Organic Acid Test Panel (OAT), Dr. Weyrich's Naturopathic Functional Medicine Notebook

Test Overview of Organic Acid Test Panel (OAT)

The Organic Acid Test (OAT) Panel examines metabolites in a patient's urine that are products of body metabolism and gut microbes. It can reveal imbalances in metabolic pathways, nutritional imbalances, and abnormal microbial overgrowth in the small and large intestines. The OAT Panel complements the Comprehensive Digestive Stool Analysis Panel, which can reveal abnormal microbial overgrowth in the large intestine.

Test Indications of Organic Acid Test Panel (OAT)

According to Go to That's Health

That's Health OAT indications include:

First-line test for evaluating Autism Spectrum Disorder (ASD), Pervasive Developmental Delay (PDD), Asperger's Syndrome, Attention-Deficit Hyperactivity Disorder (ADD, ADHD), learning disability, depression, anxiety and other mood disorders, Small Intestinal Bacteria Overgrowth (SIBO), and environmental toxicity,
Seizure disorders,
Chronic Fatigue Syndrome,
Methyl-tetrahydrofolate reductase (MTHFR) deficiency.

Theory of Organic Acid Test Panel (OAT)

Yeast/Fungal Metabolites

Elevated yeast/fungal metabolites suggest a yeast or fungal overgrowth in the gastrointestinal tract [GP2010].

Citramalic (Methylmalic) Acid

Citramalic acid is a byproduct of a Saccharomyces yeast or Propionibacterium species and suggests dysbiosis MosaicDX.
As an analogue of the Krebs cycle compound malic acid, it may interfere with the production of malic acid in the Krebs cycle.
Consider treating with probiotics and other naturopathic techniques.

5-Hydroxymethyl-2-furoic Acid

5-hydroxymethyl-2-furoic acid is a byproduct of the fungus Aspergillus and probably other fungi and yeast species, suggesting dysbiosis MosaicDX.
Consider treating with probiotics and other naturopathic techniques.

3-Oxoglutaric Acid

3-Oxoglutaric acid is an analogue of the Krebs cycle compound 2-oxoglutaric (alpha-ketoglutaric) acid.
Elevated titers suggest yeast overgrowth in the GI tract MosaicDX.
Slightly elevated titers are found in autism and other disorders.
Elevated 3-oxoglutaric acid may correlate with low 2-oxoglutaric acid, indicating an interference with 3-oxoglutaric acid in the Krebs cycle.
It is presumably formed from the amino acids lysine and tryptophan.
Consider treating with probiotics and other naturopathic techniques.

Furan-2,5-dicarboxylic Acid

Furan-2,5-dicarboxylic acid is a byproduct of the fungus Aspergillus and probably other fungi and yeast species, suggesting dysbiosis MosaicDX.
Consider treating with probiotics and other naturopathic techniques.

Furancarbonylglycine

Furancarbonylglycine is a conjugate of furancarboxylic acid and the amino acid glycine produced by Aspergillus and possibly other fungal species, which suggests dysbiosis MosaicDX.
Consider treating with probiotics and other naturopathic techniques.

Tartaric Acid (3-Hydroxymalic Acid or 2,3-Hydroxy-succinic acid)

Tartaric acid is an analogue of the Krebs cycle intermediate malic acid that inhibits the Krebs cycle enzyme fumarase that converts fumaric acid to malic acid [Shaw2008].
It is a toxic fermentation product of Saccharomyces yeast [need citation].
It is a product of Candida hyaluronidase that damages muscles and kidneys [Robertson1968 🕮 ], MosaicDX.
It is also found in grapes, cream of tartar, and as a food additive.
High titers are associated with autism and fibromyalgia [Shaw2008].
The FDA generally Recognizes Tartaric Acid as safe (GRAS) in low doses, but a 12 g dose may be fatal [Shaw2008].
Consider treating with antifungal pharmaceuticals, probiotics, and other naturopathic techniques.

Arabinose

Arabinose is a product of Candida hyaluronidase and damages muscles and kidneys [Robertson1968 🕮 ], MosaicDX.
Arabinose is a metabolite produced in the liver from arabitol (also called arabinitol); arabitol is produced by various yeast species such as Candida albicans, Candida tropicalis, Candida parapsilosis, etc. [need Citaton].
Arabinose is a 5-carbon aldose sugar that is not made in significant quantity by human metabolism but can be found in apples, grapes, and pears and can serve as a marker for yeast overgrowth [Kiehn1979 🕮 ], [Wong1990 🕮 ], [Larsson1994 🕮 ], [Roboz1992 🕮 ].
Arabinose may be a particular problem for patients with a defect in their pentose metabolism; this defect can be tested for [Shaw2008].
Consider treating with antifungal pharmaceuticals, probiotics, and other naturopathic techniques.

Carboxycitric Acid

Carboxycitric acid is an analogue of the Krebs cycle compound citric acid; as such, it may interfere with the metabolism of citric acid in the Krebs cycle.
Elevated titers of yeast/fungal metabolites suggest dysbiosis MosaicDX.
Consider treating with antifungal pharmaceuticals, probiotics, and other naturopathic techniques.

Carboxycitric Acid

Carboxycitric acid is a byproduct released from mycotoxins called fumonisins in the gastrointestinal tract MosaicDX.
Fumonisins are produced primarily by Fusarium verticillioides, a plant parasite. Elevated titers can be caused by eating contaminated corn [Brown2007 🕮 ].

Bacterial Metabolites

Hippuric Acid

Hippuric acid is a conjugate of benzoic acid and glycine formed in the liver as part of the normal phase-II detoxification pathway [need cite] and is a bacterial product of phenylalanine metabolism MosaicDX.
Titers may be elevated due to bacteria overgrowth of the GI tract producing benzoic acid; other sources of benzoic acid are the solvent toluene, the food preservative sodium benzoate, apples, pears, tea, coffee, sunflower seeds, carrots, blueberries, cherries, potatoes, tomatoes, eggplant, sweet potatoes, peaches [GP2010].
Low titers of hippuric acid may be due to depletion of glycine due to competing detoxification reactions or low amounts of bacteria after antibiotic use.
Consider treating with probiotics such as Lactobacillus rhamnosus and other naturopathic techniques [GP2010].

