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Blood Interpretation

From Lab Interpretation & Nutritional Therapy Workshop by Michael Taylor, DC

Cholesterol

Cholesterol values should only be analyzed after a 12 hour fast. Further, the physician must be aware that the patient�s posture prior to the blood draw is significant. If the patient has been in a recumbent posture for more than 20 minutes, cholesterol values may be up to 15% lower than normal.

Cholesterol is a blood fat which is the prime building block component to make hormones, enzymes, and antibodies along with iodine and protein.

Also, most of the information relative to increased or decreased cholesterol can be extrapolated to triglycerides. However, in general, cholesterol is in

If cholesterol is low: (some of the sickest of patients have low cholesterol values)

• If low cholesterol is present, rule out hyperthyroidism
• Rule out hypometabolic/fatty liver (low SGPT)
• Suspect autoimmune disease: consider ANA, SED rate, C-reactive protein, and rheumatoid factor tests
• Free radical pathology (possible cancer or other chronic degenerative diseases). If cholesterol is low with a normal or low total WBC, low albumin, high globulin, high ferritin, high platelets, and high LDH or SGPT (which may not be elevated early on), and occasionally the lymphocyte count is low.
• Uremia (patient is swollen and BUN is elevated)
• Hemolytic jaundice (total bilirubin is elevated)
• Acute infections (burns up cholesterol and the patient has elevated WBC's)
• Vegetarian diets
• The first ominous sign is a cholesterol less than 140
• Other: Protein malnutrition, anemias, anorexia, intestinal obstruction, epilepsy
• Drugs that can cause a low cholesterol: thyroxine and heparin
  

The following nutritional agents may be considered for those with low cholesterol values:

• If fatty liver is suspected

• Iodine if hyperthyroidism is suspect

• Lithium

• If due to other disease state (cancer or advanced degenerative disease states), treat accordingly

If cholesterol is elevated: (Note: 80% of all circulating cholesterol is manufactured by the liver)

• Suspect hypothyroidism (low thyroid function: low T3, T4, and/or T7, or TSH greater than 4.0, and/or low basal temperature below 97.6F)
• If increased with a TSH below 2.5, and T3 and T4 is low, suspect anterior pituitary hypo-function
• If increased with a normal TSH, suspect a diet high in carbs and saturated fat. If glucose is also elevated, hyperinsulinemia is possible
• Excess dietary protein if elevated cholesterol, increased BUN/creatinine ratio with normal triglycerides
• Liver/biliary hyperfunction especially if GGT, SGPT, or SGOT is greater than 30
• Diabetes, nephrosis, atherosclerosis, multiple sclerosis, leukemia, eclampsia, and pregnancy, and immune dysfunction all may increase cholesterol values

The following nutritional agents may be considered for those with elevated serum cholesterol values:

Note: Lowering dietary cholesterol may have some effect on the overall lowering of serum cholesterol such as found in the Pritikin Diet (low fat, low protein, and high complex carbohydrates). Refined carbs should be limited to 40-50 grams per day, and fresh/raw foods should compose the majority of the diet. Limit the amount of lean meat to 4-6 ounces per day especially if digestive problems are present. With that stated, addressing other factors such as exercise, reducing coffee consumption, smoking, and obesity are of utmost importance.

If fatty liver is suspected

• Choline, Inositol, methionine

Iodine if hyperthyroidism is suspect

• Lithium

• If due to other disease state (cancer or advanced degenerative disease states), treat accordingly

HDL Cholesterol

(range should be 55 - 120 ideal range is 37 - 70)

HDL cholesterol is comprised mostly of protein and phospholipid. HDL along with APO-E will redistribute cholesterol to our cells for growth and steroid synthesis, and will return cholesterol to the hepatocytes. Normal range for HDL is 50 to 55 and greater. If HDL is too elevated, one will suspect the possibility of autoimmune disease. If it is too low (less than 35) cardiovascular risk climbs rapidly. It is found to be decreased in essential fatty acid deficit and liver dysfunction.

The following nutritional agents may be considered for those with low HDL cholesterol values:

• Niacin Sustained Release - 1-2 tablets 3 times daily
• Vitamin E
  

• EPA/DHA

• L-Carnitine with Chromium (picolinate or glucose tolerance factor): Note: chromium travels on transferrin as does iron. Before arbitrarily giving large doses of chromium, make sure that there is adequate transferrin levels.

• Exercise
• Restrict intake of hydrogenated oils
  

Cholesterol/HDL cholesterol ratio is an important indicator of CVD risk. A ratio less than 3.1 is considered ideal. Ratios of 4.0 down to 3.1 are considered adequate. Ratios higher than 4.0 create an environment for increasing risk of CVD.

LDL Cholesterol

(range should be 50 - 110)

Typically, as LDL increases, HDL will decrease. LDL is mostly cholesterol. It is usually estimated by utilizing the following formula: cholesterol - (HDL + triglycerides/5). However, if the triglycerides are greater than 400, the formula cannot be utilized and the LDL will be undetermined. Elevated levels of LDL correlates well to increased risk of atherosclerosis and the patient is likely to also be diabetes.

Elevated LDL is treated utilizing the same treatment agents recommended in treating elevated total serum cholesterol and low HDL levels.

HDL/LDL cholesterol ratio is also an important indicator of CVD risk. An LDL/HDL ratio less than 2 is considered ideal. An LDL/HDL ratio between 3 and 2 is considered adequate.

Lipoprotein a (Lp(a))

Lipoproteins are high-molecular weight particles that transport water-insoluble lipids (primarily triglycerides and cholesterol esters) through the blood plasma. Lp(a) consists of an LDL molecule that is covalently bound to the protein component apolipoprotein(a). Research over the last 20 years has underscored the critical relationship between Lp(a) and CAD, delineating its causative role in atherothrombogenesis and its strong association with both coronary and peripheral cardiac events.

Lp(a) is largely an inherited trait. Lp(a) has been cited as a better predictor of coronary disease severity than most other lipid parameters. Doetch, Roheim, and Thompson referred to Lp(a) as the most important genetic factor associated with early atherosclerosis and CAD. Lp(a) binds to endothelial and macrophage cells, fibrinogen and fibrin, promoting the deposit of cholesterol and other fatty waste in the vascular endothelium. Lp(a) also prevents clot lysis (dissolution), adding fibrin and other debris to atherosclerotic plaque.

Lp(a) is also an accurate indicator for assessing the extent of carotid atherosclerosis, and an elevated serum level can serve as the most significant indicator of patients in which cerebral infarction is a concern. Further, elevated Lp(a) may impair normal vasodilation mechanisms

The following nutritional agents may be considered for those who have elevated Lp(a) values:

• Cardioauxin - 2 tablets twice daily

• Cardiogenics Intensive Care - 2 tablets daily in-between meals

• Vitamin C, L-lysine, L-proline: 39% reduction

• Reduce consumption of partially hydrogenated oils

Apolipoprotein A-l (Apo A-1)

Apo A-1 is the primary protein matrix for HDL, and higher levels of this protein are predictive of a decreased incidence of CVD. French researchers found that in young men, Apo A-1 is the analyte most highly correlated with early MI. However, in young women, it remains HDL. In a Mayo Clinic study, cardiovascular specialists argued that plasma apoliproprotien levels - particularly A-1 and A-2 - may be considerably better markers than traditional lipid determinants.

The following nutritional agents may be considered for those who have lowered levels of Apo-A1:

1. Stress reduction
2. Exercise
3. Dietary modification
4. Reduce consumption of partially hydrogenated oils
5. EPA/DHA
• EPA-DHA Extra Strength - 1 softgel 3 times daily
  
6. Garlic
• Super Garlic 6000 - 1-2 tablets daily

Apolipoprotein B (Apo B)

Apo B is the primary substance in LDL and is thus associated with an increased incidence of CAD. Reinhart and others concluded that both Apo A-1 and B provide important information about the presence of CAD. It is also associated with an increased risk of arterial stenosis of the carotids.

The following nutritional agents may be considered for those who have elevated levels of Apo B:

• Increase soluble fiber

• Limit fats to 15-20% of calories with emphasis on monounsaturates and EPA/DHA

• Limit simple carbohydrates

Apo B/Apo A-1 Ratio:

Apo B/Apo A-1 Ratio is highly predictive with future CAD in children and adults.

