. In pathological states, elevated levels indicate damage to the above areas and is used to determine myocardial and pulmonary infarction. In physiological states, LDH catalyzes the conversion of pyruvate ( the final step in glycolysis) to lactate and back, as it converts NADH to NAD+ and back. A dehydrogenase is an enzyme that transfers a hydride from one molecule to another. When sugar and water (fatty acid metabolism) are exchanged across a muscle cell interface, a by-product called lactic acid is produced. When lactic acid combines with the carbon dioxide of the venous blood you have a hydrogen displacement. Lactic acid now becomes lactic acid dehydrogenase. Lactic acid dehydrogenase, therefore, is a glycolytic enzyme that functions as a catalyst in carbohydrate metabolism to produce energy. The pancreas via insulin and the posterior pituitary via ADH are responsible for this sugar and water exchange across the muscle cell interface. Lactic acid dehydrogenase indicates the active exchange of sugar across the membrane (muscle cell interface) utilizing chloride, zinc, and selenium. The utilization of these minerals creates glycolysis. LDH then from a physiological perspective determines pancreatic function regulating the amount of glucose into muscle. It is also important to note that sugar metabolism is very complex and does involve a series of other organs. Ranges for LDH are between 0-220; again it is rather obvious that LDH is a by-product of sugar metabolism and a 0 figure could not be construed as a low normal range. I feel that the range should start at 80. You will find many patients with a low LDH having problems with decreased function causing heart, skeletal muscle (weakness, loss of strength, muscle wasting), kidney and liver dysfunction, and eventual wasting away of these organs.	62.86
AST (SGOT) AST (SGOT) SERUM GLUTAMIC OXALACETIC TRANSAMINASE (SGOT) (AST) SGOT is highly concentrated in organs and glands of high metabolic activity and in descending order: heart, liver, skeletal muscle, brain, kidneys, pancreas, spleen and lungs. In pathological states, when you have high levels it means that cell damage has occurred in one or more of these areas and there is a release of this enzyme in circulation, elevating in 12 hours and remaining there for 5 days. In physiologic states, we know it is a tissue enzyme present in tissues of high metabolic activity, and concerned with the transfer of nitrogen between aspartic acid, and alpha-keto-glutamic acid, resulting in the synthesis of glutamic acid, alpha keto acid and oxalacetic acid. SGOT, therefore, is the catalyst that creates amino acid metabolism during glycolysis, for the production of energy. Since there are high concentrations of SGOT in skeletal muscle/heart, and the brain, it gives you an idea of the metabolic output of each system. The sex organs via the output of testosterone, estrogen, progesterone (which are formed on the gonadal epithelium by binding cholesterol to protein) are used to maintain muscle mass and strength. Therefore having a dramatic effect on muscle and nerve metabolism. Since amino acid metabolism also affects muscle mass, muscle strength, and the energy to fuel the muscular system, it is apparent that SGOT is the indicator of choice. Not to mention the energy necessary to run the central nervous system which utilizes 60 percent of the available energy necessary to run your body. Please note that most lab ranges start at 0 and since this is a measurement of the metabolic activity of the above organs 0 would mean death. The low range for SGOT should be 15. You will find physiological conditions where there are low levels of SGOT (15-20). This is due to the exhaustion of the above organs. Low levels indicated heart, skeletal muscle and diminished brain function/damage. These patients are usually physically weak/exhausted whether they exercise or not, lack mental clarity, cannot think straight and have brain fatigue/fog. They also have sex hormonal problems and require HRT or erectile dysfunction treatment. Many of these patients have a weak flabby heart, setting the stage for many types of conditions down the road. Low levels may also mean decreased liver function affecting, protein synthesis, detoxification, sluggish metabolism, cholesterol production to name a few of the 500 know liver functions.	25.71
ALT (SGPT) ALT (SGPT) SERUM GLUTAMIC PYRUVIC TRANSAMINASE (SGPT) (ALT) SGPT is primarily a liver function test. It has a maximum concentration in the liver (fatty membranes) sinusoids. Low concentrations of SGPT are also found in the kidneys, heart, and skeletal muscle. In pathological states, elevations indicate liver disease. ALT is found in serum and in various bodily tissues but is most commonly associated with the liver. It catalyzes the transfer of an amino group from alanine to alpha-ketoglutarate, and the products of this reversible transamination reaction being pyruvate and glutamate. glutamate + pyruvate ⇌ alpha-ketoglutarate + alanine Alanine transaminase delivers skeletal muscle carbon and nitrogen in the form of alanine to the liver. In skeletal muscle, pyruvate is transaminated to alanine, thus affording an additional route of nitrogen transport from muscle to liver. In the liver, alanine transaminase transfers the ammonia to A-KG and regenerates pyruvate. The pyruvate can then be diverted into gluconeogenesis. This process is referred to as the glucose-alanine cycle. The glucose-alanine cycle is used primarily as a mechanism for skeletal muscle to eliminate nitrogen as the muscles replenish their energy supply. Within the liver, alanine is converted back to pyruvate and is then a source of carbon atoms for gluconeogenesis. The newly formed glucose can then enter the bloodstream for delivery back to the muscle. The amino group transported from the muscle to the liver, in the form of alanine, is converted to urea in the urea cycle and then excreted. In physiological states SGPT is a primary kreb cycle expressant and as a result causes the release of catabolic fats. SGPT occurs in serum as a consequence of substances being released by the fatty membranes of the liver sinusoids, and lymphatic ducts. The liver sinusoids store food, and the lymphatic ducts house toxins. Picture a layer of fat that holds foods or toxins in the cell. Now as that layer of fat is being burned off, foods and toxins are being released in a controlled manner. This allows foods or toxins to be directed to their next destination. Please note that most lab ranges for this test start at 0, which in actuality is false since this is a measurement of liver function, and 0 would mean that the liver was not functioning at all. A low range then should be around 15. Therefore, from a physiological perspective, a low SGPT between 15-20 would indicate a sluggish liver causing many metabolic disturbances. Typically these people have no energy, get sick a lot, cannot tolerate food well and have a slow metabolism.	31.43
GGT GGT GAMMA GLUTAMYL TRANSPEPTIDASE (GGT) Is a biliary enzyme useful in the diagnosis of obstructive jaundice, intrahepatic cholestasis and pancreatitis. GGT is more responsive to biliary obstruction than are aspartate aminotransferase (AST) (SGOT) and alanine aminotransferase (ALT) (SGPT). 1. GGT is increased in hepatoma and carcinoma of the pancreas and useful in the diagnosis of metastatic carcinoma of the liver. Increasing levels in carcinoma patients relate to tumor progression and a dubious outcome. 1. CEA, alkaline phosphatase and GGT together are useful markers for hepatic metastasis from the breast and colon. 2. May be useful in the diagnosis of chronic alcoholic liver disease. Follow-up blood chemistries of serum GGT, AST and ALT levels can distinguish recovering alcoholics who resume drinking from those who do not. 3. Increase in body mass correlates with increased GGT levels. 4. GGT along with MCV is a useful test for alcoholism. 5. GGT is the test of choice for pregnant females who may have cholestasis. 6. GGT levels are elevated in cirrhosis and hepatitis. 7. The transaminases, AST and ALT rise higher in acute viral hepatitis; then GGT. 8. Increased in systemic lupus erythematosus GGT IS HIGH WHEN General considerations: If patient has been on a very low-fat diet for long periods of time then increase fat intake	-40
Ferritin Ferritin A ferritin test can help a doctor determine if a person has enough iron in their body. Low ferritin levels can indicate that the body doesn't have enough iron, while high levels can indicate too much iron. FERRITIN Men 20-250 ng/mL 20-250 ug/L Women 10-120 ng/mL 10-120 ug/L Children 7-140 ng/mL 7-140 ug/L Newborns 25-200 ng/mL 25-200 ug/L	-16.4
Total Iron Total Iron Total Iron Binding Capacity (TBIC)—measures the amount of transferrin, which is a blood protein that transports iron from the digestive system to cells that will be utilizing the iron. Your body produces transferrin in relationship to the body’s need for iron. When iron stores are low, transferrin levels will increase and when transferrin levels are low, too much iron is present. Usually, about one third of the transferrin is being used to transport iron at any one time. Because of this, your blood serum has considerable extra iron-binding capacity, which is called the Unsaturated Iron Biding Capacity (UIBC). The TIBC then equals UIBC plus serum iron measurement. Some laboratories may measure UIBC, some measure TIBC and others measure transferrin. TIBC is increased in iron- deficiency, acute hepatitis, during pregnancy or when oral contraceptives are used. TIBC is decreased in hypoproteinemia from many causes, cirrhosis of the liver, nephrosis and thalassemia or from a number of inflammatory states. TOTAL IRON IRON Men 65-175ug/dL 11.6-31.3 umol/L Women 50-170ug/dL 9.0 -30.4 umol/L Children 50-120ug/dL 9.0-21.5 umol/L Newborns 100-250 ug/dL 17.9-44.8 umol/L	-40
Cholesterol, Total Cholesterol, Total SERUM LIPIDS Serum lipids serve as a primary source of energy along with glucose. The functions are many, such as the production of cell membranes, precursors to hormones, and bile acids. Lipids are first broken down in the duodenum, along with bile, which emulsifies the fats, and prepares them for absorption into the lymphatic system. Pancreatic lipase hydrolyzes cholesterol, and triglycerides into fatty acids, and glycerol. The fatty acids and glycerol are then reconverted back into triglycerides by the intestinal cells and then discharged into the lymphatic or portal blood system, which is then sent to the liver. Cholesterol is also absorbed in both the free and esterified forms into the lymphatics. Cholesterol is also synthesized in the reticular cells and histiocytes throughout the body but mainly formed in the liver. Under the influence of iodine via the thyroid, carbohydrates, amino acids, and other fats are converted to cholesterol via multiple molecules of acetyl coenzyme A creating a sterol nucleus. Triglycerides are also assembled in the liver from glycerol and fatty acids. The liver is the main organ regulating blood lipids. So the liver can degrade fatty acids for energy, synthesize triglycerides from carbohydrates and proteins. The liver can then hydrolyzes the triglycerides back into three fatty acids, and glycerol then degrades the fatty acids into acetyl coenzyme A via beta-oxidation. Then acetyl coenzyme A is then oxidized to release ATP. The liver also synthesizes phospholipids, lecithin, cephalins (that produce thromboplastin), and sphingomyelin (produces the myelin sheath) are formed in the liver and transported via lipoproteins. An increase in triglycerides or choline/inositol increases phospholipid production. Phospholipids are also important in the production of cell membranes. CHOLESTEROL Cholesterol is a byproduct of protein metabolism. Bonding oily fat (fat-soluble vitamins) to nitrogen via oxidation forms cholesterol. This process utilizes vitamins, D, E, K, A, and T. These are your fat-soluble vitamins that are bound to the nitrogen portion of foods. The basic purpose of fat-soluble vitamins is to lubricate membranes. The vitamin (oil) prevents oxygen from reaching the membrane, which may inhibit its function. Fat-soluble vitamins also provide the substance necessary to make hormones, enzymes, and antibodies. For example, Vitamin D. lubricates all gross membranes that are exposed to air, such as your skin, respiratory passages, and the digestive membranes. This is your antioxidant lubricator Vitamin A. lubricates secondary membranes that are exposed to the blood, such as the liver, kidney, lungs and spleen. Vitamin A. is called your hydrogen lubricator. Vitamin K. lubricates cell membranes that are exposed to water. Vitamin F. fatty acids are used to make enzymes. Vitamin E. is used to make hormones. Vitamin T. which, is sesame seed oil, is used to make antibodies Lecithin prevents oil and fat from going rancid. So the purpose of fat-soluble vitamins is to oxidize and combust with protein to form cholesterol, which then transposes it into a lubricator, a hormone, antibody, or enzyme. Low-density lipoproteins are rich in cholesterol and carry some triglycerides and are used to produce sex hormones. High-density lipoproteins are rich in triglycerides and carry some fat. Please note that at any one time, the body can dictate the percentage of low-density lipoproteins vs. high-density lipoproteins. It's obvious that an imbalance can create multiple diseases in the body. Please note that these lipoproteins also engulf toxins and then are stored in tissue cells. At a later time, the body gradually detoxifies these deposits unless the amount is overwhelming. Similar to glucose, cholesterol is affected by many organs and glands and in itself is not a reliable indicator as to what is going on in the body. Over the years, the labs went from a normal cholesterol reading of 300, down to 250, then down to 200, and now down to 150. If they continue this nonsense they will create a whole new list of diseases. I recommend that your cholesterol levels be between 175-275mg/dL.	-192
Triglycerides Triglycerides SERUM LIPIDS Serum lipids serve as a primary source of energy along with glucose. The functions are many, such as the production of cell membranes, precursors to hormones, and bile acids. Lipids are first broken down in the duodenum, along with bile, which emulsifies the fats, and prepares them for absorption into the lymphatic system. Pancreatic lipase hydrolyzes cholesterol, and triglycerides into fatty acids, and glycerol. The fatty acids and glycerol are then reconverted back into triglycerides by the intestinal cells and then discharged into the lymphatic or portal blood system, which is then sent to the liver. Cholesterol is also absorbed in both the free and esterified forms into the lymphatics. Cholesterol is also synthesized in the reticular cells and histiocytes throughout the body but mainly formed in the liver. Under the influence of iodine via the thyroid, carbohydrates, amino acids, and other fats are converted to cholesterol via multiple molecules of acetyl coenzyme A creating a sterol nucleus. Triglycerides are also assembled in the liver from glycerol and fatty acids. The liver is the main organ regulating blood lipids. So the liver can degrade fatty acids for energy, synthesize triglycerides from carbohydrates and proteins. The liver can then hydrolyzes the triglycerides back into three fatty acids, and glycerol then degrades the fatty acids into acetyl coenzyme A via beta-oxidation. Then acetyl coenzyme A is then oxidized to release ATP. The liver also synthesizes phospholipids, lecithin, cephalins (that produce thromboplastin), and sphingomyelin (produces the myelin sheath) are formed in the liver and transported via lipoproteins. An increase in triglycerides or choline/inositol increases phospholipid production. Phospholipids are also important in the production of cell membranes. TRIGLYCERIDES Triglycerides compromise 95% of fat stored in adipose tissue and stored as glycerol, fatty acids, and monoglycerides. The liver reconvert's these back to triglycerides. 80% of your triglycerides make up VLDL, and 15% form LDL’S. From a pathological viewpoint, this test evaluates atherosclerosis and measures the bodies ability to utilize fat. From the physiologic perspective, triglycerides are nothing more than three fatty acids, and esters of glycerol. Fatty acids are composed of sugar and alcohol. Triglycerides travel with cholesterol (LDL/HDL) to combust cholesterol at the appropriate time.Triglycerides are needed for calculation of LDLC (low-density lipoprotein cholesterol) concentration. Triglycerides are the matches or “the spark” that ignites and combusts the cholesterol. Triglycerides are implanted in the cell membrane of all neurological and glandular tissue. Triglycerides create the energy for a neurological impulse to occur. When the neurological impulse occurs triglycerides actually “explode” causing the active exchange of electrolytes. Primary glands involved in triglyceride metabolism are the posterior pituitary, the hypophyseal stalk, adrenals, and the head of the pancreas.Therefore, any condition affecting these organs can affect triglyceride levels. High levels are a greater risk for a heart attack then a high cholesterol. Low triglyceride levels from the physiologic perspective cause low energy. Triglycerides Normally Range From 0-199. It Is Rather Obvious That 0 Triglycerides Could Not Be Achieved Physiologically. My Ranges Are From 75-200 mg/dL	66.4
TSH TSH T-4, T-3, T3 uptake and TSH Thyroid-stimulating hormone (TSH) from the anterior pituitary, stimulates the production of thyroxin, and triiodothyronine, therefore, having a dramatic effect on the T4/T3 test results. Thyrotrophs makeup 5% of the anterior pituitary and produce between 100-400mU/day of TSH. Circadian peaks with the onset of sleep are between 9 pm-5am and a minimum between 4-7pm. TSH is regulated by an open feedback loop via thyroxin whereby thyroxin passes into the CSF of the lateral ventricles and is taken up by the epithelial cells of the choroid plexus, which when thyroxin levels are low, stimulates TRH-secreting neurons in the hypothalamus. TSH does the following: 1. Stimulates phospholipid metabolism 2. Stimulates purine and pyrimidine precursors and their incorporation into nucleic acids. T-4 and 3 indicate the denitrification power of iodine via thyroxin with T3 being much more powerful than T4. All food contains active biological nutrients that are bound with nitrogen. When this food reaches the liver, the iodine is used to cleave the nitrogen from the nutrient. Therefore, thyroxin and T3 are important in fat and protein digestion, absorption, and growth and endocrine function. This catabolic activity begins once aerobic bound substances become totally anaerobic and lose the need for nitrogen bonding. Nitrogen is cleaved by T3 or T4 in the liver for example as in glycogen storage. Other substances are needed by specific cells and are transported via total binding globulin to the cells where at that point, the nitrogen bonds are cleaved. Less than 1% of T3 is unbound. A high T-3 uptake indicates a hypothyroid, where a low T-3 uptake indicates a hyperthyroid.	-118.96
Thyroxine (T4) Thyroxine (T4) T-4, T-3, T3 uptake and TSH Thyroid-stimulating hormone (TSH) from the anterior pituitary, stimulates the production of thyroxin, and triiodothyronine, therefore, having a dramatic effect on the T4/T3 test results. Thyrotrophs makeup 5% of the anterior pituitary and produce between 100-400mU/day of TSH. Circadian peaks with the onset of sleep are between 9 pm-5am and a minimum between 4-7pm. TSH is regulated by an open feedback loop via thyroxin whereby thyroxin passes into the CSF of the lateral ventricles and is taken up by the epithelial cells of the choroid plexus, which when thyroxin levels are low, stimulates TRH-secreting neurons in the hypothalamus. TSH does the following: 1. Stimulates phospholipid metabolism 2. Stimulates purine and pyrimidine precursors and their incorporation into nucleic acids. T-4 and 3 indicate the denitrification power of iodine via thyroxin with T3 being much more powerful than T4. All food contains active biological nutrients that are bound with nitrogen. When this food reaches the liver, the iodine is used to cleave the nitrogen from the nutrient. Therefore, thyroxin and T3 are important in fat and protein digestion, absorption, and growth and endocrine function. This catabolic activity begins once aerobic bound substances become totally anaerobic and lose the need for nitrogen bonding. Nitrogen is cleaved by T3 or T4 in the liver for example as in glycogen storage. Other substances are needed by specific cells and are transported via total binding globulin to the cells where at that point, the nitrogen bonds are cleaved. Less than 1% of T3 is unbound. A high T-3 uptake indicates a hypothyroid, where a low T-3 uptake indicates a hyperthyroid.	84
T3 Total T3 Total T-4, T-3, T3 uptake and TSH Thyroid-stimulating hormone (TSH) from the anterior pituitary, stimulates the production of thyroxin, and triiodothyronine, therefore, having a dramatic effect on the T4/T3 test results. Thyrotrophs makeup 5% of the anterior pituitary and produce between 100-400mU/day of TSH. Circadian peaks with the onset of sleep are between 9 pm-5am and a minimum between 4-7pm. TSH is regulated by an open feedback loop via thyroxin whereby thyroxin passes into the CSF of the lateral ventricles and is taken up by the epithelial cells of the choroid plexus, which when thyroxin levels are low, stimulates TRH-secreting neurons in the hypothalamus. TSH does the following: 1. Stimulates phospholipid metabolism 2. Stimulates purine and pyrimidine precursors and their incorporation into nucleic acids. T-4 and 3 indicate the denitrification power of iodine via thyroxin with T3 being much more powerful than T4. All food contains active biological nutrients that are bound with nitrogen. When this food reaches the liver, the iodine is used to cleave the nitrogen from the nutrient. Therefore, thyroxin and T3 are important in fat and protein digestion, absorption, and growth and endocrine function. This catabolic activity begins once aerobic bound substances become totally anaerobic and lose the need for nitrogen bonding. Nitrogen is cleaved by T3 or T4 in the liver for example as in glycogen storage. Other substances are needed by specific cells and are transported via total binding globulin to the cells where at that point, the nitrogen bonds are cleaved. Less than 1% of T3 is unbound. A high T-3 uptake indicates a hypothyroid, where a low T-3 uptake indicates a hyperthyroid.	-43.33
T3 Uptake T3 Uptake T-4, T-3, T3 uptake and TSH Thyroid-stimulating hormone (TSH) from the anterior pituitary, stimulates the production of thyroxin, and triiodothyronine, therefore, having a dramatic effect on the T4/T3 test results. Thyrotrophs makeup 5% of the anterior pituitary and produce between 100-400mU/day of TSH. Circadian peaks with the onset of sleep are between 9 pm-5am and a minimum between 4-7pm. TSH is regulated by an open feedback loop via thyroxin whereby thyroxin passes into the CSF of the lateral ventricles and is taken up by the epithelial cells of the choroid plexus, which when thyroxin levels are low, stimulates TRH-secreting neurons in the hypothalamus. TSH does the following: 1. Stimulates phospholipid metabolism 2. Stimulates purine and pyrimidine precursors and their incorporation into nucleic acids. T-4 and 3 indicate the denitrification power of iodine via thyroxin with T3 being much more powerful than T4. All food contains active biological nutrients that are bound with nitrogen. When this food reaches the liver, the iodine is used to cleave the nitrogen from the nutrient. Therefore, thyroxin and T3 are important in fat and protein digestion, absorption, and growth and endocrine function. This catabolic activity begins once aerobic bound substances become totally anaerobic and lose the need for nitrogen bonding. Nitrogen is cleaved by T3 or T4 in the liver for example as in glycogen storage. Other substances are needed by specific cells and are transported via total binding globulin to the cells where at that point, the nitrogen bonds are cleaved. Less than 1% of T3 is unbound. A high T-3 uptake indicates a hypothyroid, where a low T-3 uptake indicates a hyperthyroid.
T3 Free T3 Free A free T3 test, or free triiodothyronine test, measures the amount of free triiodothyronine in your blood. Triiodothyronine (T3) is a hormone produced by the thyroid gland that helps regulate metabolism and energy levels. A normal free T3 level is typically between 2.5–4.0 ng/dL, but reference values may vary by lab. A higher-than-normal level of T3 may indicate an overactive thyroid, while a lower-than-normal level may indicate an underactive thyroid.	5.26
T4 Free T4 Free Free T4 is the amount of thyroxine (T4) in the blood that is not attached to proteins. T4 is a hormone produced by the thyroid gland that helps control metabolism and growth. A free T4 test measures the amount of free T4 in your blood.	86.21
Urine pH Urine pH URINE PH A high urine pH may be due to: Kidney failure Urinary tract infections Vomiting A low urine pH may be due to: Diarrhea Too much acid in the body fluids such as metabolic acidosis and diabetic ketoacidosis Starvation	-100
Bun/Creatin Ratio Bun/Creatin Ratio BUN/CREATININE RATIO BUN plus creatinine are residue byproducts of protein and muscle metabolism respectively. They are kept in continual balance by the water content of your body. The kidneys flush out the excessive BUN/creatinine concentration when it gets too high. The kidneys are under the influence of the posterior pituitary via antidiuretic hormone, which regulates the amount of water leaving the body. Therefore, the posterior pituitary through potassium regulates water balance. The posterior pituitary then regulates the amount of water in any one place of the body. So, therefore, it can either increase or decrease the water content in the blood, thus altering pH. The posterior pituitary besides balancing water also regulates sugar and mineral concentration. BUN/CREATININE IS HIGH WHEN General considerations: ¬ Decrease high protein intake ¬ Or increase water intake ¬ BUN/CREATININE is high when you have a high BUN or a low CREATININE or both BUN/CREATININE IS DECREASED WHEN General considerations: ¬ Increase protein intake ¬ Or decrease water intake ¬ BUN/CREATININE is low when either you have a low BUN or a high CREATININE or both	203.58
COQ10 Coenzyme COQ10 Coenzyme Coenzyme Q10 (CoQ10 also known as ubiquinone, is a natural coenzyme and an antioxidant produced by the body. It is also obtained from dietary sources, such as meat, fish, seed oils, vegetables, and dietary supplements. CoQ10 plays a role in mitochondrial oxidative phosphorylation, aidingthe production of adenosine triphosphate (ATP), which is involved in energy transfer within cells. The structure of CoQ10 consists of a benzoquinone moiety and an isoprenoid side chain, with the "10" referring to the number of isoprenyl chemical subunits in its tail. Biological function CoQ10 is a component of the mitochondrial electron transport chain (ETC), where it plays a role in oxidative phosphorylation, a process required for the biosynthesis of adenosine triphosphate, the primary energy source of cells. CoQ10 is a lipophilic molecule that is located in all biological membranes of the human body and serves as a component for the synthesis of ATP and is a life-sustaining cofactor for the three complexes (complex I, complex II, and complex III) of the ETC in the mitochondria. CoQ10 has a role in the transport of protons across lysosomal membranes to regulate pH in lysosome functions. The mitochondrial oxidative phosphorylation process occurs in the inner mitochondrial membrane of eukaryotic cells. This membrane is highly folded into structures called cristae, which increase the surface area available for oxidative phosphorylation. CoQ10 plays a role in this process as an essential cofactor of the ETC located in the inner mitochondrial membrane and serves the following functions: electron transport in the mitochondrial ETC, by shuttling electrons from mitochondrial complexes like nicotinamide adenine dinucleotide (NADH), ubiquinone reductase (complex I), and succinate ubiquinone reductase (complex II), the fatty acids and branched-chain amino acids oxidation (through flavin-linked dehydrogenases) to ubiquinol–cytochrome-c reductase (complex III) of the ETC: CoQ10 participates in fatty acid and glucose metabolism by transferring electrons generated from the reduction of fatty acids and glucose to electron acceptors; antioxidant activity as a lipid-soluble antioxidant together with vitamin E, scavenging reactive oxygen species and protecting cells against oxidative stress, inhibiting the oxidation of proteins, DNA, and use of vitamin E.			10
Fibrinogen Fibrinogen FIBRINOGEN- BLOOD TEST RANGES 200 and 400 mg/dL (2.0 to 4.0 g/L) (coagulation factor I) is a glycoprotein complex that is synthesized by the liver and circulates in the blood stream. During tissue and or vascular injury, it is converted enzymatically by thrombin to fibrin which creates a blood clot The primary function is to occlude blood vessels thus stopping bleeding. Fibrin also binds and reduces the activity of thrombin. This activity referred to as antithrombin I, which limits clot formation. Fibrin also mediates and is important in blood platelet, endothelial cell spreading, capillary tube formation, tissue fibroblast proliferation, and angiogenesis thereby promoting revascularization and wound healing. Thrombin is synthesized in the liver and secreted into the general circulation in an inactive zymogen form (prothrombin), a complex multidomain glycoprotein that is activated to yield thrombin at sites of vascular injury by limited proteolysis following upstream activation of the coagulation cascade.			10
LPA LPA LPA- BLOOD TEST LEVELS 30-50 mg/dL (75-125 nmol/L Lipoprotein (a) or Lp(a) levels are measured in milligrams per deciliter (mg/dL) or nanomoles per liter (nmol/L). A lipoprotein(a) (Lp(a)) blood test measures the amount of Lp(a) in your blood, which is lipoprotein that carries cholesterol. Thus elevated Lp(a) levels are associated with an increased risk of cardiovascular disease. Recommended for individuals with a family history of heart disease or other risk factors. High levels of lipoprotein (a) (Lp(a), may cause heart attack, stroke, and or aortic stenosis LPA is produced through multiple mechanisms within cells and in biological fluids like plasma and serum. Lysophosphatidic acid (LPA) is primarily produced by the enzyme autotaxin (ATX). ATX, which is a secreted lysophospholipase D, converts lysophospholipids, primarily lysophosphatidylcholine (LPC), into LPA. This extracellular production pathway is considered the major source of bioactive LPA.			10
Apo B Apo B Apolipoprotein B (ApoB) is a protein that plays a crucial role in the transport of fats and cholesterol in the blood. It is a key component of low-density lipoproteins (LDL) and other lipoproteins that carry triglycerides, cholesterol, and cholesterol esters. Elevated ApoB levels are associated with an increased risk of cardiovascular disease. Key aspects of ApoB: Role in Lipoprotein Formation: ApoB is a primary protein on the surface of various lipoproteins, including LDL, VLDL, chylomicrons, and lipoprotein(a). Atherogenic Particle Indicator: ApoB measurement helps determine the number of atherogenic particles circulating in the bloodstream, which are linked to plaque buildup in arteries. Cardiovascular Risk: Elevated ApoB levels are a significant indicator of increased cardiovascular risk, particularly atherosclerosis. ApoB Test: An ApoB test measures the amount of ApoB in the blood and is often used to assess the risk of heart disease. Two Forms: ApoB exists in two forms: ApoB100 (primarily in the liver) and ApoB48 (primarily in the intestine). Apo High levels of apolipoprotein B (ApoB) are often associated with elevated levels of LDL cholesterol (LDL-C) and can be caused by a variety of factors, including diet, lifestyle, underlying medical conditions, and genetics.			10
Gland Totals		5	5	50	25	10	5	5
Gland Totals (%)		50%	38%	169.5%	375.6%	24.5%	38%	16%

Results by Digestive

Gland	Result
Ileum Ileum	270%
Pancreas Pancreas THE PANCREAS The pancreas is composed of a head and a tail. The purpose of the pancreatic head is used to secrete pancreatic enzymes. The purpose of the pancreatic tail is to produce insulin. For more information check the pancreatic head and tail sections.	204%
Stomach Alkaline Stomach Alkaline THE STOMACH Phosphorus works in the stomach to stabilize sugars and activate starches by the twofold process of phosphorylation. Phosphorus in conjunction with HCl, pepsin, zinc, and vitamin C via the thymus helps in the: 1. Stabilization of sugar-simple sugars are easily oxidized (combusted) before they reach the liver, resulting in low sugar levels. Pepsin stabilizes these simple sugars, so they can be transferred to the liver for storage. 2. Activation of starches-HCl is necessary to breakdown oily carbohydrates (grains), which are difficult to oxidize (combust), thus making them readily available for oxidation. The above two mechanisms establish an HCl-pepsin balance in the stomach for proper pH digestion. The presence of both HCl and pepsin in the stomach are critical for preparing carbohydrates and proteins for further digestion in the small intestines. Phosphorus indicates the amount of acid balance in the body. It does this by regulating secretions of HCl and pepsin in the stomach by the foods you eat. For example, when you eat foods that are high in phosphoric acid, there will be a release of pepsin to neutralize the acid. On the other hand, foods low in phosphoric acid content will cause large amounts of HCl to be released. Phosphorus then carries carbohydrates across the intestinal wall for absorption by the liver. Phosphorus also affects the intrinsic factor function by releasing alkaline B vitamins into inorganic foods, converting them into organic foods for storage in the liver sinusoids. Patients that have an acid pH in their stomach should avoid excessive amounts of acid forming foods such as meats, dairy, grains and junk foods. Patients that have an alkaline pH should avoid excessive amounts of alkaline forming foods such as fruits and vegetables. Diet has a dramatic affect on the acidity or alkalinity of the stomach and is usually the culprit in stomach conditions. The 3 Phases Of Gastric Secretion 1. The Cephalic Phase- which is the result of hunger, sight, smell and thought about food neurologically controlled by the cerebral cortex that project to appetite centers in the amygdala or hypothalamus. This phase accounts for 1/5th of the digestive juices produced. 2. The Gastric Phase- when the food enters the stomach it excites long vasovagal and local enteric nerves that stimulate the release of gastric juices accounting for 2/3rds of the 1500 ml’s released daily. 3. The Intestinal Phase – once the food enters the duodenum, it triggers the release of gastrin from the intestinal mucosa thus inhibiting the release of gastric juices. The presence of food in the small intestines initiates an enterogastric reflex, which also inhibits gastric secretions. The presence of secretin and cholecystokinin are responsible for pancreatic enzyme release. Cholecystokinin releases bile via the gallbladder and also inhibits gastric function. Acids, protein by-products, gastric inhibitory peptide, vasoactive intestinal polypeptide, and somatostatin all inhibit gastric secretions. Since the stomach is poor at absorption, very little takes place. It is only when you reach the small intestines that you find folds known as valvulae conniventes, which increase the surface area of the small intestines 3 fold. Extending from these conniventes are small projections called villi, which increase the absorption another 10 fold. These villi are close together and their outer epithelial cells form a brush border protruding into the chyme. This increases the absorptive power another 600 fold. This makes the surface of the small intestines 250 sq. meters (About the size of a tennis court). The absorptive capacity of the small intestines is astounding. It can absorb several kilograms of carbohydrates, 500-1000 grams of fat (20-40 ounces), 500-700 grams (20-28 ounces) of protein, and 20 or more liters of water daily. There are four types of glands that are found in the gastrointestinal tract: 1. Salivary cells are found in the mouth, pancreas, and the liver 2. Mucous glands- Mucous contains, water, electrolytes, glycoproteins, and HCO3 ions. The function of mucous is to adhere tightly to the food while it coats the intestinal wall. Mucous prevents food from contacting the mucosa. Mucous also causes fecal particles to adhere together to form a mass. Mucous is also very resistant to digestive juices, and can buffer acids or alkaline enzymes. The esophagus also secretes mucous. The mucous glands secrete mucous in response to vagal stimulation, gastrointestinal enzymes, and irritating factors. Mucous glands that are in the upper duodenal area between the pylorus and papilla of vata are called “Brunner’s glands”. Crypts of Lieberkuhn are found in the small intestines. 3. Tubular cells- are found in the stomach and are of 2 types: the oxyntic or gastric and the pyloric. The first, oxyntic, are your parietal and chief cells. The parietal cells secrete HCl, intrinsic factor for B12 absorption, and histamine. The chief cells secrete pepsinogen, intrinsic factor and mucous. The second type of tubular gland is called the pyloric gland. The pyloric glands mainly secrete mucous but also pepsinogen and gastrin. The oxyntic glands are located in the body and fundus of the stomach comprising 80% of the stomach; the pyloric glands are found in the antral portion of the stomach. These tubular cells are also found in the upper part of the small intestines. Pepsinogen, which is not reactive, is activated and transformed into pepsin by coming in contact with HCl. Pepsin is a proteolytic enzyme that is highly reactive in an acid media between (1.8-3.5). Therefore, both HCl and pepsin are responsible for protein digestion. Other enzymes of the stomach include gastric lipase and amylase; both are extremely weak and play a minor role in the digestion of fats and starches. Gelatinase, another enzyme, is responsible for liquification of proteoglycans found in meat. The stomach also secretes intrinsic factor, which is responsible for B12 absorption in the ileum. B12 is responsible for red blood cell maturation. Gastric secretions have a pH of 1.0-3.5. 4. The stomach also secretes gastric amylase and lipase. The Neurotransmitters Affecting Gastric Secretions Are: 1. Acetylcholine-which is responsible for pepsinogen via peptic cells, gastrin via gastric cells, HCl via parietal cells and mucous secretions. 2. Gastrin (2 types G17 and G34) named for the number of amino acids that make them up, and histamine (an amino acid derivative) both stimulate HCl production. When gastric or acetylcholine are present histamine has a much stronger effect on acid production. All of these neurotransmitters activate receptor sites on secretory cells, which stimulate the secretory process. Amino acids, caffeine and alcohol can also stimulate gastric secretory activity. Neural Control Of The Gastrointestinal System The GI tract is controlled by: A. Reflex activity between the brain stem (vagus nerve dorsal motor nuclei), such as the stomach motor and secretory activity, pain and strong powerful colonic contractions. B. The spinal cord via the autonomic nervous system. The sympathetic division extends from T5-L3 forming the celiac and mesenteric plexuses and the sympathetic chain ganglion, which inhibits peristalsis and digestive secretions by the inhibition of the myenteric and submucosal plexus with norepinephrine. Usually, they control long range communication between the stomach, small intestine, ileocecal valve and the colon, by controlled slowing or speeding up of movement of food and fecal material. C. The parasympathetic outflow division originates from S1-S3 and stimulates the movement of fecal material and reabsorption of H2O and electrolytes. Remember that almost all sympathetic or parasympathetic activity is afferent in nature. This means that distention, mucosal irritation from foods, drugs, preservatives, pH etc. send afferent messages to the brain stem initiating the proper course of action to occur. D. The GI tract has its own nervous system called the enteric nervous system and is found in the gut wall extending from the esophagus to the anus (100 million neurons are the number of neurons in the spinal cord). The enteric nervous system releases the following neurotransmitters: acetylcholine, norepinephrine, ATP, serotonin, dopamine, cholecystokinin, substance P, vasoactive intestinal polypeptide, somatostatin, and leu-enkephalin. Acetylcholine stimulates intestinal activity norepinephrine inhibits intestinal activity. The enteric nervous system is composed of 2 plexuses 1. myenteric plexus (Auerbach’s) found between the circular and longitudinal fibers and controls peristaltic movement. The myenteric plexus is composed of linear chains of interconnecting neurons. When stimulated it increases: • Tonic contractions • Rhythmic contractions • Velocity of conduction • Rate of rhythm · · · Please note that the myenteric plexus does play a role in inhibition of the pyloric sphincter and the ileocecal valve. 2. Submucosal plexus (Meissner’s plexus) is found in the submucosa and is responsible for digestive secretions and blood flow. The purpose of the enteric nervous system is to control peristalsis and digestive secretions short range over small distances. This is most beneficial since the body uses a finer control over the local digestive process. Digestion And Absorption In The Gastrointestinal Tract Carbohydrate Digestion- There are 3 major sources of carbohydrates in the diet Sucrose, a disaccharide known as cane sugar Lactose, a disaccharide known as milk sugar Starches (grains), which are long polysaccharides When monosaccharides form disaccharides, hydrogen is removed from one monosaccharide and a hydroxyl group is removed from the other monosaccharide, forming water in a process (condensation). When disaccharides split into monosaccharides the process is called hydrolysis (the addition of water to form the 2 monosaccharides). Humans cannot digest cellulose. Carbohydrate digestion starts in the mouth via an alpha amylase known as ptyalin, secreted by the parotid glands. This enzyme hydrolyzes starches into maltose and other small polymers of glucose (3-9 glucose molecules long.). 3-5% of all starches are digested in the mouth. As the food enters the stomach ptyalin continues to digest the carbohydrates so that within 1 hour, upon entering the stomach, most of the carbohydrates are converted into maltose. When the pH falls below 4.0 ptyalin starts to become inactive. By the time the chyme reaches the duodenum and jejunum, pancreatic amylase, which is much more potent then ptyalin (more concentrated), converts the remaining polymers into maltose. In the lining membranes of the intestinal lumen (microvilli brush border) there are four enzymes produced: Lactase, which splits lactose into galactose and glucose Sucrase, which splits sucrose into fructose and glucose Maltase, which splits maltose into glucose. Alpha Dextrinase, which splits all of the above as well as dextrins 2. Protein Digestion-Protein digestion starts in the stomach via pepsin. Pepsin is also important for digesting collagen, an albuminoid found in meats. Pepsin is most active at a pH of 2-3. The HCl produced by the body has a pH of .8. When proteins leave the stomach they are mostly in the form of proteases, peptones, and large polypeptides. When the chyme reaches the small intestines the pancreatic enzymes trypsin and chymotrypsin split proteins into small peptides and carboxypolypeptidase then split a small percentage of these into amino acids. The bulk of the peptides are broken down by the multiple peptidases located in the brush border of the intestinal membrane. The most important peptidases are aminopolypeptidase and several dipeptidases. These split the proteins down to di and tri-peptides, which enter the microvilli membrane into the interior of the epithelial cell where other peptidases break up the remaining di and tripeptides into amino acids to be absorbed into the blood stream. Please note that di, tri, and polypeptides can still enter the blood stream and can cause allergic reactions. 99 % of all protein is absorbed as amino acids. 3. Fat Digestion The most abundant fat in the diet is in the form of triglycerides, which contains a glycerol nucleus and 3 fatty acids (stearic, and palmitic acid, which are saturated and oleic acid which is unsaturated). All 3 come from animal and not plant origin. The usual diet contains phospholipids, cholesterol and cholesterol esters. Cholesterol is formed in the liver from degraded products of fatty acid molecules, which give cholesterol its fatty characteristics. Fat (butterfat) is digested in the stomach via gastric lipase (tributyrase) in very small amounts. 99% of fat digestion takes place in the intestines via bile. Bile contains bile salts and a phospholipid known as lecithin in the form of ionized sodium salts. Bile salts have the ability to form micelles, small globules of fat attached to the bile salt. This occurs because the sterol portion of the bile salt is highly soluble in fat and a polar portion of the bile salts and lecithin are highly soluble in water. This reducing and changing the polarity reduces the interfacial tension between the fat cells so digestive enzymes can continue to break down the fat. This increases the total surface area of the fat a 1000 fold. Pancreatic lipase is responsible for splitting 99% of the triglycerides into 3 fatty acids and 2 monossachrides. Cholesterol, its ester (cholesterol +1 molecule of a fatty acid) and phosopholipids (via cholesterol ester hydrolase and phospholipidase respectively) are broken down via hydrolysis of the fatty acids from their molecular structures. The bile salts, when attached to lipids create micelles, which are highly charged and increase the absorption of these fatty acids, glycerol, free cholesterol and the remaining portion of the phospholipids. Please note that without bile salts much of the fat will be blocked from entering the blood stream.	192.67%
Cecum Cecum	133.33%
Stomach Acid Stomach Acid THE STOMACH Phosphorus works in the stomach to stabilize sugars and activate starches by the twofold process of phosphorylation. Phosphorus in conjunction with HCl, pepsin, zinc, and vitamin C via the thymus helps in the: 1. Stabilization of sugar-simple sugars are easily oxidized (combusted) before they reach the liver, resulting in low sugar levels. Pepsin stabilizes these simple sugars, so they can be transferred to the liver for storage. 2. Activation of starches-HCl is necessary to breakdown oily carbohydrates (grains), which are difficult to oxidize (combust), thus making them readily available for oxidation. The above two mechanisms establish an HCl-pepsin balance in the stomach for proper pH digestion. The presence of both HCl and pepsin in the stomach are critical for preparing carbohydrates and proteins for further digestion in the small intestines. Phosphorus indicates the amount of acid balance in the body. It does this by regulating secretions of HCl and pepsin in the stomach by the foods you eat. For example, when you eat foods that are high in phosphoric acid, there will be a release of pepsin to neutralize the acid. On the other hand, foods low in phosphoric acid content will cause large amounts of HCl to be released. Phosphorus then carries carbohydrates across the intestinal wall for absorption by the liver. Phosphorus also affects the intrinsic factor function by releasing alkaline B vitamins into inorganic foods, converting them into organic foods for storage in the liver sinusoids. Patients that have an acid pH in their stomach should avoid excessive amounts of acid forming foods such as meats, dairy, grains and junk foods. Patients that have an alkaline pH should avoid excessive amounts of alkaline forming foods such as fruits and vegetables. Diet has a dramatic affect on the acidity or alkalinity of the stomach and is usually the culprit in stomach conditions. The 3 Phases Of Gastric Secretion 1. The Cephalic Phase- which is the result of hunger, sight, smell and thought about food neurologically controlled by the cerebral cortex that project to appetite centers in the amygdala or hypothalamus. This phase accounts for 1/5th of the digestive juices produced. 2. The Gastric Phase- when the food enters the stomach it excites long vasovagal and local enteric nerves that stimulate the release of gastric juices accounting for 2/3rds of the 1500 ml’s released daily. 3. The Intestinal Phase – once the food enters the duodenum, it triggers the release of gastrin from the intestinal mucosa thus inhibiting the release of gastric juices. The presence of food in the small intestines initiates an enterogastric reflex, which also inhibits gastric secretions. The presence of secretin and cholecystokinin are responsible for pancreatic enzyme release. Cholecystokinin releases bile via the gallbladder and also inhibits gastric function. Acids, protein by-products, gastric inhibitory peptide, vasoactive intestinal polypeptide, and somatostatin all inhibit gastric secretions. Since the stomach is poor at absorption, very little takes place. It is only when you reach the small intestines that you find folds known as valvulae conniventes, which increase the surface area of the small intestines 3 fold. Extending from these conniventes are small projections called villi, which increase the absorption another 10 fold. These villi are close together and their outer epithelial cells form a brush border protruding into the chyme. This increases the absorptive power another 600 fold. This makes the surface of the small intestines 250 sq. meters (About the size of a tennis court). The absorptive capacity of the small intestines is astounding. It can absorb several kilograms of carbohydrates, 500-1000 grams of fat (20-40 ounces), 500-700 grams (20-28 ounces) of protein, and 20 or more liters of water daily. There are four types of glands that are found in the gastrointestinal tract: 1. Salivary cells are found in the mouth, pancreas, and the liver 2. Mucous glands- Mucous contains, water, electrolytes, glycoproteins, and HCO3 ions. The function of mucous is to adhere tightly to the food while it coats the intestinal wall. Mucous prevents food from contacting the mucosa. Mucous also causes fecal particles to adhere together to form a mass. Mucous is also very resistant to digestive juices, and can buffer acids or alkaline enzymes. The esophagus also secretes mucous. The mucous glands secrete mucous in response to vagal stimulation, gastrointestinal enzymes, and irritating factors. Mucous glands that are in the upper duodenal area between the pylorus and papilla of vata are called “Brunner’s glands”. Crypts of Lieberkuhn are found in the small intestines. 3. Tubular cells- are found in the stomach and are of 2 types: the oxyntic or gastric and the pyloric. The first, oxyntic, are your parietal and chief cells. The parietal cells secrete HCl, intrinsic factor for B12 absorption, and histamine. The chief cells secrete pepsinogen, intrinsic factor and mucous. The second type of tubular gland is called the pyloric gland. The pyloric glands mainly secrete mucous but also pepsinogen and gastrin. The oxyntic glands are located in the body and fundus of the stomach comprising 80% of the stomach; the pyloric glands are found in the antral portion of the stomach. These tubular cells are also found in the upper part of the small intestines. Pepsinogen, which is not reactive, is activated and transformed into pepsin by coming in contact with HCl. Pepsin is a proteolytic enzyme that is highly reactive in an acid media between (1.8-3.5). Therefore, both HCl and pepsin are responsible for protein digestion. Other enzymes of the stomach include gastric lipase and amylase; both are extremely weak and play a minor role in the digestion of fats and starches. Gelatinase, another enzyme, is responsible for liquification of proteoglycans found in meat. The stomach also secretes intrinsic factor, which is responsible for B12 absorption in the ileum. B12 is responsible for red blood cell maturation. Gastric secretions have a pH of 1.0-3.5. 4. The stomach also secretes gastric amylase and lipase. The Neurotransmitters Affecting Gastric Secretions Are: 1. Acetylcholine-which is responsible for pepsinogen via peptic cells, gastrin via gastric cells, HCl via parietal cells and mucous secretions. 2. Gastrin (2 types G17 and G34) named for the number of amino acids that make them up, and histamine (an amino acid derivative) both stimulate HCl production. When gastric or acetylcholine are present histamine has a much stronger effect on acid production. All of these neurotransmitters activate receptor sites on secretory cells, which stimulate the secretory process. Amino acids, caffeine and alcohol can also stimulate gastric secretory activity. Neural Control Of The Gastrointestinal System The GI tract is controlled by: A. Reflex activity between the brain stem (vagus nerve dorsal motor nuclei), such as the stomach motor and secretory activity, pain and strong powerful colonic contractions. B. The spinal cord via the autonomic nervous system. The sympathetic division extends from T5-L3 forming the celiac and mesenteric plexuses and the sympathetic chain ganglion, which inhibits peristalsis and digestive secretions by the inhibition of the myenteric and submucosal plexus with norepinephrine. Usually, they control long range communication between the stomach, small intestine, ileocecal valve and the colon, by controlled slowing or speeding up of movement of food and fecal material. C. The parasympathetic outflow division originates from S1-S3 and stimulates the movement of fecal material and reabsorption of H2O and electrolytes. Remember that almost all sympathetic or parasympathetic activity is afferent in nature. This means that distention, mucosal irritation from foods, drugs, preservatives, pH etc. send afferent messages to the brain stem initiating the proper course of action to occur. D. The GI tract has its own nervous system called the enteric nervous system and is found in the gut wall extending from the esophagus to the anus (100 million neurons are the number of neurons in the spinal cord). The enteric nervous system releases the following neurotransmitters: acetylcholine, norepinephrine, ATP, serotonin, dopamine, cholecystokinin, substance P, vasoactive intestinal polypeptide, somatostatin, and leu-enkephalin. Acetylcholine stimulates intestinal activity norepinephrine inhibits intestinal activity. The enteric nervous system is composed of 2 plexuses 1. myenteric plexus (Auerbach’s) found between the circular and longitudinal fibers and controls peristaltic movement. The myenteric plexus is composed of linear chains of interconnecting neurons. When stimulated it increases: • Tonic contractions • Rhythmic contractions • Velocity of conduction • Rate of rhythm · · · Please note that the myenteric plexus does play a role in inhibition of the pyloric sphincter and the ileocecal valve. 2. Submucosal plexus (Meissner’s plexus) is found in the submucosa and is responsible for digestive secretions and blood flow. The purpose of the enteric nervous system is to control peristalsis and digestive secretions short range over small distances. This is most beneficial since the body uses a finer control over the local digestive process. Digestion And Absorption In The Gastrointestinal Tract Carbohydrate Digestion- There are 3 major sources of carbohydrates in the diet Sucrose, a disaccharide known as cane sugar Lactose, a disaccharide known as milk sugar Starches (grains), which are long polysaccharides When monosaccharides form disaccharides, hydrogen is removed from one monosaccharide and a hydroxyl group is removed from the other monosaccharide, forming water in a process (condensation). When disaccharides split into monosaccharides the process is called hydrolysis (the addition of water to form the 2 monosaccharides). Humans cannot digest cellulose. Carbohydrate digestion starts in the mouth via an alpha amylase known as ptyalin, secreted by the parotid glands. This enzyme hydrolyzes starches into maltose and other small polymers of glucose (3-9 glucose molecules long.). 3-5% of all starches are digested in the mouth. As the food enters the stomach ptyalin continues to digest the carbohydrates so that within 1 hour, upon entering the stomach, most of the carbohydrates are converted into maltose. When the pH falls below 4.0 ptyalin starts to become inactive. By the time the chyme reaches the duodenum and jejunum, pancreatic amylase, which is much more potent then ptyalin (more concentrated), converts the remaining polymers into maltose. In the lining membranes of the intestinal lumen (microvilli brush border) there are four enzymes produced: Lactase, which splits lactose into galactose and glucose Sucrase, which splits sucrose into fructose and glucose Maltase, which splits maltose into glucose. Alpha Dextrinase, which splits all of the above as well as dextrins 2. Protein Digestion-Protein digestion starts in the stomach via pepsin. Pepsin is also important for digesting collagen, an albuminoid found in meats. Pepsin is most active at a pH of 2-3. The HCl produced by the body has a pH of .8. When proteins leave the stomach they are mostly in the form of proteases, peptones, and large polypeptides. When the chyme reaches the small intestines the pancreatic enzymes trypsin and chymotrypsin split proteins into small peptides and carboxypolypeptidase then split a small percentage of these into amino acids. The bulk of the peptides are broken down by the multiple peptidases located in the brush border of the intestinal membrane. The most important peptidases are aminopolypeptidase and several dipeptidases. These split the proteins down to di and tri-peptides, which enter the microvilli membrane into the interior of the epithelial cell where other peptidases break up the remaining di and tripeptides into amino acids to be absorbed into the blood stream. Please note that di, tri, and polypeptides can still enter the blood stream and can cause allergic reactions. 99 % of all protein is absorbed as amino acids. 3. Fat Digestion The most abundant fat in the diet is in the form of triglycerides, which contains a glycerol nucleus and 3 fatty acids (stearic, and palmitic acid, which are saturated and oleic acid which is unsaturated). All 3 come from animal and not plant origin. The usual diet contains phospholipids, cholesterol and cholesterol esters. Cholesterol is formed in the liver from degraded products of fatty acid molecules, which give cholesterol its fatty characteristics. Fat (butterfat) is digested in the stomach via gastric lipase (tributyrase) in very small amounts. 99% of fat digestion takes place in the intestines via bile. Bile contains bile salts and a phospholipid known as lecithin in the form of ionized sodium salts. Bile salts have the ability to form micelles, small globules of fat attached to the bile salt. This occurs because the sterol portion of the bile salt is highly soluble in fat and a polar portion of the bile salts and lecithin are highly soluble in water. This reducing and changing of the polarity reduces the interfacial tension between the fat cells so digestive enzymes can continue to break down the fat. This increases the total surface area of the fat a 1000 fold. Pancreatic lipase is responsible for splitting 99% of the triglycerides into 3 fatty acids and 2 monossachrides. Cholesterol, its ester (cholesterol +1 molecule of a fatty acid) and phosopholipids (via cholesterol ester hydrolase and phospholipidase respectively) are broken down via hydrolysis of the fatty acids from their molecular structures. The bile salts, when attached to lipids create micelles, which are highly charged and increase the absorption of these fatty acids, glycerol, free cholesterol and the remaining portion of the phospholipids. Please note that without bile salts much of the fat will be blocked from entering the blood stream.	115.33%
Liver Liver LIVER The liver has at least 500 separate functions. If we looked at the classification of these functions we could narrow them down to 2 classifications. The first classification would be one of food processing. The liver is responsible for changing inorganic food to organic food, via the process of denitrification, in which thyroxin is necessary. Lipid metabolism of cholesterol, triglycerides and phospholipids occurs mainly in the liver. Such is the case with carbohydrate, as well as lipoprotein metabolism. 1. CLASSIFICATION ONE-FOOD PROCESSING For example, when it comes to carbohydrate metabolism the liver does the following: • Causes gluconeogenesis from fats and proteins • Acts as a storage center for glycogen and balances blood sugar by the method called “glucose buffer function.” As far as fat metabolism is concerned, the liver does the following: • Forms lipoproteins, phospholipids, and cholesterol, of which 80% is used to make bile salts. Both phospholipids and cholesterol are used to make cell membranes, hormones, and intracellular structures. The liver also converts carbohydrates and proteins into fats. The liver also oxidizes fatty acids quickly. Fat is quickly turned into glycerol and three fatty acids, and then through beta-oxidation, becomes acetyl coenzyme A, via the Kreb cycle. It is then sent to other cells in the form of acetoacetic acid, which cells convert back to acetyl coenzyme A. As far as protein metabolism is concerned: • The liver forms all major plasma proteins except for gamma globulins. The liver also forms fibrinogen, prothrombin and accelerator globulin. As far as vitamins and minerals are concerned: • The liver also stores vitamin A, D, and B12 • The liver also stores iron as ferritin, by using apoferritin to attach to the iron forming ferritin. When there is a decrease of iron in the blood, ferritin releases the iron from the liver. According to Dr. Brockman, iodine is responsible for catabolism, which is a release of the foods from the liver sinusoids. Vanadium is responsible for anabolism, by storing foods in the liver sinusoids. 2. CLASSIFICATION TWO-IMMUNITY AND TOXIC REMOVAL-The endo-reticular portion, which is the most distal area, is responsible for blood filtration of all poisons, toxins, bacteria, virus, parasites, environmental pollutants, pesticides, industrial chemicals, food additives, metabolic wastes, excessive hormones, medications, and any and all filth that one can put into their body. At the present time, there are thought to be 200,000 foreign chemicals in the environment. The liver, through its various enzyme pathways, is responsible for neutralization of the various poisons. The first system is the cytochrome P450 group of enzymes known to contain 500 different enzymes. This group of enzymes is also known as the “Phase 1” system. Phase 1 enzymes chemically oxidize substances into more toxic compounds. It is interesting to note that these intermediates can be very reactive and carcinogenic. The substrates that make up the cytochrome P450 group are thought to originate from steroids, sterols, and fatty acids. The second system, known as the Phase 2 system, converts these substances into nontoxic and readily excreted substances. So, the cytochrome P450 group oxidizes a substance with oxygen, and the Phase 2 system often uses the oxygen site for further metabolism. The phase 2 conjugation pathway system is the addition of an endogenous substance, such as a carbohydrate derivative (glucuronic acid), or amino acids glycine and glutathione, or sulfate, to a foreign compound. This conjugated compound is now less polar and less lipid soluble, thus facilitating excretion and reducing the likelihood of toxicity. There are three conjugation systems: glycine, sulfate, and glucuronides conjugation. The liver must identify food from toxins. It must program and reconstruct those substances that the thyroid has prepared. Through the use of copper and iron (cytochromes), the liver tags the microbe or toxin. The iron is used to fight infection and for transportation for beneficial hosting. An example of this would be monocytes attacking a virus and engulfing it and transporting it away from the liver. Copper is used to neutralize toxins. Once a substance leaves the liver, whether it is food, microbe, or chemical poison, the process of oxidation starts. Iron or copper, prior to its proper destination, must not oxidize the substance. Antioxidants, such as cholesterol and triglycerides, surround the substance so that you can have sufficient time for oxidation and proper combustion of the surrounded substance at the proper time. Premature oxidation is what allows toxins, microbes, food and metabolic wastes to be released into the system before it reaches its destination.	104.13%
Gallbladder Gallbladder THE GALLBLADDER The purpose of the gallbladder is to store bile, which was produced via the liver (600-1200 mL are produced daily) and received the precursors from the spleen and the adrenals. Biliverdin and bilirubin are pigments that are used in red blood cell production. When red blood cells reach the 120-day mark, they are broken down via the spleen and tissue macrophages (reticuloendothelial cells). These pigments are released and utilized to form bile. Hemoglobin is also split into globin and heme. The heme is transferred in the blood with transferrin to form with the pyrrole nuclei. Biliverdin is then reduced to form bilirubin. The salts that help produce bile for emulsification of fat are produced via the adrenal glands. The precursor of bile salts is cholesterol, which is also produced via the liver and then converted into cholic acid or chendodeoxycholic acid equally. 80% of all cholesterol is converted into these two acids. These acids combined with glycine and taurine to form glyco and tauro conjugated bile acids, with the salts of the acids being secreted in the bile. The release of bile via gallbladder contractions is caused by cholecystokinin. The purpose of bile is three-fold: • The first is to transform a fat into soap via saponification (oxidation of fat), which leads to emulsification. In order for the salts to be infused into the fat, lecithin must be present. This decreases the surface tension of the fat molecule allowing agitation to break up the fat into small sizes. Therefore, the components of bile are lecithin, which are choline and inositol, cholesterol and bile salts. • The second thing bile salts do is to help absorb fatty acids, monoglycerides, cholesterol and other lipids by forming minute complexes called “micelles.” These are highly soluble, highly charged and are easily absorbed, increasing absorption of fat by 40 percent. • The third purpose of bile is to excrete waste products, such as excessive cholesterol produced by the liver and bilirubin, which is the end product of hemoglobin degradation. The following tests determine liver function: 1. SGPT (SERUM GLUTAMIC PYRUVIC TRANSAMINASE) (ALT) -SGPT has a maximum concentration in the liver sinusoid membranes. SGPT is also found in large amounts in the kidneys, heart and skeletal muscle. SGPT is the primary Krebs cycle expresser. It occurs as the result of the catabolic release of fat. Pyruvates are those substances that balance fats in an anti-oxidant media. The oxygen from the iron, and the antioxidant media from fat, which is the lubricator vitamin known as vitamin A, is balanced by pyruvates. Vitamin A is also used in the sinusoids of the lungs, spleen, kidney, sinuses and lymphatic tissue. SGPT exists in the blood serum as a consequence of substances being released by the fatty membranes of the liver sinusoids and lymphatic ducts. The liver sinusoids store food while the lymphatic ducts house toxins. Picture a layer of vitamin A that holds food or toxins in the cell. Now, as that layer of fat (vitamin A) is being burned off, oxidized via iron, foods or toxins are released from the sinusoids or lymphatic in a controlled manner, allowing foods or toxins to be released and directed to the next destination. SGPT shows the fat and the fatty acid storage ability that takes place in the liver. SGPT is the primary kreb cycle expresser, which occurs as the result of the release of catabolic fats from the liver. 2. TOTAL IRON-is the indicator of the process of oxidation vs. the antioxidation (fat). This occurs in the liver, as mentioned above. 3. GGTP-SERUM GAMMA GLUTAMYL TRANSFERASE (TRANSPEPTIDASE) is another liver enzyme test that is more concerned with liver/gallbladder/pancreatic problems and alcoholism. SGPT is more concerned with the release of foodstuffs from the liver. 4. TOTAL BILIRUBIN-as mentioned above, bilirubin is formed by the destruction of hemoglobin by the liver (kupfer cells), bone marrow and spleen. Impaired production or excretion of hemoglobin results in jaundice/liver disease. Total bilirubin is made up of direct and in-direct bilirubin. Direct bilirubin is what is called the post hepatic form, which has already been reacted on by the liver (conjugated). The elevation is usually caused by biliary obstruction. Indirect bilirubin is the pre-hepatic form, which has not been reacted on by the liver (unconjugated) and elevation occurs during liver failure. As you can see, SGPT and total iron are liver function tests, and GGTP and total bilirubin are related more to gallbladder dysfunction.	51%
Appendix Appendix	50%
Transverse colon Transverse colon	50%
Pancreatic Head Pancreatic Head THE PANCREAS The pancreas is composed of a head and a tail. The purpose of the pancreatic head is used to secrete pancreatic enzymes. The purpose of the pancreatic tail is to produce insulin. I will first discuss the pancreatic head. THE PANCREATIC HEAD The pancreatic head synthesizes and produces the following enzymes, which are released by the acini cells: 1. Trypsinogen 2. Chymotrypsinogen 3. Pro carboxy polypeptidase All are enzymatically inactive until they are activated by enterokinase when they enter the intestinal tract. Once these enzymes are activated, they are called trypsin and chymotrypsin, which cleave proteins into peptides. Carboxypolypeptidase, which is now the activated form of pro carboxy polypeptidase, then splits these peptides into amino acids. Pancreatic lipases include cholesterol esterase, which hydrolyzes cholesterol esters and phospholipase, which splits fatty acids from phospholipids. The pancreas also secretes pancreatic amylase, which breaks down carbohydrates. Bicarbonate ions (sodium) also make up a portion of pancreatic secretions, which alkalize the gastric secretions of the stomach. If necessary, bicarbonate ions can be increased by five times the normal amount. There are four stimuli of pancreatic secretions: 1. The first is acetylcholine via the vagus nerve 2. The second is gastrin produced by the stomach 3. The third is cholecystokinin secreted by the duodenum, which is responsible for pancreatic enzyme release 4. The fourth is secretin, which increases sodium bicarbonate ions The primary job of pancreatic enzymes is to oxidize fatty acids (complex sugars) through the use of chromium via amylase. Chromium is trivalent and is very acceptable to oxygen. Chromium, therefore, causes immediate oxidation (injects oxygen between the oil and sugar of the fatty acid causing pre-combustion, which readies the fatty acids for combustion and energy exchange. The head of the pancreas regulates the most alkaline substance, which is starch, and when there is an increased alkalinity of the blood, there is an increase in fatty acid oxidation via chromium. It is worth mentioning that there are three steps necessary in the breakdown of fatty acids, which are as follows: 1. Fatty acids are first prepared via ptyalin in the saliva, (which contains large amounts of potassium), activated by having the mumps. 2. The second step is through aerobic enzymation in the small intestines, which is the chromium oxidation step I just spoke about. According to Dr. Brockman having the chickenpox activates this step. 3. The final step is an anaerobic step, which occurs, between the liver-gallbladder and the head of the pancreas (duct of worsung) where trypsin and chymotrypsin are secreted. According to Dr. Brockman, this is stimulated or activated by having the measles. The measles encourages the expression, appropriate potency, and types of pancreatic enzymes. Patients who continually contract the measles are trying to kick in their pancreas to release the pancreatic enzymes. The following blood tests are used to determine pancreatic head conditions: 1. CALCIUM-besides bonding to lipoproteins, calcium also bonds to the oily portion of fatty acids. This is necessary if the fatty acids want to pass through the intestinal wall. If there is poor oxidation of fatty acids, then there will be a certain amount of calcium, which will be needed to bond to the fatty acids, decreasing the calcium levels in the blood. 2. LACTIC ACID DEHYDROGENASE (LDH)-is a glycolytic enzyme that functions as a catalyst in carbohydrate metabolism, which aids the pyruvic and lactic acid interchange. LDH is a byproduct of muscle metabolism. When sugar and water (fatty acid metabolism) are exchanged across a muscle cell interface, the byproduct left is called lactic acid. Lactic acid is also a byproduct of fatty acid metabolism via the alkalizing and oxidizing affects of the pancreatic head. When lactic acid combines with the venous blood (carbon dioxide), there is a hydrogen displacement. The lactic acid then bonds to a double hydrogen forming lactic acid dehydrogenase. LDH is then a byproduct of carbohydrate and fatty acid metabolism. The organs and glands that that are most responsible for sugar and water interchange across the muscle cell interface are the pancreas and the posterior pituitary (via antidiuretic hormone.) LDH is found chiefly in the heart, kidneys, liver, skeletal muscles, as well as all tissues. LDH is a normal component of cerebral spinal fluid.	46.33%
Ascending colon Ascending colon	33%
Duodenum Duodenum	25.5%