2-Hydroxyphenylacetic Acid

2-Hydroxyphenylacetic acid is produced by the overgrowth of several species of bacteria in the GI tract by metabolizing the amino acid tyrosine.
Elevated titers are seen in PKU [GP2010].
Very elevated titers are present in celiac disease and enteritis.
Consider treating with probiotics and other naturopathic techniques [GP2010].

4-Hydroxybenzoic Acid (p-Hydroxybenzoic acid)

Elevated titers of 4-Hydroxybenzoic acid may be due to bacterial overgrowth or may be due to fruits such as blueberries [GP2010].
4-Hydroxybenzoic acid is also a metabolite of parabens that are additives in food, cosmetics, and toiletries. Parabens have estrogenic activity and may be associated with breast cancer [GP2010], [Routledge1998]. Parabens may uncouple oxidative phosphorylation, leading to mitochondrial dysfunction [GP2010].
Treatment is by avoidance of parabens.

4-Hydroxyhippuric Acid (p-Hydroxyhippuric Acid)

Elevated titers may be due to bacterial overgrowth or may be due to fruits such as blueberries [GP2010].
4-Hydroxyhippuric acid is also a metabolite of parabens that are additives in food, cosmetics, and toiletries. Parabens have estrogenic activity and may be associated with breast cancer [GP2010], [Routledge1998]. Parabens may uncouple oxidative phosphorylation, leading to mitochondrial dysfunction [GP2010].
Treatment is by avoidance of parabens.

Dihydroxyphenylpropionic Acid (DHPPA)

DHPPA is a metabolite of chlorogenic acid, which is in many fruits and vegetables MosaicDX.
Chlorogenic acid is metabolized to DHPPA by commensal bacteria such as Lactobacilli, Bifidobacteria, and Escherichia coli; therefore, DHPPA is a marker for beneficial gut microbiome MosaicDX

Phenylcarboxylic Acid

Elevated titers of phenylcarboxylic acid suggest the overgrowth of GI bacteria.
[Dr. Weyrich: this is not a single compound - the carboxylic acid can be acetic acid (yielding phenylacetic acid) or any other carboxylic acid].

Indole-like Compound Acids

Indole-like compound acids are most likely derived from tryptophan.
Elevated titers suggest the overgrowth of GI bacteria and are commonly elevated along with 3-indoleacetic acid [need cite].

Clostridia Bacterial Markers

4-Hydroxyphenylacetic Acid

4-Hydroxyphenylacetic acid is produced by the overgrowth of bacteria in the GI tract by metabolizing the amino acid tyrosine MosaicDX.
Elevated titers are associated with Clostridia overgrowth, small intestinal bowel overgrowth (SIBO), or small bowel disease MosaicDX.
Very elevated titers are present in celiac disease, enteritis, and intestinal resection.
Treatment with the antibiotic neomycin can significantly lower urine titers; also consider naturopathic treatments.

3-(3-Hydroxyphenyl)-3-hydroxypropionic acid (HPHPA)

HPHPA is produced by Clostridium species, including but not limited to Clostridium difficile [GP2010], Clostridium sporogenes MosaicDX, Clostridium botulinum MosaicDX, Clostridium caloritolerans MosaicDX, Clostridium mangenoyi [also known as Clostridioides mangenoyi], Clostridium ghoni, Clostridium bifermentans [also known as Paraclostridium bifermentans], and Clostridium sordellii [GP2010].
HPHPA inhibits the enzyme dopamine-beta-hydroxylase, leading to derangement of neurotransmitter balance.
Elevated titers are common in autism, depression, schizophrenia, seizures, chronic fatigue syndrome, colitis, tic disorders, and muscle weakness or paralysis [Shaw2008], [GP2010] (particularly when its level exceeds 500mmol/mol creatinine) [GP2010] MosaicDX.
Antibiotics such as vancomycin or metronidazole (Flagyl) can significantly lower the HPHPA level in urine [GP2010]. Adding probiotics such as Lactobacillus acidophilus GG, Lactobacillus rhamnosus [also known as Lacticaseibacillus rhamnosus], or Saccharomyces boulardii is also recommended [Shaw2008], [GP2010]; also consider naturopathic treatments.
According to [Shaw2008, pg 14], Clostridium spp. deaminate the amino acid phenylalanine (which is the precursor of the important neurotransmitters dopamine, norepinephrine, and epinephrine) to form 3-phenylpropionic acid, which is then hydroxylated in the meta position by Clostridium spp. to form 3-(3-hydroxyphenyl)-propionic acid [Elsden1976 🕮 ] [Bhala1993 🕮 ]. This intermediate is then subjected to human beta-oxidation to form 3-(3-hydroxyphenyl)-3-hydroxypropionic acid (HPHPA), which is detectable in the urine.
An alternative pathway for the formation of HPHPA from phenylalanine is via microbial meta-hydroxylation of phenylalanine to form 3-hydroxyphenylalanine (an analogue of tyrosine, which is 4-hydroxyphenylalanine), which is then deaminated to form 3-(3-hydroxyphenyl)-propionic acid, which then proceeds to HPHPA as above [Shaw2008].

4-Cresol

An elevated titer of 4-cresol suggests an overgrowth of Clostridium difficile in the GI tract MosaicDX.
4-Cresol is often elevated in autism, psychiatric disorders, and GI disorders MosaicDX.
4-Cresol inhibits the enzyme dopamine-beta-hydroxylase, causing derangement of neurotransmitter balance MosaicDX.

Vanillylmandelic Acid (VMA) Analogue

VMA is a metabolite of the amino acid tyrosine produced by Clostridium species.
Clostridial overgrowth may interfere with the body's production and metabolism of the neurotransmitters dopamine and norepinephrine, which are made from tyrosine.
Elevated titers are common in autism, depression, schizophrenia, seizures, and chronic fatigue syndrome.
Treatment with the antibiotics vancomycin or metronidazole (Flagyl) can significantly lower titers in urine; also consider naturopathic treatments.

Oxalate Related Metabolites

Glyceric Acid

Elevated titers of glyceric acid are associated with autism, vulvar pain, fibromyalgia [GP2010].
Elevated titers may be due to microbial sources such as yeast (Aspergillus, Penicillium, and probably Candida) [GP2010] or due to dietary sources containing glycerol (glycerin).
Elevated titers may also indicate the inborn error of metabolism genetic hyperoxaluria type II; titers of glyceric acid within the reference range rule out genetic causes of oxaluria MosaicDX.