Triglycerides

(Normal range is 80 - 115)

Triglycerides are esterified fatty oils that predominate in the core of chylomicrons and VDL. It is essentially 10% fat and 90% sugar. Triglycerides are metabolized by the CNS and are essentially the fuel that runs the nervous system. They have been associated with an impaired fibrinolytic system and are implicated in the progression of both coronary and peripheral atherosclerosis, independent of LDL. Further, elevated serum trigycerides have been specifically tied to the occurrence of atherothrombotic stroke and TIA's. A diet high in saturated fats can raise serum triglycerides as can a diet high in carbohydrates.

Certainly, low thyroid function can contribute to elevated triglyceride values.

A person who is correctly metabolizing their fats, proteins, and carbs will generally have about half as much triglycerides as cholesterol.

If triglycerides are elevated:

• As well as LDH and glucose, suspect a tendency towards diabetes
• With an increased TSH greater than 4.0, suspect hypothyroidism
• If increased with a TSH below 2.5, suspect hypo-function of the anterior pituitary
• Some other conditions may increase the triglycerides including most endocrine hypofunctioning glands, liver-biliary dysfunction, immune dysfunction, severe free radical pathology, pregnancy, and pancreatitis
• If elevated above 500, consider pancreatitis and/or an alcoholic
• Triglyceride/HDL ratio is >5, suspect insulin resistance
• Genetically elevated as found in Dys-B-lipoproteinemia, lipoprotein lipase deficiency, and lipoprotein lipase cofactor (Apo C-II) deficiency
• Drugs that can cause an elevated triglyceride value include caffeine, corticosteroids, diuretics, oral contraceptives, dopamine, epinephrine
  

The following nutritional agents may be considered for those with elevated triglyceride values:

• Cardioauxin - 2 tablets twice daily

• L-Carnitine 500 - 1-4 capsules daily in between meals
• MetaGlycemXâ„¢ - 1 tablet three times daily

• EPA-DHA 720 - 2 softgels twice daily

• Increase soluble fiber

• Limit fats to 15 - 20% of calories with emphasis on EPA/DHA and monounsaturates
• Limit carbohydrates (simple) including fruits and fruit juices
• Treat low thyroid, if found, accordingly (rule out halogen sensitivities)
• Treat low anterior pituitary, if found, accordingly
  

• Exercise

If triglycerides are found to be low, consider:

• Hyperthyroidism, especially is the TSH is found to be below 0.5 and if T3 and T4 are elevated
• Autoimmune disease if found with a low or normal cholesterol. May need to order ESR, ANA, C-reactive protein, and RF factor to rule out. Also check hair for heavy metals
• Vegetarians
• Lipase deficiency, if found with an elevated LDH, and depressed calcium
  

The following nutritional agents may be considered for those with low triglycerides:

• Iodine (kelp) and lithium

• Lipase

• Dietary change
• Treat the autoimmune disease accordingly
  

Fibrinogen:

Fibrinogen is a globulin synthesized in the liver. It strongly effects blood coagulation, viscosity, blood rheology, and platelet aggregation. It has a direct effect on the vascular wall and is a prominent acute-phse reactant. Fibrinogen plays a key role in arterial occlusion by promoting atherosclerotic plaque, thrombus formation, endothelial injury, and hyperviscosity. A positive correlation exists between fibrinogen levels and mortality from brain infarction. Those with a higher risk of vascular related events are those with elevated fibrinogen with high total cholesterol/HDL ratio or elevated triglycerides. Fibrinogen will increase with smoking, oral contraceptive use, obesity, stress, and aging. Fibrinogen may be elevated in nephrosis, carcinoma, pneumonia, acute infection, and pregnancy.

The following nutritional agents may be considered for those with elevated fibrinogen:

• Garlic, ginkgo, EPA, GLA, nattokinase

• Turmeric, proteolytic enzymes, ginger

• Vitamins E and C

• Glycyrrhizin

• Coumarin-containing botanicals (bupleurum, khella, red clover, yellow clover)

• Dietary pectin

• Reduce weight to ideal weight
• Stop smoking
• Consider stopping oral contraceptives

C-Reactive Protein

C-Reactive Protein is a very sensitive marker for inflammation, including the inflammation from the immunologic diseases, infection, or cell injury. It has been determined that inflammation is a crucial factor in the pathogenesis of atherothrombosis. It is a marker associated with production of inflammatory cytokines. These cytokines appear to encourage coagulation and damage to the vascular endothelium.

A recent study published in the New England Journal of Medicine found that plasma C-reactive protein (CRP), is a strong predictor of myocardial infarction and stroke. Men with CRP values in the highest quartile had three (3) times the incidence of myocardial infarction and two (2) times the incidence of ischemic stroke. These relationships remained steady over long periods, and were independent of other lipid and non-lipid factors, including smoking. Clearly, CRP is a strong predictor of the risk of future MI.

Separate from the cardiovascular and peripheral vascular issues, elevated CRP is almost always present in rheumatic fever, rheumatoid arthritis, acute bacterial infections, and viral hepatitis. It is frequently seen in gout, advanced malignant tumors, active cirrhosis, peritonitis, and burns, and carotenoid deficiency. It is sometimes seen to be elevated in MS, guillain-barre syndrome, IUDs, chicken pox, and scarlet fever.

The following nutritional agents may be considered for those with elevated CRP levels:

• Address causes of acute-phase response (ie. Infections, inflammation, smoking)
• Test for antibodies to infectious agents such as C. pneumoniae or H. pylori
• Manage systemic inflammation
• UltraInflamX® Plus 360 - 2 scoops twice daily
  

• EPA-DHA 6:1â„¢ Enteric Coated - 2 softgels three times daily.

• Clinically address the suspected condition contributing to the elevated CRP

Homocysteine

(normal range is <7.2)

Homocysteine is an intermediate amino-acid metabolite which is at the crossroads of two critical pathways in the body including methylation reactions and trans-sulfuration reactions. Indeed, it is an intermediate in the biosynthesis of cysteine from methionine, via cystathionine. Deficiency of vitamin B12, folic acid, and/or B6 can affect the enzyme pathways involved in cysteine formation, resulting in increased circulating homocysteine levels in the blood. It is an amino acid that acts as a molecular abrasive or cocklebur as it floats down the vessel raking the endothelium. This may be the event that begins the initial stage of athrogenesis.

It is estimated that the United States loses 150,000 per year due to heart attack and stroke from elevated homocysteine values. We have known about this critical player in cardiovascular health since the 1950's. Homocysteine is an independent risk factor for cardiovascular disease separate from the other clinical entities listed above. In fact, for each 3.0 increment above 7.2, ones risk for heart attack increases by 35%. One study found that 4 years post-MI, 3.8% of patients with homocysteine levels below 9 had died, while 24% of those with levels of 15 or higher, had died.
Homocysteine may be elevated in other conditions. Some of these clinical conditions include deep vein thrombosis, diabetes, RA, osteoporosis, birth defects, kidney dialysis patients, depression, MS, Alzheimers disease, etc.

The following nutritional agents may be considered for those with elevated homocysteine levels:

• B12, folic acid, B6 (tri-methyl glycine)

• N-acetyl cysteine

• EPA, DHA

• Address hepatic toxicity interfering with methylation pathway

Fasting Glucose

(normal range is 80 - 100; ideal range is 65-85)

Glucose is very acidic. This is why diabetics have a tendency towards acidosis. The whole system surrounding how our bodies utilize glucose as well as the organs that participate in that utilization, is quite involved.

If glucose is elevated, consider the following:

• Diabetes. Be sure to run a fasting serum glucose and a Hemoglobin A-1C (protein bound glucose), and a simple urinalysis (glucosuria usually does not occur until plasma value reaches 180)
• Along with elevated cholesterol (>220) and triglycerides (150) suspect hyperinsulinemia (syndromeX)
• Along with decreased CO2 (<25) and an increased anion gap (>12), suspect thiamine (B1) deficiency
  

Other disease processes/conditions that may elevate glucose include: infections (if WBC count is >18,000), chronic renal disease, hyperthyroid, hyper function of the adrenals (Cushings disease), MI, occasionally pregnancy, inflammatory bowel conditions, asthma, pancreatitis, brain trauma, severe trauma of any sort, convulsions, severe liver disease, and the first 24 hours after a severe burn.

