Patient: Age: 48 Sex: M MRN: SAMPLE PATIENT Order Number: Completed: Received: Collected: SAMPLE REPORT Plasma Representativeness Index Ref Range 5. 6. 1. Arginine 9.5 Histidine 7.7 Isoleucine 7.7 Leucine 15. Lysine 19.9 Methionine 2.4 Phenylalanine 6.28 Taurine 4.42 Threonine 6.36 Tryptophan 3.66 Valine 27.6 7.5-13. 7.9-12.1 5.4-1.5 1.5-18. 15.5-27.5 2.5-4.9 4.6-7.9 5.25-9. 6.4-14. 3.3-6.5 19.-36. Anserine (dipeptide) Carnosine (dipeptide) <=.7 <=.9 1-Methylhistidine.6 <= 1.65 Beta-alanine <=.4
Page 2 Alanine 43 Asparagine 3.7 Aspartic Acid.42 Cyst(e)ine 6.3 Glutamic Acid 1.9 Glutamine 51 Glycine 16 Proline 28 Serine 7.7 Tyrosine 9.6 26-55 4.-7.2.2-.6 4.9-8..5-7. 5-7 19-43 1-32 8.-15.5 5.1-1. Alpha-amino-N-butyric acid 2.96 Citrulline 4.3 Ethanolamine.44 Ornithine 5.85 Phosphoethanolamine.58 Phosphoserine.74 Urea 57 1.25-3.5 2.8-5.6.5-1.2 4.25-11.5.15-.45.31-.74 32-97 Alpha-aminoadipic acid.15 <=.8 Argininosuccinic acid Beta-aminoisobutyric acid Cystathionine Gamma-aminobutyric acid Homocystine Hydroxyproline Sarcosine <=.25 <=.3 <=.3 <=.2 <=.3 <= 2.5 <=.15 3-Methylhistidine.96 <=.75
Page 3 Glutamine/Glutamate 5 >= 8 Asparagine/Aspartate 9 Ammonia Concentration 1.8 >= 6 <= 6.5 = Unable to calculate results due to less than detectable levels of analyte. REPRESENTATIVENESS INDEX GSDL uses a new, much improved procedure for preserving plasma amino acids. Nevertheless, spoilage and decay could occur. To check this, two key ratios and the ammonia concentration are monitored by computer and portrayed at the beginning of the report. The glutamine/glutamate ratio can indicate specimen decay. When aged, heated, or improperly preserved, plasma glutamine decays to glutamic acid and ammonia. Hence, low glutamine/glutamate ratio may reflect decay. A high glutamine/glutamate ratio is metabolic and does not reflect on specimen representativeness. The asparagine/aspartic acid ratio may also indicate improperly preserved plasma. Decay causes asparagine to become aspartic acid and ammonia. The ammonia concentration, if elevated, usually indicates overall decay of amino acids. An exception would be elevated ammonia concentration with hyperammonemia of metabolic or bacterial origin. Because mail-in specimens should not be used to quantitatively assess blood ammonia levels, this determination is qualitative only and is used solely for checking specimen quality. The representativeness of the plasma is rated in the Representativeness Index Section of the Report. Histidine is low in the plasma. As a semiessential amino acid, histidine is the precursor of histamine which mediates some inflammatory responses and which initiates gastric secretions for digestion of food. Nutritional essentiality of histidine often is accentuated in infants and young children whose digestive enzyme capacity is immature. Histidine is a necessary carrier of copper in blood, and deficient blood plasma levels of histidine are implicated in peripheral deficiency of superoxide dismutase activity and in rheumatoid arthritis. Deficient histidine can contribute to gastric hypochlorhydria, and gastrointestinal dysfunction can, in turn, perpetuate histidine insufficiency. Histidine is found in all protein foods, especially cheeses, legumes, almonds, cashews, veal and beef. Rarely, low blood levels of histidine coincide with singular hyperhistidinuria. A 24-hour urine amino acid analysis can be used to assess hyperhistidinuria. Low plasma histidine may also occur in generalized hyperaminoaciduria (urinary wasting) which can be secondary to: nephrotic syndrome, hyperthyroidism, chemical toxicity, heavy element excess (Pb, Cd, U), Wilson's disease, Fanconi syndrome and some hereditary diseases. Methionine, an essential amino acid, is measured to be low in the plasma. Methionine brings sulfur and methyl groups into the body. Sulfur is needed for formation of body tissues, for metabolism of carbohydrates, lipids and amino acids, and for antioxidant and detoxication processes. Insulin, coenzyme A, and glutathione contain cysteine that may have been derived from methionine. Methylation (via S-adenosylmethionine) is essential to muscle metabolism, adrenal catecholamine balance, and formation of methylated bases in DNA and RNA which assist genetic expression. Major dietary sources of methionine include meat, fish, poultry, cheese, seeds and seed meals, and Brazil nuts. Low methionine can result from a low protein or poor quality diet or from gastrointestinal dysfunction, especially gastric insufficiency or hypochlorhydria. Taurine, measured to be low in the plasma, is a semiessential amino acid for infants and children. In the body taurine accomplishes multiple functions. It conjugates hydroxylated cholesterol to form taurocholic acid, a component
