1. 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.

1. 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.

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.

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

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

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.

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

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

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

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

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

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

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.

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

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.

 

 

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

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

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.

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.

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.

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.

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.

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

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

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

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.

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

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.

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.

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.

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.

 

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.

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

 

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