Drugs that may also cause ones serum glucose levels to elevate include: ACTH, corticosteroids, epinephrine, furosamide, thiazides, phenytoin.

The following nutritional agents may be considered for those with an elevated serum glucose:

• Modify the diet. Diets low in calories high in fiber but low in simple carbohydrates and saturated or trans-fatty acids may help. (FirstLine® Therapy Diet)
• Exercise: The uptake of glucose into muscle is a significant means of glucose disposal and takes place independently from the action of insulin.
• B complex, including B6 to convert tryptophan to niacin and for gluconeogenesis), B1 (for conversion of pyruvic acid to acetyl CoA), B12 (for methylmalonate conversion to succinate for carbohydrate and fat metabolism), Niacin (B3 to make GTF and NAD), magnesium, zinc (for insulin synthesis by pancreatic B cells and to address the post-receptor defect), chromium (to make glucose tolerance factor and address the pre-receptor defect), copper (for insulin binding), biotin (needed for glucose utilization in the cells), vanadium (has possible insulintropic effects)
  

• Botanicals including: gymnema, trigonella (fenugreek seeds), momordica (bitter melon), ficus (fig leaf)

If glucose is low, consider the following:

• Hypoglycemia (reactive). 60% of the population is hypoglycemic and the majority of those individuals will possess food allergies, particularly to the grains. Not uncommonly, the LDH will be decreased (below 150). LDH activity represents the active exchange of chloride with glucose and glucose with zinc and sodium (glycolysis), therefore, LDH activity is associated with pancreatic function and glucose metabolism.
• Many nutritional medicine IV infusions can cause a reactive hypoglycemic event. Follow protocol.
• Insulinoma: Tumors should be ruled out with unexplained decreased fasting glucose. An insulin/glucose ratio of greater than .03 is presumptive of insulinoma.
• Possible sprue or celiac disease especially with a flat curve on GTT (25mg/100ml) although a flat curve on a GTT has also been seen with hypothyroidism and pituitary insufficiency, addisons disease (with a concurrent decreased sodium and increased potassium)
  

Other conditions may cause a low, fasting glucose including: Protein malnutrition, occasionally pregnancy, hypoadrenia, hypochlorhydria, and liver disease (destruction or insufficiency), certain types of heavy metal burdens.

Several medications may also cause low blood glucose levels including: Acetohexamine allopurinol, aminosalicylic acid, amodiaquine amphotericin B, steroids, androgens, choorpropamide, cyclophosphamide, desipramine, erythroycin, glycopyrrolate, haloperidol, halothane, hydrazine, imipramine, indomethacin, isoniazid, lincomycin, MAO inhibitors, mercaptopurine, metaxalone, methoxsalen, methoxyflurane, methyldopa, methly-thiouracil, nicotinic acid, nitrofurantoin, novobiocin, oleandomycin, oxazepam, oxyphenbutazone, paraldehyde, paramethadione, phenacemide, phenacetin, phenothiazines, phenybutazone, progestins and estrogens, propranolol, propylthiouracil, quinacrine, sulfonamides, tetracyclines thiosemicarbazones thiothixene, tolazamide, trimethadione, uracil.

The following nutritional agents may be considered for those who exhibit low serum glucose levels:

• Diet. Eat numerous small meals throughout the day. Be aware that hypochlorhydria, biliary stasis and hepatic insufficiency are common with glycemic problems (both high and low). A diet high in protein may be contraindicated. Refined carbs should be stopped, and fresh, raw fruits such as berries and leafy green vegetables should be a staple. If digestive problems are present, limit lean meat to 4 to 6 ounces per day.
• The same vitamins and minerals and herbals as listed above with elevated glucose values
• Address the underlying clinical condition that may be contributing
• Address the underlying drug therapy that may be influencing the low blood sugar status.
  

Clinical observations:

One may need to run a Reinch test (hair mineral analysis for toxic, heavy metals). Some studies implicate heavy metals has a contributing factor in dysglycemic conditions.

Fasting blood glucose is generally able to identify (initial) hyperglycemic conditions, although in hypoglycemia, the blood glucose is often not below homeostatic ranges. A 5 to 6 hour glucose tolerance test (GTT) can be performed to identify reactive hypoglycemia. One must note that within that test that can be quite symptomatic for the patient being tested, that a GTT value of 15 points or more below the fasting level is indicative of reactive hypoglycemia.

Those diabetic patients (Type I - insulin dependant or Type II) need to be monitored with a test called glycohemoglobin A-1C. This test will tell us what the patients blood sugar levels are averaging over a period of 4 to 8 weeks.

Fasting Serum Insulin

(ideal range is 0-15 mcIU/ml)

Insulin levels should be taken following a 12 hour fast and also 2 hours post-prandial (following a meal). The intake of excess calories and refined carbohydrates over a period of time will repeatedly stimulate insulin release and leads to dysinsulinemia. Prolonged dysinsulinemia then leads eventually to insulin resistance. Insulin resistance is generally associated with a relative glucose intolerance elevated triglyceride levels, central obesity, hypertension low levels of HDL, and elevated uric acid.

The phenomenon of insulin resistance (Metabolic syndrome) then increases the risk of developing diabetes Type II, obesity, cardiovascular disease, hypertension, malignancies, chronic inflammatory states.

If the patient exhibits an elevated fasting serum insuin level:

We may suspect the clinical condition called Metabolic syndrome. There is certainly a higher insulin output that may lead to Type II diabetes mellitus. This will likewise, increase cardiovascular risk.

The following nutritional agents may be considered for those patients exhibiting elevated, fasting insulin levels:

• Increase exercise. Even moderate exercise will improve ones insulin sensitivity.
• Increase mineral intake of chromium, magnesium, vanadium, and zinc that are all important for the efficient manufacture and use of insulin (see details discussed above in the glucose section)
  

• Increase B complex biotin, and inositol for improved insulin response (again, see above)

If the patient exhibits a low fasting serum insulin level:

We may suspect the clinical condition of Type I diabetes mellitus with an associated elevation in fasting glucose or the phenomenon may in fact be a benign individual pattern.

The following nutritional agents may be considered for those patients exhibiting a low, fasting insulin level:

• Increase the same minerals listed above
• L-arginine

• Botanicals: Gymnema S. Trigonella f. (fenugreek seeds) and insulin-mimetics such as Momordica c. (bitter melon)

If the patient exhibits an elevated 2 hour post-prandial serum insulin:

The patient may have Metabolic syndrome/Insulin resistance or possibly, if already clinically a Type I diabetic, they may require an adjustment of their insulin dosing.

The following nutritional agents may be considered for those patients exhibiting an elevated 2 hour post-prandial serum insulin:

• Again, increase those minerals and vitamins listed above
• N-acetylcysteine
  

• Dietary: lower the caloric intake, increase fiber, and consume fewer concentrated carbs
• Exercise
  

If the patient exhibits a decreased 2 hour post-prandial serum insulin:

The patient may either be a Type I diabetes mellitus individual or simply possesses a benign idiopathic decreased insulin event.

The following nutritional agents may be considered for those patients exhibiting a decreased 2 hour, post-prandial serum insulin:

• Antioxidant support for the pancreatic islet cells (especially if recent onset) including vitamin E, C, carotenoids, selenium, and taurine.

• Botanicals: bitter melons, fenugreek seeds, green tea, all may improve insulin output
  

• Increase exercise.

Sodium

(normal range is 140 - 144)

Sodium is the primary acidifying mineral of the body and is antagonistic to potassium. It is essential to the acid/base (pH) balance and intra-cellular fluid exchange for body water distribution affecting the heart, kidney, and adrenal cortex. Sodium pumps water and nutrients into the cell wall and is primarily under the control of the adrenal cortex. Chloride pumps water and nutrients through the cell wall and the potassium essentially moves them about inside of the cell.

Sodium works in a very narrow range and is excreted readily by the kidneys. Sick kidneys will let too much pass through or not enough. Sodium is the most abundant cation in the extra-cellular fluid. It is the most important osmotic regulator of the extra-cellular fluid balance.

