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T91 Urine Organic Profile


Methodology: GC/Mass Spectroscopy^^COBAS FARA II

Energy Production
Results Reference Limit
1. Citrate 541 Ág/mg creatinine 500-2300
2. Cis-Aconitate 24 5-250
3. Isocitrate` 286 50-800
4. a-Ketoglutarate 3 3-25
5. Succinate 40.5 H 5-35
6. Fumarate 0.07 L 0.2-1.2
7. Malate 1.4 <6
8. Lactate 191 H 4-30
9. Pyruvate 0.81 H <0.7
Functional Cofactor
10. a-Ketoisovalerate 0.1 <1.5
11. a-Ketoisocaproate <0.1 <2
12. a-Keto-▀-Methylvalerate 0.33 <1.2
13. Methylmalonate <0.15 <3
14. ▀-Hydroxyisovalerate 22.5 H <20
15. Hydroxymethylglutarate <0.2 L 0.2-1
Carbohydrate Metabolism
16. ▀-Hydroxybutyrate 1 <40
17. a-Hydroxybutyrate 1.7 <50
Detoxification Indicators
18. p-Hydroxyphenyllactate 0.02 <0.5
19. 2-Methylhippurate 1.1 H <1
20. Glucarate <0.1 <4
21. Orotate 76.1 <180
22. Pyroglutamate 90.1 H <80
23. Sulfate/Creatinine Ratio 207.1 >180
Fatty Acid Oxidation
24. Adipate 5.4 H <3
25. Suberate 5.1 H <4
26. Ethylmalonate 3.3 <4
27. Vanilmandelate 33.76 H 0.2-2
28. Homovanillate 3 1-5
29. 5-Hydroxyindoleacetate 4.9 0.8-5
30. Quinolinate <0.1 <5
Dysbiosis Markers
31. p-Hydroxybenzoate 0.23 <1
32. p-Hydroxyphenylacetate 6.1 <60
33. ▀-Ketoglutarate 46.3 <70
34. Dihydroxyphenylpropionate 3.91 <5
35. Tartarate <2 <50
36. Citramalate 1.2 <3.5
37. Arabinose 73 <80
38. Arabinitol 9.7 <35
39. Tricarballylate 0.5 <5

Urinary Creatinine = 111   mg/dl


Georgia Lab Lic. Code # 067-007
CLIA ID# 11D0255349
New York Clinical Lab Permit Code #811767AO
Florida Clinical Lab Lic. #800008124
Laboratory Directors
J. Alexander Bralley, PhD & Robert M. David, PhD



Energy Production
1. Citrate L Aspartic acid, 500mg 1
2. Cis-aconitate H Iron, 18mg; Cysteine, 1000mg BID 1
3. Isocitrate H a-KG, 300mg TID; B3, 100mg
Magnesium, 400mg; Manganese, 20mg
4. a-Ketoglutarate L

a-KG, 300mg; Arginine, 1000mg;
B-complex, 1 TID; Lipoic acid 100mg
Citric Acid Cycle Intermediate 1
5. Succinate L