Glycolic Acid

Elevated glycolic acid titers without elevated oxalic acid are most likely a result of GI yeast overgrowth (Aspergillus, Penicillium, probably Candida) [GP2010] or dietary sources containing glycerol (glycerin).
Associated with autism, vulvar pain, fibromyalgia [GP2010].
Elevated titers may also indicate the inborn error of metabolism genetic hyperoxaluria type I; titers of glyceric acid within the reference range rule out genetic causes of oxaluria MosaicDX.

Oxalic Acid (Oxalate)

Elevated titers of oxalic acid may be due to many causes, including:
- Primary hyperoxaluria (genetic),
- Diabetes mellitus,
- Cirrhosis,
- Vitamin B6 deficiency,
- Sarcoidosis,
- Steatorrhea due to pancreatic insufficiency,
- Celiac disease,
- Bacteria overgrowth,
- Aspergillus, Penicillium, and possibly Candida overgrowth [GP2010],
- Ileal resection,
- Biliary tract disease,
- Small bowel disease,
- Ethylene glycol poisoning MosaicDX,
- Increased intake of foods high in oxalate, including rhubarb, spinach, raspberries, beets, chocolate, wheat bran, tea, cashews, pecans, almonds, and peanuts [Great Plains Laboratories - link no longer available],
- High doses of vitamin C MosaicDX,
- Poor fat absorption, perhaps due to excessive fat intake or inadequate bile flow, increases calcium binding to fatty acids in the gut and concomitant reduction in calcium binding to oxalate [GP2010].
If glycolic acid is also elevated, it suggests the genetic disease hyperoxaluria type I.
If glyceric acid is also elevated, it suggests the genetic disease hyperoxaluria type II.
Elevated oxalic acid titers have been associated with:
- Autism [GP2010],
- Vulvar pain [GP2010],
- Fibromyalgia and muscle pain [GP2010],
- Anemia unresponsive to treatment [GP2010],
- Skin ulcers [GP2010],
- Heart abnormalities [GP2010],
- Decreased osteoblast activity and increased bone resorption [GP2010],
- Kidney stone formation [GP2010],
- Painful oxalic acid deposition in various tissues, including joints, eyes, muscles, blood vessels, brain, and heart [GP2010].
Antifungal therapy may reduce oxalates if yeast or fungal markers are elevated MosaicDX.

Glycolysis Intermediates

Lactic Acid (Lactate)

Elevated lactic acid titers may indicate infection, recent vigorous exercise, B vitamin deficiency, shock, poor perfusion, intestinal bacterial overgrowth, or mitochondrial dysfunction MosaicDX.
Extremely elevated titers (over 300 mmol/mol creatinine) suggest genetic diseases such as pyruvate dehydrogenase deficiency, glycogen storage diseases, disorders of fructose metabolism MosaicDX, severe trauma, or life-threatening infections.

Pyruvic Acid (Pyruvate)

Elevated pyruvic acid titers may indicate infection, recent vigorous exercise, B vitamin deficiency, shock, poor perfusion, intestinal bacterial overgrowth, mitochondrial dysfunction, or anemia MosaicDX.
Extremely elevated titers (over 100 mmol/mol creatinine) indicate genetic diseases such as pyruvate dehydrogenase deficiency, glycogen storage diseases, disorders of fructose metabolism MosaicDX, severe trauma, or life-threatening infections.

2-Hydroxybutyric Acid

2-hydroxybutyric acid is a metabolite of cystathionine MosaicDX.
Moderately elevated titers may indicate infection, recent vigorous exercise, poor perfusion, oxidative stress, toxic exposures, or deficiencies of methyl tetrahydrofolate, methyl B12, or betaine MosaicDX.
Considerably elevated titers may indicate genetic diseases such as pyruvate dehydrogenase deficiency, glycogen storage disease, disorders of fructose metabolism, disorders of the methylation pathway, severe trauma, life-threatening infections.

Krebs Cycle Intermediates

The Krebs cycle is also called citric acid cycle or the tricarboxylic acid cycle. It is a series of 10 enzymatic reactions that occur within the mitochondria in the body, and is key to proper energy metabolism [Nelson2000, pg 572], Go to Wikipedia Wikipedia.

Citric Acid (Citrate)

Citric acid is produced by the Krebs cycle enzyme citrate synthase acting on the precursors acetyl-CoA and oxaloacetic acid [Nelson2000, pg 572], Wikipedia.
When citric, 2-Oxoglutaric, fumaric, and malic acid titers are all elevated, a mitochondrial energy pathway dysfunction is likely MosaicDX.
Do not confuse citric acid with ascorbic acid (vitamin C). They are both found in citrus fruit but are not the same compound.
Elevated citric acid may be due to dietary intake, intestinal yeast producing citric acid, intestinal yeast metabolites inhibiting the human Krebs Cycle, the depletion of glutathione, which is a required cofactor for the enzyme aconitase that metabolizes cis-aconitic and citric acids) [GP2010] MosaicDX.
Consider supplementing glutathione or n-acetyl-cysteine if pyroglutamic acid titers are low MosaicDX.

cis-Aconitic Acid

cis-aconitic acid is produced by the Krebs cycle enzyme aconitase acting on the precursor citric acid [Nelson2000, pg 572], Wikipedia.
Its titer may be elevated due to a deficiency in glutathione since the enzyme aconitase requires reduced glutathione [need cite] to metabolize cis-aconitic to citric acid or mitochondrial dysfunction (e.g., Complex I and Pierson Syndrome) MosaicDX.

D-Isocitric Acid (D-Isocitrate)

D-isocitric acid is produced by the Krebs cycle enzyme aconitase acting on the precursor cis-aconitic acid [Nelson2000, pg 572], Wikipedia.

2-Oxoglutaric Acid (alpha-Ketoglutaric Acid, alpha-Ketoglutarate, AKG)

AKG is produced by the Krebs cycle enzyme isocitrate dehydrogenase acting on the precursor D-Isocitric acid. This process requires the co-factor NAD⁺ (derived from vitamin B3) [Nelson2000, pg 572], Wikipedia.
When citric, 2-Oxoglutaric, fumaric, and malic acid titers are all elevated, a mitochondrial energy pathway dysfunction is likely MosaicDX.
Alternatively, 2-oxoglutaric acid may be derived from converting glutamic acid to 2-oxoglutaric by deamination or transamination.
Elevated urine titers of AKG may be due to vitamin deficiencies (vitamins B1, B2, B5) blocking the conversion of 2-oxoglutaric acid to succinyl-CoA or dietary intake of 2-ketoglutaric acid MosaicDX.
Very low titers are associated with chronic fatigue syndrome.
Anecdotal reports indicate that autistic symptoms sometimes improve with AKG supplementation in response to low titers of this metabolite.