Show Expanded

#		Appendix	Ascending colon	Cecum	Duodenum	Gallbladder	Ileum	Jejunum	Liver	Pancreas	Pancreatic Head	Stomach	Stomach Acid	Stomach Alkaline	Transverse colon
Glucose Glucose GLUCOSE Glucose is an important fuel for the body, which affects all tissues, organs, and systems. Glucose also affects the acid/alkaline balance in the body. Breakdown of glucose or starch starts in the mouth via ptyalin, then in the stomach via HCL, and then by pancreatic amylase, lactase and other enzymes. Glucose is then absorbed in the small intestines and is then stored as glycogen in the liver. The liver is the primary site of glucose production. The liver converts lactic acid to glycogen and back to glucose via epinephrine. The liver converts fats and proteins via gluconeogenesis into glucose or glycogen. The head of the pancreas controls chromium, which controls insulin levels and assists in the enzyme action of fats via bile salts. The tail of the pancreas controls zinc, which maintains and sustains levels of insulin. Blood sugar depends on: 1. The liver which stores and releases glycogen 2. The pancreas, which produces insulin that transfers sugar from the blood to the extracellular fluid 3. The adrenal glands, which produced glucocorticoids that, cause the liver to release glycogen into the blood as glucose 4. The sex organs, which deliver the extracellular glucose to the cell 5. The thyroid, which affects the storage of glycogen in the liver 6. The thymus and spleen, which affect the levels of iron and copper in the liver which, determine the liver's ability to handle glucose As you can see there are many organs, or combinations of these organs and glands, which affect glucose levels in the body. Therefore, glucose in itself cannot specifically determine where the problem may lie. Other indicators are necessary to pinpoint the problem.	-28
Uric Acid Uric Acid URIC ACID Uric acid is the principal end product of purine, nucleic acid, and nucleoprotein metabolism. Uric acid is transported by the blood from the liver to the kidney’s which filter out and secretes about 70% and the remainder excreted via the GI tract. From a pathological view, uric acid is elevated when there is cell breakdown as in leukemia and catabolism of nucleic acids as in gout, or removal via the kidneys is decreased due to renal failure. From a physiologic view, we look at every level of protein combustion where there remain two by-products which are a Mucous (oily residue) and Uric acid (carbon ash) In order for protein to be fully combusted, it must first be influenced in the duodenum by trypsin, chymotrypsin, carboxypolypeptidase, and bile emulsification. Trypsin and chymotrypsin cleave proteins into peptides and carboxypolypeptidase split the peptides into amino acids. The pancreas synthesizes trypsinogen, chymotrypsinogen, and procarboxypolypeptidase, which are enzymatically inactive. When they are released into the duodenum they are all activated by enterokinase. Which now readies the proteins for assimilation in the liver. Therefore, if the proteins are not prepared properly the two end products, uric acid, and mucous, will be out of balance. URIC ACID IS HIGH WHEN General considerations: ¬ Decrease fatty proteins and rich foods ¬ Decrease alcohol and simple sugars ¬ Increase water intake	303.64
Bun Bun BLOOD UREA NITROGEN Blood urea nitrogen is formed entirely by liver deamination from protein metabolism. BUN is a byproduct due to the release of nitrogen bonds (and measures the nitrogen portion of urea) from protein substances in the liver. From a pathological perspective, an increased blood urea nitrogen would indicate renal disease, tissue necrosis, increased adrenal gland activity, and rapid protein catabolism. From a physiologic perspective, the purpose of nitrogen is to carry a substance through an aerobic media preventing oxidation, and eventually back into an anaerobic environment. Once in the liver the thyroid through the use of iodine, releases the nitrogen bond, releasing the nitrogen from the protein, allowing the protein to combust into hormones, enzymes and antibodies. The adrenals and anterior pituitary play a vital role in the combustion of this protein. The urea is now sent to the kidneys and is converted into urine. Urea is produced when amino acids, which are not used for protein synthesis, are broken down via hepatic metabolism. These amino acids are de-aminated producing ammonia, which is converted to urea immediately since ammonia levels become toxic. When this metabolic conversion is affected due to faulty metabolism or liver disease ammonia is not converted causing excessive levels of ammonia with possible hepatic encephalopathy. Renal malfunction/failure may also cause a high BUN due to its affect on the removal of urea causing uremia. Uremic wastes usually impair platelet function, and patients may show an increased tendency towards bleeding. BUN IS HIGH WHEN General considerations: ¬ High protein diets can cause increased BUN ¬ Increase water intake if no edema	880.95
Creatinine Creatinine CREATININE Creatinine ash is a basic byproduct in the breakdown of muscle creatine phosphate resulting from energy metabolism. From a pathological perspective the kidneys primarily remove creatinine and when there are elevated levels it indicates reduced kidney function. Thus creatine levels give an approximate for the GFR. From a physiological perspective, creatine is a by-product of actin metabolism after being exposed to acetylcholine combustion. The actin fiber joins two stable protein blocks (myosin), which combusts to produce muscle contraction, primarily for activity and secondarily for tonicity. During a muscle contraction, an action potential travels along a motor nerve to a muscle fiber. Acetylcholine is released at the motor endplate, causing multiple acetylcholine lined gated protein channels to open. This causes sodium ions to flow to the interior of the muscle, which initiates an action potential of that muscle. This then leads to depolarization releasing large amounts of calcium into the myofibrils. This initiates a contractive force between the actin and myosin filaments via ATP causing them to slide together, which is the contractile process. After a fraction of a second, calcium is pumped back into the sarcoplasmic reticulum, until the next muscle contraction. The actin fiber is then oxidized (H displaced) via acetylcholine, leaving an oily waxy residue known as creatinine. GABA (Glutamic amino benzoic acid), which is part of the actin fiber, helps it burn better. Creatine becomes creatinine with the release of ATP. Low creatinine levels would indicate muscle loss and weakness.	455.56
Sodium Sodium ELECTROLYTES The blood electrolytes include sodium, potassium, chloride, and the bicarbonate (HCO3) ion. Sodium, potassium, and chloride enter the body via ingestion of food. Carbon dioxide, on the other hand, originates within the body via the metabolic process of carbohydrates, fats, and proteins. Normally the excretion of sodium, potassium, and water is equal to their intake. The kidneys secrete 80-90 percent of all electrolytes. Excessive carbon dioxide stimulates the respiratory centers in the brainstem to increase respiration. Therefore, the kidneys and the lungs control sodium, chloride, potassium, water, and carbon dioxide thus exerting control over the acid/alkaline balance in the body. There are also many other organs, and glands involved in this process, such as the posterior pituitary, adrenals, bowel, and uterus/prostate. The purpose of electrolytes is to set up a shifting mechanism in the cell membrane via oxidation, allowing increased or decreased permeability to that membrane site. Sodium, which is found in high concentration outside the cell, has the ability to gather up substances (foods) and bring them to active membrane sites. Chloride is found in the cell membrane and acts as a “doorman” allowing or disallowing exchanges between the intracellular and extracellular fluids. Potassium, which is found in high concentrations within cells, oxidizes chloride, and allows sodium, with the food to cross the cell membrane and enter the cell. Sodium, potassium, chloride, calcium, and hydrogen are all transported via active transport. SODIUM Sodium is the most abundant cation (90%) and is the major base in the body. Sodium is either implanted into the food via saliva or is found in the food and has the following functions: 1. Sodium is an alkaline mineral that helps maintain alkaline activity. Therefore, it helps in acid-alkaline balance, which affect intracellular/extracellular fluid exchange, osmotic pressure, via the sodium/potassium pump and does this in conjunction with antidiuretic hormone and aldosterone. 2. Sodium gathers, and aggregates (polarizes) all substances necessary to be exchanged by semi-permeable membranes. Sodium pumps proteins and sugars into the cell membranes. 3. Sodium also affects the renal tubules for the activity of discharging toxins. It literally aggregates toxins and holds them in suspension. 4. Sodium is controlled by the adrenal cortex and as mentioned above is extremely alkaline and therefore, can cause migration of substances towards its polarity, as well as causing these migrated substances to achieve permeability in an acid antioxidant type media known as a fatty membrane. Sodium is the substance necessary to polarize foods into storage according to that permeable membranes needs. 5. Sodium is also necessary for the transmission of neurological impulses by creating action potentials across neurological membranes. 6. Sodium concentration in and out of cells remains constant due to renal blood flow, carbonic anhydrase enzyme activity, aldosterone, and other steroids controlled by the anterior pituitary, rennin enzyme secretion, hypothalamus, and posterior pituitary control of ADH and vasopressin secretion	-33.33
Potassium Potassium ELECTROLYTES The blood electrolytes include sodium, potassium, chloride, and the bicarbonate (HCO3) ion. Sodium, potassium, and chloride enter the body via ingestion of food. Carbon dioxide, on the other hand, originates within the body via the metabolic process of carbohydrates, fats, and proteins. Normally the excretion of sodium, potassium, and water is equal to their intake. The kidneys secrete 80-90 percent of all electrolytes. Excessive carbon dioxide stimulates the respiratory centers in the brainstem to increase respiration. Therefore, the kidneys and the lungs control sodium, chloride, potassium, water, and carbon dioxide thus exerting control over the acid/alkaline balance in the body. There are also many other organs, and glands involved in this process, such as the posterior pituitary, adrenals, bowel, and uterus/prostate. The purpose of electrolytes is to set up a shifting mechanism in the cell membrane via oxidation, allowing increased or decreased permeability to that membrane site. Sodium, which is found in high concentration outside the cell, has the ability to gather up substances (foods), and bring them to active membrane sites. Chloride is found in the cell membrane and acts as a “doorman” allowing or disallowing exchanges between the intracellular and extracellular fluids. Potassium, which is found in high concentrations within cells, oxidizes chloride, and allows sodium, with the food to cross the cell membrane and enter the cell. Sodium, potassium, chloride, calcium, and hydrogen are all transported via active transport. POTASSIUM Potassium is intracellular, lining the inside of all cell membranes and affecting intracellular fluids, osmotic pressure, buffering viscosity (potassium bicarbonate is the primary intracellular inorganic buffer). When there is a decrease in potassium bicarbonate you have acid cells, which excites the respiratory centers so the patient hyperventilates. Metabolic acidosis or diabetic ketoacidosis drives potassium out of the cells, affecting electrolyte balance, water retention and carbon dioxide transport in red blood cells. Potassium is responsible via the posterior pituitary for oxidizing secondary hydrogen chloride (affecting adrenal function), allowing the sodium-aggregated substances to cross the cell membrane by affecting the membranes permeability. Potassium is the only substance, which allows oxygen into unoxygenated tissue. About 90% of the body’s potassium supply is intracellular with only a small percent in the serum. 80% of that is found in the muscles (used for muscular contraction) and in the bones. Potassium levels are regulated by the Na/K ATPase pump which requires magnesium for proper function. Potassium is necessary for proper function of mineralocorticoids, (aldosterone and deoxycorticosterone) thus maintaining sodium concentration and alkaline reserve. Therefore, potassium is of great value to the posterior pituitary (ADH/oxytocin), the pineal, and the adrenal cortex via aldosterone secretion. Potassium along with sodium regulate renal acid-base balance, by substituting hydrogen ions for sodium and potassium in the renal tubules. Potassium also facilitates oxygen to the myocardium and oxidizes the S.A. node of the heart. The heart has the highest potassium concentration in the body. Potassium along with calcium and magnesium controls the rate and force of contraction in heart muscle. It is the primary oxidizer of the body capable of expressing all cellular needs. Potassium also regulates neurological impulses via osmotic pressure gradients throughout the nervous system. Potassium directs carbohydrate digestion by polarizing minerals associated with carbohydrate digestion, from the time the carbohydrate enters the body until the cell utilizes it. Potassium also makes proteins soluble and regulates protein synthesis. 80-90 percent of potassium in the cells is excreted by the kidneys (resulting in the loss of 40-50 mEq/L per day even during fasting) with the remainder excreted by the stool and through sweating POTASSIUM IS LOW WHEN General considerations: ¬ Increase water intake ¬ Increase magnesium intake ¬ Decrease calcium intake ¬ Increase potassium intake ¬ Decrease carbohydrate intake	-50	5	5	5											5
Chloride Chloride ELECTROLYTES The blood electrolytes include sodium, potassium, chloride, and the bicarbonate (HCO3) ion. Sodium, potassium, and chloride enter the body via ingestion of food. Carbon dioxide, on the other hand, originates within the body via the metabolic process of carbohydrates, fats, and proteins. Normally the excretion of sodium, potassium, and water is equal to their intake. The kidneys secrete 80-90 percent of all electrolytes. Excessive carbon dioxide stimulates the respiratory centers in the brainstem to increase respiration. Therefore, the kidneys and the lungs control sodium, chloride, potassium, water, and carbon dioxide thus exerting control over the acid/alkaline balance in the body. There are also many other organs, and glands involved in this process, such as the posterior pituitary, adrenals, bowel, and uterus/prostate. The purpose of electrolytes is to set up a shifting mechanism in the cell membrane via oxidation, allowing increased or decreased permeability to that membrane site. Sodium, which is found in high concentration outside the cell, has the ability to gather up substances (foods) and bring them to active membrane sites. Chloride is found in the cell membrane and acts as a “doorman” allowing or disallowing exchanges between the intracellular and extracellular fluids. Potassium, which is found in high concentrations within cells, oxidizes chloride, and allows sodium, with the food to cross the cell membrane and enter the cell. Sodium, potassium, chloride, calcium, and hydrogen are all transported via active transport. CHLORIDE Chloride a blood electrolyte, and is the major anion and exists in the extracellular spaces as part of the sodium chloride or HCl molecules. Chloride is used for assessing pH, and electrolyte balance. From a physiologic perspective, the primary purpose of chloride is to regulate the quantity of carbohydrates and proteins entering into the cells, by inhibiting the exchange of mineral controlled substances across the cell membrane and responds to the oxidative power of potassium. Chloride the major anion is predominantly found in the extracellular spaces as part of sodium chloride or in the stomach as hydrochloric acid. Chloride maintains cellular integrity by its influence on acid-base and water balance as well as osmotic pressure. Chloride has a reciprocal power with other anions by decreasing or increasing when there are too many or not enough anions. Aldosterone has a direct effect of reabsorption of sodium and an indirect effect on the increased absorption of chloride. Chlorides are lost via the GI tract through vomiting or diarrhea and thru the kidneys during times of diuresis. Chloride also responds to the antioxidant media (cell membrane) by mobilizing, and collecting sodium/food aggregates on a selectively permeable basis. This reaction is under the influence of the adrenal medulla/epinephrine/norepinephrine thereby maintaining energy stores. Chloride also assists in the production of HCl via the chief cells in the stomach. In the bowel, chloride is important in preventing the passage of water out of the body. Therefore, chloride literally blocks the flow of water/gas exchange across a cell membrane. This is extremely important in the intestines and bladder. Chloride plays a vital role during the conduction of a neurological impulse where sodium lines up on the outside of a cell membrane, and potassium on the inside of the cell membrane, during the resting stage or polarized state. In a normal nerve fiber, the permeability of the membrane to potassium is about 100 times that of sodium. The sodium-potassium pump moves three sodium ions to the exterior of the cell, for every two potassium ions that are moved to the interior of the cell, creating a net positive charge to the outside of the cell membrane for each revolution of the sodium-potassium pump. This creates a positively charged external membrane and a negatively charged internal membrane, which sets up a membrane electrical potential. As a neurological impulse is transmitted down the nerve, (which is the excitation phase of an impulse), sodium crosses the cell membrane, and enters into the cell, while potassium moves to the external portion of the membrane. This then creates the depolarization of the cell membrane, thereby creating a negative charge on the outside, and a positive charge on the inside. The transmission of each impulse along the nerve fiber reduces infinitesimally as the concentration differences of sodium and potassium between the inside and outside of the cell membrane change slightly. In so doing allows the nerve fiber to transmit between 100, 000 to 50, 000, 000 impulses before the concentration differences are rundown. As the neurological impulse passes, the sodium-potassium ATPase pump re-establishes the sodium-potassium ratio back to normal (repolarization). The pumping activity is dramatically increased approximately eightfold to restore the membrane back to the polarized state. The chloride shift to the inside of the cell membrane during the final stages makes the inside of the cell, even more, negative, which further helps repolarize the cell. Chloride generally increases and decreases with plasma or serum sodium levels. CHLORIDE IS HIGH WHEN General considerations: ¬ Drink plenty of water ¬ Decrease sodium levels ¬ Increase fat-soluble vitamins D, E, K, and A	-38.46				5								10	5
CO2 CO2 CARBON DIOXIDE Carbon dioxide is created as a byproduct when potassium forces water into fat. So carbon dioxide is the acid gas factor, which binds fats and selenium creating the intelligent metabolic activity between the water and fat. 80-90 percent of the carbon dioxide found in plasma is bound to protein and is represented as bicarbonate ions (HCO3-) which first exists in the extracellular spaces as CO2 then as H2CO3 and finally is buffered by the plasma and erythrocytes into sodium bicarbonate NaHCO3) and is regulated by the kidneys. The other 10 to 20 percent is dissolved CO2 gas (removed by the lungs), which is bound to protein as CO3 (2), and carbonic acid (H2CO3). The total CO2 comes from dissolved CO2, H2CO3, HCO3- and carbaminohemoglobin (CO2HHb). This occurs in the following way, carbon dioxide in the blood reacts with water in the red blood cells to form carbonic acid. In the blood cells, there is an enzyme called carbonic anhydrase that catalyzes the water and carbon dioxide 5,000 fold, creating a rapid exchange into carbonic acid. This allows tremendous amounts of carbon dioxide reacting with the water in the red blood cells, even before the blood leaves the tissue capillaries. So a red blood cell creates carbonic acid from water and carbon dioxide. In another small fraction of a second, the carbonic acid formed in the red blood cell now disassociates into hydrogen and bicarbonate ions. The hydrogen ions combine with hemoglobin, as the bicarbonate ions diffuse out into the plasma while chloride ions diffuse into the red blood cells taking the place of the bicarbonate ions. This is made possible by the presence of a bicarbonate/chloride carrier protein in the red blood cell membrane, which acts as a shuttle for these two ions. Thus, the chloride content of venous red blood cells is greater than that of arterial cells. This is known as the chloride shift. In addition, carbon dioxide can react directly with hemoglobin to form the compound carbaminohemoglobin. This carbaminohemoglobin creates the reversible reaction releasing carbon dioxide into the alveoli of the lungs. Carbon dioxide then is the venous capillary exchange product after diffusion takes place. The active pressure intake of oxygen relies upon this diffusion. This active process realizes the ability of forced metabolism and is the ash byproduct. Carbon dioxide is vital to pH balance and is controlled by the respiratory, renal, and posterior pituitary adrenal axis. Therefore, any of these glands or organs or combinations thereof can affect carbon dioxide levels. CARBON DIOXIDE IS HIGH WHEN General considerations: ¬ Water loss- increase water intake ¬ Protein loss- increase protein intake ¬ Hypomagnesemia or hypokalemia causes increased CO2- increase potassium and magnesium CARBON DIOXIDE IS LOW WHEN ¬ Water loss- increase water intake ¬ Hypermagnesemia or hyperkalemia causes decreased CO2- decrease potassium and magnesium support	-16.67		5
Calcium Calcium CALCIUM Calcium is the largest most nonpolar, alkaline and most abundant of all minerals with 99% of all calcium found in the bones and teeth. Calcium exists in the ionized state 55 percent of the time and 45 percent of the time in the non-diffusible state, bound to either albumin, prealbumin or thyroglobulin. Therefore, if there is a decrease in serum albumin then there will be a decrease in serum calcium. Calcium has many functions: ¬ Provides the mobilizing factor in trauma, infections and stress for tissue repair, along with vitamins A, C, manganese, phosphorus, and fatty acids. ¬ Causes vasoconstriction, while potassium, sodium, magnesium, hydrogen ions, and carbon dioxide cause vasodilatation. ¬ Is necessary for bone formation along with phosphorus, collagen, hydroxyapatite (gives bone its hardness) and bone salts of magnesium, sodium, potassium, carbonate, uranium, plutonium, and strontium. ¬ Calcium is used to create action potentials across smooth and striated muscles leading to contraction. ¬ Calcium is used as an intracellular communicator via calcium ion gated channels. ¬ Calcium collects and gather up lipoproteins, and move them across the intestinal membrane. Attaches to oils, fats, fatty acids and waxes. Calcium is absorbed in the upper portion of the small intestines (duodeneum), and the amount absorbed depends on the "acidity" of the intestinal content, via phosphorylation and protein content. When the ratio of calcium to magnesium (which is found in the intestinal membrane as well as cell membranes) is greater than 2-1, fat is drawn through the intestinal and cell membranes. Calcium also requires vitamin D. and HCl for optimal metabolism. The glands involved with calcium are: 1. The stomach via the release of HCL, which affects the preparation and absorption of calcium. 2. The parathyroids- via parathormone control of calcium ion concentration by controlling intestinal absorption, excretion via the kidneys and the release of calcium from the bones. 3. The liver/gallbladder- via bile emulsification of lipoproteins, preparing them for intestinal absorption. 4. The spleen- which stores and ages fats or lipoproteins. 5. The parotids- due to their ability to program foodstuffs. 6. The thyroid glands-via "calcitonin", promoting deposition of calcium in the bones, while decreasing calcium concentration in the extra-cellular fluids and the blood. 7. The anterior pituitary via its control of magnesium regulating calcium uptake, which regulates protein transport thru the cell membranes. 8. The pancreas- via its ability to oxidize fatty acids Therefore, any of the above glands or organs or combinations thereof has a great impact on calcium levels. CALCIUM IS HIGH WHEN General considerations ¬ Your patient should drink plenty of water ¬ Make sure they are not hypervitaminosis on Vitamins A or D ¬ Very high protein diets may increase calcium levels ¬ Magnesium and phosphates may also increase calcium levels ¬ Using sea salt can help to reduce calcium levels. CALCIUM IS LOW WHEN General considerations: ¬ Increase Vitamin A and D intake ¬ Increase albumin and protein intake ¬ Increase magnesium intake ¬ Increase phosphorus	-13.04				5						5
Phosphorus Phosphorus PHOSPHORUS 85% of the total phosphorus exists as phosphates or esters in the body and is found chiefly in the skeleton and is combined with calcium. 14% of the phosphorus is found in intracellular tissues and 1 % is found in the extracellular fluid. Therefore phosphorus levels are a poor indicator of levels of phosphates in the body. Phosphorus runs inversely to calcium levels in the body at a calcium to phosphorus ratio of 10 to 4. Therefore, calcium can be a great indicator for phosphorus as well. As calcium levels increase in the serum, phosphorus levels decrease, and when calcium levels decrease phosphorus levels increase. In fact, causes of high calcium also cause low phosphorus. The controlling factor of phosphorus is parathormone (PTH), which is also the calcium-controlling factor. Phosphorus helps calcium through the cell membrane by increasing the permeability of the cell membrane via oxygen displacement. 1. Phosphorus is responsible for growth and development by way of: ✓ bonding ✓ polymer function ✓ hydration ✓ chemical transport, and ✓ buffering 2. Phosphorus is also responsible for bone formation 3. Phosphorus and metabolism of glucose Phosphorus is also required for the metabolism of glucose via phosphorylation. Phosphorylation is when a phosphate radical promoted by glucokinase in the liver, or hexokinase in other cells captures the glucose and once inside the cells keeps it there. The exception to this occurs in the liver, the kidneys, and the intestinal epithelial cells. Ingestion of carbohydrates causes phosphorus to enter RBC’s with glucose causing a reduction of serum phosphorus levels and lipids. Phosphorus also works in the stomach to stabilize sugars and activate starches by the twofold process of phosphorylation. Phosphorylation and its counterpart, dephosphorylation, turn many protein enzymes on and off, thereby altering their function and activity. By altering pepsin/HCL levels phosphorus can: a. Stabilize simple sugars-simple sugars are easily oxidized (combusted) before they reach the liver, resulting in low sugar levels. Pepsin stabilizes these simple sugars, so they can be transferred to the liver for storage. b. Activation of starches- HCl is necessary to breakdown oily carbohydrates (grains), which are difficult to oxidize (combust). Thus making them readily available for oxidation. The above two mechanisms establish an HCl-pepsin balance in the stomach for proper pH digestion. The presence of both HCl and pepsin in the stomach are critical for preparing carbohydrates, as well as proteins for further digestion in the small intestines. 4. The regulation and maintenance of the acid-base balance in the body by maintaining glandular acidity. 5. The storage and transfer of energy from one part of the body to the other. 6. Used in the Production of phospholipids (90 % produced by the liver): lecithin, A cephalin, and sphingomyelin Phospholipids are necessary for: Proper brain function (sphingomyelins) Phospholipids are a major constituent of lipoproteins which can affect function, formation and transport of these lipoproteins causing serious cholesterol abnormalities Production of cell membranes Thromboplastin production produced from A cephalin 7. Intracellular phosphorus is used for: Energy transport formation of ATP from ADP and creatine phosphate via oxidative phosphorylation. Major constituent of plasma membranes (phospholipids) Major constituent of DNA and RNA (nucleic acids) Calcium transport and osmotic fluid pressure General nutritional considerations when phosphorus is high: 1. Patient should increase water intake 2. Reduce fat intake 3. Reduce Vitamin D intake if overdosing 4. An isotonic saline solution (sea salt) will decrease phosphorus levels 5. Also, decrease phosphorus in the diet and add calcium carbonate to your diet General considerations when phosphorous is low: 1. Vitamin D deficiency 2. Calcium deficiency 3. Magnesium deficiency 4. Patient needs a high protein diet	270			5			5						5	10
Magnesium Magnesium MAGNESIUM Serum magnesium constitutes only a small fraction of the total body stores and may not predict magnesium status correctly. From a physiologic perspective, magnesium directs protein digestion, by polarizing minerals associated with protein digestion, from the entrance of protein into the body to its final deposition in the cell. Approximately 40-60 % of the magnesium is found in the skeleton for bone formation, 20% is found in the muscle, 30% is found in the intracellular cytoplasm, with only 1 % of the magnesium found in the serum. Magnesium affects membrane permeability, nerve impulses, muscle contraction, intracellular fluid regulation, activation of enzyme systems, where magnesium acts as a metallic cofactor in over 300 enzymatic reactions. Regulates protein synthesis, carbohydrate metabolism, nucleic acid synthesis, and blood viscosity. Magnesium along with sodium, potassium and calcium regulate neuromuscular irritability and the mechanism for clotting. Less then 2% of calcium, magnesium and phosphates are found in the plasma and extracellular fluid and are controlled in narrow limits. Albumin accounts for 70% of the bound calcium. Magnesium also binds to albumin and since it has a lower specificity for the receptors it creates more free magnesium in the plasma. Magnesium and calcium are very much linked in their body functions and a deficiency in either one will have an adverse affect on the other. Especially since calcium needs magnesium to be absorbed thru the intestinal membrane as well as needing magnesium for calcium metabolism. For example, a magnesium deficiency will cause calcium to migrate out of the bone and into soft tissues such as the aorta and kidneys. 95% of all magnesium that is filtered thru the glomerulus is reabsorbed by the tubules where parathormone enhances tubular reabsorption of magnesium. When there is a deficiency of magnesium you will see a decrease in urine stores before serum stores. Please note that even when magnesium is in a 20% depleted state, magnesium levels in the serum will appear normal. Calcium, magnesium and phosphates continuously enter the plasma via the kidney, the intestinal brush borders, and the ruffled border from the bones. Steady states of calcium, magnesium, and phosphorus approximate urine loss against intestinal absorption and skeletal mineral apposition against mineral absorption. Magnesium in the cells is complexed to phosphates, citrates and anions such as ATP, AMP and ADP (such as MgATP2-) Magnesium also plays a key role in the hormonal regulation of insulin, estrogen and thyroid hormones. Magnesium also stimulates secretions from the parathyroids and adrenal cortex (corticosteroids). Magnesium is also affected just the way calcium is to parathormone (enhances distal tubular reabsorption of magnesium) and to a lesser degree calcitonin. In fact, calcium, magnesium, and phosphates are depressed in vitamin D deficiencies and increased with vitamin D excess. Magnesium is used in the treatment of elevated cholesterol and triglycerides, muscular contraction, hypertension (A causal relation between decreased Mg2+ content of cardiac muscle/coronary arteries and nonocclusive sudden-death ischemic heart disease has been proposed) and premenstrual syndrome. Magnesium is indicated in collagen and connective tissue diseases, inflammatory disorders, migraines, general endocrine function and neurological and psychosomatic disorders.	-80			5
Total Protein Total Protein TOTAL PROTEIN Total proteins are divided into two fractions: albumin, and globulin (alpha, beta, and gamma). Please note that total protein also includes fibrinogen. Therefore total protein is made up of albumin, globulin and fibrinogen, all produced in the liver. These are the plasma proteins necessary to produce enzymes, antibodies, clotting factors, kinin precursors, and transport substances for hormones, vitamins, minerals, fats, etc. For example, plasma proteins combine with cholesterol forming lipoproteins such as VLDL, LDL’s, HDL’s etc. The lipoproteins then combine with minerals via enzyme metabolism to form and renew sex hormones such as testosterone, estrogen, progesterone etc. Other deaminated proteins produced in the liver, combusts at the mitochondrial level to form cell structures. These are your tissue building proteins known as nucleoproteins, DNA and RNA (your proteins of mitosis and meiosis). Since there are many glands involved in protein digestion, it is very difficult to make a determination from total protein alone. Glands and organs involved with protein control are as follows: The anterior pituitary, which controls all glands of protein digestion, such as the adrenals, thyroid, pancreatic head, sex organs, and spleen That parotid glands which tag lipoproteins with copper The parathyroids via the calcium/magnesium mobilization of lipoproteins The thyroid which denitrifies protein in the liver The pancreas by trypsin and chymotrypsin which, prepares the protein for assimilation into the bloodstream The sex organs that prepare protein for final deposition into the cells * Any combination of the above TOTAL PROTEIN IS LOW WHEN General considerations: o Increase protein intake o Increase B acid vitamins	20
Albumin Albumin ALBUMIN In pathological levels albumin is used to evaluate: 1. Liver and renal disease 2. Blood osmotic pressure 3. Chronic disease states, which most patients have 4. Dehydration 5. Albumin decreases in acute inflammatory infectious processes From a physiological standpoint, albumin is produced in the liver and is a primary byproduct of sterols and waxes. Its function is used to build and repair tissue. Albumin is responsible for 80 percent of the colloidal osmotic pressure between body tissues and blood cells. 75% of this control occurs inside the cells since most of the protein is intracellular. When you have a decrease in albumin, the osmotic pressure becomes disturbed resulting in fluid transfer and edema. Since albumin influences water movement, it will also influence nutrient and mineral movement. Albumin creates the permeability of the membrane to the osmolarity of the membrane. Therefore, substances can pass from a lesser concentration to a greater concentration. The flow is from the arterial capillaries to extracellular fluid, then from the extracellular fluid to the intracellular fluid, then from the intracellular fluid to the mitochondria. Then back via the same pathway in reverse via osmotic absorption into the veins. Albumin is also a part of a complex buffer system, which accounts for 75% of things that need to be buffered to maintain acid-alkaline balance in the body. The most powerful buffer system out of the four including, the bicarbonate system (HCO3-), the phosphate buffer system, and the liver (nitrogen/urea), the proteins of the cells and plasma, rein supreme. The protein buffer system works by controlling blood Hydrogen (H+) ion homeostasis. Both intracellular and extracellular proteins have negative charges and can serve as buffers for alterations in hydrogen ion concentration. However, because most proteins are inside cells, this primarily is an intracellular buffer system. Hemoglobin (Hb) a globular protein is an excellent intracellular buffer because of it's ability to bind with Hydrogen ions forming a weak acid and carbon dioxide (CO2) bond. After oxygen is released in the peripheral tissues, hemoglobin binds with CO2 and H+ ions. As the blood reaches the lungs these actions reverse themselves. Hemoglobin binds with oxygen, releasing the CO2 and H+ ions. The H+ ions then combine with bicarbonate (HCO3) ions to form carbonic acid (H2CO3). The H2CO3 breaks down to form water (H2O) and carbon dioxide (CO2), which are excreted via expiration through the lungs. Increases in albumin cause arteries to sclerose and a decrease in albumin causes veins to sclerose. Albumin is also a transporter of minerals and accounts for 70% of the bound calcium. Magnesium also binds to albumin and since it has a lower specificity for the receptors it creates more free magnesium in the plasma. Calcium, magnesium, and phosphates continuously enter the plasma via the kidneys, the intestinal brush borders and the ruffled border of the bone. Albumin is also responsible for transporting copper, zinc, and nickel. By controlling the transport of these minerals, albumin is the carrier of choice. The following glands are associated with albumin: 1. The parotids 2. The head of the pancreas 3. The endo-reticular portion of the liver 4. Kidneys Therefore, the function or malfunction of anyone of those glands/organs or combinations thereof can lead to imbalances in albumin levels.	-30
Globulin Total Globulin Total GLOBULIN Organs that are responsible for globulin production are the liver, thyroid, spleen and the rest the immune system. There are four types of globulins alpha 1,2, beta and Gamma. There a few groups of gamma globulins with one group being the immunoglobulins (IgA, IgG. IgM), which produce our antibodies. The thymus produces α and β globulins know as thymoglobulin using Vitamin T and copper for its production. The thyroid produces thyroglobulins that form thyroxin and triiodothyronine via vitamin K and iodine. The spleen produces spleenoglobulins that require vitamin E and iron for its production. Globulin also acts as a polarized colloidal substance necessary for specific glandular hormonal function by acting as a transport mechanism for many hormones such as sex hormone binding globulin. Globulin also assists in: Toxin neutralization by binding soluble antigens in the blood and intracellular spaces Red blood cell production Antibody formation Protection of the gastrointestinal mucosa And is also necessary via the intrinsic factor for digestion and absorption. Globular proteins can be affected via: Nutrition- lack of protein Liver Thyroid Spleen Thymus	15.79
A/G Ratio A/G Ratio A/G RATIO The A/G ratio is the ratio of albumin to globulin, and along with fibrinogen (produced by the liver) literally measures the thickness or “collagen factor” of the blood. The A/G ratio then is also a representation of the fibrinogen content in the blood and regulates the amount of protein being utilized at any time in the body. The liver forms prothrombin, which requires vitamin K. for its production. Prothrombin is a plasma protein, which is changed into thrombin via prothrombin activator and calcium. Thrombin, transposes fibrinogen into fibrin, continually causing clotting throughout the body along with blood platelets. Fibrinogen, therefore, provides the clotting thickness (collagen factor) in the blood. These polarized protein fibrous strands are necessary to maintain blood viscosity, which regulates the amount of capillary exchange from the artery to the extracellular fluid. Collagen a protein strand (albuminoid) and proteoglycan filaments also regulate exchange by causing a very slow diffusion of molecules via kinetic motion moving substances through the extracellular fluid either to the cell membrane or back into the circulatory or lymphatic systems. Collagen is also the main structural protein in connective tissue and found in the extracellular spaces. Collagen and proteoglycan filaments are used in the interstitium to provide tensile strength and for healing. As the main component of connective tissue, it makes up from 25% to 35% of the whole-body protein content. Collagen is formed in the sternum and iliac crest. A/G RATIO IS INCREASED WHEN Anything that would decrease globulin would increase the A/G ratio and anything that would increase albumin would also increase the A/G ratio so also look at all the possibilities under low globulin or high albumin THE A/G RATIO IS DECREASED WHEN Anything that would increase globulin would decrease the A/G ratio and anything that would decrease albumin would decrease the A/G ratio so also look at all the possibilities under high globulin or low albumin	1645.45
Bilirubin, Total Bilirubin, Total TOTAL BILIRUBIN Bilirubin comes from the breakdown of hemoglobin and is the byproduct of hemolysis. Bilirubin is produced by the RE portion of the liver and is excreted with the bile. Pathologically elevations in total bilirubin occur when there is a massive amount of destruction of RBC’s, or the liver is congested and unable to excrete bilirubin. From a physiologic perspective, the components of bile are inositol, choline, lecithin, cholesterol, and bilirubin/biliverdin. Cholesterol, which is produced by the liver, is converted into bile salts via the influence of the adrenal glands. The bile salts are converted into cholic acid or chenodeoxycholic acid equally. Approximately 60 percent of all cholesterol is converted into these two acids. These acids then combine with glycine and taurine to form glyco and tauro conjugated bile acids. The salts of these acids are secreted in the bile. These salts do two things: 1. They act like "soap" creating saponification and emulsification of fat. This decreases the surface tension of the fat allowing agitation to break the fat up into smaller sizes. 2. Bile salts help absorb fatty acids, monoglycerides, cholesterol, and other lipids, by forming minute complexes called micelles. Micelles are highly soluble, highly charged, and easily absorbed, increasing absorption by 40 percent. The liver secretes about 600-1,200 milliliters of bile per day. The purpose of bile is to: 1. Digest, emulsify and absorb fats. 2. To excrete waste products, such as excessive cholesterol, and bilirubin, which is the end product of hemoglobin degradation. Bilirubin is the predominant pigment of bile, and is formed from hemoglobin, and destroyed red blood cells. The red blood cells are destroyed by the reticulo-endothelial system (liver and spleen), including the kupfer cells of the liver. If the spleen/liver are hyperactive, the bile production is increased. This allows the passive function of bile production to elevate. As the spleen, liver, and bone marrow destroy hemoglobin it passes into the bloodstream with a protein creating a colloidal state. This creates hemolytic jaundice when there is excessive destruction or impaired production of red blood cells, leading to excessive amounts of prehepatic bilirubin. The liver cells are unable to withdraw the bilirubin from the blood as fast as it is formed. Therefore consequently there is an increase in prehepatic bilirubin (indirect form). Remember total bilirubin = the direct and indirect forms. The direct is elevated in biliary obstruction, which is conjugated and reacted on by the liver. The indirect form is elevated in liver failure, which is unconjugated and not reacted on by the liver. Since the liver, spleen, adrenals and diet play a role in total bilirubin production from a physiologic perspective we must evaluate those glands as well.	-77.78					10			5
Alkaline Phosphatase Alkaline Phosphatase ALKALINE PHOSPHATASE Bone osteoblasts, liver cells, and the placenta all produce high levels of alkaline phosphatase, with some activity in the kidneys and intestines. Alkaline phosphatase is called alkaline because it aids in maintaining and works best in an alkaline pH of 9-10. From a pathological perspective, alkaline phosphatase levels rise in liver disease due to impaired excretion of this enzyme from obstruction in the biliary tract, and bone disease via increased osteoclastic activity due to bone breakdown as in cancer. From a physiological perspective alkaline phosphatase is responsible for the balancing of water, and mineral metabolism controlled by the glands below. This exchange of water and mineral metabolism occurs at the cell membranes of ligaments, tendons and disc structures. The balance is created by, setting the minerals involved with electrolyte balance into motion. These minerals, along with proper neurological control, cause the shifting of food thru the membranes. The glands responsible for this balance are as follows: • The adrenal cortex via mineralocorticoids causes excretion of sodium and potassium by the kidney. • The adrenal medulla via epinephrine and norepinephrine increase metabolism, and cellular exchange via the chloride shift at the level of the membrane. • The posterior pituitary via antidiuretic hormone and its effect on potassium (oxidizer) and the water content within the cell. • Prostate/uterus via selenium acts as an oxidative mineral to insure proper membrane exchange in conjunction with the above. Alkaline phosphatase is a member of a family of zinc metalloprotein enzymes whose purpose is to split off a terminal phosphate group from an organic phosphate ester. Enzyme activity is localized in the brush border of the proximal convoluted tubules of the kidney, intestinal mucosal epithelial cells, hepatic sinusoidal membranes, vascular endothelial cells and osteoblasts of bone as mentioned above. It is the introduction of an alkaline media for bone growth. When there is an increased alkaline phosphatase you have too much acidity. In “bone pathology” there is usually a hyper-acidic state, since the foundation of a cell, is nucleic acid. The nucleic acid is composed of phosphoric acid. Phosphoric acid is a component of alkaline phosphatase, therefore, the adrenals regulate the acid/alkaline balance for energy, and growth. Alkaline phosphatase controls the alkaline substance, which controls energy, and the acid substance, which controls growth. Over the years, the laboratory low range has been steadily decreasing from 60, down to 40 now down to the mid 20's. Since this test does measure metabolic output of the adrenals, going to low is not the answer. I recommend that the low range is 70.	-66.32
LDH LDH LACTIC ACID DEHYDROGENASE Lactic acid dehydrogenase is found chiefly in the heart, skeletal muscles, kidneys, and liver, as well as all cells. In pathological states, elevated levels indicate damage to the above areas and is used to determine myocardial and pulmonary infarction. In physiological states, LDH catalyzes the conversion of pyruvate ( the final step in glycolysis) to lactate and back, as it converts NADH to NAD+ and back. A dehydrogenase is an enzyme that transfers a hydride from one molecule to another. When sugar and water (fatty acid metabolism) are exchanged across a muscle cell interface, a by-product called lactic acid is produced. When lactic acid combines with the carbon dioxide of the venous blood you have a hydrogen displacement. Lactic acid now becomes lactic acid dehydrogenase. Lactic acid dehydrogenase, therefore, is a glycolytic enzyme that functions as a catalyst in carbohydrate metabolism to produce energy. The pancreas via insulin and the posterior pituitary via ADH are responsible for this sugar and water exchange across the muscle cell interface. Lactic acid dehydrogenase indicates the active exchange of sugar across the membrane (muscle cell interface) utilizing chloride, zinc, and selenium. The utilization of these minerals creates glycolysis. LDH then from a physiological perspective determines pancreatic function regulating the amount of glucose into muscle. It is also important to note that sugar metabolism is very complex and does involve a series of other organs. Ranges for LDH are between 0-220; again it is rather obvious that LDH is a by-product of sugar metabolism and a 0 figure could not be construed as a low normal range. I feel that the range should start at 80. You will find many patients with a low LDH having problems with decreased function causing heart, skeletal muscle (weakness, loss of strength, muscle wasting), kidney and liver dysfunction, and eventual wasting away of these organs.	62.86										10
AST (SGOT) AST (SGOT) SERUM GLUTAMIC OXALACETIC TRANSAMINASE (SGOT) (AST) SGOT is highly concentrated in organs and glands of high metabolic activity and in descending order: heart, liver, skeletal muscle, brain, kidneys, pancreas, spleen and lungs. In pathological states, when you have high levels it means that cell damage has occurred in one or more of these areas and there is a release of this enzyme in circulation, elevating in 12 hours and remaining there for 5 days. In physiologic states, we know it is a tissue enzyme present in tissues of high metabolic activity, and concerned with the transfer of nitrogen between aspartic acid, and alpha-keto-glutamic acid, resulting in the synthesis of glutamic acid, alpha keto acid and oxalacetic acid. SGOT, therefore, is the catalyst that creates amino acid metabolism during glycolysis, for the production of energy. Since there are high concentrations of SGOT in skeletal muscle/heart, and the brain, it gives you an idea of the metabolic output of each system. The sex organs via the output of testosterone, estrogen, progesterone (which are formed on the gonadal epithelium by binding cholesterol to protein) are used to maintain muscle mass and strength. Therefore having a dramatic effect on muscle and nerve metabolism. Since amino acid metabolism also affects muscle mass, muscle strength, and the energy to fuel the muscular system, it is apparent that SGOT is the indicator of choice. Not to mention the energy necessary to run the central nervous system which utilizes 60 percent of the available energy necessary to run your body. Please note that most lab ranges start at 0 and since this is a measurement of the metabolic activity of the above organs 0 would mean death. The low range for SGOT should be 15. You will find physiological conditions where there are low levels of SGOT (15-20). This is due to the exhaustion of the above organs. Low levels indicated heart, skeletal muscle and diminished brain function/damage. These patients are usually physically weak/exhausted whether they exercise or not, lack mental clarity, cannot think straight and have brain fatigue/fog. They also have sex hormonal problems and require HRT or erectile dysfunction treatment. Many of these patients have a weak flabby heart, setting the stage for many types of conditions down the road. Low levels may also mean decreased liver function affecting, protein synthesis, detoxification, sluggish metabolism, cholesterol production to name a few of the 500 know liver functions.	25.71
ALT (SGPT) ALT (SGPT) SERUM GLUTAMIC PYRUVIC TRANSAMINASE (SGPT) (ALT) SGPT is primarily a liver function test. It has a maximum concentration in the liver (fatty membranes) sinusoids. Low concentrations of SGPT are also found in the kidneys, heart, and skeletal muscle. In pathological states, elevations indicate liver disease. ALT is found in serum and in various bodily tissues but is most commonly associated with the liver. It catalyzes the transfer of an amino group from alanine to alpha-ketoglutarate, and the products of this reversible transamination reaction being pyruvate and glutamate. glutamate + pyruvate ⇌ alpha-ketoglutarate + alanine Alanine transaminase delivers skeletal muscle carbon and nitrogen in the form of alanine to the liver. In skeletal muscle, pyruvate is transaminated to alanine, thus affording an additional route of nitrogen transport from muscle to liver. In the liver, alanine transaminase transfers the ammonia to A-KG and regenerates pyruvate. The pyruvate can then be diverted into gluconeogenesis. This process is referred to as the glucose-alanine cycle. The glucose-alanine cycle is used primarily as a mechanism for skeletal muscle to eliminate nitrogen as the muscles replenish their energy supply. Within the liver, alanine is converted back to pyruvate and is then a source of carbon atoms for gluconeogenesis. The newly formed glucose can then enter the bloodstream for delivery back to the muscle. The amino group transported from the muscle to the liver, in the form of alanine, is converted to urea in the urea cycle and then excreted. In physiological states SGPT is a primary kreb cycle expressant and as a result causes the release of catabolic fats. SGPT occurs in serum as a consequence of substances being released by the fatty membranes of the liver sinusoids, and lymphatic ducts. The liver sinusoids store food, and the lymphatic ducts house toxins. Picture a layer of fat that holds foods or toxins in the cell. Now as that layer of fat is being burned off, foods and toxins are being released in a controlled manner. This allows foods or toxins to be directed to their next destination. Please note that most lab ranges for this test start at 0, which in actuality is false since this is a measurement of liver function, and 0 would mean that the liver was not functioning at all. A low range then should be around 15. Therefore, from a physiological perspective, a low SGPT between 15-20 would indicate a sluggish liver causing many metabolic disturbances. Typically these people have no energy, get sick a lot, cannot tolerate food well and have a slow metabolism.	31.43					5			10
GGT GGT GAMMA GLUTAMYL TRANSPEPTIDASE (GGT) Is a biliary enzyme useful in the diagnosis of obstructive jaundice, intrahepatic cholestasis and pancreatitis. GGT is more responsive to biliary obstruction than are aspartate aminotransferase (AST) (SGOT) and alanine aminotransferase (ALT) (SGPT). 1. GGT is increased in hepatoma and carcinoma of the pancreas and useful in the diagnosis of metastatic carcinoma of the liver. Increasing levels in carcinoma patients relate to tumor progression and a dubious outcome. 1. CEA, alkaline phosphatase and GGT together are useful markers for hepatic metastasis from the breast and colon. 2. May be useful in the diagnosis of chronic alcoholic liver disease. Follow-up blood chemistries of serum GGT, AST and ALT levels can distinguish recovering alcoholics who resume drinking from those who do not. 3. Increase in body mass correlates with increased GGT levels. 4. GGT along with MCV is a useful test for alcoholism. 5. GGT is the test of choice for pregnant females who may have cholestasis. 6. GGT levels are elevated in cirrhosis and hepatitis. 7. The transaminases, AST and ALT rise higher in acute viral hepatitis; then GGT. 8. Increased in systemic lupus erythematosus GGT IS HIGH WHEN General considerations: If patient has been on a very low-fat diet for long periods of time then increase fat intake	-40					10			5
Ferritin Ferritin A ferritin test can help a doctor determine if a person has enough iron in their body. Low ferritin levels can indicate that the body doesn't have enough iron, while high levels can indicate too much iron. FERRITIN Men 20-250 ng/mL 20-250 ug/L Women 10-120 ng/mL 10-120 ug/L Children 7-140 ng/mL 7-140 ug/L Newborns 25-200 ng/mL 25-200 ug/L	-16.4
Total Iron Total Iron Total Iron Binding Capacity (TBIC)—measures the amount of transferrin, which is a blood protein that transports iron from the digestive system to cells that will be utilizing the iron. Your body produces transferrin in relationship to the body’s need for iron. When iron stores are low, transferrin levels will increase and when transferrin levels are low, too much iron is present. Usually, about one third of the transferrin is being used to transport iron at any one time. Because of this, your blood serum has considerable extra iron-binding capacity, which is called the Unsaturated Iron Biding Capacity (UIBC). The TIBC then equals UIBC plus serum iron measurement. Some laboratories may measure UIBC, some measure TIBC and others measure transferrin. TIBC is increased in iron- deficiency, acute hepatitis, during pregnancy or when oral contraceptives are used. TIBC is decreased in hypoproteinemia from many causes, cirrhosis of the liver, nephrosis and thalassemia or from a number of inflammatory states. TOTAL IRON IRON Men 65-175ug/dL 11.6-31.3 umol/L Women 50-170ug/dL 9.0 -30.4 umol/L Children 50-120ug/dL 9.0-21.5 umol/L Newborns 100-250 ug/dL 17.9-44.8 umol/L	-40					5			5
Cholesterol, Total Cholesterol, Total SERUM LIPIDS Serum lipids serve as a primary source of energy along with glucose. The functions are many, such as the production of cell membranes, precursors to hormones, and bile acids. Lipids are first broken down in the duodenum, along with bile, which emulsifies the fats, and prepares them for absorption into the lymphatic system. Pancreatic lipase hydrolyzes cholesterol, and triglycerides into fatty acids, and glycerol. The fatty acids and glycerol are then reconverted back into triglycerides by the intestinal cells and then discharged into the lymphatic or portal blood system, which is then sent to the liver. Cholesterol is also absorbed in both the free and esterified forms into the lymphatics. Cholesterol is also synthesized in the reticular cells and histiocytes throughout the body but mainly formed in the liver. Under the influence of iodine via the thyroid, carbohydrates, amino acids, and other fats are converted to cholesterol via multiple molecules of acetyl coenzyme A creating a sterol nucleus. Triglycerides are also assembled in the liver from glycerol and fatty acids. The liver is the main organ regulating blood lipids. So the liver can degrade fatty acids for energy, synthesize triglycerides from carbohydrates and proteins. The liver can then hydrolyzes the triglycerides back into three fatty acids, and glycerol then degrades the fatty acids into acetyl coenzyme A via beta-oxidation. Then acetyl coenzyme A is then oxidized to release ATP. The liver also synthesizes phospholipids, lecithin, cephalins (that produce thromboplastin), and sphingomyelin (produces the myelin sheath) are formed in the liver and transported via lipoproteins. An increase in triglycerides or choline/inositol increases phospholipid production. Phospholipids are also important in the production of cell membranes. CHOLESTEROL Cholesterol is a byproduct of protein metabolism. Bonding oily fat (fat-soluble vitamins) to nitrogen via oxidation forms cholesterol. This process utilizes vitamins, D, E, K, A, and T. These are your fat-soluble vitamins that are bound to the nitrogen portion of foods. The basic purpose of fat-soluble vitamins is to lubricate membranes. The vitamin (oil) prevents oxygen from reaching the membrane, which may inhibit its function. Fat-soluble vitamins also provide the substance necessary to make hormones, enzymes, and antibodies. For example, Vitamin D. lubricates all gross membranes that are exposed to air, such as your skin, respiratory passages, and the digestive membranes. This is your antioxidant lubricator Vitamin A. lubricates secondary membranes that are exposed to the blood, such as the liver, kidney, lungs and spleen. Vitamin A. is called your hydrogen lubricator. Vitamin K. lubricates cell membranes that are exposed to water. Vitamin F. fatty acids are used to make enzymes. Vitamin E. is used to make hormones. Vitamin T. which, is sesame seed oil, is used to make antibodies Lecithin prevents oil and fat from going rancid. So the purpose of fat-soluble vitamins is to oxidize and combust with protein to form cholesterol, which then transposes it into a lubricator, a hormone, antibody, or enzyme. Low-density lipoproteins are rich in cholesterol and carry some triglycerides and are used to produce sex hormones. High-density lipoproteins are rich in triglycerides and carry some fat. Please note that at any one time, the body can dictate the percentage of low-density lipoproteins vs. high-density lipoproteins. It's obvious that an imbalance can create multiple diseases in the body. Please note that these lipoproteins also engulf toxins and then are stored in tissue cells. At a later time, the body gradually detoxifies these deposits unless the amount is overwhelming. Similar to glucose, cholesterol is affected by many organs and glands and in itself is not a reliable indicator as to what is going on in the body. Over the years, the labs went from a normal cholesterol reading of 300, down to 250, then down to 200, and now down to 150. If they continue this nonsense they will create a whole new list of diseases. I recommend that your cholesterol levels be between 175-275mg/dL.	-192
Triglycerides Triglycerides SERUM LIPIDS Serum lipids serve as a primary source of energy along with glucose. The functions are many, such as the production of cell membranes, precursors to hormones, and bile acids. Lipids are first broken down in the duodenum, along with bile, which emulsifies the fats, and prepares them for absorption into the lymphatic system. Pancreatic lipase hydrolyzes cholesterol, and triglycerides into fatty acids, and glycerol. The fatty acids and glycerol are then reconverted back into triglycerides by the intestinal cells and then discharged into the lymphatic or portal blood system, which is then sent to the liver. Cholesterol is also absorbed in both the free and esterified forms into the lymphatics. Cholesterol is also synthesized in the reticular cells and histiocytes throughout the body but mainly formed in the liver. Under the influence of iodine via the thyroid, carbohydrates, amino acids, and other fats are converted to cholesterol via multiple molecules of acetyl coenzyme A creating a sterol nucleus. Triglycerides are also assembled in the liver from glycerol and fatty acids. The liver is the main organ regulating blood lipids. So the liver can degrade fatty acids for energy, synthesize triglycerides from carbohydrates and proteins. The liver can then hydrolyzes the triglycerides back into three fatty acids, and glycerol then degrades the fatty acids into acetyl coenzyme A via beta-oxidation. Then acetyl coenzyme A is then oxidized to release ATP. The liver also synthesizes phospholipids, lecithin, cephalins (that produce thromboplastin), and sphingomyelin (produces the myelin sheath) are formed in the liver and transported via lipoproteins. An increase in triglycerides or choline/inositol increases phospholipid production. Phospholipids are also important in the production of cell membranes. TRIGLYCERIDES Triglycerides compromise 95% of fat stored in adipose tissue and stored as glycerol, fatty acids, and monoglycerides. The liver reconvert's these back to triglycerides. 80% of your triglycerides make up VLDL, and 15% form LDL’S. From a pathological viewpoint, this test evaluates atherosclerosis and measures the bodies ability to utilize fat. From the physiologic perspective, triglycerides are nothing more than three fatty acids, and esters of glycerol. Fatty acids are composed of sugar and alcohol. Triglycerides travel with cholesterol (LDL/HDL) to combust cholesterol at the appropriate time.Triglycerides are needed for calculation of LDLC (low-density lipoprotein cholesterol) concentration. Triglycerides are the matches or “the spark” that ignites and combusts the cholesterol. Triglycerides are implanted in the cell membrane of all neurological and glandular tissue. Triglycerides create the energy for a neurological impulse to occur. When the neurological impulse occurs triglycerides actually “explode” causing the active exchange of electrolytes. Primary glands involved in triglyceride metabolism are the posterior pituitary, the hypophyseal stalk, adrenals, and the head of the pancreas.Therefore, any condition affecting these organs can affect triglyceride levels. High levels are a greater risk for a heart attack then a high cholesterol. Low triglyceride levels from the physiologic perspective cause low energy. Triglycerides Normally Range From 0-199. It Is Rather Obvious That 0 Triglycerides Could Not Be Achieved Physiologically. My Ranges Are From 75-200 mg/dL	66.4
TSH TSH T-4, T-3, T3 uptake and TSH Thyroid-stimulating hormone (TSH) from the anterior pituitary, stimulates the production of thyroxin, and triiodothyronine, therefore, having a dramatic effect on the T4/T3 test results. Thyrotrophs makeup 5% of the anterior pituitary and produce between 100-400mU/day of TSH. Circadian peaks with the onset of sleep are between 9 pm-5am and a minimum between 4-7pm. TSH is regulated by an open feedback loop via thyroxin whereby thyroxin passes into the CSF of the lateral ventricles and is taken up by the epithelial cells of the choroid plexus, which when thyroxin levels are low, stimulates TRH-secreting neurons in the hypothalamus. TSH does the following: 1. Stimulates phospholipid metabolism 2. Stimulates purine and pyrimidine precursors and their incorporation into nucleic acids. T-4 and 3 indicate the denitrification power of iodine via thyroxin with T3 being much more powerful than T4. All food contains active biological nutrients that are bound with nitrogen. When this food reaches the liver, the iodine is used to cleave the nitrogen from the nutrient. Therefore, thyroxin and T3 are important in fat and protein digestion, absorption, and growth and endocrine function. This catabolic activity begins once aerobic bound substances become totally anaerobic and lose the need for nitrogen bonding. Nitrogen is cleaved by T3 or T4 in the liver for example as in glycogen storage. Other substances are needed by specific cells and are transported via total binding globulin to the cells where at that point, the nitrogen bonds are cleaved. Less than 1% of T3 is unbound. A high T-3 uptake indicates a hypothyroid, where a low T-3 uptake indicates a hyperthyroid.	-118.96
Thyroxine (T4) Thyroxine (T4) T-4, T-3, T3 uptake and TSH Thyroid-stimulating hormone (TSH) from the anterior pituitary, stimulates the production of thyroxin, and triiodothyronine, therefore, having a dramatic effect on the T4/T3 test results. Thyrotrophs makeup 5% of the anterior pituitary and produce between 100-400mU/day of TSH. Circadian peaks with the onset of sleep are between 9 pm-5am and a minimum between 4-7pm. TSH is regulated by an open feedback loop via thyroxin whereby thyroxin passes into the CSF of the lateral ventricles and is taken up by the epithelial cells of the choroid plexus, which when thyroxin levels are low, stimulates TRH-secreting neurons in the hypothalamus. TSH does the following: 1. Stimulates phospholipid metabolism 2. Stimulates purine and pyrimidine precursors and their incorporation into nucleic acids. T-4 and 3 indicate the denitrification power of iodine via thyroxin with T3 being much more powerful than T4. All food contains active biological nutrients that are bound with nitrogen. When this food reaches the liver, the iodine is used to cleave the nitrogen from the nutrient. Therefore, thyroxin and T3 are important in fat and protein digestion, absorption, and growth and endocrine function. This catabolic activity begins once aerobic bound substances become totally anaerobic and lose the need for nitrogen bonding. Nitrogen is cleaved by T3 or T4 in the liver for example as in glycogen storage. Other substances are needed by specific cells and are transported via total binding globulin to the cells where at that point, the nitrogen bonds are cleaved. Less than 1% of T3 is unbound. A high T-3 uptake indicates a hypothyroid, where a low T-3 uptake indicates a hyperthyroid.	84
T3 Total T3 Total T-4, T-3, T3 uptake and TSH Thyroid-stimulating hormone (TSH) from the anterior pituitary, stimulates the production of thyroxin, and triiodothyronine, therefore, having a dramatic effect on the T4/T3 test results. Thyrotrophs makeup 5% of the anterior pituitary and produce between 100-400mU/day of TSH. Circadian peaks with the onset of sleep are between 9 pm-5am and a minimum between 4-7pm. TSH is regulated by an open feedback loop via thyroxin whereby thyroxin passes into the CSF of the lateral ventricles and is taken up by the epithelial cells of the choroid plexus, which when thyroxin levels are low, stimulates TRH-secreting neurons in the hypothalamus. TSH does the following: 1. Stimulates phospholipid metabolism 2. Stimulates purine and pyrimidine precursors and their incorporation into nucleic acids. T-4 and 3 indicate the denitrification power of iodine via thyroxin with T3 being much more powerful than T4. All food contains active biological nutrients that are bound with nitrogen. When this food reaches the liver, the iodine is used to cleave the nitrogen from the nutrient. Therefore, thyroxin and T3 are important in fat and protein digestion, absorption, and growth and endocrine function. This catabolic activity begins once aerobic bound substances become totally anaerobic and lose the need for nitrogen bonding. Nitrogen is cleaved by T3 or T4 in the liver for example as in glycogen storage. Other substances are needed by specific cells and are transported via total binding globulin to the cells where at that point, the nitrogen bonds are cleaved. Less than 1% of T3 is unbound. A high T-3 uptake indicates a hypothyroid, where a low T-3 uptake indicates a hyperthyroid.	-43.33
T3 Uptake T3 Uptake T-4, T-3, T3 uptake and TSH Thyroid-stimulating hormone (TSH) from the anterior pituitary, stimulates the production of thyroxin, and triiodothyronine, therefore, having a dramatic effect on the T4/T3 test results. Thyrotrophs makeup 5% of the anterior pituitary and produce between 100-400mU/day of TSH. Circadian peaks with the onset of sleep are between 9 pm-5am and a minimum between 4-7pm. TSH is regulated by an open feedback loop via thyroxin whereby thyroxin passes into the CSF of the lateral ventricles and is taken up by the epithelial cells of the choroid plexus, which when thyroxin levels are low, stimulates TRH-secreting neurons in the hypothalamus. TSH does the following: 1. Stimulates phospholipid metabolism 2. Stimulates purine and pyrimidine precursors and their incorporation into nucleic acids. T-4 and 3 indicate the denitrification power of iodine via thyroxin with T3 being much more powerful than T4. All food contains active biological nutrients that are bound with nitrogen. When this food reaches the liver, the iodine is used to cleave the nitrogen from the nutrient. Therefore, thyroxin and T3 are important in fat and protein digestion, absorption, and growth and endocrine function. This catabolic activity begins once aerobic bound substances become totally anaerobic and lose the need for nitrogen bonding. Nitrogen is cleaved by T3 or T4 in the liver for example as in glycogen storage. Other substances are needed by specific cells and are transported via total binding globulin to the cells where at that point, the nitrogen bonds are cleaved. Less than 1% of T3 is unbound. A high T-3 uptake indicates a hypothyroid, where a low T-3 uptake indicates a hyperthyroid.
T3 Free T3 Free A free T3 test, or free triiodothyronine test, measures the amount of free triiodothyronine in your blood. Triiodothyronine (T3) is a hormone produced by the thyroid gland that helps regulate metabolism and energy levels. A normal free T3 level is typically between 2.5–4.0 ng/dL, but reference values may vary by lab. A higher-than-normal level of T3 may indicate an overactive thyroid, while a lower-than-normal level may indicate an underactive thyroid.	5.26
T4 Free T4 Free Free T4 is the amount of thyroxine (T4) in the blood that is not attached to proteins. T4 is a hormone produced by the thyroid gland that helps control metabolism and growth. A free T4 test measures the amount of free T4 in your blood.	86.21
Urine pH Urine pH URINE PH A high urine pH may be due to: Kidney failure Urinary tract infections Vomiting A low urine pH may be due to: Diarrhea Too much acid in the body fluids such as metabolic acidosis and diabetic ketoacidosis Starvation	-100
Bun/Creatin Ratio Bun/Creatin Ratio BUN/CREATININE RATIO BUN plus creatinine are residue byproducts of protein and muscle metabolism respectively. They are kept in continual balance by the water content of your body. The kidneys flush out the excessive BUN/creatinine concentration when it gets too high. The kidneys are under the influence of the posterior pituitary via antidiuretic hormone, which regulates the amount of water leaving the body. Therefore, the posterior pituitary through potassium regulates water balance. The posterior pituitary then regulates the amount of water in any one place of the body. So, therefore, it can either increase or decrease the water content in the blood, thus altering pH. The posterior pituitary besides balancing water also regulates sugar and mineral concentration. BUN/CREATININE IS HIGH WHEN General considerations: ¬ Decrease high protein intake ¬ Or increase water intake ¬ BUN/CREATININE is high when you have a high BUN or a low CREATININE or both BUN/CREATININE IS DECREASED WHEN General considerations: ¬ Increase protein intake ¬ Or decrease water intake ¬ BUN/CREATININE is low when either you have a low BUN or a high CREATININE or both	203.58									1
COQ10 Coenzyme COQ10 Coenzyme Coenzyme Q10 (CoQ10 also known as ubiquinone, is a natural coenzyme and an antioxidant produced by the body. It is also obtained from dietary sources, such as meat, fish, seed oils, vegetables, and dietary supplements. CoQ10 plays a role in mitochondrial oxidative phosphorylation, aidingthe production of adenosine triphosphate (ATP), which is involved in energy transfer within cells. The structure of CoQ10 consists of a benzoquinone moiety and an isoprenoid side chain, with the "10" referring to the number of isoprenyl chemical subunits in its tail. Biological function CoQ10 is a component of the mitochondrial electron transport chain (ETC), where it plays a role in oxidative phosphorylation, a process required for the biosynthesis of adenosine triphosphate, the primary energy source of cells. CoQ10 is a lipophilic molecule that is located in all biological membranes of the human body and serves as a component for the synthesis of ATP and is a life-sustaining cofactor for the three complexes (complex I, complex II, and complex III) of the ETC in the mitochondria. CoQ10 has a role in the transport of protons across lysosomal membranes to regulate pH in lysosome functions. The mitochondrial oxidative phosphorylation process occurs in the inner mitochondrial membrane of eukaryotic cells. This membrane is highly folded into structures called cristae, which increase the surface area available for oxidative phosphorylation. CoQ10 plays a role in this process as an essential cofactor of the ETC located in the inner mitochondrial membrane and serves the following functions: electron transport in the mitochondrial ETC, by shuttling electrons from mitochondrial complexes like nicotinamide adenine dinucleotide (NADH), ubiquinone reductase (complex I), and succinate ubiquinone reductase (complex II), the fatty acids and branched-chain amino acids oxidation (through flavin-linked dehydrogenases) to ubiquinol–cytochrome-c reductase (complex III) of the ETC: CoQ10 participates in fatty acid and glucose metabolism by transferring electrons generated from the reduction of fatty acids and glucose to electron acceptors; antioxidant activity as a lipid-soluble antioxidant together with vitamin E, scavenging reactive oxygen species and protecting cells against oxidative stress, inhibiting the oxidation of proteins, DNA, and use of vitamin E.								5
Fibrinogen Fibrinogen FIBRINOGEN- BLOOD TEST RANGES 200 and 400 mg/dL (2.0 to 4.0 g/L) (coagulation factor I) is a glycoprotein complex that is synthesized by the liver and circulates in the blood stream. During tissue and or vascular injury, it is converted enzymatically by thrombin to fibrin which creates a blood clot The primary function is to occlude blood vessels thus stopping bleeding. Fibrin also binds and reduces the activity of thrombin. This activity referred to as antithrombin I, which limits clot formation. Fibrin also mediates and is important in blood platelet, endothelial cell spreading, capillary tube formation, tissue fibroblast proliferation, and angiogenesis thereby promoting revascularization and wound healing. Thrombin is synthesized in the liver and secreted into the general circulation in an inactive zymogen form (prothrombin), a complex multidomain glycoprotein that is activated to yield thrombin at sites of vascular injury by limited proteolysis following upstream activation of the coagulation cascade.								5
LPA LPA LPA- BLOOD TEST LEVELS 30-50 mg/dL (75-125 nmol/L Lipoprotein (a) or Lp(a) levels are measured in milligrams per deciliter (mg/dL) or nanomoles per liter (nmol/L). A lipoprotein(a) (Lp(a)) blood test measures the amount of Lp(a) in your blood, which is lipoprotein that carries cholesterol. Thus elevated Lp(a) levels are associated with an increased risk of cardiovascular disease. Recommended for individuals with a family history of heart disease or other risk factors. High levels of lipoprotein (a) (Lp(a), may cause heart attack, stroke, and or aortic stenosis LPA is produced through multiple mechanisms within cells and in biological fluids like plasma and serum. Lysophosphatidic acid (LPA) is primarily produced by the enzyme autotaxin (ATX). ATX, which is a secreted lysophospholipase D, converts lysophospholipids, primarily lysophosphatidylcholine (LPC), into LPA. This extracellular production pathway is considered the major source of bioactive LPA.
Apo B Apo B Apolipoprotein B (ApoB) is a protein that plays a crucial role in the transport of fats and cholesterol in the blood. It is a key component of low-density lipoproteins (LDL) and other lipoproteins that carry triglycerides, cholesterol, and cholesterol esters. Elevated ApoB levels are associated with an increased risk of cardiovascular disease. Key aspects of ApoB: Role in Lipoprotein Formation: ApoB is a primary protein on the surface of various lipoproteins, including LDL, VLDL, chylomicrons, and lipoprotein(a). Atherogenic Particle Indicator: ApoB measurement helps determine the number of atherogenic particles circulating in the bloodstream, which are linked to plaque buildup in arteries. Cardiovascular Risk: Elevated ApoB levels are a significant indicator of increased cardiovascular risk, particularly atherosclerosis. ApoB Test: An ApoB test measures the amount of ApoB in the blood and is often used to assess the risk of heart disease. Two Forms: ApoB exists in two forms: ApoB100 (primarily in the liver) and ApoB48 (primarily in the intestine). Apo High levels of apolipoprotein B (ApoB) are often associated with elevated levels of LDL cholesterol (LDL-C) and can be caused by a variety of factors, including diet, lifestyle, underlying medical conditions, and genetics.								5
Gland Totals		5	10	15	10	30	5	0	40	1	15	0	15	15	5
Gland Totals (%)		50%	33%	133.33%	25.5%	51%	270%	%	104.13%	204%	46.33%	%	115.33%	192.67%	50%