If the patient exhibits an elevated serum sodium level, consider:

• Dehydration (patient did not drink enough water during their 12 hour fast prior to blood draw)
• Nephritis: look for elevated BUN and/or creatinine
• If elevated with a low potassium consider adrenal hyperfunction. Adrenal adenoma?
• If elevated with elevated chloride, possible over use of aspirin or softened drinking water
• Other factors that may elevate sodium include: diabetes, pyoric obstruction, CHF

The following drugs may elevate sodium levels:

• estrogen corticosteroids
• contraceptives.
  

The following nutritional agents may be considered for those with an elevated serum sodium level:

• Restrict sodium intake
• Raw, glandular kidney and L-arginine
  

• If drug related, consider removal

If the patient exhibits a low serum sodium level, consider:

• Hypoadrenia especially if concurrent increased potassium, but not totally necessary. Perform postural raglands blood pressure or pupillary raglands test.
• Possibly, full-blown Addisons disease
• Myxedema (hypothyroid)
• Acute infections
• If low with low chloride and elevated potassium, consider hypochlorhydria
• If low with low or high chloride and elevated potassium, consider bowel dysfunction
• Other factors that may cause a lowered sodium level include: pyloric spasm, diabetes, diarrhea, and may be observed as secondary to cirrhosis, CHF and nephrosis.
  

The following drug category may cause low serum sodium levels:

• the diuretics

The following nutritional agents may be considered for those patients exhibiting a low serum sodium value:

• Adrenal glandular

• Celery and/or celery juice
• Reduction or elimination of diuretics where appropriate
• Treatment of the underlying contributing disease process
  

Potassium

(range should be 4.0 - 4.6)

Potassium is the chief ion found in the intracellular compartment. Only a small part of the total body potassium stores are contained in the serum. The concentration inside the RBC is at least 15 to 20 times greater than that found in the serum/plasma. Therefore, significantly lowered serum values can be considered very serious. Further, it serves as the primary oxidizing mineral of the body. It attracts water and nutrients into the cells. Potassium is also essential to maintenance of pH (blood and urine) and maintenance of osmotic pressure. And potassium should always be viewed in relation to the other electrolytes.

If the patient exhibits a low serum potassium level, consider the following:

• If low with low BUN, suspect a diet that is high in refined carbohydrates
• If low with an increased sodium and/or chloride, suspect adrenal hyperfunction. Adrenal adenoma?
• Other factors that may contribute to a low potassium serum level include: diarrhea and/or vomiting, fatigue, chronic fatigue, benign essential hypertension, metabolic alkalosis, several types of anemia, familial periodic paralysis, malignant growths, chronic nephritis, weak myocardium, dry mouth
  

The following drugs may cause a low serum potassium level:

• diuretics
• desoxycorticosterone
• testosterone
  

The following nutritional agents may be considered for those patients exhibiting a low serum potassium level:

• Potassium

• Reduce refined carbohydrate consumption
• Reduction or elimination of diuretics where possible
• Treat the underlying contributing clinical condition/disease
  

If a patient exhibits an elevated serum potassium value, consider the following:

• Adrenal cortical hypofunction: aldosterone will be decreased, sodium and chloride normal to decreased, plasma and salivary cortisol decreased plasma renin increased, and urinary 17 ketosteroids decreased.
• Renal dysfunction if elevated BUN and creatinine and other electrolytes are out of range
• If high with increased Alpha 1 and 2 globulin, tissue destruction (cancer?) is possible. Look further to see if there is a low albumin, elevated globulin, elevated ferritin, platelets, and LDH or SGPT.
• Bradycardia and/or congestive heart cells which may manifest as an abnormal T wave on EKG
• Other conditions that may contribute to an elevated potassium include: metabolic acidosis, acute bronchial asthma, diabetes, acute infections, and accidental hemolysis during venipuncture may increase potassium levels as much as 10 - 20%.
  

The following nutritional agents may be considered for those patients exhibiting an elevated serum potassium value:

• Adrenal glandular

• Raw kidney glandular and L-arginine

• Treat the underlying contributing clinical condition/disease

Chloride

(normal range is 100 - 106)

If the patient exhibits a disturbed chloride value, this indicates an imbalance of the water shifting mechanism. Elevated chlorides would mean that too much water is crossing the membrane. Decreased chloride value along with decreased albumin (marked edema if albumin is below 3.5) means that there is deficient water creossing the membranes and will yeild a pitting edema.

If the patient exhibits a low value for chloride, you may want to consider the following:

• If low with CO2 increased then metabolic alkalosis is probable
• If low with BUN or creatinine increased and other electrolytes imbalanced renal dysfunction is probable
• If low with low sodium then adrenal hypofunction is possible
• If low with sow sodium and high potassium, bowel dysfunction/constipation is possible
• If low with low chloride and high potassium then hypochlorhydria is possible
• Other conditions that may exhibit a decreased chloride include: pyloric spasm diabetes, respiratory distress. Also excessive vomiting, acute and chronic fevers, excessive perspiration, emphysema, diabetic acidosis, heat cramps, diarrhea, pneumonia, infection.
  

The following nutritional agents may be considered for those patients exhibiting a decreased chloride value:

• Adrenal glandular

• Digestive enzymes and butyrate
  

• Kidney glandular along with l-arginine

• Betaine HCL (remember, chloride assists in the production of HCL by the chief cells of the stomach)

• Table salt
• Treat the underlying condition
  

If the patient exhibits an elevated chloride value, you may want to consider the following:

• If high with low CO2, then metabolic acidosis is probable (along with an elevated anion gap, source of acidosis is from renal dysfunction, diabetic ketoacidosis, lactic acidosis, or exogenous poisons ethylene glycol, salicylates, methanol, paraldehydel) or (with a normal anion gap the cause is GI alkali loss due to diarrhea, ileostomy or colostomy, renal tubular acidosis, selective hypoaldosteronism, ingestion of acetazolamide or ammonium chloride)
• If high with increased BUN and creatinine, and other electrolytes imbalanced, renal dysfunction (nephritis) is probable.
• Rule out excess use of salicyates or table salt.
• Other conditions that may exhibit an increased chloride value include: adrenal cortical hyperfunction, dehydration, hyperparathyroidism, cardiac decompensation, anemia, prostatic and other types of urinary obstruction.

Carbon Dioxide (CO2)

(normal range is 26 - 28)

Generally speaking, if the patient exhibits an elevated CO2, the patient is considered to be in a state of alkalosis (anything above 32 mEq/L, further, always order a pulmonary function test if elevated above 32). Often in cases of metabolic alkalosis, there is need for HCL and associated factors including zinc, thiamine, and potassium. If CO2 is high with low chloride, then metabolic alkalosis is probable. However, if CO2 is elevated along with high LDH, and basophils, then asthma or some other obstructive lung condition may be possible. Other factors may cause an increased CO2 value including: fever, hot baths, loss of HCL through vomiting, respiratory distress, adrenal cortical hyperfunction. Remember, alkalosis is a common finding in patients with food and environmental sensitivities.

If the patient exhibits a low CO2 value, the patient is considered to be in a state of acidosis. Mild acidosis is considered to run between 18 - 24. Moderate acidosis is considered to run between 18 - 14. Severe acidosis is less than 14. The patient may be in a state of metabolic acidosis due to lactic acid or pyruvic acid or due to toxins. Other factors that may decrease CO2 include renal dysfunction, dehydration, diabetes (remember, sugar is very acidic), or respiratory alkalosis.

BUN (Blood Urea Nitrogen)

(normal range is 13 - 18)

Nitrogen (N2) is split off of protein in the liver, the result is urea nitrogen. BUN is a by-product of protein metabolism. BUN also assesses renal changes much faster in the less serious cases than creatinine. BUN is an excellent tool for determining renal dysfunction in the early stages. It will also assess amino acid and protein need during pregnancy. It is important that BUN be determined only on a 12 hour fast since there is an increase in blood values after ingestion of protein.

The clinician must also be aware of the sign of 88. This is where the BUN value falls to 8 and the serum protein value climbs to 8 thus making the sign of 88. This circumstance creates a favorable environment for the future development of cancer in the patient.