Succinal-Co-A

Succinal-Co-A is produced by the Krebs cycle enzyme alpha-ketoglutarate dehydrogenase acting on the precursor AKG This process requires the co-factors NAD⁺ (derived from vitamin B3) and CoA-SH (derived from vitamin B5) [Nelson2000, pg 572], Wikipedia.

Succinic Acid (Succinate)

Succinic acid is produced by the Krebs cycle enzyme succinyl-CoA synthase acting on the precursor succinyl-CoA. This process requires the co-factors GDP (interchangable with ADP) and inorganic phosphorus [Nelson2000, pg 572], Wikipedia.
Succinic acid titers may be elevated due to environmental toxicity, riboflavin deficiency, coenzyme Q-10 deficiency, bacterial conversion of dietary glutamine to succinic acid in the gastrointestinal tract MosaicDX, or inborn error of metabolism.
Low titers of succinic acid suggest inadequate consumption of the essential branched-chain amino acids leucine and isoleucine MosaicDX.

Fumaric Acid (Fumarate)

Fumaric acid is produced by the Krebs cycle enzyme succinic dehydrogenase acting on the precursor succinic acid. This process requires the co-factors Co-Q10 (ubiquinone) and FAD (derived from vitamin B2) [Nelson2000, pg 572], Wikipedia.
When citric, 2-Oxoglutaric, fumaric, and malic acid titers are all elevated, a mitochondrial energy pathway dysfunction is likely MosaicDX.
Elevated titers of fumaric acid suggest impaired function of fumarase (the following enzyme in the Krebs cycle) or mitochondrial dysfunction MosaicDX.
Supplements to support mitochondrial function include "coenzyme Q10, nicotinamide adenine dinucleotide (NAD+), L-carnitine and acetyl-L-carnitine, riboflavin, nicotinamide, biotin, and vitamin E" MosaicDX.

Malic Acid (Malate)

Malic acid is produced by the Krebs cycle enzyme fumaease acting on the precursor fumaric acid [Nelson2000, pg 572], Wikipedia.
When citric, 2-Oxoglutaric, fumaric, and malic acid titers are all elevated, a mitochondrial energy pathway dysfunction is likely MosaicDX.
Slightly elevated titers of malic acid suggest niacin deficiency or coenzyme Q10 deficiency MosaicDX.

Oxaloacetic Acid (Oxaloacetate)

Oxaloacetic acid is produced by the Krebs cycle enzyme malate dehydrogenase acting on the precursor malic acid. This process requires the co-factor NAD⁺ (derived from vitamin B3) [Nelson2000, pg 572], Wikipedia.
Alternatively, oxaloacetic acid can be produced by the enzyme pyruvate carboxylase acting on the precursor pyruvic acid (pyruvate). This process requires the co-factor bicarbonate (HCO⁺₃ (derived from CO₂ Wikipedia.

Amino Acid Metabolites (Mitochondria)

3-Methylglutaric Acid and 3-Methylglutaconic Acid

Elevated titers of these metabolites suggest a reduced ability to metabolize leucine due to the genetic diseases 3-hydroxy-3-methylglutaric aciduria and 3-methylglutaconic aciduria MosaicDX.
Supplements to support mitochondrial function include "coenzyme Q10, niacin, L-carnitine and acetyl-L-carnitine, riboflavin, nicotinamide, biotin, and vitamin E" MosaicDX.

3-Hydroxyglutaric Acid

A slight elevation in 3-Hydroxyglutaric Acid titer suggests mitochondrial dysfunction MosaicDX.
Larger elevations suggest a deficiency in glutaryl CoA dehydrogenase, which metabolizes tryptophan, lysine, and hydroxylysine. This defect is associated with the genetic disease glutaric aciduria type 1 MosaicDX.
Elevated 3-hydroxyglutaric acid may occur concomitantly with glutaric and glutaconic acids MosaicDX.
Symptoms vary but include "encephalopathy, autism, cerebral palsy, and additional neurological abnormalities" MosaicDX.
Treatment is a diet low in lysine and supplementation with carnitine MosaicDX.

Amino Acid Metabolites

2-Hydroxyisovaleric Acid

Slight elevations may be due to thiamine or lipoic acid deficiencies, lactic acidosis, or episodic ketosis MosaicDX.
Elevated titers are also associated with the genetic diseases maple syrup urine disease and pyruvate dehydrogenase deficiency MosaicDX.

2-Oxoisovaleric Acid

Slight elevations may be due to thiamine or lipoic acid deficiencies, lactic acidosis, or episodic ketosis MosaicDX.
Elevated titers are also associated with the genetic disorders maple syrup urine disease and pyruvate dehydrogenase deficiency MosaicDX.

3-Methyl-2-oxovaleric Acid

Slight elevations may be due to thiamine or lipoic acid deficiencies.
Elevated titers are also associated with the genetic diseases maple syrup urine disease and pyruvate dehydrogenase deficiency MosaicDX.

2-Hydroxyisocaproic Acid

Slight elevations may be due to thiamine or lipoic acid deficiencies, lactic acidosis, or episodic ketosis MosaicDX.
Elevated titers are also associated with short bowel syndrome or the genetic diseases maple syrup urine disease and pyruvate dehydrogenase deficiency MosaicDX.

2-Oxoisocaproic Acid

Slight elevations may be due to thiamine or lipoic acid deficiencies, lactic acidosis, or episodic ketosis MosaicDX.
Elevated titers are also associated with the genetic diseases maple syrup urine disease and pyruvate dehydrogenase deficiency MosaicDX.

2-Oxo-4-methylbutyric Acid

Elevated in methioninemia, the genetic disease methionine metabolism, which is associated with myopathy and mental deficiency [Gaull1981 🕮 ].

Mandelic Acid

Elevated in the genetic diseases phenylketonuria (PKU) and tyrosinemia.
Slight elevations may result from increased dietary intake of phenylalanine or exposure to styrene MosaicDX.

Phenylacetic Acid

Elevated in the genetic diseases phenylketonuria (PKU) and tyrosinemia.
Slight elevations may result from increased dietary intake of phenylalanine.