Results by Endocrine

Gland	Result
Anterior Pituitary Anterior Pituitary THE PITUITARY GLAND The pituitary, the existence of which has been known for 2000 years, sits in the sella turcica of the sphenoid bone. The sella turcica forms the roof of the sphenoid sinus. The lateral walls are comprised of durra or bone, which abut the cavernous sinuses and can affect the 3rd, 4th, and 6th cranial nerves and the internal carotid arteries since they transverse thru this area. The cavernous sinuses can exert a great deal of CSF pressure but, due to the diaphragm sellae, the gland will not become compressed nor will the optic chiasm and tracts, which lie immediately above the diaphragm sellae. Also lying in close proximity to the cavernous sinuses are the internal carotid arteries, cranial nerves 3, 4, 5 and 6, the third ventricle and the optic chiasm, which lies above the diaphragm sellae. The pituitary is divided into three parts: 1. ADENOHYPOPHYSIS-is the anterior portion, which is derived from Rathke’s pouch. This is divided into three lobes: the pars distalis (anterior lobe,) the pars inter-media (intermediate lobe) and the pars tuberalis. 2. NEUROHYPOPHYSIS-is the posterior portion and is composed of the pars nervosa, the infundibular stalk, and the median eminence. The major supply of axons to the neural lobe is the magnicellular secretory neurons from the paraventricular and supraoptic nuclei of the hypothalamus. These axon terminals also secrete AVP (regulating blood osmolarity, pressure, and fluid balance) and oxytocin into the surrounding capillary beds leading into the hypophyseal veins. The infundibular stalk is surrounded by the pars tuberalis, and together they make up the hypophyseal stalk. 3. VESTIGIAL INTERMEDIATE LOBE . The pituitary gland is regulated by the hypothalamus via feedback mechanisms of hormones and from paracrine and autocrine secretions from the pituitary itself. It attaches to the hypothalamus via the stalk thru the diaphragm sellae and into the median eminence. The pituitary is derived from the: • ECTODERM-which forms the pars distalis/tuberalis and the intermediate lobe • NEURAL PORTION-which forms the infundibulum, posterior pituitary, and neural stalk The pituitary weighs between 4-900 mgs (during pregnancy up to 1 gram), is bean shaped and brownish in color with dimensions of 9 mm A/P, 6mm S/I, 13 mm laterally. The hypothalamus receives its blood supply from the superior (provides 10-20 % of the blood supply) and inferior hypophyseal arteries (supply blood to the posterior pituitary), which are derived from the internal carotid arteries. These arteries form a capillary network in the median eminence (external to the blood-brain barrier). This capillary network picks up hypothalamic secretions from the hypothalamic nerve endings delivering them into the long and short hypophyseal portal veins, which are now transported to the anterior pituitary. Please note that retrograde blood flow causes bi-directional movement of blood between the hypothalamus and pituitary. Once the hypothalamic releasing hormones reach the pituitary, they activate G protein receptors on the cell membrane, creating a cascading chain reaction for the production of their pituitary hormone counterparts. Blood drainage of the pituitary leaves through the cavernous sinuses and the petrosal veins and out the jugular foramina via the jugular vein. Note that the blood supply to the pituitary via the hypothalamus is not unidirectional and can flow both ways creating ultra-short biofeedback loops. The hypothalamus releases its secretions via hypothalamic neurons, which end in the infundibulum and permeate into the fenestrations at the perigomitolar capillaries. This enters the portal vein, which enters the capillary circulation of the anterior pituitary (which provides 80-90 % of the blood supply to the pituitary). The pituitary, as stated above, is attached to the hypothalamus via the pituitary infundibulum. The diaphragm sellae has a 5mm opening for the hypophyseal stalk and allows transmission of pulsations of CSF. The purpose of the pituitary infundibulum is to act as a direct pathway for hormonal secretion between the hypothalamus and the pituitary. Pituitary hormones are released as pulsations, which does affect hormonal levels minute, by minute, which may give false positives when measuring hormonal levels. Each releasing factor (hormone) that is released from the hypothalamus causes a release of a hormone from the anterior pituitary. The hypothalamus also produces two hormones called anti-diuretic hormone and oxytocin. The anti-diuretic hormone is formed primarily by the supraoptic nuclei, whereas oxytocin is formed primarily in the paraventricular nuclei. The major nerve tracts of the neurohypophysis arise from these two nuclei, from large cells termed magnocellular cells forming the supra optico hypophyseal tract and the paraventricular hypophyseal tract. AVP and oxytocin tracts are also distributed widely and project into the brain stem affecting the vagal nuclei, glossopharyngeal nuclei, and the spinal cord, sending information to the ANS to evaluate blood pressure. Vasopressinergic and oxytocin fiber pathways (which have different effects than those that end in the posterior pituitary) also terminate in the choroid plexus, which influences salt and water exchange between the brain (especially regions associated with emotion and memory) and the CSF. Neurological impulses from the two nuclei above, cause a secretory granular release of these two hormones into the posterior pituitary, which are then released into the adjacent capillaries. It is interesting to note that the differences between oxytocin and anti-diuretic hormone are two amino acids. Otherwise, the chains are identical. The functions are entirely different, as you will see. The anterior pituitary is controlled by the hypothalamus in a slightly different manner than the posterior pituitary. Oxytocin and anti-diuretic hormone (AVP) are produced in the hypothalamus and are released into the posterior pituitary, via the neurological tracts of those nuclei mentioned above in the hypothalamus. Other neurological tracts secrete other neuropeptides called TRH (thyrotrophin releasing factor), CRH (corticotrophin releasing hormone), VIP and neurotensin. Paraventricular hypophyseal tracts located on either side of the ventricles are both unmylenated and descend thru the infundibulum. The releasing factors from the hypothalamus are transmitted to nerve endings, which then release these factors into a primary plexus of veins known as the hypophyseal portal system. These veins are located in the pituitary infundibulum and travel into the anterior pituitary, releasing the hypothalmic hormones into and stimulating the anterior pituitary. THE ANTERIOR PITUITARY (PARS DISTALIS, PARS GLANDULARIS) The anterior lobe is composed of 3 divisions: 1. PARS DISTALIS – largest and produces most of the hormones 2. THE INTERMEDIA-the least developed 3. TUBERALIS-attached to the pituitary stalk and produces many of the glycoproteins. At this poin, there are cells that produce specific hormones, from specific releasing factors released from specific areas in the hypothalamus. There are 5 specific secreting cells that arise from totipotential pituitary stem cells of the anterior pituitary. They are: • CORTICOTROPHIC CELLS-which express POMC (pro-opiomelanocortin) peptides including ACTH • SOMATOTROPH CELLS-which express growth hormone • THYROTROPHS-which express TSH • GONADOTROPHS-which express FSH and LH • LACTOTROPH CELLS-which produce prolactin These hormones are produced in the anterior pituitary and are now released into the hypophyseal portal veins. They continue down through the circulatory system to target sites in the body. Any hormones that are now released from the target sites reenter the bloodstream and are transported back to the hypothalamus via the hypothalamic artery and to the pituitary via the hypophyseal artery. This is why it should be looked at as a “neuroendocrine axis” due to this dual control mechanism. It makes much more sense and is more reliable to have each system checking and balancing each other. The following hormones are released from the anterior pituitary: 1. FOLLICLE STIMULATING HORMONE (GONADOTROPHINS) -are released by lutenizing hormone-releasing hormone (LHRH) via the hypothalamus. Gonadotrophin cells make up 10-15 % of the anterior pituitary. FSH and LH regulate gonadal steroid hormone biosynthesis and germ cell production. FSH, LH, TSH, and HCG are all glycoproteins. The purpose of follicle stimulating hormone is to stimulate the growth of the follicle on the ovary. FSH, LH, TSH AND HCG all have identical alpha subunit chains. These are polypeptides containing 92 amino acids, whereas the beta subunit chains contain 117, 121, and 145 amino acids. LHRH synthesizes these alpha and beta gonadotrophin subunits forming and secreting FSH, LH, CRH (corticotrophin releasing hormone) and progesterone. The follicle-stimulating hormone increases estrogen levels. As estrogen levels rise in the bloodstream, they enter the hypothalamic artery and decrease the output of LHRH from the hypothalamus. There are also a group of peptide hormones produced by the gonads called inhibins, which are produced by the follicular-luteal and sertoli cells of the gonads that inhibit FSH secretion, without affecting LH secretion. Activins also produced by the above cells stimulate GnRF, which induces FSH production. Activins and inhibins regulate granulose cell growth, differentiation, steroid hormone production, oocyte maturation and follicular development. You will notice that most hormones either increase or decrease the output of other hormones through this kind of a feedback mechanism. If a hormone increases the output of another hormone, then it is said to be a positive feedback mechanism. On the other hand, if a hormone decreases the output of another hormone, then it is said to be a negative feedback mechanism. 2. CORTOCOTROPHIN STIMULATING HORMONE (ADRENO-CORTICOTROPHIC STIMULATING HORMONE) (ACTH)-ACTH production is inhibited by angiotensin 2, activins, inhibins, cytokines and cell-to-cell communication. Corticotrophs constitute 20% of the anterior pituitary. ACTH is a 39 amino acid peptide made from a 241 amino acid structure called pro-opiomelanocortin (POMC). This is cleaved in tissue-specific fashion to yield small peptide hormones. POMC is also transcribed in other tissues such as the brain, liver, kidney, gonads and the placenta. POMC expression within the hypothalamus is cleaved into MSH and is thought to regulate hair color and appetite control. POMC is controlled by CRH, arginine, vasopressin, stress, circadian rhythms and the negative feedback of cortisol. Pro-inflammatory cytokines (interleukins 1 and 6, TNF (tumor necrosing factor) and physical stress increases ACTH release. ACTH circadian rhythms begin at 4 am and peak at 7 am, and are generated by the supra chiasmic nucleus, which signals CRH release. ACTH is secreted in bursts and increases in frequency 3-5 hours after sleep and is highest upon awakening. Adrenal steroid hormones reach their peak between 11 pm and 3 am. ACTH circadian rhythms are entrained by visual cues and the light/dark reactions. The rhythms are affected by sleep/wake, light/dark reactions, spontaneous bursts and stress via CRH. Glucocorticoids inhibit while CRH stimulates the synthesis of ACTH by binding to high-affinity receptors stimulating cyclic-AMP activating protein kinase A of the POMC mRNA (pro-opiomelanocortin). POMC undergoes post-translation processing including glycosylation, enzymatic cleavage, phosphorylation, NH2 terminal acetylation, and COOH amidation via amidase, which catalyzes the formation of a monocarboxylic acid and ammonia by cleavage of the C-N bond of a monocarboxylic acid amide. ACTH is also cleaved into beta-MSH and beta-endorphin. The actions of ACTH on the adrenals is to maintain adrenal size, function and adrenal steroid genesis thru specific cell membrane receptors, which requires a G protein-coupled melanocyte 2 receptor (3500 on each adrenal cell) and calcium ion channels for ACTH to bind. This activates adenyl cylclase, which increases cAMP and protein kinase A activity and phosphorylation of many proteins. ACTH secretion activates the conversion of cholesterol into pregneolone (hormone production) and protein synthesis via p450 enzyme transcription for cortisol, aldosterone and 17-hydro progesterone, which is necessary to produce steroid hormones. Exercise, which is exhausting and for short durations increases ACTH immensely. Pain, infection, trauma and hypoglycemia also affect ACTH. ACTH is controlled by a 3-tier system: 1. Hypothalamic secretions such as CRH and vasopressin 2. Intra pituitary cytokines and growth factors 3. Glucocorticoid negative feedback on the hypothalamus Glucocorticoid target neurons lie outside the hypothalamus in the hippocampus, septum, and amygdale nucleus, and are part of the visceral brain involved in emotional states. At the hippocampus glucocorticoid receptors determine the set point for cortisol. Glucocorticoids affect cerebral vascular permeability, choroid transport of H20 and electrolytes, regulating CSF synthesis and brain volume. Although most steroids that affect the brain come from the circulation, these steroids produced in the brain are called neurosteroids (estradiol, pregnenolone, dehydroepiandosterone located in the oligodendroglial cells). Glucocorticoids inhibit the release of CRH and AVP. Morphine stimulates the release of ACTH. 3. THYROID STIMULATING HORMONE (TSH) -Thyrotrophs make up 5% of the anterior pituitary. TSH is a glycoprotein where the cells are located in the anteromedial portion of the anterior pituitary. TSH is composed of two subunits an: • Alpha subunit-which is similar to lh, fsh, and hcg • Beta subunit-which is 112 amino acids long TRH increases transcription of both alpha and beta units, whereas dopamine inhibits them. TRH stimulates glycosylation of TSH within the rough endoplasmic reticulum, which is then sent to the Golgi apparatus, folded and put into secretory granules. Estrogens, glucocorticoids, and GH modify TSH secretion. Stress also inhibits the release of TSH and GH. TRH binds to the thyrotrophin membranes, and through calcium ion channels and cGMP (cyclic guanosine monophosphate), which act as secondary messengers, produce between 100-400mU/day of TSH. TSH secretion is pulsating in nature, pulsing every 2-3 hours. Circadian peaks with the onset of sleep are between 9 pm-5am, are at a minimum between 4-7pm, and do not appear to be sleep entrained. This is also accompanied by an ultradian rhythm of 90-180 minutes. TSH stimulates the thyroid to produce thyroxin, which determines metabolic rate with pulsating variations of thyroxin at 1-2 hour intervals. TSH is decreased by warm temperature, starvation, and infection via tumor necrosing factor. TSH does the following: a. Stimulates phospholipid metabolism b. Stimulates purine and pyrimidine precursors and their incorporation into nucleic acids TSH is regulated by an open loop feedback via thyroxin, whereby thyroxin passes into the CSF of the lateral ventricles and is taken up by the epithelial cells of the choroids plexus. When thyroxin levels are low, these stimulate TRH-secreting neurons in the hypothalamus. TSH may be modified by estrogens, glucocorticoids, and GH and are inhibited by the pituitary and hypothalamic cytokines. Thyrotrophin is also inhibited by somatostatin and dopamine. 4. LUTEINIZING HORMONE-plays an important role in ovulation and the release of estrogen in the female and testosterone in the male. 5. LUTEOTROPHIC STIMULATING HORMONE (PROLACTIN) -lactotroph cells comprise 15-25 % of the anterior pituitary, and most come from GH-producing cells. Prolactin is 199 amino acids long, closely resembles GH, and is produced in the pituitary by small polyhedral cells. Approximately 100 ugs of prolactin are produced daily as compared to 50 times this for GH. Dopamine secretions via the tuber infundibular pathways inhibit prolactin, by inhibiting adenyl cylclase activity and the release and synthesis of prolactin. Prolactin is also inhibited by calcitonin and transforming growth factor. Prolactin-releasing factors include GnRH, TRH, VIP, oxytocin and estrogen (which increases gene transcription and secretion.) Prolactin is released in moderate amounts during mid-day and increase around bedtime. Prolactin stimulates the development of breast tissue (along with growth hormone and IGF 1) and the secretion of milk. During pregnancy, the pituitary doubles due to PRL producing cells. Prolactin levels can increase from 200 micrograms to 500 micrograms and ammonic PRL may increase to 100 times that of the blood. Suckling causes the mechanoreceptors in the breasts to stimulate nerves in the nipple, which travel to the spinal cord, stimulating the release of prolactin. Then they travel to the spinal cord up through the spin thalamic tract to the lateral cervical nucleus, and to the medulla. Neurological impulses ascend to the oxytocin neurons of the magnicellular cells, to the supraoptic nuclei and the paraventricular nucleus, finally affecting the pituitary. Oxytocin is affected by mating, emotional and physical stress, and cycles related to sleep. The principle inhibitor of prolactin is dopamine. Prolactin is neurologically controlled by many tuber hypophyseal neurons, where the set point is controlled by dopamine secretion (inhibits PRL where serotoninergic stimulates the release). The posterior pituitary also affects PRL release via oxytocin, AVP, and TRH. Prolactin acts through receptors in the liver, breast, adrenal cortex, kidneys, epidermis, lungs, myocardium, pancreatic islets, brain, lymphocytes, ovaries/uterus and testicle/prostate. These are the same receptors used for GH reception. Prolactin and oxytocin together regulate milk production, whereas oxytocin is used for milk let down. Both hormones are under the control of the gonadal steroidal hormones. Milk is synthesized in the glandular cells of the alveoli. Oxytocin receptors are found on these glandular cells, which cause these cells to contract expelling milk into the ducts, where oxytocin causes a widening and contracting of these same ducts. REGULATION OF THE MENSTRUAL CYCLE On the first day of menstrual bleeding, the follicles are small, accompanied by low levels of estradiol. Pulsations of LH are fast, about 1 every 60 seconds. FSH levels are high, which increase follicular size and estradiol production. As estradiol production increases, it acts as a negative feedback loop on the hypothalamus, decreasing LH to 1 pulsation every 90 seconds. At the 15th, day estradiol, which is at a peak, triggers the hypothalamus to release GnRH and high amounts of FSH and LH, which then stimulates the dissolution of the follicular wall, releasing the ovum into the fallopian tube. The Follicular cells now undergo differentiation and become the corpus luteum (yellow body) that secretes large amounts of progesterone. This will maintain pregnancy due to its negative feedback on GnRH, FSH and LH production. The time frame is fixed for the corpus luteum. This also produces small amounts of estradiol. If the egg is not fertilized and implanted in the endometrial lining, then the corpus luteum digresses due to prostaglandin F production, which causes luteolysis, decreasing progesterone and estradiol production. This causes a sloughing off of the endometrium within 28-30 days, or at the end of pregnancy prior to parturition. Just prior to parturition, there is an increase in FSH and LH production and oxytocin is released in an explosive pulsating fashion. Stresses on reproduction include: • Mental • Diet chemical • Physical exercise • Pain and injury • Infection All create reductions in GnRH, FSH, LH, and gonadotrophins. Fuels essential for reproductive function are glucose and fatty acids. 6. MELANOCYTE-STIMULATING HORMONE-This stimulates the melanocytes to produce melatonin for skin pigmentation and sexual drive. 7. SOMATOTROPHIN (GROWTH HORMONE) (GH)-Makes up 50% of the cells of the anterior pituitary and produces between .25-52 mgs every 24 hours with a storage capacity of 5-10 mgs at any time. Somatotrophin is a 191 amino acid chain with a molecular weight of 22,005 and a half-life between 9-27 minutes. The purpose of growth hormone is to create growth in the body. It does this by: • Promoting protein synthesis, amino acid transport, increased urinary nitrogen retention, increases lean muscle tissue and energy expenditure • Increases fatty-acid breakdown for energy • Decreasing glucose utilization, by enhancing glycogen deposition and insulin secretion • Increasing bone growth through osteoclastic activity, epiphysis growth, osteoclastic differentiation, and activity and increases bone mass by endochondral bone formation. • Having acute insulin-like effect followed by lipolysis, decreased glucose transport, decreased lipogenesis (by inhibiting lipoprotein lipase) and increased lipolysis. GH has been described as being, anabolic, lipolytic and diabetogenic. GH does the following: a. Stimulates the Liver-RNA synthesis, plasma protein synthesis, somatomedin release and replication b. Stimulates Muscles-amino acid transport and incorporation c. Stimulates vascular outgrowth of blood vessels d. Stimulates hemopoeitic centers via increasing mitosis e. Stimulates adipose tissue lipolysis GHRH, GH secretagogues, and SRIF receptor subtypes 2 and 5, mediate GH secretion and controls GH. GHRH induces GH gene transcription and hormone release whereas SRIF inhibits GHRH but not GH biosynthesis. Ghrelin, which is 28 amino acids long, induces GHRH and GH production. Ghrelin is synthesized in peripheral tissues, especially the gastric mucosa neuroendocrine cells. GH release is from rhythms, with a maximum of 2 mgs per day in late puberty, to 20 micrograms in older or obese people. Most GH is released during nocturnal times, irrespective of sleep, with the highest release during slow wave sleep and lowest during REM sleep. Feedback mechanisms also increase GH release such as: • Exercise • Physical and emotional stress • Slow wave sleep • Fasting • High-protein meals • Specific amino acids such as arginine and leucine • High carbohydrate meals when blood sugar is falling. • The sex hormones estrogen, progesterone, testosterone, and TSH also modify GH High levels of glucocorticoids suppress GH. 3 inhibitory peptides, GH itself, somatostatin, and IGF 1 also regulate GH. Other factors that stimulate GH release are insulin in hypoglycemia (which can also suppress GH), arginine, leucine, lysine, norepinephrine, AVP, alpha-MSH, glucagon, epinephrine, 5-hydroxytryptophane, melatonin, and potassium. Other factors that inhibit GH are acetylcholine, progesterone, morphine, melatonin and increased intake of free fatty acids. GH secretion is low in obese people due to high somatostatin levels. Depression also leads to decreased levels of GH. GH has an inverse relationship to insulin and GHRH containing nerve fibers that arise from the arcuate and ventromedial nucleus. GHRH via GHRH cell membrane receptors increase adenyl cyclase, cAMP, protein kinase C and intra calcium ion concentration whereby somatostatin has the opposite dominant effect on these same receptors. IGF 1 (somatostatin C) also influences the hypothalamus to reduce GHRH via the hippocampus (and are excitatory), from the amygdale, which can be excitory (basso lateral amygdale) and inhibitory (corticomedial amygdale). The ventromedial nucleus regulates fat and carbohydrate metabolism. This nucleus contains gluco receptors stimulating insulin secretion and GH release. From a biochemical blood chemistry perspective, the pituitary hormones deal with the growth of the body. This is accomplished by hormones of the anterior pituitary controlling lipoprotein digestion and placement for growth and repair, via the control of all organs and glands that control digestion, assimilation, and metabolism. Without digestion and proper placement of the prepared foods by the body, you have no growth. The primary purpose of the pituitary is one of anabolism, rather than catabolism. This means that any catabolic disease that overcomes the human body may have their roots in the anterior pituitary. The following blood tests are used to determine anterior pituitary function: 1. CHOLESTEROL-This is a byproduct of protein metabolism, which is the bonding of oily fats to nitrogen and is produced by every cell in the body. This is called your endogenous cholesterol. Exogenous cholesterol comes from dietary intake. It is the combination of the above two that shows cholesterol levels. Did you know that the majority of cholesterol produced and taken in through diet forms an enzyme called cholic acid? Cholic acid is an enzyme, which is released by the gallbladder to emulsify fats, which you take in through your diet. If you do not take in any fat, then your body does not need any cholic acid. Since 50-60% of your cholesterol is used to produce cholic acid, your cholesterol levels will rise. Such is the case with all the people on low-fat diets trying to reduce their cholesterol levels. 25-35% of the cholesterol is used as a precursor to make your sex hormones, estrogen, progesterone, and testosterone. Cholesterol is also used to make antibodies and acts as a mucous lubricant for mucus, synovial, and cellular membranes. Since the anterior pituitary controls protein digestion and placement, you can see why cholesterol, which is a byproduct of protein metabolism, can be of use in determining a problem with the anterior pituitary. 2. BLOOD UREA NITROGEN-This is an end product of protein metabolism. When lipoproteins enter the liver via the calcium magnesium gradient, the liver changes the foodstuff from an inorganic to an organic state, and can now process the food. Cleaving a nitrogen atom (breaking a bond) from the amino acid molecule does this. Thyroxin, which is produced by the thyroid, is what “cleaves off” this nitrogen atom from the protein. So, thyroxin oxidizes the protein molecule via iodine, by splitting off one nitrogen atom. When the nitrogen is released, it is converted into ammonia, then to urea, via the ornithine cycle. From the liver, it is sent to the kidneys, via the blood stream, to be released in the urine. 3. MAGNESIUM AND CALCIUM-Calcium is the substance that pushes proteins, fatty acids, and triglycerides through the intestinal wall and through the cell membrane of each cell. When the calcium to magnesium ratio is greater than two-parts calcium to one-part magnesium, there is a movement of the above through the intestinal wall. This calcium to magnesium phenomenon creates an electrical osmotic gradient that draws the calcium and lipoprotein across the membrane of the cell. Magnesium is also very abundant within the cell, approximately one-sixth the amount of potassium. The calcium magnesium ratio within the cells is five to one. In plasma, 75 percent of the magnesium is in the ionic state, with the remainder bound to protein. Magnesium, within the cell, acts as a catalyst for enzymes associated with carbohydrate metabolism. Increased extracellular magnesium decreases neurological and muscular-skeletal activity. The anterior pituitary and its hormones are used to control the mineral magnesium in this endeavor. Calcium, due to its “ratio effect,” can also be looked at when determining anterior pituitary function.	267.88%
Parathyroids Parathyroids THE PARATHYROIDS Located on the posterior portion of the thyroid are four-five parathyroid glands weighing 120 grams total, with an ellipsoidal shape having the dimensions of 6x5x2 millimeters. The blood supply for the parathyroids is the inferior thyroid artery. The chief cells, which are the major cells of the parathyroids, synthesize and secrete parathormone (PTH) (which is 84 amino acid’s long) that comes from a pre-proparathormone, which is 110 amino acids long. Though calcium is the major factor controlling the secretion of PTH, secretion of newly synthesized PTH is from preformed pools of PTH, where cAMP only stimulates these pools. cAMP is the major regulator of PTH secretion. Beta-androgenic catecholamines, dopamine, secretin and prostaglandin E can activate adenylate cylclase and increase cAMP, thereby stimulating PTH regulation. The basic function of PTH is to control calcium concentration in the extracellular fluid (ECF). Parathyroid hormone, calcitonin and calciferous are the principle calcitrope hormones. Sodium, calcium, and potassium play a central role in the transmission of information between cells. Phosphates act as: • Cytoplasmic buffers • Participate in energy exchange • Makeup membranes and nucleic acids The bulk of calcium, phosphates, and magnesium in the body are found in the skeleton. RDA’s of calcium is between 8-1200 mgs, for magnesium 4-600 mgs and 8-1200 mgs for phosphate. Less than 2% of calcium, magnesium and phosphates are found in the plasma and extracellular fluid and are controlled in narrow limits. Steady states of calcium, magnesium and phosphorus approximate urine loss against intestinal absorption and skeletal mineral apposition against mineral absorption. Magnesium in the cells is complexed to phosphate, citrates and anions such as ATP, AMP, and ADP (such as MgATP2). Phosphates are covalently incorporated into proteins, lipids, and nucleic acids. Many enzymes go thru dramatic shifts in activity via phosphorylation and dephosphorylation. Ionized cellular calcium regulates secondary cell messengers. Calcium can increase in a cell due to electrical impulses, hormones, and intracellular signals. Calcium also interacts with proteins such as protein kinase C, and ion channels found in plasma membranes and the sarcoplasmic reticulum. Parathormone levels elevate cell calcium levels in the renal tubules and the osteoblasts. Calcium is transported from the cytoplasm by exchange with sodium. Contracted striated muscle relaxes with rapid removal of calcium from the cytoplasm into the sarcoplasmic reticulum. Plasma membranes undergo many complex interactions with cellular calcium via membrane permeability and pump activity. In erythrocytes, cellular calcium increases potassium permeability. Mitochondria contain most of the intracellular calcium. There are many cytoplasmic enzyme changes via calcium such as adenylate cylclase, guanylate cylclase, cAMP, ATPase and protein C kinase. Since calcium can regulate contractile proteins, it can affect striated muscle, secretory granule contraction, exocytosis, mitotic spindle function and ciliary beating. Calcium concentrations can be reduced quickly via repetitive nerve stimulation. Albumin accounts for 70% of the protein binding of calcium. Magnesium bonds to the same site on the albumin molecule as calcium, but with a lower affinity, thereby having more magnesium in a diffusible form. Magnesium is also affected just the way calcium is to parathormone, and to a lesser degree calcitonin. 70 % of phosphates are bound to phospholipids and phosphoproteins and are also affected in and out of plasma compartments by parathormone, calcitonin, and calciferols. PTH enhances phosphate secretion and inhibits sodium reabsorption in the proximal tubules. PTH stimulates both bone formation and reabsorption (catabolism and anabolism) via influencing osteoclasts, osteoblasts, and osteocytes. PTH enhances synthesis of hyaluronate and inhibits citrate decarboxylation and collagen synthesis while it increases alkaline phosphatase levels. Other affects of PTH include changes in blood flow, mitosis of lymphocytes, enhanced lipolysis and increased gluconeogenesis from the liver and kidney. PTH reacts with specific receptors on the bone and kidney (renal cortex) activating adenylate cylclase and intracellular messenger cAMP According to Guyton’s Physiology on the physiology of calcium and phosphate “phosphates act as buffers, participate in energy exchange, and are an essential component of membranes and nucleic acids. 70 % of phosphates are bound to phospholipids and phosphoproteins.” Phosphates do not affect PTH or calcitonin (CT) levels, but PTH and CT affect phosphate levels. The function of vitamin D and the formation of bone and teeth are all tied together in a common system, along with the two regulatory hormones parathyroid hormone (parathormone), calcitonin and the calciferols. In mammals, the bulk of calcium, phosphates and magnesium are found in the skeleton as hydroxyapatite. Less than 2% are found in the extracellular fluid. Plasma calcium is used for clotting and kinin formation, regulates plasma membrane potential and exocytosis. As stated above, albumin accounts for 70% of the bound calcium. Magnesium also binds to albumin, and since it has a lower specificity for the receptors, it creates more free magnesium in the plasma. Calcium, magnesium, and phosphates continuously enter the plasma via the kidneys (intestinal brush borders) and the ruffled border of bones. Calcium, phosphates, and magnesium are depressed in vitamin D deficiencies. Phosphates are reabsorbed by the proximal convoluted tubules due to PTH, and PTH also absorbs magnesium and calcium from the distal tubules. Calcium is poorly absorbed in the intestinal tract, as are most other bivalent cations. Calcium absorption can be dramatically affected by vitamin D, which has a potent effect on increased calcium absorption in the intestinal tract. In fact calcium, magnesium and phosphates are depressed in vitamin D deficiencies and increased with vitamin D excess. Calcium absorption is also increased by dietary sugars. The D vitamins (calciferols) are steroid molecules of 4 rings. Calciferols are absorbed in the chylomicrons of the small intestines (60-90%) and are bound to alpha globulins. Vitamin D is also stored in the adipose tissue. It is not actually vitamin D, but a vitamin D compound that is formed between the liver and the kidneys, known as 1,2,5-dihydroxycholecalciferol. This 1,2,5-dihydroxycholecalciferol is also stimulated by parathyroid hormone. Another vitamin D compound that is important is D3 (cholecalciferol), found in the skin. BONE FORMATION Skeletal tissue consists of an extracellular matrix 55% organic and 45% inorganic and cells. The purpose on the skeletal system is to regulate the distribution of inorganic compounds, such as calcium, for the remodeling and the formation and reabsorption of the matrix. There are 3 types of cells 1. Osteoblasts-derived from pre-osteoblasts from the mesenchyme. They are cuboid in shape, have a lot of Golgi apparatus for collagen processing, and lots of alkaline phosphatase. Osteoblasts are located in the bone-forming surface and are responsible for elaborating organic compounds from the extracellular matrix and the mineralized bone. The unmineralized matrix forms the osteoid zone and is separated from the mineralized bone via the calcification front. Osteoblasts form bone by the release of alkaline phosphatase, which increases the concentration of phosphate into the bone matrix. 2. Osteocytes-once osteoblasts, they are surrounded by an organic matrix and are now called osteocytes. 3. Osteoclasts-are also found on the bone surface. They are multinucleated, highly mobile moving along the bone surface reabsorbing bone. Osteoclasts break bone down. The cytoplasm contains abundant mitochondria, vacuoles, and lysosomes containing acid hydrolases such as carbonic anhydrate. Other cells found in bone are endothelial cells, fibroblasts, preosteoclasts, and preosteoblasts. Other inorganic components that make up the inorganic matrix are calcium, phosphate in a crystalline structure known as hydroxyapatite, with fluorine, sodium, potassium, magnesium and carbonate. 80% of the skeletal mass is made of cortical (compact) bone (long bones). Cortical bone is composed of packed osteons (haversian systems) surrounding a central canal, and volkmann canals, which radiate from the central canal connecting neighboring osteons to form an anatomizing network for blood and lymph. 20% is trabeculae bone (spongy) (vertebra, the ends of long bones and flat bones.) In trabeculae bone, lamellas are arranged in longitudinal bundles and anastomose with the marrow cavity. Please note that the surface area of trabeculae bone is 5 times that of compact bone. Bone formation is controlled by osteoblast differentiation, proliferation, matrix formation and mineralization (by alkaline phosphatase cleaving phosphate groups.) Bone contains many growth factors such as: • Transforming growth factor B produced by the osteoblasts, which stimulate mitogenesis and collagen synthesis • IGF 1 and IGF 2 Bone proteins consist of 13 forms of collagen, osteonectin (a carbohydrate containing protein), osteocalcin, osteopontin (produced by osteoblasts) and proteoglycans (glycosaminoglycans), which are controlled by autocrine, paracrine and systemic hormone regulation. Osteocalcin is a protein making up 1-2% of the total bone protein and depends on vitamins D, K, and C. PROMOTERS OF BONE FORMATION • INSULIN • IGF 1 and 2 • ESTROGENS/ANDROGENS • GROWTH HORMONE • THYROID HORMONE • PTH PROMOTERS OF BONE REABSORPTION • PTH • Interleukin 1 • Prostaglandins • Thyroid hormone • Epidermal growth factor • Vitamin A • Tumor necrosing factor INHIBITS BONE REABSORPTION • Calcitonin • Phosphate • Glucocorticoids FORMATION OF THE CALCIFEROLS 7-DEHYDRO CHOLESTEROL OR ERGOSTEROL PLUS LIGHT LUMSTEROL PREVITAMIN D TACHYSTEROL VITAMIN D2 D3 (CHOLECALCIFEROL) (ERGOCALCIFEROL) DIHYDROTACHYSTEROL D3 is formed through irradiation of 7 dehydrocholesterol. Dihydroxycholecalciferol lines the intestinal epithelium, absorbing large quantities of calcium when needed in the blood or bone. On the other hand, phosphorus is easily absorbed, unless there are large quantities of calcium that combine with phosphate creating an insoluble calcium phosphate compound that is excreted from the bowel. Ninety percent of all calcium loss is from the bowel. Ten percent is excreted in the urine. The ten percent that is excreted in the urine is controlled by parathyroid hormone, which also causes the excretion of phosphorus. Plasma calcium is found in three different forms: • 40% is combined with plasma proteins • 10% is bound to phosphates and is not usable • 50% is in the ionized and diffusible state necessary for heart function, bone formation, and nervous system control. Phosphates exist in two states HPO4, HPO4. When the pH of the extracellular fluid becomes acid, there is an increase in HPO4 and a decrease in HPO4, with the reverse also being true. Phosphorus levels can dramatically change without affecting function. On the other hand, increased amounts of calcium in the blood can cause central nervous system depression. Decreased calcium in the blood can lead to tetney. Parathormone controls calcium ion concentration in the extracellular fluid by controlling calcium absorption in the intestines, excretion via the kidneys (increases distal tubular reabsorption of calcium and magnesium) and release of calcium from the bones. Magnesium can exert control over PTH retention. Calcitonin (CT) is secreted by the parafollicular cells of the thyroid gland as mentioned above, has the opposite effect of parathormone. Although the effect is much weaker than parathormone, there is still that balance necessary to be maintained. Calcium also stimulates the secretion of CT, as does beta androgenic catecholamines, gastrin, and cholecystokinin. CT decreases alkaline phosphatase, pyrophosphatase activity, and hydroxyproline production. CT inhibits calcium reabsorption from bone. Therefore parathormone, which is a polypeptide (110 amino acids long), together with calcitonin (32 amino acid’s long), regulates the calcium-phosphorus ratio. If you lack calcium/phosphorus in the blood, then parathormone will shift them out of the bone and decrease excretion from the distal kidney tubules. Bone is composed of: • 90-95% collagen (protein) • 5% ground substance, which is composed of fluid, proteoglycans, chondroitin sulfate and hyaluronic acid. • 5% bone salts composed of calcium and phosphorus. The major crystalline salt is hydroxyapatite (CA10 (PO4) 6 (OH) 2), along with other bone salts such as magnesium, sodium, carbonate, uranium, plutonium, strontium and K. PHOSPHORUS AND CALCIUM INVOLVEMENT IN DIGESTION Phosphorus is also the regulator of the stomach. Phosphorus regulates the amount of HCl and pepsin in the stomach, which controls carbohydrate metabolism via the process of phosphorylation. Phosphorylation is the process that hydrogenates the carbohydrate, which alters the pH for glycogen storage in the liver. Oxygen, on the other hand, oxidizes carbohydrates for immediate use. The thymus, which will be covered later, assists the parathyroids in the process of phosphorylation. If the phosphorus in the stomach is too low, then the carbohydrate cannot be hydrogenated and the HCl content of the stomach increases, causing an acid stomach. When the phosphorus content is too high, there is a depletion of HCl content in the stomach. This creates an alkaline stomach. Calcium is the regulator of the small intestines. Calcium, along with B12 and folic acid, attach to lipoproteins so that they can be polarized through the intestinal wall, via magnesium. At the proper time, the calcium will be severed from the lipoprotein when needed for hormone, enzyme, and antibody formation. At that point, the calcium will be released back into the body. The following tests can be used to assess parathyroid function: 1. CALCIUM 2. PHOSPHORUS	141.5%
Posterior Pituitary Posterior Pituitary THE PITUITARY GLAND The pituitary, the existence of which has been known for 2000 years, sits in the sella turcica of the sphenoid bone. The sella turcica forms the roof of the sphenoid sinus. The lateral walls are comprised of durra or bone, which abut the cavernous sinuses and can affect the 3rd, 4th, and 6th cranial nerves and the internal carotid arteries since they transverse thru this area. The cavernous sinuses can exert a great deal of CSF pressure but, due to the diaphragm sellae, the gland will not become compressed nor will the optic chiasm and tracts, which lie immediately above the diaphragm sellae. Also lying in close proximity to the cavernous sinuses are the internal carotid arteries, cranial nerves 3, 4, 5 and 6, the third ventricle and the optic chiasm, which lies above the diaphragm sellae. The pituitary is divided into three parts: 1. ADENOHYPOPHYSIS-is the anterior portion, which is derived from Rathke’s pouch. This is divided into three lobes: the pars distalis (anterior lobe,) the pars intermedia (intermediate lobe) and the pars tuberalis. 2. NEUROHYPOPHYSIS-is the posterior portion and is composed of the pars nervosa, the infundibular stalk, and the median eminence. The major supply of axons to the neural lobe is the magnocellular secretory neurons from the paraventricular and supraoptic nuclei of the hypothalamus. These axon terminals also secrete AVP (regulating blood osmolarity, pressure, and fluid balance) and oxytocin into the surrounding capillary beds leading into the hypophyseal veins. The infundibular stalk is surrounded by the pars tuberalis, and together they make up the hypophyseal stalk. 3. VESTIGIAL INTERMEDIATE LOBE . The pituitary gland is regulated by the hypothalamus via feedback mechanisms of hormones and from paracrine and autocrine secretions from the pituitary itself. It attaches to the hypothalamus via the stalk thru the diaphragm sellae and into the median eminence. The pituitary is derived from the: • ECTODERM-which forms the pars distalis/tuberalis and the intermediate lobe • NEURAL PORTION-which forms the infundibulum, posterior pituitary, and neural stalk The pituitary weighs between 4-900 mgs (during pregnancy up to 1 gram), is bean shaped and brownish in color with dimensions of 9 mm A/P, 6mm S/I, 13 mm laterally. The hypothalamus receives its blood supply from the superior (provides 10-20 % of the blood supply) and inferior hypophyseal arteries (supply blood to the posterior pituitary), which are derived from the internal carotid arteries. These arteries form a capillary network in the median eminence (external to the blood-brain barrier). This capillary network picks up hypothalamic secretions from the hypothalamic nerve endings delivering them into the long and short hypophyseal portal veins, which are now transported to the anterior pituitary. Please note that retrograde blood flow causes bi-directional movement of blood between the hypothalamus and pituitary. Once the hypothalamic releasing hormones reach the pituitary, they activate G protein receptors on the cell membrane, creating a cascading chain reaction for the production of their pituitary hormone counterparts. Blood drainage of the pituitary leaves through the cavernous sinuses and the petrosal veins and out the jugular foramina via the jugular vein. Note that the blood supply to the pituitary via the hypothalamus is not unidirectional and can flow both ways creating ultra-short biofeedback loops. The hypothalamus releases its secretions via hypothalamic neurons, which end in the infundibulum and permeate into the fenestrations at the perigomitolar capillaries. This enters the portal vein, which enters the capillary circulation of the anterior pituitary (which provides 80-90 % of the blood supply to the pituitary). The pituitary, as stated above, is attached to the hypothalamus via the pituitary infundibulum. The diaphragm sellae has a 5mm opening for the hypophyseal stalk and allows transmission of pulsations of CSF. The purpose of the pituitary infundibulum is to act as a direct pathway for hormonal secretion between the hypothalamus and the pituitary. Pituitary hormones are released as pulsations, which does affect hormonal levels minute, by minute, which may give false positives when measuring hormonal levels. Each releasing factor (hormone) that is released from the hypothalamus causes a release of a hormone from the anterior pituitary. The hypothalamus also produces two hormones called antidiuretic hormone and oxytocin. Anti-diuretic hormone is formed primarily by the supraoptic nuclei, whereas oxytocin is formed primarily in the paraventricular nuclei. The major nerve tracts of the neurohypophysis arise from these two nuclei, from large cells termed magnocellular cells forming the supra optico hypophyseal tract and the paraventricular hypophyseal tract. AVP and oxytocin tracts are also distributed widely and project into the brain stem affecting the vagal nuclei, glossopharyngeal nuclei, and the spinal cord, sending information to the ANS to evaluate blood pressure. Vasopressinergic and oxytocin fiber pathways (which have different effects than those that end in the posterior pituitary) also terminate in the choroid plexus, which influences salt and water exchange between the brain (especially regions associated with emotion and memory) and the CSF. Neurological impulses from the two nuclei above, cause secretory granular release of these two hormones into the posterior pituitary, which are then released into the adjacent capillaries. It is interesting to note that the differences between oxytocin and anti-diuretic hormone are two amino acids. Otherwise, the chains are identical. The functions are entirely different, as you will see. The anterior pituitary is controlled by the hypothalamus in a slightly different manner than the posterior pituitary. Oxytocin and anti-diuretic hormone (AVP) are produced in the hypothalamus and are released into the posterior pituitary, via the neurological tracts of those nuclei mentioned above in the hypothalamus. Other neurological tracts secrete other neuropeptides called TRH (thyrotrophin releasing factor), CRH (corticotrophin releasing hormone), VIP and neurotensin. Paraventricular hypophyseal tracts located on either side of the ventricles are both unmylenated and descend thru the infundibulum. The releasing factors from the hypothalamus are transmitted to nerve endings, which then release these factors into a primary plexus of veins known as the hypophyseal portal system. These veins are located in the pituitary infundibulum and travel into the anterior pituitary, releasing the hypothalmic hormones into and stimulating the anterior pituitary. THE POSTERIOR PITUITARY (NEUROHYPOPHYSIS, INFUNDIBULAR PROCESS) The posterior pituitary includes the pars nervosa, infundibular stalk, and the median eminence, and is directly innervated by the supraoptic hypophyseal and the tuber hypophyseal neurological tracts. The median eminence, which lies in the tuber cinereum, has an internal zone from which the supraoptic and paraventricular magna cellular neurons control the posterior pituitary and an external zone, which receives information from the hypophyseal trophic neurons (sensory trophic neurons.) The magnocellular neurons embrionically arise out of neuroepithelial cells lining the third ventricle, which form the supraoptic nuclei above the optic chiasm, and the paraventricular nucleus located in the third ventricle. A third structure, which is also considered part of the median eminence, is the pars tuberalis, which surrounds the infundibulum and pituitary stalk. The median eminence is composed of nerve endings and blood vessels and is truly the functional link between the hypothalamus and the pituitary. The median eminence receives blood supply from the posterior communicating and superior hypophyseal artery (from the internal carotid) and drains thru the cavernous sinuses. The blood then flows thru capillary loops, which anastomose and drain into the sinusoids, which become the pituitary portal veins. The pituitary portal veins drain into the pituitary, the neural stalk and specialized neuro tissues that lie at the base of the hypothalmic pituitary juncture. This forms the base of the third ventricle, creating a funnel (infundibulum), and literally draining into the CSF as well as releasing neurosecretions into the anterior pituitary. The 2 major hypothalamic/posterior pituitary nerve tracts, which arise from magnicellular cells, are the bilateral supraoptic nucleus and the paraventricular nucleus and they produce (via ribosome protein synthesis) a pre-prohormone. Then, via glycosylation in the Golgi apparatus, the pre-prohormone is made into the prohormone and transported via neurosecretory granules (inactive state), where the secretory granular membrane adheres to the plasma membrane, releasing the granular material into the cell. It is then stored in the posterior pituitary as a neurophysin. Then, through the process of exocytosis, anti-diuretic hormone (AVP) and neurophysin 2 are released via neuron bombardment into the blood stream. There are two receptor sites: V1 found in smooth muscle, and V2 found in renal epithelial. V2 activates antidiuretic activity by activation of adenylate cylclase. Once the neurophysin is cleaved, the hormones are released. Capillaries and glue like non-secretory cells (pituicytes) help bind together the posterior pituitary. The capillaries are different in that they allow diffusion of the neurosecretory cells into the blood stream, unlike other capillaries in the brain that are subject to the blood brain barrier, preventing diffusion into circulation. The purpose of the posterior pituitary is to regulate body cell osmolarity by regulating sodium concentration, and by effective extracellular fluid regulation via osmoreceptors. Osmoreceptors for thirst and AVP release respond to slight changes in extracellular fluid osmolarity. The primary osmoreceptors that are triggered are triggered by urea and glucose for sensing changes in osmolarity and are found in the brain and outside the blood brain barrier. For example, an increase in ECF (extracellular fluid) osmolarity causes shrinkage of the cells, stimulating the osmoreceptors inside the cells to stimulate the release of AVP and angiotensin 2, conserving H20. Bar receptors are of two types: • Low pressure found in the right side and left atrium of the heart • High pressure found in the carotid sinus and aortic arch. This stimulates the vagus nerve and the glossly pharyngeal to the nucleus tractus solitarius then via noradrengic projections into the PVN and SON, which then inhibits the release of AVP To a lesser degree, a drop in blood volume stimulates angiotensin 2 and AVP release, stimulating thirst and increasing blood volume. Once blood volume is up, the oropharyngeal reflex and the release of atrial natriuretic peptide suppresses thirst. In actuality, the purpose then becomes regulating cell volume against extracellular fluid. The goal is to create a balance in Intra and extracellular osmolarity, whereby permeability would be perfect for passive and active transport (keeping the highways open between the cells and the extracellular fluids they bathe in.) This allows cell metabolites, CO2, hormones, enzymes and antibodies to diffuse with ease out of the cell while letting food, enzymes, hormones and oxygen to enter the cell. From an active standpoint, sodium constantly leaks into the cell, and potassium leaks out of the cell. This is due to their respective concentration gradients. Via active transport, the sodium-potassium ATPase extrudes the sodium to outside the membrane, and at the same time potassium is pulled back in. As potassium is leaking out via passive diffusion, it is being pulled back in via active transport. The following hormones, which are octal peptides with similar structural formulas, are released from the posterior pituitary: 1. ANTI-DIURETIC HORMONE (AKA VASOPRESSIN, ARGININE VASOPRESSIN, AVP) and its related neurophysin one (propressophysin, prohormone) cause the kidneys to retain water, excrete sodium while retaining potassium, and raising blood pressure through vasoconstriction. The most important factor regulating vasopressin is blood osmolarity and circulating blood volume. Increases in osmolarity and decreases in volume both increase vasopressin release. Blood osmolarity is kept within a fine range +- 1.8% of 282 mmo/kg. Other factors that affect blood osmolarity include emotional stress, nausea and blood pressure. 1) Aldosterone has the opposite effect, as well as constricting blood vessels and elevating blood pressure. The glucocorticoids and mineral corticoids, released by the adrenal cortex, counteract the function of antidiuretic hormone. Since glucocorticoids control sugar levels in the body, you can see how diabetes insipidus can occur. AVP release is also enhanced by prostaglandin E 2, morphine, nicotine, acetylcholine, histamine, barbiturates and hypoxia. Other factors that suppress AVP are alcohol and atrial natriuretic peptide. DIABETES INSIPIDUS This is a condition where there is a large volume of urine that is dilute (hypotonic) and tasteless (insipidus.) In diabetes mellitus, the urine is hypertonic and sweet tasting like honey (mellitus.) 1. OXYTOCIN AND ITS RELATED NEUROPHYSIN 2 (PROOXYPHYSIN) causes contraction of the uterus during the birth process and causes the contraction of the myo-epithelial cells in the breasts when the baby suckles. Oxytocin is also involved in maintaining the uterus in a quiet state during pregnancy. Oxytocin is also responsible for maternal behavior. Oxytocin is found in the ovary, placenta, testis, renal medulla, thymus and anterior pituitary. Oxytocin may also affect feeding behavior, gonadotrophin secretion, response to stress (decreasing stress), stimulation of the tubules in the spermatic ducts, regulating blood pressure, temperature, and heart rate. Just like AVP, oxytocin release is stimulated by plasma hypertonicity and suppressed by plasma hypotonicity via binding to high-affinity receptors. It stimulates cAMP, which increases natriferic and hydro-osmotic responses of the tissue. 4. 4. The posterior pituitary and the adrenal glands regulate mineral, water and sugar levels in the body. Factors that stimulate oxytocin secretion are nausea, saity, cholecystokinin and angiotensin 2. Factors that inhibit oxytocin are opiods, relaxing and ANP. Both oxytocin and AVP and their related neurophysin are synthesized in both the supra-optical (most oxytocinergic) (dorsal portion) and vasopressin (ventral portion), which project into the posterior pituitary and via the paraventricular nucleus, which is divided into 3 distinct magno cellular divisions consisting of: • Oxytocinergic neurons • Vasopressin neurons • Par cellular division that synthesizes peptides, corticotrophin releasing hormone, thyrotrophin releasing hormone, somatostatin, and opiods. Projections from pare cellular neurons project into the median eminence, brain stem and the spinal cord for autonomic function. The supra chiasmic nucleus in the third ventricle secretes only vasopressin and controls circadian and seasonal rhythms. Ventricular neurons triggered by nerve action potentials, via cholinergic and noradrenergic neurotransmitters, and several other neuropeptides including angiotension 2, atrial peptide (AP), and atrial natriuretic factor (ANF) cause an influx of calcium. This induces movement of the neuro secretory granules to the membrane surface, causing a release of the hormones from the granules into per vascular space. From there, it enters into the capillary system of the posterior pituitary, or via microtubule tracts. Acetylcholine stimulates AVP via nicotinic acid receptor stimulation and oxytocin release where adrenergic influences inhibit oxytocin and AVP secretion thru beta androgenic receptors. They are then transported via vesicles into the axons to the neural lobe. Both hormones and their neurophysins are released in fixed ratios. Other substances released from the posterior pituitary include: • Somatostatin • SRIF (somatotrophin release inhibiting factor) • TRH • Substance P • LHRH • GNRH (gonadotrophin- releasing hormone) • Dopamine • Serotonin • Histamine • Beta-melanocyte-stimulating hormone (b-MSH) • An opium peptide named dynorphin a 1-8, which is present in AVP-containing neurons From a biochemical perspective, the posterior pituitary controls biochemistry by maintaining potassium levels in all cells. As you may already be aware, potassium levels are highest within the cell. The purpose of potassium within cells is to maintain water levels. Potassium has been coined the “oxidative life principle” of the body. If this balance is affected, cells can either burst or shrink. In so doing, potassium literally pulls foodstuffs (that are stored in the cell membrane) through the membrane of the cell and into the mitochondria for energy. Now, via the demand of the cell, the potassium, which is controlled by the posterior pituitary, donates oxygen to this hydrogenated foodstuff on the membrane and draws it into the cell. When the pressure gradient of potassium becomes too high on the inside of the cell, potassium, along with metabolic waste products, is transported out of the cell. Therefore, by balancing water levels in body, the posterior pituitary can balance the body’s pH. The posterior pituitary also balances the pH of the body by affecting sugar levels (which are acids) and minerals (which are alkaline). So, in essence, the posterior pituitary, the pancreas, and adrenals dramatically affect the above. The following blood tests assess the functions of the posterior pituitary: 1. POTASSIUM as mentioned above is the primary indicator for posterior pituitary function. 2. TRIGLYCERIDES are composed of a molecule of glycerol and three molecules of fatty acids. The energy necessary for active transport across a cell membrane, via the influence of potassium, is supplied by fatty acids. 3. GLUCOSE although affected by many other organs and glands, glucose is also affected by the posterior pituitary. 4. BUN/CREATININE RATIO blood urea nitrogen and creatinine are residue byproducts found at the end of protein and muscle metabolism. They are kept in continual balance via the water content in our body. The kidneys flush out the blood urea nitrogen and creatinine when the concentrations get too high, via antidiuretic hormone release from the posterior pituitary.	127%
Pancreatic Tail Pancreatic Tail THE PANCREAS The pancreas is composed of a head and a tail. The purpose of the pancreatic head is used to secrete pancreatic enzymes. The purpose of the pancreatic tail is to produce insulin. I will first discuss the pancreatic head. THE PANCREATIC TAIL The pancreatic tail (islets of Langerhan) produces the following hormones: 1. Insulin-which has a molecular weight of 5,808, is produced by the beta cells and has the following functions: a. Inhibits liver phosphorylate for prevention of glycogen breakdown b. Increases activities of enzymes that promote glycogen synthesis a. Increases the flow of glucose to the liver b. Increases sugar flow into fat cells, causing the production of glycerol for fat production with fatty acids c. Increases membrane permeability for glucose, amino acids, potassium, magnesium, and phosphates f. Increases translation of messenger RNA and the formation of proteins g. Decreases the rate of gluconeogenesis in the liver h. Decreases catabolism of proteins It is interesting to note that gastrin, secretin, cholecystokinin, somatotrophin, cortisol, glucagon, progesterone and estrogen all affect the release of insulin. It is also interesting that resting muscles use fatty acids for energy and, when working hard, use glucose for energy. 2. Glucagon-which has a molecular weight of 3,485 and is 29 amino acids long, is produced by the alpha cells and has the following functions: a. Promotes the breakdown of glycogen in the liver (glucogenesis) by the following process. Glycogen is activated by adenyl cylclase, which is found in the hepatic cell membranes. This forms cAMP (adenosine mono-phosphate), which activates the protein kinase. The protein kinase then activates phosphorylate B kinase, which is converted into phosphorylate A kinase, which causes the degradation of glycogen into glucose 1 phosphate, which is then dephosphorylated into glucose and released into the bloodstream. b. Promotes gluconeogenesis in the liver 3. Somatostatin-which is 14 amino acids long, produced by delta cells and does the following: a. Decreases insulin and glucagon secretion b. Decreased motility, secretions of the stomach and the GI tract It is interesting that somatostatin is the same chemical substance as somatotrophin inhibiting hormone, which is released by the hypothalamus and suppresses the anterior pituitary from releasing growth hormone. 4. Pancreatic polypeptide secreted by the PP cells and has uncertain functions. The overall purpose of the pancreatic tail is to regulate muscle tone by balancing sugar and water across the muscle cell interface (membrane.) The pancreas via insulin utilizes zinc as a carrier mechanism to create this effect. As you may recall, actin is the active fiber that is burning and myosin, the stable protein block that contracts and is dramatically affected by this process. If sugar and water are not balanced accurately, then we have a loss or increased amount of insulin penetration into the cell. This will cause the body great difficulty with sugar metabolism. This may lead to a crystalline blockage, especially at the level of the motor end plate, creating neurological problems. The true pancreatic patient does not have stamina and ages quickly. One of the first complaints of a diabetic is that they sweat a lot and have increased urination, which causes the diabetic to drink a lot of water. The hypoglycemic, on the other hand, has poor circulation and muscle coordination. The tone of the blood vessels is poor and causes the blood vessel walls to prolapse, allowing blood to pool in the central cavity of the body. The hypoglycemic patient breaks out into cold sweats with spastic trembling to get sugar across the muscle wall. Hypoglycemics also hold fluid, as the kidneys go alkaline which prevents urination. In order for sugar to be handled properly it must go through the following four processes: Reaction 1-Copper via the parotids must first tag the carbohydrate. The parathyroids, through the process of “phosphorylation,” add phosphorus to the carbohydrate. So, the first thing that takes place with the preparation of sugar is the phosphorus injecting ability of choline and inositol into the sugar, creating the proper acid-alkaline balance within that sugar for further breakdown. Therefore, the first step in preparing the sugar zinc compound (insulin) occurs in the stomach via pepsin. Chlorine is then added to the compound via HCl acid/pepsin release in the stomach, which is controlled by the adrenal medulla. Once the carbohydrate is properly prepared, it now enters the bloodstream and travels to the liver. Reaction 2-Once in the liver, the thyroid converts sugar into glycogen by removing nitrogen via iodine. Then glycogen is released by epinephrine and is then activated on by adenyl cylclase that is found in the hepatic cell membranes. This forms cAMP (adenosine mono-phosphate), which activates protein kinase. The protein kinase then activates phosphorylate B kinase, which is converted into phosphorylate A kinase, which causes the degradation of glycogen into glucose 1 phosphate, which is then dephosphorylated into glucose and released into the bloodstream. This only occurs if there are sufficient amounts of zinc and selenium (insulin) outside the liver, which will draw the sugar out of the liver and into the blood. Zinc is also used to make peptidases for protein digestion and is a component part of LDH via inter-conversion of pyruvic acid into lactic acid. Zinc is also an integral part of carbonic anhydrase, which is found in red blood cells. The purpose of carbonic anhydrase is to adhere to carbon dioxide and water so that it can be expired by the lungs. Carbonic anhydrase is also found in the gastrointestinal tract and kidneys. Reaction 3-In order for the insulin/sugar compound to leave the blood and enter the extracellular fluid, glucagon is now necessary for this to occur. When zinc is in higher quantities in the extracellular fluid, in combination with selenium, they draw sugar out of the blood and into the extracellular fluid. The uterus and prostate control selenium. This will be discussed later. Reaction 4-When the sugar/insulin compound reaches the cell membrane, the selenium draws the sugar into the membrane. At this point, there is a selenium and potassium regulator known as oxytocin, which is released by the posterior pituitary (and closely resembles antidiuretic hormone), which holds the sugar for storage in the cell membrane. This membrane oxytocin is the regulator at every cell membrane for sugar and water entry into the cell to be metabolized. The oxytocin now causes the internal potassium to oxidize the chloride, shifting chloride out of the way, allowing the sugar and water to pass into the cell, which is then combusted to form lactic acid and converted back into lactic acid dehydrogenase in the veins. The following blood tests determine pancreatic tail function: 1. PHOSPHORUS-indicates the amount of acid balance in the body. It does this via regulating secretions of HCl/pepsin ratios in the stomach. For example, if the food you eat contains large amounts of phosphoric acid, pepsin will be released to neutralize the acid. If the food contains very little phosphoric acid, large amounts of HCl will be released. Phosphoric acid, as explained before, creates the proper balance of choline and inositol into the sugar, affecting sugar metabolism from this point forward. Increases in blood acidity may be due to an increase of zinc and sugar. Alkaline blood is due to a decrease of zinc and sugar. The pancreatic tail regulates this acidity/alkalinity via insulin/glucagon. 2. LACTIC ACID DEHYDROGENASE-is a byproduct of sugar metabolism, as mentioned above. Lactic acid dehydrogenase (LDH) is a glycolytic enzyme that functions as a catalyst in carbohydrate metabolism, which aids the pyruvic and lactic acid interchange. LDH is a byproduct of muscle metabolism. When sugar and water (fatty acid metabolism) are exchanged across a muscle cell interface, a byproduct known as lactic acid is produced. Lactic acid is a byproduct of fatty acid metabolism via the alkalizing and oxidizing effect of the pancreatic head. When lactic acid combines with the venous blood (carbon dioxide), there is a hydrogen displacement. Lactic acid then bonds to a double hydrogen, forming lactic acid dehydrogenase. The organs and glands most responsible for the sugar and water interchange across a muscle cell interface are the pancreas and posterior pituitary (via antidiuretic hormone.) LDH is chiefly found in the heart, kidneys, liver, skeletal muscle, as well as all tissues. LDH is a normal component of the cerebral spinal fluid.	110.67%
Hypothalamus Hypothalamus THE HYPOTHALAMUS The hypothalamus is located right above the pituitary gland that sits in the sella turcica of the sphenoid bone. The hypothalamus is attached to the pituitary gland by the pituitary infundibulum. The hypothalamus is the “major player” in the function of the endocrine system, where neurological energy is transposed into chemical energy (HORMONE RELEASING HORMONES.) The hypophyseal vein transports these releasing hormones to the anterior pituitary. In other words, all neurological transmission and communication that is directed toward the hypothalamus help determine what hormones are to be released. In fact, the pons varoli, medulla oblongata and the hypothalamus, form a network of visceral trophic sensors that receive information from many hormones (estrogen, testosterone, thyroid, etc.) and all sensory tropic nerves, including but not limited to all the cranial nerve nuclei, located in the medulla oblongata. Therefore, all cranial nerve activity, such as sight, smell, taste, hearing, and balance, influences hypothalamic secretions. The hypothalamus also receives all sensory trophic information through the thalamus via the spinal cord and brain stem. Neurological control over the hypothalamus comes from many other sources such as: 1. The limbic system and brain stem which connect to the periventricular and arcuate nuclei which stimulate GHRH 2. Emotional stress triggers thru the red nucleus, stria terminalis, and amygdale complex 3. Circadian rhythms are regulated via the supra chiasmatic nucleus 4. GH and sleep are regulated by the cortex and sub cortical nuclei 5. Dopa minergic and histaminergic in the arcuate and mammilla nuclei, respectively 6. Catechol minergic ascend and arise from the ventral lateral medulla and the tractus solitarius 7. Serotoninergic fibers from the raphae nucleus There are also peripheral hormones, metabolic signals, and cytokines that affect hypothalamic secretions, via the medial basal hypothalamus and the pituitary gland (acetyl choline stimulates GH secretion.) The hypothalamus also produces anti-diuretic hormone and oxytocin, which are made up of small peptides that are attached to large proteins found along the neural tracts from the hypothalamus to the posterior pituitary. Let us not forget the vagus nerve that affects all parasympathetic outflow to all organs from the heart to the descending colon. The hypothalamus also receives communications from the external environment, such as light, pain, temperature, and odorants. As you can see, there is a multitude of information directed toward the hypothalamus. The hypothalamus then serves as the link between the endocrine and nervous systems. In fact, the hypothalamus is composed of both nervous and endocrine tissue. The hormones that the hypothalamus produces are peptides, except for dopamine, which is a biogenic amine. The neurological tissue stimulates the endocrine tissue to produce the following hormones: 1. GONADOTROPHIN RELEASING HORMONE GnRH (FOLLICLE STIMULATING HORMONE RELEASING HORMONE) GnRH is a ten amino acid protein that stimulates the pituitary to produce follicle-stimulating hormone. There are 2 genes encoding GnRH, and they are: • GnRH 1-stimulates the release of the pituitary hormone • GnRH 2- serves as a neurotransmitter in the forebrain GnRH binds to a membrane receptor on the pituitrophes (G-protein-coupled receptor), which stimulates LH and FSH synthesis and secretion. GnRH receptors on the hypothalamus are affected and suppressed by steroids, estrogens, progesterones, and gonadotrophins. GnRH receptors are stimulated by calcium and protein C kinase. Calcium is important in GnRH stimulation and the release of gonadotrophins. GnRH receptors can increase or decrease uptake regulation or self-priming based on seasonal periods, malnutrition, and lactation or by GnRH downgrade due to high levels of GnRH. GnRH from the hypothalamus sends neurons to the portal circulation in the median eminence in coordinated, repetitive and spasmodic pulses into the portal blood. Neurological control is via neurotransmitter systems in the brain stem and limbic system, which includes norepinephrine and glutamate, which drive the reproductive axis, dopamine, GABA and opioids, which then inhibit GnRH neurons and serotonin. 2. ADRENOCORTICO-TROPHIC HORMONE RELEASING HORMONE (CORTICOTROPHIN RELEASING HORMONE) (CRH) CRH stimulates the pituitary to produce the adrenocorticotrophic hormone. CRH neurons are located in the parvi-cellular division of the hypothalamus. They send projections into the median eminence. Glucocorticoids inhibit the release of CRH and AVP. CRH neurons, which contain AVP, arise from the periventricular nucleus, SC nucleus, amygdala, and raphae nucleus in the brain stem. Inhibition of CRH is from the hippocampus and locus ceruleus of the midbrain. Neurotransmitters that are cholinergic and serotoninergic excite CRH release and noradrenergic inhibit CRH release. The HPA axis ‘s primary job is to maintain homeostasis in the body, as internal and external stressors affect it. The system is comprised of neurological control causing the release of catacholamines from the adrenal medulla, as well as hypothalamic-pituitary control over ACTH. This axis also controls behavioral response to stress via CRH-like peptides called urocortin 1, 2 and 3. CRH binds to a specific receptor and stimulates hormonal release only in the presence of Ca++ increasing cAMP and enhances the transcription rate of ACTH and its pro hormone POMC (pro-opiomelanocortin). CRH is also found in the limbic system and is used in the processing of sensory information and in the regulation of ANS function. CRH is also located in the amygdale, substantia nigra, solitary tract nucleus, cerebral cortex, pineal, spinal cord, lungs, and liver. GI tract and is also found in the human placenta. CRH increases sympathetic activity, blood pressure, heart -rate, cardiac output and suppresses GH and hunger. CRH and AVP play important roles in regulating inflammatory responses in the body via cytokines due to their extinguishing effects on inflammation. CRH also acts as a vasodilator on the uterine lining, regulating decidulization or implantation of the fertilized egg. The human placenta has the largest concentration of CRH outside the hypothalamus. The CRH system is also regulated by a CRH-binding hormone, which inhibits CRH action. Glucocorticoids are lipid soluble, inhibit CRH and can enter thru the blood brain barrier and bind to two receptors which are the: 1. Mineral corticoid receptors for aldosterone and glucocorticoids 2. Gluco corticoid receptors which have low affinity for mineral corticoids It has been said that the type mineral corticoid receptors regulate basal activity, and the glucocorticoid receptors are responsible for stress reactions. CRH runs on a circadian rhythm, which peaks in the early morning and falls during the day until midnight, then starts to increase at 1:00 pm. Glucocorticoids inhibit the release of CRH and AVP. 3. THYROID STIMULATING HORMONE RELEASING HORMONE (THYROTROPHIN RELEASING HORMONE (TRH) TRH is a tripeptide that stimulates the pituitary to produce thyroid-stimulating hormone (thyrotropin) via glycosylation of thyrotrophin. This happens with a maximum circadian rhythm between 9pm-5am, and a minimum circadian rhythm between 4 pm and 7 pm, accompanied by an ultradian rhythm of 90-180 minutes. TRH is also a potent releaser of prolactin and may in some cases cause the release of growth hormone and corticotropin. The binding sites are on the plasma membrane of the pituitary cells where TRH hydrolyzing phosphatidylinositol and phosphorylation via protein kinases, stimulate mRNA coding for thyrotrophin. TRH is also found in all parts of the brain, cerebral cortex, circum ventricular structures, posterior pituitary, pineal, spinal cord, islets of Langerhan, myocardium, prostate/testes and various parts of the GI tract. The TSH of these tissues far exceeds that in the hypothalamus. TRH receives nerve supply from catecholamines, neuropeptide Y and somatostatin-containing axons, and is released thru peptidergic neurons into the portal hypothalamic pituitary circulation. TSH has many affects on the CNS such as: • Increasing and improving motor function and activity, good for ALS patients (amyotrophic lateral sclerosis). • Altering sleep • Increasing blood pressure • Producing anoxia • Releasing norepinephrine and dopamine • Ameliorating human behavior disorders • Protecting against spinal shock 4. MELANOTROPHIC STIMULATING HORMONE RELEASING HORMONE Which stimulates the pituitary to produce the melanocyte-stimulating hormone. 5. LUTENIZING HORMONE RELEASING HORMONE (LHRH) LHRH is a deca peptide, which is derived from a precursor molecule called pre-pro LHRH (92 aa’s long), which stimulates the pituitary. LHRH neurons from the hypothalamus more specifically the arcuate nucleus, medial basilar hypothalamus and the pre-optic nuclei from the anterior hypothalamus, project into the median eminence (about 1-3000 neurons) and terminate in capillaries of the portal vein descending into the pituitary stalk to produce the lutenizing hormone in the anterior pituitary. LHRH is also found in the limbic system (hippocampus, cingulated cortex and olfactory bulb) and has been implicated in sexual drive, mating behavior, and emotional expression. Pituitary receptors are found on the plasma membrane, which then increases calcium concentration, hydrolysis of inositol phosphates and phosphorylation of protein C kinase. LHRH binds to the receptor, which initiates transcription of subunit genes, translated to subunit mRNA. This is followed by post-transitional modification of the precursor subunits and subunit folding and combination, followed by mature hormone packaging and secretion. LHRH also stimulates gonadotrophin synthesis. Dopamine, norepinephrine, serotonin, opioids, estrogen and progesterone produced by the brain regulate LHRH secretion. LHRH secretion by the hypothalamus causes the pituitary to produce FSH and LH. It appears that pulse frequency of LHRH influences LH and FSH secretion, whereby fast pulses favors LH secretion and slow pulses favor FSH secretion. Pulse frequencies affect the receptor concentration on the cell membranes of the pituitary gland, which increases receptor concentration with pulsations of 30 minutes and decreases the number of receptors when pulsations (every two hours) decrease. The half-life of LHRH is 2-4 minutes, which depends on a number of carbohydrate residues making up the glycoprotein and sialic acid content of the gonadotrophin. Ovarian steroids and peptides modify the secretions of FSH and LH. LH stimulates androstenedione production of the theca cells where FSH regulates estradiol production in the granulose cells, as well as follicular growth. The release of the egg from the follicle is due to sudden bursts of LH during mid-cycle. After ovulation, the follicle becomes a corpus luteum that secretes both estradiol and progesterone, which is also under the control of FSH and LH. The endometrium of the uterus has many receptors for estrogen, which increases endometrial growth Progesterone limits the estrogenic effect on the endometrium, but increases cell differentiation. Both a withdrawal of either estrogen or progesterone causes a sloughing off of the functional portion of the endometrium called the functionalist layer and the deeper remaining layer, the basal layer is regenerated due to estrogen. The entire reproductive function (no more oocytes), and most of the endocrine function is lost after menopause. Menses occurs approximately every 24-35 days. 6. LUTEOTROPHIC HORMONE RELEASING HORMONE Unlike other hypothalamic hormones that stimulate the pituitary to release hormones, this hormone inhibits prolactin (PRL) secretion by the pituitary. Prolactin inhibiting factor (PIF) with dopamine is the most important. PIF is a secretory product of the tuber infundibular dopaminergic pathways. Y-amino butyric acid (GABA) and prolactin releasing factors such as TRH, AVP, VIP, oxytocin, PHI-27 (peptide-histodine-isoleucine-27), EGF (epidermal growth factor), angiotensin 2, substance P and interleukin 6 stimulate the pituitary to produce the leutotrophic hormone. Prolactin secretion is also affected by autocrine/paracrine factors in the anterior and neuro intermediate lobe, whereby these factors gain access thru the sinusoids via short portal vessels. PRL is reduced by acetylcholine and calcitonin. PRL is also affected by estrogens, pregnancy, lactation, menstrual cycle, light, olfactory cues, and stress. Neurological control comes from serotoninergic neurons from the dorsal raphae nucleus, which activate PRL neurons in the paraventricular nucleus. 7. SOMATOTROPHIC HORMONE RELEASING HORMONE (GHRH) GHRH stimulates the pituitary via a circadian rhythm that is reactive to stress, and the pituitary stalk can block its action. Negative feedback control of GHRH is mediated by GH and IGF-1, which is synthesized by the liver under the control of GH. IGF-1 is a critical growth factor that is responsible for the growth promoting activities of GH. IGF-1 now via negative feedback stops production of GH by directly influencing the pituitary receptors. The GHRH receptor is a G-protein coupled receptor. GHRH stimulates GH secretion via calcium channels, which activate adenyl cyclase and the phosphatidylinositol cycle, thereby stimulating transcription of GH mRNA. Somatostatin (growth hormone-release inhibiting factor) blocks the effect of GHRH and inhibits TSH secretion, as well. On the other hand, glucocorticoids enhance GHRH secretion. Somatostatin also acts as a neurotransmitter and neuromodulator in the CNS and PNS. In the gut, somatostatin is found in the myenteric plexus where it acts as a neurotransmitter on the epithelial cells, which influence adjacent cells (paracrine function such as the islet pancreas cells). Somatostatin also acts in an autocrine fashion, where it can stimulate surrounding cells to produce it. A gut exocrine secretion, which is modulated by the intraluminal action called a lumone.. Somatostatin-14 is found in the brain (cortex, lateral septum, amygdale, brain stem nuclei, thalamus, and hippocampus) and inhibits GH and somatostatin. There is a wealth of data linking decreased levels of somatostatin in the CSF of the forebrain with Alzheimer’s, major depression and neuro psychiatric disorders. Somatostatin 28 is found in the GI tract (especially in the duodenum and jejunum) and inhibits the secretion of the salivary glands, parathyroid glands, calcitonin via the thyroid, PRL and ACTH. It also inhibits all pancreatic and gall bladder endocrine and exocrine gland function such as gastrin, secretin, motilin, insulin, glucagon, VIP, rennin, and glucentin (enteroglucagon). Somatostatin 28 also inhibits gastric acid and jejuna fluid secretion and emptying, pancreatic bicarbonate and enzyme secretion, intestinal absorption, bile flow and GI blood flow. Somatostatin can inhibit immune cell function and also inhibits the growth of tumor cells. Please note that these releasing hormones are peptides, with the exception of dopamine, which is the principle PRL (release inhibiting factor.) These do not, by themselves, act as sole controllers of each pituitary secretion, but are performed by a combination of releasing hormones that either inhibit or stimulate hormone release from the anterior pituitary. For example, TRH can release PRL, TSH, ACTH, GH, and LHRH. PRL inhibits TSH and GH. FAT STORAGE, THE BRAIN GUT ADIPOSE AXIS LEPTINS Long term energy and fat storage is controlled by the hypothalamic axis. Energy homeostasis is regulated via the triune of behavior, autonomic and hormonal inputs. Lepton, which is 167 AA’s long, is secreted by adipocytes with minor levels secreted by the skeletal muscle, placenta, and stomach. A decrease in fat deposits due to starvation and anorexia nervosa decreases lepton levels. Lepton also triggers puberty and fertility. Lepton is actively taken up by the capillary endothelial and microvascular system of the choroids plexus of the brain. Once it passes the blood-brain barrier, there are specific receptors (which are cytokine) found in the arcuate, ventromedial, and dorsal medial nuclei of the hypothalamus. Lepton also appears to inhibit feeding and increases metabolism. As far as the neurological circuitry is concerned, below is a brief description from Guyton’s physiology as to the hypothalamus’s far-reaching effects. Not only does it affect the body chemically, and physically, but mentally and emotionally, as well. As you will note, the hypothalamus is considered to be part of a system known as the limbic system. THE LIMBIC SYSTEM The limbic system refers to all the neuronal circuitry necessary to control emotional behavior and motivational drives. A major part of the limbic system is the hypothalamus but it also consists of the: 1. SEPTUM 2. PARAOLFACTORY AREA 3. EPITHALAMUS 4. ANTERIOR NUCLEUS OF THE THALAMUS 5. PORTIONS OF THE BASAL GANGLIA 6. HIPPOCAMPUS 7. AMYGDALA The purpose of this system is to affect behavioral control, body temperature, body weight, appetite and osmolality of body fluids. The portion of the cerebral cortex that lies directly above the limbic system is known as the limbic cortex. The purpose of this cortex is to form a two-way communication system between the limbic system and the cerebral cortex. Also, note that the reticular nuclei, and their associated nuclei in the brainstem (cranial nerve nuclei), mediate control over the limbic system, which elicit many behavioral functions and patterns such as rage, anger, grief, pain, etc. They also exert influence over the autonomic nervous system, via the hypothalamus. PITUITARY PINEAL *I have included the pituitary and pineal, which are involved in the endocrine axis that is affected/or affects the hypothalamus. The hypothalamus, through hormonal release, causes the pituitary to release/store hormones that can affect our emotions, as well as maintaining biochemical balance throughout the body. The pineal, through sensory feedback from the eye (light), acts as an environmental sensor or third eye and produces a hormone called melatonin, which inhibits the release of sex hormones affecting sexual drive and behavior. The hypothalamus is made up of an anterior, posterior and lateral portion with each portion consisting of the following: THE ANTERIOR HYPOTHALAMUS The anterior hypothalamus is divided into the: 1. PARAVENTRICULAR NUCLEUS (PVN)-which is composed of neurons from the: a. Magnicellular nucleus, which contain oxytocin and vasopressin neurons that extend into the posterior pituitary and regulate fluid balance, blood pressure, lactation, and parturition. The magnocellular division also releases the following hormones peptides and neurotransmitters: • Angiotension 2 • Cholecystokinin • Glucagon • Oxytocin • Peptide 782 • Pro encephalin B (dynorphin, rimorphin, alpha-neo-endorphin) • Vasopressin b. Neurons projecting into the brain stem and spinal cord regulating a variety of ANS responses c. Parvicellular nucleus (PVN), which is composed of CRH neurons that project into the median eminence regulating ACTH synthesis and release. Visceral sensory output to the PVN occurs thru the nucleus of the solitary tract via the thoracic abdominal viscera, which send dense catecholaminergic projections to the PVH thru the ventro lateral medulla. The parvicellular division releases the following hormones/peptides and neurotransmitters • Y-amino butyric acid • Angiotension 2 stimulates drinking thirst reflex. • Atrial natriuretic factor • Cholecystokinin • CRH • Dopamine • FSHRH • Glucagon • Neuropeptide Y • Neurotensin • Peptide 782 • Pro encephalin A (met and leu-enkephalins, BAM 22P, metorphamide) • Somatostatin • TRH • Vasopressin • Vasoactive intestinal peptide/peptide-histidine-isoleucine (PHI) 2. MEDIAL PREOPTIC AREA-decreases heart rate, blood pressure and bladder contraction. 3. SUPRAOPTIC NUCLEI-for release of vasopressin 4. OPTIC CHIASMA 5. INFUNDIBULUM 6. POSTERIOR PREOPTIC AND ANTERIOR HYPOTHALAMIC AREA-for the regulation of body temperature through panting, sweating and thyrotropin inhibition. THE POSTERIOR HYPOTHALAMUS The posterior hypothalamus controls shivering, increases blood pressure and pupil dilation. The posterior hypothalamus is composed of the: 1. DORSOMEDIAL NUCLEI-for gastrointestinal stimulation 2. PERIFORNICAL NUCLEUS-for hunger, rage and increased blood pressure 3. VENTROMEDIAL NUCLEUS-for neuro-endocrine control and satiety 4. MAMILLARY BODY-for the feeding reflex. 5. ARCUATE NUCLEI AND PERIVENTRICULAR ZONE-Dopamine fibers from this nucleus project into the median eminence and releases the following hormones/ peptides and neurotransmitters: • Acetylcholine • Y-amino butyric acid • Dopamine • GHRH • Neuropeptide Y • Neurotensin • Pancreatic polypeptide • Pro encephalin A • Prolactin • Pro-opiomelanocortin (ACTH, beta-lipotropin, Y-melanocyte stimulating hormone, beta-endorphins) • Somatostatin • Substance P • THE LATERAL HYPOTHALAMUS The lateral hypothalamic area is for thirst and hunger. THE BLOOD BRAIN BARRIER THE ROLE OF THE CIRCUMVENTRICULAR ORGANS The role of the circum ventricular organs (CVOs) is to act as doormen, so to speak, about what vital information crosses into the brain and what does not. More specifically, vital sensory chemical information (hormones, metabolites, toxins, bacteria, etc) to maintain homeostasis needs to be allowed to pass thru into these CVOs, which have a rich blood supply and can give vital information to the glial cells and neurons that reside in these blood vessels This is done thru key junctures (CVOs) that lie in the midline of the brain in the third and fourth ventricles, and include the: • Median eminence that gives sensory input to adjacent nuclei such as the arcuate, ventro medial, dorsal medial and para ventricular nuclei. The para ventricular nucleus then sends magnicellular neuron projections to the posterior pituitary to release arginine, vasopressin or oxytocin • Area post rema lies in the fourth ventricle and sends efferent projections into the nucleus of the solitary and ventral lateral medulla. It receives sensory input from the vagus and gloss pharyngeal nerves and the carotid sinus nerve. The area post rema can induce vomiting in response to foreign substances and control of blood pressure. • Posterior pituitary (see posterior pituitary) • Sub commissural organ located at the junction of the 3rd ventricle and cerebral aqueduct below the pineal that is composed of ependymal cells that secrete glycosylated protein. These extrude thru the aqueduct of the 4th ventricle, down the spinal cord lumen, and terminate in the caudal equine. • Subfornical organ located in the third ventricle having receptors for angiotensin 2 and atrial natriuretic peptide that project into sites of the hypothalamus, producing oxytocin and AVP. The SFO is also a blood pressure fluid regulator. The SFO innervates the parvicellular neurons of the para ventricular nucleus, which project into the median eminence releasing CRH and regulating neuroendocrine and autonomic control. • Organium vasculosum of the lamina terminalis is located in the third ventricle and is innervated by neurons that secrete many neurotransmitters and peptides such as LHRH, somatostatin, dopamine, serotonin, acetylcholine, oxytocin, vasopressin and TRH. The organium vasculosum has a dramatic effect on fluid regulation (osmolality), electrolyte balance, reproduction, and thermoregulation. So the CVOs act as a critical link between the chemical cues from the body, transposing them into neurological cues (communications) to regulate hormonal, autonomic and behavioral responses. This is where the vascular endothelial cells of the brain prevent passage of polarized macromolecules (hormones, peptides.) Perimicroglial cells, neurons and glial cells that arise in the CVOs contribute neurological intelligence to the integrity of this complex by transposing this chemical information into neurological information, stimulating key neuronal cell groups of the median eminence, posterior pituitary, and the hypothalamus, maintaining homeostasis. Blood chemistry tests that determine the function of the hypothalamus: 1. CALCIUM is the largest and most abundant mineral in the body. The purpose of calcium is to attach to all lipoproteins, fatty acids, and triglycerides within the digestive tract. All minerals that are involved in biochemical reactions within the body are in an ionic state. They will have a positive or negative charge. The purpose of these electrically charged ions is to act as magnets, repelling and attracting biochemical substances through the body. The purpose of hormones and releasing factors is to direct these mineral magnets and their biochemical substances throughout the body to specific sites, at specific times, creating growth/repair, energy and all the chemicals necessary for your survival. The mineral calcium (which is a cation) is the substance that pushes proteins, fatty acids, and triglycerides through the intestinal wall. When the calcium to magnesium ratio is greater than two-part calcium to one-part magnesium, there is movement of food substances through the intestinal wall. This calcium to magnesium phenomenon creates an electrical osmotic gradient that draws the calcium/lipoprotein across the cell membrane. The hypothalamus, through its releasing factors, creates growth, reproduction, digestion, assimilation, metabolism and protein deposition in cells. You can see why calcium would be dramatically affected by hypothalamic malfunctions. The releasing factors are all geared for protein deposition in cells, as well as controlling triglycerides, cholesterol, and fatty acid distribution throughout the body. These releasing factors also influence the production of energy and the creation of hormones, enzymes, and antibodies. It’s rather obvious that other blood tests such as protein, cholesterol and triglycerides can all be used and are affected by hypothalamic malfunctions. 2. POTASSIUM AND SODIUM The purpose of potassium is to create an action potential with sodium across a neurological membrane. When a neurological impulse passes through a cell membrane, there is a large influx of potassium out of the cell, and a large inflow of sodium into the cell, allowing the propagation of the neurological impulse, which then must be repolarized (sodium pumped out of the cell and potassium pumped in.) Since the hypothalamus is neurologically controlled via a vast network of sensory trophic nerves, sodium and potassium, levels must be observed as indicators of hypothalamic function, since they literally control neurological activity on a chemical level. This then would have a dramatic effect on communication between the body and hypothalamus, creating improper hormonal release to the pituitary.	95.43%
Testicles/Ovaries Testicles/Ovaries THE TESTICLES MALE REPRODUCTIVE PHYSIOLOGY Genes on the short arm of the Y chromosome control testicular differentiation. There are three principle cell types that make up the testis: 1. Germ cells-from primitive ectodermal cells 2. Supporting cells-derived from coelomic epithelium, which make up the Sertoli cells or granulosa cells of the ovary 3. Stromal (interstitial cells)-from the mesenchyme, which differentiate into the Leydig cells Sexual dimorphism comes 6-8 weeks after gestation, when the testes are totally developed, within 3 months post gestation. Testicular descent occurs within 7 months and is controlled by dihydrotestosterone and androgens, which may enhance the release of calcitonin gene-related peptide from the genital femoral nerve promoting descent. The INSL3 gene is a member of the insulin-like superfamily that can affect the descent as well. The anti-mullarian (AMH) hormone may also affect this as well. The testes are a network of tubules from Sertoli or germ cells and are used for the production and transport of sperm thru these ducts. Sertoli cells produce AMH, inhibins, activins, prodynorphin, and factors that affect spermatogenesis, such as transferrin. At the same time, it produces androgens from the interstitial or Leydig cells, which consistently produce testosterone. The cytoplasm has a soapy appearance due to the cytoplasm being totally filled with esterified cholesterol. This will be hydrolyzed and the free cholesterol moved to the mitochondria where, under the control of StAR (steroidogenic acute regulatory protein), is converted into pregnenolone, which is then converted into testosterone in the endoplasmic reticulum. The preoptic area and the medial basal area of the hypothalamus and the arcuate nucleus are responsible for GnRH (gonadotrophin releasing hormone) (LHRH luteinizing hormone releasing hormone) in pulsations. The amplitude of pulsations is also affected by catecholamine, dopamine and endomorphic related mechanisms. LH and FSH also control testicular function. LH receptors are found on the membrane of the Leydig cells and are members of the G-protein-coupled seven transmembrane domain receptor families. The binding of LH activates both adenylate cyclase-cyclic AMP and phospholipase. Cyclic AMP binds to protein kinase, which activates the synthesis of enzymes to produce testosterone. The primary site of action for FSH is on the plasma membrane of the Sertoli cells, where it binds to a receptor and uses the same channels as LH to convert testosterone into estradiol. Testosterone and estradiol influence FSH secretion. PATHWAYS OF TESTOSTERONE PRODUCTION CHOLESTEROL StAR CHOLESTEROL SIDE CHAIN CLEAVAGE ENZYME PREGNENOLONE ADRENALS AND TESTES 3 BETA-HYDROYSTEROID DEHYDROGENASE PROGESTERONE 17 ALPHA HYDROXYLASE OH-PROGESTERONE 17,20-LYASE ANDROSTENEDIONE TESTES 17 BETA-HYDROXYSTEROID DEHYDROGENASE TESTOSTERONE 5ALPHA REDUCTASE AROMATASE PERIPHERAL TISSUES DIHYDROTESTOSTERONE ESTRADIOL There is also much paracrine control in the testes such as: 1. Testicular peptides inhibins and activins 2. Growth factors such as transforming growth factor, IGF-1 and fibro growth factor 3. Immune-derived cytokines, TNF and interleukins 4. Vasopeptides, angiotensin 2 and natriuretic peptide When testosterone reaches the plasma, it is either bound to albumin 54% of the time, sex hormone binding globulin 44% of the time, and 2% will be found as free testosterone.	74%
Glans Penis Clitoris Glans Penis Clitoris	50%
Prostate/Uterus Prostate/Uterus UTERUS PROSTATE The uterus and prostate play a vital role in oxygen/carbon dioxide/water balance in the body. It does this via a relationship between the mineral potassium and carbon dioxide. The actual function of the uterus and the prostate is to bind fat with water. The catalyst, which creates this blending of fat and water, is selenium and potassium. The selenium has an affinity for fat and water creating sexual energy and sexual desire. This energy is coined the “expression of life force.” Selenium is usually found with high quantities of vitamin F. Vitamin F is also used in the production of the three fatty acids known as linolenic, linoleic and arachidonic acid. When these fatty acids are in combination, they are called the combusted fats. Fats are activated by selenium, and that activation causes a blending of these oils (fats) and water, which occurs at the cell membrane level. Potassium then draws these fatty acids into the cell forcing water into the fat causing a combustion activity with oxygen, creating energy, and a byproduct called carbon dioxide. As you may have noted in practice, most female patients with uterine problems complain of water retention, lack of energy and excessive fatty deposition, especially in the hips, buttocks and thighs. The proverbial cellulite is a typical uterine condition. Please note that the bladder, bowel, prostate, and uterus are organs that are also concerned with water balance. THE ENDOMETRIUM Implantation occurs in the uterus via the endometrium, which develops spiral arteries in the formation of uteroplacental vessels. Menstruation occurs when the endometrium hemorrhages due to blood flow directed changes via sterogenic hormones The endometrium is composed of two layers: 1. A FUNCTUNALIS LAYER-which prepares for implantation of the blastocyst (proliferation, and degradation) 2. A LOWER BASALIS LAYER-which is to provide a regenerative functional layer to prepare for the next implantation There are 5 cycles to the endometrial cycle: 1. MENSTRUAL-postmenstrual reepithelialization 2. ENDOMETRIAL PROLIFERATION-due to estradiol 3. ABUNDANT EPITHELIAL SECRETION-due to estradiol and progesterone 4. PREMENSTRUAL ISCHEMIA-due to volume involution, causes a stasis of blood in the spiral arteries via steroid hormones. Degradation of the stromal reticular network via stromal infiltration by polymorphonuclear, mononuclear leukocytes and secretory exhaustion, which helps shrink the endometrium 5. MENSTRUATION-via progesterone withdrawal causes a severe vasoconstriction of the spiral arteries followed by desquamation. Bleeding occurs once the arteries relax leading to hypoxia-reperfusion injury, creating hematomas and fissures leading to detachment, fragmentation, lysis, and apoptosis. The bleeding is fragments of endometrium, blood and liquefied cellular debris. Estrogen and progesterone receptors are found in the cells of the endometrium and are reached via blood supply. Progesterone acts as an anti-estradiol hormone by limiting the synthesis of estradiol receptors, converting estradiol into estrone and increasing inactivation of estradiol via sulfonation. The following tests indicate a uterus prostate problem: 1. Potassium-regulates this fat/water/carbon dioxide exchange 2. Carbon dioxide is released when potassium forces water into the fat	38.67%
Pineal Pineal THE PINEAL Calcification of the pineal is from an appetite form of calcium phosphate that is laid down in a matrix of ground substance secreted by pinealocytes (primordial photoreceptor cells) and has no effect on the pineal. Lining the ventricles (especially the third and fourth) and the central canal of the spinal cord are ependymal cells that are ciliated, which are then modified forming secretory tissues. The most well known is the pineal. The pineal is derived from the roof of the third ventricle and is composed of two types of cells pinealocytes and glial-like cells. The pineal integrates information encoded by light into organized secretions of rhythmic character. It receives its light encoded information from norandrogenic sympathetic nerve terminals regulating melatonin production. The pathway for melatonin production starts at the retina and then proceeds to the supra chiasmic nucleus (SCN) of the hypothalamus via the retina hypophyseal tract. The supra chiasmic nucleus neurons are inhibited by melatonin. Melatonin regulates circadian rhythms thru its effect on the supraoptic nucleus, which has been called the master circadian pacemaker. This is why melatonin can be used for jet lag and seasonal disorders. The SCN also provides input to the paraventricular nucleus providing direct innervations to the cervical sympathetic pre-ganglionic, extending into the upper thoracic to the postganglionic noradrengic, extending into the pineal. Lack of light causes a release of norepinephrine from the postganglionic that act on beta androgenic receptors in the pinealocytes. Other structures formed by the third ventricle are the: • Sub commissural organ-its cells secrete an insoluble fluid into the lumen of the aqua duct. This secretion forms a cord-like structure extending down to the caudal spinal canal. • Sub formic organ which contains neurosecretory neurons and receives cholinergic fibers from the midbrain. This contains neuropeptide, angiotensin 2 (converted from angiotension one), which is produced from its precursor angiotensinogen and atriopeptin. The sub formic organ plays an important role in water regulation by regulating and controlling thirst and AVP release. • Organium vasculosum of the lamina terminalis-this entire structure has its own circulation independent from the other organs. Its nerve ending contains LHRH, somatostatin, and neurophisms, from the median eminence. The roof of the fourth ventricle forms the area post rema. All of these tissues have large interstitial spaces so large molecules can leave the blood and enter these spaces lacking the blood brain barrier condition. The pineal weighs between .1-.18 grams. The pineal gland is a true secretory structure, which contains many biologically active substances and is occasionally the site of significant human disease. It is now known from comparative anatomy that the pineal gland is a vestigial remnant of what was the third eye (a light sensitive organ) in lower animals. The superior cervical ganglion via postganglionic sympathetic nerves also influences the pineal. Preganglionic fibers from the superior sympathetic chain found in the lateral column of the spinal cord receive impulses from descending branches of the supra chiasmic nucleus located in the hypothalamus. This nucleus receives nerve input from the retina, called the retina hypothalamic tract, which stimulates pineal secretions. Light dark shifts are the most important rhythm makers of the pineal. The pineal gland, as noted above, is controlled by the amount/types of light that pass through our eyes. Also crucial to the pineal regulation is noradrenergic fibers that end in the interstitial spaces or on the plasma membrane of the pinealocytes (secretory cells.) All pineal parenchymal cells are regulated by beta-adrenergic receptors. The pineal plays an important role in regulating sexual and reproductive function. The pineal gland also secretes: • Biogenic amines such as norepinephrine, serotonin, histamine, melatonin and dopamine • Peptides-LHRH, TRH, somatostatin, vasotocin (oxytocin) and the inhibitory neurotransmitter GABA • Pinealin-insulin-like substance that lowers blood sugar. • Melatonin-produces sleepiness via increasing the number of alpha waves, a feeling of well-being, elation and increased REM sleep. Lack of melatonin causes sleeplessness and depression. Melatonin is also used to regulate the reproductive axis and the onset of puberty. Melatonin mediates its effects thru G-protein receptors affecting circadian rhythms via inhibition of the SCN of the hypothalamus, which is the circadian pacemaker. Melatonin is also used to treat immune conditions and jet lag as mentioned above. Melatonin is made from tryptophan and serotonin via the melatonin, producing enzyme hydroxyindole-O-methyltransferase, which is also found in the retina and in red blood cells. L-tryptophan is converted into 5-hydroxytryptophan by tryptophan hydroxylase. 5-hydroxytryptophan is converted into serotonin by 5-hydroxytryptophan decarboxylase. Serotonin is then converted into n-acetyl serotonin by n-acetyl transferase + acetyl-CoA and n-acetyl serotonin is converted into melatonin. The pineal also produces monoamine oxidase and histamine N-methyl transferase. Melatonin is stimulated thru increased sympathetic activity, hypoglycemia, L-dopa and can be affected by sleep, diet activity, and posture. Melatonin receptors are dense in the SC nucleus, and in the ovaries inhibit gonadotropin secretions as well as GH secretions from the pituitary. During the evening, melatonin is high and serotonin in the pineal is low. Serotonin is also released into sympathetic nerve endings, as is dopamine and norepinephrine. The melatonin and similar substances pass either by way of the blood or through the fluid of the third ventricle to the anterior pituitary gland, which controls gonad trophic hormone secretion. As mentioned above, the pineal works as the body’s antenna. It becomes the media between the body’s internal environment and the external surrounding environment. The pineal is used greatly by deaf or blind people, psychics, and top grade athletes. The pineal works with vision, smell, taste, touch, and hearing. The pineal forms a reticular formation with the posterior pituitary to deal with humidity in the external environment and water balance within the body. It also sets up a reticular formation with the various cranial nerves and influences sex organs and their development, brain maturity, puberty and the onset of menopause. It also retards sexual development by inhibition of the hypothalamic releasing factors. According to Dr. Brockman, the mineral of the pineal is silica, a mineral that reflects vibration in a hormonal circuit. Silica picks up light and sound waves (vibrations), which then reflect into the eyes/ears triggering a cascade of events mentioned above. It should be noted that pulsating or artificial light influence the pineal and confuses it, resulting in multiple disease states. The pineal is known as the biological clock of the body and can be affected by traumatic emotional or physical shocks. It can also adjust the pH of your body to external environmental changes. It does this by balancing sodium (which is acid and controlled by the adrenal cortex) and chloride (which is alkaline and is controlled by the adrenal medulla.) It is interesting to note that silica, which is found in sand and sodium, and chloride, found in salt water, have a calming and relaxing effect on the body. Ask anyone who is relaxing at the beach. Sodium and chloride are very responsive to the movement of light and sound in the body. The following blood chemistries assess the function of the pineal: 1. SODIUM 2. CHLORIDE	35.5%
Hypothalamic/Hypophyseal Stalk Hypothalamic/Hypophyseal Stalk THE PITUITARY STALK (INFUNDIBULUM) HYPOPHYSEAL STALK MEDIAN EMINENCE, TUBEROINFUNDIBULAR AND TUBEROHYPOPHYSEAL NEURONS The median eminence lies in the center of the tuber cinereum and is the site of an array of blood vessels, from the superior hypophyseal artery (which is a branch of the internal carotid) from which the pituitary portal vessels arise. This drains into the pituitary sinus and is the site where hypothalamic neurons from the ventral hypothalamus (tuber hypophyseal neurons) regulate the release of hormones from the anterior pituitary into the hypophyseal-portal system. The pars tuberalis, which is a thin glandular tissue sheath around the infundibulum that can secrete LH and TSH, makes up part of the median eminence and is a subdivision of the adenohypophysis. This surrounds the infundibular stalk and together they make up the hypophyseal stalk. The median eminence is considered to be the functional link between the hypothalamus and the pituitary. There are three zones that make up the median eminence and they are: 1. EPENDYMAL LAYER-which is made from ependymal cells that form the floor of the third ventricle. This ependymal layer contains tanycytes, which act as the blood brain barrier between itself and the third ventricle (CSF and blood.) 2. INTERNAL ZONE-which is composed of axons from the supraoptic and paraventricular magnocellular neurons heading to the posterior pituitary. 3. EXTERNAL ZONE-is the exchange point of the hypothalamic releasing factors. There are two types of tuber hypophyseal neurons that project into this zone. a. Peptides neurons which release thyrotrophin releasing hormone, corticotrophin releasing hormone, luteinizing hormone releasing hormone and somatostatin b. Monoamines and bio-amines such as dopamine, serotonin, and norepinephrine, which come in contact with the pituitary portal veins. These tuber hypophyseal neurons synthesize the neurotransmitters in the following way: 1. There is an uptake of amino acids into aminergic neurons such as tyrosine that are the precursor for dopamine, epinephrine, and norepinephrine. 2. Enzymatic synthesis, whereby tyrosine is hydroxylated by tyrosine hydroxylase to form L-dopa, which is decarboxylated to form dopamine, which is hydroxylated to form norepinephrine which is methylated to form epinephrine. 3. Storage phase 4. Released of preformed granules in response to neural depolarization, whereby granules are extruded thru the nerve endings. 5. Interaction with the catecholamines with receptors located on the postsynaptic neuron. 6. Reuptake process after the release of the preformed hormones and neurotransmitters, any unused hormones/neurotransmitters that are still left in the synaptic cleft, are taken up into the presynaptic neuron. 7. Degradation of neurotransmitters, dopamine, and norepinephrine, which are bound to postsynaptic membranes are freed into presynaptic membranes, which are then destroyed by monoamine oxidase. 8. Monoamine oxidase inhibitors (parglycine, isocarboxazid) then make up more neurotransmitters and hormones. There are distinct pathways within the median eminence and they include: DOPAMINERGIC PATHWAYS-most of the cells that synthesize dopamine arise from the midbrain, project to the forebrain and the basal ganglia (causing Parkinson’s), and to the cerebral cortex, causing schizophrenia. They also project to the arcuate nucleus of the hypothalamus and to the median eminence. NORADRENERGIC PATHWAYS-originate from the midbrain, locus ceruleus, and project to the forebrain (cerebral cortex), the limbic system, hypothalamus, brain stem, and spinal cord. They play a role in visceral homeostasis, regulating sleep, appetite, emotional happiness and physical activity. This is the site of action for amphetamines and antidepressant drugs. CENTRAL ADRENERGIC PATHWAYS-are the least plentiful and are the cell bodies that originate in the midbrain. They are extensive in the hypothalamus and the median eminence. CENTRAL SEROTONINERGIC PATHWAYS-all originate from the raphae nucleus in, which fibers ascend to innervate the forebrain and the diencephalons. These fibers also terminate in the hypothalamus (paraventricular nucleus, median eminence and the lumen of the 3rd ventricle). Fibers also project downward into the brain stem and the spinal cord. CENTRAL CHOLINERGIC PATHWAYS-(muscarine and nicotinic receptors) are found in the brain and hypothalamus, with some fibers originating from the nucleus basalis of the forebrain to the hippocampus. Loss of these neurons causes Alzheimer’s. These pathways control AVP, ACTH, and GH secretion. AMINO ACID TRANSMITTERS-glutamine, aspartate, glycine and inhibitory GABA is found in hypothalamic neurons and can modify tuber hypophyseal function. The medial eminence then can be said to consist of three components: • Neural • Vascular blood supply from the hypophyseal artery, which is a branch of the internal carotid and drains via the portal veins, which drain into the pituitary sinus. • Epithelial-The nerve endings, basement membranes, interstitial space and the capillary wall of the median eminence release all the neuropeptides and can be stimulated by increasing potassium in the presence of calcium. This also increases anterior pituitary secretions. The extra and per vascular spaces of the median eminence are where billions of neurons are bathed in interstitial fluid in a multitude of hormones and neurotransmitters. The supraoptic and paraventricular hypophyseal tracts pass thru the eminence and some tracts end here as well. The purpose of the pituitary infundibulum is to make sure all chemical and neurological information from the hypothalamus, and through many neurological pathways with the brain, can communicate and control the pituitary gland properly. The nervous and endocrine systems communicate thru pulsations (circulatory disturbances of blood and CSF) and vibrations (neurological transmissions.) If the pituitary infundibulum has adhesions (via the diaphragm sellae) can lead to improper communication with the pituitary. The pituitary infundibulum is derived from the posterior wall of Rathke pouch. The intermediate lobe produces melanocyte-stimulating hormone (MSH), which increases skin pigmentation by stimulating melanin granules in melanocytes. MSH is synthesized by pro-opiomelanocortin (POMC) a precursor of ACTH. Beta-lipotropin and beta-endorphin also produce melatonin and serotonin that create a phenomenon similar to photosynthesis in plants, called biosynthesis in humans. During biosynthesis, you also have a light and dark reaction, which is controlled by melatonin and serotonin. Melatonin controls response of tissue to light and darkness, and the more melatonin in the skin, the more the skin coloration changes when exposed to light. High-density fats such as cholesterol always cause browning of the skin. Low-density fats such as triglycerides always cause lightening of the skin. Serotonin, on the other hand, controls the waking and sleeping reactions within our bodies. Sleeping relates to darkness or nighttime, and waking relates to daylight or daytime. During the light reaction, we have our waking hours and fatty acid combustion (which is the breakdown of triglycerides to yield energy for body metabolism.) This relates to the catabolic phase of metabolism. The dark reaction, which is during the sleep hours, is the anabolic phase, utilizing cholesterol for growth and repair. The following blood chemistries assess the function of the pituitary infundibulum: 1. CHOLESTEROL: 2. TRIGLYCERIDES: Any imbalance in either cholesterol or triglycerides can be affected by the pituitary infundibulum, as mentioned above.	33%