If the patient exhibits an increased (because the body is either splitting off too much N2, or the body is not excreting it like it should) BUN value, consider the following:

• Renal impairment due to uremia, renal destruction, nephritis (acute or chronic), metallic poisoning of the kidneys (as found in patients receiving improperly supervised chelation therapy patients), or polycystic kidney.
• In cases of augmented nitrogen catabolism (the body is breaking down protein) as in intestinal obstruction, dehydration, pneumonia, peritonitis, bleeding from any occult source.
• Other causes including addisons disease, uncontrolled diabetes, gout, rheumatoid arthritis, CHF, pregnancy.
• Certain drugs may increase BUN including: alkaline antacids, antimony salts, arsenicals, cephaloridine, furosemide, gentamicin, kanamycin, methyldopa, neomycin.
  

If the patient exhibits a decreased BUN value (not splitting off enough N2), consider the following:

• Acute liver destruction
• Acute hepatic insufficiency
• Nephrosis (the patient is losing everything through the kidney)
• Chronic wasting disease
• Amylosidosis
• Pregnancy
  

In both cases (elevated values or decreased values, the clinician must determine the underlying cause and clinically address it.

Creatinine

(normal range is .6 - 1.0)

Creatinine is also a by product of protein metabolism. It serves well as a glomerular filtration assessment test. Creatinine is found in skeletal muscle and heart muscle. Creatinine may be slightly lower in children and during pregnancy. Creatinine has a diurnal variation with the lowest values at about 7AM and the peak values around 7PM.

If the patient exhibits an elevated serum creatinine value, consider the following:

• If high along with BUN, and the patients electrolytes are out of range, then poor kidney function is possible
• If high with increased monocytes, normal BUN and electroytes then prostatic hypertrophy is possible. A creatinine at 1.2 or higher in men, and subjective symptoms (urinary infrequency urgency, nocturia due to incomplete emptying, hesitancy and intermittence with decreased size and force of the urinary stream, incontinence, terminal dribbling, sensation of incomplete emptying, or complete urinary retention may ensue) may indicate BPH, especially in males over 45 years of age. Further, in cases of BPH, always rule out food allergies.
• Elevated levels will occur while the body is clearing heavy metals if pushed too fast. (DO NOT CHELATE IF CREATININE IS > 1.1)
• Other clinical factors that may elevate BUN include: CHF, starvation-dehydration, uncontrolled diabetes.
  

Creatinine may be low in the patient with amyotonia congenita (usually a child)

Again, the clinician must establish the reason(s) for the elevated creatinine and treat accordingly.

BUN/Creatinine Ratio

(normal range is 13 - 17)

If the patient exhibits an elevated BUN/Creatinine ratio, consider the following:

• Catabolic states including fever, tissue trauma, burns, internal bleeding, circulatory failure leading to fall in renal blood flow and then to shock and acute CHF
• Acute and chronic renal failure
• Urinary tract obstruction (BPH)
• High protein diet.
• Diabetes insipidus
• Whenever antidiuretic hormone (vasopressin) produced in the hypothalamus is deficient, it causes the kidneys to decrease the reabsorption of water, thus decreasing the fluid content of the body, increasing the BUN/Creatinine ratio.
  

If the patient exhibits a decreased BUN/creatinine value, consider the following:

• If low, suspect edema due to posterior pituitary dysfunction (check for low sodium and chloride). There will be an inappropriate secretion of anti-diuretic hormone (ADH). Remember, ADH (vasopressin) is produced in the hypothalamus and stored in the posterior pituitary. When released, it increases water reabsorption by te kidneys, thus increasing the fluid content of the body and decreasing BUN/creatinine ratio.
• Other factors that may decrease BUN/creatinine ratio include: pregnancy, low protein - high carbohydrate diets, hypochorhydria.
  

Remember, normal concentrations of BUN and creatinine are: 10x BUN; .1x creatinine

If BUN and creatinine raise together adhering to the above ratio in the presence of an elevated uric acid, the patient is experiencing renal failure. If however, the BUN is rising exponentially and the creatinine is remaining stationary, the patient may have hardening of the arteries, perirenal azotemia (no calcium, could kill the patient), or internal bleeding.

Uric Acid

(normal range is 4 - 6)

Uric acid is the ash of protein digestion (liver deaminization). Further, uric acid is stored in the kidneys, hence there is an increase along with BUN in renal dysfunction and sometimes in liver dyfunction.

If the patient exhibits an elevated uric acid value, consider the following:

(indicates increased purine cataboism and metaboic block before nitrogenous waste can be excreted as urea):

• Gout (rule out hypochlorhydria in gout)
• If high with high ESR and basophils, atherosclerosis is possible.
• Possible heavy metal burden (run hair analysis)
• Other conditions that may elevate uric acid include: RA, liver dysfunction, renal dysfunction (such as acute or chronic nephritis, urinary obstruction, metallic poisoning of the kidney), cancer (conditions accompanied by massive and rapid destruction of cell nuclei as when the body is feeding on itself), pernicious anemia, hyperparathyroidism, polycythemia, diabetes, CHF, hypertension
• Possible use of prescription or recreational drugs including adrenocortical steroids, busulfan nitrogen mustard, purine analogue antimetaboilites, pyhrazinamide, quinethazone, thiazides, vencristine sufate.
  

The following nutritional agents may be considered for those patients exhibiting an elevated uric acid value:

• For gout, 30 black cherries/D. Also consider HCL if hypochlorhydric

• Pancreatic enzymes

• Folic acid

If the patient exhibits a decreased uric acid value, consider the following:

• If low, suspect poor enzymation
• Also, if low, suspect Molybdenum deficiency leading to a sulfur detox pathway impairment (may have a history of allergic reaction to the sulfur based antibiotics (Septra or Bactrim) or wine due to the urinary sulfites. Can be readily checked with a urinary sulfite dipstick. There should be no urinary sulfites showing up an a UA. Sulfites, in the presence of a normal functioning pathway would be oxidized all the way to sulfates. Further, is uric acid is low along with a low MCV (less than 88) and MCH, then molybdenum need is even more probable.
• If low along with elevated MCV, MCH, MCCHC, and RDW, suspect B12 and/or folate deficiency
  

The following nutritional agents may be considered for those patients exhibiting a decreased uric acid value:

• Molybdenum

• Broad spectrum, plant based digestive enzymes

• B complex

Calcium

(normal range is 9.7 - 10.1)

99% of our bodys calcium is stored in our bones. It is the most abundant macro-mineral in the body. Calcium is absorbed from the upper small intestines and the amount of absorption depends upon the acidity in that region as well as the amount of phosphate present.

Serum proteins influence the calcium level. Generally, calcium is increased in hyper-proteinemia and decreased in hypo-proteinemia.

Calcium is used rapidly for tissue repair due to trauma and infections. It is used in conjunction with vitamin A, C, magnesium, phosphorus, iodine, and unsaturated fatty acids.

About 55% of serum calcium is in the ionized form and 45% is the non-diffusible form which is bound to protein (mostly albumin).

A physician must make sure that a patients calcium level never goes above 11.0 (indicating an extremely morbid clinical condition).

Lactose and vitamin D will enhance calcium absorption. High fiber, phytates, cellulose, oxylates, hyaluronic acid, and low hydrochloric acid output will all hinder calcium absorption.

If a patient exhibits an increased calcium value, consider the following:

• Hyperplasia or tumor of the thyroid
• Hyperparathyroidism
• Hypervitaminosis D
• Multiple myeloma
• Bone metastases
  

The following nutritional agents may be considered for those patients exhibiting an increased calcium value:

• HCl

• Calcium citrate

• Decrease vitamin D
• Treat underlying disease state
  

If a patient exhibits a decreased calcium value, consider the following:

• Diarrhea
• Malnutrition
• Hypoparathyroidism
• Vitamin D deficiency
• Nephrosis
• Pneumonia
• Severe infections of any type
• Low calcium and elevated phosphorus may be poor gall bladder emulsification
• Low calcium and triglycerides and elevated LDH may be pancreatic enzyme deficiency as may altered calcium, elevated uric acid and protein.
  