Phenylpyruvic Acid

Elevated in the genetic diseases phenylketonuria (PKU) and tyrosinemia.
Slight elevations may result from increased dietary intake of phenylalanine or a deficiency in biopterin production, a cofactor required for phenylalanine metabolism MosaicDX.

Homogentisic Acid

Homogentisic acid is elevated in the genetic disease homogentisic aciduria (alkaptonuria).

4-Hydroxyphenyllactic Acid

Significantly elevated in the genetic diseases tyrosinemia and phenylketonuria.
A slight increase may be due to increased tyrosine intake, "bacterial gut metabolism, short bowel syndrome, or liver disease" MosaicDX.
Associated with post-COVID-19 syndrome [Sobolev2023 🕮 ].

N-acetylaspartic Acid

High titers suggest Carnavan's disease, a potentially fatal genetic disease that causes spongy degeneration of the brain MosaicDX.

Malonic Acid

Elevated titers may be associated with the genetic disease malonyl-CoA decarboxylase deficiency MosaicDX.
Mild elevations are unlikely to be clinically significant MosaicDX.

3-Indoleacetic Acid

A metabolite of the amino acid tryptophan.
Elevated titers are associated with Hartnup disease, a genetic neurological disease due to defective renal and intestinal transport of certain neutral amino acids.
Elevations of lesser magnitude appear to be of bacterial origin.

Neurotransmitter Metabolites

Homovanillic Acid (HVA, Homovanillate)

Metabolite of the catecholamine neurotransmitter dopamine; therefore, can serve as a surrogate marker of dopamine titers in circulation [GP2010].
HVA may be elevated due to:

Stress or sympathetic nervous stimulation (elevated adrenal output)[PA-OAT]
Lead toxicity MosaicDX.
Deficiency of Cu or Vitamin C [PA-OAT]
Administration of catecholamine precursors such as L-dopa, tyrosine, or phenylalanine [PA-OAT]
Neuroblastoma, ganglioneuroblastoma, or pheochromocytoma tumors (consider 24-hour VMA and HVA test if OAT results exceed twice the reference range) [GP2010]
MAO inhibitors [PA-OAT]
Dopaminergic medications (L-dopa, Levodopa, Sinemet, Methyldopa) [PA-OAT]
Dopamine-containing foods/supplements (Mucuna pruriens, bananas) [PA-OAT]
SNRI (Wellbutrin) [PA-OAT]
Tricyclic antidepressants [PA-OAT]
Amphetamines [PA-OAT]
Appetite suppressants [PA-OAT]
Caffeine [PA-OAT]
Quercetin [PA-OAT]

Low titers of HVA can be due to:

Low titers of dopamine secondary to deficiencies of tetrahydrobiopterin (BH₄), Fe, or tyrosine [PA-OAT]
Low adrenal function [PA-OAT]
Poor conversion of dopamine to HVA secondary to deficiencies of SAM, Mg, FADH₂, or NADH [PA-OAT]

If HVA titers are significantly higher than VMA titers, the patient may be having trouble converting dopamine to norepinephrine due to a copper or vitamin C deficiency or trouble converting norepinephrine to VMA due to low COMT (Catecholamine O-Methyl Transferase) or MAO (Monoamine Oxidase) enzyme activity [PA-OAT]
Signs of low dopamine titers include:

Sleepiness [PA-OAT]
Fatigue [PA-OAT]
Low motivation [PA-OAT]
Low mood [PA-OAT]
Depression [PA-OAT]
Addiction issues [PA-OAT]
Cravings [PA-OAT]
Pleasure-seeking (to boost level) [PA-OAT]

Signs of elevated dopamine titers include:

Loss of memory [PA-OAT]
Insomnia [PA-OAT]
Agitation [PA-OAT]
Hyperactivity [PA-OAT]
Mania [PA-OAT]
Hyper-focus [PA-OAT]
High stress [PA-OAT]
Anxiety [PA-OAT]
Addictions [PA-OAT]
Cravings [PA-OAT]
Pleasure-seeking (to maintain high)[PA-OAT]

Vanillylmandelic Acid (VMA, Vanillylmandelate)

Metabolite of catecholamine neurotransmitters norepinephrine and epinephrine; can serve as a surrogate marker of norepinephrine/epinephrine titers in circulation [GP2010].
VMA may be elevated due to:

Physical or psychological stress or sympathetic nervous stimulation (elevated adrenal output) [PA-OAT]),
Lead toxicity MosaicDX,
Administration of catecholamine precursors such as dopamine, L-dopa, tyrosine, or phenylalanine MosaicDX,
Drugs (see HVA),
Neuroblastoma, ganglioneuroblastoma, and pheochromocytoma tumors, (consider 24-hour VMA and HVA test if OAT results exceed twice twice the upper bound of the reference range) [GP2010],
Clostridia metabolites MosaicDX.

Low titers of VMA can be due to:

Low titers of dopamine precursor.
Trouble converting norepinephrine to VMA secondary to low COMT (catechol-O-methyltransferase) enzyme activity [PA-OAT].
Trouble converting norepinephrine to VMA secondary to low MAO (monoamine oxidase) enzyme activity, including MAO-inhibitor (MAO) drugs [PA-OAT]

Signs of low norepinephrine/epinephrine titers include:

Addictions [PA-OAT]
Cravings [PA-OAT]
Fatigue [PA-OAT]
Low blood pressure [PA-OAT]
Low muscle tone [PA-OAT]
Intolerance to exercise [PA-OAT]
Depression [PA-OAT]
Loss of alertness [PA-OAT]

Signs of elevated norepinephrine/epinephrine titers include:

Feeling stressed [PA-OAT]
Aggression [PA-OAT]
Violence [PA-OAT]
Impatience [PA-OAT]
Anxiety [PA-OAT]
Panic [PA-OAT]
Worry [PA-OAT]
Insomnia [PA-OAT]
Paranoia [PA-OAT]
Increased tingling/burning [PA-OAT]
Loss of memory [PA-OAT]
Pain sensitivity [PA-OAT]
High blood pressure [PA-OAT]
Heart palpitations [PA-OAT]

HVA/VMA Ratio

An elevated ratio suggests decreased conversion of dopamine to norepinephrine by dopamine beta-hydroxylase, which is often due to Clostridia metabolites such as HPHPA, 4-hydroxyphenylacetic acid, or 4-cresol MosaicDX.