Isoleucine, 1000mg TID; Valine, 1000mg TID
Magnesium, 500mg
6. Fumarate L Tyrosine, 1000mg BID; Phenylalanine, 500mg BID 1
7. Malate H B3, 100mg TID 1
8. Lactate  H Coenzyme Q10, 50mg TID 2
9. Pyruvate H B-complex, 1 capsule TID;
B1, 100mg TID; Lipoic acid, 100mg TID
Aerobic/anaerobic energy production and acid/base balance 2
Functional Cofactor Indicators
10. a-Ketoisovalerate H B-complex, 1 capsule TID; B1, 100mg TID;
11. a-Ketoisocaproate H Lipoic acid, 100mg TID Amino acid catabolism 3
12. a-Keto-▀-methylvalerate H utilizing B-complex vitamins
13. Methylmalonate H B12, 1000mcg TID BCAA input to Krebs cycle 4
14. ▀-Hydroxyisovalerate H Biotin, 5mg BID; Magnesium, 100mg BID Dicarboxylic acid metabolism requiring biotin 5
15. Hydroxymethylglutarate H/L Coenzyme Q10, 50mg TID Co-Q10 synthesis 6
Carbohydrate Metabolism
16. ▀-Hydroxybutyrate H Chromium picolinate, 200mcg BID Balance of fat and CHO metabolism 7
17. a-Hydroxybutyrate  H
Detoxication Indicators
18. p-Hydroxyphenyllactate H Vit. C, up to 100mg/kg/day Pro-oxidant and carcinogen 8
19. 2-Methylhippurate H Avoidance of toxin Hepatic conjugation 9
20. Glucarate H Glycine, GSH, NAC, 500-5000mg/day Liver enzyme induction due to toxins 10
21. Orotate H a-KG, 300mg TID; Arginine, 1-3gm/day;
Aspartic Acid, 500mg BID; Magnesium, 300mg
Urea synthesis and
ammonia detox.
22. Pyroglutamate L/H NAC, 1000mg, glutathione, 300mg Renal amino acid recovery- required for glutathione synthesis 12
23. Sulfate/Creatinine Ratio H Taurine, 500mg BID; Glutathione, 300mg Detox & anti-oxidant functions using sulfur compounds 11
Fatty Acid Oxidation
24. Adipate H L-carnitine, 250mg TID; B2, 100mg BID; 14
25. Suberate H B5, 500mg BID; choline, 100mg TID Fatty acid oxidation 14
26. Ethylmalonate  H C, 1000mg TID: CoQ10, 150mg 15
Neurotransmitter Metabolism
27. Vanilmandelate L/H Tyrosine, 1000mg two or three times daily, between meals. (Contraindicated for patients taking MAO inhibitors) Catecholamine catabolism, neurotransmitter metabolites 16
28. Homovanillate L/H
29. 5-hydroxyindolacetate L 5-hydroxytryptophan, 100mg TID 17
30. Quinolinate H Magnesium, 300mg Serotonin catabolism 18
Dysbiosis Markers (Products of Abnormal Gut Microflora)
31. p-Hydroxybenzoate H 19
32. p-Hydroxyphenylacetate H 19
33. ▀-Ketoglutarate H If any of these compounds are high, the 20
34. Hydrocaffeate H possibility of dysbiosis is reinforced. 20
35. Tartarate  H Glutamine, 10-30gm daily and free form Numerous interferences in energy 20
36. Citramalate  H amino acids normalize gut permeability pathways and cellular control 20
37. Arabinose  H Take appropriate steps to ensure favorable mechanisms. 20
38. Arabinitol H gut microflora population. 20
39. Tricarballylate H 20


Comments (Numbered)



Citric acid cycle intermediates:
These components represent the core metabolic engine of the body which generates cellular energy. The Krebs citric acid cycle (CAC) not only is the final common pathway of food components, but is also the source of basic structural or anabolic molecules that feed and support organ metabolism. Therefore, the CAC serves both anabolic and catabolic functions of the body, representing the "crossroads" of food conversion and utilization.

As can be seen from the pathway diagram (Stages in Extraction of Energy from Food), the CAC intermediates can be derived from amino acids. This would explain the energy-boosting effect people often report when they take free form amino acid supplements. The fatigue-reducing effect of supplementation of aspartate salts and a-ketoglutaric acid may also be explained in this way.4,5 Supplementation of the precursors (see table above) serves to drive the cycle and generate reducing equivalents used in the electron transport chain where ATP is produced via oxidative phosphorylation. Low levels of a specific metabolite may be indicative of suboptimal amino acid availability and need for supplemental amounts of these specific amino acids for improved function.

Functional Cofactor Assessment: Citric Acid Cycle

Conversion of one CAC intermediate to another uses enzymes that often require vitamin and mineral cofactors for improved function. Elevations of any CAC intermediate may reflect a functional need for these nutrients in supplemental dosages to overcome the metabolic block (see pathway diagram).

Low levels of CAC intermediates may reflect an increased need for precursor amino acids. (See pathway diagram) Amino acid supplementation often results in increased energy levels experienced by the individual. This effect is most likely due to the ability of amino acids to be converted directly to CAC intermediates that drive this energy cycle.6

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Lactate, Pyruvate:
These two compounds provide useful insight to basic metabolic factors due to their position in the energy production process. Pyruvate is the breakdown product of glucose and requires the enzyme pyruvate dehydrogenase for its conversion to acetyl-CoA and further metabolism either in the citric acid cycle or into fatty acids. Pyruvate dehydrogenase requires B1, Lipoic acid, B2, B3, and B5 for optimal function. Elevated levels of pyruvate may reflect a functional need for increased B vitamins, particularly B1 and lipoic acid.

Elevated lactate may reflect suboptimal metabolism and/or inactivation of citric acid cycle due to inadequate oxidative phosphorylation (ox/phos). Coenzyme Q10 has been used in cases of lactic acidosis associated with ox/phos impairments.7,8 Increased lactate is a common acidotic condition that can be caused by a variety of metabolic problems. Decreased lactate is seen in people with very little physical activity, and occasionally in well-conditioned athletes.