The following nutritional agents may be considered for those patients exhibiting a decreased calcium value:

• HCl

• Calcium citrate

• Dietary modification to avoid agents responsible for poor absorption
• Pancreatic enzymes (plant based)
  

• Vitamin D

• Treat underlying disease process.

Much has been written about the type of calcium to be used based upon urinary pH measured 2 hours after a typical meal.

• If the urinary pH is >7.5 consider: HCL, ascorbic acid, calcium chloride, lactate, or phytate. (Cal-Mag 750)
• If the urinary pH is 6.8 - 7.5 consider: calcium orotate, lactate, ascorbic acid. (Cal-Mag 750)
• If the urinary pH is 6.4 - 6.8 consider: calcium citrate, phosphate, or proteinate (Osteo-Citrate or Cal-Min)
• If the urinary pH is 6.0 - 6.4 consider: calcium citrate, gluconate, or carbonate (Osteo-Citrate or Trace-Min Plus)
• If the urinary pH is 5.6 - 6.0 consider: calcium citrate, gluconate, carbonate, or vitamin D (Osteo Citrate or Trace Min Plus)
• If the urinary pH is 5.1 - 5.6 consider: calcium citrate (don't use vitamin for 24 - 36 hours, then you may use a buffered vitamin C. (Osteo-Citrate)
  

Phosphorus

(normal range 3.4 - 4.0)

Phosphorus is quite important in bone physiology and also in the formation of biologically active compounds such as phospholipids, nucleic acids, ATP, creatine phosphate, and complexes required for the utilization of glucose within the body.

Generally speaking, phosphorus is an indicator of digestive function. Further, it is a good indicator of intestinal pH. If low the gut is acid, if elevated, the gut is alkaline. However, certainly, several factors are important players in regulating serum phosphorus , including PTH and the functional state of the kidneys as well as diet (soft drinks?)

If the patient exhibits an increased serum phosphorus level, consider the following:

• Hypoparathyroidism
• Renal insufficiency
• Hypervitaminosis D
• Normally found elevated in children and bone repair
• Portal cirrhosis
• Bone neoplasm
• Edema
• Diabetes
• Ovarian hyper-function
• When elevated with elevated Calcium, consider hydrochloric acid deficiency or #3
• When elevated with decreased calcium, consider poor gall bladder emulsification
  

The following nutritional agents may be considered for those patients exhibiting an elevated phosphorus:

• Hydrochloric acid

• Folic acid
  

• B12
• Bile salts
  

• Reduce Vitamin D supplementation
• Treat the underlying disease
  

If the patient exhibits a decreased serum phosphorus level, you may want to consider the following:

• Osteomalacia
• Myxedema (thyroid problems)
• Hyperparathyroidism
• Lobar pneumonia
• Decreased duodenal pH with lack of pancreatic bicarbonate
• Low phos., low Calcium, low bilirubin, consider poor fat absorption
• Commonly, vitamin D deficiency
• If low, with an altered (high or low) serum globulin, hypochlorhydria is probable
• Diets high in refined sugars
• Elevated blood viscosity
• Ovarian hypo-function
• Diabetes
• Protein malnutrition
  

The following nutritional agents may be considered for those patients exhibiting a decreased serum phosphorus:

• Vitamin D (some patients may require up to 60,000 IU/D for a short period)

• Pepsin-bromelain-lactase

• Lipase

• HCl

• Reduce refined carbs
• Treat underlying disease process
  

Note: the normal calcium to phosphorus ratio is 10 parts of calcium to 4 parts of phosphorus. This ratio may be heavier on the calcium side in sub-acute primary hypothyroidism and also in secondary hypothyroidism due to the anterior pituitary.

Usable calcium = 2.5 x phosphorus (normal range is 7.9 - 10.1)

Calcium-phosphorus index = usable calcium (above) x phosphorus (or) phosphorus squared x 2.5 (normal range is 30.0 - 40.0)

Alkaline Phosphatase

(normal range 60 - 80)

Alkaline phosphatase is one member of a group of zinc metalloprotein enzymes. Therefore, it is a zinc dependant enzyme. Alkaline phosphatase is found in several tissues including liver, bone, intestinal mucosa, and placenta.

If the patient exhibits an increased alkaline phosphatase level, consider the following possible clinical scenarios:

• Primary bone lesions including carcinoma of bone, sarcoma, osteomalacia, metastatic disease to the bone, paget's disease, hodgkin's with bone involvement, multiple myeloma
• Liver involvement including liver abcesses, hepatitis (viral or toxic), primary liver disease (cirrhosis, liver cancer, primary sclerosing cholingitis, parenchymal jaundice, etc.)
• Biliary duct obstruction
• Normally increased in 2 to 4 hours after a fatty meal
• Normally increased in patients who are Lewis positive secretors of blood type O and B
• Normally found in growing children (bones are growing)
• Normally elevated in bone fracture healing (may be increased up to 500 to 800)
• During attempts at bone repair (osteoporosis)
  

The following nutritional agents may be considered for those patients exhibiting an elevated alkaline phosphatase:

• Herbal Liver Support & Raw liver glandular

• Ascorbates

• Treat the underlying disease process

If the patient exhibits a decreased alkaline phosphatase level, consider the following:

• Anemia
• Hypothyroidism
• Celiac disease
• Severe chronic nephritis
• Usually a zinc deficiency
• Estrogen therapy
• Hypothyroidism occasionally
  

The following nutritional agents may be considered for those patients with a decreased alkaline phosphatase:

• Zinc (may take 18 months for alkaline phosphatase to achieve a normal range while on Zn)
  

• Consider removing from HRT
• Treat underlying disease process

Total Protein

(normal range is 7.1 - 7.6)

Albumin and total globulin are the components that make up total protein. One can see that it is possible to have a normal total protein, yet have abnormal indices of globulin or albumin.

If a patient exhibits elevated total serum protein levels, you may consider the following:

• Neoplasm
• Multiple myeloma
• Pneumonia
• Poor enzymation (low protease enzyme output), when elevated protein, elevated uric acid, and altered calcium level
• Hypochlorhydria
• Dehydration
• High protein and high calorie diet if elevated protein, elevated A/G ratio, and elevated cholesterol
• Liver/biliary dysfunction
• Rheumatoid arthritis
  

Note: a climbing total protein level is a serious clinical condition

The following nutritional agents may be considered for those patients with an elevated serum protein level:

• Protease enzymes (plant based)

• HCl

• Possibly reduce protein consumption
• Calcium, vitamin D
  

• Treat underlying disease process

If the patient exhibits a decreased serum protein level, you may consider the following:

• Hyperthyroidism
• Birth control pills
• Edema (gross edema will manifest when the patient's serum protein level falls below 5)
• Malnutrition
• Leukemia
• Liver disease: (fatty liver congestion when decresed protein, decreased cholesterol and SGPT), (hepatic insufficiency when decreased protein and BUN and altered SGPT)
• Digestive tract inflammatory disease states (colitis, crohn's, gastritis, ileitis, etc.)
• CHF
• Renal dysfunction (usually due to diabetes or hypertension)
• Poor protein assimilation when decreased protein and calcium
  

The following nutritional agents may be considered for those patients with a decreased serum total protein level:

• If due to hyperthyroid, consider iodine

• If due to birth control pills, consider alternate forms of birth control
• If due to liver disease (fatty liver), consider inositol and choline
  

• If the kidneys are involved, consider L-arginine, and raw kidney glandular

• If due to hypertension, consider diet

• Treat the underlying disease process

Albumin

(normal range is 4 - 4.5)

The albumin within the body is almost entirely produced by the liver. Albumin is responsible for approximately 80% of the colloid-osmotic pressure between blood and tissue fluids.

If the patient exhibits an increased serum albumin level, you may consider the following:

• Dehydration

The following may be considered in the treatment for the dehydrated patient:

• increase fluids.