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#		Anterior Pituitary	Glans Penis Clitoris	Hypothalamic /Hypophyseal Stalk	Hypothalamus	Pancreatic Tail	Parathyroids	Pineal	Posterior Pituitary	Prostate /Uterus	Testicles /Ovaries
Glucose Glucose GLUCOSE Glucose is an important fuel for the body, which affects all tissues, organs, and systems. Glucose also affects the acid/alkaline balance in the body. Breakdown of glucose or starch starts in the mouth via ptyalin, then in the stomach via HCL, and then by pancreatic amylase, lactase and other enzymes. Glucose is then absorbed in the small intestines and is then stored as glycogen in the liver. The liver is the primary site of glucose production. The liver converts lactic acid to glycogen and back to glucose via epinephrine. The liver converts fats and proteins via gluconeogenesis into glucose or glycogen. The head of the pancreas controls chromium, which controls insulin levels and assists in the enzyme action of fats via bile salts. The tail of the pancreas controls zinc, which maintains and sustains levels of insulin. Blood sugar depends on: 1. The liver which stores and releases glycogen 2. The pancreas, which produces insulin that transfers sugar from the blood to the extracellular fluid 3. The adrenal glands, which produced glucocorticoids that, cause the liver to release glycogen into the blood as glucose 4. The sex organs, which deliver the extracellular glucose to the cell 5. The thyroid, which affects the storage of glycogen in the liver 6. The thymus and spleen, which affect the levels of iron and copper in the liver which, determine the liver's ability to handle glucose As you can see there are many organs, or combinations of these organs and glands, which affect glucose levels in the body. Therefore, glucose in itself cannot specifically determine where the problem may lie. Other indicators are necessary to pinpoint the problem.	-28				0	5
Uric Acid Uric Acid URIC ACID Uric acid is the principal end product of purine, nucleic acid, and nucleoprotein metabolism. Uric acid is transported by the blood from the liver to the kidney’s which filter out and secretes about 70% and the remainder excreted via the GI tract. From a pathological view, uric acid is elevated when there is cell breakdown as in leukemia and catabolism of nucleic acids as in gout, or removal via the kidneys is decreased due to renal failure. From a physiologic view, we look at every level of protein combustion where there remain two by-products which are a Mucous (oily residue) and Uric acid (carbon ash) In order for protein to be fully combusted, it must first be influenced in the duodenum by trypsin, chymotrypsin, carboxypolypeptidase, and bile emulsification. Trypsin and chymotrypsin cleave proteins into peptides and carboxypolypeptidase split the peptides into amino acids. The pancreas synthesizes trypsinogen, chymotrypsinogen, and procarboxypolypeptidase, which are enzymatically inactive. When they are released into the duodenum they are all activated by enterokinase. Which now readies the proteins for assimilation in the liver. Therefore, if the proteins are not prepared properly the two end products, uric acid, and mucous, will be out of balance. URIC ACID IS HIGH WHEN General considerations: ¬ Decrease fatty proteins and rich foods ¬ Decrease alcohol and simple sugars ¬ Increase water intake	303.64
Bun Bun BLOOD UREA NITROGEN Blood urea nitrogen is formed entirely by liver deamination from protein metabolism. BUN is a byproduct due to the release of nitrogen bonds (and measures the nitrogen portion of urea) from protein substances in the liver. From a pathological perspective, an increased blood urea nitrogen would indicate renal disease, tissue necrosis, increased adrenal gland activity, and rapid protein catabolism. From a physiologic perspective, the purpose of nitrogen is to carry a substance through an aerobic media preventing oxidation, and eventually back into an anaerobic environment. Once in the liver the thyroid through the use of iodine, releases the nitrogen bond, releasing the nitrogen from the protein, allowing the protein to combust into hormones, enzymes and antibodies. The adrenals and anterior pituitary play a vital role in the combustion of this protein. The urea is now sent to the kidneys and is converted into urine. Urea is produced when amino acids, which are not used for protein synthesis, are broken down via hepatic metabolism. These amino acids are de-aminated producing ammonia, which is converted to urea immediately since ammonia levels become toxic. When this metabolic conversion is affected due to faulty metabolism or liver disease ammonia is not converted causing excessive levels of ammonia with possible hepatic encephalopathy. Renal malfunction/failure may also cause a high BUN due to its affect on the removal of urea causing uremia. Uremic wastes usually impair platelet function, and patients may show an increased tendency towards bleeding. BUN IS HIGH WHEN General considerations: ¬ High protein diets can cause increased BUN ¬ Increase water intake if no edema	880.95	10
Creatinine Creatinine CREATININE Creatinine ash is a basic byproduct in the breakdown of muscle creatine phosphate resulting from energy metabolism. From a pathological perspective the kidneys primarily remove creatinine and when there are elevated levels it indicates reduced kidney function. Thus creatine levels give an approximate for the GFR. From a physiological perspective, creatine is a by-product of actin metabolism after being exposed to acetylcholine combustion. The actin fiber joins two stable protein blocks (myosin), which combusts to produce muscle contraction, primarily for activity and secondarily for tonicity. During a muscle contraction, an action potential travels along a motor nerve to a muscle fiber. Acetylcholine is released at the motor endplate, causing multiple acetylcholine lined gated protein channels to open. This causes sodium ions to flow to the interior of the muscle, which initiates an action potential of that muscle. This then leads to depolarization releasing large amounts of calcium into the myofibrils. This initiates a contractive force between the actin and myosin filaments via ATP causing them to slide together, which is the contractile process. After a fraction of a second, calcium is pumped back into the sarcoplasmic reticulum, until the next muscle contraction. The actin fiber is then oxidized (H displaced) via acetylcholine, leaving an oily waxy residue known as creatinine. GABA (Glutamic amino benzoic acid), which is part of the actin fiber, helps it burn better. Creatine becomes creatinine with the release of ATP. Low creatinine levels would indicate muscle loss and weakness.	455.56
Sodium Sodium ELECTROLYTES The blood electrolytes include sodium, potassium, chloride, and the bicarbonate (HCO3) ion. Sodium, potassium, and chloride enter the body via ingestion of food. Carbon dioxide, on the other hand, originates within the body via the metabolic process of carbohydrates, fats, and proteins. Normally the excretion of sodium, potassium, and water is equal to their intake. The kidneys secrete 80-90 percent of all electrolytes. Excessive carbon dioxide stimulates the respiratory centers in the brainstem to increase respiration. Therefore, the kidneys and the lungs control sodium, chloride, potassium, water, and carbon dioxide thus exerting control over the acid/alkaline balance in the body. There are also many other organs, and glands involved in this process, such as the posterior pituitary, adrenals, bowel, and uterus/prostate. The purpose of electrolytes is to set up a shifting mechanism in the cell membrane via oxidation, allowing increased or decreased permeability to that membrane site. Sodium, which is found in high concentration outside the cell, has the ability to gather up substances (foods) and bring them to active membrane sites. Chloride is found in the cell membrane and acts as a “doorman” allowing or disallowing exchanges between the intracellular and extracellular fluids. Potassium, which is found in high concentrations within cells, oxidizes chloride, and allows sodium, with the food to cross the cell membrane and enter the cell. Sodium, potassium, chloride, calcium, and hydrogen are all transported via active transport. SODIUM Sodium is the most abundant cation (90%) and is the major base in the body. Sodium is either implanted into the food via saliva or is found in the food and has the following functions: 1. Sodium is an alkaline mineral that helps maintain alkaline activity. Therefore, it helps in acid-alkaline balance, which affect intracellular/extracellular fluid exchange, osmotic pressure, via the sodium/potassium pump and does this in conjunction with antidiuretic hormone and aldosterone. 2. Sodium gathers, and aggregates (polarizes) all substances necessary to be exchanged by semi-permeable membranes. Sodium pumps proteins and sugars into the cell membranes. 3. Sodium also affects the renal tubules for the activity of discharging toxins. It literally aggregates toxins and holds them in suspension. 4. Sodium is controlled by the adrenal cortex and as mentioned above is extremely alkaline and therefore, can cause migration of substances towards its polarity, as well as causing these migrated substances to achieve permeability in an acid antioxidant type media known as a fatty membrane. Sodium is the substance necessary to polarize foods into storage according to that permeable membranes needs. 5. Sodium is also necessary for the transmission of neurological impulses by creating action potentials across neurological membranes. 6. Sodium concentration in and out of cells remains constant due to renal blood flow, carbonic anhydrase enzyme activity, aldosterone, and other steroids controlled by the anterior pituitary, rennin enzyme secretion, hypothalamus, and posterior pituitary control of ADH and vasopressin secretion	-33.33			5	5			5
Potassium Potassium ELECTROLYTES The blood electrolytes include sodium, potassium, chloride, and the bicarbonate (HCO3) ion. Sodium, potassium, and chloride enter the body via ingestion of food. Carbon dioxide, on the other hand, originates within the body via the metabolic process of carbohydrates, fats, and proteins. Normally the excretion of sodium, potassium, and water is equal to their intake. The kidneys secrete 80-90 percent of all electrolytes. Excessive carbon dioxide stimulates the respiratory centers in the brainstem to increase respiration. Therefore, the kidneys and the lungs control sodium, chloride, potassium, water, and carbon dioxide thus exerting control over the acid/alkaline balance in the body. There are also many other organs, and glands involved in this process, such as the posterior pituitary, adrenals, bowel, and uterus/prostate. The purpose of electrolytes is to set up a shifting mechanism in the cell membrane via oxidation, allowing increased or decreased permeability to that membrane site. Sodium, which is found in high concentration outside the cell, has the ability to gather up substances (foods), and bring them to active membrane sites. Chloride is found in the cell membrane and acts as a “doorman” allowing or disallowing exchanges between the intracellular and extracellular fluids. Potassium, which is found in high concentrations within cells, oxidizes chloride, and allows sodium, with the food to cross the cell membrane and enter the cell. Sodium, potassium, chloride, calcium, and hydrogen are all transported via active transport. POTASSIUM Potassium is intracellular, lining the inside of all cell membranes and affecting intracellular fluids, osmotic pressure, buffering viscosity (potassium bicarbonate is the primary intracellular inorganic buffer). When there is a decrease in potassium bicarbonate you have acid cells, which excites the respiratory centers so the patient hyperventilates. Metabolic acidosis or diabetic ketoacidosis drives potassium out of the cells, affecting electrolyte balance, water retention and carbon dioxide transport in red blood cells. Potassium is responsible via the posterior pituitary for oxidizing secondary hydrogen chloride (affecting adrenal function), allowing the sodium-aggregated substances to cross the cell membrane by affecting the membranes permeability. Potassium is the only substance, which allows oxygen into unoxygenated tissue. About 90% of the body’s potassium supply is intracellular with only a small percent in the serum. 80% of that is found in the muscles (used for muscular contraction) and in the bones. Potassium levels are regulated by the Na/K ATPase pump which requires magnesium for proper function. Potassium is necessary for proper function of mineralocorticoids, (aldosterone and deoxycorticosterone) thus maintaining sodium concentration and alkaline reserve. Therefore, potassium is of great value to the posterior pituitary (ADH/oxytocin), the pineal, and the adrenal cortex via aldosterone secretion. Potassium along with sodium regulate renal acid-base balance, by substituting hydrogen ions for sodium and potassium in the renal tubules. Potassium also facilitates oxygen to the myocardium and oxidizes the S.A. node of the heart. The heart has the highest potassium concentration in the body. Potassium along with calcium and magnesium controls the rate and force of contraction in heart muscle. It is the primary oxidizer of the body capable of expressing all cellular needs. Potassium also regulates neurological impulses via osmotic pressure gradients throughout the nervous system. Potassium directs carbohydrate digestion by polarizing minerals associated with carbohydrate digestion, from the time the carbohydrate enters the body until the cell utilizes it. Potassium also makes proteins soluble and regulates protein synthesis. 80-90 percent of potassium in the cells is excreted by the kidneys (resulting in the loss of 40-50 mEq/L per day even during fasting) with the remainder excreted by the stool and through sweating POTASSIUM IS LOW WHEN General considerations: ¬ Increase water intake ¬ Increase magnesium intake ¬ Decrease calcium intake ¬ Increase potassium intake ¬ Decrease carbohydrate intake	-50		5						10	10
Chloride Chloride ELECTROLYTES The blood electrolytes include sodium, potassium, chloride, and the bicarbonate (HCO3) ion. Sodium, potassium, and chloride enter the body via ingestion of food. Carbon dioxide, on the other hand, originates within the body via the metabolic process of carbohydrates, fats, and proteins. Normally the excretion of sodium, potassium, and water is equal to their intake. The kidneys secrete 80-90 percent of all electrolytes. Excessive carbon dioxide stimulates the respiratory centers in the brainstem to increase respiration. Therefore, the kidneys and the lungs control sodium, chloride, potassium, water, and carbon dioxide thus exerting control over the acid/alkaline balance in the body. There are also many other organs, and glands involved in this process, such as the posterior pituitary, adrenals, bowel, and uterus/prostate. The purpose of electrolytes is to set up a shifting mechanism in the cell membrane via oxidation, allowing increased or decreased permeability to that membrane site. Sodium, which is found in high concentration outside the cell, has the ability to gather up substances (foods) and bring them to active membrane sites. Chloride is found in the cell membrane and acts as a “doorman” allowing or disallowing exchanges between the intracellular and extracellular fluids. Potassium, which is found in high concentrations within cells, oxidizes chloride, and allows sodium, with the food to cross the cell membrane and enter the cell. Sodium, potassium, chloride, calcium, and hydrogen are all transported via active transport. CHLORIDE Chloride a blood electrolyte, and is the major anion and exists in the extracellular spaces as part of the sodium chloride or HCl molecules. Chloride is used for assessing pH, and electrolyte balance. From a physiologic perspective, the primary purpose of chloride is to regulate the quantity of carbohydrates and proteins entering into the cells, by inhibiting the exchange of mineral controlled substances across the cell membrane and responds to the oxidative power of potassium. Chloride the major anion is predominantly found in the extracellular spaces as part of sodium chloride or in the stomach as hydrochloric acid. Chloride maintains cellular integrity by its influence on acid-base and water balance as well as osmotic pressure. Chloride has a reciprocal power with other anions by decreasing or increasing when there are too many or not enough anions. Aldosterone has a direct effect of reabsorption of sodium and an indirect effect on the increased absorption of chloride. Chlorides are lost via the GI tract through vomiting or diarrhea and thru the kidneys during times of diuresis. Chloride also responds to the antioxidant media (cell membrane) by mobilizing, and collecting sodium/food aggregates on a selectively permeable basis. This reaction is under the influence of the adrenal medulla/epinephrine/norepinephrine thereby maintaining energy stores. Chloride also assists in the production of HCl via the chief cells in the stomach. In the bowel, chloride is important in preventing the passage of water out of the body. Therefore, chloride literally blocks the flow of water/gas exchange across a cell membrane. This is extremely important in the intestines and bladder. Chloride plays a vital role during the conduction of a neurological impulse where sodium lines up on the outside of a cell membrane, and potassium on the inside of the cell membrane, during the resting stage or polarized state. In a normal nerve fiber, the permeability of the membrane to potassium is about 100 times that of sodium. The sodium-potassium pump moves three sodium ions to the exterior of the cell, for every two potassium ions that are moved to the interior of the cell, creating a net positive charge to the outside of the cell membrane for each revolution of the sodium-potassium pump. This creates a positively charged external membrane and a negatively charged internal membrane, which sets up a membrane electrical potential. As a neurological impulse is transmitted down the nerve, (which is the excitation phase of an impulse), sodium crosses the cell membrane, and enters into the cell, while potassium moves to the external portion of the membrane. This then creates the depolarization of the cell membrane, thereby creating a negative charge on the outside, and a positive charge on the inside. The transmission of each impulse along the nerve fiber reduces infinitesimally as the concentration differences of sodium and potassium between the inside and outside of the cell membrane change slightly. In so doing allows the nerve fiber to transmit between 100, 000 to 50, 000, 000 impulses before the concentration differences are rundown. As the neurological impulse passes, the sodium-potassium ATPase pump re-establishes the sodium-potassium ratio back to normal (repolarization). The pumping activity is dramatically increased approximately eightfold to restore the membrane back to the polarized state. The chloride shift to the inside of the cell membrane during the final stages makes the inside of the cell, even more, negative, which further helps repolarize the cell. Chloride generally increases and decreases with plasma or serum sodium levels. CHLORIDE IS HIGH WHEN General considerations: ¬ Drink plenty of water ¬ Decrease sodium levels ¬ Increase fat-soluble vitamins D, E, K, and A	-38.46							5
CO2 CO2 CARBON DIOXIDE Carbon dioxide is created as a byproduct when potassium forces water into fat. So carbon dioxide is the acid gas factor, which binds fats and selenium creating the intelligent metabolic activity between the water and fat. 80-90 percent of the carbon dioxide found in plasma is bound to protein and is represented as bicarbonate ions (HCO3-) which first exists in the extracellular spaces as CO2 then as H2CO3 and finally is buffered by the plasma and erythrocytes into sodium bicarbonate NaHCO3) and is regulated by the kidneys. The other 10 to 20 percent is dissolved CO2 gas (removed by the lungs), which is bound to protein as CO3 (2), and carbonic acid (H2CO3). The total CO2 comes from dissolved CO2, H2CO3, HCO3- and carbaminohemoglobin (CO2HHb). This occurs in the following way, carbon dioxide in the blood reacts with water in the red blood cells to form carbonic acid. In the blood cells, there is an enzyme called carbonic anhydrase that catalyzes the water and carbon dioxide 5,000 fold, creating a rapid exchange into carbonic acid. This allows tremendous amounts of carbon dioxide reacting with the water in the red blood cells, even before the blood leaves the tissue capillaries. So a red blood cell creates carbonic acid from water and carbon dioxide. In another small fraction of a second, the carbonic acid formed in the red blood cell now disassociates into hydrogen and bicarbonate ions. The hydrogen ions combine with hemoglobin, as the bicarbonate ions diffuse out into the plasma while chloride ions diffuse into the red blood cells taking the place of the bicarbonate ions. This is made possible by the presence of a bicarbonate/chloride carrier protein in the red blood cell membrane, which acts as a shuttle for these two ions. Thus, the chloride content of venous red blood cells is greater than that of arterial cells. This is known as the chloride shift. In addition, carbon dioxide can react directly with hemoglobin to form the compound carbaminohemoglobin. This carbaminohemoglobin creates the reversible reaction releasing carbon dioxide into the alveoli of the lungs. Carbon dioxide then is the venous capillary exchange product after diffusion takes place. The active pressure intake of oxygen relies upon this diffusion. This active process realizes the ability of forced metabolism and is the ash byproduct. Carbon dioxide is vital to pH balance and is controlled by the respiratory, renal, and posterior pituitary adrenal axis. Therefore, any of these glands or organs or combinations thereof can affect carbon dioxide levels. CARBON DIOXIDE IS HIGH WHEN General considerations: ¬ Water loss- increase water intake ¬ Protein loss- increase protein intake ¬ Hypomagnesemia or hypokalemia causes increased CO2- increase potassium and magnesium CARBON DIOXIDE IS LOW WHEN ¬ Water loss- increase water intake ¬ Hypermagnesemia or hyperkalemia causes decreased CO2- decrease potassium and magnesium support	-16.67									5
Calcium Calcium CALCIUM Calcium is the largest most nonpolar, alkaline and most abundant of all minerals with 99% of all calcium found in the bones and teeth. Calcium exists in the ionized state 55 percent of the time and 45 percent of the time in the non-diffusible state, bound to either albumin, prealbumin or thyroglobulin. Therefore, if there is a decrease in serum albumin then there will be a decrease in serum calcium. Calcium has many functions: ¬ Provides the mobilizing factor in trauma, infections and stress for tissue repair, along with vitamins A, C, manganese, phosphorus, and fatty acids. ¬ Causes vasoconstriction, while potassium, sodium, magnesium, hydrogen ions, and carbon dioxide cause vasodilatation. ¬ Is necessary for bone formation along with phosphorus, collagen, hydroxyapatite (gives bone its hardness) and bone salts of magnesium, sodium, potassium, carbonate, uranium, plutonium, and strontium. ¬ Calcium is used to create action potentials across smooth and striated muscles leading to contraction. ¬ Calcium is used as an intracellular communicator via calcium ion gated channels. ¬ Calcium collects and gather up lipoproteins, and move them across the intestinal membrane. Attaches to oils, fats, fatty acids and waxes. Calcium is absorbed in the upper portion of the small intestines (duodeneum), and the amount absorbed depends on the "acidity" of the intestinal content, via phosphorylation and protein content. When the ratio of calcium to magnesium (which is found in the intestinal membrane as well as cell membranes) is greater than 2-1, fat is drawn through the intestinal and cell membranes. Calcium also requires vitamin D. and HCl for optimal metabolism. The glands involved with calcium are: 1. The stomach via the release of HCL, which affects the preparation and absorption of calcium. 2. The parathyroids- via parathormone control of calcium ion concentration by controlling intestinal absorption, excretion via the kidneys and the release of calcium from the bones. 3. The liver/gallbladder- via bile emulsification of lipoproteins, preparing them for intestinal absorption. 4. The spleen- which stores and ages fats or lipoproteins. 5. The parotids- due to their ability to program foodstuffs. 6. The thyroid glands-via "calcitonin", promoting deposition of calcium in the bones, while decreasing calcium concentration in the extra-cellular fluids and the blood. 7. The anterior pituitary via its control of magnesium regulating calcium uptake, which regulates protein transport thru the cell membranes. 8. The pancreas- via its ability to oxidize fatty acids Therefore, any of the above glands or organs or combinations thereof has a great impact on calcium levels. CALCIUM IS HIGH WHEN General considerations ¬ Your patient should drink plenty of water ¬ Make sure they are not hypervitaminosis on Vitamins A or D ¬ Very high protein diets may increase calcium levels ¬ Magnesium and phosphates may also increase calcium levels ¬ Using sea salt can help to reduce calcium levels. CALCIUM IS LOW WHEN General considerations: ¬ Increase Vitamin A and D intake ¬ Increase albumin and protein intake ¬ Increase magnesium intake ¬ Increase phosphorus	-13.04	5					5
Phosphorus Phosphorus PHOSPHORUS 85% of the total phosphorus exists as phosphates or esters in the body and is found chiefly in the skeleton and is combined with calcium. 14% of the phosphorus is found in intracellular tissues and 1 % is found in the extracellular fluid. Therefore phosphorus levels are a poor indicator of levels of phosphates in the body. Phosphorus runs inversely to calcium levels in the body at a calcium to phosphorus ratio of 10 to 4. Therefore, calcium can be a great indicator for phosphorus as well. As calcium levels increase in the serum, phosphorus levels decrease, and when calcium levels decrease phosphorus levels increase. In fact, causes of high calcium also cause low phosphorus. The controlling factor of phosphorus is parathormone (PTH), which is also the calcium-controlling factor. Phosphorus helps calcium through the cell membrane by increasing the permeability of the cell membrane via oxygen displacement. 1. Phosphorus is responsible for growth and development by way of: ✓ bonding ✓ polymer function ✓ hydration ✓ chemical transport, and ✓ buffering 2. Phosphorus is also responsible for bone formation 3. Phosphorus and metabolism of glucose Phosphorus is also required for the metabolism of glucose via phosphorylation. Phosphorylation is when a phosphate radical promoted by glucokinase in the liver, or hexokinase in other cells captures the glucose and once inside the cells keeps it there. The exception to this occurs in the liver, the kidneys, and the intestinal epithelial cells. Ingestion of carbohydrates causes phosphorus to enter RBC’s with glucose causing a reduction of serum phosphorus levels and lipids. Phosphorus also works in the stomach to stabilize sugars and activate starches by the twofold process of phosphorylation. Phosphorylation and its counterpart, dephosphorylation, turn many protein enzymes on and off, thereby altering their function and activity. By altering pepsin/HCL levels phosphorus can: a. Stabilize simple sugars-simple sugars are easily oxidized (combusted) before they reach the liver, resulting in low sugar levels. Pepsin stabilizes these simple sugars, so they can be transferred to the liver for storage. b. Activation of starches- HCl is necessary to breakdown oily carbohydrates (grains), which are difficult to oxidize (combust). Thus making them readily available for oxidation. The above two mechanisms establish an HCl-pepsin balance in the stomach for proper pH digestion. The presence of both HCl and pepsin in the stomach are critical for preparing carbohydrates, as well as proteins for further digestion in the small intestines. 4. The regulation and maintenance of the acid-base balance in the body by maintaining glandular acidity. 5. The storage and transfer of energy from one part of the body to the other. 6. Used in the Production of phospholipids (90 % produced by the liver): lecithin, A cephalin, and sphingomyelin Phospholipids are necessary for: Proper brain function (sphingomyelins) Phospholipids are a major constituent of lipoproteins which can affect function, formation and transport of these lipoproteins causing serious cholesterol abnormalities Production of cell membranes Thromboplastin production produced from A cephalin 7. Intracellular phosphorus is used for: Energy transport formation of ATP from ADP and creatine phosphate via oxidative phosphorylation. Major constituent of plasma membranes (phospholipids) Major constituent of DNA and RNA (nucleic acids) Calcium transport and osmotic fluid pressure General nutritional considerations when phosphorus is high: 1. Patient should increase water intake 2. Reduce fat intake 3. Reduce Vitamin D intake if overdosing 4. An isotonic saline solution (sea salt) will decrease phosphorus levels 5. Also, decrease phosphorus in the diet and add calcium carbonate to your diet General considerations when phosphorous is low: 1. Vitamin D deficiency 2. Calcium deficiency 3. Magnesium deficiency 4. Patient needs a high protein diet	270					5	5
Magnesium Magnesium MAGNESIUM Serum magnesium constitutes only a small fraction of the total body stores and may not predict magnesium status correctly. From a physiologic perspective, magnesium directs protein digestion, by polarizing minerals associated with protein digestion, from the entrance of protein into the body to its final deposition in the cell. Approximately 40-60 % of the magnesium is found in the skeleton for bone formation, 20% is found in the muscle, 30% is found in the intracellular cytoplasm, with only 1 % of the magnesium found in the serum. Magnesium affects membrane permeability, nerve impulses, muscle contraction, intracellular fluid regulation, activation of enzyme systems, where magnesium acts as a metallic cofactor in over 300 enzymatic reactions. Regulates protein synthesis, carbohydrate metabolism, nucleic acid synthesis, and blood viscosity. Magnesium along with sodium, potassium and calcium regulate neuromuscular irritability and the mechanism for clotting. Less then 2% of calcium, magnesium and phosphates are found in the plasma and extracellular fluid and are controlled in narrow limits. Albumin accounts for 70% of the bound calcium. Magnesium also binds to albumin and since it has a lower specificity for the receptors it creates more free magnesium in the plasma. Magnesium and calcium are very much linked in their body functions and a deficiency in either one will have an adverse affect on the other. Especially since calcium needs magnesium to be absorbed thru the intestinal membrane as well as needing magnesium for calcium metabolism. For example, a magnesium deficiency will cause calcium to migrate out of the bone and into soft tissues such as the aorta and kidneys. 95% of all magnesium that is filtered thru the glomerulus is reabsorbed by the tubules where parathormone enhances tubular reabsorption of magnesium. When there is a deficiency of magnesium you will see a decrease in urine stores before serum stores. Please note that even when magnesium is in a 20% depleted state, magnesium levels in the serum will appear normal. Calcium, magnesium and phosphates continuously enter the plasma via the kidney, the intestinal brush borders, and the ruffled border from the bones. Steady states of calcium, magnesium, and phosphorus approximate urine loss against intestinal absorption and skeletal mineral apposition against mineral absorption. Magnesium in the cells is complexed to phosphates, citrates and anions such as ATP, AMP and ADP (such as MgATP2-) Magnesium also plays a key role in the hormonal regulation of insulin, estrogen and thyroid hormones. Magnesium also stimulates secretions from the parathyroids and adrenal cortex (corticosteroids). Magnesium is also affected just the way calcium is to parathormone (enhances distal tubular reabsorption of magnesium) and to a lesser degree calcitonin. In fact, calcium, magnesium, and phosphates are depressed in vitamin D deficiencies and increased with vitamin D excess. Magnesium is used in the treatment of elevated cholesterol and triglycerides, muscular contraction, hypertension (A causal relation between decreased Mg2+ content of cardiac muscle/coronary arteries and nonocclusive sudden-death ischemic heart disease has been proposed) and premenstrual syndrome. Magnesium is indicated in collagen and connective tissue diseases, inflammatory disorders, migraines, general endocrine function and neurological and psychosomatic disorders.	-80	5			5
Total Protein Total Protein TOTAL PROTEIN Total proteins are divided into two fractions: albumin, and globulin (alpha, beta, and gamma). Please note that total protein also includes fibrinogen. Therefore total protein is made up of albumin, globulin and fibrinogen, all produced in the liver. These are the plasma proteins necessary to produce enzymes, antibodies, clotting factors, kinin precursors, and transport substances for hormones, vitamins, minerals, fats, etc. For example, plasma proteins combine with cholesterol forming lipoproteins such as VLDL, LDL’s, HDL’s etc. The lipoproteins then combine with minerals via enzyme metabolism to form and renew sex hormones such as testosterone, estrogen, progesterone etc. Other deaminated proteins produced in the liver, combusts at the mitochondrial level to form cell structures. These are your tissue building proteins known as nucleoproteins, DNA and RNA (your proteins of mitosis and meiosis). Since there are many glands involved in protein digestion, it is very difficult to make a determination from total protein alone. Glands and organs involved with protein control are as follows: The anterior pituitary, which controls all glands of protein digestion, such as the adrenals, thyroid, pancreatic head, sex organs, and spleen That parotid glands which tag lipoproteins with copper The parathyroids via the calcium/magnesium mobilization of lipoproteins The thyroid which denitrifies protein in the liver The pancreas by trypsin and chymotrypsin which, prepares the protein for assimilation into the bloodstream The sex organs that prepare protein for final deposition into the cells * Any combination of the above TOTAL PROTEIN IS LOW WHEN General considerations: o Increase protein intake o Increase B acid vitamins	20
Albumin Albumin ALBUMIN In pathological levels albumin is used to evaluate: 1. Liver and renal disease 2. Blood osmotic pressure 3. Chronic disease states, which most patients have 4. Dehydration 5. Albumin decreases in acute inflammatory infectious processes From a physiological standpoint, albumin is produced in the liver and is a primary byproduct of sterols and waxes. Its function is used to build and repair tissue. Albumin is responsible for 80 percent of the colloidal osmotic pressure between body tissues and blood cells. 75% of this control occurs inside the cells since most of the protein is intracellular. When you have a decrease in albumin, the osmotic pressure becomes disturbed resulting in fluid transfer and edema. Since albumin influences water movement, it will also influence nutrient and mineral movement. Albumin creates the permeability of the membrane to the osmolarity of the membrane. Therefore, substances can pass from a lesser concentration to a greater concentration. The flow is from the arterial capillaries to extracellular fluid, then from the extracellular fluid to the intracellular fluid, then from the intracellular fluid to the mitochondria. Then back via the same pathway in reverse via osmotic absorption into the veins. Albumin is also a part of a complex buffer system, which accounts for 75% of things that need to be buffered to maintain acid-alkaline balance in the body. The most powerful buffer system out of the four including, the bicarbonate system (HCO3-), the phosphate buffer system, and the liver (nitrogen/urea), the proteins of the cells and plasma, rein supreme. The protein buffer system works by controlling blood Hydrogen (H+) ion homeostasis. Both intracellular and extracellular proteins have negative charges and can serve as buffers for alterations in hydrogen ion concentration. However, because most proteins are inside cells, this primarily is an intracellular buffer system. Hemoglobin (Hb) a globular protein is an excellent intracellular buffer because of it's ability to bind with Hydrogen ions forming a weak acid and carbon dioxide (CO2) bond. After oxygen is released in the peripheral tissues, hemoglobin binds with CO2 and H+ ions. As the blood reaches the lungs these actions reverse themselves. Hemoglobin binds with oxygen, releasing the CO2 and H+ ions. The H+ ions then combine with bicarbonate (HCO3) ions to form carbonic acid (H2CO3). The H2CO3 breaks down to form water (H2O) and carbon dioxide (CO2), which are excreted via expiration through the lungs. Increases in albumin cause arteries to sclerose and a decrease in albumin causes veins to sclerose. Albumin is also a transporter of minerals and accounts for 70% of the bound calcium. Magnesium also binds to albumin and since it has a lower specificity for the receptors it creates more free magnesium in the plasma. Calcium, magnesium, and phosphates continuously enter the plasma via the kidneys, the intestinal brush borders and the ruffled border of the bone. Albumin is also responsible for transporting copper, zinc, and nickel. By controlling the transport of these minerals, albumin is the carrier of choice. The following glands are associated with albumin: 1. The parotids 2. The head of the pancreas 3. The endo-reticular portion of the liver 4. Kidneys Therefore, the function or malfunction of anyone of those glands/organs or combinations thereof can lead to imbalances in albumin levels.	-30
Globulin Total Globulin Total GLOBULIN Organs that are responsible for globulin production are the liver, thyroid, spleen and the rest the immune system. There are four types of globulins alpha 1,2, beta and Gamma. There a few groups of gamma globulins with one group being the immunoglobulins (IgA, IgG. IgM), which produce our antibodies. The thymus produces α and β globulins know as thymoglobulin using Vitamin T and copper for its production. The thyroid produces thyroglobulins that form thyroxin and triiodothyronine via vitamin K and iodine. The spleen produces spleenoglobulins that require vitamin E and iron for its production. Globulin also acts as a polarized colloidal substance necessary for specific glandular hormonal function by acting as a transport mechanism for many hormones such as sex hormone binding globulin. Globulin also assists in: Toxin neutralization by binding soluble antigens in the blood and intracellular spaces Red blood cell production Antibody formation Protection of the gastrointestinal mucosa And is also necessary via the intrinsic factor for digestion and absorption. Globular proteins can be affected via: Nutrition- lack of protein Liver Thyroid Spleen Thymus	15.79
A/G Ratio A/G Ratio A/G RATIO The A/G ratio is the ratio of albumin to globulin, and along with fibrinogen (produced by the liver) literally measures the thickness or “collagen factor” of the blood. The A/G ratio then is also a representation of the fibrinogen content in the blood and regulates the amount of protein being utilized at any time in the body. The liver forms prothrombin, which requires vitamin K. for its production. Prothrombin is a plasma protein, which is changed into thrombin via prothrombin activator and calcium. Thrombin, transposes fibrinogen into fibrin, continually causing clotting throughout the body along with blood platelets. Fibrinogen, therefore, provides the clotting thickness (collagen factor) in the blood. These polarized protein fibrous strands are necessary to maintain blood viscosity, which regulates the amount of capillary exchange from the artery to the extracellular fluid. Collagen a protein strand (albuminoid) and proteoglycan filaments also regulate exchange by causing a very slow diffusion of molecules via kinetic motion moving substances through the extracellular fluid either to the cell membrane or back into the circulatory or lymphatic systems. Collagen is also the main structural protein in connective tissue and found in the extracellular spaces. Collagen and proteoglycan filaments are used in the interstitium to provide tensile strength and for healing. As the main component of connective tissue, it makes up from 25% to 35% of the whole-body protein content. Collagen is formed in the sternum and iliac crest. A/G RATIO IS INCREASED WHEN Anything that would decrease globulin would increase the A/G ratio and anything that would increase albumin would also increase the A/G ratio so also look at all the possibilities under low globulin or high albumin THE A/G RATIO IS DECREASED WHEN Anything that would increase globulin would decrease the A/G ratio and anything that would decrease albumin would decrease the A/G ratio so also look at all the possibilities under high globulin or low albumin	1645.45
Bilirubin, Total Bilirubin, Total TOTAL BILIRUBIN Bilirubin comes from the breakdown of hemoglobin and is the byproduct of hemolysis. Bilirubin is produced by the RE portion of the liver and is excreted with the bile. Pathologically elevations in total bilirubin occur when there is a massive amount of destruction of RBC’s, or the liver is congested and unable to excrete bilirubin. From a physiologic perspective, the components of bile are inositol, choline, lecithin, cholesterol, and bilirubin/biliverdin. Cholesterol, which is produced by the liver, is converted into bile salts via the influence of the adrenal glands. The bile salts are converted into cholic acid or chenodeoxycholic acid equally. Approximately 60 percent of all cholesterol is converted into these two acids. These acids then combine with glycine and taurine to form glyco and tauro conjugated bile acids. The salts of these acids are secreted in the bile. These salts do two things: 1. They act like "soap" creating saponification and emulsification of fat. This decreases the surface tension of the fat allowing agitation to break the fat up into smaller sizes. 2. Bile salts help absorb fatty acids, monoglycerides, cholesterol, and other lipids, by forming minute complexes called micelles. Micelles are highly soluble, highly charged, and easily absorbed, increasing absorption by 40 percent. The liver secretes about 600-1,200 milliliters of bile per day. The purpose of bile is to: 1. Digest, emulsify and absorb fats. 2. To excrete waste products, such as excessive cholesterol, and bilirubin, which is the end product of hemoglobin degradation. Bilirubin is the predominant pigment of bile, and is formed from hemoglobin, and destroyed red blood cells. The red blood cells are destroyed by the reticulo-endothelial system (liver and spleen), including the kupfer cells of the liver. If the spleen/liver are hyperactive, the bile production is increased. This allows the passive function of bile production to elevate. As the spleen, liver, and bone marrow destroy hemoglobin it passes into the bloodstream with a protein creating a colloidal state. This creates hemolytic jaundice when there is excessive destruction or impaired production of red blood cells, leading to excessive amounts of prehepatic bilirubin. The liver cells are unable to withdraw the bilirubin from the blood as fast as it is formed. Therefore consequently there is an increase in prehepatic bilirubin (indirect form). Remember total bilirubin = the direct and indirect forms. The direct is elevated in biliary obstruction, which is conjugated and reacted on by the liver. The indirect form is elevated in liver failure, which is unconjugated and not reacted on by the liver. Since the liver, spleen, adrenals and diet play a role in total bilirubin production from a physiologic perspective we must evaluate those glands as well.	-77.78
Alkaline Phosphatase Alkaline Phosphatase ALKALINE PHOSPHATASE Bone osteoblasts, liver cells, and the placenta all produce high levels of alkaline phosphatase, with some activity in the kidneys and intestines. Alkaline phosphatase is called alkaline because it aids in maintaining and works best in an alkaline pH of 9-10. From a pathological perspective, alkaline phosphatase levels rise in liver disease due to impaired excretion of this enzyme from obstruction in the biliary tract, and bone disease via increased osteoclastic activity due to bone breakdown as in cancer. From a physiological perspective alkaline phosphatase is responsible for the balancing of water, and mineral metabolism controlled by the glands below. This exchange of water and mineral metabolism occurs at the cell membranes of ligaments, tendons and disc structures. The balance is created by, setting the minerals involved with electrolyte balance into motion. These minerals, along with proper neurological control, cause the shifting of food thru the membranes. The glands responsible for this balance are as follows: • The adrenal cortex via mineralocorticoids causes excretion of sodium and potassium by the kidney. • The adrenal medulla via epinephrine and norepinephrine increase metabolism, and cellular exchange via the chloride shift at the level of the membrane. • The posterior pituitary via antidiuretic hormone and its effect on potassium (oxidizer) and the water content within the cell. • Prostate/uterus via selenium acts as an oxidative mineral to insure proper membrane exchange in conjunction with the above. Alkaline phosphatase is a member of a family of zinc metalloprotein enzymes whose purpose is to split off a terminal phosphate group from an organic phosphate ester. Enzyme activity is localized in the brush border of the proximal convoluted tubules of the kidney, intestinal mucosal epithelial cells, hepatic sinusoidal membranes, vascular endothelial cells and osteoblasts of bone as mentioned above. It is the introduction of an alkaline media for bone growth. When there is an increased alkaline phosphatase you have too much acidity. In “bone pathology” there is usually a hyper-acidic state, since the foundation of a cell, is nucleic acid. The nucleic acid is composed of phosphoric acid. Phosphoric acid is a component of alkaline phosphatase, therefore, the adrenals regulate the acid/alkaline balance for energy, and growth. Alkaline phosphatase controls the alkaline substance, which controls energy, and the acid substance, which controls growth. Over the years, the laboratory low range has been steadily decreasing from 60, down to 40 now down to the mid 20's. Since this test does measure metabolic output of the adrenals, going to low is not the answer. I recommend that the low range is 70.	-66.32
LDH LDH LACTIC ACID DEHYDROGENASE Lactic acid dehydrogenase is found chiefly in the heart, skeletal muscles, kidneys, and liver, as well as all cells. In pathological states, elevated levels indicate damage to the above areas and is used to determine myocardial and pulmonary infarction. In physiological states, LDH catalyzes the conversion of pyruvate ( the final step in glycolysis) to lactate and back, as it converts NADH to NAD+ and back. A dehydrogenase is an enzyme that transfers a hydride from one molecule to another. When sugar and water (fatty acid metabolism) are exchanged across a muscle cell interface, a by-product called lactic acid is produced. When lactic acid combines with the carbon dioxide of the venous blood you have a hydrogen displacement. Lactic acid now becomes lactic acid dehydrogenase. Lactic acid dehydrogenase, therefore, is a glycolytic enzyme that functions as a catalyst in carbohydrate metabolism to produce energy. The pancreas via insulin and the posterior pituitary via ADH are responsible for this sugar and water exchange across the muscle cell interface. Lactic acid dehydrogenase indicates the active exchange of sugar across the membrane (muscle cell interface) utilizing chloride, zinc, and selenium. The utilization of these minerals creates glycolysis. LDH then from a physiological perspective determines pancreatic function regulating the amount of glucose into muscle. It is also important to note that sugar metabolism is very complex and does involve a series of other organs. Ranges for LDH are between 0-220; again it is rather obvious that LDH is a by-product of sugar metabolism and a 0 figure could not be construed as a low normal range. I feel that the range should start at 80. You will find many patients with a low LDH having problems with decreased function causing heart, skeletal muscle (weakness, loss of strength, muscle wasting), kidney and liver dysfunction, and eventual wasting away of these organs.	62.86					10					10
AST (SGOT) AST (SGOT) SERUM GLUTAMIC OXALACETIC TRANSAMINASE (SGOT) (AST) SGOT is highly concentrated in organs and glands of high metabolic activity and in descending order: heart, liver, skeletal muscle, brain, kidneys, pancreas, spleen and lungs. In pathological states, when you have high levels it means that cell damage has occurred in one or more of these areas and there is a release of this enzyme in circulation, elevating in 12 hours and remaining there for 5 days. In physiologic states, we know it is a tissue enzyme present in tissues of high metabolic activity, and concerned with the transfer of nitrogen between aspartic acid, and alpha-keto-glutamic acid, resulting in the synthesis of glutamic acid, alpha keto acid and oxalacetic acid. SGOT, therefore, is the catalyst that creates amino acid metabolism during glycolysis, for the production of energy. Since there are high concentrations of SGOT in skeletal muscle/heart, and the brain, it gives you an idea of the metabolic output of each system. The sex organs via the output of testosterone, estrogen, progesterone (which are formed on the gonadal epithelium by binding cholesterol to protein) are used to maintain muscle mass and strength. Therefore having a dramatic effect on muscle and nerve metabolism. Since amino acid metabolism also affects muscle mass, muscle strength, and the energy to fuel the muscular system, it is apparent that SGOT is the indicator of choice. Not to mention the energy necessary to run the central nervous system which utilizes 60 percent of the available energy necessary to run your body. Please note that most lab ranges start at 0 and since this is a measurement of the metabolic activity of the above organs 0 would mean death. The low range for SGOT should be 15. You will find physiological conditions where there are low levels of SGOT (15-20). This is due to the exhaustion of the above organs. Low levels indicated heart, skeletal muscle and diminished brain function/damage. These patients are usually physically weak/exhausted whether they exercise or not, lack mental clarity, cannot think straight and have brain fatigue/fog. They also have sex hormonal problems and require HRT or erectile dysfunction treatment. Many of these patients have a weak flabby heart, setting the stage for many types of conditions down the road. Low levels may also mean decreased liver function affecting, protein synthesis, detoxification, sluggish metabolism, cholesterol production to name a few of the 500 know liver functions.	25.71										10
ALT (SGPT) ALT (SGPT) SERUM GLUTAMIC PYRUVIC TRANSAMINASE (SGPT) (ALT) SGPT is primarily a liver function test. It has a maximum concentration in the liver (fatty membranes) sinusoids. Low concentrations of SGPT are also found in the kidneys, heart, and skeletal muscle. In pathological states, elevations indicate liver disease. ALT is found in serum and in various bodily tissues but is most commonly associated with the liver. It catalyzes the transfer of an amino group from alanine to alpha-ketoglutarate, and the products of this reversible transamination reaction being pyruvate and glutamate. glutamate + pyruvate ⇌ alpha-ketoglutarate + alanine Alanine transaminase delivers skeletal muscle carbon and nitrogen in the form of alanine to the liver. In skeletal muscle, pyruvate is transaminated to alanine, thus affording an additional route of nitrogen transport from muscle to liver. In the liver, alanine transaminase transfers the ammonia to A-KG and regenerates pyruvate. The pyruvate can then be diverted into gluconeogenesis. This process is referred to as the glucose-alanine cycle. The glucose-alanine cycle is used primarily as a mechanism for skeletal muscle to eliminate nitrogen as the muscles replenish their energy supply. Within the liver, alanine is converted back to pyruvate and is then a source of carbon atoms for gluconeogenesis. The newly formed glucose can then enter the bloodstream for delivery back to the muscle. The amino group transported from the muscle to the liver, in the form of alanine, is converted to urea in the urea cycle and then excreted. In physiological states SGPT is a primary kreb cycle expressant and as a result causes the release of catabolic fats. SGPT occurs in serum as a consequence of substances being released by the fatty membranes of the liver sinusoids, and lymphatic ducts. The liver sinusoids store food, and the lymphatic ducts house toxins. Picture a layer of fat that holds foods or toxins in the cell. Now as that layer of fat is being burned off, foods and toxins are being released in a controlled manner. This allows foods or toxins to be directed to their next destination. Please note that most lab ranges for this test start at 0, which in actuality is false since this is a measurement of liver function, and 0 would mean that the liver was not functioning at all. A low range then should be around 15. Therefore, from a physiological perspective, a low SGPT between 15-20 would indicate a sluggish liver causing many metabolic disturbances. Typically these people have no energy, get sick a lot, cannot tolerate food well and have a slow metabolism.	31.43
GGT GGT GAMMA GLUTAMYL TRANSPEPTIDASE (GGT) Is a biliary enzyme useful in the diagnosis of obstructive jaundice, intrahepatic cholestasis and pancreatitis. GGT is more responsive to biliary obstruction than are aspartate aminotransferase (AST) (SGOT) and alanine aminotransferase (ALT) (SGPT). 1. GGT is increased in hepatoma and carcinoma of the pancreas and useful in the diagnosis of metastatic carcinoma of the liver. Increasing levels in carcinoma patients relate to tumor progression and a dubious outcome. 1. CEA, alkaline phosphatase and GGT together are useful markers for hepatic metastasis from the breast and colon. 2. May be useful in the diagnosis of chronic alcoholic liver disease. Follow-up blood chemistries of serum GGT, AST and ALT levels can distinguish recovering alcoholics who resume drinking from those who do not. 3. Increase in body mass correlates with increased GGT levels. 4. GGT along with MCV is a useful test for alcoholism. 5. GGT is the test of choice for pregnant females who may have cholestasis. 6. GGT levels are elevated in cirrhosis and hepatitis. 7. The transaminases, AST and ALT rise higher in acute viral hepatitis; then GGT. 8. Increased in systemic lupus erythematosus GGT IS HIGH WHEN General considerations: If patient has been on a very low-fat diet for long periods of time then increase fat intake	-40
Ferritin Ferritin A ferritin test can help a doctor determine if a person has enough iron in their body. Low ferritin levels can indicate that the body doesn't have enough iron, while high levels can indicate too much iron. FERRITIN Men 20-250 ng/mL 20-250 ug/L Women 10-120 ng/mL 10-120 ug/L Children 7-140 ng/mL 7-140 ug/L Newborns 25-200 ng/mL 25-200 ug/L	-16.4
Total Iron Total Iron Total Iron Binding Capacity (TBIC)—measures the amount of transferrin, which is a blood protein that transports iron from the digestive system to cells that will be utilizing the iron. Your body produces transferrin in relationship to the body’s need for iron. When iron stores are low, transferrin levels will increase and when transferrin levels are low, too much iron is present. Usually, about one third of the transferrin is being used to transport iron at any one time. Because of this, your blood serum has considerable extra iron-binding capacity, which is called the Unsaturated Iron Biding Capacity (UIBC). The TIBC then equals UIBC plus serum iron measurement. Some laboratories may measure UIBC, some measure TIBC and others measure transferrin. TIBC is increased in iron- deficiency, acute hepatitis, during pregnancy or when oral contraceptives are used. TIBC is decreased in hypoproteinemia from many causes, cirrhosis of the liver, nephrosis and thalassemia or from a number of inflammatory states. TOTAL IRON IRON Men 65-175ug/dL 11.6-31.3 umol/L Women 50-170ug/dL 9.0 -30.4 umol/L Children 50-120ug/dL 9.0-21.5 umol/L Newborns 100-250 ug/dL 17.9-44.8 umol/L	-40
Cholesterol, Total Cholesterol, Total SERUM LIPIDS Serum lipids serve as a primary source of energy along with glucose. The functions are many, such as the production of cell membranes, precursors to hormones, and bile acids. Lipids are first broken down in the duodenum, along with bile, which emulsifies the fats, and prepares them for absorption into the lymphatic system. Pancreatic lipase hydrolyzes cholesterol, and triglycerides into fatty acids, and glycerol. The fatty acids and glycerol are then reconverted back into triglycerides by the intestinal cells and then discharged into the lymphatic or portal blood system, which is then sent to the liver. Cholesterol is also absorbed in both the free and esterified forms into the lymphatics. Cholesterol is also synthesized in the reticular cells and histiocytes throughout the body but mainly formed in the liver. Under the influence of iodine via the thyroid, carbohydrates, amino acids, and other fats are converted to cholesterol via multiple molecules of acetyl coenzyme A creating a sterol nucleus. Triglycerides are also assembled in the liver from glycerol and fatty acids. The liver is the main organ regulating blood lipids. So the liver can degrade fatty acids for energy, synthesize triglycerides from carbohydrates and proteins. The liver can then hydrolyzes the triglycerides back into three fatty acids, and glycerol then degrades the fatty acids into acetyl coenzyme A via beta-oxidation. Then acetyl coenzyme A is then oxidized to release ATP. The liver also synthesizes phospholipids, lecithin, cephalins (that produce thromboplastin), and sphingomyelin (produces the myelin sheath) are formed in the liver and transported via lipoproteins. An increase in triglycerides or choline/inositol increases phospholipid production. Phospholipids are also important in the production of cell membranes. CHOLESTEROL Cholesterol is a byproduct of protein metabolism. Bonding oily fat (fat-soluble vitamins) to nitrogen via oxidation forms cholesterol. This process utilizes vitamins, D, E, K, A, and T. These are your fat-soluble vitamins that are bound to the nitrogen portion of foods. The basic purpose of fat-soluble vitamins is to lubricate membranes. The vitamin (oil) prevents oxygen from reaching the membrane, which may inhibit its function. Fat-soluble vitamins also provide the substance necessary to make hormones, enzymes, and antibodies. For example, Vitamin D. lubricates all gross membranes that are exposed to air, such as your skin, respiratory passages, and the digestive membranes. This is your antioxidant lubricator Vitamin A. lubricates secondary membranes that are exposed to the blood, such as the liver, kidney, lungs and spleen. Vitamin A. is called your hydrogen lubricator. Vitamin K. lubricates cell membranes that are exposed to water. Vitamin F. fatty acids are used to make enzymes. Vitamin E. is used to make hormones. Vitamin T. which, is sesame seed oil, is used to make antibodies Lecithin prevents oil and fat from going rancid. So the purpose of fat-soluble vitamins is to oxidize and combust with protein to form cholesterol, which then transposes it into a lubricator, a hormone, antibody, or enzyme. Low-density lipoproteins are rich in cholesterol and carry some triglycerides and are used to produce sex hormones. High-density lipoproteins are rich in triglycerides and carry some fat. Please note that at any one time, the body can dictate the percentage of low-density lipoproteins vs. high-density lipoproteins. It's obvious that an imbalance can create multiple diseases in the body. Please note that these lipoproteins also engulf toxins and then are stored in tissue cells. At a later time, the body gradually detoxifies these deposits unless the amount is overwhelming. Similar to glucose, cholesterol is affected by many organs and glands and in itself is not a reliable indicator as to what is going on in the body. Over the years, the labs went from a normal cholesterol reading of 300, down to 250, then down to 200, and now down to 150. If they continue this nonsense they will create a whole new list of diseases. I recommend that your cholesterol levels be between 175-275mg/dL.	-192				5						5
Triglycerides Triglycerides SERUM LIPIDS Serum lipids serve as a primary source of energy along with glucose. The functions are many, such as the production of cell membranes, precursors to hormones, and bile acids. Lipids are first broken down in the duodenum, along with bile, which emulsifies the fats, and prepares them for absorption into the lymphatic system. Pancreatic lipase hydrolyzes cholesterol, and triglycerides into fatty acids, and glycerol. The fatty acids and glycerol are then reconverted back into triglycerides by the intestinal cells and then discharged into the lymphatic or portal blood system, which is then sent to the liver. Cholesterol is also absorbed in both the free and esterified forms into the lymphatics. Cholesterol is also synthesized in the reticular cells and histiocytes throughout the body but mainly formed in the liver. Under the influence of iodine via the thyroid, carbohydrates, amino acids, and other fats are converted to cholesterol via multiple molecules of acetyl coenzyme A creating a sterol nucleus. Triglycerides are also assembled in the liver from glycerol and fatty acids. The liver is the main organ regulating blood lipids. So the liver can degrade fatty acids for energy, synthesize triglycerides from carbohydrates and proteins. The liver can then hydrolyzes the triglycerides back into three fatty acids, and glycerol then degrades the fatty acids into acetyl coenzyme A via beta-oxidation. Then acetyl coenzyme A is then oxidized to release ATP. The liver also synthesizes phospholipids, lecithin, cephalins (that produce thromboplastin), and sphingomyelin (produces the myelin sheath) are formed in the liver and transported via lipoproteins. An increase in triglycerides or choline/inositol increases phospholipid production. Phospholipids are also important in the production of cell membranes. TRIGLYCERIDES Triglycerides compromise 95% of fat stored in adipose tissue and stored as glycerol, fatty acids, and monoglycerides. The liver reconvert's these back to triglycerides. 80% of your triglycerides make up VLDL, and 15% form LDL’S. From a pathological viewpoint, this test evaluates atherosclerosis and measures the bodies ability to utilize fat. From the physiologic perspective, triglycerides are nothing more than three fatty acids, and esters of glycerol. Fatty acids are composed of sugar and alcohol. Triglycerides travel with cholesterol (LDL/HDL) to combust cholesterol at the appropriate time.Triglycerides are needed for calculation of LDLC (low-density lipoprotein cholesterol) concentration. Triglycerides are the matches or “the spark” that ignites and combusts the cholesterol. Triglycerides are implanted in the cell membrane of all neurological and glandular tissue. Triglycerides create the energy for a neurological impulse to occur. When the neurological impulse occurs triglycerides actually “explode” causing the active exchange of electrolytes. Primary glands involved in triglyceride metabolism are the posterior pituitary, the hypophyseal stalk, adrenals, and the head of the pancreas.Therefore, any condition affecting these organs can affect triglyceride levels. High levels are a greater risk for a heart attack then a high cholesterol. Low triglyceride levels from the physiologic perspective cause low energy. Triglycerides Normally Range From 0-199. It Is Rather Obvious That 0 Triglycerides Could Not Be Achieved Physiologically. My Ranges Are From 75-200 mg/dL	66.4
TSH TSH T-4, T-3, T3 uptake and TSH Thyroid-stimulating hormone (TSH) from the anterior pituitary, stimulates the production of thyroxin, and triiodothyronine, therefore, having a dramatic effect on the T4/T3 test results. Thyrotrophs makeup 5% of the anterior pituitary and produce between 100-400mU/day of TSH. Circadian peaks with the onset of sleep are between 9 pm-5am and a minimum between 4-7pm. TSH is regulated by an open feedback loop via thyroxin whereby thyroxin passes into the CSF of the lateral ventricles and is taken up by the epithelial cells of the choroid plexus, which when thyroxin levels are low, stimulates TRH-secreting neurons in the hypothalamus. TSH does the following: 1. Stimulates phospholipid metabolism 2. Stimulates purine and pyrimidine precursors and their incorporation into nucleic acids. T-4 and 3 indicate the denitrification power of iodine via thyroxin with T3 being much more powerful than T4. All food contains active biological nutrients that are bound with nitrogen. When this food reaches the liver, the iodine is used to cleave the nitrogen from the nutrient. Therefore, thyroxin and T3 are important in fat and protein digestion, absorption, and growth and endocrine function. This catabolic activity begins once aerobic bound substances become totally anaerobic and lose the need for nitrogen bonding. Nitrogen is cleaved by T3 or T4 in the liver for example as in glycogen storage. Other substances are needed by specific cells and are transported via total binding globulin to the cells where at that point, the nitrogen bonds are cleaved. Less than 1% of T3 is unbound. A high T-3 uptake indicates a hypothyroid, where a low T-3 uptake indicates a hyperthyroid.	-118.96	5			10
Thyroxine (T4) Thyroxine (T4) T-4, T-3, T3 uptake and TSH Thyroid-stimulating hormone (TSH) from the anterior pituitary, stimulates the production of thyroxin, and triiodothyronine, therefore, having a dramatic effect on the T4/T3 test results. Thyrotrophs makeup 5% of the anterior pituitary and produce between 100-400mU/day of TSH. Circadian peaks with the onset of sleep are between 9 pm-5am and a minimum between 4-7pm. TSH is regulated by an open feedback loop via thyroxin whereby thyroxin passes into the CSF of the lateral ventricles and is taken up by the epithelial cells of the choroid plexus, which when thyroxin levels are low, stimulates TRH-secreting neurons in the hypothalamus. TSH does the following: 1. Stimulates phospholipid metabolism 2. Stimulates purine and pyrimidine precursors and their incorporation into nucleic acids. T-4 and 3 indicate the denitrification power of iodine via thyroxin with T3 being much more powerful than T4. All food contains active biological nutrients that are bound with nitrogen. When this food reaches the liver, the iodine is used to cleave the nitrogen from the nutrient. Therefore, thyroxin and T3 are important in fat and protein digestion, absorption, and growth and endocrine function. This catabolic activity begins once aerobic bound substances become totally anaerobic and lose the need for nitrogen bonding. Nitrogen is cleaved by T3 or T4 in the liver for example as in glycogen storage. Other substances are needed by specific cells and are transported via total binding globulin to the cells where at that point, the nitrogen bonds are cleaved. Less than 1% of T3 is unbound. A high T-3 uptake indicates a hypothyroid, where a low T-3 uptake indicates a hyperthyroid.	84	5			5
T3 Total T3 Total T-4, T-3, T3 uptake and TSH Thyroid-stimulating hormone (TSH) from the anterior pituitary, stimulates the production of thyroxin, and triiodothyronine, therefore, having a dramatic effect on the T4/T3 test results. Thyrotrophs makeup 5% of the anterior pituitary and produce between 100-400mU/day of TSH. Circadian peaks with the onset of sleep are between 9 pm-5am and a minimum between 4-7pm. TSH is regulated by an open feedback loop via thyroxin whereby thyroxin passes into the CSF of the lateral ventricles and is taken up by the epithelial cells of the choroid plexus, which when thyroxin levels are low, stimulates TRH-secreting neurons in the hypothalamus. TSH does the following: 1. Stimulates phospholipid metabolism 2. Stimulates purine and pyrimidine precursors and their incorporation into nucleic acids. T-4 and 3 indicate the denitrification power of iodine via thyroxin with T3 being much more powerful than T4. All food contains active biological nutrients that are bound with nitrogen. When this food reaches the liver, the iodine is used to cleave the nitrogen from the nutrient. Therefore, thyroxin and T3 are important in fat and protein digestion, absorption, and growth and endocrine function. This catabolic activity begins once aerobic bound substances become totally anaerobic and lose the need for nitrogen bonding. Nitrogen is cleaved by T3 or T4 in the liver for example as in glycogen storage. Other substances are needed by specific cells and are transported via total binding globulin to the cells where at that point, the nitrogen bonds are cleaved. Less than 1% of T3 is unbound. A high T-3 uptake indicates a hypothyroid, where a low T-3 uptake indicates a hyperthyroid.	-43.33	5			5
T3 Uptake T3 Uptake T-4, T-3, T3 uptake and TSH Thyroid-stimulating hormone (TSH) from the anterior pituitary, stimulates the production of thyroxin, and triiodothyronine, therefore, having a dramatic effect on the T4/T3 test results. Thyrotrophs makeup 5% of the anterior pituitary and produce between 100-400mU/day of TSH. Circadian peaks with the onset of sleep are between 9 pm-5am and a minimum between 4-7pm. TSH is regulated by an open feedback loop via thyroxin whereby thyroxin passes into the CSF of the lateral ventricles and is taken up by the epithelial cells of the choroid plexus, which when thyroxin levels are low, stimulates TRH-secreting neurons in the hypothalamus. TSH does the following: 1. Stimulates phospholipid metabolism 2. Stimulates purine and pyrimidine precursors and their incorporation into nucleic acids. T-4 and 3 indicate the denitrification power of iodine via thyroxin with T3 being much more powerful than T4. All food contains active biological nutrients that are bound with nitrogen. When this food reaches the liver, the iodine is used to cleave the nitrogen from the nutrient. Therefore, thyroxin and T3 are important in fat and protein digestion, absorption, and growth and endocrine function. This catabolic activity begins once aerobic bound substances become totally anaerobic and lose the need for nitrogen bonding. Nitrogen is cleaved by T3 or T4 in the liver for example as in glycogen storage. Other substances are needed by specific cells and are transported via total binding globulin to the cells where at that point, the nitrogen bonds are cleaved. Less than 1% of T3 is unbound. A high T-3 uptake indicates a hypothyroid, where a low T-3 uptake indicates a hyperthyroid.	5
T3 Free T3 Free A free T3 test, or free triiodothyronine test, measures the amount of free triiodothyronine in your blood. Triiodothyronine (T3) is a hormone produced by the thyroid gland that helps regulate metabolism and energy levels. A normal free T3 level is typically between 2.5–4.0 ng/dL, but reference values may vary by lab. A higher-than-normal level of T3 may indicate an overactive thyroid, while a lower-than-normal level may indicate an underactive thyroid.	5.26
T4 Free T4 Free Free T4 is the amount of thyroxine (T4) in the blood that is not attached to proteins. T4 is a hormone produced by the thyroid gland that helps control metabolism and growth. A free T4 test measures the amount of free T4 in your blood.	86.21
Urine pH Urine pH URINE PH A high urine pH may be due to: Kidney failure Urinary tract infections Vomiting A low urine pH may be due to: Diarrhea Too much acid in the body fluids such as metabolic acidosis and diabetic ketoacidosis Starvation	-100
Bun/Creatin Ratio Bun/Creatin Ratio BUN/CREATININE RATIO BUN plus creatinine are residue byproducts of protein and muscle metabolism respectively. They are kept in continual balance by the water content of your body. The kidneys flush out the excessive BUN/creatinine concentration when it gets too high. The kidneys are under the influence of the posterior pituitary via antidiuretic hormone, which regulates the amount of water leaving the body. Therefore, the posterior pituitary through potassium regulates water balance. The posterior pituitary then regulates the amount of water in any one place of the body. So, therefore, it can either increase or decrease the water content in the blood, thus altering pH. The posterior pituitary besides balancing water also regulates sugar and mineral concentration. BUN/CREATININE IS HIGH WHEN General considerations: ¬ Decrease high protein intake ¬ Or increase water intake ¬ BUN/CREATININE is high when you have a high BUN or a low CREATININE or both BUN/CREATININE IS DECREASED WHEN General considerations: ¬ Increase protein intake ¬ Or decrease water intake ¬ BUN/CREATININE is low when either you have a low BUN or a high CREATININE or both	203.58					1			10
COQ10 Coenzyme COQ10 Coenzyme Coenzyme Q10 (CoQ10 also known as ubiquinone, is a natural coenzyme and an antioxidant produced by the body. It is also obtained from dietary sources, such as meat, fish, seed oils, vegetables, and dietary supplements. CoQ10 plays a role in mitochondrial oxidative phosphorylation, aidingthe production of adenosine triphosphate (ATP), which is involved in energy transfer within cells. The structure of CoQ10 consists of a benzoquinone moiety and an isoprenoid side chain, with the "10" referring to the number of isoprenyl chemical subunits in its tail. Biological function CoQ10 is a component of the mitochondrial electron transport chain (ETC), where it plays a role in oxidative phosphorylation, a process required for the biosynthesis of adenosine triphosphate, the primary energy source of cells. CoQ10 is a lipophilic molecule that is located in all biological membranes of the human body and serves as a component for the synthesis of ATP and is a life-sustaining cofactor for the three complexes (complex I, complex II, and complex III) of the ETC in the mitochondria. CoQ10 has a role in the transport of protons across lysosomal membranes to regulate pH in lysosome functions. The mitochondrial oxidative phosphorylation process occurs in the inner mitochondrial membrane of eukaryotic cells. This membrane is highly folded into structures called cristae, which increase the surface area available for oxidative phosphorylation. CoQ10 plays a role in this process as an essential cofactor of the ETC located in the inner mitochondrial membrane and serves the following functions: electron transport in the mitochondrial ETC, by shuttling electrons from mitochondrial complexes like nicotinamide adenine dinucleotide (NADH), ubiquinone reductase (complex I), and succinate ubiquinone reductase (complex II), the fatty acids and branched-chain amino acids oxidation (through flavin-linked dehydrogenases) to ubiquinol–cytochrome-c reductase (complex III) of the ETC: CoQ10 participates in fatty acid and glucose metabolism by transferring electrons generated from the reduction of fatty acids and glucose to electron acceptors; antioxidant activity as a lipid-soluble antioxidant together with vitamin E, scavenging reactive oxygen species and protecting cells against oxidative stress, inhibiting the oxidation of proteins, DNA, and use of vitamin E.
Fibrinogen Fibrinogen FIBRINOGEN- BLOOD TEST RANGES 200 and 400 mg/dL (2.0 to 4.0 g/L) (coagulation factor I) is a glycoprotein complex that is synthesized by the liver and circulates in the blood stream. During tissue and or vascular injury, it is converted enzymatically by thrombin to fibrin which creates a blood clot The primary function is to occlude blood vessels thus stopping bleeding. Fibrin also binds and reduces the activity of thrombin. This activity referred to as antithrombin I, which limits clot formation. Fibrin also mediates and is important in blood platelet, endothelial cell spreading, capillary tube formation, tissue fibroblast proliferation, and angiogenesis thereby promoting revascularization and wound healing. Thrombin is synthesized in the liver and secreted into the general circulation in an inactive zymogen form (prothrombin), a complex multidomain glycoprotein that is activated to yield thrombin at sites of vascular injury by limited proteolysis following upstream activation of the coagulation cascade.
LPA LPA LPA- BLOOD TEST LEVELS 30-50 mg/dL (75-125 nmol/L Lipoprotein (a) or Lp(a) levels are measured in milligrams per deciliter (mg/dL) or nanomoles per liter (nmol/L). A lipoprotein(a) (Lp(a)) blood test measures the amount of Lp(a) in your blood, which is lipoprotein that carries cholesterol. Thus elevated Lp(a) levels are associated with an increased risk of cardiovascular disease. Recommended for individuals with a family history of heart disease or other risk factors. High levels of lipoprotein (a) (Lp(a), may cause heart attack, stroke, and or aortic stenosis LPA is produced through multiple mechanisms within cells and in biological fluids like plasma and serum. Lysophosphatidic acid (LPA) is primarily produced by the enzyme autotaxin (ATX). ATX, which is a secreted lysophospholipase D, converts lysophospholipids, primarily lysophosphatidylcholine (LPC), into LPA. This extracellular production pathway is considered the major source of bioactive LPA.
Apo B Apo B Apolipoprotein B (ApoB) is a protein that plays a crucial role in the transport of fats and cholesterol in the blood. It is a key component of low-density lipoproteins (LDL) and other lipoproteins that carry triglycerides, cholesterol, and cholesterol esters. Elevated ApoB levels are associated with an increased risk of cardiovascular disease. Key aspects of ApoB: Role in Lipoprotein Formation: ApoB is a primary protein on the surface of various lipoproteins, including LDL, VLDL, chylomicrons, and lipoprotein(a). Atherogenic Particle Indicator: ApoB measurement helps determine the number of atherogenic particles circulating in the bloodstream, which are linked to plaque buildup in arteries. Cardiovascular Risk: Elevated ApoB levels are a significant indicator of increased cardiovascular risk, particularly atherosclerosis. ApoB Test: An ApoB test measures the amount of ApoB in the blood and is often used to assess the risk of heart disease. Two Forms: ApoB exists in two forms: ApoB100 (primarily in the liver) and ApoB48 (primarily in the intestine). Apo High levels of apolipoprotein B (ApoB) are often associated with elevated levels of LDL cholesterol (LDL-C) and can be caused by a variety of factors, including diet, lifestyle, underlying medical conditions, and genetics.
Gland Totals		40	5	5	35	21	10	10	20	15	25
Gland Totals (%)		267.88%	50%	33%	95.43%	110.67%	141.5%	35.5%	127%	38.67%	74%