Page 4 of bile and a major process of cholesterol utilization. At the plasma membrane of cells, taurine participates in the control of magnesium, calcium, potassium and sodium transport. Of all body organs, heart muscle cells have the highest concentration of taurine. Taurine is magnesium sparing and low taurine in heart muscle cells can lead to arrhythmia. In the central nervous system taurine performs neurotransmitter activities. In leukocytes, taurine scavenges excess hypochlorite ion (OCl-) which is generated during phagocytosis. Deficient taurine may lead to increased inflammatory response to: toxins, foreign proteins, and xenobiotic chamicals including aldehydes, alcohols, amines, petroleum solvents, and chlorine or chlorite (bleach). Dietary taurine comes from seafood, especially shellfish, and from liver and organ meats. Human mothers' milk contains taurine; cows' milk does not. Endogenous taurine comes from cysteine and requires oxygenation and pyridoxal phosphate coenzyme activity. Low taurine may be coincident with renal wasting, perhaps due to elevated levels of beta-alanine which impair renal conservation of taurine. Threonine is measured to be low in the plasma. Threonine is an essential amino acid needed for formation of body proteins, enzymes, peptides and hormones. Also, it is the precursor of other important protein-forming amino acids, glycine and serine. Threonine is needed for some glycoproteins where it becomes the link between the protein and a carbohydrate or sugar molecule. Glycoproteins are involved in collagen and globulin formation and in immune function. Agglutinins that determine blood group are glycoproteins, some of which require threonine. Cheeses (especially Swiss), meat, fish, poultry, seeds, walnuts, cashews, almonds and peanuts contain relatively high levels of threonine. Low threonine can result from a poor quality diet or from gastrointestinal dysfunction, particularly intestinal malabsorption. In the small intestine, threonine absorption occurs slowly and is sensitive to disturbances in mucosal transport. Asparagine, a protein amino acid, is measured to be low. This amino acid has dietary sources - vegetable protein foods such as soy, peanuts and other legumes - and it can be formed endogenously from glutamine and aspartic acid. Endogenous formation is magnesium dependent and requires an energy-coupled ATP step. Deficient asparagine may result from a low protein diet in general, from a diet that is deficient in vegetable protein, from gastrointestinal dysfunction and poor uptake of amino acids, or it may be a consequence of magnesium deficiency or dysfunction. Normal or high levels of aspartic acid and glutamine with low asparagine are consistent with magnesium dysfunction. Asparagine can be a limiting amino acid for leukocyte formation and low asparagine may contribute to immune dysfunction. In leukemia, (acute histocytic and chronic lymphocytic), blood plasma levels of asparagine have been observed to be depressed. Low asparagine can be an artifact of specimen decay. This is monitored and reflected by the Representativeness section of the Report. Glycine, a major nonessential, protein-forming amino acid, is low. Glycine comes from digestion of dietary protein, and it has multiple routes for endogenous formation and removal. The amino acids threonine and serine are important sources of glycine as is glycolysis. After two days of fasting or in early stages of starvation, elevated glycine may occur from catabolism of body protein. Later, as body muscle and protein are depleted, decreased glycine occurs. Negative nitrogen balance and deficiencies of threonine and serine may accompany low glycine. Subnormal blood levels of glycine also may coincide with renal wasting (hyperglycinuria) as determined by 24-hour urine amino acid analysis. Blood glycine can be depleted by conjugation with benzoic acid for detoxication if benzoic acid is consumed in excess. Benzoic acid (benzoate) is commonly used as a food/drink preservative. Serine, a