If the patient exhibits a decreased serum albumin level, you may consider the following:

• Since most of the albumin is produced by the liver, if low, clearly liver disease must be considered, including hepatitis, cirrhosis, or acute cholecystitis
• Kidney related disorders including nephrosis, and nephritis
• Malnutrition or visceral protein loss
• Below 3.5 indicates a possible serious pathology (neoplasm)
• Digestive inflammatory diseases (usually secondary to the need for HCL)
• Hyperthyroidism
• Pregnancy
  

The following nutritional agents may be considered for those patients with a decreased albumin level:

• Address liver condition(s) appropriately (methionine, choline,and inositol)

• If kidney, consider L-arginine and raw kidney glandular
  

• If digestive inflammatory disease, consider
  

• Treat underlying disease process

Note: Albumin levels and ratios with other entities, play a significant role in assessing the patient's morbidity risk. Three (3) of the ominous signs include albumin in the equation. Perhaps the most ominous of the 4 ominous signs is an albumin that is 3.5 or below, with a total absolute lymphocyte count less than 1,500. The patient with this ominous sign possesses a 4 times greater risk for morbidity and a 20 times greater risk for mortality than the general population.

Globulin

(normal range is 2.8 - 3.5)

Several components make up the total globulin serum level of the patient. They include the alpha 1 fraction, alpha 2 fraction, beta fraction, and the gamma fraction. Therefore, varying levels of any of these fractions can influence total globulin levels. Globulin is a sophisticated form of protein. It indicates the amount of circulating colloidal protein that is used to manufacture antibodies, blood cells, and enzymes. Globulin will combines with phosphorus, copper, iodine, and iron in order to have functioning IgG,A,M, and E immunoglobulins

If the patient exhibits an increased globulin level, you may consider:

• Infection
• Neoplasm (early malignancy or multiple myeloma)
• Parasitic infections
• Hepatitis
• HCL deficiency
  

Note: a climbing total globulin is a serious clinical matter.

The following nutritional agents may be considered for those patients with an increased globulin level:

• If due to infection, must discern what type and treat accordingly
• If due to neoplasm, see treatment protocols within the Cancer Modules of 300 hour Diplomate Internist course or chiropractic injectable nutrient pharmacotherapy course.
• If due to infectious hepatitis, consider Wright and Gaby protocol
  

• Betaine HC

If the patient exhibits a decreased globulin level, you may consider:

• Anemia
• Chronic viral or bacterial infections
• Hemorrhage
• Liver dysfunction
  

Note: A decreased total globulin may suggest increased use of globulin by the liver, spleen, thymus, kidneys, or heart.

The following nutritional agents may be considered for those patients with a decreased globulin level:

• If due to anemia, is it secondary to an “occultâ€� bleed? Treat accordingly
• If due to chronic viral or bacterial infections, upregulate immune status with C, Zn, Germanium, CoQ10, colostrums, thymus, etc.
  

• If due to hemorrhage within upper GI tract, consider olive oil, gastromet, gastricumeel, elhasecalin
• If due to liver dysfunction, discern what type and treat accordingly.
  

Albumin/Globulin Ratio: (A/G Ratio)

(normal value is 1.2 - 1.5)

NOTE: A low (reversed, or inverted) A/G ratio less than 1.0, is one of the 4 ominous signs. These people may have a serious, developing, or currently manifesting pathological process.

If the patient exhibits a decreased A/G ratio, consider the following:

• Neoplasm, including multiple myeloma or metastatic disease
• Infectious disease including AIDS
• Intestinal disease
• Liver disease
• Renal disease
• The cachexic patient
• CHF
  

The following nutritional agents may be considered for those patients with a decreased A/G ratio:

• The physician must determine what pathology is developing or already present, and treat accordingly.

NOTE: If the patient possesses an elevated A/G ratio, this phenomenon is not considered to be clinically significant.

Calcium/Albumin Ratio: (Ca/A ratio)

(normal value is 2.2 - 2.5)

If the patient exhibits a decreased Ca/A ratio, it is consider usually as clinically insignificant

NOTE: If the ratio is elevated greater than 2.7, this is considered one of the 4 ominous signs, due to malnutrition or visceral protein loss secondary to a potential pathological process.

GGT (Gamma-glutamyl transferase)

(normal range is 1 - 40)

GGT is generally considered to not be quite as sensitive a marker as SGPT. GGT is responsible for transporting amino acids across the cell membranes from the extracellular to the intracellular component. This function requires 3 molecules of ATP and 1 molecule of glutathione. GGT is commonly elevated in alcoholics.

If the patient exhibits an increased GGT level, consider the following:

• Hepatic disease
• Pancreatic disease especially if > 300.
• Cardiovascular disease
• Diabetes
• Epilepsy
• Severe trauma
  

The following nutritional agents may be considered for those patients possessing an elevated GGT:

• If due to biliary tree obstruction, follow gallbladder protocol.
• If due to liver disease, treat accordingly (methionine, raw liver, hepatoplex, etc.)
  

• If due to pancreatitis, no alcohol, digestive enzymes
  

• Treat the responsible disease process.

NOTE: There is no significant clinical concern with a lowered level of GGT.

SGOT: (also known as AST)

(normal levels are 18 - 26)

SGOT is found in liver, skeletal muscle, brain, heart, and kidneys. It will elevate with degenerative destructive organ processes. *In cardiac related conditions, SGOT will not return to normal as quickly as SGPT.

If the patient exhibits an elevated SGOT level, one may consider the following:

• Myocardial infarction (confirm with treponin)
• Hepatic conditions (parenchymal damage)
• Pancreatitis
• Pulmonary embolism
• Myositis / skeletal muscle damage
• Mono
• Neoplasm
• Alcoholics
• Diabetes
• Essential hypertension
• Rheumatoid arthritis
  

The following nutritional agents may be considered for those patients possessing an elevated SGOT:

• Broad spectrum, plant based enzymes [amylase, protease, lipase, cellulase] for pancreatic involvement.

• If liver is involved, consider the pathology and treat accordingly.
• If cardiac (MI or coronary artery insuff.), consider IV chelation, DMSO and glutathione for free radical damage control for the expanding infracted penumbra. Also magnesium, taurine, Co-Q10, L-carnitine, hawthorne, cralonin, cor compositum.
  

• Ascertain the underlying clinical condition, and treat accordingly

If the patient exhibits a decreased SGOT level, one must consider the following:

• Vitamin B6 deficiency (pyridoxine)
  

Note: SGOT is a B6 dependent enzyme. In other words, for the body to manufacture SGOT, there must be adequate levels of circulating B6.

The following chiropractic nutritional pharmacotherapy agent may be considered for the patient with decreased SGOT:

• Pyridoxine (B6)

SGPT: (also known as ALT)

(normal range is 18 – 26)

SGPT is an enzyme that is found in liver, kidneys, heart, and skeletal muscle.

If the patient exhibits an elevated SGPT level, one may consider the following:

• Hepatic related disorders where the liver is swollen, alkaline, and inflamed (especially hepatitis)
• Pancreatic conditions
• Neoplasm
• Alcoholism
• CHF
• MI
• Hypertension
• RA
• Asthma
  

The following nutritional agents may be considered for the patient with elevated SGPT:

• If due to hepatitis, silymarin, hepataplex, beta carotene, germanium, etc.

• If due to pancreatic problems, place on broad spectrum, plant based digestive enzymes

• If due to adult onset asthma

• Determine the underlying pathology and treat accordingly

If the patient exhibits a decreased SGPT level, one may consider the following:

• Fatty liver congestion

The following nutritional agents may be considered for the patient with decreased SGPT levels:

• Lipotrophic factors including methionine, inositol, choline

• Alkaline B vitamins

NOTE: When SGPT is greater than SGOT (and must be higher than the laboratory reference ranges,....not our homeostatic ranges that we quote), this typically indicates an extra-hepatic condition such as hepatitis, extra-hepatic obstruction (ie. Gall stones in bile duct), and toxic hepatitis. When SGOT is greater than SGPT (and again, it is higher than the laboratory reference ranges) we are typically looking at an intra-hepatic condition such as primary liver cancer, cirrhosis, primary sclerosing cholengitis. Clearly, the latter scenario is associated with increased risk for mortality.

LDH

(normal range is 120 – 160)

Total LDH may elevate in virtually any destructive process or trauma in the body. The enzyme is widely distributed in heart and skeletal muscle, liver, kidney, and red blood cells. Anytime an elevated total LDH is discovered, it is clinically prudent to order an LDH isoenzymes study. There are 5 isoenzymes with some cross-over noted between sets.