Results by Immune

Gland	Result
Thymus Thymus THE THYMUS The thymus is a ductless gland located in the anterior mediastinal cavity, which reaches its maximum development in early childhood. As you leave early childhood, the thymus starts its process of involution. The hormone produced by the thymus is called thymosin A. The purpose of thymosin A is to cause further proliferation and increased the activity of lymphocytes. The lymphatic system, spleen, thymus and bone marrow produce lymphocytes. The thymus gland produces T lymphocytes, which are mainly produced within a few months of life. The purpose of these T lymphocytes is to increase cell-mediated immunity. These T lymphocytes are specifically designed to destroy foreign agents. Lymphocytes are located most extensively in the lymph nodes but are also found in the spleen, the submucosa of the gastrointestinal tract and the bone marrow. The purpose of this lymphoid tissue is to intercept invading organisms or toxins before they spread. For example, the lymphoid tissue of the gastrointestinal tract is exposed to antigens coming in through your food and drink. The lymphoid tissues in your throat are your tonsils and adenoids, which are the first line of defense in your upper respiratory tract. Your peripheral lymph nodes are responsible for protecting the peripheral body when traumatized and cut. The lymphoid tissue in the spleen and bone marrow intercept invading organisms and toxins once they reach the blood stream. Please note that there is also a humeral immunity called B cell immunity. B cell immunity utilizes the liver and bone marrow to process and creates antibodies (B cells) for specific antigens. The antibodies are made up from gamma globulin molecules called immunoglobulins, which have molecular weights between 150,000 and 900,000. These immunoglobulins constitute 20 % of all plasma proteins. They are respectively named: IgM, IgG, IgA, IgD, and IgE For a substance to be antigenic, it must have a molecular weight of 8,000 or more. Antibodies work in two different ways to protect the body. They either directly attack the invading agent, or they activate a complementary system that destroys the invading agent. Direct action is through the following methods: 1. AGGLUTINATION-when the antigens stick and clump together on the surface of the antibodies 2. PRECIPITATION-when the molecular weight of the antibody and antigen becomes too large precipitates out and is rendered insoluble 3. NEUTRALIZATION-where the antibody covers the toxic site on the antigen 1. LYSIS-is where the antibody attacks the cell membrane of the antigen causing it to rupture When antibodies work with complementary systems, they attach to antigens and form long antigen-anti-body molecules that are now broken down by a cascade of biochemical reactions. Both humoral and mediated immunity are under the heading of acquired immunity. According to Dr. Brockman, the primary mineral of the thymus is uranium. The function of uranium is to create a radioactive bond or isotope tracker for all substances that enter the body through all membranes, including the skin. When an invasive substance enters the body, it is directed by magnetic control via uranium. The body hooks this invasive substance to uranium, which then tracks and targets this compound, directing it to the appropriate area for degradation and/or elimination. Another function of the thymus, states Brockman, is to extract bioflavonoids from ascorbic acid to create an acid pH on cell membranes, increasing their permeability for toxic disposal. This acts as a membrane resistant factor. If this is improperly handled, you loose acid maintenance and detoxification power. This will now affect the secondary gland of acid maintenance, which is the pancreas via sugar balance. The pancreas now tries to increase blood acidity, causing the alkaline oxidizing enzymes from the head of the pancreas to become more acidic and less potent. The following tests can be used to assess thymus function: 1. GLOBULIN-since the thymus is used to produce immunoglobulins, globulin is affected by thymus function 2. A/G RATIO-the albumin globulin ratio will also be affected by the thymus’s affect on globulin offsetting this ratio Albumin is considered the colloidal protein of osmosis since it regulates the flow of substances from the capillaries to the interstitial tissue. Globulin is the colloidal protein of momentum since it transports substances throughout the body, such as hemoglobin. Fibrinogen is considered the colloidal protein of clotting since it regulates the clotting ability of the blood. When a foreign substance enters the body through the skin via cuts, or through mucous membranes, uranium is sent by the thymus to program the foreign substance. Depending on the foreign substance, whether it is toxic or a pathogen, the thymus, and spleen will help dictate whether there should be a buildup of white blood cells and or breakdown of red blood cells to increase globulin production for thymus or spleen globulin to fight off the infection. Fibrinogen, which is transposed into fibrin via thrombin, will aid in clot formation, helping to wall off the infection. The A/G ratio is also a representation of the fibrinogen content in the blood. 3. TOTAL BILIRUBIN-when globulins are needed to produce immunoglobulins, the body relies on the red blood cells to fulfill this need. Since the blood cells are composed of globulin, iron, biliverdin and bilirubin, they are the perfect source for additional globulins. The spleen and liver hemolyze the red blood cells for the globulin and, at the same time, release bilirubin into the bloodstream, affecting total bilirubin levels.	454%
Parotids Parotids THE PAROTIDS The principal glands of salivation are the parotids, which are the submandibular, sublingual and buccal glands. The daily secretion of saliva normally ranges between eight hundred to fifteen hundred milliliters. The saliva contains two major protein secretions. The first is a serous secretion containing ptyalin, which is an enzyme necessary for digesting starches. The second is a mucous secretion containing mucin for lubricating purposes. The parotid glands secrete entirely the serous type while the submandibular and sublingual glands secrete both serous and mucous. The buccal glands secrete only mucus. The pH of saliva is between 6.0 and 7.0. Saliva also contains the following ions: Under resting conditions, the sodium and chloride ions are approximately 1/7-1/10 of that found in plasma. During maximum salivation, the sodium and chloride concentrations elevate to 1/2 to two-thirds that of the plasma. Potassium, on the other hand, is seven times more concentrated than in the plasma but during maximum salivation, it is reduced to four times the concentration of the plasma. The purpose of potassium is to push food into the cells. The only other ion found in saliva is the bicarbonate ion. Besides the function of carbohydrate digestion, saliva also plays an important role in oral hygiene. The mouth is loaded with pathogenic bacteria that can easily destroy tissue. Saliva prevents this by first washing the bacteria away. Secondly, saliva contains several factors that destroy bacteria. These include thiocyanate ions, and several proteolytic enzymes, the most important being lysozyme. Lysozyme attacks the bacteria and aids the thiocyanate ions to enter the bacteria, where it becomes bactericidal. Saliva also digests food particles that help to remove bacterial metabolic support. The saliva also contains significant amounts of protein antibodies that can destroy all bacteria. According to Dr. Brockman, the primary function of the parotids is through the mineral copper, which tags all incoming substances through the mouth and nasal pharynx. The following substances are tagged and taken to the following areas: • FOOD-programmed and taken to the liver • TOXINS-sent to the lymphatic • MICROBES-taken to the point of beneficial hosting • PROGRAMS PROTEINS-there are two types of proteins. The first type of protein is called colloidal albumin, which is used for an osmotic gradient, which keeps things in passive motion. The second is called colloidal globulin, which is the momentum protein that moves toxins and infections throughout the body so the body can balance what it wants and what it does not want. There are certain organisms that may not be needed at another area. So the purpose of globulin is to serve as the sub-protein transport system for these organisms, which is necessary for chemical momentum in the body. This keeps the toxin and infection mechanisms moving throughout the system. What makes the globulin colloidal is the electrical copper implant, which steers it through the system. • ANY MAN-MADE PRODUCTS such as pesticides attenuated viruses, which contain no nucleic affinity, which the body cannot tag or identify. In turn. your body has no idea what to do with this compound. These are the man-made distortions that cause sickness and disease that our bodies have difficulty in overcoming. It is also interesting to note that potassium cannot work without copper and that salivary glands are activated via the mumps. The mumps are a normal childhood disease, which activate this parotid copper phenomenon. The following blood tests indicate a possible problem with the parotids: 1. GLOBULIN-which is joined with copper to create programming of ingested or inhaled substances. 2. POTASSIUM- which is secreted by the salivary glands, and is necessary for the programming process and drawing food into the cells. 3. A/G RATIO-the albumin globulin ratio will also be altered if the globulin is affected by the malfunctioning parotid gland. 4. ALBUMIN-albumin levels will also be affected via a malfunctioning parotid gland.	358.4%
Thyroid Thyroid THE THYROID Diseases of the thyroid are the most common of all the endocrine glands, notably due to iodine deficiencies in North America, as compared to Japan. This is due to a reduction of salt intake in this country and people living in iodine-depleted areas such as mountainous regions. Iodine deficiencies during pregnancy can lead to CNS damage and cretinism. A minimum dosage of iodine should be 100 micrograms per day. Iodine is lost through urine as glucuronides (500 micrograms per day), the stool, skin, and lungs. The GI tract reabsorbs digested iodine with little lost in the stool. Iodine is also found in saliva, red blood cells, and extracellular fluid. Embryogenesis and certain functions of the thyroid are interlinked with the GI tract, such as salivary and gastric glands. These are both able to concentrate iodine in their secretions just like the thyroid. The only difference is that TSH does not affect these glands. The thyroid, one of the larger endocrine glands weighing 15- 20 grams, stores excessive amounts of thyroxine as compared to other hormonal levels. The thyroid is composed of 2 lobes, each 2.5cm thick and 4cm in length, with the right being more vascular then the left. A thin band called the isthmus, which is right below the cricoid cartilage and affixed to the trachea via loose connective tissue, joins the two lobes. Two pairs of parathyroid glands sit on the posterior surface of the lobes. Blood supply comes from the external carotid artery via the superior thyroid artery and the inferior thyroid artery via the subclavian artery. The thyroid receives approximately two times the blood supply as the kidneys. Nerve supply comes from the cervical ganglion (androgenic) and vagus nerve (cholinergic), which regulates blood flow to the thyroid. There is a rich lymphatic drainage with high iodoproteins (metabolic substrates), as compared to venous blood. The metabolic processes of the body are divided into an anabolic building up phase and a catabolic breaking down phase. The thyroid, as mentioned above, is largely dependent on the pituitary via the release of thyroid stimulating hormone. This stimulates the thyroid to produce 90% thyroxin and 10% triiodothyronine. The triiodothyronine is four times as powerful as thyroxin and all thyroxin will eventually become triiodothyronine. It is of interest to note that each minute, the blood supply to the thyroid is five times the weight of the gland. The thyroid gland is seen as packed sacs called acini or follicles, lined by columnar cells and filled with a protein acetous colloid that is mostly thyroglobulin, invested in a rich capillary supply. The thyroid also contains parafollicular cells that produce calcitonin. These protein acetous colloids that are thyroglobulin via endocytosis collect as vesicles and are brought to the cell membrane and released into the bloodstream. The production of thyroxin occurs in the following way. Iodide (normal levels are 800 micrograms and 90 % is in the organic form) under TSH influence (also found and concentrated in the salivary, mammary, choroid plexus and gastric glands) is pumped via active transport (closely related to the Na, K, ATPase systems) into the thyroid via the iodide pump and diffuses along electrochemical gradients into the lumina. The iodide is oxidized and converted into iodine, via peroxidase and hydrogen peroxide. Human thyroid peroxidase, which is the oxidant of iodide, is generated by autooxidation of flavin enzymes that act on NADH and NADPH oxidase. The thyroid synthesizes approximately 110 nmoles (85 micrograms) per day, 65% of it is T4 and 35% of it is T3. Iodide, both inorganic and organic, is taken in by the diet, is absorbed by the GI tract and salivary glands and is then sent to the extracellular fluid where it is highly concentrated. Iodide is also found in RBCs. The endoplasmic reticulum and Golgi apparatus produce a glycoprotein called thyroglobulin, which is made up of 140 tyrosine molecules. This thyroglobulin molecule combines with iodine to form the thyroid hormones. The biosynthesis of thyroid hormones requires three steps: 1. Iodide is pumped into the thyroid via active transport via iodine trapping by a membrane protein called the sodium iodine symporter, which is 643 amino acids long and has a 13 membrane-spanning domain, which gives up two sodium ions for entry of one iodide atom against an electrochemical gradient. 2. Iodide is then oxidized and tyros residues are iodinated within the thyroglobulin molecule (Tg), which yield the thyroid inactive iodotyrosine precursors. 3. The coupling (peptide linkages) of the iodoprecursors forms the active T4 and T3 hormones. Below is a more in-depth explanation. Thyroglobulin (Tg) contains tyrosine residues that are then iodinated to form monoiodotyrosine (MIT) and diiodotyrosine (DIT), which are stored as colloids. Thyroid perodoxase then catalyzes coupling of two molecules of DIT to form T4 or one of MIT and DIT to form T3 in the apical portion of the thyroid cell. TYROSINE→ 3-MONOIODOTYROSINE (MIT) → 3, 5-DIIODOTYROSINE, (DIT) (thyroid iodotyrosine hormone precursors) → (3, 5, 3′-TRIIODOTYROSINE → THYROXIN (active thyroid hormones) TSH then stimulates the TSH receptor, which is a member of the gycoprotein G protein-coupled receptor family. TSH can also increase the growth of the thyroid. TSH then causes pinocytosis of the colloid with the action of phagolysomes, which digest the colloid and as it reaches the cell membrane T3, T4, MIT and DIT are released. At this point, T4 and T3 leave the cell and MIT and DIT are deiodinated via iodotyrosine deiodinase. This allows the recycling of iodide back into Tg colloids. The ratio of T4 to T3 in thyroglobulin is 13-1 and in secreted hormone, 10-1. T4 is solely released from the thyroid and T 3 is released from peripheral tissues and slightly from the thyroid. The peripheral tissues, via enzymatic removal of an iodide atom from T4, convert it back into T3. When T4 and T3 enter the blood, they bond to several proteins produced by the liver. T4 bonds to: • TBG (T4-binding inter-α-globulin)—the TBG binding sites have a 20-fold affinity for T4 as compared to T3. • TBPA (T4-binding pre-albumin)—now called transthyretin (TR), whereas T3 mainly bonds to TBG transthyretin as part of a retinal (vitamin A) binding protein. It is expressed via the choroid plexus and is the major thyroid hormone binder in the CSF. T3 has a 15 fold binding affinity for TR as compared to T4. • Albumin has the weakest affinity for T3 and T4, then the above. • 3-6% of the T4/T3 in the plasma can also bind to lipoproteins. . This carrier mediated transport, transports T4 and T3 to hepatocytes and fibroblasts, in which extracellular sodium is required for uptake. The cells release thyroglobulins when they are hydrolyzed by thyroid proteases and peptidases, which release T4 and T3 into the blood Thyroid hormones have great diversity in the metabolic process, from influencing activation and concentration of many enzymes, metabolism of all foodstuffs, influencing the production and release of hormones and stimulating cell receptors to increase the activity of all other hormones. There is no organ, gland, or tissue that is not affected by the thyroid. The thyroid increases the use of oxygen use in the whole body, therefore increasing the exchange of ADP/ATP across membranes. Thyroxin accomplishes this by creating a 3-fold increase of mRNA for α/β subunits of Na, K, and ATPase, which alters membrane permeability. This then increases caloric-genesis and protein synthesis (via enzyme (lysosomal)/hormonal control). A second hormone produced by the thyroid is calcitonin, which is produced by parafollicular or C cells. Calcitonin decreases calcium levels in blood and decreases osteoclastic absorption and formation. A more thorough explanation will be covered when discussing the parathyroid glands. The functions of the thyroid are as follows: 1. Increases the basal metabolic rate by increasing the rate of protein, fat, and carbohydrate metabolism. 2. Thyroxin also stimulates cholesterol synthesis and regulates excretion from the body via bile salt conversion, which also affects triglycerides and phospholipids. The sum total effect causes a decrease in cholesterol. Thyroxin does this by increasing lipolysis of adipose tissue via the adenylate cyclase-cycle AMP system and potentiating other hormones such as catecholamines, glucocorticoids, growth hormone and glucagons. This increases fatty acids in the blood, which then enhances triglyceride formation in the liver. 3. Thyroxin also stimulates carbohydrate storage and metabolism by potentiating catecholamines and insulin, causing the rapid degradation of glycogen into glucose. 4. Thyroxin also influences epinephrine probably via enhancing the adenyl-cyclase-cycle AMP system. 5. Thyroxin also increases mitochondrial enzymes α-glycerol phosphate dehydrogenase. Thyroxin also enhances synthesis of oxaloacetic acid and malate from pyruvate. In the liver, thyroid hormone stimulates pyruvate carboxylic, phosphenol pyruvate, carboxyl kinase and glucose-6-phosphatase. At the same time, the thyroid also increases intracellular enzyme activity via thiamine, riboflavin, vitamin B12 and vitamin C. Vitamin A, which is manufactured from carotene through vitamin A synthesis, is used by the retina for dark adaptation and also for covering liver sinusoids. According to Dr. Brockman, the thyroid is responsible for the sum total of catabolism and anabolism via the use of iodine. The top left lobe affects and is affected by the anterior pituitary, the right lobe by the posterior pituitary, the superior medial lobe by the parotids, the medial left lobe by the spleen and the medial right lobe by the endo reticular portion of the liver. The primary problem that causes thyroid problems is infections and toxins because both do not have polarity. Chemically, the thyroxin molecule functions in the following way: thyroxin is responsible for the conversion of inorganic food that is sent to the liver, into organic food, which the body can now utilize. In other words, the function of the liver is to bring food from an aerobic state, convert it into an anaerobic state and program the food so it knows where to go. The active site of the thyroxin molecule is iodine. Iodine acts as an emulsifier of fats, oils and waxes by removing the oils, striping the waxes and loosening the fatty substance from its adherent surface. Iodine accomplishes this by activating lecithin. Lecithin is made up of choline, inositol, and phosphorus. The purpose of lecithin is to release alkaline B vitamins into food preparing the food for the organic state. A perfect example of this occurs in the liver. The liver is composed of sinusoids. The sinusoids are where food, toxins and poisons are stored. The surfaces of the sinusoids are covered with fat-soluble vitamins A and D (fat), which prevents oxidation of food or poison before its time. Iodine loosens the vitamin A covering by activating lecithin, to emulsify the fatty layer over the sinusoid. Therefore, iodine raises and emulsifies the storage lubricant of the sinusoid surfactant (vitamins A and D), thereby creating a catabolic release when needed and an anabolic combining when needed. A sort of caldron effect, a bubbling on the surface of the sinusoid, allows foods/toxins to enter and leave the sinusoids, which are governed by the thyroid. Iodine then breaks (cleaves) the nitrogen bond from the inorganic food (anaerobic state), converting it into organic food by adding oxygen (aerobic state). This is a critical process, because if not properly executed, food may combust too soon, too late or not at all. The thyroid also has a dramatic effect on other sinusoidal organs such as the sinuses, lungs, kidneys and lymphatic system, including the spleen. It does this by encapsulating toxins and poisons that are collected via the intercellular fluid. The poisons are stored in the fat membrane of the lymphatic tissue until iodine flushes them out, as explained above. Iodine also works in the lungs in a similar fashion, allowing proper transport of carbon dioxide out of the body and oxygen into the body. This caldron effect also regulates the production of hormones and antibodies by storing fats and preparing them via oxidation, to form active hormones and antibodies. The following tests are necessary to determine thyroid function: 1. T 4—has the highest concentration in blood and the only one that arises solely from the thyroid, whereas 80% of T3 is derived from peripheral tissues. T4 is a measurement of the amount of thyroxin that is circulating in your bloodstream. This is a direct indicator of thyroid function. When you have too much thyroxin, you have a hyperactive thyroid and vice versa. 2. T3—is a radioactive isotope of iodine. In the blood, thyroxin is bound to a protein molecule called thyroglobulin (TBG). TBG can be present in the bloodstream without thyroxin. If there is little thyroxin output, then there will be a lot of free thyroglobulins. The higher the T3 uptake, the more sluggish the thyroid becomes and the less T3 uptake, the more hyperactive the thyroid becomes. Therefore, a high T3 indicates a sluggish thyroid and a low T3 indicates an overactive thyroid. 3. Phosphorus—phosphorus is necessary to release alkaline B vitamins into inorganic foods, transposing them into organic foods for storage in sinusoids of the liver. The thyroid then uses iodine on stored food to release food for any metabolic processes needed by the body. If you lack calcium/phosphorus in the bone, then calcitonin will shift them out of blood and into bone. This affects the phosphorus/calcium balance. Please note that calcium can also be used to assess thyroid function.	87.14%
Adrenal Cortex Adrenal Cortex THE ADRENAL CORTEX The adrenal glands, or “suprarenal glands” as they are sometimes referred to, sit on top of the posteromedial surface of the kidneys. The adrenal glands weigh approximately 4 grams, are 2cms wide, 5cms long, and 1 cm thick. The adrenal glands are composed of the adrenal cortex and the adrenal medulla. Each has specific hormones and functions, which will now be discussed. Under the capsule, you have the cortex, which is divided into 3 zones: 1. ZONA GLOMERULOSA-makes up 15% of the cortex and this depends on sodium intake 2. ZONA FASCICULATE-makes up 75% of the cortex is large and lipid-laden 3. The innermost zone, which is sharply demarcated from the other two zones, is called the ZONA RETICULARIS Blood supply for the cortex comes from 12 arteries off the aorta, phrenic, renal and intercostals. They form a subcapsular plexus, which radiate and penetrate the cortex zones. At the reticular zone, a sinusoidal plexus empties into the inferior vena cava on the right and the renal vein on the left. . THE ADRENAL CORTEX The adrenal cortex produces the following hormones, which are divided into three classifications: CLASSIFICATION 1-called the glucocorticoids, with the most important one being cortisol. Cortisol is very potent and accounts for about 95% of glucocorticoid activity. The second glucocorticoid is called corticosterone, which is much less potent, than cortisol. Cortisol has multiple metabolic functions for control of the metabolism of proteins, carbohydrates and fat’s. Cortisol is elevated thru fever, burns, psychological stress, injury, hypoglycemia, hypotension, and depression. Glucocorticoids themselves inhibit POMC gene transcription in the anterior pituitary. Glucocorticoids increase blood glucose levels by their action on glycogen, protein and lipids. Cortisol, for example, increases glycogen storage via increasing glycogen synthesis and inhibiting glycogen phosphorylate. Key liver enzymes such as glucose-6-phosphatase start gluconeogenesis. In muscle, cortisol inhibits glucose uptake and utilization. In adipose, tissue lipolysis is activated by the stimulation of adiposities, creating transcriptional activity in key genes, including lipoprotein lipase, glycerol-3-phosphate dehydrogenase, and lepton, all releasing fatty acids into circulation. Glucocorticoids, in concert with catecholamines and glucagon, create insulin resistance, elevating blood sugar and creating a catabolic effect on proteins and lipids. Glucocorticoids also cause catabolic changes in the: • Skin via inhibiting epidermal cell division due to the affects of DNA and collagen synthesis • Muscle and connective tissue atrophy via reduced muscle and connective tissue synthesis • Bone-glucocorticoids inhibit osteoblastic activity; inhibit intestinal calcium absorption, and increase renal calcium secretion. Glucocorticoids affect glomerular filtration rate, proximal tubular epithelial sodium transport, and free water clearance. Angiotensinogen synthesis is also increased via glucocorticoids. Glucocorticoids suppress immunology responses by suppressing: • T and B lymphocytes • Eosinophils • Cytokine production • Monocyte differentiation into macrophages and • Prostaglandin synthesis CLASSIFICATION 2-mineral corticoids, of which aldosterone is the most important, followed by deoxycorticosterone. Aldosterone decreases sodium excretion and increases potassium excretion, via the kidneys. This increases sodium in the body while decreasing the amount of potassium. Aldosterone is secreted by the zonal glomeruli and is controlled by angiotensin 2 secretagogues, potassium and, to a lesser extent, by ACTH. The adrenal cortex, through the use of mineral corticoids and glucocorticoids, balance minerals (alkaline), and sugar (acid) metabolism in the following manner: The mineral corticoids regulate sodium and potassium, thereby drawing foodstuffs (proteins, carbohydrates, and fats) thru the cell membranes. At the membrane level, there is an effervescent (bubbling effect) due to the sodium and food mixture. The adrenal cortex regulates the sodium pump and, in turn, actively moves a substance across the cell membrane. Now, as the chloride shift takes place, the membrane is opened and the food is allowed to pass into the cell. The adrenals control where, when and what minerals are on any membrane at any given time. The purpose of a mineral, in this case, is to transport foods/chemical (magnetic effect) from one area to the next, across a fatty membrane. The adrenals make sure that the minerals are in the right place at the right time. Besides this, the adrenal cortex balances minerals, which are alkaline and sugar, which is acid. The adrenals also regulate the pH within the body. This allows the proper transport of substances through cell membranes and through the body. This momentum is absolutely necessary for transport of substances through the body. There are two types of transport mechanisms (momentum) within the body: One is called visceral and the other is called chemical. Visceral is created by a neurological source, and the chemical is caused by an endocrine mineral source. Whenever a mineral is in momentum, it will work and affect ligaments, tendons, and cartilage (discs.) If there is a need for chemical momentum sufficient enough to produce stamina in the body, then the adrenal cortex will be kicked in. Stamina is the ability to maintain strength under certain amounts of stress. This is due to a balance of minerals and water. The posterior pituitary also plays a dramatic role in this balance via its effect on water levels in the body. Aldosterone and cortisol enter intracellular fluids and attach to glucocorticoid and mineral corticoid receptors, which are members of the thyroid/steroid hormone receptor superfamily. These affect transcription of DNA sequences of targeted genes that either stimulate or repress the genes. The principal sites of aldosterone and cortisol metabolism are in the liver and the kidneys. Some genes induced by glucocorticoids include: • Immune-hepatic globulin and lipocortin • Metabolic-glutamine synthesis, glycogen synthesis, gluco-6-phosphatase, lepton, fibrinogen, cholesterol 7 alpha-hydroxylase and tyrosine aminotransferase • Bone-androgen and calcitonin receptors and alkaline phosphatase. • Channels and transporters-sodium • Endocrine-vasoactive intestinal peptide, GHRH receptors and fibroblastic growth factor Some genes repressed by glucocorticoids are: • Immune-interleukins, tumor necrosing factor-alpha, interferon and cyclooxygenase 2 • Metabolic-metalloproteins • Bone-collagenase • Endocrine-GH, PRL, POMC/CRH, parathyroid-related protein and vasopressin • Growth-fibronectin, nerve growth factor and erythropoietin CLASSIFICATION 3-these are your steroid hormones called: • Estrogen-(18 carbon chain), • Progestins-progesterone (steroid derivatives) • Androgens-(19 carbon chain) Over 30 steroid compounds have been isolated from the cortex. All steroid hormones are derived from the cyclopentanoperhydrophenanthrene structure, which is composed of three cyclohexane and one cyclopentane ring. The precursor of these steroid hormones is cholesterol (mostly the LDLs). LDL receptors on the adrenal glands that come in contact with LDLs cause a pinocytosis entrapping the LDLs. They fuse lysosomes with this droplet, which hydrolyzes and frees the LDLs. These then enter the mitochondria and are converted into pregnenolone by many enzyme systems, which shuttle electrons that oxidize and further hydrolyze the compound via the P450 cytochromes in the cytoplasm. Pregnenolone is converted to progesterone via hydrogenation enzymes, and progesterone can be further hydroxylated for glucocorticoid synthesis. Please note that cholesterol, mostly LDLs, are the precursor for all steroid agenesis Below is a pathway analysis of hormone production via cholesterol: CHOLESTEROL 17alpha-hydroxylase 17alpha-hydroxylase 17,20 lyase 17,20 lyase PREGNENOLONE 17-OH-PREGNENOLONE DEHYDROEPIANDROSTERONE 3 betahydroxysteroid 3 betahydroxysteroid dehydrogenase dehydrogenase PROGESTERONE 17-OH-PROGESTERONE ANDROSTENEDIONE 21 hydroxylase 21 hydroxylase DEOXYCORTICOSTERONE 11-DEOXYCORTISOL 11-beta-hydroxylase 11-beta-hydroxylase CORTICOSTERONE CORTISOL Aldosterons synthase ALDOSTERONE MINERALCORTICOID GLUCOCORTICOID ANDROGENS Estrogen and androgens are necessary to promote secondary sexual characteristics, such as muscle mass, hair growth, voice, and external genitalia. Glucocorticoids are secreted at a rate of 10-20 milligrams per day from the zona fasciculate, via ACTH, and mineral corticoids are secreted at a rate of 100-150 micrograms per day from the zonal glomeruli via angiotensin 2, and to a lesser degree via ACTH. The steroid hormones DHEA and androstenedione, which are sulfonated in the reticular, are both secreted at a rate greater than 20 milligrams per day.	81.4%
Spleen Spleen THE SPLEEN The spleen is a highly vascular organ breaking down red blood cells and all other cells. In fetal life, the spleen produces red and white blood cells. In adults, it acts as a blood reservoir. As blood passes through the pulp of the spleen, fragile red blood cells are destroyed via being squeezed through. The reticuloendothelial portion of the spleen contains large phagocytes and venous sinuses, which remove bacteria, debris, and parasites. The spleen can enlarge like any other lymph node to improve the cleansing function of the body. The spleen also contains a white pulp, which is filled with plasma cells and lymphocytes, creating lymphocyte immunity against toxins, debris, and bacteria. The spleen also stimulates hormone production, by storing and aging fats to produce spleen globulin, thyroglobulin, and thymoglobulin. Taking fats that are combined with B12 and calcium and storing them in the membrane of each cell accomplish this. The spleen is also involved with the balance of an oxidant (iron) and an antioxidant (fat), since its stores both. The iron attaches to fat for storage in the spleen. When fat combines with iron hemopoiesis is the result. The spleen, therefore, balances fat and iron, and the byproduct of that balance is the formation of red blood cells and/or the production of white blood cells. The primary job of white blood cells is to keep as thin a membrane as possible, so it can magnetize substances to it. When there is an increase of fat in the bloodstream, we have an abundance of white blood cells, where the fats are used to restore and repair white blood cell membranes. When there is no escalation of membrane repair, toxins may be blocking the process. As far as red blood cells are concerned, they have a thick and pliable membrane to hold iron within the cell, to prevent oxidation. Therefore increased amounts of iron in the bloodstream increases red blood cell production. When red blood cells die, you decrease the number of red blood cells, which causes an increase in red blood cell production from the iron and fat stored in the spleen. This, in turn, decreases the amount of fat and iron in the blood to refill the spleen. So, a decrease of fat in the blood is due to white blood cell production, and a decrease of iron in the blood is due to red blood cell production. The following tests indicate a problem with the spleen: 1. TOTAL IRON-This indicates the amount of iron in the blood, indicating a red blood cell production/breakdown. 2. TOTAL BILIRUBIN-Bilirubin forms bile, which emulsifies fats. Emulsification or non-emulsification can affect levels of both fats (cholesterol) and total bilirubin. 3. CHOLESTEROL-HDLs, LDLs. These can help determine if there is a spleen/immune system condition affecting your cholesterol levels.	79.8%
Adrenal Medulla Adrenal Medulla THE ADRENAL MEDULLA The adrenal glands, or “suprarenal glands” as they are sometimes referred to, sit on top of the posteromedial surface of the kidneys. The adrenal glands weigh approximately 4 grams, are 2cms wide, 5cms long, and 1 cm thick. The adrenal glands are composed of the adrenal cortex and the adrenal medulla. Each has specific hormones and functions, which will now be discussed. Under the capsule, you have the cortex, which is divided into 3 zones: 1. ZONA GLOMERULOSA-makes up 15% of the cortex and this depends on sodium intake 2. ZONA FASCICULATE-makes up 75% of the cortex is large and lipid-laden 3. The innermost zone, which is sharply demarcated from the other two zones, is called the ZONA RETICULARIS Blood supply for the cortex comes from 12 arteries off the aorta, phrenic, renal and intercostals. They form a subcapsular plexus, which radiate and penetrate the cortex zones. At the reticular zone, a sinusoidal plexus empties into the inferior vena cava on the right and the renal vein on the left. . THE ADRENAL MEDULLA The adrenal medulla is part of the sympathetic portion of the autonomic nervous system. The principal secretion of the sympathetic nervous system is norepinephrine (which builds up glycogen) from the peripheral nerves and the CNS and epinephrine (which breaks down glycogen), from the adrenal medulla. Peripheral sympathetic nerves also secrete catecholamines and dopamine. Preganglionic neurons synapse in the sympathetic chain, preaortic, celiac and superior/inferior mesenteric ganglion, and can ascend via the sympathetic chain to the pons, medulla and then to the hypothalamus. Lower thoracic and upper lumbar preganglionic innervate the adrenal medulla and secrete acetylcholine in the ganglion synapses, whereas postganglionic innervations can be cholinergic, noradrenergic or both. Androgenic nerves can also secrete substance P, neuropeptide Y and somatostatin. The adrenal medulla is derived from the nervous system, specifically from chromatin tissue, which is an extension of the sympathetic nervous system. It is also found everywhere along the sympathetic chain. You can live without the adrenal medulla, but not without the cortex. The arterial blood supply is from the aorta to the inferior phrenic, and renal artery and drains via the renal vein on the left, and the vena cava on the right. Glucocorticoids influence the production of epinephrine (which is stored in the adrenal medulla) by the enzyme phenylethanolamine N-Methyl transferase. Norepinephrine is synthesized and stored in the nerve endings. Catecholamines are formed by the hydroxylation and decarboxylation of tyrosine via tyrosine hydroxylase. The adrenal medulla has an affinity for chromium, which is a blood sugar regulator. These two hormones also help regulate the sympathetic and parasympathetic nervous systems controlling fat and fatty acid metabolism in the following way. It is the acid depositing mineral chloride, from the stomach (HCL) that attaches to the food substance, which stores the food (fats and fatty acids) in the cell membrane. Food then is stored in the membrane and needs chloride to shift out of the way, allowing the foods to enter the cell and the toxins to leave. In order for the chloride shift to occur, epinephrine must be present. Epinephrine is then necessary for fatty acid combustion, is sympathetically controlled and is a daylight phenomenon (catabolism). Norepinephrine is the nighttime phenomenon (anabolism) for fat/hormone growth/storage and is controlled via the parasympathetic nervous system. The following blood tests are used to determine adrenal dysfunction: 1. CHLORIDE-as mentioned above, chloride is the regulatory mechanism for food storage in cell membranes to increase the potency for body utilization. It is the epinephrine and nor-epinephrine effect on chloride that regulates the shift. 2. SODIUM-as mentioned above, is controlled by the adrenal cortex and is extremely alkaline. Therefore, it causes migration of substances towards its polarity, as well as causing these migrated substances to achieve permeability in an acid antioxidant type media known as a fatty membrane. This is the substance necessary for polarizing substances into storage, according to the needs of the membrane. 3. POTASSIUM-which has prime importance in controlling membrane permeability by displacing the chloride ion as well as epinephrine for the next stage, which permits sodium aggregated substances to cross the cell membrane. It is the only substance necessary to allow oxygen into unoxygenated tissue. 4. ALKALINE PHOSPHATASE-is an enzyme that affects phosphorus. Therefore, we are looking at the phosphoric acid component of the alkaline phosphatase. There are high concentrations found in the intestinal mucosa, liver, and bone. Alkaline phosphatase aids in maintaining the alkaline pH of the blood and works best at a pH of ten (10). Alkaline phosphatase is a member of a family of metalloid protein enzymes that split off phosphate groups from organic phosphate esters. The enzyme activity usually occurs in the brush borders of the proximal convoluted tubules of the kidneys, the intestinal mucosa, the hepatic sinusoidal membranes and the vascular endothelial cells of the osteoblasts. Since the adrenals are responsible for mineral/alkaline and sugar/acid pH balance, you can see how pH levels may affect, and are affected by, alkaline phosphatase, since it is a very powerful alkaline enzyme.	55%