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These analytes are the keto-acids of the branched chain amino acids, isoleucine, leucine and valine, respectively. They are formed by the removal of the amine group in the first step of their metabolism and further metabolized by enzymes similar to pyruvate dehydrogenase that use the B-complex cofactors, B1, B2, B3, B5 and lipoic acid. Therefore, elevations of these metabolites provide a functional assessment of the sufficiency of these B vitamins.

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This compound is converted into succinic acid using a B12-dependent enzyme, methylmalonyl CoA mutase. A high level indicates a functional deficiency of B12. A differential diagnosis can be made when considering both methylmalonate and homocysteine concentrations. If homocysteine is also elevated, both B12 and folate functional deficiencies are indicated. If only homocysteine is high, folate and B6 supplementation are suggested. If methylmalonate only is elevated, B12 supplementation is needed.9

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Excretion of this compound in urine is an early and sensitive indicator of biotin deficiency.10 This is a compound that is elevated in multiple carboxylase insufficiency. Symptoms of these disorders include: alopecia, skin rash, Candida dermatitis, unusual odor to the urine, immune deficiencies and muscle weakness. Other possible indications are elevations of lactate and alanine in urine and accumulations of odd-chain fatty acids in plasma or red cell membranes.11,12 There are three mitochondrial carboxylase enzymes which use biotin as a cofactor. Supplementation of biotin may improve these conditions.

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Hydroxymethylglutarate (HMG):
This compound is the metabolic precursor of cholesterol and coenzyme Q10 (CoQ10). Low levels may reflect inadequate synthesis and possible deficiency of coenzyme Q10. Cholesterol lowering drugs that block utilization of HMG for cholesterol synthesis also lower coenzyme Q10 levels.
13 Therefore, low levels of HMG may indicate suboptimal synthesis of CoQ10. CoQ10 is utilized in the mitochondrial oxidative phosphorylation pathway for ATP synthesis and is a potent anti-oxidant. It has been used extensively as a cardiovascular protective agent.14 Coenzyme Q10 has been used successfully to improve mitochondrial function in several clinical situations15,16 and may be useful in the treatment of fatigue particularly when both lactate and pyruvate are elevated. This could reflect the inability of mitochrondrial oxidative phosphorylation to proceed efficiently possibly due to CoQ10 insufficiency. (see diagram)

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These two compounds are ketone bodies. Ketone body production occurs in conditions of impaired carbohydrate metabolism where the liver breaks down free fatty acids as an energy source. Ketone bodies are a byproduct of this process. Slight elevations seen in an overnight urine collection may indicate inefficient utilization or mobilization of carbohydrate stores. Chromium supplementation may support the carbohydrate utilization by improving the action of insulin.

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HPLA-is a carcinogenic metabolite of tyrosine that increases lipid peroxidation in the liver.17 Methyl p-Hydroxy- phenyllactate (MeHPLA) is an important cell growth-regulating agent and tumor cells contain esterase activities that hydrolyze the compound to the free acid, HPLA.18 HPLA is an important regulator of normal and malignant cell growth and it appears to mediate the cancer promoting effects of estrogen. MeHPLA blocks uterine growth in vivo and inhibits MCF-7 human breast cancer cell growth in vitro.19 High doses of ascorbic acid (100 mg/kg body weight daily) were shown to arrest or significantly inhibit the excretion of HPLA in patients with hemoblastoses and nephroblastoma.20 HPLA is produced by some microbes that could inhabit the gut 21, but the recently-discovered cell proliferative and pro-oxidant functions are of far greater clinical relevance.

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This compound is a metabolite of the detoxification of the common solvents xylene and toluene. Elevations indicate an exposure to these potentially toxic compounds.22,23 Patient counseling in avoidance of these compounds would be indicated.

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Glucaric acid (glucarate) is a by-product of the liver Phase II detoxification reactions involving glucuronic acid conjugation. Elevations are thought to be a marker of enzyme induction due to toxic exposures and/or pharmaceutical use.24,25

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Sulfation pathways in Phase II liver detoxification are important in biotransforming drugs, steroid hormones, and phenolic compounds, among others. The ratio of sulfate to creatinine is an assessment of the bodyĺs reserves of sulfur-containing compounds (including glutathione, below) used in Phase II. When this ratio is low, these stores need replenishment.26,27

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In the kidney pyroglutamate is formed from the utilization of glutathione in a cyclic process that serves to recover amino acids and prevent their loss in urine.28 Up to 70% of plasma glutathione can enter this pathway in the kidney. Most of the glutathione is normally recovered, but failure of the energy-dependent steps of the cycle leads to accumulation of pyroglutamate at the expense of glutathione. Thus glutathione depletion is indicated by high urinary pyroglutamate.