Dihydroxyphenylacetic Acid (DOPAC)

DOPAC is a metabolite of dopamine.
DOPAC titers may be elevated due to the following: MosaicDX:

Inhibition of dopamine beta-hydroxylase (DBH) by Clostridia metabolites,
Inhibition of DBH by the mold metabolite fusaric acid,
Pharmaceuticals such as disulfiram,
Food additives such as aspartame,
Deficiency of cofactors copper, vitamin C, or malic acid.

DOPAC titers may be low due to the following: MosaicDX:

Decreased intake or absorption of dopamine's precursor amino acids phenylalanine and tyrosine,
Deficiency cofactors needed for the biosynthesis of dopamine, such as tetrahydrobiopterin or vitamin B6,
Pharmaceuticals such as monoamine oxidase (MAO) inhibitors,
Genetic polymorphisms (SNPs) of MAO or aldehyde dehydrogenase.

HVA/DOPAC Ratio

The HVA/DOPAC ratio can be increased by the increased availability of S-adenosyl methionine (SAMe) due to SAMe supplementation or factors of SAMe production, such as methyltetrahydrofolate or methylcobalamin MosaicDX.
The HVA/DOPAC ratio can be reduced by decreased conversion of DOPAC to HVA due to a genetic deficiency of catechol-O-methyltransferase (COMT) or a deficiency of SAMe MosaicDX.

5-Hydroxyindoleacetic Acid (5-hydroxyindoleacetate, 5-HIAA)

This serotonin metabolite is a surrogate marker of serotonin titers in circulation [GP2010], MosaicDX.
5-HIAA may be elevated due to:

Ingestion of tryptophan or 5-hydroxytryptophan (5-HTP) supplements,
Increased turnover of serotonin secondary to SSRI use,
Carcinoid syndrome [GP2010],
Bronchial adenoma of carcinoid type [GP2010],
Carcinoid tumor (very high titer) [PA-OAT],
Celiac sprue [GP2010],
Tropical sprue [GP2010],
Whipple's disease [GP2010],
Oat cell carcinoma of the bronchus [GP2010],
Intake of foods high in hydroxyindoles such as walnuts, avocado, eggplant, plums, tomatoes [GP2010], butternuts, black walnuts, plantain, pecans, [PA-OAT], pineapple, bananas [PA-OAT] [GP2010].

Low titers of 5-HIAA can be due to:

Decreased intake of tryptophan or 5-HTP,
Depressive illnesses [GP2010],
Small intestine resection [GP2010],
Mastocytosis [GP2010],
PKU [GP2010],
Hartnup disease [GP2010],
Decreased availability of tryptophan (caused by elevated estrogen [?], cortisol, or inflammation. These push tryptophan down the kynurenine pathway rather than the serotonin pathway) [PA-OAT],
Low titers of estrogen [?] because the estrogen receptor beta (ER-beta) induces tryptophan hydroxylase, which is the rate-limiting step for making 5-HTP (a precursor of serotonin).

Only 1% of the serotonin in circulation is made in the brain; 80% is made in the gut [PA-OAT].
Serotonin promotes gut motility and activates smooth muscle [PA-OAT].
Serotonin is found in several areas of the brain, including:

Dorsal raphe nucleus (DRN) in the brain stem, which is also rich in estrogen receptors [PA-OAT]
Forebrain (cerebrum, thalamus, hypothalamus, pituitary, limbic) [PA-OAT]

Quinolinic Acid

Elevated titers of Quinolinic acid suggest chronic inflammation due to microbial infections, central nervous system degeneration, excessive tryptophan supplementation, or exposure to phthalates MosaicDX.
This chronic inflammation can induce brain damage but may be mitigated by supplementing with acetyl L-carnitine, melatonin, vitamin B6, turmeric, or garlic MosaicDX.

Kynurenic Acid (KYNA)

The reaction by which kynurenine is converted to hydroxyanthranilate is catalyzed by an enzyme requiring vitamin B6. Thus, elevations of kynurenic acid may indicate a vitamin B6 deficiency.
Other causes of high titers are yeast overgrowth syndrome, other chronic infections, or genetic disorders affecting kynureninase MosaicDX.

6-Hydroxymelatonin Sulfate (6-OHMS)

6-OHMS is a metabolite of melatonin that can act as a surrogate marker of melatonin titers in circulation [PA-OAT].

Pyrimidines

Uracil

Folic acid acts as a methyl donor in converting uracil to thymine, so elevated uracil titers suggest a problem in folic acid metabolism MosaicDX.
About 10% of children with autism have elevated uracil MosaicDX.
Uracil and thymine are pyrimidines that are elevated in the mitochondrial genetic disease dihydropyrimidine dehydrogenase deficiency.
Uracil and orotic acid are also elevated in the genetic diseases of ornithine transcarbamylase (OTC) deficiency and citrullinemia.

Thymine

Uracil and thymine are pyrimidines that are elevated in the mitochondrial genetic disease dihydropyrimidine dehydrogenase deficiency.
High titers of thymine are also associated with inflammatory diseases, cancer, seizures, and autism MosaicDX.

Phosphoric Acid

Excess urinary phosphate excretion may correlate with dietary intake of processed foods such as sodas, commercially baked goods, and meats MosaicDX.
Excess urinary excretion of phosphate may also suggest metabolic problems such as hyperparathyroidism, vitamin D-resistant rickets, bone resorption, vitamin D overdose, renal tubular damage, familial hypophosphatemia, or metabolic acidosis MosaicDX.
Low urinary phosphate is most common in low phosphate intake and vitamin D deficiency" MosaicDX.

Fatty Acid Metabolites

3-hydroxybutyric Acid

3-hydroxybutyric Acid is associated with excessive fatty acid oxidation.
It may be elevated due to fasting or starvation, protein malnutrition, diabetes mellitus, high-fat (ketogenic) diet use, vitamin B12 deficiency, severe GI Candida overgrowth, pulmonary infections, and several genetic diseases [GP2010], MosaicDX.

Acetoacetic Acid

Acetoacetic acid is associated with excessive fatty acid oxidation.
It may be elevated due to fasting or starvation, protein malnutrition, diabetes mellitus, high-fat (ketogenic) diets, vitamin B12 deficiency, severe GI Candida overgrowth, pulmonary infections, nausea, influenza, or genetic diseases [GP2010], MosaicDX.

4-hydroxybutyric Acid

Elevated titers may indicate the genetic diseases 3-methylglutaconic aciduria or succinic semialdehyde dehydrogenase MosaicDX.
Elevated titers may also indicate excessive intake of the muscle builder 4-hydroxybutyric acid (also called gamma-hydroxybutyric acid), which can cause severe myalgia or death.