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#		Adrenal Cortex	Adrenal Medulla	Parotids	Spleen	Thymus	Thyroid
Glucose Glucose GLUCOSE Glucose is an important fuel for the body, which affects all tissues, organs, and systems. Glucose also affects the acid/alkaline balance in the body. Breakdown of glucose or starch starts in the mouth via ptyalin, then in the stomach via HCL, and then by pancreatic amylase, lactase and other enzymes. Glucose is then absorbed in the small intestines and is then stored as glycogen in the liver. The liver is the primary site of glucose production. The liver converts lactic acid to glycogen and back to glucose via epinephrine. The liver converts fats and proteins via gluconeogenesis into glucose or glycogen. The head of the pancreas controls chromium, which controls insulin levels and assists in the enzyme action of fats via bile salts. The tail of the pancreas controls zinc, which maintains and sustains levels of insulin. Blood sugar depends on: 1. The liver which stores and releases glycogen 2. The pancreas, which produces insulin that transfers sugar from the blood to the extracellular fluid 3. The adrenal glands, which produced glucocorticoids that, cause the liver to release glycogen into the blood as glucose 4. The sex organs, which deliver the extracellular glucose to the cell 5. The thyroid, which affects the storage of glycogen in the liver 6. The thymus and spleen, which affect the levels of iron and copper in the liver which, determine the liver's ability to handle glucose As you can see there are many organs, or combinations of these organs and glands, which affect glucose levels in the body. Therefore, glucose in itself cannot specifically determine where the problem may lie. Other indicators are necessary to pinpoint the problem.	-28
Uric Acid Uric Acid URIC ACID Uric acid is the principal end product of purine, nucleic acid, and nucleoprotein metabolism. Uric acid is transported by the blood from the liver to the kidney’s which filter out and secretes about 70% and the remainder excreted via the GI tract. From a pathological view, uric acid is elevated when there is cell breakdown as in leukemia and catabolism of nucleic acids as in gout, or removal via the kidneys is decreased due to renal failure. From a physiologic view, we look at every level of protein combustion where there remain two by-products which are a Mucous (oily residue) and Uric acid (carbon ash) In order for protein to be fully combusted, it must first be influenced in the duodenum by trypsin, chymotrypsin, carboxypolypeptidase, and bile emulsification. Trypsin and chymotrypsin cleave proteins into peptides and carboxypolypeptidase split the peptides into amino acids. The pancreas synthesizes trypsinogen, chymotrypsinogen, and procarboxypolypeptidase, which are enzymatically inactive. When they are released into the duodenum they are all activated by enterokinase. Which now readies the proteins for assimilation in the liver. Therefore, if the proteins are not prepared properly the two end products, uric acid, and mucous, will be out of balance. URIC ACID IS HIGH WHEN General considerations: ¬ Decrease fatty proteins and rich foods ¬ Decrease alcohol and simple sugars ¬ Increase water intake	303.64
Bun Bun BLOOD UREA NITROGEN Blood urea nitrogen is formed entirely by liver deamination from protein metabolism. BUN is a byproduct due to the release of nitrogen bonds (and measures the nitrogen portion of urea) from protein substances in the liver. From a pathological perspective, an increased blood urea nitrogen would indicate renal disease, tissue necrosis, increased adrenal gland activity, and rapid protein catabolism. From a physiologic perspective, the purpose of nitrogen is to carry a substance through an aerobic media preventing oxidation, and eventually back into an anaerobic environment. Once in the liver the thyroid through the use of iodine, releases the nitrogen bond, releasing the nitrogen from the protein, allowing the protein to combust into hormones, enzymes and antibodies. The adrenals and anterior pituitary play a vital role in the combustion of this protein. The urea is now sent to the kidneys and is converted into urine. Urea is produced when amino acids, which are not used for protein synthesis, are broken down via hepatic metabolism. These amino acids are de-aminated producing ammonia, which is converted to urea immediately since ammonia levels become toxic. When this metabolic conversion is affected due to faulty metabolism or liver disease ammonia is not converted causing excessive levels of ammonia with possible hepatic encephalopathy. Renal malfunction/failure may also cause a high BUN due to its affect on the removal of urea causing uremia. Uremic wastes usually impair platelet function, and patients may show an increased tendency towards bleeding. BUN IS HIGH WHEN General considerations: ¬ High protein diets can cause increased BUN ¬ Increase water intake if no edema	880.95
Creatinine Creatinine CREATININE Creatinine ash is a basic byproduct in the breakdown of muscle creatine phosphate resulting from energy metabolism. From a pathological perspective the kidneys primarily remove creatinine and when there are elevated levels it indicates reduced kidney function. Thus creatine levels give an approximate for the GFR. From a physiological perspective, creatine is a by-product of actin metabolism after being exposed to acetylcholine combustion. The actin fiber joins two stable protein blocks (myosin), which combusts to produce muscle contraction, primarily for activity and secondarily for tonicity. During a muscle contraction, an action potential travels along a motor nerve to a muscle fiber. Acetylcholine is released at the motor endplate, causing multiple acetylcholine lined gated protein channels to open. This causes sodium ions to flow to the interior of the muscle, which initiates an action potential of that muscle. This then leads to depolarization releasing large amounts of calcium into the myofibrils. This initiates a contractive force between the actin and myosin filaments via ATP causing them to slide together, which is the contractile process. After a fraction of a second, calcium is pumped back into the sarcoplasmic reticulum, until the next muscle contraction. The actin fiber is then oxidized (H displaced) via acetylcholine, leaving an oily waxy residue known as creatinine. GABA (Glutamic amino benzoic acid), which is part of the actin fiber, helps it burn better. Creatine becomes creatinine with the release of ATP. Low creatinine levels would indicate muscle loss and weakness.	455.56
Sodium Sodium ELECTROLYTES The blood electrolytes include sodium, potassium, chloride, and the bicarbonate (HCO3) ion. Sodium, potassium, and chloride enter the body via ingestion of food. Carbon dioxide, on the other hand, originates within the body via the metabolic process of carbohydrates, fats, and proteins. Normally the excretion of sodium, potassium, and water is equal to their intake. The kidneys secrete 80-90 percent of all electrolytes. Excessive carbon dioxide stimulates the respiratory centers in the brainstem to increase respiration. Therefore, the kidneys and the lungs control sodium, chloride, potassium, water, and carbon dioxide thus exerting control over the acid/alkaline balance in the body. There are also many other organs, and glands involved in this process, such as the posterior pituitary, adrenals, bowel, and uterus/prostate. The purpose of electrolytes is to set up a shifting mechanism in the cell membrane via oxidation, allowing increased or decreased permeability to that membrane site. Sodium, which is found in high concentration outside the cell, has the ability to gather up substances (foods) and bring them to active membrane sites. Chloride is found in the cell membrane and acts as a “doorman” allowing or disallowing exchanges between the intracellular and extracellular fluids. Potassium, which is found in high concentrations within cells, oxidizes chloride, and allows sodium, with the food to cross the cell membrane and enter the cell. Sodium, potassium, chloride, calcium, and hydrogen are all transported via active transport. SODIUM Sodium is the most abundant cation (90%) and is the major base in the body. Sodium is either implanted into the food via saliva or is found in the food and has the following functions: 1. Sodium is an alkaline mineral that helps maintain alkaline activity. Therefore, it helps in acid-alkaline balance, which affect intracellular/extracellular fluid exchange, osmotic pressure, via the sodium/potassium pump and does this in conjunction with antidiuretic hormone and aldosterone. 2. Sodium gathers, and aggregates (polarizes) all substances necessary to be exchanged by semi-permeable membranes. Sodium pumps proteins and sugars into the cell membranes. 3. Sodium also affects the renal tubules for the activity of discharging toxins. It literally aggregates toxins and holds them in suspension. 4. Sodium is controlled by the adrenal cortex and as mentioned above is extremely alkaline and therefore, can cause migration of substances towards its polarity, as well as causing these migrated substances to achieve permeability in an acid antioxidant type media known as a fatty membrane. Sodium is the substance necessary to polarize foods into storage according to that permeable membranes needs. 5. Sodium is also necessary for the transmission of neurological impulses by creating action potentials across neurological membranes. 6. Sodium concentration in and out of cells remains constant due to renal blood flow, carbonic anhydrase enzyme activity, aldosterone, and other steroids controlled by the anterior pituitary, rennin enzyme secretion, hypothalamus, and posterior pituitary control of ADH and vasopressin secretion	-33.33	5
Potassium Potassium ELECTROLYTES The blood electrolytes include sodium, potassium, chloride, and the bicarbonate (HCO3) ion. Sodium, potassium, and chloride enter the body via ingestion of food. Carbon dioxide, on the other hand, originates within the body via the metabolic process of carbohydrates, fats, and proteins. Normally the excretion of sodium, potassium, and water is equal to their intake. The kidneys secrete 80-90 percent of all electrolytes. Excessive carbon dioxide stimulates the respiratory centers in the brainstem to increase respiration. Therefore, the kidneys and the lungs control sodium, chloride, potassium, water, and carbon dioxide thus exerting control over the acid/alkaline balance in the body. There are also many other organs, and glands involved in this process, such as the posterior pituitary, adrenals, bowel, and uterus/prostate. The purpose of electrolytes is to set up a shifting mechanism in the cell membrane via oxidation, allowing increased or decreased permeability to that membrane site. Sodium, which is found in high concentration outside the cell, has the ability to gather up substances (foods), and bring them to active membrane sites. Chloride is found in the cell membrane and acts as a “doorman” allowing or disallowing exchanges between the intracellular and extracellular fluids. Potassium, which is found in high concentrations within cells, oxidizes chloride, and allows sodium, with the food to cross the cell membrane and enter the cell. Sodium, potassium, chloride, calcium, and hydrogen are all transported via active transport. POTASSIUM Potassium is intracellular, lining the inside of all cell membranes and affecting intracellular fluids, osmotic pressure, buffering viscosity (potassium bicarbonate is the primary intracellular inorganic buffer). When there is a decrease in potassium bicarbonate you have acid cells, which excites the respiratory centers so the patient hyperventilates. Metabolic acidosis or diabetic ketoacidosis drives potassium out of the cells, affecting electrolyte balance, water retention and carbon dioxide transport in red blood cells. Potassium is responsible via the posterior pituitary for oxidizing secondary hydrogen chloride (affecting adrenal function), allowing the sodium-aggregated substances to cross the cell membrane by affecting the membranes permeability. Potassium is the only substance, which allows oxygen into unoxygenated tissue. About 90% of the body’s potassium supply is intracellular with only a small percent in the serum. 80% of that is found in the muscles (used for muscular contraction) and in the bones. Potassium levels are regulated by the Na/K ATPase pump which requires magnesium for proper function. Potassium is necessary for proper function of mineralocorticoids, (aldosterone and deoxycorticosterone) thus maintaining sodium concentration and alkaline reserve. Therefore, potassium is of great value to the posterior pituitary (ADH/oxytocin), the pineal, and the adrenal cortex via aldosterone secretion. Potassium along with sodium regulate renal acid-base balance, by substituting hydrogen ions for sodium and potassium in the renal tubules. Potassium also facilitates oxygen to the myocardium and oxidizes the S.A. node of the heart. The heart has the highest potassium concentration in the body. Potassium along with calcium and magnesium controls the rate and force of contraction in heart muscle. It is the primary oxidizer of the body capable of expressing all cellular needs. Potassium also regulates neurological impulses via osmotic pressure gradients throughout the nervous system. Potassium directs carbohydrate digestion by polarizing minerals associated with carbohydrate digestion, from the time the carbohydrate enters the body until the cell utilizes it. Potassium also makes proteins soluble and regulates protein synthesis. 80-90 percent of potassium in the cells is excreted by the kidneys (resulting in the loss of 40-50 mEq/L per day even during fasting) with the remainder excreted by the stool and through sweating POTASSIUM IS LOW WHEN General considerations: ¬ Increase water intake ¬ Increase magnesium intake ¬ Decrease calcium intake ¬ Increase potassium intake ¬ Decrease carbohydrate intake	-50		5	10
Chloride Chloride ELECTROLYTES The blood electrolytes include sodium, potassium, chloride, and the bicarbonate (HCO3) ion. Sodium, potassium, and chloride enter the body via ingestion of food. Carbon dioxide, on the other hand, originates within the body via the metabolic process of carbohydrates, fats, and proteins. Normally the excretion of sodium, potassium, and water is equal to their intake. The kidneys secrete 80-90 percent of all electrolytes. Excessive carbon dioxide stimulates the respiratory centers in the brainstem to increase respiration. Therefore, the kidneys and the lungs control sodium, chloride, potassium, water, and carbon dioxide thus exerting control over the acid/alkaline balance in the body. There are also many other organs, and glands involved in this process, such as the posterior pituitary, adrenals, bowel, and uterus/prostate. The purpose of electrolytes is to set up a shifting mechanism in the cell membrane via oxidation, allowing increased or decreased permeability to that membrane site. Sodium, which is found in high concentration outside the cell, has the ability to gather up substances (foods) and bring them to active membrane sites. Chloride is found in the cell membrane and acts as a “doorman” allowing or disallowing exchanges between the intracellular and extracellular fluids. Potassium, which is found in high concentrations within cells, oxidizes chloride, and allows sodium, with the food to cross the cell membrane and enter the cell. Sodium, potassium, chloride, calcium, and hydrogen are all transported via active transport. CHLORIDE Chloride a blood electrolyte, and is the major anion and exists in the extracellular spaces as part of the sodium chloride or HCl molecules. Chloride is used for assessing pH, and electrolyte balance. From a physiologic perspective, the primary purpose of chloride is to regulate the quantity of carbohydrates and proteins entering into the cells, by inhibiting the exchange of mineral controlled substances across the cell membrane and responds to the oxidative power of potassium. Chloride the major anion is predominantly found in the extracellular spaces as part of sodium chloride or in the stomach as hydrochloric acid. Chloride maintains cellular integrity by its influence on acid-base and water balance as well as osmotic pressure. Chloride has a reciprocal power with other anions by decreasing or increasing when there are too many or not enough anions. Aldosterone has a direct effect of reabsorption of sodium and an indirect effect on the increased absorption of chloride. Chlorides are lost via the GI tract through vomiting or diarrhea and thru the kidneys during times of diuresis. Chloride also responds to the antioxidant media (cell membrane) by mobilizing, and collecting sodium/food aggregates on a selectively permeable basis. This reaction is under the influence of the adrenal medulla/epinephrine/norepinephrine thereby maintaining energy stores. Chloride also assists in the production of HCl via the chief cells in the stomach. In the bowel, chloride is important in preventing the passage of water out of the body. Therefore, chloride literally blocks the flow of water/gas exchange across a cell membrane. This is extremely important in the intestines and bladder. Chloride plays a vital role during the conduction of a neurological impulse where sodium lines up on the outside of a cell membrane, and potassium on the inside of the cell membrane, during the resting stage or polarized state. In a normal nerve fiber, the permeability of the membrane to potassium is about 100 times that of sodium. The sodium-potassium pump moves three sodium ions to the exterior of the cell, for every two potassium ions that are moved to the interior of the cell, creating a net positive charge to the outside of the cell membrane for each revolution of the sodium-potassium pump. This creates a positively charged external membrane and a negatively charged internal membrane, which sets up a membrane electrical potential. As a neurological impulse is transmitted down the nerve, (which is the excitation phase of an impulse), sodium crosses the cell membrane, and enters into the cell, while potassium moves to the external portion of the membrane. This then creates the depolarization of the cell membrane, thereby creating a negative charge on the outside, and a positive charge on the inside. The transmission of each impulse along the nerve fiber reduces infinitesimally as the concentration differences of sodium and potassium between the inside and outside of the cell membrane change slightly. In so doing allows the nerve fiber to transmit between 100, 000 to 50, 000, 000 impulses before the concentration differences are rundown. As the neurological impulse passes, the sodium-potassium ATPase pump re-establishes the sodium-potassium ratio back to normal (repolarization). The pumping activity is dramatically increased approximately eightfold to restore the membrane back to the polarized state. The chloride shift to the inside of the cell membrane during the final stages makes the inside of the cell, even more, negative, which further helps repolarize the cell. Chloride generally increases and decreases with plasma or serum sodium levels. CHLORIDE IS HIGH WHEN General considerations: ¬ Drink plenty of water ¬ Decrease sodium levels ¬ Increase fat-soluble vitamins D, E, K, and A	-38.46	5	5
CO2 CO2 CARBON DIOXIDE Carbon dioxide is created as a byproduct when potassium forces water into fat. So carbon dioxide is the acid gas factor, which binds fats and selenium creating the intelligent metabolic activity between the water and fat. 80-90 percent of the carbon dioxide found in plasma is bound to protein and is represented as bicarbonate ions (HCO3-) which first exists in the extracellular spaces as CO2 then as H2CO3 and finally is buffered by the plasma and erythrocytes into sodium bicarbonate NaHCO3) and is regulated by the kidneys. The other 10 to 20 percent is dissolved CO2 gas (removed by the lungs), which is bound to protein as CO3 (2), and carbonic acid (H2CO3). The total CO2 comes from dissolved CO2, H2CO3, HCO3- and carbaminohemoglobin (CO2HHb). This occurs in the following way, carbon dioxide in the blood reacts with water in the red blood cells to form carbonic acid. In the blood cells, there is an enzyme called carbonic anhydrase that catalyzes the water and carbon dioxide 5,000 fold, creating a rapid exchange into carbonic acid. This allows tremendous amounts of carbon dioxide reacting with the water in the red blood cells, even before the blood leaves the tissue capillaries. So a red blood cell creates carbonic acid from water and carbon dioxide. In another small fraction of a second, the carbonic acid formed in the red blood cell now disassociates into hydrogen and bicarbonate ions. The hydrogen ions combine with hemoglobin, as the bicarbonate ions diffuse out into the plasma while chloride ions diffuse into the red blood cells taking the place of the bicarbonate ions. This is made possible by the presence of a bicarbonate/chloride carrier protein in the red blood cell membrane, which acts as a shuttle for these two ions. Thus, the chloride content of venous red blood cells is greater than that of arterial cells. This is known as the chloride shift. In addition, carbon dioxide can react directly with hemoglobin to form the compound carbaminohemoglobin. This carbaminohemoglobin creates the reversible reaction releasing carbon dioxide into the alveoli of the lungs. Carbon dioxide then is the venous capillary exchange product after diffusion takes place. The active pressure intake of oxygen relies upon this diffusion. This active process realizes the ability of forced metabolism and is the ash byproduct. Carbon dioxide is vital to pH balance and is controlled by the respiratory, renal, and posterior pituitary adrenal axis. Therefore, any of these glands or organs or combinations thereof can affect carbon dioxide levels. CARBON DIOXIDE IS HIGH WHEN General considerations: ¬ Water loss- increase water intake ¬ Protein loss- increase protein intake ¬ Hypomagnesemia or hypokalemia causes increased CO2- increase potassium and magnesium CARBON DIOXIDE IS LOW WHEN ¬ Water loss- increase water intake ¬ Hypermagnesemia or hyperkalemia causes decreased CO2- decrease potassium and magnesium support	-16.67
Calcium Calcium CALCIUM Calcium is the largest most nonpolar, alkaline and most abundant of all minerals with 99% of all calcium found in the bones and teeth. Calcium exists in the ionized state 55 percent of the time and 45 percent of the time in the non-diffusible state, bound to either albumin, prealbumin or thyroglobulin. Therefore, if there is a decrease in serum albumin then there will be a decrease in serum calcium. Calcium has many functions: ¬ Provides the mobilizing factor in trauma, infections and stress for tissue repair, along with vitamins A, C, manganese, phosphorus, and fatty acids. ¬ Causes vasoconstriction, while potassium, sodium, magnesium, hydrogen ions, and carbon dioxide cause vasodilatation. ¬ Is necessary for bone formation along with phosphorus, collagen, hydroxyapatite (gives bone its hardness) and bone salts of magnesium, sodium, potassium, carbonate, uranium, plutonium, and strontium. ¬ Calcium is used to create action potentials across smooth and striated muscles leading to contraction. ¬ Calcium is used as an intracellular communicator via calcium ion gated channels. ¬ Calcium collects and gather up lipoproteins, and move them across the intestinal membrane. Attaches to oils, fats, fatty acids and waxes. Calcium is absorbed in the upper portion of the small intestines (duodeneum), and the amount absorbed depends on the "acidity" of the intestinal content, via phosphorylation and protein content. When the ratio of calcium to magnesium (which is found in the intestinal membrane as well as cell membranes) is greater than 2-1, fat is drawn through the intestinal and cell membranes. Calcium also requires vitamin D. and HCl for optimal metabolism. The glands involved with calcium are: 1. The stomach via the release of HCL, which affects the preparation and absorption of calcium. 2. The parathyroids- via parathormone control of calcium ion concentration by controlling intestinal absorption, excretion via the kidneys and the release of calcium from the bones. 3. The liver/gallbladder- via bile emulsification of lipoproteins, preparing them for intestinal absorption. 4. The spleen- which stores and ages fats or lipoproteins. 5. The parotids- due to their ability to program foodstuffs. 6. The thyroid glands-via "calcitonin", promoting deposition of calcium in the bones, while decreasing calcium concentration in the extra-cellular fluids and the blood. 7. The anterior pituitary via its control of magnesium regulating calcium uptake, which regulates protein transport thru the cell membranes. 8. The pancreas- via its ability to oxidize fatty acids Therefore, any of the above glands or organs or combinations thereof has a great impact on calcium levels. CALCIUM IS HIGH WHEN General considerations ¬ Your patient should drink plenty of water ¬ Make sure they are not hypervitaminosis on Vitamins A or D ¬ Very high protein diets may increase calcium levels ¬ Magnesium and phosphates may also increase calcium levels ¬ Using sea salt can help to reduce calcium levels. CALCIUM IS LOW WHEN General considerations: ¬ Increase Vitamin A and D intake ¬ Increase albumin and protein intake ¬ Increase magnesium intake ¬ Increase phosphorus	-13.04				5
Phosphorus Phosphorus PHOSPHORUS 85% of the total phosphorus exists as phosphates or esters in the body and is found chiefly in the skeleton and is combined with calcium. 14% of the phosphorus is found in intracellular tissues and 1 % is found in the extracellular fluid. Therefore phosphorus levels are a poor indicator of levels of phosphates in the body. Phosphorus runs inversely to calcium levels in the body at a calcium to phosphorus ratio of 10 to 4. Therefore, calcium can be a great indicator for phosphorus as well. As calcium levels increase in the serum, phosphorus levels decrease, and when calcium levels decrease phosphorus levels increase. In fact, causes of high calcium also cause low phosphorus. The controlling factor of phosphorus is parathormone (PTH), which is also the calcium-controlling factor. Phosphorus helps calcium through the cell membrane by increasing the permeability of the cell membrane via oxygen displacement. 1. Phosphorus is responsible for growth and development by way of: ✓ bonding ✓ polymer function ✓ hydration ✓ chemical transport, and ✓ buffering 2. Phosphorus is also responsible for bone formation 3. Phosphorus and metabolism of glucose Phosphorus is also required for the metabolism of glucose via phosphorylation. Phosphorylation is when a phosphate radical promoted by glucokinase in the liver, or hexokinase in other cells captures the glucose and once inside the cells keeps it there. The exception to this occurs in the liver, the kidneys, and the intestinal epithelial cells. Ingestion of carbohydrates causes phosphorus to enter RBC’s with glucose causing a reduction of serum phosphorus levels and lipids. Phosphorus also works in the stomach to stabilize sugars and activate starches by the twofold process of phosphorylation. Phosphorylation and its counterpart, dephosphorylation, turn many protein enzymes on and off, thereby altering their function and activity. By altering pepsin/HCL levels phosphorus can: a. Stabilize simple sugars-simple sugars are easily oxidized (combusted) before they reach the liver, resulting in low sugar levels. Pepsin stabilizes these simple sugars, so they can be transferred to the liver for storage. b. Activation of starches- HCl is necessary to breakdown oily carbohydrates (grains), which are difficult to oxidize (combust). Thus making them readily available for oxidation. The above two mechanisms establish an HCl-pepsin balance in the stomach for proper pH digestion. The presence of both HCl and pepsin in the stomach are critical for preparing carbohydrates, as well as proteins for further digestion in the small intestines. 4. The regulation and maintenance of the acid-base balance in the body by maintaining glandular acidity. 5. The storage and transfer of energy from one part of the body to the other. 6. Used in the Production of phospholipids (90 % produced by the liver): lecithin, A cephalin, and sphingomyelin Phospholipids are necessary for: Proper brain function (sphingomyelins) Phospholipids are a major constituent of lipoproteins which can affect function, formation and transport of these lipoproteins causing serious cholesterol abnormalities Production of cell membranes Thromboplastin production produced from A cephalin 7. Intracellular phosphorus is used for: Energy transport formation of ATP from ADP and creatine phosphate via oxidative phosphorylation. Major constituent of plasma membranes (phospholipids) Major constituent of DNA and RNA (nucleic acids) Calcium transport and osmotic fluid pressure General nutritional considerations when phosphorus is high: 1. Patient should increase water intake 2. Reduce fat intake 3. Reduce Vitamin D intake if overdosing 4. An isotonic saline solution (sea salt) will decrease phosphorus levels 5. Also, decrease phosphorus in the diet and add calcium carbonate to your diet General considerations when phosphorous is low: 1. Vitamin D deficiency 2. Calcium deficiency 3. Magnesium deficiency 4. Patient needs a high protein diet	270						5
Magnesium Magnesium MAGNESIUM Serum magnesium constitutes only a small fraction of the total body stores and may not predict magnesium status correctly. From a physiologic perspective, magnesium directs protein digestion, by polarizing minerals associated with protein digestion, from the entrance of protein into the body to its final deposition in the cell. Approximately 40-60 % of the magnesium is found in the skeleton for bone formation, 20% is found in the muscle, 30% is found in the intracellular cytoplasm, with only 1 % of the magnesium found in the serum. Magnesium affects membrane permeability, nerve impulses, muscle contraction, intracellular fluid regulation, activation of enzyme systems, where magnesium acts as a metallic cofactor in over 300 enzymatic reactions. Regulates protein synthesis, carbohydrate metabolism, nucleic acid synthesis, and blood viscosity. Magnesium along with sodium, potassium and calcium regulate neuromuscular irritability and the mechanism for clotting. Less then 2% of calcium, magnesium and phosphates are found in the plasma and extracellular fluid and are controlled in narrow limits. Albumin accounts for 70% of the bound calcium. Magnesium also binds to albumin and since it has a lower specificity for the receptors it creates more free magnesium in the plasma. Magnesium and calcium are very much linked in their body functions and a deficiency in either one will have an adverse affect on the other. Especially since calcium needs magnesium to be absorbed thru the intestinal membrane as well as needing magnesium for calcium metabolism. For example, a magnesium deficiency will cause calcium to migrate out of the bone and into soft tissues such as the aorta and kidneys. 95% of all magnesium that is filtered thru the glomerulus is reabsorbed by the tubules where parathormone enhances tubular reabsorption of magnesium. When there is a deficiency of magnesium you will see a decrease in urine stores before serum stores. Please note that even when magnesium is in a 20% depleted state, magnesium levels in the serum will appear normal. Calcium, magnesium and phosphates continuously enter the plasma via the kidney, the intestinal brush borders, and the ruffled border from the bones. Steady states of calcium, magnesium, and phosphorus approximate urine loss against intestinal absorption and skeletal mineral apposition against mineral absorption. Magnesium in the cells is complexed to phosphates, citrates and anions such as ATP, AMP and ADP (such as MgATP2-) Magnesium also plays a key role in the hormonal regulation of insulin, estrogen and thyroid hormones. Magnesium also stimulates secretions from the parathyroids and adrenal cortex (corticosteroids). Magnesium is also affected just the way calcium is to parathormone (enhances distal tubular reabsorption of magnesium) and to a lesser degree calcitonin. In fact, calcium, magnesium, and phosphates are depressed in vitamin D deficiencies and increased with vitamin D excess. Magnesium is used in the treatment of elevated cholesterol and triglycerides, muscular contraction, hypertension (A causal relation between decreased Mg2+ content of cardiac muscle/coronary arteries and nonocclusive sudden-death ischemic heart disease has been proposed) and premenstrual syndrome. Magnesium is indicated in collagen and connective tissue diseases, inflammatory disorders, migraines, general endocrine function and neurological and psychosomatic disorders.	-80
Total Protein Total Protein TOTAL PROTEIN Total proteins are divided into two fractions: albumin, and globulin (alpha, beta, and gamma). Please note that total protein also includes fibrinogen. Therefore total protein is made up of albumin, globulin and fibrinogen, all produced in the liver. These are the plasma proteins necessary to produce enzymes, antibodies, clotting factors, kinin precursors, and transport substances for hormones, vitamins, minerals, fats, etc. For example, plasma proteins combine with cholesterol forming lipoproteins such as VLDL, LDL’s, HDL’s etc. The lipoproteins then combine with minerals via enzyme metabolism to form and renew sex hormones such as testosterone, estrogen, progesterone etc. Other deaminated proteins produced in the liver, combusts at the mitochondrial level to form cell structures. These are your tissue building proteins known as nucleoproteins, DNA and RNA (your proteins of mitosis and meiosis). Since there are many glands involved in protein digestion, it is very difficult to make a determination from total protein alone. Glands and organs involved with protein control are as follows: The anterior pituitary, which controls all glands of protein digestion, such as the adrenals, thyroid, pancreatic head, sex organs, and spleen That parotid glands which tag lipoproteins with copper The parathyroids via the calcium/magnesium mobilization of lipoproteins The thyroid which denitrifies protein in the liver The pancreas by trypsin and chymotrypsin which, prepares the protein for assimilation into the bloodstream The sex organs that prepare protein for final deposition into the cells * Any combination of the above TOTAL PROTEIN IS LOW WHEN General considerations: o Increase protein intake o Increase B acid vitamins	20
Albumin Albumin ALBUMIN In pathological levels albumin is used to evaluate: 1. Liver and renal disease 2. Blood osmotic pressure 3. Chronic disease states, which most patients have 4. Dehydration 5. Albumin decreases in acute inflammatory infectious processes From a physiological standpoint, albumin is produced in the liver and is a primary byproduct of sterols and waxes. Its function is used to build and repair tissue. Albumin is responsible for 80 percent of the colloidal osmotic pressure between body tissues and blood cells. 75% of this control occurs inside the cells since most of the protein is intracellular. When you have a decrease in albumin, the osmotic pressure becomes disturbed resulting in fluid transfer and edema. Since albumin influences water movement, it will also influence nutrient and mineral movement. Albumin creates the permeability of the membrane to the osmolarity of the membrane. Therefore, substances can pass from a lesser concentration to a greater concentration. The flow is from the arterial capillaries to extracellular fluid, then from the extracellular fluid to the intracellular fluid, then from the intracellular fluid to the mitochondria. Then back via the same pathway in reverse via osmotic absorption into the veins. Albumin is also a part of a complex buffer system, which accounts for 75% of things that need to be buffered to maintain acid-alkaline balance in the body. The most powerful buffer system out of the four including, the bicarbonate system (HCO3-), the phosphate buffer system, and the liver (nitrogen/urea), the proteins of the cells and plasma, rein supreme. The protein buffer system works by controlling blood Hydrogen (H+) ion homeostasis. Both intracellular and extracellular proteins have negative charges and can serve as buffers for alterations in hydrogen ion concentration. However, because most proteins are inside cells, this primarily is an intracellular buffer system. Hemoglobin (Hb) a globular protein is an excellent intracellular buffer because of it's ability to bind with Hydrogen ions forming a weak acid and carbon dioxide (CO2) bond. After oxygen is released in the peripheral tissues, hemoglobin binds with CO2 and H+ ions. As the blood reaches the lungs these actions reverse themselves. Hemoglobin binds with oxygen, releasing the CO2 and H+ ions. The H+ ions then combine with bicarbonate (HCO3) ions to form carbonic acid (H2CO3). The H2CO3 breaks down to form water (H2O) and carbon dioxide (CO2), which are excreted via expiration through the lungs. Increases in albumin cause arteries to sclerose and a decrease in albumin causes veins to sclerose. Albumin is also a transporter of minerals and accounts for 70% of the bound calcium. Magnesium also binds to albumin and since it has a lower specificity for the receptors it creates more free magnesium in the plasma. Calcium, magnesium, and phosphates continuously enter the plasma via the kidneys, the intestinal brush borders and the ruffled border of the bone. Albumin is also responsible for transporting copper, zinc, and nickel. By controlling the transport of these minerals, albumin is the carrier of choice. The following glands are associated with albumin: 1. The parotids 2. The head of the pancreas 3. The endo-reticular portion of the liver 4. Kidneys Therefore, the function or malfunction of anyone of those glands/organs or combinations thereof can lead to imbalances in albumin levels.	-30			5
Globulin Total Globulin Total GLOBULIN Organs that are responsible for globulin production are the liver, thyroid, spleen and the rest the immune system. There are four types of globulins alpha 1,2, beta and Gamma. There a few groups of gamma globulins with one group being the immunoglobulins (IgA, IgG. IgM), which produce our antibodies. The thymus produces α and β globulins know as thymoglobulin using Vitamin T and copper for its production. The thyroid produces thyroglobulins that form thyroxin and triiodothyronine via vitamin K and iodine. The spleen produces spleenoglobulins that require vitamin E and iron for its production. Globulin also acts as a polarized colloidal substance necessary for specific glandular hormonal function by acting as a transport mechanism for many hormones such as sex hormone binding globulin. Globulin also assists in: Toxin neutralization by binding soluble antigens in the blood and intracellular spaces Red blood cell production Antibody formation Protection of the gastrointestinal mucosa And is also necessary via the intrinsic factor for digestion and absorption. Globular proteins can be affected via: Nutrition- lack of protein Liver Thyroid Spleen Thymus	15.79			5		5
A/G Ratio A/G Ratio A/G RATIO The A/G ratio is the ratio of albumin to globulin, and along with fibrinogen (produced by the liver) literally measures the thickness or “collagen factor” of the blood. The A/G ratio then is also a representation of the fibrinogen content in the blood and regulates the amount of protein being utilized at any time in the body. The liver forms prothrombin, which requires vitamin K. for its production. Prothrombin is a plasma protein, which is changed into thrombin via prothrombin activator and calcium. Thrombin, transposes fibrinogen into fibrin, continually causing clotting throughout the body along with blood platelets. Fibrinogen, therefore, provides the clotting thickness (collagen factor) in the blood. These polarized protein fibrous strands are necessary to maintain blood viscosity, which regulates the amount of capillary exchange from the artery to the extracellular fluid. Collagen a protein strand (albuminoid) and proteoglycan filaments also regulate exchange by causing a very slow diffusion of molecules via kinetic motion moving substances through the extracellular fluid either to the cell membrane or back into the circulatory or lymphatic systems. Collagen is also the main structural protein in connective tissue and found in the extracellular spaces. Collagen and proteoglycan filaments are used in the interstitium to provide tensile strength and for healing. As the main component of connective tissue, it makes up from 25% to 35% of the whole-body protein content. Collagen is formed in the sternum and iliac crest. A/G RATIO IS INCREASED WHEN Anything that would decrease globulin would increase the A/G ratio and anything that would increase albumin would also increase the A/G ratio so also look at all the possibilities under low globulin or high albumin THE A/G RATIO IS DECREASED WHEN Anything that would increase globulin would decrease the A/G ratio and anything that would decrease albumin would decrease the A/G ratio so also look at all the possibilities under high globulin or low albumin	1645.45			5		5
Bilirubin, Total Bilirubin, Total TOTAL BILIRUBIN Bilirubin comes from the breakdown of hemoglobin and is the byproduct of hemolysis. Bilirubin is produced by the RE portion of the liver and is excreted with the bile. Pathologically elevations in total bilirubin occur when there is a massive amount of destruction of RBC’s, or the liver is congested and unable to excrete bilirubin. From a physiologic perspective, the components of bile are inositol, choline, lecithin, cholesterol, and bilirubin/biliverdin. Cholesterol, which is produced by the liver, is converted into bile salts via the influence of the adrenal glands. The bile salts are converted into cholic acid or chenodeoxycholic acid equally. Approximately 60 percent of all cholesterol is converted into these two acids. These acids then combine with glycine and taurine to form glyco and tauro conjugated bile acids. The salts of these acids are secreted in the bile. These salts do two things: 1. They act like "soap" creating saponification and emulsification of fat. This decreases the surface tension of the fat allowing agitation to break the fat up into smaller sizes. 2. Bile salts help absorb fatty acids, monoglycerides, cholesterol, and other lipids, by forming minute complexes called micelles. Micelles are highly soluble, highly charged, and easily absorbed, increasing absorption by 40 percent. The liver secretes about 600-1,200 milliliters of bile per day. The purpose of bile is to: 1. Digest, emulsify and absorb fats. 2. To excrete waste products, such as excessive cholesterol, and bilirubin, which is the end product of hemoglobin degradation. Bilirubin is the predominant pigment of bile, and is formed from hemoglobin, and destroyed red blood cells. The red blood cells are destroyed by the reticulo-endothelial system (liver and spleen), including the kupfer cells of the liver. If the spleen/liver are hyperactive, the bile production is increased. This allows the passive function of bile production to elevate. As the spleen, liver, and bone marrow destroy hemoglobin it passes into the bloodstream with a protein creating a colloidal state. This creates hemolytic jaundice when there is excessive destruction or impaired production of red blood cells, leading to excessive amounts of prehepatic bilirubin. The liver cells are unable to withdraw the bilirubin from the blood as fast as it is formed. Therefore consequently there is an increase in prehepatic bilirubin (indirect form). Remember total bilirubin = the direct and indirect forms. The direct is elevated in biliary obstruction, which is conjugated and reacted on by the liver. The indirect form is elevated in liver failure, which is unconjugated and not reacted on by the liver. Since the liver, spleen, adrenals and diet play a role in total bilirubin production from a physiologic perspective we must evaluate those glands as well.	-77.78				10	10
Alkaline Phosphatase Alkaline Phosphatase ALKALINE PHOSPHATASE Bone osteoblasts, liver cells, and the placenta all produce high levels of alkaline phosphatase, with some activity in the kidneys and intestines. Alkaline phosphatase is called alkaline because it aids in maintaining and works best in an alkaline pH of 9-10. From a pathological perspective, alkaline phosphatase levels rise in liver disease due to impaired excretion of this enzyme from obstruction in the biliary tract, and bone disease via increased osteoclastic activity due to bone breakdown as in cancer. From a physiological perspective alkaline phosphatase is responsible for the balancing of water, and mineral metabolism controlled by the glands below. This exchange of water and mineral metabolism occurs at the cell membranes of ligaments, tendons and disc structures. The balance is created by, setting the minerals involved with electrolyte balance into motion. These minerals, along with proper neurological control, cause the shifting of food thru the membranes. The glands responsible for this balance are as follows: • The adrenal cortex via mineralocorticoids causes excretion of sodium and potassium by the kidney. • The adrenal medulla via epinephrine and norepinephrine increase metabolism, and cellular exchange via the chloride shift at the level of the membrane. • The posterior pituitary via antidiuretic hormone and its effect on potassium (oxidizer) and the water content within the cell. • Prostate/uterus via selenium acts as an oxidative mineral to insure proper membrane exchange in conjunction with the above. Alkaline phosphatase is a member of a family of zinc metalloprotein enzymes whose purpose is to split off a terminal phosphate group from an organic phosphate ester. Enzyme activity is localized in the brush border of the proximal convoluted tubules of the kidney, intestinal mucosal epithelial cells, hepatic sinusoidal membranes, vascular endothelial cells and osteoblasts of bone as mentioned above. It is the introduction of an alkaline media for bone growth. When there is an increased alkaline phosphatase you have too much acidity. In “bone pathology” there is usually a hyper-acidic state, since the foundation of a cell, is nucleic acid. The nucleic acid is composed of phosphoric acid. Phosphoric acid is a component of alkaline phosphatase, therefore, the adrenals regulate the acid/alkaline balance for energy, and growth. Alkaline phosphatase controls the alkaline substance, which controls energy, and the acid substance, which controls growth. Over the years, the laboratory low range has been steadily decreasing from 60, down to 40 now down to the mid 20's. Since this test does measure metabolic output of the adrenals, going to low is not the answer. I recommend that the low range is 70.	-66.32	10	10
LDH LDH LACTIC ACID DEHYDROGENASE Lactic acid dehydrogenase is found chiefly in the heart, skeletal muscles, kidneys, and liver, as well as all cells. In pathological states, elevated levels indicate damage to the above areas and is used to determine myocardial and pulmonary infarction. In physiological states, LDH catalyzes the conversion of pyruvate ( the final step in glycolysis) to lactate and back, as it converts NADH to NAD+ and back. A dehydrogenase is an enzyme that transfers a hydride from one molecule to another. When sugar and water (fatty acid metabolism) are exchanged across a muscle cell interface, a by-product called lactic acid is produced. When lactic acid combines with the carbon dioxide of the venous blood you have a hydrogen displacement. Lactic acid now becomes lactic acid dehydrogenase. Lactic acid dehydrogenase, therefore, is a glycolytic enzyme that functions as a catalyst in carbohydrate metabolism to produce energy. The pancreas via insulin and the posterior pituitary via ADH are responsible for this sugar and water exchange across the muscle cell interface. Lactic acid dehydrogenase indicates the active exchange of sugar across the membrane (muscle cell interface) utilizing chloride, zinc, and selenium. The utilization of these minerals creates glycolysis. LDH then from a physiological perspective determines pancreatic function regulating the amount of glucose into muscle. It is also important to note that sugar metabolism is very complex and does involve a series of other organs. Ranges for LDH are between 0-220; again it is rather obvious that LDH is a by-product of sugar metabolism and a 0 figure could not be construed as a low normal range. I feel that the range should start at 80. You will find many patients with a low LDH having problems with decreased function causing heart, skeletal muscle (weakness, loss of strength, muscle wasting), kidney and liver dysfunction, and eventual wasting away of these organs.	62.86
AST (SGOT) AST (SGOT) SERUM GLUTAMIC OXALACETIC TRANSAMINASE (SGOT) (AST) SGOT is highly concentrated in organs and glands of high metabolic activity and in descending order: heart, liver, skeletal muscle, brain, kidneys, pancreas, spleen and lungs. In pathological states, when you have high levels it means that cell damage has occurred in one or more of these areas and there is a release of this enzyme in circulation, elevating in 12 hours and remaining there for 5 days. In physiologic states, we know it is a tissue enzyme present in tissues of high metabolic activity, and concerned with the transfer of nitrogen between aspartic acid, and alpha-keto-glutamic acid, resulting in the synthesis of glutamic acid, alpha keto acid and oxalacetic acid. SGOT, therefore, is the catalyst that creates amino acid metabolism during glycolysis, for the production of energy. Since there are high concentrations of SGOT in skeletal muscle/heart, and the brain, it gives you an idea of the metabolic output of each system. The sex organs via the output of testosterone, estrogen, progesterone (which are formed on the gonadal epithelium by binding cholesterol to protein) are used to maintain muscle mass and strength. Therefore having a dramatic effect on muscle and nerve metabolism. Since amino acid metabolism also affects muscle mass, muscle strength, and the energy to fuel the muscular system, it is apparent that SGOT is the indicator of choice. Not to mention the energy necessary to run the central nervous system which utilizes 60 percent of the available energy necessary to run your body. Please note that most lab ranges start at 0 and since this is a measurement of the metabolic activity of the above organs 0 would mean death. The low range for SGOT should be 15. You will find physiological conditions where there are low levels of SGOT (15-20). This is due to the exhaustion of the above organs. Low levels indicated heart, skeletal muscle and diminished brain function/damage. These patients are usually physically weak/exhausted whether they exercise or not, lack mental clarity, cannot think straight and have brain fatigue/fog. They also have sex hormonal problems and require HRT or erectile dysfunction treatment. Many of these patients have a weak flabby heart, setting the stage for many types of conditions down the road. Low levels may also mean decreased liver function affecting, protein synthesis, detoxification, sluggish metabolism, cholesterol production to name a few of the 500 know liver functions.	25.71
ALT (SGPT) ALT (SGPT) SERUM GLUTAMIC PYRUVIC TRANSAMINASE (SGPT) (ALT) SGPT is primarily a liver function test. It has a maximum concentration in the liver (fatty membranes) sinusoids. Low concentrations of SGPT are also found in the kidneys, heart, and skeletal muscle. In pathological states, elevations indicate liver disease. ALT is found in serum and in various bodily tissues but is most commonly associated with the liver. It catalyzes the transfer of an amino group from alanine to alpha-ketoglutarate, and the products of this reversible transamination reaction being pyruvate and glutamate. glutamate + pyruvate ⇌ alpha-ketoglutarate + alanine Alanine transaminase delivers skeletal muscle carbon and nitrogen in the form of alanine to the liver. In skeletal muscle, pyruvate is transaminated to alanine, thus affording an additional route of nitrogen transport from muscle to liver. In the liver, alanine transaminase transfers the ammonia to A-KG and regenerates pyruvate. The pyruvate can then be diverted into gluconeogenesis. This process is referred to as the glucose-alanine cycle. The glucose-alanine cycle is used primarily as a mechanism for skeletal muscle to eliminate nitrogen as the muscles replenish their energy supply. Within the liver, alanine is converted back to pyruvate and is then a source of carbon atoms for gluconeogenesis. The newly formed glucose can then enter the bloodstream for delivery back to the muscle. The amino group transported from the muscle to the liver, in the form of alanine, is converted to urea in the urea cycle and then excreted. In physiological states SGPT is a primary kreb cycle expressant and as a result causes the release of catabolic fats. SGPT occurs in serum as a consequence of substances being released by the fatty membranes of the liver sinusoids, and lymphatic ducts. The liver sinusoids store food, and the lymphatic ducts house toxins. Picture a layer of fat that holds foods or toxins in the cell. Now as that layer of fat is being burned off, foods and toxins are being released in a controlled manner. This allows foods or toxins to be directed to their next destination. Please note that most lab ranges for this test start at 0, which in actuality is false since this is a measurement of liver function, and 0 would mean that the liver was not functioning at all. A low range then should be around 15. Therefore, from a physiological perspective, a low SGPT between 15-20 would indicate a sluggish liver causing many metabolic disturbances. Typically these people have no energy, get sick a lot, cannot tolerate food well and have a slow metabolism.	31.43
GGT GGT GAMMA GLUTAMYL TRANSPEPTIDASE (GGT) Is a biliary enzyme useful in the diagnosis of obstructive jaundice, intrahepatic cholestasis and pancreatitis. GGT is more responsive to biliary obstruction than are aspartate aminotransferase (AST) (SGOT) and alanine aminotransferase (ALT) (SGPT). 1. GGT is increased in hepatoma and carcinoma of the pancreas and useful in the diagnosis of metastatic carcinoma of the liver. Increasing levels in carcinoma patients relate to tumor progression and a dubious outcome. 1. CEA, alkaline phosphatase and GGT together are useful markers for hepatic metastasis from the breast and colon. 2. May be useful in the diagnosis of chronic alcoholic liver disease. Follow-up blood chemistries of serum GGT, AST and ALT levels can distinguish recovering alcoholics who resume drinking from those who do not. 3. Increase in body mass correlates with increased GGT levels. 4. GGT along with MCV is a useful test for alcoholism. 5. GGT is the test of choice for pregnant females who may have cholestasis. 6. GGT levels are elevated in cirrhosis and hepatitis. 7. The transaminases, AST and ALT rise higher in acute viral hepatitis; then GGT. 8. Increased in systemic lupus erythematosus GGT IS HIGH WHEN General considerations: If patient has been on a very low-fat diet for long periods of time then increase fat intake	-40
Ferritin Ferritin A ferritin test can help a doctor determine if a person has enough iron in their body. Low ferritin levels can indicate that the body doesn't have enough iron, while high levels can indicate too much iron. FERRITIN Men 20-250 ng/mL 20-250 ug/L Women 10-120 ng/mL 10-120 ug/L Children 7-140 ng/mL 7-140 ug/L Newborns 25-200 ng/mL 25-200 ug/L	-16.4
Total Iron Total Iron Total Iron Binding Capacity (TBIC)—measures the amount of transferrin, which is a blood protein that transports iron from the digestive system to cells that will be utilizing the iron. Your body produces transferrin in relationship to the body’s need for iron. When iron stores are low, transferrin levels will increase and when transferrin levels are low, too much iron is present. Usually, about one third of the transferrin is being used to transport iron at any one time. Because of this, your blood serum has considerable extra iron-binding capacity, which is called the Unsaturated Iron Biding Capacity (UIBC). The TIBC then equals UIBC plus serum iron measurement. Some laboratories may measure UIBC, some measure TIBC and others measure transferrin. TIBC is increased in iron- deficiency, acute hepatitis, during pregnancy or when oral contraceptives are used. TIBC is decreased in hypoproteinemia from many causes, cirrhosis of the liver, nephrosis and thalassemia or from a number of inflammatory states. TOTAL IRON IRON Men 65-175ug/dL 11.6-31.3 umol/L Women 50-170ug/dL 9.0 -30.4 umol/L Children 50-120ug/dL 9.0-21.5 umol/L Newborns 100-250 ug/dL 17.9-44.8 umol/L	-40				5
Cholesterol, Total Cholesterol, Total SERUM LIPIDS Serum lipids serve as a primary source of energy along with glucose. The functions are many, such as the production of cell membranes, precursors to hormones, and bile acids. Lipids are first broken down in the duodenum, along with bile, which emulsifies the fats, and prepares them for absorption into the lymphatic system. Pancreatic lipase hydrolyzes cholesterol, and triglycerides into fatty acids, and glycerol. The fatty acids and glycerol are then reconverted back into triglycerides by the intestinal cells and then discharged into the lymphatic or portal blood system, which is then sent to the liver. Cholesterol is also absorbed in both the free and esterified forms into the lymphatics. Cholesterol is also synthesized in the reticular cells and histiocytes throughout the body but mainly formed in the liver. Under the influence of iodine via the thyroid, carbohydrates, amino acids, and other fats are converted to cholesterol via multiple molecules of acetyl coenzyme A creating a sterol nucleus. Triglycerides are also assembled in the liver from glycerol and fatty acids. The liver is the main organ regulating blood lipids. So the liver can degrade fatty acids for energy, synthesize triglycerides from carbohydrates and proteins. The liver can then hydrolyzes the triglycerides back into three fatty acids, and glycerol then degrades the fatty acids into acetyl coenzyme A via beta-oxidation. Then acetyl coenzyme A is then oxidized to release ATP. The liver also synthesizes phospholipids, lecithin, cephalins (that produce thromboplastin), and sphingomyelin (produces the myelin sheath) are formed in the liver and transported via lipoproteins. An increase in triglycerides or choline/inositol increases phospholipid production. Phospholipids are also important in the production of cell membranes. CHOLESTEROL Cholesterol is a byproduct of protein metabolism. Bonding oily fat (fat-soluble vitamins) to nitrogen via oxidation forms cholesterol. This process utilizes vitamins, D, E, K, A, and T. These are your fat-soluble vitamins that are bound to the nitrogen portion of foods. The basic purpose of fat-soluble vitamins is to lubricate membranes. The vitamin (oil) prevents oxygen from reaching the membrane, which may inhibit its function. Fat-soluble vitamins also provide the substance necessary to make hormones, enzymes, and antibodies. For example, Vitamin D. lubricates all gross membranes that are exposed to air, such as your skin, respiratory passages, and the digestive membranes. This is your antioxidant lubricator Vitamin A. lubricates secondary membranes that are exposed to the blood, such as the liver, kidney, lungs and spleen. Vitamin A. is called your hydrogen lubricator. Vitamin K. lubricates cell membranes that are exposed to water. Vitamin F. fatty acids are used to make enzymes. Vitamin E. is used to make hormones. Vitamin T. which, is sesame seed oil, is used to make antibodies Lecithin prevents oil and fat from going rancid. So the purpose of fat-soluble vitamins is to oxidize and combust with protein to form cholesterol, which then transposes it into a lubricator, a hormone, antibody, or enzyme. Low-density lipoproteins are rich in cholesterol and carry some triglycerides and are used to produce sex hormones. High-density lipoproteins are rich in triglycerides and carry some fat. Please note that at any one time, the body can dictate the percentage of low-density lipoproteins vs. high-density lipoproteins. It's obvious that an imbalance can create multiple diseases in the body. Please note that these lipoproteins also engulf toxins and then are stored in tissue cells. At a later time, the body gradually detoxifies these deposits unless the amount is overwhelming. Similar to glucose, cholesterol is affected by many organs and glands and in itself is not a reliable indicator as to what is going on in the body. Over the years, the labs went from a normal cholesterol reading of 300, down to 250, then down to 200, and now down to 150. If they continue this nonsense they will create a whole new list of diseases. I recommend that your cholesterol levels be between 175-275mg/dL.	-192				5
Triglycerides Triglycerides SERUM LIPIDS Serum lipids serve as a primary source of energy along with glucose. The functions are many, such as the production of cell membranes, precursors to hormones, and bile acids. Lipids are first broken down in the duodenum, along with bile, which emulsifies the fats, and prepares them for absorption into the lymphatic system. Pancreatic lipase hydrolyzes cholesterol, and triglycerides into fatty acids, and glycerol. The fatty acids and glycerol are then reconverted back into triglycerides by the intestinal cells and then discharged into the lymphatic or portal blood system, which is then sent to the liver. Cholesterol is also absorbed in both the free and esterified forms into the lymphatics. Cholesterol is also synthesized in the reticular cells and histiocytes throughout the body but mainly formed in the liver. Under the influence of iodine via the thyroid, carbohydrates, amino acids, and other fats are converted to cholesterol via multiple molecules of acetyl coenzyme A creating a sterol nucleus. Triglycerides are also assembled in the liver from glycerol and fatty acids. The liver is the main organ regulating blood lipids. So the liver can degrade fatty acids for energy, synthesize triglycerides from carbohydrates and proteins. The liver can then hydrolyzes the triglycerides back into three fatty acids, and glycerol then degrades the fatty acids into acetyl coenzyme A via beta-oxidation. Then acetyl coenzyme A is then oxidized to release ATP. The liver also synthesizes phospholipids, lecithin, cephalins (that produce thromboplastin), and sphingomyelin (produces the myelin sheath) are formed in the liver and transported via lipoproteins. An increase in triglycerides or choline/inositol increases phospholipid production. Phospholipids are also important in the production of cell membranes. TRIGLYCERIDES Triglycerides compromise 95% of fat stored in adipose tissue and stored as glycerol, fatty acids, and monoglycerides. The liver reconvert's these back to triglycerides. 80% of your triglycerides make up VLDL, and 15% form LDL’S. From a pathological viewpoint, this test evaluates atherosclerosis and measures the bodies ability to utilize fat. From the physiologic perspective, triglycerides are nothing more than three fatty acids, and esters of glycerol. Fatty acids are composed of sugar and alcohol. Triglycerides travel with cholesterol (LDL/HDL) to combust cholesterol at the appropriate time.Triglycerides are needed for calculation of LDLC (low-density lipoprotein cholesterol) concentration. Triglycerides are the matches or “the spark” that ignites and combusts the cholesterol. Triglycerides are implanted in the cell membrane of all neurological and glandular tissue. Triglycerides create the energy for a neurological impulse to occur. When the neurological impulse occurs triglycerides actually “explode” causing the active exchange of electrolytes. Primary glands involved in triglyceride metabolism are the posterior pituitary, the hypophyseal stalk, adrenals, and the head of the pancreas.Therefore, any condition affecting these organs can affect triglyceride levels. High levels are a greater risk for a heart attack then a high cholesterol. Low triglyceride levels from the physiologic perspective cause low energy. Triglycerides Normally Range From 0-199. It Is Rather Obvious That 0 Triglycerides Could Not Be Achieved Physiologically. My Ranges Are From 75-200 mg/dL	66.4
TSH TSH T-4, T-3, T3 uptake and TSH Thyroid-stimulating hormone (TSH) from the anterior pituitary, stimulates the production of thyroxin, and triiodothyronine, therefore, having a dramatic effect on the T4/T3 test results. Thyrotrophs makeup 5% of the anterior pituitary and produce between 100-400mU/day of TSH. Circadian peaks with the onset of sleep are between 9 pm-5am and a minimum between 4-7pm. TSH is regulated by an open feedback loop via thyroxin whereby thyroxin passes into the CSF of the lateral ventricles and is taken up by the epithelial cells of the choroid plexus, which when thyroxin levels are low, stimulates TRH-secreting neurons in the hypothalamus. TSH does the following: 1. Stimulates phospholipid metabolism 2. Stimulates purine and pyrimidine precursors and their incorporation into nucleic acids. T-4 and 3 indicate the denitrification power of iodine via thyroxin with T3 being much more powerful than T4. All food contains active biological nutrients that are bound with nitrogen. When this food reaches the liver, the iodine is used to cleave the nitrogen from the nutrient. Therefore, thyroxin and T3 are important in fat and protein digestion, absorption, and growth and endocrine function. This catabolic activity begins once aerobic bound substances become totally anaerobic and lose the need for nitrogen bonding. Nitrogen is cleaved by T3 or T4 in the liver for example as in glycogen storage. Other substances are needed by specific cells and are transported via total binding globulin to the cells where at that point, the nitrogen bonds are cleaved. Less than 1% of T3 is unbound. A high T-3 uptake indicates a hypothyroid, where a low T-3 uptake indicates a hyperthyroid.	-118.96
Thyroxine (T4) Thyroxine (T4) T-4, T-3, T3 uptake and TSH Thyroid-stimulating hormone (TSH) from the anterior pituitary, stimulates the production of thyroxin, and triiodothyronine, therefore, having a dramatic effect on the T4/T3 test results. Thyrotrophs makeup 5% of the anterior pituitary and produce between 100-400mU/day of TSH. Circadian peaks with the onset of sleep are between 9 pm-5am and a minimum between 4-7pm. TSH is regulated by an open feedback loop via thyroxin whereby thyroxin passes into the CSF of the lateral ventricles and is taken up by the epithelial cells of the choroid plexus, which when thyroxin levels are low, stimulates TRH-secreting neurons in the hypothalamus. TSH does the following: 1. Stimulates phospholipid metabolism 2. Stimulates purine and pyrimidine precursors and their incorporation into nucleic acids. T-4 and 3 indicate the denitrification power of iodine via thyroxin with T3 being much more powerful than T4. All food contains active biological nutrients that are bound with nitrogen. When this food reaches the liver, the iodine is used to cleave the nitrogen from the nutrient. Therefore, thyroxin and T3 are important in fat and protein digestion, absorption, and growth and endocrine function. This catabolic activity begins once aerobic bound substances become totally anaerobic and lose the need for nitrogen bonding. Nitrogen is cleaved by T3 or T4 in the liver for example as in glycogen storage. Other substances are needed by specific cells and are transported via total binding globulin to the cells where at that point, the nitrogen bonds are cleaved. Less than 1% of T3 is unbound. A high T-3 uptake indicates a hypothyroid, where a low T-3 uptake indicates a hyperthyroid.	84						10
T3 Total T3 Total T-4, T-3, T3 uptake and TSH Thyroid-stimulating hormone (TSH) from the anterior pituitary, stimulates the production of thyroxin, and triiodothyronine, therefore, having a dramatic effect on the T4/T3 test results. Thyrotrophs makeup 5% of the anterior pituitary and produce between 100-400mU/day of TSH. Circadian peaks with the onset of sleep are between 9 pm-5am and a minimum between 4-7pm. TSH is regulated by an open feedback loop via thyroxin whereby thyroxin passes into the CSF of the lateral ventricles and is taken up by the epithelial cells of the choroid plexus, which when thyroxin levels are low, stimulates TRH-secreting neurons in the hypothalamus. TSH does the following: 1. Stimulates phospholipid metabolism 2. Stimulates purine and pyrimidine precursors and their incorporation into nucleic acids. T-4 and 3 indicate the denitrification power of iodine via thyroxin with T3 being much more powerful than T4. All food contains active biological nutrients that are bound with nitrogen. When this food reaches the liver, the iodine is used to cleave the nitrogen from the nutrient. Therefore, thyroxin and T3 are important in fat and protein digestion, absorption, and growth and endocrine function. This catabolic activity begins once aerobic bound substances become totally anaerobic and lose the need for nitrogen bonding. Nitrogen is cleaved by T3 or T4 in the liver for example as in glycogen storage. Other substances are needed by specific cells and are transported via total binding globulin to the cells where at that point, the nitrogen bonds are cleaved. Less than 1% of T3 is unbound. A high T-3 uptake indicates a hypothyroid, where a low T-3 uptake indicates a hyperthyroid.	-43.33						10
T3 Uptake T3 Uptake T-4, T-3, T3 uptake and TSH Thyroid-stimulating hormone (TSH) from the anterior pituitary, stimulates the production of thyroxin, and triiodothyronine, therefore, having a dramatic effect on the T4/T3 test results. Thyrotrophs makeup 5% of the anterior pituitary and produce between 100-400mU/day of TSH. Circadian peaks with the onset of sleep are between 9 pm-5am and a minimum between 4-7pm. TSH is regulated by an open feedback loop via thyroxin whereby thyroxin passes into the CSF of the lateral ventricles and is taken up by the epithelial cells of the choroid plexus, which when thyroxin levels are low, stimulates TRH-secreting neurons in the hypothalamus. TSH does the following: 1. Stimulates phospholipid metabolism 2. Stimulates purine and pyrimidine precursors and their incorporation into nucleic acids. T-4 and 3 indicate the denitrification power of iodine via thyroxin with T3 being much more powerful than T4. All food contains active biological nutrients that are bound with nitrogen. When this food reaches the liver, the iodine is used to cleave the nitrogen from the nutrient. Therefore, thyroxin and T3 are important in fat and protein digestion, absorption, and growth and endocrine function. This catabolic activity begins once aerobic bound substances become totally anaerobic and lose the need for nitrogen bonding. Nitrogen is cleaved by T3 or T4 in the liver for example as in glycogen storage. Other substances are needed by specific cells and are transported via total binding globulin to the cells where at that point, the nitrogen bonds are cleaved. Less than 1% of T3 is unbound. A high T-3 uptake indicates a hypothyroid, where a low T-3 uptake indicates a hyperthyroid.						10
T3 Free T3 Free A free T3 test, or free triiodothyronine test, measures the amount of free triiodothyronine in your blood. Triiodothyronine (T3) is a hormone produced by the thyroid gland that helps regulate metabolism and energy levels. A normal free T3 level is typically between 2.5–4.0 ng/dL, but reference values may vary by lab. A higher-than-normal level of T3 may indicate an overactive thyroid, while a lower-than-normal level may indicate an underactive thyroid.	5.26
T4 Free T4 Free Free T4 is the amount of thyroxine (T4) in the blood that is not attached to proteins. T4 is a hormone produced by the thyroid gland that helps control metabolism and growth. A free T4 test measures the amount of free T4 in your blood.	86.21
Urine pH Urine pH URINE PH A high urine pH may be due to: Kidney failure Urinary tract infections Vomiting A low urine pH may be due to: Diarrhea Too much acid in the body fluids such as metabolic acidosis and diabetic ketoacidosis Starvation	-100
Bun/Creatin Ratio Bun/Creatin Ratio BUN/CREATININE RATIO BUN plus creatinine are residue byproducts of protein and muscle metabolism respectively. They are kept in continual balance by the water content of your body. The kidneys flush out the excessive BUN/creatinine concentration when it gets too high. The kidneys are under the influence of the posterior pituitary via antidiuretic hormone, which regulates the amount of water leaving the body. Therefore, the posterior pituitary through potassium regulates water balance. The posterior pituitary then regulates the amount of water in any one place of the body. So, therefore, it can either increase or decrease the water content in the blood, thus altering pH. The posterior pituitary besides balancing water also regulates sugar and mineral concentration. BUN/CREATININE IS HIGH WHEN General considerations: ¬ Decrease high protein intake ¬ Or increase water intake ¬ BUN/CREATININE is high when you have a high BUN or a low CREATININE or both BUN/CREATININE IS DECREASED WHEN General considerations: ¬ Increase protein intake ¬ Or decrease water intake ¬ BUN/CREATININE is low when either you have a low BUN or a high CREATININE or both	203.58	5
COQ10 Coenzyme COQ10 Coenzyme Coenzyme Q10 (CoQ10 also known as ubiquinone, is a natural coenzyme and an antioxidant produced by the body. It is also obtained from dietary sources, such as meat, fish, seed oils, vegetables, and dietary supplements. CoQ10 plays a role in mitochondrial oxidative phosphorylation, aidingthe production of adenosine triphosphate (ATP), which is involved in energy transfer within cells. The structure of CoQ10 consists of a benzoquinone moiety and an isoprenoid side chain, with the "10" referring to the number of isoprenyl chemical subunits in its tail. Biological function CoQ10 is a component of the mitochondrial electron transport chain (ETC), where it plays a role in oxidative phosphorylation, a process required for the biosynthesis of adenosine triphosphate, the primary energy source of cells. CoQ10 is a lipophilic molecule that is located in all biological membranes of the human body and serves as a component for the synthesis of ATP and is a life-sustaining cofactor for the three complexes (complex I, complex II, and complex III) of the ETC in the mitochondria. CoQ10 has a role in the transport of protons across lysosomal membranes to regulate pH in lysosome functions. The mitochondrial oxidative phosphorylation process occurs in the inner mitochondrial membrane of eukaryotic cells. This membrane is highly folded into structures called cristae, which increase the surface area available for oxidative phosphorylation. CoQ10 plays a role in this process as an essential cofactor of the ETC located in the inner mitochondrial membrane and serves the following functions: electron transport in the mitochondrial ETC, by shuttling electrons from mitochondrial complexes like nicotinamide adenine dinucleotide (NADH), ubiquinone reductase (complex I), and succinate ubiquinone reductase (complex II), the fatty acids and branched-chain amino acids oxidation (through flavin-linked dehydrogenases) to ubiquinol–cytochrome-c reductase (complex III) of the ETC: CoQ10 participates in fatty acid and glucose metabolism by transferring electrons generated from the reduction of fatty acids and glucose to electron acceptors; antioxidant activity as a lipid-soluble antioxidant together with vitamin E, scavenging reactive oxygen species and protecting cells against oxidative stress, inhibiting the oxidation of proteins, DNA, and use of vitamin E.
Fibrinogen Fibrinogen FIBRINOGEN- BLOOD TEST RANGES 200 and 400 mg/dL (2.0 to 4.0 g/L) (coagulation factor I) is a glycoprotein complex that is synthesized by the liver and circulates in the blood stream. During tissue and or vascular injury, it is converted enzymatically by thrombin to fibrin which creates a blood clot The primary function is to occlude blood vessels thus stopping bleeding. Fibrin also binds and reduces the activity of thrombin. This activity referred to as antithrombin I, which limits clot formation. Fibrin also mediates and is important in blood platelet, endothelial cell spreading, capillary tube formation, tissue fibroblast proliferation, and angiogenesis thereby promoting revascularization and wound healing. Thrombin is synthesized in the liver and secreted into the general circulation in an inactive zymogen form (prothrombin), a complex multidomain glycoprotein that is activated to yield thrombin at sites of vascular injury by limited proteolysis following upstream activation of the coagulation cascade.
LPA LPA LPA- BLOOD TEST LEVELS 30-50 mg/dL (75-125 nmol/L Lipoprotein (a) or Lp(a) levels are measured in milligrams per deciliter (mg/dL) or nanomoles per liter (nmol/L). A lipoprotein(a) (Lp(a)) blood test measures the amount of Lp(a) in your blood, which is lipoprotein that carries cholesterol. Thus elevated Lp(a) levels are associated with an increased risk of cardiovascular disease. Recommended for individuals with a family history of heart disease or other risk factors. High levels of lipoprotein (a) (Lp(a), may cause heart attack, stroke, and or aortic stenosis LPA is produced through multiple mechanisms within cells and in biological fluids like plasma and serum. Lysophosphatidic acid (LPA) is primarily produced by the enzyme autotaxin (ATX). ATX, which is a secreted lysophospholipase D, converts lysophospholipids, primarily lysophosphatidylcholine (LPC), into LPA. This extracellular production pathway is considered the major source of bioactive LPA.
Apo B Apo B Apolipoprotein B (ApoB) is a protein that plays a crucial role in the transport of fats and cholesterol in the blood. It is a key component of low-density lipoproteins (LDL) and other lipoproteins that carry triglycerides, cholesterol, and cholesterol esters. Elevated ApoB levels are associated with an increased risk of cardiovascular disease. Key aspects of ApoB: Role in Lipoprotein Formation: ApoB is a primary protein on the surface of various lipoproteins, including LDL, VLDL, chylomicrons, and lipoprotein(a). Atherogenic Particle Indicator: ApoB measurement helps determine the number of atherogenic particles circulating in the bloodstream, which are linked to plaque buildup in arteries. Cardiovascular Risk: Elevated ApoB levels are a significant indicator of increased cardiovascular risk, particularly atherosclerosis. ApoB Test: An ApoB test measures the amount of ApoB in the blood and is often used to assess the risk of heart disease. Two Forms: ApoB exists in two forms: ApoB100 (primarily in the liver) and ApoB48 (primarily in the intestine). Apo High levels of apolipoprotein B (ApoB) are often associated with elevated levels of LDL cholesterol (LDL-C) and can be caused by a variety of factors, including diet, lifestyle, underlying medical conditions, and genetics.
Gland Totals		25	20	25	25	20	35
Gland Totals (%)		81.4%	55%	358.4%	79.8%	454%	87.14%

Results by Membarnes

Gland	Result
Serous Membranes Serous Membranes	456%
Mucous Membranes Mucous Membranes	304%