nonessential protein-forming amino acid, is low. Serine comes from digestion of dietary protein and from endogenous sources that include threonine, glycine, and glycolysis. Vitamin B6 or magnesium dysfunctions can limit the glycolysis route, and malabsorption or poor quality diet can limit serine formation from glycine. Depression, and loss of libido, may accompany serine deficiency. Long -term serine deficiency may contribute to cardiovascular disease if it provokes homocystinuria which is assessed by 24-hour urine amino acid analysis. Serine may also be depleted in urinary wasting conditions, including generalized hyperaminoaciduria, hyperglycinuria, and nephrosis or nephrotic syndromes.
Page 5 Ethanolamine, an intermediate of the serine-to-choline metabolism sequence, is measured to be low. Ethanolamine is formed metabolically from serine and phosphatidylethanolamine; this endogenous formation is pyridoxal phosphate dependent and requires adequate serine. Consequences of ethanolamine insufficiency may be limited or insufficient levels of phosphoethanolamine, phosphatidylcholine and choline. Acetylcholine, the neurotransmitter, is formed from choline. Dietary lecithin provides an independent source of the neurotransmitter precursors. Ethanolamine insufficiency is significant if cholinergic functions are limited. 3-Methylhistidine is elevated. This methylated form of histidine comes from muscle tissue, both dietary and endogenous, where it is part of the muscle proteins actin and myosin. A slight elevation of plasma 3-methylhistidine is not abnormal. Elevated levels suggest either an inordinately high intake of dietary actin/myosin or accelerated catabolism of muscle tissue in this individual. 3-Methylhistidine levels may be temporarily increased after strenuous physical exercise. Physiological and pathological conditions featuring 3-methylhistidinemia include muscle wasting due to extended bedrest or physical inactivity, muscular dystrophy, and terminal stages of serious illness. Elevated 3-methylhistidine is observed in some cases of arthritis, Lyme disease, and neuromuscular disorders. Convulsions and seizures also feature increased 3-methylhistidine. There is some correlation between elevated 3-methylhistidine and increased need for vitamin B12, folic acid, methionine and perhaps histidine if it is marginal or low. Glutamic acid is measured to be elevated. The known conditions consistent with glutamic acidemia are as follows. 1. Recent ingestion of excessive levels of monosodium glutamate "MSG" (non-fasting blood) 2. Ingestion of nutritional supplements containing large amounts of glutamic acid 3. Gout or pregout; check blood/urine uric acid levels 4. Some imbalance or impairment in purine metabolism Conditions (1) and (2) are expected to normalize soon after the dietary source is discontinued. Conditions (3) and (4) are often best corrected by a low purine diet. Purine metabolism disorders are uncommon and differential diagnosis is difficult. Decayed blood specimens almost always feature falsely high glutamic acid and falsely low glutamine secondary to the decay process. This prospect is monitored by computer analysis and is reflected in the "Representativeness" section at the beginning of this report. Phosphoethanolamine is elevated. Metabolically, phosphoethanolamine is an intermediate of the serine-to-choline sequence. Impairment of this sequence beyond phosphoethanolamine is not documented except for presumptive evidence of impaired methylation. Triple methylation by S-adenosylmethionine (SAM) of phosphatidylethanolamine produces choline. If methionine is deficient or elevated, limited SAM or rate-limited methylation could contribute to elevated phosphoethanolamine. Conditions consistent with elevated phosphoethanolamine due to impaired methylation by SAM include: mood swings, mental depression, cognitive and memory impairments, cholinergic dysfunction. Other, more commonly-encountered conditions featuring elevated plasma phosphoethanolamine are - 1. Hypophosphatasia: genetic or acquired deficiency in the enzyme alkaline phosphatase (measured in blood serum/plasma) 2. Intestinal dysbiosis with increased formation and absorption of phosphoethanolamine from gut flora. 3. Unspecified imbalances in calcium/phosphorus levels, osteomalacia or bone metabolism disorder, hypervitaminosis D, and parathyroid disorders.