Adipic Acid (Adipate)

Adipic Acid is a fatty acid metabolite (6-carbon dicarboxylic acid).
It is a product of peroxisomal fatty acid oxidation [MetaMetrix2010].
Titre may be elevated in the following:

Fasting [GP2010], ketosis [GP2010] or metabolic acidosis [MetaMetrix2010],
Excessive intake of adipic acid-containing foods such as Jell-O, particularly if suberic acid is not elevated [GP2010]; [MetaMetrix2010],
Increased intake of foods containing medium chain triglycerides such as coconut oil [GP2010],
Functional deficiency of the fat-transporting molecule carnitine may prevent the entry of long-chain fatty acids into mitochondria, leading to incomplete fatty acid oxidation [GP2010], For carnitine deficiency, consider supplementation with L-carnitine (CI with certain thyroid medications) (500 to 1000mg) TID or L-lysine (precursor to carnitine) (1000mg QD to TID); also consider SAMe, vitamin B6, Mg, vitamin C, iron, niacin, and adequate protein intake [MetaMetrix2010].
Mitochondrial dysfunction. Consider vitamin B2 (100mg BID) [MetaMetrix2010].
Genetic deficiencies of fatty acid metabolism [GP2010],
Genetic disease multiple acyl dehydrogenase deficiency [GP2010],
Environmental toxins [MetaMetrix2010],
Periodic mild weakness [MetaMetrix2010],
Nausea [MetaMetrix2010],
Fatigue [MetaMetrix2010].
Hypoglycemia [MetaMetrix2010],
Recurrent infections [MetaMetrix2010],
Sweaty foot odor [MetaMetrix2010],
Reye syndrome (inhibition of fatty acid oxidation associated with aspirin, viral infections, and genetic mutations) [MetaMetrix2010],
Elevated titers of adipic acid but not suberic acid are associated with patients having ADD, lethargy, or seizures [GP2010].

For carnitine deficiency, consider supplementation with L-carnitine (CI with certain thyroid medications) (500 to 1000mg) TID or L-lysine (precursor to carnitine) (1000mg QD to TID); also consider SAMe, vitamin B6, Mg, vitamin C, iron, niacin, and adequate protein intake [MetaMetrix2010]..

Suberic Acid (Suberate)

Suberic acid is a fatty acid metabolite (8-carbon dicarboxylic acid) that is a product of peroxisomal fatty acid oxidation [MetaMetrix2010].
Titres may be elevated in:

Fasting [GP2010], ketosis [GP2010] or metabolic acidosis [MetaMetrix2010],
Functional deficiency of the fat-transporting molecule carnitine [GP2010], [MetaMetrix2010]. See adipic acid (above) for treatment [MetaMetrix2010],
Mitochondrial dysfunction. Consider Vitamin B2 100mg BID [MetaMetrix2010],
Genetic deficiencies of fatty acid metabolism [GP2010],
Genetic disease multiple acyl dehydrogenase deficiency [GP2010],
Increased intake of foods containing medium chain triglycerides, such as coconut oil or some infant formulas [GP2010], MosaicDX,
Environmental toxins [MetaMetrix2010],
Periodic mild weakness [MetaMetrix2010],
Nausea [MetaMetrix2010],
Fatigue [MetaMetrix2010],
Hypoglycemia [MetaMetrix2010], MosaicDX,
Lethargy MosaicDX,
Recurrent infections [MetaMetrix2010],
Sweaty foot odor [MetaMetrix2010],
Reye syndrome (inhibiting fatty acid oxidation associated with aspirin, viral infections, and genetic mutations) [MetaMetrix2010].

Sebacic Acid

Fatty acid metabolite.
Titre may be elevated in ketosis, fasting, deficiency of the fat-transporting molecule carnitine, genetic deficiencies of fatty acid metabolism and the genetic disease multiple acyl dehydrogenase deficiency, consumption of adipic acid-containing foods, such as Jell-O, consumption of foods containing medium-chain triglycerides, such as coconut oil and some infant formulas MosaicDX.
Defects in sebacic acid metabolism are associated with hypoglycemia and lethargy MosaicDX.

Ethylmalonic Acid

Ethylmalonic acid is a five-carbon branched chain dicarboxylic acid formed in isoleucine metabolism [MetaMetrix2010].
This is a product of fatty acid metabolism.
Titers may be elevated:

In ketosis,
Fasting, functional deficiency of the fat-transporting molecule carnitine,
Genetic deficiencies of fatty acid metabolism, such as multiple acyl dehydrogenase deficiency,
Consumption of adipic acid-containing foods, such as Jell-O, consumption of foods containing medium-chain triglycerides, such as coconut oil and some infant formulas MosaicDX,
A compromise of short-chain fatty acid oxidation, leading to the elevation of butyrate, which may be converted to ethylmalonic acid [MetaMetrix2010],
Riboflavin deficiency [MetaMetrix2010],
Inability to form or oxidize butyrylcarnitine [MetaMetrix2010].

Defects in ethylmalonic acid metabolism are associated with hypoglycemia and lethargy MosaicDX.
See adipic acid (above) for treatment [MetaMetrix2010].

Methylsuccinic Acid

Methylsuccinic acid is a fatty acid metabolite.
Titre may be elevated in ketosis, fasting, deficiency of the fat-transporting molecule carnitine, genetic deficiencies of fatty acid metabolism, the genetic disease multiple acyl dehydrogenase deficiency, consumption of adipic acid-containing foods, such as Jell-O, consumption of foods containing medium-chain triglycerides, such as coconut oil, and some infant formulas MosaicDX,
Defects in methylsuccinic acid metabolism are associated with hypoglycemia and lethargy MosaicDX.

Vitamin Indicators and Metabolites

Methylmalonic Acid (Ethylmalonate) (Vitamin B12)

Moderate increases may be due to vitamin B12 deficiency, pernicious anemia, GI bacterial metabolism, malabsorption, or gastroenteritis MosaicDX,
Greatly elevated titers may also be due to the genetic disorder methylmalonic aciduria [GP2010].

Pyridoxic Acid (Vitamin B6)

Pyridoxic acid is the primary urinary metabolite of pyridoxine (vitamin B6) and measures recent dietary intake.
Low titers of pyridoxic acid in the urine indicate low recent intake, while high titers indicate high recent dietary intake.
High titers are not necessarily undesirable.
Vitamin B6 deficiency is associated with high oxalate titers and low neurotransmitter titers MosaicDX.