Show Expanded

#		Mucous Membranes	Serous Membranes
Glucose Glucose GLUCOSE Glucose is an important fuel for the body, which affects all tissues, organs, and systems. Glucose also affects the acid/alkaline balance in the body. Breakdown of glucose or starch starts in the mouth via ptyalin, then in the stomach via HCL, and then by pancreatic amylase, lactase and other enzymes. Glucose is then absorbed in the small intestines and is then stored as glycogen in the liver. The liver is the primary site of glucose production. The liver converts lactic acid to glycogen and back to glucose via epinephrine. The liver converts fats and proteins via gluconeogenesis into glucose or glycogen. The head of the pancreas controls chromium, which controls insulin levels and assists in the enzyme action of fats via bile salts. The tail of the pancreas controls zinc, which maintains and sustains levels of insulin. Blood sugar depends on: 1. The liver which stores and releases glycogen 2. The pancreas, which produces insulin that transfers sugar from the blood to the extracellular fluid 3. The adrenal glands, which produced glucocorticoids that, cause the liver to release glycogen into the blood as glucose 4. The sex organs, which deliver the extracellular glucose to the cell 5. The thyroid, which affects the storage of glycogen in the liver 6. The thymus and spleen, which affect the levels of iron and copper in the liver which, determine the liver's ability to handle glucose As you can see there are many organs, or combinations of these organs and glands, which affect glucose levels in the body. Therefore, glucose in itself cannot specifically determine where the problem may lie. Other indicators are necessary to pinpoint the problem.	-28
Uric Acid Uric Acid URIC ACID Uric acid is the principal end product of purine, nucleic acid, and nucleoprotein metabolism. Uric acid is transported by the blood from the liver to the kidney’s which filter out and secretes about 70% and the remainder excreted via the GI tract. From a pathological view, uric acid is elevated when there is cell breakdown as in leukemia and catabolism of nucleic acids as in gout, or removal via the kidneys is decreased due to renal failure. From a physiologic view, we look at every level of protein combustion where there remain two by-products which are a Mucous (oily residue) and Uric acid (carbon ash) In order for protein to be fully combusted, it must first be influenced in the duodenum by trypsin, chymotrypsin, carboxypolypeptidase, and bile emulsification. Trypsin and chymotrypsin cleave proteins into peptides and carboxypolypeptidase split the peptides into amino acids. The pancreas synthesizes trypsinogen, chymotrypsinogen, and procarboxypolypeptidase, which are enzymatically inactive. When they are released into the duodenum they are all activated by enterokinase. Which now readies the proteins for assimilation in the liver. Therefore, if the proteins are not prepared properly the two end products, uric acid, and mucous, will be out of balance. URIC ACID IS HIGH WHEN General considerations: ¬ Decrease fatty proteins and rich foods ¬ Decrease alcohol and simple sugars ¬ Increase water intake	303.64	5
Bun Bun BLOOD UREA NITROGEN Blood urea nitrogen is formed entirely by liver deamination from protein metabolism. BUN is a byproduct due to the release of nitrogen bonds (and measures the nitrogen portion of urea) from protein substances in the liver. From a pathological perspective, an increased blood urea nitrogen would indicate renal disease, tissue necrosis, increased adrenal gland activity, and rapid protein catabolism. From a physiologic perspective, the purpose of nitrogen is to carry a substance through an aerobic media preventing oxidation, and eventually back into an anaerobic environment. Once in the liver the thyroid through the use of iodine, releases the nitrogen bond, releasing the nitrogen from the protein, allowing the protein to combust into hormones, enzymes and antibodies. The adrenals and anterior pituitary play a vital role in the combustion of this protein. The urea is now sent to the kidneys and is converted into urine. Urea is produced when amino acids, which are not used for protein synthesis, are broken down via hepatic metabolism. These amino acids are de-aminated producing ammonia, which is converted to urea immediately since ammonia levels become toxic. When this metabolic conversion is affected due to faulty metabolism or liver disease ammonia is not converted causing excessive levels of ammonia with possible hepatic encephalopathy. Renal malfunction/failure may also cause a high BUN due to its affect on the removal of urea causing uremia. Uremic wastes usually impair platelet function, and patients may show an increased tendency towards bleeding. BUN IS HIGH WHEN General considerations: ¬ High protein diets can cause increased BUN ¬ Increase water intake if no edema	880.95
Creatinine Creatinine CREATININE Creatinine ash is a basic byproduct in the breakdown of muscle creatine phosphate resulting from energy metabolism. From a pathological perspective the kidneys primarily remove creatinine and when there are elevated levels it indicates reduced kidney function. Thus creatine levels give an approximate for the GFR. From a physiological perspective, creatine is a by-product of actin metabolism after being exposed to acetylcholine combustion. The actin fiber joins two stable protein blocks (myosin), which combusts to produce muscle contraction, primarily for activity and secondarily for tonicity. During a muscle contraction, an action potential travels along a motor nerve to a muscle fiber. Acetylcholine is released at the motor endplate, causing multiple acetylcholine lined gated protein channels to open. This causes sodium ions to flow to the interior of the muscle, which initiates an action potential of that muscle. This then leads to depolarization releasing large amounts of calcium into the myofibrils. This initiates a contractive force between the actin and myosin filaments via ATP causing them to slide together, which is the contractile process. After a fraction of a second, calcium is pumped back into the sarcoplasmic reticulum, until the next muscle contraction. The actin fiber is then oxidized (H displaced) via acetylcholine, leaving an oily waxy residue known as creatinine. GABA (Glutamic amino benzoic acid), which is part of the actin fiber, helps it burn better. Creatine becomes creatinine with the release of ATP. Low creatinine levels would indicate muscle loss and weakness.	455.56		5
Sodium Sodium ELECTROLYTES The blood electrolytes include sodium, potassium, chloride, and the bicarbonate (HCO3) ion. Sodium, potassium, and chloride enter the body via ingestion of food. Carbon dioxide, on the other hand, originates within the body via the metabolic process of carbohydrates, fats, and proteins. Normally the excretion of sodium, potassium, and water is equal to their intake. The kidneys secrete 80-90 percent of all electrolytes. Excessive carbon dioxide stimulates the respiratory centers in the brainstem to increase respiration. Therefore, the kidneys and the lungs control sodium, chloride, potassium, water, and carbon dioxide thus exerting control over the acid/alkaline balance in the body. There are also many other organs, and glands involved in this process, such as the posterior pituitary, adrenals, bowel, and uterus/prostate. The purpose of electrolytes is to set up a shifting mechanism in the cell membrane via oxidation, allowing increased or decreased permeability to that membrane site. Sodium, which is found in high concentration outside the cell, has the ability to gather up substances (foods) and bring them to active membrane sites. Chloride is found in the cell membrane and acts as a “doorman” allowing or disallowing exchanges between the intracellular and extracellular fluids. Potassium, which is found in high concentrations within cells, oxidizes chloride, and allows sodium, with the food to cross the cell membrane and enter the cell. Sodium, potassium, chloride, calcium, and hydrogen are all transported via active transport. SODIUM Sodium is the most abundant cation (90%) and is the major base in the body. Sodium is either implanted into the food via saliva or is found in the food and has the following functions: 1. Sodium is an alkaline mineral that helps maintain alkaline activity. Therefore, it helps in acid-alkaline balance, which affect intracellular/extracellular fluid exchange, osmotic pressure, via the sodium/potassium pump and does this in conjunction with antidiuretic hormone and aldosterone. 2. Sodium gathers, and aggregates (polarizes) all substances necessary to be exchanged by semi-permeable membranes. Sodium pumps proteins and sugars into the cell membranes. 3. Sodium also affects the renal tubules for the activity of discharging toxins. It literally aggregates toxins and holds them in suspension. 4. Sodium is controlled by the adrenal cortex and as mentioned above is extremely alkaline and therefore, can cause migration of substances towards its polarity, as well as causing these migrated substances to achieve permeability in an acid antioxidant type media known as a fatty membrane. Sodium is the substance necessary to polarize foods into storage according to that permeable membranes needs. 5. Sodium is also necessary for the transmission of neurological impulses by creating action potentials across neurological membranes. 6. Sodium concentration in and out of cells remains constant due to renal blood flow, carbonic anhydrase enzyme activity, aldosterone, and other steroids controlled by the anterior pituitary, rennin enzyme secretion, hypothalamus, and posterior pituitary control of ADH and vasopressin secretion	-33.33
Potassium Potassium ELECTROLYTES The blood electrolytes include sodium, potassium, chloride, and the bicarbonate (HCO3) ion. Sodium, potassium, and chloride enter the body via ingestion of food. Carbon dioxide, on the other hand, originates within the body via the metabolic process of carbohydrates, fats, and proteins. Normally the excretion of sodium, potassium, and water is equal to their intake. The kidneys secrete 80-90 percent of all electrolytes. Excessive carbon dioxide stimulates the respiratory centers in the brainstem to increase respiration. Therefore, the kidneys and the lungs control sodium, chloride, potassium, water, and carbon dioxide thus exerting control over the acid/alkaline balance in the body. There are also many other organs, and glands involved in this process, such as the posterior pituitary, adrenals, bowel, and uterus/prostate. The purpose of electrolytes is to set up a shifting mechanism in the cell membrane via oxidation, allowing increased or decreased permeability to that membrane site. Sodium, which is found in high concentration outside the cell, has the ability to gather up substances (foods), and bring them to active membrane sites. Chloride is found in the cell membrane and acts as a “doorman” allowing or disallowing exchanges between the intracellular and extracellular fluids. Potassium, which is found in high concentrations within cells, oxidizes chloride, and allows sodium, with the food to cross the cell membrane and enter the cell. Sodium, potassium, chloride, calcium, and hydrogen are all transported via active transport. POTASSIUM Potassium is intracellular, lining the inside of all cell membranes and affecting intracellular fluids, osmotic pressure, buffering viscosity (potassium bicarbonate is the primary intracellular inorganic buffer). When there is a decrease in potassium bicarbonate you have acid cells, which excites the respiratory centers so the patient hyperventilates. Metabolic acidosis or diabetic ketoacidosis drives potassium out of the cells, affecting electrolyte balance, water retention and carbon dioxide transport in red blood cells. Potassium is responsible via the posterior pituitary for oxidizing secondary hydrogen chloride (affecting adrenal function), allowing the sodium-aggregated substances to cross the cell membrane by affecting the membranes permeability. Potassium is the only substance, which allows oxygen into unoxygenated tissue. About 90% of the body’s potassium supply is intracellular with only a small percent in the serum. 80% of that is found in the muscles (used for muscular contraction) and in the bones. Potassium levels are regulated by the Na/K ATPase pump which requires magnesium for proper function. Potassium is necessary for proper function of mineralocorticoids, (aldosterone and deoxycorticosterone) thus maintaining sodium concentration and alkaline reserve. Therefore, potassium is of great value to the posterior pituitary (ADH/oxytocin), the pineal, and the adrenal cortex via aldosterone secretion. Potassium along with sodium regulate renal acid-base balance, by substituting hydrogen ions for sodium and potassium in the renal tubules. Potassium also facilitates oxygen to the myocardium and oxidizes the S.A. node of the heart. The heart has the highest potassium concentration in the body. Potassium along with calcium and magnesium controls the rate and force of contraction in heart muscle. It is the primary oxidizer of the body capable of expressing all cellular needs. Potassium also regulates neurological impulses via osmotic pressure gradients throughout the nervous system. Potassium directs carbohydrate digestion by polarizing minerals associated with carbohydrate digestion, from the time the carbohydrate enters the body until the cell utilizes it. Potassium also makes proteins soluble and regulates protein synthesis. 80-90 percent of potassium in the cells is excreted by the kidneys (resulting in the loss of 40-50 mEq/L per day even during fasting) with the remainder excreted by the stool and through sweating POTASSIUM IS LOW WHEN General considerations: ¬ Increase water intake ¬ Increase magnesium intake ¬ Decrease calcium intake ¬ Increase potassium intake ¬ Decrease carbohydrate intake	-50
Chloride Chloride ELECTROLYTES The blood electrolytes include sodium, potassium, chloride, and the bicarbonate (HCO3) ion. Sodium, potassium, and chloride enter the body via ingestion of food. Carbon dioxide, on the other hand, originates within the body via the metabolic process of carbohydrates, fats, and proteins. Normally the excretion of sodium, potassium, and water is equal to their intake. The kidneys secrete 80-90 percent of all electrolytes. Excessive carbon dioxide stimulates the respiratory centers in the brainstem to increase respiration. Therefore, the kidneys and the lungs control sodium, chloride, potassium, water, and carbon dioxide thus exerting control over the acid/alkaline balance in the body. There are also many other organs, and glands involved in this process, such as the posterior pituitary, adrenals, bowel, and uterus/prostate. The purpose of electrolytes is to set up a shifting mechanism in the cell membrane via oxidation, allowing increased or decreased permeability to that membrane site. Sodium, which is found in high concentration outside the cell, has the ability to gather up substances (foods) and bring them to active membrane sites. Chloride is found in the cell membrane and acts as a “doorman” allowing or disallowing exchanges between the intracellular and extracellular fluids. Potassium, which is found in high concentrations within cells, oxidizes chloride, and allows sodium, with the food to cross the cell membrane and enter the cell. Sodium, potassium, chloride, calcium, and hydrogen are all transported via active transport. CHLORIDE Chloride a blood electrolyte, and is the major anion and exists in the extracellular spaces as part of the sodium chloride or HCl molecules. Chloride is used for assessing pH, and electrolyte balance. From a physiologic perspective, the primary purpose of chloride is to regulate the quantity of carbohydrates and proteins entering into the cells, by inhibiting the exchange of mineral controlled substances across the cell membrane and responds to the oxidative power of potassium. Chloride the major anion is predominantly found in the extracellular spaces as part of sodium chloride or in the stomach as hydrochloric acid. Chloride maintains cellular integrity by its influence on acid-base and water balance as well as osmotic pressure. Chloride has a reciprocal power with other anions by decreasing or increasing when there are too many or not enough anions. Aldosterone has a direct effect of reabsorption of sodium and an indirect effect on the increased absorption of chloride. Chlorides are lost via the GI tract through vomiting or diarrhea and thru the kidneys during times of diuresis. Chloride also responds to the antioxidant media (cell membrane) by mobilizing, and collecting sodium/food aggregates on a selectively permeable basis. This reaction is under the influence of the adrenal medulla/epinephrine/norepinephrine thereby maintaining energy stores. Chloride also assists in the production of HCl via the chief cells in the stomach. In the bowel, chloride is important in preventing the passage of water out of the body. Therefore, chloride literally blocks the flow of water/gas exchange across a cell membrane. This is extremely important in the intestines and bladder. Chloride plays a vital role during the conduction of a neurological impulse where sodium lines up on the outside of a cell membrane, and potassium on the inside of the cell membrane, during the resting stage or polarized state. In a normal nerve fiber, the permeability of the membrane to potassium is about 100 times that of sodium. The sodium-potassium pump moves three sodium ions to the exterior of the cell, for every two potassium ions that are moved to the interior of the cell, creating a net positive charge to the outside of the cell membrane for each revolution of the sodium-potassium pump. This creates a positively charged external membrane and a negatively charged internal membrane, which sets up a membrane electrical potential. As a neurological impulse is transmitted down the nerve, (which is the excitation phase of an impulse), sodium crosses the cell membrane, and enters into the cell, while potassium moves to the external portion of the membrane. This then creates the depolarization of the cell membrane, thereby creating a negative charge on the outside, and a positive charge on the inside. The transmission of each impulse along the nerve fiber reduces infinitesimally as the concentration differences of sodium and potassium between the inside and outside of the cell membrane change slightly. In so doing allows the nerve fiber to transmit between 100, 000 to 50, 000, 000 impulses before the concentration differences are rundown. As the neurological impulse passes, the sodium-potassium ATPase pump re-establishes the sodium-potassium ratio back to normal (repolarization). The pumping activity is dramatically increased approximately eightfold to restore the membrane back to the polarized state. The chloride shift to the inside of the cell membrane during the final stages makes the inside of the cell, even more, negative, which further helps repolarize the cell. Chloride generally increases and decreases with plasma or serum sodium levels. CHLORIDE IS HIGH WHEN General considerations: ¬ Drink plenty of water ¬ Decrease sodium levels ¬ Increase fat-soluble vitamins D, E, K, and A	-38.46
CO2 CO2 CARBON DIOXIDE Carbon dioxide is created as a byproduct when potassium forces water into fat. So carbon dioxide is the acid gas factor, which binds fats and selenium creating the intelligent metabolic activity between the water and fat. 80-90 percent of the carbon dioxide found in plasma is bound to protein and is represented as bicarbonate ions (HCO3-) which first exists in the extracellular spaces as CO2 then as H2CO3 and finally is buffered by the plasma and erythrocytes into sodium bicarbonate NaHCO3) and is regulated by the kidneys. The other 10 to 20 percent is dissolved CO2 gas (removed by the lungs), which is bound to protein as CO3 (2), and carbonic acid (H2CO3). The total CO2 comes from dissolved CO2, H2CO3, HCO3- and carbaminohemoglobin (CO2HHb). This occurs in the following way, carbon dioxide in the blood reacts with water in the red blood cells to form carbonic acid. In the blood cells, there is an enzyme called carbonic anhydrase that catalyzes the water and carbon dioxide 5,000 fold, creating a rapid exchange into carbonic acid. This allows tremendous amounts of carbon dioxide reacting with the water in the red blood cells, even before the blood leaves the tissue capillaries. So a red blood cell creates carbonic acid from water and carbon dioxide. In another small fraction of a second, the carbonic acid formed in the red blood cell now disassociates into hydrogen and bicarbonate ions. The hydrogen ions combine with hemoglobin, as the bicarbonate ions diffuse out into the plasma while chloride ions diffuse into the red blood cells taking the place of the bicarbonate ions. This is made possible by the presence of a bicarbonate/chloride carrier protein in the red blood cell membrane, which acts as a shuttle for these two ions. Thus, the chloride content of venous red blood cells is greater than that of arterial cells. This is known as the chloride shift. In addition, carbon dioxide can react directly with hemoglobin to form the compound carbaminohemoglobin. This carbaminohemoglobin creates the reversible reaction releasing carbon dioxide into the alveoli of the lungs. Carbon dioxide then is the venous capillary exchange product after diffusion takes place. The active pressure intake of oxygen relies upon this diffusion. This active process realizes the ability of forced metabolism and is the ash byproduct. Carbon dioxide is vital to pH balance and is controlled by the respiratory, renal, and posterior pituitary adrenal axis. Therefore, any of these glands or organs or combinations thereof can affect carbon dioxide levels. CARBON DIOXIDE IS HIGH WHEN General considerations: ¬ Water loss- increase water intake ¬ Protein loss- increase protein intake ¬ Hypomagnesemia or hypokalemia causes increased CO2- increase potassium and magnesium CARBON DIOXIDE IS LOW WHEN ¬ Water loss- increase water intake ¬ Hypermagnesemia or hyperkalemia causes decreased CO2- decrease potassium and magnesium support	-16.67
Calcium Calcium CALCIUM Calcium is the largest most nonpolar, alkaline and most abundant of all minerals with 99% of all calcium found in the bones and teeth. Calcium exists in the ionized state 55 percent of the time and 45 percent of the time in the non-diffusible state, bound to either albumin, prealbumin or thyroglobulin. Therefore, if there is a decrease in serum albumin then there will be a decrease in serum calcium. Calcium has many functions: ¬ Provides the mobilizing factor in trauma, infections and stress for tissue repair, along with vitamins A, C, manganese, phosphorus, and fatty acids. ¬ Causes vasoconstriction, while potassium, sodium, magnesium, hydrogen ions, and carbon dioxide cause vasodilatation. ¬ Is necessary for bone formation along with phosphorus, collagen, hydroxyapatite (gives bone its hardness) and bone salts of magnesium, sodium, potassium, carbonate, uranium, plutonium, and strontium. ¬ Calcium is used to create action potentials across smooth and striated muscles leading to contraction. ¬ Calcium is used as an intracellular communicator via calcium ion gated channels. ¬ Calcium collects and gather up lipoproteins, and move them across the intestinal membrane. Attaches to oils, fats, fatty acids and waxes. Calcium is absorbed in the upper portion of the small intestines (duodeneum), and the amount absorbed depends on the "acidity" of the intestinal content, via phosphorylation and protein content. When the ratio of calcium to magnesium (which is found in the intestinal membrane as well as cell membranes) is greater than 2-1, fat is drawn through the intestinal and cell membranes. Calcium also requires vitamin D. and HCl for optimal metabolism. The glands involved with calcium are: 1. The stomach via the release of HCL, which affects the preparation and absorption of calcium. 2. The parathyroids- via parathormone control of calcium ion concentration by controlling intestinal absorption, excretion via the kidneys and the release of calcium from the bones. 3. The liver/gallbladder- via bile emulsification of lipoproteins, preparing them for intestinal absorption. 4. The spleen- which stores and ages fats or lipoproteins. 5. The parotids- due to their ability to program foodstuffs. 6. The thyroid glands-via "calcitonin", promoting deposition of calcium in the bones, while decreasing calcium concentration in the extra-cellular fluids and the blood. 7. The anterior pituitary via its control of magnesium regulating calcium uptake, which regulates protein transport thru the cell membranes. 8. The pancreas- via its ability to oxidize fatty acids Therefore, any of the above glands or organs or combinations thereof has a great impact on calcium levels. CALCIUM IS HIGH WHEN General considerations ¬ Your patient should drink plenty of water ¬ Make sure they are not hypervitaminosis on Vitamins A or D ¬ Very high protein diets may increase calcium levels ¬ Magnesium and phosphates may also increase calcium levels ¬ Using sea salt can help to reduce calcium levels. CALCIUM IS LOW WHEN General considerations: ¬ Increase Vitamin A and D intake ¬ Increase albumin and protein intake ¬ Increase magnesium intake ¬ Increase phosphorus	-13.04
Phosphorus Phosphorus PHOSPHORUS 85% of the total phosphorus exists as phosphates or esters in the body and is found chiefly in the skeleton and is combined with calcium. 14% of the phosphorus is found in intracellular tissues and 1 % is found in the extracellular fluid. Therefore phosphorus levels are a poor indicator of levels of phosphates in the body. Phosphorus runs inversely to calcium levels in the body at a calcium to phosphorus ratio of 10 to 4. Therefore, calcium can be a great indicator for phosphorus as well. As calcium levels increase in the serum, phosphorus levels decrease, and when calcium levels decrease phosphorus levels increase. In fact, causes of high calcium also cause low phosphorus. The controlling factor of phosphorus is parathormone (PTH), which is also the calcium-controlling factor. Phosphorus helps calcium through the cell membrane by increasing the permeability of the cell membrane via oxygen displacement. 1. Phosphorus is responsible for growth and development by way of: ✓ bonding ✓ polymer function ✓ hydration ✓ chemical transport, and ✓ buffering 2. Phosphorus is also responsible for bone formation 3. Phosphorus and metabolism of glucose Phosphorus is also required for the metabolism of glucose via phosphorylation. Phosphorylation is when a phosphate radical promoted by glucokinase in the liver, or hexokinase in other cells captures the glucose and once inside the cells keeps it there. The exception to this occurs in the liver, the kidneys, and the intestinal epithelial cells. Ingestion of carbohydrates causes phosphorus to enter RBC’s with glucose causing a reduction of serum phosphorus levels and lipids. Phosphorus also works in the stomach to stabilize sugars and activate starches by the twofold process of phosphorylation. Phosphorylation and its counterpart, dephosphorylation, turn many protein enzymes on and off, thereby altering their function and activity. By altering pepsin/HCL levels phosphorus can: a. Stabilize simple sugars-simple sugars are easily oxidized (combusted) before they reach the liver, resulting in low sugar levels. Pepsin stabilizes these simple sugars, so they can be transferred to the liver for storage. b. Activation of starches- HCl is necessary to breakdown oily carbohydrates (grains), which are difficult to oxidize (combust). Thus making them readily available for oxidation. The above two mechanisms establish an HCl-pepsin balance in the stomach for proper pH digestion. The presence of both HCl and pepsin in the stomach are critical for preparing carbohydrates, as well as proteins for further digestion in the small intestines. 4. The regulation and maintenance of the acid-base balance in the body by maintaining glandular acidity. 5. The storage and transfer of energy from one part of the body to the other. 6. Used in the Production of phospholipids (90 % produced by the liver): lecithin, A cephalin, and sphingomyelin Phospholipids are necessary for: Proper brain function (sphingomyelins) Phospholipids are a major constituent of lipoproteins which can affect function, formation and transport of these lipoproteins causing serious cholesterol abnormalities Production of cell membranes Thromboplastin production produced from A cephalin 7. Intracellular phosphorus is used for: Energy transport formation of ATP from ADP and creatine phosphate via oxidative phosphorylation. Major constituent of plasma membranes (phospholipids) Major constituent of DNA and RNA (nucleic acids) Calcium transport and osmotic fluid pressure General nutritional considerations when phosphorus is high: 1. Patient should increase water intake 2. Reduce fat intake 3. Reduce Vitamin D intake if overdosing 4. An isotonic saline solution (sea salt) will decrease phosphorus levels 5. Also, decrease phosphorus in the diet and add calcium carbonate to your diet General considerations when phosphorous is low: 1. Vitamin D deficiency 2. Calcium deficiency 3. Magnesium deficiency 4. Patient needs a high protein diet	270
Magnesium Magnesium MAGNESIUM Serum magnesium constitutes only a small fraction of the total body stores and may not predict magnesium status correctly. From a physiologic perspective, magnesium directs protein digestion, by polarizing minerals associated with protein digestion, from the entrance of protein into the body to its final deposition in the cell. Approximately 40-60 % of the magnesium is found in the skeleton for bone formation, 20% is found in the muscle, 30% is found in the intracellular cytoplasm, with only 1 % of the magnesium found in the serum. Magnesium affects membrane permeability, nerve impulses, muscle contraction, intracellular fluid regulation, activation of enzyme systems, where magnesium acts as a metallic cofactor in over 300 enzymatic reactions. Regulates protein synthesis, carbohydrate metabolism, nucleic acid synthesis, and blood viscosity. Magnesium along with sodium, potassium and calcium regulate neuromuscular irritability and the mechanism for clotting. Less then 2% of calcium, magnesium and phosphates are found in the plasma and extracellular fluid and are controlled in narrow limits. Albumin accounts for 70% of the bound calcium. Magnesium also binds to albumin and since it has a lower specificity for the receptors it creates more free magnesium in the plasma. Magnesium and calcium are very much linked in their body functions and a deficiency in either one will have an adverse affect on the other. Especially since calcium needs magnesium to be absorbed thru the intestinal membrane as well as needing magnesium for calcium metabolism. For example, a magnesium deficiency will cause calcium to migrate out of the bone and into soft tissues such as the aorta and kidneys. 95% of all magnesium that is filtered thru the glomerulus is reabsorbed by the tubules where parathormone enhances tubular reabsorption of magnesium. When there is a deficiency of magnesium you will see a decrease in urine stores before serum stores. Please note that even when magnesium is in a 20% depleted state, magnesium levels in the serum will appear normal. Calcium, magnesium and phosphates continuously enter the plasma via the kidney, the intestinal brush borders, and the ruffled border from the bones. Steady states of calcium, magnesium, and phosphorus approximate urine loss against intestinal absorption and skeletal mineral apposition against mineral absorption. Magnesium in the cells is complexed to phosphates, citrates and anions such as ATP, AMP and ADP (such as MgATP2-) Magnesium also plays a key role in the hormonal regulation of insulin, estrogen and thyroid hormones. Magnesium also stimulates secretions from the parathyroids and adrenal cortex (corticosteroids). Magnesium is also affected just the way calcium is to parathormone (enhances distal tubular reabsorption of magnesium) and to a lesser degree calcitonin. In fact, calcium, magnesium, and phosphates are depressed in vitamin D deficiencies and increased with vitamin D excess. Magnesium is used in the treatment of elevated cholesterol and triglycerides, muscular contraction, hypertension (A causal relation between decreased Mg2+ content of cardiac muscle/coronary arteries and nonocclusive sudden-death ischemic heart disease has been proposed) and premenstrual syndrome. Magnesium is indicated in collagen and connective tissue diseases, inflammatory disorders, migraines, general endocrine function and neurological and psychosomatic disorders.	-80
Total Protein Total Protein TOTAL PROTEIN Total proteins are divided into two fractions: albumin, and globulin (alpha, beta, and gamma). Please note that total protein also includes fibrinogen. Therefore total protein is made up of albumin, globulin and fibrinogen, all produced in the liver. These are the plasma proteins necessary to produce enzymes, antibodies, clotting factors, kinin precursors, and transport substances for hormones, vitamins, minerals, fats, etc. For example, plasma proteins combine with cholesterol forming lipoproteins such as VLDL, LDL’s, HDL’s etc. The lipoproteins then combine with minerals via enzyme metabolism to form and renew sex hormones such as testosterone, estrogen, progesterone etc. Other deaminated proteins produced in the liver, combusts at the mitochondrial level to form cell structures. These are your tissue building proteins known as nucleoproteins, DNA and RNA (your proteins of mitosis and meiosis). Since there are many glands involved in protein digestion, it is very difficult to make a determination from total protein alone. Glands and organs involved with protein control are as follows: The anterior pituitary, which controls all glands of protein digestion, such as the adrenals, thyroid, pancreatic head, sex organs, and spleen That parotid glands which tag lipoproteins with copper The parathyroids via the calcium/magnesium mobilization of lipoproteins The thyroid which denitrifies protein in the liver The pancreas by trypsin and chymotrypsin which, prepares the protein for assimilation into the bloodstream The sex organs that prepare protein for final deposition into the cells * Any combination of the above TOTAL PROTEIN IS LOW WHEN General considerations: o Increase protein intake o Increase B acid vitamins	20
Albumin Albumin ALBUMIN In pathological levels albumin is used to evaluate: 1. Liver and renal disease 2. Blood osmotic pressure 3. Chronic disease states, which most patients have 4. Dehydration 5. Albumin decreases in acute inflammatory infectious processes From a physiological standpoint, albumin is produced in the liver and is a primary byproduct of sterols and waxes. Its function is used to build and repair tissue. Albumin is responsible for 80 percent of the colloidal osmotic pressure between body tissues and blood cells. 75% of this control occurs inside the cells since most of the protein is intracellular. When you have a decrease in albumin, the osmotic pressure becomes disturbed resulting in fluid transfer and edema. Since albumin influences water movement, it will also influence nutrient and mineral movement. Albumin creates the permeability of the membrane to the osmolarity of the membrane. Therefore, substances can pass from a lesser concentration to a greater concentration. The flow is from the arterial capillaries to extracellular fluid, then from the extracellular fluid to the intracellular fluid, then from the intracellular fluid to the mitochondria. Then back via the same pathway in reverse via osmotic absorption into the veins. Albumin is also a part of a complex buffer system, which accounts for 75% of things that need to be buffered to maintain acid-alkaline balance in the body. The most powerful buffer system out of the four including, the bicarbonate system (HCO3-), the phosphate buffer system, and the liver (nitrogen/urea), the proteins of the cells and plasma, rein supreme. The protein buffer system works by controlling blood Hydrogen (H+) ion homeostasis. Both intracellular and extracellular proteins have negative charges and can serve as buffers for alterations in hydrogen ion concentration. However, because most proteins are inside cells, this primarily is an intracellular buffer system. Hemoglobin (Hb) a globular protein is an excellent intracellular buffer because of it's ability to bind with Hydrogen ions forming a weak acid and carbon dioxide (CO2) bond. After oxygen is released in the peripheral tissues, hemoglobin binds with CO2 and H+ ions. As the blood reaches the lungs these actions reverse themselves. Hemoglobin binds with oxygen, releasing the CO2 and H+ ions. The H+ ions then combine with bicarbonate (HCO3) ions to form carbonic acid (H2CO3). The H2CO3 breaks down to form water (H2O) and carbon dioxide (CO2), which are excreted via expiration through the lungs. Increases in albumin cause arteries to sclerose and a decrease in albumin causes veins to sclerose. Albumin is also a transporter of minerals and accounts for 70% of the bound calcium. Magnesium also binds to albumin and since it has a lower specificity for the receptors it creates more free magnesium in the plasma. Calcium, magnesium, and phosphates continuously enter the plasma via the kidneys, the intestinal brush borders and the ruffled border of the bone. Albumin is also responsible for transporting copper, zinc, and nickel. By controlling the transport of these minerals, albumin is the carrier of choice. The following glands are associated with albumin: 1. The parotids 2. The head of the pancreas 3. The endo-reticular portion of the liver 4. Kidneys Therefore, the function or malfunction of anyone of those glands/organs or combinations thereof can lead to imbalances in albumin levels.	-30
Globulin Total Globulin Total GLOBULIN Organs that are responsible for globulin production are the liver, thyroid, spleen and the rest the immune system. There are four types of globulins alpha 1,2, beta and Gamma. There a few groups of gamma globulins with one group being the immunoglobulins (IgA, IgG. IgM), which produce our antibodies. The thymus produces α and β globulins know as thymoglobulin using Vitamin T and copper for its production. The thyroid produces thyroglobulins that form thyroxin and triiodothyronine via vitamin K and iodine. The spleen produces spleenoglobulins that require vitamin E and iron for its production. Globulin also acts as a polarized colloidal substance necessary for specific glandular hormonal function by acting as a transport mechanism for many hormones such as sex hormone binding globulin. Globulin also assists in: Toxin neutralization by binding soluble antigens in the blood and intracellular spaces Red blood cell production Antibody formation Protection of the gastrointestinal mucosa And is also necessary via the intrinsic factor for digestion and absorption. Globular proteins can be affected via: Nutrition- lack of protein Liver Thyroid Spleen Thymus	15.79
A/G Ratio A/G Ratio A/G RATIO The A/G ratio is the ratio of albumin to globulin, and along with fibrinogen (produced by the liver) literally measures the thickness or “collagen factor” of the blood. The A/G ratio then is also a representation of the fibrinogen content in the blood and regulates the amount of protein being utilized at any time in the body. The liver forms prothrombin, which requires vitamin K. for its production. Prothrombin is a plasma protein, which is changed into thrombin via prothrombin activator and calcium. Thrombin, transposes fibrinogen into fibrin, continually causing clotting throughout the body along with blood platelets. Fibrinogen, therefore, provides the clotting thickness (collagen factor) in the blood. These polarized protein fibrous strands are necessary to maintain blood viscosity, which regulates the amount of capillary exchange from the artery to the extracellular fluid. Collagen a protein strand (albuminoid) and proteoglycan filaments also regulate exchange by causing a very slow diffusion of molecules via kinetic motion moving substances through the extracellular fluid either to the cell membrane or back into the circulatory or lymphatic systems. Collagen is also the main structural protein in connective tissue and found in the extracellular spaces. Collagen and proteoglycan filaments are used in the interstitium to provide tensile strength and for healing. As the main component of connective tissue, it makes up from 25% to 35% of the whole-body protein content. Collagen is formed in the sternum and iliac crest. A/G RATIO IS INCREASED WHEN Anything that would decrease globulin would increase the A/G ratio and anything that would increase albumin would also increase the A/G ratio so also look at all the possibilities under low globulin or high albumin THE A/G RATIO IS DECREASED WHEN Anything that would increase globulin would decrease the A/G ratio and anything that would decrease albumin would decrease the A/G ratio so also look at all the possibilities under high globulin or low albumin	1645.45
Bilirubin, Total Bilirubin, Total TOTAL BILIRUBIN Bilirubin comes from the breakdown of hemoglobin and is the byproduct of hemolysis. Bilirubin is produced by the RE portion of the liver and is excreted with the bile. Pathologically elevations in total bilirubin occur when there is a massive amount of destruction of RBC’s, or the liver is congested and unable to excrete bilirubin. From a physiologic perspective, the components of bile are inositol, choline, lecithin, cholesterol, and bilirubin/biliverdin. Cholesterol, which is produced by the liver, is converted into bile salts via the influence of the adrenal glands. The bile salts are converted into cholic acid or chenodeoxycholic acid equally. Approximately 60 percent of all cholesterol is converted into these two acids. These acids then combine with glycine and taurine to form glyco and tauro conjugated bile acids. The salts of these acids are secreted in the bile. These salts do two things: 1. They act like "soap" creating saponification and emulsification of fat. This decreases the surface tension of the fat allowing agitation to break the fat up into smaller sizes. 2. Bile salts help absorb fatty acids, monoglycerides, cholesterol, and other lipids, by forming minute complexes called micelles. Micelles are highly soluble, highly charged, and easily absorbed, increasing absorption by 40 percent. The liver secretes about 600-1,200 milliliters of bile per day. The purpose of bile is to: 1. Digest, emulsify and absorb fats. 2. To excrete waste products, such as excessive cholesterol, and bilirubin, which is the end product of hemoglobin degradation. Bilirubin is the predominant pigment of bile, and is formed from hemoglobin, and destroyed red blood cells. The red blood cells are destroyed by the reticulo-endothelial system (liver and spleen), including the kupfer cells of the liver. If the spleen/liver are hyperactive, the bile production is increased. This allows the passive function of bile production to elevate. As the spleen, liver, and bone marrow destroy hemoglobin it passes into the bloodstream with a protein creating a colloidal state. This creates hemolytic jaundice when there is excessive destruction or impaired production of red blood cells, leading to excessive amounts of prehepatic bilirubin. The liver cells are unable to withdraw the bilirubin from the blood as fast as it is formed. Therefore consequently there is an increase in prehepatic bilirubin (indirect form). Remember total bilirubin = the direct and indirect forms. The direct is elevated in biliary obstruction, which is conjugated and reacted on by the liver. The indirect form is elevated in liver failure, which is unconjugated and not reacted on by the liver. Since the liver, spleen, adrenals and diet play a role in total bilirubin production from a physiologic perspective we must evaluate those glands as well.	-77.78
Alkaline Phosphatase Alkaline Phosphatase ALKALINE PHOSPHATASE Bone osteoblasts, liver cells, and the placenta all produce high levels of alkaline phosphatase, with some activity in the kidneys and intestines. Alkaline phosphatase is called alkaline because it aids in maintaining and works best in an alkaline pH of 9-10. From a pathological perspective, alkaline phosphatase levels rise in liver disease due to impaired excretion of this enzyme from obstruction in the biliary tract, and bone disease via increased osteoclastic activity due to bone breakdown as in cancer. From a physiological perspective alkaline phosphatase is responsible for the balancing of water, and mineral metabolism controlled by the glands below. This exchange of water and mineral metabolism occurs at the cell membranes of ligaments, tendons and disc structures. The balance is created by, setting the minerals involved with electrolyte balance into motion. These minerals, along with proper neurological control, cause the shifting of food thru the membranes. The glands responsible for this balance are as follows: • The adrenal cortex via mineralocorticoids causes excretion of sodium and potassium by the kidney. • The adrenal medulla via epinephrine and norepinephrine increase metabolism, and cellular exchange via the chloride shift at the level of the membrane. • The posterior pituitary via antidiuretic hormone and its effect on potassium (oxidizer) and the water content within the cell. • Prostate/uterus via selenium acts as an oxidative mineral to insure proper membrane exchange in conjunction with the above. Alkaline phosphatase is a member of a family of zinc metalloprotein enzymes whose purpose is to split off a terminal phosphate group from an organic phosphate ester. Enzyme activity is localized in the brush border of the proximal convoluted tubules of the kidney, intestinal mucosal epithelial cells, hepatic sinusoidal membranes, vascular endothelial cells and osteoblasts of bone as mentioned above. It is the introduction of an alkaline media for bone growth. When there is an increased alkaline phosphatase you have too much acidity. In “bone pathology” there is usually a hyper-acidic state, since the foundation of a cell, is nucleic acid. The nucleic acid is composed of phosphoric acid. Phosphoric acid is a component of alkaline phosphatase, therefore, the adrenals regulate the acid/alkaline balance for energy, and growth. Alkaline phosphatase controls the alkaline substance, which controls energy, and the acid substance, which controls growth. Over the years, the laboratory low range has been steadily decreasing from 60, down to 40 now down to the mid 20's. Since this test does measure metabolic output of the adrenals, going to low is not the answer. I recommend that the low range is 70.	-66.32
LDH LDH LACTIC ACID DEHYDROGENASE Lactic acid dehydrogenase is found chiefly in the heart, skeletal muscles, kidneys, and liver, as well as all cells. In pathological states, elevated levels indicate damage to the above areas and is used to determine myocardial and pulmonary infarction. In physiological states, LDH catalyzes the conversion of pyruvate ( the final step in glycolysis) to lactate and back, as it converts NADH to NAD+ and back. A dehydrogenase is an enzyme that transfers a hydride from one molecule to another. When sugar and water (fatty acid metabolism) are exchanged across a muscle cell interface, a by-product called lactic acid is produced. When lactic acid combines with the carbon dioxide of the venous blood you have a hydrogen displacement. Lactic acid now becomes lactic acid dehydrogenase. Lactic acid dehydrogenase, therefore, is a glycolytic enzyme that functions as a catalyst in carbohydrate metabolism to produce energy. The pancreas via insulin and the posterior pituitary via ADH are responsible for this sugar and water exchange across the muscle cell interface. Lactic acid dehydrogenase indicates the active exchange of sugar across the membrane (muscle cell interface) utilizing chloride, zinc, and selenium. The utilization of these minerals creates glycolysis. LDH then from a physiological perspective determines pancreatic function regulating the amount of glucose into muscle. It is also important to note that sugar metabolism is very complex and does involve a series of other organs. Ranges for LDH are between 0-220; again it is rather obvious that LDH is a by-product of sugar metabolism and a 0 figure could not be construed as a low normal range. I feel that the range should start at 80. You will find many patients with a low LDH having problems with decreased function causing heart, skeletal muscle (weakness, loss of strength, muscle wasting), kidney and liver dysfunction, and eventual wasting away of these organs.	62.86
AST (SGOT) AST (SGOT) SERUM GLUTAMIC OXALACETIC TRANSAMINASE (SGOT) (AST) SGOT is highly concentrated in organs and glands of high metabolic activity and in descending order: heart, liver, skeletal muscle, brain, kidneys, pancreas, spleen and lungs. In pathological states, when you have high levels it means that cell damage has occurred in one or more of these areas and there is a release of this enzyme in circulation, elevating in 12 hours and remaining there for 5 days. In physiologic states, we know it is a tissue enzyme present in tissues of high metabolic activity, and concerned with the transfer of nitrogen between aspartic acid, and alpha-keto-glutamic acid, resulting in the synthesis of glutamic acid, alpha keto acid and oxalacetic acid. SGOT, therefore, is the catalyst that creates amino acid metabolism during glycolysis, for the production of energy. Since there are high concentrations of SGOT in skeletal muscle/heart, and the brain, it gives you an idea of the metabolic output of each system. The sex organs via the output of testosterone, estrogen, progesterone (which are formed on the gonadal epithelium by binding cholesterol to protein) are used to maintain muscle mass and strength. Therefore having a dramatic effect on muscle and nerve metabolism. Since amino acid metabolism also affects muscle mass, muscle strength, and the energy to fuel the muscular system, it is apparent that SGOT is the indicator of choice. Not to mention the energy necessary to run the central nervous system which utilizes 60 percent of the available energy necessary to run your body. Please note that most lab ranges start at 0 and since this is a measurement of the metabolic activity of the above organs 0 would mean death. The low range for SGOT should be 15. You will find physiological conditions where there are low levels of SGOT (15-20). This is due to the exhaustion of the above organs. Low levels indicated heart, skeletal muscle and diminished brain function/damage. These patients are usually physically weak/exhausted whether they exercise or not, lack mental clarity, cannot think straight and have brain fatigue/fog. They also have sex hormonal problems and require HRT or erectile dysfunction treatment. Many of these patients have a weak flabby heart, setting the stage for many types of conditions down the road. Low levels may also mean decreased liver function affecting, protein synthesis, detoxification, sluggish metabolism, cholesterol production to name a few of the 500 know liver functions.	25.71
ALT (SGPT) ALT (SGPT) SERUM GLUTAMIC PYRUVIC TRANSAMINASE (SGPT) (ALT) SGPT is primarily a liver function test. It has a maximum concentration in the liver (fatty membranes) sinusoids. Low concentrations of SGPT are also found in the kidneys, heart, and skeletal muscle. In pathological states, elevations indicate liver disease. ALT is found in serum and in various bodily tissues but is most commonly associated with the liver. It catalyzes the transfer of an amino group from alanine to alpha-ketoglutarate, and the products of this reversible transamination reaction being pyruvate and glutamate. glutamate + pyruvate ⇌ alpha-ketoglutarate + alanine Alanine transaminase delivers skeletal muscle carbon and nitrogen in the form of alanine to the liver. In skeletal muscle, pyruvate is transaminated to alanine, thus affording an additional route of nitrogen transport from muscle to liver. In the liver, alanine transaminase transfers the ammonia to A-KG and regenerates pyruvate. The pyruvate can then be diverted into gluconeogenesis. This process is referred to as the glucose-alanine cycle. The glucose-alanine cycle is used primarily as a mechanism for skeletal muscle to eliminate nitrogen as the muscles replenish their energy supply. Within the liver, alanine is converted back to pyruvate and is then a source of carbon atoms for gluconeogenesis. The newly formed glucose can then enter the bloodstream for delivery back to the muscle. The amino group transported from the muscle to the liver, in the form of alanine, is converted to urea in the urea cycle and then excreted. In physiological states SGPT is a primary kreb cycle expressant and as a result causes the release of catabolic fats. SGPT occurs in serum as a consequence of substances being released by the fatty membranes of the liver sinusoids, and lymphatic ducts. The liver sinusoids store food, and the lymphatic ducts house toxins. Picture a layer of fat that holds foods or toxins in the cell. Now as that layer of fat is being burned off, foods and toxins are being released in a controlled manner. This allows foods or toxins to be directed to their next destination. Please note that most lab ranges for this test start at 0, which in actuality is false since this is a measurement of liver function, and 0 would mean that the liver was not functioning at all. A low range then should be around 15. Therefore, from a physiological perspective, a low SGPT between 15-20 would indicate a sluggish liver causing many metabolic disturbances. Typically these people have no energy, get sick a lot, cannot tolerate food well and have a slow metabolism.	31.43
GGT GGT GAMMA GLUTAMYL TRANSPEPTIDASE (GGT) Is a biliary enzyme useful in the diagnosis of obstructive jaundice, intrahepatic cholestasis and pancreatitis. GGT is more responsive to biliary obstruction than are aspartate aminotransferase (AST) (SGOT) and alanine aminotransferase (ALT) (SGPT). 1. GGT is increased in hepatoma and carcinoma of the pancreas and useful in the diagnosis of metastatic carcinoma of the liver. Increasing levels in carcinoma patients relate to tumor progression and a dubious outcome. 1. CEA, alkaline phosphatase and GGT together are useful markers for hepatic metastasis from the breast and colon. 2. May be useful in the diagnosis of chronic alcoholic liver disease. Follow-up blood chemistries of serum GGT, AST and ALT levels can distinguish recovering alcoholics who resume drinking from those who do not. 3. Increase in body mass correlates with increased GGT levels. 4. GGT along with MCV is a useful test for alcoholism. 5. GGT is the test of choice for pregnant females who may have cholestasis. 6. GGT levels are elevated in cirrhosis and hepatitis. 7. The transaminases, AST and ALT rise higher in acute viral hepatitis; then GGT. 8. Increased in systemic lupus erythematosus GGT IS HIGH WHEN General considerations: If patient has been on a very low-fat diet for long periods of time then increase fat intake	-40
Ferritin Ferritin A ferritin test can help a doctor determine if a person has enough iron in their body. Low ferritin levels can indicate that the body doesn't have enough iron, while high levels can indicate too much iron. FERRITIN Men 20-250 ng/mL 20-250 ug/L Women 10-120 ng/mL 10-120 ug/L Children 7-140 ng/mL 7-140 ug/L Newborns 25-200 ng/mL 25-200 ug/L	-16.4
Total Iron Total Iron Total Iron Binding Capacity (TBIC)—measures the amount of transferrin, which is a blood protein that transports iron from the digestive system to cells that will be utilizing the iron. Your body produces transferrin in relationship to the body’s need for iron. When iron stores are low, transferrin levels will increase and when transferrin levels are low, too much iron is present. Usually, about one third of the transferrin is being used to transport iron at any one time. Because of this, your blood serum has considerable extra iron-binding capacity, which is called the Unsaturated Iron Biding Capacity (UIBC). The TIBC then equals UIBC plus serum iron measurement. Some laboratories may measure UIBC, some measure TIBC and others measure transferrin. TIBC is increased in iron- deficiency, acute hepatitis, during pregnancy or when oral contraceptives are used. TIBC is decreased in hypoproteinemia from many causes, cirrhosis of the liver, nephrosis and thalassemia or from a number of inflammatory states. TOTAL IRON IRON Men 65-175ug/dL 11.6-31.3 umol/L Women 50-170ug/dL 9.0 -30.4 umol/L Children 50-120ug/dL 9.0-21.5 umol/L Newborns 100-250 ug/dL 17.9-44.8 umol/L	-40
Cholesterol, Total Cholesterol, Total SERUM LIPIDS Serum lipids serve as a primary source of energy along with glucose. The functions are many, such as the production of cell membranes, precursors to hormones, and bile acids. Lipids are first broken down in the duodenum, along with bile, which emulsifies the fats, and prepares them for absorption into the lymphatic system. Pancreatic lipase hydrolyzes cholesterol, and triglycerides into fatty acids, and glycerol. The fatty acids and glycerol are then reconverted back into triglycerides by the intestinal cells and then discharged into the lymphatic or portal blood system, which is then sent to the liver. Cholesterol is also absorbed in both the free and esterified forms into the lymphatics. Cholesterol is also synthesized in the reticular cells and histiocytes throughout the body but mainly formed in the liver. Under the influence of iodine via the thyroid, carbohydrates, amino acids, and other fats are converted to cholesterol via multiple molecules of acetyl coenzyme A creating a sterol nucleus. Triglycerides are also assembled in the liver from glycerol and fatty acids. The liver is the main organ regulating blood lipids. So the liver can degrade fatty acids for energy, synthesize triglycerides from carbohydrates and proteins. The liver can then hydrolyzes the triglycerides back into three fatty acids, and glycerol then degrades the fatty acids into acetyl coenzyme A via beta-oxidation. Then acetyl coenzyme A is then oxidized to release ATP. The liver also synthesizes phospholipids, lecithin, cephalins (that produce thromboplastin), and sphingomyelin (produces the myelin sheath) are formed in the liver and transported via lipoproteins. An increase in triglycerides or choline/inositol increases phospholipid production. Phospholipids are also important in the production of cell membranes. CHOLESTEROL Cholesterol is a byproduct of protein metabolism. Bonding oily fat (fat-soluble vitamins) to nitrogen via oxidation forms cholesterol. This process utilizes vitamins, D, E, K, A, and T. These are your fat-soluble vitamins that are bound to the nitrogen portion of foods. The basic purpose of fat-soluble vitamins is to lubricate membranes. The vitamin (oil) prevents oxygen from reaching the membrane, which may inhibit its function. Fat-soluble vitamins also provide the substance necessary to make hormones, enzymes, and antibodies. For example, Vitamin D. lubricates all gross membranes that are exposed to air, such as your skin, respiratory passages, and the digestive membranes. This is your antioxidant lubricator Vitamin A. lubricates secondary membranes that are exposed to the blood, such as the liver, kidney, lungs and spleen. Vitamin A. is called your hydrogen lubricator. Vitamin K. lubricates cell membranes that are exposed to water. Vitamin F. fatty acids are used to make enzymes. Vitamin E. is used to make hormones. Vitamin T. which, is sesame seed oil, is used to make antibodies Lecithin prevents oil and fat from going rancid. So the purpose of fat-soluble vitamins is to oxidize and combust with protein to form cholesterol, which then transposes it into a lubricator, a hormone, antibody, or enzyme. Low-density lipoproteins are rich in cholesterol and carry some triglycerides and are used to produce sex hormones. High-density lipoproteins are rich in triglycerides and carry some fat. Please note that at any one time, the body can dictate the percentage of low-density lipoproteins vs. high-density lipoproteins. It's obvious that an imbalance can create multiple diseases in the body. Please note that these lipoproteins also engulf toxins and then are stored in tissue cells. At a later time, the body gradually detoxifies these deposits unless the amount is overwhelming. Similar to glucose, cholesterol is affected by many organs and glands and in itself is not a reliable indicator as to what is going on in the body. Over the years, the labs went from a normal cholesterol reading of 300, down to 250, then down to 200, and now down to 150. If they continue this nonsense they will create a whole new list of diseases. I recommend that your cholesterol levels be between 175-275mg/dL.	-192
Triglycerides Triglycerides SERUM LIPIDS Serum lipids serve as a primary source of energy along with glucose. The functions are many, such as the production of cell membranes, precursors to hormones, and bile acids. Lipids are first broken down in the duodenum, along with bile, which emulsifies the fats, and prepares them for absorption into the lymphatic system. Pancreatic lipase hydrolyzes cholesterol, and triglycerides into fatty acids, and glycerol. The fatty acids and glycerol are then reconverted back into triglycerides by the intestinal cells and then discharged into the lymphatic or portal blood system, which is then sent to the liver. Cholesterol is also absorbed in both the free and esterified forms into the lymphatics. Cholesterol is also synthesized in the reticular cells and histiocytes throughout the body but mainly formed in the liver. Under the influence of iodine via the thyroid, carbohydrates, amino acids, and other fats are converted to cholesterol via multiple molecules of acetyl coenzyme A creating a sterol nucleus. Triglycerides are also assembled in the liver from glycerol and fatty acids. The liver is the main organ regulating blood lipids. So the liver can degrade fatty acids for energy, synthesize triglycerides from carbohydrates and proteins. The liver can then hydrolyzes the triglycerides back into three fatty acids, and glycerol then degrades the fatty acids into acetyl coenzyme A via beta-oxidation. Then acetyl coenzyme A is then oxidized to release ATP. The liver also synthesizes phospholipids, lecithin, cephalins (that produce thromboplastin), and sphingomyelin (produces the myelin sheath) are formed in the liver and transported via lipoproteins. An increase in triglycerides or choline/inositol increases phospholipid production. Phospholipids are also important in the production of cell membranes. TRIGLYCERIDES Triglycerides compromise 95% of fat stored in adipose tissue and stored as glycerol, fatty acids, and monoglycerides. The liver reconvert's these back to triglycerides. 80% of your triglycerides make up VLDL, and 15% form LDL’S. From a pathological viewpoint, this test evaluates atherosclerosis and measures the bodies ability to utilize fat. From the physiologic perspective, triglycerides are nothing more than three fatty acids, and esters of glycerol. Fatty acids are composed of sugar and alcohol. Triglycerides travel with cholesterol (LDL/HDL) to combust cholesterol at the appropriate time.Triglycerides are needed for calculation of LDLC (low-density lipoprotein cholesterol) concentration. Triglycerides are the matches or “the spark” that ignites and combusts the cholesterol. Triglycerides are implanted in the cell membrane of all neurological and glandular tissue. Triglycerides create the energy for a neurological impulse to occur. When the neurological impulse occurs triglycerides actually “explode” causing the active exchange of electrolytes. Primary glands involved in triglyceride metabolism are the posterior pituitary, the hypophyseal stalk, adrenals, and the head of the pancreas.Therefore, any condition affecting these organs can affect triglyceride levels. High levels are a greater risk for a heart attack then a high cholesterol. Low triglyceride levels from the physiologic perspective cause low energy. Triglycerides Normally Range From 0-199. It Is Rather Obvious That 0 Triglycerides Could Not Be Achieved Physiologically. My Ranges Are From 75-200 mg/dL	66.4
TSH TSH T-4, T-3, T3 uptake and TSH Thyroid-stimulating hormone (TSH) from the anterior pituitary, stimulates the production of thyroxin, and triiodothyronine, therefore, having a dramatic effect on the T4/T3 test results. Thyrotrophs makeup 5% of the anterior pituitary and produce between 100-400mU/day of TSH. Circadian peaks with the onset of sleep are between 9 pm-5am and a minimum between 4-7pm. TSH is regulated by an open feedback loop via thyroxin whereby thyroxin passes into the CSF of the lateral ventricles and is taken up by the epithelial cells of the choroid plexus, which when thyroxin levels are low, stimulates TRH-secreting neurons in the hypothalamus. TSH does the following: 1. Stimulates phospholipid metabolism 2. Stimulates purine and pyrimidine precursors and their incorporation into nucleic acids. T-4 and 3 indicate the denitrification power of iodine via thyroxin with T3 being much more powerful than T4. All food contains active biological nutrients that are bound with nitrogen. When this food reaches the liver, the iodine is used to cleave the nitrogen from the nutrient. Therefore, thyroxin and T3 are important in fat and protein digestion, absorption, and growth and endocrine function. This catabolic activity begins once aerobic bound substances become totally anaerobic and lose the need for nitrogen bonding. Nitrogen is cleaved by T3 or T4 in the liver for example as in glycogen storage. Other substances are needed by specific cells and are transported via total binding globulin to the cells where at that point, the nitrogen bonds are cleaved. Less than 1% of T3 is unbound. A high T-3 uptake indicates a hypothyroid, where a low T-3 uptake indicates a hyperthyroid.	-118.96
Thyroxine (T4) Thyroxine (T4) T-4, T-3, T3 uptake and TSH Thyroid-stimulating hormone (TSH) from the anterior pituitary, stimulates the production of thyroxin, and triiodothyronine, therefore, having a dramatic effect on the T4/T3 test results. Thyrotrophs makeup 5% of the anterior pituitary and produce between 100-400mU/day of TSH. Circadian peaks with the onset of sleep are between 9 pm-5am and a minimum between 4-7pm. TSH is regulated by an open feedback loop via thyroxin whereby thyroxin passes into the CSF of the lateral ventricles and is taken up by the epithelial cells of the choroid plexus, which when thyroxin levels are low, stimulates TRH-secreting neurons in the hypothalamus. TSH does the following: 1. Stimulates phospholipid metabolism 2. Stimulates purine and pyrimidine precursors and their incorporation into nucleic acids. T-4 and 3 indicate the denitrification power of iodine via thyroxin with T3 being much more powerful than T4. All food contains active biological nutrients that are bound with nitrogen. When this food reaches the liver, the iodine is used to cleave the nitrogen from the nutrient. Therefore, thyroxin and T3 are important in fat and protein digestion, absorption, and growth and endocrine function. This catabolic activity begins once aerobic bound substances become totally anaerobic and lose the need for nitrogen bonding. Nitrogen is cleaved by T3 or T4 in the liver for example as in glycogen storage. Other substances are needed by specific cells and are transported via total binding globulin to the cells where at that point, the nitrogen bonds are cleaved. Less than 1% of T3 is unbound. A high T-3 uptake indicates a hypothyroid, where a low T-3 uptake indicates a hyperthyroid.	84
T3 Total T3 Total T-4, T-3, T3 uptake and TSH Thyroid-stimulating hormone (TSH) from the anterior pituitary, stimulates the production of thyroxin, and triiodothyronine, therefore, having a dramatic effect on the T4/T3 test results. Thyrotrophs makeup 5% of the anterior pituitary and produce between 100-400mU/day of TSH. Circadian peaks with the onset of sleep are between 9 pm-5am and a minimum between 4-7pm. TSH is regulated by an open feedback loop via thyroxin whereby thyroxin passes into the CSF of the lateral ventricles and is taken up by the epithelial cells of the choroid plexus, which when thyroxin levels are low, stimulates TRH-secreting neurons in the hypothalamus. TSH does the following: 1. Stimulates phospholipid metabolism 2. Stimulates purine and pyrimidine precursors and their incorporation into nucleic acids. T-4 and 3 indicate the denitrification power of iodine via thyroxin with T3 being much more powerful than T4. All food contains active biological nutrients that are bound with nitrogen. When this food reaches the liver, the iodine is used to cleave the nitrogen from the nutrient. Therefore, thyroxin and T3 are important in fat and protein digestion, absorption, and growth and endocrine function. This catabolic activity begins once aerobic bound substances become totally anaerobic and lose the need for nitrogen bonding. Nitrogen is cleaved by T3 or T4 in the liver for example as in glycogen storage. Other substances are needed by specific cells and are transported via total binding globulin to the cells where at that point, the nitrogen bonds are cleaved. Less than 1% of T3 is unbound. A high T-3 uptake indicates a hypothyroid, where a low T-3 uptake indicates a hyperthyroid.	-43.33
T3 Uptake T3 Uptake T-4, T-3, T3 uptake and TSH Thyroid-stimulating hormone (TSH) from the anterior pituitary, stimulates the production of thyroxin, and triiodothyronine, therefore, having a dramatic effect on the T4/T3 test results. Thyrotrophs makeup 5% of the anterior pituitary and produce between 100-400mU/day of TSH. Circadian peaks with the onset of sleep are between 9 pm-5am and a minimum between 4-7pm. TSH is regulated by an open feedback loop via thyroxin whereby thyroxin passes into the CSF of the lateral ventricles and is taken up by the epithelial cells of the choroid plexus, which when thyroxin levels are low, stimulates TRH-secreting neurons in the hypothalamus. TSH does the following: 1. Stimulates phospholipid metabolism 2. Stimulates purine and pyrimidine precursors and their incorporation into nucleic acids. T-4 and 3 indicate the denitrification power of iodine via thyroxin with T3 being much more powerful than T4. All food contains active biological nutrients that are bound with nitrogen. When this food reaches the liver, the iodine is used to cleave the nitrogen from the nutrient. Therefore, thyroxin and T3 are important in fat and protein digestion, absorption, and growth and endocrine function. This catabolic activity begins once aerobic bound substances become totally anaerobic and lose the need for nitrogen bonding. Nitrogen is cleaved by T3 or T4 in the liver for example as in glycogen storage. Other substances are needed by specific cells and are transported via total binding globulin to the cells where at that point, the nitrogen bonds are cleaved. Less than 1% of T3 is unbound. A high T-3 uptake indicates a hypothyroid, where a low T-3 uptake indicates a hyperthyroid.
T3 Free T3 Free A free T3 test, or free triiodothyronine test, measures the amount of free triiodothyronine in your blood. Triiodothyronine (T3) is a hormone produced by the thyroid gland that helps regulate metabolism and energy levels. A normal free T3 level is typically between 2.5–4.0 ng/dL, but reference values may vary by lab. A higher-than-normal level of T3 may indicate an overactive thyroid, while a lower-than-normal level may indicate an underactive thyroid.	5.26
T4 Free T4 Free Free T4 is the amount of thyroxine (T4) in the blood that is not attached to proteins. T4 is a hormone produced by the thyroid gland that helps control metabolism and growth. A free T4 test measures the amount of free T4 in your blood.	86.21
Urine pH Urine pH URINE PH A high urine pH may be due to: Kidney failure Urinary tract infections Vomiting A low urine pH may be due to: Diarrhea Too much acid in the body fluids such as metabolic acidosis and diabetic ketoacidosis Starvation	-100
Bun/Creatin Ratio Bun/Creatin Ratio BUN/CREATININE RATIO BUN plus creatinine are residue byproducts of protein and muscle metabolism respectively. They are kept in continual balance by the water content of your body. The kidneys flush out the excessive BUN/creatinine concentration when it gets too high. The kidneys are under the influence of the posterior pituitary via antidiuretic hormone, which regulates the amount of water leaving the body. Therefore, the posterior pituitary through potassium regulates water balance. The posterior pituitary then regulates the amount of water in any one place of the body. So, therefore, it can either increase or decrease the water content in the blood, thus altering pH. The posterior pituitary besides balancing water also regulates sugar and mineral concentration. BUN/CREATININE IS HIGH WHEN General considerations: ¬ Decrease high protein intake ¬ Or increase water intake ¬ BUN/CREATININE is high when you have a high BUN or a low CREATININE or both BUN/CREATININE IS DECREASED WHEN General considerations: ¬ Increase protein intake ¬ Or decrease water intake ¬ BUN/CREATININE is low when either you have a low BUN or a high CREATININE or both	203.58
COQ10 Coenzyme COQ10 Coenzyme Coenzyme Q10 (CoQ10 also known as ubiquinone, is a natural coenzyme and an antioxidant produced by the body. It is also obtained from dietary sources, such as meat, fish, seed oils, vegetables, and dietary supplements. CoQ10 plays a role in mitochondrial oxidative phosphorylation, aidingthe production of adenosine triphosphate (ATP), which is involved in energy transfer within cells. The structure of CoQ10 consists of a benzoquinone moiety and an isoprenoid side chain, with the "10" referring to the number of isoprenyl chemical subunits in its tail. Biological function CoQ10 is a component of the mitochondrial electron transport chain (ETC), where it plays a role in oxidative phosphorylation, a process required for the biosynthesis of adenosine triphosphate, the primary energy source of cells. CoQ10 is a lipophilic molecule that is located in all biological membranes of the human body and serves as a component for the synthesis of ATP and is a life-sustaining cofactor for the three complexes (complex I, complex II, and complex III) of the ETC in the mitochondria. CoQ10 has a role in the transport of protons across lysosomal membranes to regulate pH in lysosome functions. The mitochondrial oxidative phosphorylation process occurs in the inner mitochondrial membrane of eukaryotic cells. This membrane is highly folded into structures called cristae, which increase the surface area available for oxidative phosphorylation. CoQ10 plays a role in this process as an essential cofactor of the ETC located in the inner mitochondrial membrane and serves the following functions: electron transport in the mitochondrial ETC, by shuttling electrons from mitochondrial complexes like nicotinamide adenine dinucleotide (NADH), ubiquinone reductase (complex I), and succinate ubiquinone reductase (complex II), the fatty acids and branched-chain amino acids oxidation (through flavin-linked dehydrogenases) to ubiquinol–cytochrome-c reductase (complex III) of the ETC: CoQ10 participates in fatty acid and glucose metabolism by transferring electrons generated from the reduction of fatty acids and glucose to electron acceptors; antioxidant activity as a lipid-soluble antioxidant together with vitamin E, scavenging reactive oxygen species and protecting cells against oxidative stress, inhibiting the oxidation of proteins, DNA, and use of vitamin E.
Fibrinogen Fibrinogen FIBRINOGEN- BLOOD TEST RANGES 200 and 400 mg/dL (2.0 to 4.0 g/L) (coagulation factor I) is a glycoprotein complex that is synthesized by the liver and circulates in the blood stream. During tissue and or vascular injury, it is converted enzymatically by thrombin to fibrin which creates a blood clot The primary function is to occlude blood vessels thus stopping bleeding. Fibrin also binds and reduces the activity of thrombin. This activity referred to as antithrombin I, which limits clot formation. Fibrin also mediates and is important in blood platelet, endothelial cell spreading, capillary tube formation, tissue fibroblast proliferation, and angiogenesis thereby promoting revascularization and wound healing. Thrombin is synthesized in the liver and secreted into the general circulation in an inactive zymogen form (prothrombin), a complex multidomain glycoprotein that is activated to yield thrombin at sites of vascular injury by limited proteolysis following upstream activation of the coagulation cascade.
LPA LPA LPA- BLOOD TEST LEVELS 30-50 mg/dL (75-125 nmol/L Lipoprotein (a) or Lp(a) levels are measured in milligrams per deciliter (mg/dL) or nanomoles per liter (nmol/L). A lipoprotein(a) (Lp(a)) blood test measures the amount of Lp(a) in your blood, which is lipoprotein that carries cholesterol. Thus elevated Lp(a) levels are associated with an increased risk of cardiovascular disease. Recommended for individuals with a family history of heart disease or other risk factors. High levels of lipoprotein (a) (Lp(a), may cause heart attack, stroke, and or aortic stenosis LPA is produced through multiple mechanisms within cells and in biological fluids like plasma and serum. Lysophosphatidic acid (LPA) is primarily produced by the enzyme autotaxin (ATX). ATX, which is a secreted lysophospholipase D, converts lysophospholipids, primarily lysophosphatidylcholine (LPC), into LPA. This extracellular production pathway is considered the major source of bioactive LPA.
Apo B Apo B Apolipoprotein B (ApoB) is a protein that plays a crucial role in the transport of fats and cholesterol in the blood. It is a key component of low-density lipoproteins (LDL) and other lipoproteins that carry triglycerides, cholesterol, and cholesterol esters. Elevated ApoB levels are associated with an increased risk of cardiovascular disease. Key aspects of ApoB: Role in Lipoprotein Formation: ApoB is a primary protein on the surface of various lipoproteins, including LDL, VLDL, chylomicrons, and lipoprotein(a). Atherogenic Particle Indicator: ApoB measurement helps determine the number of atherogenic particles circulating in the bloodstream, which are linked to plaque buildup in arteries. Cardiovascular Risk: Elevated ApoB levels are a significant indicator of increased cardiovascular risk, particularly atherosclerosis. ApoB Test: An ApoB test measures the amount of ApoB in the blood and is often used to assess the risk of heart disease. Two Forms: ApoB exists in two forms: ApoB100 (primarily in the liver) and ApoB48 (primarily in the intestine). Apo High levels of apolipoprotein B (ApoB) are often associated with elevated levels of LDL cholesterol (LDL-C) and can be caused by a variety of factors, including diet, lifestyle, underlying medical conditions, and genetics.
Gland Totals		5	5
Gland Totals (%)		304%	456%