Patient: Age: 48 Sex: M MRN: SAMPLE PATIENT Order Number: Completed: Received: Collected: AMINO ACID SUPPLEMENT SCHEDULE Amino Acid Milligrams/day Arginine. Asparagine 291. Cystine. Glutamine 5. Glycine 12. Histidine 352. Isoleucine. Leucine. Lysine. Methionine 334. Phenylalanine. Serine 441. Taurine 522. Threonine 262. Tryptophan 72. Tyrosine. Valine. The Amino Acid Supplement Schedule presented above is based upon a comparison of the measured levels with an optimal level. The optimal level is set at 1.25 X the lower limit of the reference range. Thus, a given amino acid listed for supplementation may be deficient for this individual, or it may be within the reference range but at a low-normal level. The purpose of the Amino Acid Supplement Schedule is to provide guidelines for individual or custom formulation (blending) by qualified, knowledgeable pharmacies. Only pure, L-configured amino acids should be used. Quantities stated are for daily, oral supplementation only. Amino acids are best taken with meals if food reactivities have been alleviated by avoidance, rotation and/or neutralization-desensitization therapy. Otherwise, amino acids are best taken away from meals. Adequate vitamin and mineral nutriture is required for proper metabolism of amino acids. The Amino Acid Supplement Schedule presented here is not intended for pregnant females, and such use of the schedule is not recommended. An overriding circumstance is renal insufficiency or renal failure. If this individual is known to have or
Page 7 suspected of having renal insufficiency, disregard the above and do not implement amino acid supplementation. Such supplementation is contraindicated in renal insufficiency in spite of low plasma levels of amino acids. Regardless of the cystine entry in the above supplement schedule, supplementation of cystine or cysteine is contraindicated in cystinuria, even when cyst(e)ine is measured to be low in plasma. Cystinuria is assessed by 24-hour urine amino acid analysis and should be considered if plasma cyst(e)ine is deficient.
Page 8 Patient: Age: 48 Sex: M MRN: SAMPLE PATIENT Order Number: Completed: Received: Collected: 4 5 8 2 8 1 8 4 8 4 4 3 5
Page 1 S. RESULTS RELATING TO GASTROINTESTINAL DYSFUNCTION: * Deficient histidine together with marginal or subnormal levels of essential amino acids is measured. If this individual is consuming an adequate protein diet, then consider gastric hypochlorhydria. An assessment of digestive function is suggested. * Threonine, the most slowly absorbed essential amino acid, is subnormal together with relatively low levels of at least two other essentials. Consider malabsorption. Assessments of digestion and absorption are suggested. T. RESULTS RELATING TO ENDOCRINE DYSFUNCTIONS OR HORMONAL IMBALANCES: * Deficient histidine is measured. Histamine insufficiency is possible. U. RESULTS RELATING TO INFECTION OR GUT DYSBIOSIS: * None