Xanthurenic Acid (Xanthurenate) (Vitamin B6)

Xanthurenic acid is a tryptophan metabolite that may be elevated with vitamin B6 deficiency (conversion of tryptophan to NAD requires B6; in the absence of B6, xanthurenic acid is produced instead [PA-OAT].
Elevated titers are a functional marker of intracellular vitamin B6 deficiency, inflammation, excess estrogen, or excess cortisol [PA-OAT].
Complexes with insulin and decreases insulin sensitivity [PA-OAT].
Complexes with iron and causes oxidative damage to DNA (increases 8-hydroxydeoxyguanosine (8-OHdG) marker for oxidative damage) [PA-OAT].

Pantothenic Acid (Vitamin B5)

Urinary excretion reflects dietary intake.
High titers are not necessarily undesirable.
Individuals may have a much higher than usual requirement for this cofactor.

Glutaric Acid (Vitamin B2)

Elevated in the genetic diseases glutaric acidemia types I and II.
Moderate increases may be due to riboflavin deficiency, coenzyme Q-10 deficiency, fatty acid oxidation defects, valproic acid (Depakene), or celiac disease MosaicDX.
Moderate increases are associated with about 10% of children with autism MosaicDX, possibly due to defective vitamin absorption or microbial production in the GI tract.
Very high titers suggest an inborn error of metabolism MosaicDX,

Ascorbic Acid (Vitamin C)

Ascorbic acid is an important antioxidant.
Low titers may indicate dietary deficiency (scurvy).
Low titers are associated with chronic fatigue syndrome.
High titers are usually due to dietary intake.
Extremely high intake (over 2000 mg/day) raises concern that in individuals with bacteria overgrowth of the GI tract, ascorbic acid may be converted to oxalic acid, which can lead to kidney stones. There is a low probability that elevated vitamin C will cause kidney stones if oxalic acid is in the normal range MosaicDX.

3-Hydroxy-3-methylglutaric Acid (HMG) (Coenzyme Q10)

HMG is the precursor of mevalonic acid, Co-Q10, and cholesterol. Statin drugs inhibit the conversion of HMG to mevalonic acid by HMG-CoA reductase and thus cause increased titers of HMG and decreased titers of Co-Q10.
Gastrointestinal yeast overgrowth may also increase HMG titers MosaicDX.
Very elevated titers of HMG suggest the genetic disorder 3-hydroxy-3-methylglutaric aciduria (HMG aciduria} MosaicDX.
Both yeast and humans produce these same compounds as a precursor of steroid hormones; moderate elevations in titer may be due to yeast overgrowth of the GI tract and may be associated with elevated serum cholesterol.

N-Acetylcysteine (NAC)

NAC is a powerful antioxidant that promotes glutathione production and is important to detoxification in the liver.

Methylcitric Acid (Biotin or Vitamin H)

High titers of methylcitric acid suggest biotin deficiency or an inborn error of metabolism affecting biotin pathways.
Low titers of methylcitric acid have no known significance.
Biotin deficiency may be due to dietary insufficiency, malabsorption, excessive intake of raw egg whites, or dysbiosis MosaicDX.

Pyroglutamic Acid (Pyroglutamate)

Pyroglutamic acid is a metabolite of the antioxidant glutathione and is highly elevated in the genetic disease pyroglutamic aciduria or following the use of the antibiotics flucloxacillin and netilmicin.
Elevated titers are a marker of Glutathione Deficiency [PA-OAT].
Low titers may be found due to glutathione depletion following oxidative stress or after exposure to toxic solvents or pesticides such as chloroform, DDT, polybrominated biphenyls (PBBs), polychlorinated biphenyls (PCBs), or an overdose of acetaminophen (Tylenol) [PA-OAT].
Glutathione is an important antioxidant and is necessary for detoxifying estrogen metabolites 4-hydroxyestrone (4-OH-E1) and 4-hydroxyestradiol (4-OH-E2) [PA-OAT].

Toxic Indicators

Orotic Acid

Elevated level suggests urea cycle defect.
Elevated titers are most commonly associated with ammonia toxicity. When ammonia is elevated, it is biochemically converted to carbamyl phosphate and then orotic acid. Elevated ammonia may occur due to liver toxicity, viral liver infection, GI bleeding, portal-systemic shunting of blood, drug toxicity, Reye's syndrome, as well as inborn errors of ammonia metabolism MosaicDX.
Elevated orotic acid may also be found in leukemias and lymphomas, possibly due to the increased production of pyrimidines.

2-Hydroxyhippuric Acid (2-hydroxybenzoylglycine)

2-Hydroxyhippuric acid is a conjugate of the amino acid glycine and hydroxybenzoic acid (salicylic acid).
Elevated2-Hydroxyhippuric acid is a g the artificial sweetener aspartame (NutraSweet) MosaicDX.

3-Hydroxyhippuric Acid (3-hydroxybenzoylglycine)

A conjugate of the amino acid glycine and 3-hydroxybenzoic acid (salicylic acid).
Elevated titers may be due to the use of aspirin (salicylates), the growth of GI bacteria producing salicylates, or after ingesting the artificial sweetener aspartame (NutraSweet) [GP2010].
According to [Shaw2008, pg 14], HPHPA, which is a metabolite derived from Clostridium spp. metabolism, can undergo further human beta-oxidation to form 3-hydroxybenzoic acid, which is then conjugated with glycine in the liver's phase-2 detoxification step to produce 3-hydroxybenzoylglycine, also known as 3-hydroxyhippuric acid.

References regarding Organic Acid Test Panel (OAT)

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      [MetaMetrix2010] MetaMetrix Handbook: Clinical Reference Manual, 2nd Edition. (2010). Full text: http://www.metametrix.com

      [PA-OAT] Precision Analytical. Dried Urine Organic Acids Test Full text: https://dutchtest.com/wp-content/uploads/2017/12/OATs-Sell-Sheet.pdf Accessed: 6/30/2018..

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Unless specifically noted above, references used in the construction of this web page include the following:

[FMU] Lecture notes from Functional Medicine University.

[SCNM] Lecture notes from Southwest College of Naturopathic Medicine.

[UT] Lecture notes from the University of Tennessee graduate programs in Chemistry, Microbiology, and Biochemistry.