Top 12 Glands/Organs test

Gland	Results	Add Supplement
Serous Membranes Serous Membranes TBC	456%	Add
Thymus Thymus THE THYMUS The thymus is a ductless gland located in the anterior mediastinal cavity, which reaches its maximum development in early childhood. As you leave early childhood, the thymus starts its process of involution. The hormone produced by the thymus is called thymosin A. The purpose of thymosin A is to cause further proliferation and increased the activity of lymphocytes. The lymphatic system, spleen, thymus and bone marrow produce lymphocytes. The thymus gland produces T lymphocytes, which are mainly produced within a few months of life. The purpose of these T lymphocytes is to increase cell-mediated immunity. These T lymphocytes are specifically designed to destroy foreign agents. Lymphocytes are located most extensively in the lymph nodes but are also found in the spleen, the submucosa of the gastrointestinal tract and the bone marrow. The purpose of this lymphoid tissue is to intercept invading organisms or toxins before they spread. For example, the lymphoid tissue of the gastrointestinal tract is exposed to antigens coming in through your food and drink. The lymphoid tissues in your throat are your tonsils and adenoids, which are the first line of defense in your upper respiratory tract. Your peripheral lymph nodes are responsible for protecting the peripheral body when traumatized and cut. The lymphoid tissue in the spleen and bone marrow intercept invading organisms and toxins once they reach the blood stream. Please note that there is also a humeral immunity called B cell immunity. B cell immunity utilizes the liver and bone marrow to process and creates antibodies (B cells) for specific antigens. The antibodies are made up from gamma globulin molecules called immunoglobulins, which have molecular weights between 150,000 and 900,000. These immunoglobulins constitute 20 % of all plasma proteins. They are respectively named: IgM, IgG, IgA, IgD, and IgE For a substance to be antigenic, it must have a molecular weight of 8,000 or more. Antibodies work in two different ways to protect the body. They either directly attack the invading agent, or they activate a complementary system that destroys the invading agent. Direct action is through the following methods: 1. AGGLUTINATION-when the antigens stick and clump together on the surface of the antibodies 2. PRECIPITATION-when the molecular weight of the antibody and antigen becomes too large precipitates out and is rendered insoluble 3. NEUTRALIZATION-where the antibody covers the toxic site on the antigen 1. LYSIS-is where the antibody attacks the cell membrane of the antigen causing it to rupture When antibodies work with complementary systems, they attach to antigens and form long antigen-anti-body molecules that are now broken down by a cascade of biochemical reactions. Both humoral and mediated immunity are under the heading of acquired immunity. According to Dr. Brockman, the primary mineral of the thymus is uranium. The function of uranium is to create a radioactive bond or isotope tracker for all substances that enter the body through all membranes, including the skin. When an invasive substance enters the body, it is directed by magnetic control via uranium. The body hooks this invasive substance to uranium, which then tracks and targets this compound, directing it to the appropriate area for degradation and/or elimination. Another function of the thymus, states Brockman, is to extract bioflavonoids from ascorbic acid to create an acid pH on cell membranes, increasing their permeability for toxic disposal. This acts as a membrane resistant factor. If this is improperly handled, you loose acid maintenance and detoxification power. This will now affect the secondary gland of acid maintenance, which is the pancreas via sugar balance. The pancreas now tries to increase blood acidity, causing the alkaline oxidizing enzymes from the head of the pancreas to become more acidic and less potent. The following tests can be used to assess thymus function: 1. GLOBULIN-since the thymus is used to produce immunoglobulins, globulin is affected by thymus function 2. A/G RATIO-the albumin globulin ratio will also be affected by the thymus's affect on globulin offsetting this ratio Albumin is considered the colloidal protein of osmosis since it regulates the flow of substances from the capillaries to the interstitial tissue. Globulin is the colloidal protein of momentum since it transports substances throughout the body, such as hemoglobin. Fibrinogen is considered the colloidal protein of clotting since it regulates the clotting ability of the blood. When a foreign substance enters the body through the skin via cuts, or through mucous membranes, uranium is sent by the thymus to program the foreign substance. Depending on the foreign substance, whether it is toxic or a pathogen, the thymus, and spleen will help dictate whether there should be a buildup of white blood cells and or breakdown of red blood cells to increase globulin production for thymus or spleen globulin to fight off the infection. Fibrinogen, which is transposed into fibrin via thrombin, will aid in clot formation, helping to wall off the infection. The A/G ratio is also a representation of the fibrinogen content in the blood. 3. TOTAL BILIRUBIN-when globulins are needed to produce immunoglobulins, the body relies on the red blood cells to fulfill this need. Since the blood cells are composed of globulin, iron, biliverdin and bilirubin, they are the perfect source for additional globulins. The spleen and liver hemolyze the red blood cells for the globulin and, at the same time, release bilirubin into the bloodstream, affecting total bilirubin levels.	454%	Add
Kidneys Kidneys THE KIDNEYS The function of the kidneys is to filter 170,000 mL of blood daily and produce about 1200 mL of urine daily. At the same time, the kidneys are used to filter out all excessive ions such as sodium, chloride, and potassium, while maintaining glucose, amino acids, water and other substances that are essential for body metabolism. The kidneys also remove the following waste products: creatinine, BUN, and uric acid. The two kidneys together contain about two million nephrons and each nephron is capable of forming urine by itself. Blood enters the kidneys thru the renal artery, enters the glomeruli through the afferent arteriole, and leaves through the efferent arteriole. The efferent arteriole is smaller in diameter than the afferent arteriole, therefore creating a hydrostatic (back) pressure forming the glomerular filtrate. (The glomeruli is a network of up to 50 parallel and anastomosing capillaries covered by epithelium cells and encased in Bowman's capsule.) The pressure of the blood into the glomeruli causes fluid to filter into Bowman's capsule. This is known as the glomerular filtrate, which then travels to the proximal/ distal tubules in the kidney cortex. As the filtrate passes along the tubules, the capillary blood and the epithelial tubular cells add more solutes. Interposed between the proximal and distal tubules is the loop of Henley, which has a thin descending limb, and a thin and a thick (impermeable to H20, but actively absorbs solutes causing filtrate to become hypotonic) ascending limb. It then travels through the distal tubules, through the corticoid-collecting duct, into the medullar-collecting duct, where things are absorbed or secreted. As the glomerular filtrate flows through the tubules, especially the cortical, medullary and papillary collecting ducts, over 99% of the water (via AVP) and varying amounts of its solutes are reabsorbed. The basic function of the nephron is to clean the blood plasma of unwanted substances, particularly the end products of metabolism (organic substances) such as urea (accounts for ½ of the total dissolved solids in urine), creatinine, uric acid, urate, BUN and inorganic dissolved solids (the highest being chloride followed by sodium and potassium.) The kidney does this through two mechanisms: filtration and secretion. Antidiuretic hormone (AVP) retains water but removes solutes. AVP binds to V2 receptor sites on renal epithelial cells of the basso lateral membrane activating protein kinase and adenylate cyclase to catalyze cAMP from ATP. The cAMP is now phosphorylated, mediating the effects of renal transport. AVP also increases transepithelial conductance and basso lateral membrane conductance of the CL ion channels. AVP also increases co transport units on other cell membranes for NA, K, and CL. Aldosterone controls potassium excretion and sodium reabsorption. Parathyroid hormone causes absorption of calcium and loss of phosphorus. The daily loss of fluid through urine is 1400 mL, 350 mL through the skin and respiratory tract, and 100 mL through sweat and feces. The rennin-angiotensin system is stimulated by decreased blood flow through the kidneys. The purpose of which is to increase blood pressure. Rennin is a small protein enzyme released by the kidney and is stored as pro rennin. When the blood pressure drops, pro rennin is converted into rennin. Rennin also works as an enzyme on another plasma globular protein called rennin substrate 1 and 2 or angiotensin (a powerful vasoconstrictor). Angiotensin 2 is the most powerful constrictor and is also found in the epithelium of the lungs. Angiotension decreases water and mineral loss through the kidneys while stimulating the adrenals. Aldosterone is strongly influenced by this rennin-angiotensin system (90% more than ACTH) causing strong reabsorption of sodium into the distal tubules to balance extracellular potassium ions. The following tests indicates kidney malfunction: 1. SODIUM-Sodium is an alkaline mineral that helps maintain alkaline activity. It helps in acid-alkaline balance, which affects intracellular/extracellular fluid exchange, and osmotic pressure, via the sodium/potassium pump. It does this in conjunction with antidiuretic hormone and aldosterone. Sodium gathers and aggregates (polarizes) all substances necessary to be exchanged by semi-permeable membranes. Sodium also affects the renal tubules for the activity of discharging toxins. It literally aggregates toxins and holds them in suspension. 2. POTASSIUM-Potassium lines the inside of all cell membranes and is responsible, via the posterior pituitary, for oxidizing secondary hydrogen chloride and allowing sodium-aggregated substances to cross the cell membrane. It is the only substance that allows oxygen into unoxygenated tissue. Potassium is necessary for proper function of mineral corticoids, (aldosterone and deoxycorticosterone) thus maintaining sodium concentration and alkaline reserve. Therefore, potassium is of great value to the posterior pituitary (ADH/oxytocin), the pineal and the adrenal cortex, via aldosterone secretion. In turn, the kidneys are greatly affected.	376%	Add
Parotids Parotids THE PAROTIDS The principal glands of salivation are the parotids, which are the submandibular, sublingual and buccal glands. The daily secretion of saliva normally ranges between eight hundred to fifteen hundred milliliters. The saliva contains two major protein secretions. The first is a serous secretion containing ptyalin, which is an enzyme necessary for digesting starches. The second is a mucous secretion containing mucin for lubricating purposes. The parotid glands secrete entirely the serous type while the submandibular and sublingual glands secrete both serous and mucous. The buccal glands secrete only mucus. The pH of saliva is between 6.0 and 7.0. Saliva also contains the following ions: Under resting conditions, the sodium and chloride ions are approximately 1/7-1/10 of that found in plasma. During maximum salivation, the sodium and chloride concentrations elevate to 1/2 to two-thirds that of the plasma. Potassium, on the other hand, is seven times more concentrated than in the plasma but during maximum salivation, it is reduced to four times the concentration of the plasma. The purpose of potassium is to push food into the cells. The only other ion found in saliva is the bicarbonate ion. Besides the function of carbohydrate digestion, saliva also plays an important role in oral hygiene. The mouth is loaded with pathogenic bacteria that can easily destroy tissue. Saliva prevents this by first washing the bacteria away. Secondly, saliva contains several factors that destroy bacteria. These include thiocyanate ions, and several proteolytic enzymes, the most important being lysozyme. Lysozyme attacks the bacteria and aids the thiocyanate ions to enter the bacteria, where it becomes bactericidal. Saliva also digests food particles that help to remove bacterial metabolic support. The saliva also contains significant amounts of protein antibodies that can destroy all bacteria. According to Dr. Brockman, the primary function of the parotids is through the mineral copper, which tags all incoming substances through the mouth and nasal pharynx. The following substances are tagged and taken to the following areas: • FOOD-programmed and taken to the liver • TOXINS-sent to the lymphatic • MICROBES-taken to the point of beneficial hosting • PROGRAMS PROTEINS-there are two types of proteins. The first type of protein is called colloidal albumin, which is used for an osmotic gradient, which keeps things in passive motion. The second is called colloidal globulin, which is the momentum protein that moves toxins and infections throughout the body so the body can balance what it wants and what it does not want. There are certain organisms that may not be needed at another area. So the purpose of globulin is to serve as the sub-protein transport system for these organisms, which is necessary for chemical momentum in the body. This keeps the toxin and infection mechanisms moving throughout the system. What makes the globulin colloidal is the electrical copper implant, which steers it through the system. • ANY MAN-MADE PRODUCTS such as pesticides attenuated viruses, which contain no nucleic affinity, which the body cannot tag or identify. In turn. your body has no idea what to do with this compound. These are the man-made distortions that cause sickness and disease that our bodies have difficulty in overcoming. It is also interesting to note that potassium cannot work without copper and that salivary glands are activated via the mumps. The mumps are a normal childhood disease, which activate this parotid copper phenomenon. The following blood tests indicate a possible problem with the parotids: 1. GLOBULIN-which is joined with copper to create programming of ingested or inhaled substances. 2. POTASSIUM- which is secreted by the salivary glands, and is necessary for the programming process and drawing food into the cells. 3. A/G RATIO-the albumin globulin ratio will also be altered if the globulin is affected by the malfunctioning parotid gland. 4. ALBUMIN-albumin levels will also be affected via a malfunctioning parotid gland.	359%	Add
Mucous Membranes Mucous Membranes TBC	304%	Add
Ileum Ileum TBC	270%	Add
Anterior Pituitary Anterior Pituitary THE PITUITARY GLAND The pituitary, the existence of which has been known for 2000 years, sits in the sella turcica of the sphenoid bone. The sella turcica forms the roof of the sphenoid sinus. The lateral walls are comprised of durra or bone, which abut the cavernous sinuses and can affect the 3rd, 4th, and 6th cranial nerves and the internal carotid arteries since they transverse thru this area. The cavernous sinuses can exert a great deal of CSF pressure but, due to the diaphragm sellae, the gland will not become compressed nor will the optic chiasm and tracts, which lie immediately above the diaphragm sellae. Also lying in close proximity to the cavernous sinuses are the internal carotid arteries, cranial nerves 3, 4, 5 and 6, the third ventricle and the optic chiasm, which lies above the diaphragm sellae. The pituitary is divided into three parts: 1. ADENOHYPOPHYSIS-is the anterior portion, which is derived from Rathke's pouch. This is divided into three lobes: the pars distalis (anterior lobe,) the pars inter-media (intermediate lobe) and the pars tuberalis. 2. NEUROHYPOPHYSIS-is the posterior portion and is composed of the pars nervosa, the infundibular stalk, and the median eminence. The major supply of axons to the neural lobe is the magnicellular secretory neurons from the paraventricular and supraoptic nuclei of the hypothalamus. These axon terminals also secrete AVP (regulating blood osmolarity, pressure, and fluid balance) and oxytocin into the surrounding capillary beds leading into the hypophyseal veins. The infundibular stalk is surrounded by the pars tuberalis, and together they make up the hypophyseal stalk. 3. VESTIGIAL INTERMEDIATE LOBE . The pituitary gland is regulated by the hypothalamus via feedback mechanisms of hormones and from paracrine and autocrine secretions from the pituitary itself. It attaches to the hypothalamus via the stalk thru the diaphragm sellae and into the median eminence. The pituitary is derived from the: • ECTODERM-which forms the pars distalis/tuberalis and the intermediate lobe • NEURAL PORTION-which forms the infundibulum, posterior pituitary, and neural stalk The pituitary weighs between 4-900 mgs (during pregnancy up to 1 gram), is bean shaped and brownish in color with dimensions of 9 mm A/P, 6mm S/I, 13 mm laterally. The hypothalamus receives its blood supply from the superior (provides 10-20 % of the blood supply) and inferior hypophyseal arteries (supply blood to the posterior pituitary), which are derived from the internal carotid arteries. These arteries form a capillary network in the median eminence (external to the blood-brain barrier). This capillary network picks up hypothalamic secretions from the hypothalamic nerve endings delivering them into the long and short hypophyseal portal veins, which are now transported to the anterior pituitary. Please note that retrograde blood flow causes bi-directional movement of blood between the hypothalamus and pituitary. Once the hypothalamic releasing hormones reach the pituitary, they activate G protein receptors on the cell membrane, creating a cascading chain reaction for the production of their pituitary hormone counterparts. Blood drainage of the pituitary leaves through the cavernous sinuses and the petrosal veins and out the jugular foramina via the jugular vein. Note that the blood supply to the pituitary via the hypothalamus is not unidirectional and can flow both ways creating ultra-short biofeedback loops. The hypothalamus releases its secretions via hypothalamic neurons, which end in the infundibulum and permeate into the fenestrations at the perigomitolar capillaries. This enters the portal vein, which enters the capillary circulation of the anterior pituitary (which provides 80-90 % of the blood supply to the pituitary). The pituitary, as stated above, is attached to the hypothalamus via the pituitary infundibulum. The diaphragm sellae has a 5mm opening for the hypophyseal stalk and allows transmission of pulsations of CSF. The purpose of the pituitary infundibulum is to act as a direct pathway for hormonal secretion between the hypothalamus and the pituitary. Pituitary hormones are released as pulsations, which does affect hormonal levels minute, by minute, which may give false positives when measuring hormonal levels. Each releasing factor (hormone) that is released from the hypothalamus causes a release of a hormone from the anterior pituitary. The hypothalamus also produces two hormones called anti-diuretic hormone and oxytocin. The anti-diuretic hormone is formed primarily by the supraoptic nuclei, whereas oxytocin is formed primarily in the paraventricular nuclei. The major nerve tracts of the neurohypophysis arise from these two nuclei, from large cells termed magnocellular cells forming the supra optico hypophyseal tract and the paraventricular hypophyseal tract. AVP and oxytocin tracts are also distributed widely and project into the brain stem affecting the vagal nuclei, glossopharyngeal nuclei, and the spinal cord, sending information to the ANS to evaluate blood pressure. Vasopressinergic and oxytocin fiber pathways (which have different effects than those that end in the posterior pituitary) also terminate in the choroid plexus, which influences salt and water exchange between the brain (especially regions associated with emotion and memory) and the CSF. Neurological impulses from the two nuclei above, cause a secretory granular release of these two hormones into the posterior pituitary, which are then released into the adjacent capillaries. It is interesting to note that the differences between oxytocin and anti-diuretic hormone are two amino acids. Otherwise, the chains are identical. The functions are entirely different, as you will see. The anterior pituitary is controlled by the hypothalamus in a slightly different manner than the posterior pituitary. Oxytocin and anti-diuretic hormone (AVP) are produced in the hypothalamus and are released into the posterior pituitary, via the neurological tracts of those nuclei mentioned above in the hypothalamus. Other neurological tracts secrete other neuropeptides called TRH (thyrotrophin releasing factor), CRH (corticotrophin releasing hormone), VIP and neurotensin. Paraventricular hypophyseal tracts located on either side of the ventricles are both unmylenated and descend thru the infundibulum. The releasing factors from the hypothalamus are transmitted to nerve endings, which then release these factors into a primary plexus of veins known as the hypophyseal portal system. These veins are located in the pituitary infundibulum and travel into the anterior pituitary, releasing the hypothalmic hormones into and stimulating the anterior pituitary. THE ANTERIOR PITUITARY (PARS DISTALIS, PARS GLANDULARIS) The anterior lobe is composed of 3 divisions: 1. PARS DISTALIS - largest and produces most of the hormones 2. THE INTERMEDIA-the least developed 3. TUBERALIS-attached to the pituitary stalk and produces many of the glycoproteins. At this poin, there are cells that produce specific hormones, from specific releasing factors released from specific areas in the hypothalamus. There are 5 specific secreting cells that arise from totipotential pituitary stem cells of the anterior pituitary. They are: • CORTICOTROPHIC CELLS-which express POMC (pro-opiomelanocortin) peptides including ACTH • SOMATOTROPH CELLS-which express growth hormone • THYROTROPHS-which express TSH • GONADOTROPHS-which express FSH and LH • LACTOTROPH CELLS-which produce prolactin These hormones are produced in the anterior pituitary and are now released into the hypophyseal portal veins. They continue down through the circulatory system to target sites in the body. Any hormones that are now released from the target sites reenter the bloodstream and are transported back to the hypothalamus via the hypothalamic artery and to the pituitary via the hypophyseal artery. This is why it should be looked at as a "neuroendocrine axis" due to this dual control mechanism. It makes much more sense and is more reliable to have each system checking and balancing each other. The following hormones are released from the anterior pituitary: 1. FOLLICLE STIMULATING HORMONE (GONADOTROPHINS) -are released by lutenizing hormone-releasing hormone (LHRH) via the hypothalamus. Gonadotrophin cells make up 10-15 % of the anterior pituitary. FSH and LH regulate gonadal steroid hormone biosynthesis and germ cell production. FSH, LH, TSH, and HCG are all glycoproteins. The purpose of follicle stimulating hormone is to stimulate the growth of the follicle on the ovary. FSH, LH, TSH AND HCG all have identical alpha subunit chains. These are polypeptides containing 92 amino acids, whereas the beta subunit chains contain 117, 121, and 145 amino acids. LHRH synthesizes these alpha and beta gonadotrophin subunits forming and secreting FSH, LH, CRH (corticotrophin releasing hormone) and progesterone. The follicle-stimulating hormone increases estrogen levels. As estrogen levels rise in the bloodstream, they enter the hypothalamic artery and decrease the output of LHRH from the hypothalamus. There are also a group of peptide hormones produced by the gonads called inhibins, which are produced by the follicular-luteal and sertoli cells of the gonads that inhibit FSH secretion, without affecting LH secretion. Activins also produced by the above cells stimulate GnRF, which induces FSH production. Activins and inhibins regulate granulose cell growth, differentiation, steroid hormone production, oocyte maturation and follicular development. You will notice that most hormones either increase or decrease the output of other hormones through this kind of a feedback mechanism. If a hormone increases the output of another hormone, then it is said to be a positive feedback mechanism. On the other hand, if a hormone decreases the output of another hormone, then it is said to be a negative feedback mechanism. 2. CORTOCOTROPHIN STIMULATING HORMONE (ADRENO-CORTICOTROPHIC STIMULATING HORMONE) (ACTH)-ACTH production is inhibited by angiotensin 2, activins, inhibins, cytokines and cell-to-cell communication. Corticotrophs constitute 20% of the anterior pituitary. ACTH is a 39 amino acid peptide made from a 241 amino acid structure called pro-opiomelanocortin (POMC). This is cleaved in tissue-specific fashion to yield small peptide hormones. POMC is also transcribed in other tissues such as the brain, liver, kidney, gonads and the placenta. POMC expression within the hypothalamus is cleaved into MSH and is thought to regulate hair color and appetite control. POMC is controlled by CRH, arginine, vasopressin, stress, circadian rhythms and the negative feedback of cortisol. Pro-inflammatory cytokines (interleukins 1 and 6, TNF (tumor necrosing factor) and physical stress increases ACTH release. ACTH circadian rhythms begin at 4 am and peak at 7 am, and are generated by the supra chiasmic nucleus, which signals CRH release. ACTH is secreted in bursts and increases in frequency 3-5 hours after sleep and is highest upon awakening. Adrenal steroid hormones reach their peak between 11 pm and 3 am. ACTH circadian rhythms are entrained by visual cues and the light/dark reactions. The rhythms are affected by sleep/wake, light/dark reactions, spontaneous bursts and stress via CRH. Glucocorticoids inhibit while CRH stimulates the synthesis of ACTH by binding to high-affinity receptors stimulating cyclic-AMP activating protein kinase A of the POMC mRNA (pro-opiomelanocortin). POMC undergoes post-translation processing including glycosylation, enzymatic cleavage, phosphorylation, NH2 terminal acetylation, and COOH amidation via amidase, which catalyzes the formation of a monocarboxylic acid and ammonia by cleavage of the C-N bond of a monocarboxylic acid amide. ACTH is also cleaved into beta-MSH and beta-endorphin. The actions of ACTH on the adrenals is to maintain adrenal size, function and adrenal steroid genesis thru specific cell membrane receptors, which requires a G protein-coupled melanocyte 2 receptor (3500 on each adrenal cell) and calcium ion channels for ACTH to bind. This activates adenyl cylclase, which increases cAMP and protein kinase A activity and phosphorylation of many proteins. ACTH secretion activates the conversion of cholesterol into pregneolone (hormone production) and protein synthesis via p450 enzyme transcription for cortisol, aldosterone and 17-hydro progesterone, which is necessary to produce steroid hormones. Exercise, which is exhausting and for short durations increases ACTH immensely. Pain, infection, trauma and hypoglycemia also affect ACTH. ACTH is controlled by a 3-tier system: 1. Hypothalamic secretions such as CRH and vasopressin 2. Intra pituitary cytokines and growth factors 3. Glucocorticoid negative feedback on the hypothalamus Glucocorticoid target neurons lie outside the hypothalamus in the hippocampus, septum, and amygdale nucleus, and are part of the visceral brain involved in emotional states. At the hippocampus glucocorticoid receptors determine the set point for cortisol. Glucocorticoids affect cerebral vascular permeability, choroid transport of H20 and electrolytes, regulating CSF synthesis and brain volume. Although most steroids that affect the brain come from the circulation, these steroids produced in the brain are called neurosteroids (estradiol, pregnenolone, dehydroepiandosterone located in the oligodendroglial cells). Glucocorticoids inhibit the release of CRH and AVP. Morphine stimulates the release of ACTH. 3. THYROID STIMULATING HORMONE (TSH) -Thyrotrophs make up 5% of the anterior pituitary. TSH is a glycoprotein where the cells are located in the anteromedial portion of the anterior pituitary. TSH is composed of two subunits an: • Alpha subunit-which is similar to lh, fsh, and hcg • Beta subunit-which is 112 amino acids long TRH increases transcription of both alpha and beta units, whereas dopamine inhibits them. TRH stimulates glycosylation of TSH within the rough endoplasmic reticulum, which is then sent to the Golgi apparatus, folded and put into secretory granules. Estrogens, glucocorticoids, and GH modify TSH secretion. Stress also inhibits the release of TSH and GH. TRH binds to the thyrotrophin membranes, and through calcium ion channels and cGMP (cyclic guanosine monophosphate), which act as secondary messengers, produce between 100-400mU/day of TSH. TSH secretion is pulsating in nature, pulsing every 2-3 hours. Circadian peaks with the onset of sleep are between 9 pm-5am, are at a minimum between 4-7pm, and do not appear to be sleep entrained. This is also accompanied by an ultradian rhythm of 90-180 minutes. TSH stimulates the thyroid to produce thyroxin, which determines metabolic rate with pulsating variations of thyroxin at 1-2 hour intervals. TSH is decreased by warm temperature, starvation, and infection via tumor necrosing factor. TSH does the following: a. Stimulates phospholipid metabolism b. Stimulates purine and pyrimidine precursors and their incorporation into nucleic acids TSH is regulated by an open loop feedback via thyroxin, whereby thyroxin passes into the CSF of the lateral ventricles and is taken up by the epithelial cells of the choroids plexus. When thyroxin levels are low, these stimulate TRH-secreting neurons in the hypothalamus. TSH may be modified by estrogens, glucocorticoids, and GH and are inhibited by the pituitary and hypothalamic cytokines. Thyrotrophin is also inhibited by somatostatin and dopamine. 4. LUTEINIZING HORMONE-plays an important role in ovulation and the release of estrogen in the female and testosterone in the male. 5. LUTEOTROPHIC STIMULATING HORMONE (PROLACTIN) -lactotroph cells comprise 15-25 % of the anterior pituitary, and most come from GH-producing cells. Prolactin is 199 amino acids long, closely resembles GH, and is produced in the pituitary by small polyhedral cells. Approximately 100 ugs of prolactin are produced daily as compared to 50 times this for GH. Dopamine secretions via the tuber infundibular pathways inhibit prolactin, by inhibiting adenyl cylclase activity and the release and synthesis of prolactin. Prolactin is also inhibited by calcitonin and transforming growth factor. Prolactin-releasing factors include GnRH, TRH, VIP, oxytocin and estrogen (which increases gene transcription and secretion.) Prolactin is released in moderate amounts during mid-day and increase around bedtime. Prolactin stimulates the development of breast tissue (along with growth hormone and IGF 1) and the secretion of milk. During pregnancy, the pituitary doubles due to PRL producing cells. Prolactin levels can increase from 200 micrograms to 500 micrograms and ammonic PRL may increase to 100 times that of the blood. Suckling causes the mechanoreceptors in the breasts to stimulate nerves in the nipple, which travel to the spinal cord, stimulating the release of prolactin. Then they travel to the spinal cord up through the spin thalamic tract to the lateral cervical nucleus, and to the medulla. Neurological impulses ascend to the oxytocin neurons of the magnicellular cells, to the supraoptic nuclei and the paraventricular nucleus, finally affecting the pituitary. Oxytocin is affected by mating, emotional and physical stress, and cycles related to sleep. The principle inhibitor of prolactin is dopamine. Prolactin is neurologically controlled by many tuber hypophyseal neurons, where the set point is controlled by dopamine secretion (inhibits PRL where serotoninergic stimulates the release). The posterior pituitary also affects PRL release via oxytocin, AVP, and TRH. Prolactin acts through receptors in the liver, breast, adrenal cortex, kidneys, epidermis, lungs, myocardium, pancreatic islets, brain, lymphocytes, ovaries/uterus and testicle/prostate. These are the same receptors used for GH reception. Prolactin and oxytocin together regulate milk production, whereas oxytocin is used for milk let down. Both hormones are under the control of the gonadal steroidal hormones. Milk is synthesized in the glandular cells of the alveoli. Oxytocin receptors are found on these glandular cells, which cause these cells to contract expelling milk into the ducts, where oxytocin causes a widening and contracting of these same ducts. REGULATION OF THE MENSTRUAL CYCLE On the first day of menstrual bleeding, the follicles are small, accompanied by low levels of estradiol. Pulsations of LH are fast, about 1 every 60 seconds. FSH levels are high, which increase follicular size and estradiol production. As estradiol production increases, it acts as a negative feedback loop on the hypothalamus, decreasing LH to 1 pulsation every 90 seconds. At the 15th, day estradiol, which is at a peak, triggers the hypothalamus to release GnRH and high amounts of FSH and LH, which then stimulates the dissolution of the follicular wall, releasing the ovum into the fallopian tube. The Follicular cells now undergo differentiation and become the corpus luteum (yellow body) that secretes large amounts of progesterone. This will maintain pregnancy due to its negative feedback on GnRH, FSH and LH production. The time frame is fixed for the corpus luteum. This also produces small amounts of estradiol. If the egg is not fertilized and implanted in the endometrial lining, then the corpus luteum digresses due to prostaglandin F production, which causes luteolysis, decreasing progesterone and estradiol production. This causes a sloughing off of the endometrium within 28-30 days, or at the end of pregnancy prior to parturition. Just prior to parturition, there is an increase in FSH and LH production and oxytocin is released in an explosive pulsating fashion. Stresses on reproduction include: • Mental • Diet chemical • Physical exercise • Pain and injury • Infection All create reductions in GnRH, FSH, LH, and gonadotrophins. Fuels essential for reproductive function are glucose and fatty acids. 6. MELANOCYTE-STIMULATING HORMONE-This stimulates the melanocytes to produce melatonin for skin pigmentation and sexual drive. 7. SOMATOTROPHIN (GROWTH HORMONE) (GH)-Makes up 50% of the cells of the anterior pituitary and produces between .25-52 mgs every 24 hours with a storage capacity of 5-10 mgs at any time. Somatotrophin is a 191 amino acid chain with a molecular weight of 22,005 and a half-life between 9-27 minutes. The purpose of growth hormone is to create growth in the body. It does this by: • Promoting protein synthesis, amino acid transport, increased urinary nitrogen retention, increases lean muscle tissue and energy expenditure • Increases fatty-acid breakdown for energy • Decreasing glucose utilization, by enhancing glycogen deposition and insulin secretion • Increasing bone growth through osteoclastic activity, epiphysis growth, osteoclastic differentiation, and activity and increases bone mass by endochondral bone formation. • Having acute insulin-like effect followed by lipolysis, decreased glucose transport, decreased lipogenesis (by inhibiting lipoprotein lipase) and increased lipolysis. GH has been described as being, anabolic, lipolytic and diabetogenic. GH does the following: a. Stimulates the Liver-RNA synthesis, plasma protein synthesis, somatomedin release and replication b. Stimulates Muscles-amino acid transport and incorporation c. Stimulates vascular outgrowth of blood vessels d. Stimulates hemopoeitic centers via increasing mitosis e. Stimulates adipose tissue lipolysis GHRH, GH secretagogues, and SRIF receptor subtypes 2 and 5, mediate GH secretion and controls GH. GHRH induces GH gene transcription and hormone release whereas SRIF inhibits GHRH but not GH biosynthesis. Ghrelin, which is 28 amino acids long, induces GHRH and GH production. Ghrelin is synthesized in peripheral tissues, especially the gastric mucosa neuroendocrine cells. GH release is from rhythms, with a maximum of 2 mgs per day in late puberty, to 20 micrograms in older or obese people. Most GH is released during nocturnal times, irrespective of sleep, with the highest release during slow wave sleep and lowest during REM sleep. Feedback mechanisms also increase GH release such as: • Exercise • Physical and emotional stress • Slow wave sleep • Fasting • High-protein meals • Specific amino acids such as arginine and leucine • High carbohydrate meals when blood sugar is falling. • The sex hormones estrogen, progesterone, testosterone, and TSH also modify GH High levels of glucocorticoids suppress GH. 3 inhibitory peptides, GH itself, somatostatin, and IGF 1 also regulate GH. Other factors that stimulate GH release are insulin in hypoglycemia (which can also suppress GH), arginine, leucine, lysine, norepinephrine, AVP, alpha-MSH, glucagon, epinephrine, 5-hydroxytryptophane, melatonin, and potassium. Other factors that inhibit GH are acetylcholine, progesterone, morphine, melatonin and increased intake of free fatty acids. GH secretion is low in obese people due to high somatostatin levels. Depression also leads to decreased levels of GH. GH has an inverse relationship to insulin and GHRH containing nerve fibers that arise from the arcuate and ventromedial nucleus. GHRH via GHRH cell membrane receptors increase adenyl cyclase, cAMP, protein kinase C and intra calcium ion concentration whereby somatostatin has the opposite dominant effect on these same receptors. IGF 1 (somatostatin C) also influences the hypothalamus to reduce GHRH via the hippocampus (and are excitatory), from the amygdale, which can be excitory (basso lateral amygdale) and inhibitory (corticomedial amygdale). The ventromedial nucleus regulates fat and carbohydrate metabolism. This nucleus contains gluco receptors stimulating insulin secretion and GH release. From a biochemical blood chemistry perspective, the pituitary hormones deal with the growth of the body. This is accomplished by hormones of the anterior pituitary controlling lipoprotein digestion and placement for growth and repair, via the control of all organs and glands that control digestion, assimilation, and metabolism. Without digestion and proper placement of the prepared foods by the body, you have no growth. The primary purpose of the pituitary is one of anabolism, rather than catabolism. This means that any catabolic disease that overcomes the human body may have their roots in the anterior pituitary. The following blood tests are used to determine anterior pituitary function: 1. CHOLESTEROL-This is a byproduct of protein metabolism, which is the bonding of oily fats to nitrogen and is produced by every cell in the body. This is called your endogenous cholesterol. Exogenous cholesterol comes from dietary intake. It is the combination of the above two that shows cholesterol levels. Did you know that the majority of cholesterol produced and taken in through diet forms an enzyme called cholic acid? Cholic acid is an enzyme, which is released by the gallbladder to emulsify fats, which you take in through your diet. If you do not take in any fat, then your body does not need any cholic acid. Since 50-60% of your cholesterol is used to produce cholic acid, your cholesterol levels will rise. Such is the case with all the people on low-fat diets trying to reduce their cholesterol levels. 25-35% of the cholesterol is used as a precursor to make your sex hormones, estrogen, progesterone, and testosterone. Cholesterol is also used to make antibodies and acts as a mucous lubricant for mucus, synovial, and cellular membranes. Since the anterior pituitary controls protein digestion and placement, you can see why cholesterol, which is a byproduct of protein metabolism, can be of use in determining a problem with the anterior pituitary. 2. BLOOD UREA NITROGEN-This is an end product of protein metabolism. When lipoproteins enter the liver via the calcium magnesium gradient, the liver changes the foodstuff from an inorganic to an organic state, and can now process the food. Cleaving a nitrogen atom (breaking a bond) from the amino acid molecule does this. Thyroxin, which is produced by the thyroid, is what "cleaves off" this nitrogen atom from the protein. So, thyroxin oxidizes the protein molecule via iodine, by splitting off one nitrogen atom. When the nitrogen is released, it is converted into ammonia, then to urea, via the ornithine cycle. From the liver, it is sent to the kidneys, via the blood stream, to be released in the urine. 3. MAGNESIUM AND CALCIUM-Calcium is the substance that pushes proteins, fatty acids, and triglycerides through the intestinal wall and through the cell membrane of each cell. When the calcium to magnesium ratio is greater than two-parts calcium to one-part magnesium, there is a movement of the above through the intestinal wall. This calcium to magnesium phenomenon creates an electrical osmotic gradient that draws the calcium and lipoprotein across the membrane of the cell. Magnesium is also very abundant within the cell, approximately one-sixth the amount of potassium. The calcium magnesium ratio within the cells is five to one. In plasma, 75 percent of the magnesium is in the ionic state, with the remainder bound to protein. Magnesium, within the cell, acts as a catalyst for enzymes associated with carbohydrate metabolism. Increased extracellular magnesium decreases neurological and muscular-skeletal activity. The anterior pituitary and its hormones are used to control the mineral magnesium in this endeavor. Calcium, due to its "ratio effect," can also be looked at when determining anterior pituitary function.	268%	Add
Pancreas Pancreas THE PANCREAS The pancreas is composed of a head and a tail. The purpose of the pancreatic head is used to secrete pancreatic enzymes. The purpose of the pancreatic tail is to produce insulin. For more information check the pancreatic head and tail sections.	204%	Add
Stomach Alkaline Stomach Alkaline THE STOMACH Phosphorus works in the stomach to stabilize sugars and activate starches by the twofold process of phosphorylation. Phosphorus in conjunction with HCl, pepsin, zinc, and vitamin C via the thymus helps in the: 1. Stabilization of sugar-simple sugars are easily oxidized (combusted) before they reach the liver, resulting in low sugar levels. Pepsin stabilizes these simple sugars, so they can be transferred to the liver for storage. 2. Activation of starches-HCl is necessary to breakdown oily carbohydrates (grains), which are difficult to oxidize (combust), thus making them readily available for oxidation. The above two mechanisms establish an HCl-pepsin balance in the stomach for proper pH digestion. The presence of both HCl and pepsin in the stomach are critical for preparing carbohydrates and proteins for further digestion in the small intestines. Phosphorus indicates the amount of acid balance in the body. It does this by regulating secretions of HCl and pepsin in the stomach by the foods you eat. For example, when you eat foods that are high in phosphoric acid, there will be a release of pepsin to neutralize the acid. On the other hand, foods low in phosphoric acid content will cause large amounts of HCl to be released. Phosphorus then carries carbohydrates across the intestinal wall for absorption by the liver. Phosphorus also affects the intrinsic factor function by releasing alkaline B vitamins into inorganic foods, converting them into organic foods for storage in the liver sinusoids. Patients that have an acid pH in their stomach should avoid excessive amounts of acid forming foods such as meats, dairy, grains and junk foods. Patients that have an alkaline pH should avoid excessive amounts of alkaline forming foods such as fruits and vegetables. Diet has a dramatic affect on the acidity or alkalinity of the stomach and is usually the culprit in stomach conditions. The 3 Phases Of Gastric Secretion 1. The Cephalic Phase- which is the result of hunger, sight, smell and thought about food neurologically controlled by the cerebral cortex that project to appetite centers in the amygdala or hypothalamus. This phase accounts for 1/5th of the digestive juices produced. 2. The Gastric Phase- when the food enters the stomach it excites long vasovagal and local enteric nerves that stimulate the release of gastric juices accounting for 2/3rds of the 1500 ml's released daily. 3. The Intestinal Phase - once the food enters the duodenum, it triggers the release of gastrin from the intestinal mucosa thus inhibiting the release of gastric juices. The presence of food in the small intestines initiates an enterogastric reflex, which also inhibits gastric secretions. The presence of secretin and cholecystokinin are responsible for pancreatic enzyme release. Cholecystokinin releases bile via the gallbladder and also inhibits gastric function. Acids, protein by-products, gastric inhibitory peptide, vasoactive intestinal polypeptide, and somatostatin all inhibit gastric secretions. Since the stomach is poor at absorption, very little takes place. It is only when you reach the small intestines that you find folds known as valvulae conniventes, which increase the surface area of the small intestines 3 fold. Extending from these conniventes are small projections called villi, which increase the absorption another 10 fold. These villi are close together and their outer epithelial cells form a brush border protruding into the chyme. This increases the absorptive power another 600 fold. This makes the surface of the small intestines 250 sq. meters (About the size of a tennis court). The absorptive capacity of the small intestines is astounding. It can absorb several kilograms of carbohydrates, 500-1000 grams of fat (20-40 ounces), 500-700 grams (20-28 ounces) of protein, and 20 or more liters of water daily. There are four types of glands that are found in the gastrointestinal tract: 1. Salivary cells are found in the mouth, pancreas, and the liver 2. Mucous glands- Mucous contains, water, electrolytes, glycoproteins, and HCO3 ions. The function of mucous is to adhere tightly to the food while it coats the intestinal wall. Mucous prevents food from contacting the mucosa. Mucous also causes fecal particles to adhere together to form a mass. Mucous is also very resistant to digestive juices, and can buffer acids or alkaline enzymes. The esophagus also secretes mucous. The mucous glands secrete mucous in response to vagal stimulation, gastrointestinal enzymes, and irritating factors. Mucous glands that are in the upper duodenal area between the pylorus and papilla of vata are called "Brunner's glands". Crypts of Lieberkuhn are found in the small intestines. 3. Tubular cells- are found in the stomach and are of 2 types: the oxyntic or gastric and the pyloric. The first, oxyntic, are your parietal and chief cells. The parietal cells secrete HCl, intrinsic factor for B12 absorption, and histamine. The chief cells secrete pepsinogen, intrinsic factor and mucous. The second type of tubular gland is called the pyloric gland. The pyloric glands mainly secrete mucous but also pepsinogen and gastrin. The oxyntic glands are located in the body and fundus of the stomach comprising 80% of the stomach; the pyloric glands are found in the antral portion of the stomach. These tubular cells are also found in the upper part of the small intestines. Pepsinogen, which is not reactive, is activated and transformed into pepsin by coming in contact with HCl. Pepsin is a proteolytic enzyme that is highly reactive in an acid media between (1.8-3.5). Therefore, both HCl and pepsin are responsible for protein digestion. Other enzymes of the stomach include gastric lipase and amylase; both are extremely weak and play a minor role in the digestion of fats and starches. Gelatinase, another enzyme, is responsible for liquification of proteoglycans found in meat. The stomach also secretes intrinsic factor, which is responsible for B12 absorption in the ileum. B12 is responsible for red blood cell maturation. Gastric secretions have a pH of 1.0-3.5. 4. The stomach also secretes gastric amylase and lipase. The Neurotransmitters Affecting Gastric Secretions Are: 1. Acetylcholine-which is responsible for pepsinogen via peptic cells, gastrin via gastric cells, HCl via parietal cells and mucous secretions. 2. Gastrin (2 types G17 and G34) named for the number of amino acids that make them up, and histamine (an amino acid derivative) both stimulate HCl production. When gastric or acetylcholine are present histamine has a much stronger effect on acid production. All of these neurotransmitters activate receptor sites on secretory cells, which stimulate the secretory process. Amino acids, caffeine and alcohol can also stimulate gastric secretory activity. Neural Control Of The Gastrointestinal System The GI tract is controlled by: A. Reflex activity between the brain stem (vagus nerve dorsal motor nuclei), such as the stomach motor and secretory activity, pain and strong powerful colonic contractions. B. The spinal cord via the autonomic nervous system. The sympathetic division extends from T5-L3 forming the celiac and mesenteric plexuses and the sympathetic chain ganglion, which inhibits peristalsis and digestive secretions by the inhibition of the myenteric and submucosal plexus with norepinephrine. Usually, they control long range communication between the stomach, small intestine, ileocecal valve and the colon, by controlled slowing or speeding up of movement of food and fecal material. C. The parasympathetic outflow division originates from S1-S3 and stimulates the movement of fecal material and reabsorption of H2O and electrolytes. Remember that almost all sympathetic or parasympathetic activity is afferent in nature. This means that distention, mucosal irritation from foods, drugs, preservatives, pH etc. send afferent messages to the brain stem initiating the proper course of action to occur. D. The GI tract has its own nervous system called the enteric nervous system and is found in the gut wall extending from the esophagus to the anus (100 million neurons are the number of neurons in the spinal cord). The enteric nervous system releases the following neurotransmitters: acetylcholine, norepinephrine, ATP, serotonin, dopamine, cholecystokinin, substance P, vasoactive intestinal polypeptide, somatostatin, and leu-enkephalin. Acetylcholine stimulates intestinal activity norepinephrine inhibits intestinal activity. The enteric nervous system is composed of 2 plexuses 1. myenteric plexus (Auerbach's) found between the circular and longitudinal fibers and controls peristaltic movement. The myenteric plexus is composed of linear chains of interconnecting neurons. When stimulated it increases: • Tonic contractions • Rhythmic contractions • Velocity of conduction • Rate of rhythm · · · Please note that the myenteric plexus does play a role in inhibition of the pyloric sphincter and the ileocecal valve. 2. Submucosal plexus (Meissner's plexus) is found in the submucosa and is responsible for digestive secretions and blood flow. The purpose of the enteric nervous system is to control peristalsis and digestive secretions short range over small distances. This is most beneficial since the body uses a finer control over the local digestive process. Digestion And Absorption In The Gastrointestinal Tract Carbohydrate Digestion- There are 3 major sources of carbohydrates in the diet Sucrose, a disaccharide known as cane sugar Lactose, a disaccharide known as milk sugar Starches (grains), which are long polysaccharides When monosaccharides form disaccharides, hydrogen is removed from one monosaccharide and a hydroxyl group is removed from the other monosaccharide, forming water in a process (condensation). When disaccharides split into monosaccharides the process is called hydrolysis (the addition of water to form the 2 monosaccharides). Humans cannot digest cellulose. Carbohydrate digestion starts in the mouth via an alpha amylase known as ptyalin, secreted by the parotid glands. This enzyme hydrolyzes starches into maltose and other small polymers of glucose (3-9 glucose molecules long.). 3-5% of all starches are digested in the mouth. As the food enters the stomach ptyalin continues to digest the carbohydrates so that within 1 hour, upon entering the stomach, most of the carbohydrates are converted into maltose. When the pH falls below 4.0 ptyalin starts to become inactive. By the time the chyme reaches the duodenum and jejunum, pancreatic amylase, which is much more potent then ptyalin (more concentrated), converts the remaining polymers into maltose. In the lining membranes of the intestinal lumen (microvilli brush border) there are four enzymes produced: Lactase, which splits lactose into galactose and glucose Sucrase, which splits sucrose into fructose and glucose Maltase, which splits maltose into glucose. Alpha Dextrinase, which splits all of the above as well as dextrins 2. Protein Digestion-Protein digestion starts in the stomach via pepsin. Pepsin is also important for digesting collagen, an albuminoid found in meats. Pepsin is most active at a pH of 2-3. The HCl produced by the body has a pH of .8. When proteins leave the stomach they are mostly in the form of proteases, peptones, and large polypeptides. When the chyme reaches the small intestines the pancreatic enzymes trypsin and chymotrypsin split proteins into small peptides and carboxypolypeptidase then split a small percentage of these into amino acids. The bulk of the peptides are broken down by the multiple peptidases located in the brush border of the intestinal membrane. The most important peptidases are aminopolypeptidase and several dipeptidases. These split the proteins down to di and tri-peptides, which enter the microvilli membrane into the interior of the epithelial cell where other peptidases break up the remaining di and tripeptides into amino acids to be absorbed into the blood stream. Please note that di, tri, and polypeptides can still enter the blood stream and can cause allergic reactions. 99 % of all protein is absorbed as amino acids. 3. Fat Digestion The most abundant fat in the diet is in the form of triglycerides, which contains a glycerol nucleus and 3 fatty acids (stearic, and palmitic acid, which are saturated and oleic acid which is unsaturated). All 3 come from animal and not plant origin. The usual diet contains phospholipids, cholesterol and cholesterol esters. Cholesterol is formed in the liver from degraded products of fatty acid molecules, which give cholesterol its fatty characteristics. Fat (butterfat) is digested in the stomach via gastric lipase (tributyrase) in very small amounts. 99% of fat digestion takes place in the intestines via bile. Bile contains bile salts and a phospholipid known as lecithin in the form of ionized sodium salts. Bile salts have the ability to form micelles, small globules of fat attached to the bile salt. This occurs because the sterol portion of the bile salt is highly soluble in fat and a polar portion of the bile salts and lecithin are highly soluble in water. This reducing and changing the polarity reduces the interfacial tension between the fat cells so digestive enzymes can continue to break down the fat. This increases the total surface area of the fat a 1000 fold. Pancreatic lipase is responsible for splitting 99% of the triglycerides into 3 fatty acids and 2 monossachrides. Cholesterol, its ester (cholesterol +1 molecule of a fatty acid) and phosopholipids (via cholesterol ester hydrolase and phospholipidase respectively) are broken down via hydrolysis of the fatty acids from their molecular structures. The bile salts, when attached to lipids create micelles, which are highly charged and increase the absorption of these fatty acids, glycerol, free cholesterol and the remaining portion of the phospholipids. Please note that without bile salts much of the fat will be blocked from entering the blood stream.	193%	Add
Heart Heart HEART Keeping it simple, the heart is a muscle that never rests. It works 24/7. From an ionic standpoint, calcium and potassium ions (calcium pump) are responsible for creating the action potential of heart cells. Potassium causes the heart to relax, and decreases the heart rate, whereas calcium has the exact opposite effect. So, any endocrine imbalance causing problems with calcium or potassium has an adverse affect on the heart. On the other hand, neurotransmitters from the autonomic nervous system and the adrenals such as acetylcholine and epinephrine inhibit and excite the heart. Stimulation of the vagus nerve (parasympathetic division) releases acetylcholine, which decreases the rhythm of the SA node and decreases the junction fiber rhythm of the AV node, due to the acetylcholine effect of increasing cell membrane permeability to potassium. For example, the heart rate of a healthy individual can go as high as 250 beats per minute via sympathetic stimulation, and can almost stop due to parasympathetic stimulation. Epinephrine, on the other hand, has the exact opposite effect on the heart. Other hormones such as vasopressin, angiotensin, oxytocin, norepinephrine, serotonin and histamine also affect all types of muscles. Each type of smooth muscle has hormonal gated excitatory or inhibitory receptors for that respective hormone. Other factors, such as lack of oxygen, and increased carbon dioxide and hydrogen, effect baroreceptors inhibiting vasoconstrictor centers in the medulla and exciting the vagus nuclei cause muscles to relax (decreased contraction) or vasodilate. Perhaps one of the most far-reaching effects on the heart is due to sugar metabolism (glucose and triglycerides.) They give the heart muscle the fuel and the spark it needs to run. Without the proper amounts of fuel, you car and heart cannot make the journey. Sugar metabolism is controlled through many glands such as the pancreas, liver, and adrenals. Let us by no means leave out protein. Listen, every time you exercise a muscle, it breaks down, and without proper protein intake, and you will not build that muscle back up again. Your heart is no different; there are many flabby heart patients due to reduced protein intake. I saved the best for last-fat. You will soon find out how important fat is in your diet, and is much more of a friend then you know. The following blood tests are used to determine a heart conditions: 1. CALCIUM-besides bonding to lipoprotein, calcium also bonds to the oily portion of fatty acids. This is necessary for fatty acids to pass through the intestinal wall. If there is poor oxidation of fatty acids, there will be a specific amount of calcium needed to bond to the fatty acids, thereby decreasing the calcium levels in the blood and decreasing heart muscle function. Calcium ions with ATP also activate the "contractile" process in both smooth and skeletal muscle. 2. POTASSIUM-has prime importance in controlling membrane permeability by displacing the chloride ion as well as epinephrine for the next stage, which permits calcium to cross the cell membrane. This causes the heart muscle to decrease in tone. It is the only substance that allows oxygen into unoxygenated tissue. 3. LACTIC ACID DEHYDROGENASE (LDH)-is a glycolytic enzyme that functions as a catalyst in carbohydrate metabolism, aiding the pyruvic and lactic acid interchange. LDH is a byproduct of muscle metabolism. When sugar and water (fatty acid metabolism) are exchanged across a muscle cell interface, the byproduct left is called lactic acid. Lactic acid is also a byproduct of fatty acid metabolism via the alkalizing and oxidizing affects of the pancreatic head. When lactic acid combines with the venous blood (carbon dioxide), there is hydrogen displacement. The lactic acid then bonds to a double hydrogen forming lactic acid dehydrogenase. LDH is then a byproduct of carbohydrate and fatty acid metabolism. The organs and glands that that are most responsible for sugar and water interchange across the muscle cell interface are the pancreas and posterior pituitary (via antidiuretic hormone.) LDH is found chiefly in the heart, kidneys, liver, skeletal muscles, as well as all tissues. LDH is a normal component of the cerebral spinal fluid. 4. TRIGLYCERIDES-High triglycerides indicate a weak heart. This is because triglycerides create the spark necessary for combustion to produce energy, in this case, muscular contraction. 5. CHOLESTEROL-HDLs clinging to arterial walls	170%	Add
Parathyroids Parathyroids THE PARATHYROIDS Located on the posterior portion of the thyroid are four-five parathyroid glands weighing 120 grams total, with an ellipsoidal shape having the dimensions of 6x5x2 millimeters. The blood supply for the parathyroids is the inferior thyroid artery. The chief cells, which are the major cells of the parathyroids, synthesize and secrete parathormone (PTH) (which is 84 amino acid's long) that comes from a pre-proparathormone, which is 110 amino acids long. Though calcium is the major factor controlling the secretion of PTH, secretion of newly synthesized PTH is from preformed pools of PTH, where cAMP only stimulates these pools. cAMP is the major regulator of PTH secretion. Beta-androgenic catecholamines, dopamine, secretin and prostaglandin E can activate adenylate cylclase and increase cAMP, thereby stimulating PTH regulation. The basic function of PTH is to control calcium concentration in the extracellular fluid (ECF). Parathyroid hormone, calcitonin and calciferous are the principle calcitrope hormones. Sodium, calcium, and potassium play a central role in the transmission of information between cells. Phosphates act as: • Cytoplasmic buffers • Participate in energy exchange • Makeup membranes and nucleic acids The bulk of calcium, phosphates, and magnesium in the body are found in the skeleton. RDA's of calcium is between 8-1200 mgs, for magnesium 4-600 mgs and 8-1200 mgs for phosphate. Less than 2% of calcium, magnesium and phosphates are found in the plasma and extracellular fluid and are controlled in narrow limits. Steady states of calcium, magnesium and phosphorus approximate urine loss against intestinal absorption and skeletal mineral apposition against mineral absorption. Magnesium in the cells is complexed to phosphate, citrates and anions such as ATP, AMP, and ADP (such as MgATP2). Phosphates are covalently incorporated into proteins, lipids, and nucleic acids. Many enzymes go thru dramatic shifts in activity via phosphorylation and dephosphorylation. Ionized cellular calcium regulates secondary cell messengers. Calcium can increase in a cell due to electrical impulses, hormones, and intracellular signals. Calcium also interacts with proteins such as protein kinase C, and ion channels found in plasma membranes and the sarcoplasmic reticulum. Parathormone levels elevate cell calcium levels in the renal tubules and the osteoblasts. Calcium is transported from the cytoplasm by exchange with sodium. Contracted striated muscle relaxes with rapid removal of calcium from the cytoplasm into the sarcoplasmic reticulum. Plasma membranes undergo many complex interactions with cellular calcium via membrane permeability and pump activity. In erythrocytes, cellular calcium increases potassium permeability. Mitochondria contain most of the intracellular calcium. There are many cytoplasmic enzyme changes via calcium such as adenylate cylclase, guanylate cylclase, cAMP, ATPase and protein C kinase. Since calcium can regulate contractile proteins, it can affect striated muscle, secretory granule contraction, exocytosis, mitotic spindle function and ciliary beating. Calcium concentrations can be reduced quickly via repetitive nerve stimulation. Albumin accounts for 70% of the protein binding of calcium. Magnesium bonds to the same site on the albumin molecule as calcium, but with a lower affinity, thereby having more magnesium in a diffusible form. Magnesium is also affected just the way calcium is to parathormone, and to a lesser degree calcitonin. 70 % of phosphates are bound to phospholipids and phosphoproteins and are also affected in and out of plasma compartments by parathormone, calcitonin, and calciferols. PTH enhances phosphate secretion and inhibits sodium reabsorption in the proximal tubules. PTH stimulates both bone formation and reabsorption (catabolism and anabolism) via influencing osteoclasts, osteoblasts, and osteocytes. PTH enhances synthesis of hyaluronate and inhibits citrate decarboxylation and collagen synthesis while it increases alkaline phosphatase levels. Other affects of PTH include changes in blood flow, mitosis of lymphocytes, enhanced lipolysis and increased gluconeogenesis from the liver and kidney. PTH reacts with specific receptors on the bone and kidney (renal cortex) activating adenylate cylclase and intracellular messenger cAMP According to Guyton's Physiology on the physiology of calcium and phosphate "phosphates act as buffers, participate in energy exchange, and are an essential component of membranes and nucleic acids. 70 % of phosphates are bound to phospholipids and phosphoproteins." Phosphates do not affect PTH or calcitonin (CT) levels, but PTH and CT affect phosphate levels. The function of vitamin D and the formation of bone and teeth are all tied together in a common system, along with the two regulatory hormones parathyroid hormone (parathormone), calcitonin and the calciferols. In mammals, the bulk of calcium, phosphates and magnesium are found in the skeleton as hydroxyapatite. Less than 2% are found in the extracellular fluid. Plasma calcium is used for clotting and kinin formation, regulates plasma membrane potential and exocytosis. As stated above, albumin accounts for 70% of the bound calcium. Magnesium also binds to albumin, and since it has a lower specificity for the receptors, it creates more free magnesium in the plasma. Calcium, magnesium, and phosphates continuously enter the plasma via the kidneys (intestinal brush borders) and the ruffled border of bones. Calcium, phosphates, and magnesium are depressed in vitamin D deficiencies. Phosphates are reabsorbed by the proximal convoluted tubules due to PTH, and PTH also absorbs magnesium and calcium from the distal tubules. Calcium is poorly absorbed in the intestinal tract, as are most other bivalent cations. Calcium absorption can be dramatically affected by vitamin D, which has a potent effect on increased calcium absorption in the intestinal tract. In fact calcium, magnesium and phosphates are depressed in vitamin D deficiencies and increased with vitamin D excess. Calcium absorption is also increased by dietary sugars. The D vitamins (calciferols) are steroid molecules of 4 rings. Calciferols are absorbed in the chylomicrons of the small intestines (60-90%) and are bound to alpha globulins. Vitamin D is also stored in the adipose tissue. It is not actually vitamin D, but a vitamin D compound that is formed between the liver and the kidneys, known as 1,2,5-dihydroxycholecalciferol. This 1,2,5-dihydroxycholecalciferol is also stimulated by parathyroid hormone. Another vitamin D compound that is important is D3 (cholecalciferol), found in the skin. BONE FORMATION Skeletal tissue consists of an extracellular matrix 55% organic and 45% inorganic and cells. The purpose on the skeletal system is to regulate the distribution of inorganic compounds, such as calcium, for the remodeling and the formation and reabsorption of the matrix. There are 3 types of cells 1. Osteoblasts-derived from pre-osteoblasts from the mesenchyme. They are cuboid in shape, have a lot of Golgi apparatus for collagen processing, and lots of alkaline phosphatase. Osteoblasts are located in the bone-forming surface and are responsible for elaborating organic compounds from the extracellular matrix and the mineralized bone. The unmineralized matrix forms the osteoid zone and is separated from the mineralized bone via the calcification front. Osteoblasts form bone by the release of alkaline phosphatase, which increases the concentration of phosphate into the bone matrix. 2. Osteocytes-once osteoblasts, they are surrounded by an organic matrix and are now called osteocytes. 3. Osteoclasts-are also found on the bone surface. They are multinucleated, highly mobile moving along the bone surface reabsorbing bone. Osteoclasts break bone down. The cytoplasm contains abundant mitochondria, vacuoles, and lysosomes containing acid hydrolases such as carbonic anhydrate. Other cells found in bone are endothelial cells, fibroblasts, preosteoclasts, and preosteoblasts. Other inorganic components that make up the inorganic matrix are calcium, phosphate in a crystalline structure known as hydroxyapatite, with fluorine, sodium, potassium, magnesium and carbonate. 80% of the skeletal mass is made of cortical (compact) bone (long bones). Cortical bone is composed of packed osteons (haversian systems) surrounding a central canal, and volkmann canals, which radiate from the central canal connecting neighboring osteons to form an anatomizing network for blood and lymph. 20% is trabeculae bone (spongy) (vertebra, the ends of long bones and flat bones.) In trabeculae bone, lamellas are arranged in longitudinal bundles and anastomose with the marrow cavity. Please note that the surface area of trabeculae bone is 5 times that of compact bone. Bone formation is controlled by osteoblast differentiation, proliferation, matrix formation and mineralization (by alkaline phosphatase cleaving phosphate groups.) Bone contains many growth factors such as: • Transforming growth factor B produced by the osteoblasts, which stimulate mitogenesis and collagen synthesis • IGF 1 and IGF 2 Bone proteins consist of 13 forms of collagen, osteonectin (a carbohydrate containing protein), osteocalcin, osteopontin (produced by osteoblasts) and proteoglycans (glycosaminoglycans), which are controlled by autocrine, paracrine and systemic hormone regulation. Osteocalcin is a protein making up 1-2% of the total bone protein and depends on vitamins D, K, and C. PROMOTERS OF BONE FORMATION • INSULIN • IGF 1 and 2 • ESTROGENS/ANDROGENS • GROWTH HORMONE • THYROID HORMONE • PTH PROMOTERS OF BONE REABSORPTION • PTH • Interleukin 1 • Prostaglandins • Thyroid hormone • Epidermal growth factor • Vitamin A • Tumor necrosing factor INHIBITS BONE REABSORPTION • Calcitonin • Phosphate • Glucocorticoids FORMATION OF THE CALCIFEROLS 7-DEHYDRO CHOLESTEROL OR ERGOSTEROL PLUS LIGHT LUMSTEROL PREVITAMIN D TACHYSTEROL VITAMIN D2 D3 (CHOLECALCIFEROL) (ERGOCALCIFEROL) DIHYDROTACHYSTEROL D3 is formed through irradiation of 7 dehydrocholesterol. Dihydroxycholecalciferol lines the intestinal epithelium, absorbing large quantities of calcium when needed in the blood or bone. On the other hand, phosphorus is easily absorbed, unless there are large quantities of calcium that combine with phosphate creating an insoluble calcium phosphate compound that is excreted from the bowel. Ninety percent of all calcium loss is from the bowel. Ten percent is excreted in the urine. The ten percent that is excreted in the urine is controlled by parathyroid hormone, which also causes the excretion of phosphorus. Plasma calcium is found in three different forms: • 40% is combined with plasma proteins • 10% is bound to phosphates and is not usable • 50% is in the ionized and diffusible state necessary for heart function, bone formation, and nervous system control. Phosphates exist in two states HPO4, HPO4. When the pH of the extracellular fluid becomes acid, there is an increase in HPO4 and a decrease in HPO4, with the reverse also being true. Phosphorus levels can dramatically change without affecting function. On the other hand, increased amounts of calcium in the blood can cause central nervous system depression. Decreased calcium in the blood can lead to tetney. Parathormone controls calcium ion concentration in the extracellular fluid by controlling calcium absorption in the intestines, excretion via the kidneys (increases distal tubular reabsorption of calcium and magnesium) and release of calcium from the bones. Magnesium can exert control over PTH retention. Calcitonin (CT) is secreted by the parafollicular cells of the thyroid gland as mentioned above, has the opposite effect of parathormone. Although the effect is much weaker than parathormone, there is still that balance necessary to be maintained. Calcium also stimulates the secretion of CT, as does beta androgenic catecholamines, gastrin, and cholecystokinin. CT decreases alkaline phosphatase, pyrophosphatase activity, and hydroxyproline production. CT inhibits calcium reabsorption from bone. Therefore parathormone, which is a polypeptide (110 amino acids long), together with calcitonin (32 amino acid's long), regulates the calcium-phosphorus ratio. If you lack calcium/phosphorus in the blood, then parathormone will shift them out of the bone and decrease excretion from the distal kidney tubules. Bone is composed of: • 90-95% collagen (protein) • 5% ground substance, which is composed of fluid, proteoglycans, chondroitin sulfate and hyaluronic acid. • 5% bone salts composed of calcium and phosphorus. The major crystalline salt is hydroxyapatite (CA10 (PO4) 6 (OH) 2), along with other bone salts such as magnesium, sodium, carbonate, uranium, plutonium, strontium and K. PHOSPHORUS AND CALCIUM INVOLVEMENT IN DIGESTION Phosphorus is also the regulator of the stomach. Phosphorus regulates the amount of HCl and pepsin in the stomach, which controls carbohydrate metabolism via the process of phosphorylation. Phosphorylation is the process that hydrogenates the carbohydrate, which alters the pH for glycogen storage in the liver. Oxygen, on the other hand, oxidizes carbohydrates for immediate use. The thymus, which will be covered later, assists the parathyroids in the process of phosphorylation. If the phosphorus in the stomach is too low, then the carbohydrate cannot be hydrogenated and the HCl content of the stomach increases, causing an acid stomach. When the phosphorus content is too high, there is a depletion of HCl content in the stomach. This creates an alkaline stomach. Calcium is the regulator of the small intestines. Calcium, along with B12 and folic acid, attach to lipoproteins so that they can be polarized through the intestinal wall, via magnesium. At the proper time, the calcium will be severed from the lipoprotein when needed for hormone, enzyme, and antibody formation. At that point, the calcium will be released back into the body. The following tests can be used to assess parathyroid function: 1. CALCIUM 2. PHOSPHORUS	142%	Add
Cecum Cecum TBC	134%	Add

General Support Plan

Product	What for?	Dosage
CELTIC SEA SALT	Micro-minerals Formulation	Season food to taste.
NANNO GREENS	Phytonutrient	As Directed
LIQUID HEALTH	Multiple vitamin Mineral	As Directed
ENDOCRINE COMPLEX	Multiple Gland/Organ	As Directed

Metabolic

Test	Results	M Type 6 M Type 6 Metabolic Type VI Diet Plan VEGETARIAN, LACTO-VEGETARIAN, OVO-VEGETARIAN, OVO- LACTO-VEGETARIAN (Poor Metabolizer) CHARACTERISTICS: Type VI people are very poor metabolizers, which means that they handle most foods poorly. They have difficulty in digestion, absorption and metabolism of all types of food. Therefore, they need the majority of their foods cooked and require a lot more supplementation then the average person. This Type should eat whole and complete foods and eliminate all refined, processed, and synthetic foods. There is usually a suppressed immune and endocrine system function. 1. Burns sugar (carbohydrates) inefficiently and uses sugar for energy. You are usually fatigued. This means that you do well with most carbohydrates that are whole and complete unrefined and cooked 2. Can eat mostly cooked vegetables and fruits avoid raw whenever possible. Your diet should be rich in, fresh cooked vegetables and fruits (as desserts), that should make up between 50-60% of you meal. 3. 50-60% of your foods should be derived from the Alkaline Forming Foods Chart and 40-50% from the Acid Forming Foods Chart. However, you must eliminate all red animal meats. Use beans, fish, and fowl as primary sources of protein. Use nuts, seeds, eggs, and cheeses as your secondary sources of protein. 4. The following foods should be stressed in your diet: A. Whole grains, including bread, cereals, pasta and rice (for carbohydrate and water requirements) B. Moderate amounts of dairy such as whole milk, natural cheeses, and eggs- (for protein fat and fat soluble vitamin {D, E, K and A} requirements) C. Whitefish (trout, catfish, orange roughy, cod, flounder, scrod), fowl (white meat) (for protein fat and fat soluble vitamin {D, E, K and A} requirements) D. All nuts and seeds (for protein fat and fat soluble vitamin {D, E, K and A} requirements) E. All beans and legumes - (for protein and carbohydrate requirements)	M Type 4 M Type 4 Metabolic Type IV Diet Plan MEDITERRANEAN (Excellent Metabolizer) CHARACTERISTICS: Type IV people usually have a genetic background from and around the Mediterranean Sea. This typically includes Spanish, Italian, Greek, Israeli, and Arabic countries. This metabolic type: 1. Burns sugar (carbohydrates) at a moderate rate and uses sugar for energy. This means that you do well with most carbohydrates including carbohydrates that have a mid-range (50-80) glycemic index. 2. Can eat mostly raw vegetables with limited amounts of fruit. Your diet should be rich in salads, fresh uncooked vegetables, and fruits (as desserts) that should make up between 40-50% of you meal. 3. 50-60% of your foods should be derived from the Alkaline Forming Foods Chart and 40-50% from the Acid Forming Foods Chart. You should limit all red animal meats to 2-4 times per week. Use beans, fish, and fowl as other primary sources of protein and nuts, seeds, eggs, and cheeses as your secondary sources of protein. 4. The following foods should be stressed in your diet: A. Whole grains, including bread, cereals, pasta, and rice (for carbohydrate and water requirements) B. Moderate amounts of dairy, such as whole milk, natural cheeses, and eggs (for protein fat and fat soluble vitamin {D, E, K and A} requirements) C. Limited amounts of red meat (2-4 times per week) (for protein fat and fat soluble vitamin {D, E, K and A} requirements) D. Whitefish (trout, catfish, orange roughy, cod, flounder, scrod), fowl (white meat) (for protein fat and fat soluble vitamin {D, E, K and A} requirements) E. All nuts and seeds (for protein fat and fat soluble vitamin {D, E, K and A} requirements) F. All beans and legumes- (for protein and carbohydrate requirements)	M Type 8 Balanced M Type 8 Metabolic Type VIII Diet Plan MEDITERRANEAN, PALEO DIET Balanced Metabolizer) CHARACTERISTICS: This Metabolic Type is a combination of a Metabolic Type IV and Type V. The person should look at both diets and either pick the one that he/she desires the most or if it is a toss up, use a combination of both diets. Metabolic Type IV Diet Plan (Excellent Metabolizer) CHARACTERISTICS: Type IV people usually have a genetic background from and around the Mediterranean Sea. This typically includes Spanish, Italian, Greek, Israeli, and Arabic countries. This metabolic type: 1. Burns sugar (carbohydrates) at a moderate rate and uses sugar for energy. This means that you do well with most carbohydrates including carbohydrates that have a mid-range (50-80) glycemic index. 2. Can eat mostly raw vegetables with limited amounts of fruit. Your diet should be rich in salads, fresh uncooked vegetables, and fruits (as desserts) that should make up between 40-50% of you meal. 3. 50-60% of your foods should be derived from the Alkaline Forming Foods Chart and 40-50% from the Acid Forming Foods Chart. You should limit all red animal meats to 2-4 times per week. Use beans, fish, and fowl as other primary sources of protein and nuts, seeds, eggs, and cheeses as your secondary sources of protein. 4. The following foods should be stressed in your diet: A. Whole grains, including bread, cereals, pasta, and rice (for carbohydrate and water requirements) B. Moderate amounts of dairy, such as whole milk, natural cheeses, and eggs (for protein fat and fat soluble vitamin {D, E, K and A} requirements) C. Limited amounts of red meat (2-4 times per week) (for protein fat and fat soluble vitamin {D, E, K and A} requirements) D. Whitefish (trout, catfish, orange roughy, cod, flounder, scrod), fowl (white meat) (for protein fat and fat soluble vitamin {D, E, K and A} requirements) E. All nuts and seeds (for protein fat and fat soluble vitamin {D, E, K and A} requirements) F. All beans and legumes- (for protein and carbohydrate requirements) Metabolic Type V-Diet Plan (Excellent Metabolizer) CHARACTERISTICS: Metabolic Type V people can tolerate a wide variety of foods. They are prone to hypoglycaemia, so they must stay away from a lot of simple sugars (junk foods) like soda, alcohol (hard liquor), fruit juices, and candy. Metabolic Type V people derive their energy more from fat than from carbohydrates. This Type does well with a lot of red meat (beef, veal, pork, wild game, and lamb) eaten several times a week. It is a true meat and potatoes, man/woman. As far as seafood is concerned, they typically like oily seafood (cold water fish, high omega oils) such as salmon, tuna, sardines, mackerel, and shellfish, with butter. In fact, they like your seafood fried. This type of metabolism: 1. Burns sugar (carbohydrates) rapidly and inefficiently causing your blood sugar to rise and fall rapidly, giving you spikes of energy followed by bouts of fatigue. This means that you do well with most carbohydrates including carbohydrates that have a mid-range (50-80) glycemic index. 2. Can eat cooked and raw vegetables and fruits. Your diet should be rich in fresh cooked and uncooked vegetables and fruits (as desserts), that should make up between 40-50-% of your meal. 3. 50-60% of your foods should be derived from the Acid Forming Foods Chart and 40-50% from the Alkaline Forming Foods Chart. Use red meats, fowl (dark meat and skin) and oily fish as your primary sources of protein. Use eggs, cheeses, nuts, seeds, and beans as your secondary sources of protein. 4. The following foods should be stressed in your diet: A. Red meats such as beef, veal, lamb, pork and wild game (for protein fat and fat soluble vitamin {D, E, K and A} requirements) B. Oily seafood (for protein fat and fat soluble vitamin {D, E, K and A} requirements) C. Fowl, dark meat with the skin (for protein fat and fat soluble vitamin {D, E, K and A} requirements) D. Moderate amounts of dairy such as whole milk, natural cheeses and eggs (for protein fat and fat soluble vitamin {D, E, K and A} requirements) E. All nuts and seeds (for protein fat and fat soluble vitamin {D, E, K and A} requirements) F. Small amounts of beans and legumes (for protein and carbohydrate requirements) G. Small to moderate amounts of whole grains, including bread, cereals, pasta and rice (for carbohydrate and water requirements)	M Type 5 M Type 5 Metabolic Type V-Diet Plan PALEO DIET (Excellent Metabolizer) CHARACTERISTICS: Metabolic Type V people can tolerate a wide variety of foods. They are prone to hypoglycaemia, so they must stay away from a lot of simple sugars (junk foods) like soda, alcohol (hard liquor), fruit juices, and candy. Metabolic Type V people derive their energy more from fat than from carbohydrates. This Type does well with a lot of red meat (beef, veal, pork, wild game, and lamb) eaten several times a week. It is a true meat and potatoes, man/woman. As far as seafood is concerned, they typically like oily seafood (cold water fish, high omega oils) such as salmon, tuna, sardines, mackerel, and shellfish, with butter. In fact, they like your seafood fried. This type of metabolism: 1. Burns sugar (carbohydrates) rapidly and inefficiently causing your blood sugar to rise and fall rapidly, giving you spikes of energy followed by bouts of fatigue. This means that you do well with most carbohydrates including carbohydrates that have a mid-range (50-80) glycemic index. 2. Can eat cooked and raw vegetables and fruits. Your diet should be rich in fresh cooked and uncooked vegetables and fruits (as desserts), that should make up between 40-50-% of your meal. 3. 50-60% of your foods should be derived from the Acid Forming Foods Chart and 40-50% from the Alkaline Forming Foods Chart. Use red meats, fowl (dark meat and skin) and oily fish as your primary sources of protein. Use eggs, cheeses, nuts, seeds, and beans as your secondary sources of protein. 4. The following foods should be stressed in your diet: A. Red meats such as beef, veal, lamb, pork and wild game (for protein fat and fat soluble vitamin {D, E, K and A} requirements) B. Oily seafood (for protein fat and fat soluble vitamin {D, E, K and A} requirements) C. Fowl, dark meat with the skin (for protein fat and fat soluble vitamin {D, E, K and A} requirements) D. Moderate amounts of dairy such as whole milk, natural cheeses and eggs (for protein fat and fat soluble vitamin {D, E, K and A} requirements) E. All nuts and seeds (for protein fat and fat soluble vitamin {D, E, K and A} requirements) F. Small amounts of beans and legumes (for protein and carbohydrate requirements) G. Small to moderate amounts of whole grains, including bread, cereals, pasta and rice (for carbohydrate and water requirements)	M Type 2 M Type 2 Metabolic Type II Diet Plan KETOGENIC DIET (Good Metabolizer) CHARACTERISTICS: Metabolic Type II people are the true carnivores and can almost live on meat alone. Their genetic background is usually from Germany, Scandinavian and northern European countries. They are extremely prone to hypoglycemia so they must stay away from a lot of simple sugars (junk foods) like soda, alcohol (hard liquor), fruit juice, and candy. Metabolic Type II people derive their energy mostly from sources of fat rather than carbohydrates. This type does well with a lot of red meat such as beef, veal, pork, wild game and lamb, every day. You are a true meat and potatoes, man/woman. As far as seafood is concerned you like oily seafood (cold water fish, high omega oils) such as salmon, tuna, sardines, mackerel, and shellfish with butter. In fact, you like your seafood fried. This metabolic type: 1. Burns sugar (carbohydrates) rapidly and inefficiently causing your blood sugar to rise and fall rapidly, giving you spikes of energy followed by bouts of fatigue. This means that you do well with most carbohydrates including carbohydrates that have a mid-range (50-80) glycemic index. 2. Can eat cooked and raw vegetables. Your diet should be rich in, fresh cooked and uncooked vegetables, that should make up between 30-40-% of you meal. Stay away from a lot of fruit and leafy green vegetables and stick with your hearty vegetables such as potatoes, yams, beets, corn and brussel sprouts 3. 60-70% of your foods should be derived from the Acid Forming Foods Chart and 30-40% from the Alkaline Forming Foods Chart. Use red meats, fowl (dark meat and skin) and oily fish as your primary sources of protein, and eggs, cheeses, nuts, seeds and beans as your secondary sources of protein. 4. The following foods should be stressed in your diet: A. Red meats such as beef, veal, lamb, pork and wild game (for protein fat and fat soluble vitamin {D, E, K and A} requirements). B. Oily seafood (for protein fat and fat soluble vitamin {D, E, K and A} requirements). C. Fowl dark meat with the skin (for protein fat and fat soluble vitamin {D, E, K and A} requirements). D. Moderate amounts of dairy such as whole milk, natural cheeses and eggs - (for protein fat and fat soluble vitamin {D, E, K and A} requirements) E. All nuts and seeds (for protein fat and fat soluble vitamin {D, E, K and A} requirements). F. Small amounts of beans and legumes- (for protein and carbohydrate requirements). G. Small amounts of whole grains, including bread, cereals, pasta and rice (for carbohydrate and water requirements).	M Type 7 M Type 7 Metabolic Type VII Diet Plan KETOGENIC DIET (Poor Metabolizer) CHARACTERISTICS: Type VII people are very poor metabolizers, which means that they handle most foods poorly. They have difficulty in digestion, absorption, and metabolism of all types of food. Therefore, they need the majority of their foods cooked and require a lot more supplementation then the average person. They should eat whole and complete foods and eliminate all refined, processed, and synthetic foods. They usually have a suppressed immune and endocrine system function. Metabolic type VII people derive their energy more from fat than from carbohydrates. This type does well with a lot of red meat such as beef, veal, pork, wild game, and lamb several times a week. It is a true meat and potatoes, man/women. As far as seafood is concerned they like oily seafood (cold water fish, high omega oils) such as salmon, tuna, sardines, mackerel, and shellfish with butter. In fact, they like their seafood fried. This type of metabolism: 1. Burns sugar (carbohydrates) rapidly and inefficiently causing your blood sugar to rise and fall rapidly, giving you spikes of energy followed by bouts of fatigue. This means that you do well with most carbohydrates including carbohydrates that have a mid-range (50-80) glycemic index. 2. Can eat cooked and raw vegetables. Your diet should be rich in fresh, cooked, and uncooked vegetables, that should make up between 30-40% of you meal. Stay away from a lot of fruit and leafy green vegetables and stick with your hearty vegetables such as your potatoes, yams, beets, corn, and brussel sprouts. 3. 60-70% of your foods should be derived from the Acid Forming Foods Chart and 30-40% from the Alkaline Forming Foods Chart. Use red meats, fowl (dark meat and skin) and oily fish as your primary sources of protein and eggs, cheeses, nuts, seeds, and beans as your secondary sources of protein. 4. The following foods should be stressed in your diet: A. Red and organ meats such as brain, liver, heart, sweetbreads, beef, veal, lamb, pork, and wild game. Meats should be made or put into soups, gravyâ€™s, or stews for easy digestion and absorption (for protein fat and fat soluble vitamin {D,E,K and A} requirements) B. Oily seafood (for protein fat and fat soluble vitamin {D, E, K and A} requirements) C. Fowl dark meat with the skin (for protein fat and fat soluble vitamin {D, E, K and A} requirements) D. Moderate amounts of dairy such as whole milk, natural cheeses and eggs - (for protein fat and fat soluble vitamin {D, E, K and A} requirements) E. All nuts and seeds (for protein fat and fat soluble vitamin {D, E, K and A} requirements) F. Small amounts of beans and legumes- (for protein and carbohydrate requirements) G. Small amounts of whole grains, including bread, cereals, pasta and rice (for carbohydrate and water requirements)
Glucose.	83	0	0	0	0	3	0
Sodium.	139	0	0	0	2	0	0
Potassium.	4	0	2	0	0	0	0
Chloride.	100	0	0	0	0	3	0
CO2.	25	0	0	3	0	0	0
Calcium.	9.5	0	0	0	2	0	0
Phosphorus.	6.2	2	0	0	0	0	0
Cholesterol, Total.	129	1	0	0	0	0	0
Triglycerides.	179	0	0	0	0	0	1
Urine pH.		0	0	0	0	0	0
Eosinophils (EOS).		0	0	0	0	0	0
Red Blood Cell (RBC) Count.		0	0	0	0	0	0
White Blood Cell (WBC) Count.		0	0	0	0	0	0
Totals		3	2	3	4	6	1

Section 2

Test	Results	Sympathic	Balanced	Parasympathic
Urine Urine URINE PH- When you have an acid pH the patient is more acid and is a sympathetic dominant patient. Likewise, if the patient is running an alkaline pH the patient is parasympathetic dominant. What this means, is when the pH of your urine is acid, you are losing fatty acids, and amino acids. So it would be important for you to increase your fatty proteins making up for this loss.	5	1	0	0
Eosinophils Eosinophils URINE PH- When you have an acid pH the patient is more acid and is a sympathetic dominant patient. Likewise, if the patient is running an alkaline pH the patient is parasympathetic dominant. What this means, is when the pH of your urine is acid, you are losing fatty acids, and amino acids. So it would be important for you to increase your fatty proteins making up for this loss.	1.7	1	0	0
RBCs RBCs RED BLOOD CELL COUNT- runs higher in parasympathetics due to stimulation of the bone marrow, the liver and the spleen.	3.29	1	0	0
WBCs WBCs WHITE BLOOD CELL COUNT- runs low in the parasympathetic and high in the sympathetic. The white blood cells are also produced in the lymph, bone marrow, and are processed by the thymus, and spleen. Apparently sympathetics run a higher white blood cell count due to their predisposition to bacterial infections. I feel that the white blood cell counts may run higher in the parasympathetics due to increased immune function and digestive capabilities.	8.4	1	0	0
Totals		4	0	0

Totals

Sympathic	Balanced	Parasympathic
9	3	11

Dominant: Parasympathetic Type 2

Metabolic Type II Ketogenic Diet

METABOLIC TYPE II DIET PLAN – KETOGENIC

(GOOD METABOLIZER)

Characteristics

Metabolic Type II people are the true carnivores (meat eaters) and can almost live on meat alone. Their genetic background is usually from Germany, Scandinavian and northern European countries.

They are extremely prone to hypoglycemia, so they must stay away from simple sugars (junk foods) like soda, alcohol (hard liquor), fruit juice, and candy. Metabolic Type II people derive their energy mostly from sources of fat rather than carbohydrates.

This type does well with a lot of red meat such as beef, veal, pork, wild game, and lamb—every day. You are a “true” meat-and-potatoes man/woman.

As far as seafood is concerned, you prefer oily seafood (cold-water fish, high omega oils) such as salmon, tuna, sardines, mackerel, and shellfish with butter. In fact, you may prefer seafood fried.

This Metabolic Type

Burns sugar (carbohydrates) rapidly and inefficiently, causing blood sugar to rise and fall quickly—leading to energy spikes followed by fatigue. You do well with most carbohydrates, including those with a mid-range (50–80) glycemic index.
You do well with cooked and raw vegetables. Your diet should be rich in fresh cooked and uncooked vegetables, making up 30–40% of your meal. Stay away from lots of fruits and green leafy vegetables and stick with hearty vegetables such as potatoes, yams, beets, corn, and Brussels sprouts.
60–70% of your foods should be derived from the Acid Forming Foods Chart and 30–40% from the Alkaline Forming Foods Chart (see About Your Blood Test manual). Use red meats, fowl (dark meat and skin), and oily fish as your primary proteins; eggs, cheeses, nuts, seeds, and beans as secondary sources.

Always personalize portions/macros to your labs, goals, and clinician guidance.

Subtype: M Type 5

Metabolic Type V Paleo Diet

METABOLIC TYPE V – PALEO DIET

(EXCELLENT METABOLIZER)

Characteristics

Metabolic Type V people can tolerate a wide variety of foods. They are prone to hypoglycemia, so they must stay away from a lot of simple sugars (junk foods) like soda, alcohol (hard liquor), fruit juices, and candy. Metabolic Type V people derive their energy more from fat than from carbohydrates.

This type does well with a lot of red meat (beef, veal, pork, wild game, and lamb) eaten several times a week. It is a true meat-and-potatoes man/woman.

As far as seafood is concerned, they typically like oily seafood (cold-water fish, high omega oils) such as salmon, tuna, sardines, mackerel, and shellfish with butter. In fact, they like their seafood fried.

This Metabolic Type

Burns sugar (carbohydrates) rapidly and inefficiently, causing your blood sugar to rise and fall rapidly, giving you spikes of energy followed by bouts of fatigue. You do well with most carbohydrates including carbohydrates that have a mid-range (50–80) glycemic index.
Can eat cooked and raw vegetables and fruits. Your diet should be rich in fresh cooked and uncooked vegetables and fruits (as desserts), making up between 40–50% of your meal.
50–60% of your foods should be derived from the Acid Forming Foods Chart and 40–50% from the Alkaline Forming Foods Chart (see About Your Blood Test manual). Use red meats, fowl (dark meat and skin) and oily fish as your primary sources of protein. Use eggs, cheeses, nuts, seeds, and beans as your secondary sources of protein.
Stress the following foods in your diet (A–G), because they all contain protein, fat and fat-soluble vitamins (D, E, K, A):

Always personalize portions/macros to your labs, goals, and clinician guidance.

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Dominant: Parasympathetic Type 2

METABOLIC TYPE II DIET PLAN – KETOGENIC

Characteristics

This Metabolic Type

Subtype: M Type 5

METABOLIC TYPE V – PALEO DIET

Characteristics

This Metabolic Type