• LDH Isoenzyme #1 is found in heart and RBC’s
• LDH Isoenzyme #2 is found in heart, lymph, and RBC’s
• LDH Isoenzyme #3 is found in pulmonary, spleen, adrenal, and kidney
• LDH Isoenzyme #4 is found in liver, skeletal muscle, prostate/uterus
• LDH Isoenzyme #5 is found in liver and skeletal muscle.

A decreased LDH Isoenzyme #5 will often occur in patients who have experienced long-term, insidious exposure to noxious gases (CO, etc.). Beware if your patient complains of unexplained illness, fatigue, loss of memory, etc. Check for leaks. Further, if this isoenzyme is decreased, it can indicate a heavy metal burden.

By ordering LDH isoenzyme study, it is possible to narrow a developing disease process by organ system early on in its development.

If the patient exhibits an elevated total LDH, run the isoenzyme study and treat the afflicted organ/tissue accordingly.

NOTE: Hemolyzed blood draw samples have a large amount of LDH, SGOT, and SGPT in them. Be aware of that when drawing blood in your offices.

If the patient exhibits a decreased LDH, one may consider the following:

• Hypoglycemia

The following nutritional agents may be considered for those patients with decreased total serum LDH levels:

• Hypoglycemic nutrients including: Cr, Zn, Vanadium, Magnesium, B vitamins, etc.

Total Bilirubin

(normal range is .5 – .7)

Total bilirubin is an end-product of hemoglobin breakdown by the spleen, liver, and bone marrow. The liver will alter bilirubin to a form that is excreted through the bile or by the kidneys. When the patient’s value goes above 1.2, consider a liver/gallbladder flush if stones are confirmed an are < 1.5 cm in diameter, and non-calcified.

If the patient exhibits an elevated total bilirubin, consider the following:

• Biliary obstruction
• Hemolytic anemia
• Liver injury
• Chronic cholecystitis
• Thymus involvement if T. bili is elevated with altered lymphocyte count
• Spleen hyperfunction if elevated T. bili, Hgb, Hct, and low RBC count
  

The following nutritional agents may be considered for those patients with an elevated T. bilirubin:

• If due to gallstones, consider abdominal DXUS to determine size(can work with them if they are <1.5 cm in diameter. Perform an abdominal flat-plate to see if stones are calcified (if calcified, and patient is acute, consider surgical referral). If stones are not calcified, begin with bile viscosity thinning agents such as apple cider for 4 to 10 days. Then proceed to liver-gallbladder flush. (see appendix)
• Raw thymus glandular

• Raw spleen glandular

• Determine the underlying pathology and treat appropriately.

There is virtually no significance with a lowered T.bilirubin with the exception of possible seconday aplastic anemia.

CPK

(creatin kinase) (normal range is 30 – 180)

Virtually any patient who possesses a significantly elevated total CPK should have a CPK isoenzyme study ordered.

CPK is elevated in cardiac conditions, muscular dystrophy, muscle damage/degeneration, brain damage/inflammation, and strenuous exercise, also other conditions include hypothyroidism, edema, and influenza.

CPK isoenzymes are broken down into three (3) categories:

1. CK:MM – derived from skeletal muscle
2. CK:MB – derived from heart muscle
3. CK:BB – derived from brain and nerve tissue and may also be a useful marker for prostate, breast, ovarian, colon, lung, and digestive tract cancers.

Serum Iron (Fe)

(normal range is 85 – 120)

Serum iron is just that, the inorganic form of circulating iron in the blood.

If the patient exhibits an increased serum iron, consider the following:

• Hemochromatosis
• The patient is on iron therapy
• Liver dysfunction (hepatitis)
• Iron conversion anemias
• Water supply? Cooking utensils?
• May result from deficiency in RBC production and/or RBC destruction
• In presence of decreased Hct, possible intrinsic factor deficiency
  

Note: Iron is vital to spleen function and reticulo-endothelial activity.

The following nutritional agents may be considered for those with elevated serum iron levels:

• Discontinue iron therapy
• Address liver involvement
• Determine the underlying cause and treat appropriately

If the patient exhibits a decreased total serum iron level, consider the following:

• If the serum iron is below 40 – 50, must rule-out pathological bleeding. (Hemoccult test?)
• Chronic infections
• Nephrosis
• Hypochromic anemias
  

The following nutritional agents may be considered for those with decreased serum iron levels.

• Spleen (raw)

• Iron

• Vitamin C

Note: must consider to run a transferrin and serum ferritin.

Thyroid Profile

T3: (tri-iodothyronine)(normal range is 36.0 – 40.0)

T3 comprises approximately 10 – 15% of the total circulating hormone. Approximately 1/3 of T4 is converted to T3. T3 is produced mainly from the peripheral conversion of T4.

Generally speaking, T3 has a higher biological activity that T4, yet will bind to protein less efficiently that T4. T3, in serum, exists in both a bound form and a free form, however, less than 1% is in the free-form.

If the patient exhibits an increased T3 value, consider the following:

• Hyperthyroidism
• Thyrotoxicosis
• Hypoproteinemia
• Nephrosis
• Neoplasm
  

If the patient exhibits a decreased T3 value, consider the following:

• Hypothyroidism
• Myxedema
• Pregnancy
• Birth control pills
  

T4: (tetra-iodothyronine)

(normal range is 7.0 – 9.0)

T4 is the major hormone secreted by the thyroid making up 85 – 90% of the hormone. T4 exists as both a bound and non-bound form. T4 is predominately bound to thyroid binding globulin (TBG), pre-albumin, and albumin.

If the patient exhibits an increased T4 value, consider the following:

• Hyperthyroidism
• Thyrotoxicosis
• Birth control pills
• Pregnancy
• Neoplasm
  

If the patient exhibits a decreased T4 value, consider the following:

• Hypothyroidism
• Myxedema
• Hypoproteinemia
• Nephrosis
• Simmonds disease

T7: (also known as FTI [free thyroid index])

(normal range is 2.6 – 3.6)

T7 essentially reflects the metabolic impact of the thyroid hormone on the body. T7 can be calculated by the following equation: T7 = T3/100 x T4.

It is interesting to note that many patients may in fact look like and complain of symptoms associated with hypothyroidism, yet have normal or nearly normal thyroid indices. When the blood work appears somewhat unremarkable, yet you still are clinically thinking that this patient has hypothyroidism, consider having the patient do the basal body temperature study.

Basal Body Temperature Studies for Thyroid Function:

Of all the problems that can affect health, none can be more common, more easily corrected, yet more untreated and unsuspected, than low thyroid gland functioning, called hypothyroidism.

Thyroid function may have an effect on many of the degenerative disease processes that we encounter, such as hardening of the arteries, cholesterol abnormalities, high blood pressure, skin disorders, menstrual abnormalities, low resistance to infections, and many other conditions.

A simple test has been devised to evaluate thyroid activity, this is performed simply by taking the axillary (under arm) temperature every morning for ten (10) consecutive days.

Instructions For Taking Basal Body Temperature:

• Use an ordinary oral or rectal thermometer.
• Shake down the thermometer the night before, and place it on your night stand.
• The first thing in the morning BEFORE you get out of bed, place the thermometer under your arm for ten (10) minutes.
• Record the temperature reading and date
  

Normal Range: 97.6 to 98.2

• Averages below indicate hypothyroidism.
• Averages above indicate hyperthyroidism.

If the patient winds up having a fairly normal thyroid panel, yet the basal temperatures are consistently less than 97.6 degrees farenheit, you may still consider treating the patient for hypothyroidism. The treatment would proceed for approximately 30 days, then re-evaluate.

The following nutritional agents may be considered for a patient exhibiting hypothyroidism:

• Thyrosol — 1 tablet three times daily
• T-100 — 1-2 tablets three times daily away from food

The following nutritional agents may be considered for a patient exhibiting hyperthyroidism:

• T-100 - 1-2 tablets three times daily
• Comprehensive Thyroid support Formula
• Thyrosol - 1-2 tablets three times daily
• Thyrosol is an exciting multi-faceted formula featuring targeted nutrients and herbs that promote healthy thyroid function.
• Wellness EssentialsTM — 1 packet twice daily.
• Base nutrition with essential fatty acids and detoxification support.