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Orotate: Orotic acid synthesis is abnormally high with hereditary deficiencies of enzymes of pyrimidine synthesis or of the urea cycle. Orotic acid excretion is elevated by arginine deficiency, ammonia intoxication and by diets with high lysine to arginine ratios.29 Magnesium is a key cofactor in the catabolism of orotic acid. Aspartic acid and ?-KG are substrates needed to prevent the ammonia accumulation that leads to orotic aciduria.

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Adipate, Suberate:
Elevations of adipate and suberate occur in dicarboxylic aciduria and reflect suboptimal fatty acid oxidation. Symptoms include periodic mild weakness, nausea, easy fatigability, hypoglycemia, "sweaty feet" odor, recurrent infections, increased free fatty acids. Patients may also exhibit a Reyes-like syndrome in dicarboxylic aciduria which has been associated with various metabolic toxins generated from viral infections that affect mitochondrial function. Mild, heterozygotic forms of dicarboxylic aciduria may be more commonly seen clinically and go unrecognized. Environmental toxin exposure prior to a viral exposure may cause subclinical damage, altered lipid metabolism and impaired immune responsiveness.30,31 Supplementation of supportive nutrients may benefit this condition, (carnitine, B-complex, vitamin C).

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Ethylmalonate: Ethylmalonate is elevated in multiple acyl-CoA dehydrogenase deficiency causing an inability to efficiently oxidize fatty acids for energy. This genetic deficiency can vary in severity and may produce no symptomology until older age. Coincident elevations of adipate can occur, further indicating the fatty acid oxidation impairment. Cofactor supplement, B2 and CoQ10, may assist in activating the enzymes involved.32

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These two compounds are metabolites of catecholamines, epinephrine and norepinephrine. Low urinary levels have been associated with low CNS levels of these neurotransmitters. Symptoms associated with this condition are depression, sleep disturbances, inability to deal with stress, fatigue. Supplementation of the amino acid precursors, tyrosine and phenylalanine, can raise these neurotransmitter levels in the CNS.33 A further indication of need for these precursors would be low fumarate in the citric acid cycle, a metabolic intermediate that can also be derived from tyrosine and phenylalanine.

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A urinary metabolite of serotonin, 5-hydroxyindolacetate (5-HIA) reflects central nervous system levels of this neurotransmitter made from tryptophan. Low levels have been associated with depression, fatigue, insomnia, suicide, attention deficit and behavioral disorders. Increased dietary tryptophan is indicated (from turkey, bananas, low fat milk, lentils, and eggs). Addition of the precursors, tryptophan or 5-HT may be helpful. Serotonin re-uptake inhibitors (Prozac, etc.) often lead to high 5HIA.

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This compound is a metabolite of tryptophan and kynurenate. Although its metabolic significance is unclear, elevated levels have been associated with inflammatory brain diseases and it appears to be synthesized upon immune stimulation. Quinolinate is neurotoxic and binds with NMDA receptors in the brain. A structural analogue of oxaloacetate, quinolinateĺs presence may also inhibit citric acid cycle activity and ATP production. Quinolinate may be converted into NAD via a multi-step, magnesium dependent reaction sequence. Consequently, magnesium sufficiency may be necessary to regulate abnormal quinolinate levels.34

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These compounds ordinarily should not be appearing in the urine due to the metabolic conservation or recycling of such phenyl group compounds. However, intestinal microorganisms do manufacture these in relatively high quantities which are absorbed in the gut to eventually appear in the urine. Several studies have used these compounds as indicators of gut dysbiosis or microbial overgrowth in the intestines. Gut dysbiosis can lead to a wide variety of symptoms due to potential pathogenic toxins elaborated by these microorganisms.35,36 Beneficial interventions include digestive aids (stomach and bile acids and pancreatic enzymes), lactobacillus inoculations by oral supplementation and diet and lifestyle modification. A bowel detoxification regimen may be indicated to normalize the microbial flora of the gut.

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Dihydroxyphenylpropiate, Tartarate,Citramalate,Arabinose, Arabinitol, Tricarballylate:
These compounds are not normal metabolites of the body but are produced by conditionally pathogenic microbes in the bowel which can proliferate due to antibiotic use creating toxic dysbiotic conditions. Arabinitol is specifically elevated by Candida overgrowth. Thought to be metabolic inhibitors of energy production enzyme systems, these compounds can dversely affect many systems in the body and are associated with the development of autism.37 These compounds will help the clinician monitor the effectiveness of treatment for gut dysbiosis. (see above)

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