- A product of tryptophan fermentation. If elevated, decrease protein intake and address digestion and GI issues. Bacteroides, Clostridia, and E. coli ferment tryptophan to produced indoleacetic acid.
- It has been found elevated in liver disease, ASD, and cancer, and has been noted as a marker of microbial activity.
- Indoleacetic acid can be degraded by Bacillus subtilis, or Pseudomonas aeruginosa.
- Indoleacetic acid has been found in many foods, such as lettuce, cherry tomato, Chinese bayberry, and okra.
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Indoleacetic acid (IAA), or indole-3-acetate, is produced by the bacterial fermentation of the amino acid tryptophan.
IAA can be formed from several common gut microbes such as Clostridia species, Escherichia coli, and Saccharomyces species.
Common Dietary Sources:
High tryptophan intake, green/black tea
References:
- Blaut M, Clavel T. Metabolic Diversity of the Intestinal Microbiota: Implications for Health and Disease. J Nutr. 2007;137(3):751S-755S.
- Russell WR, Duncan SH, Scobbie L, et al. Major phenylpropanoidderived metabolites in the human gut can arise from microbial fermentation of protein. Mol Nutr Food Res. 2013;57(3):523-535.
- Rao RP, Hunter A, Kashpur O, Normanly J. Aberrant synthesis of indole-3-acetic acid in Saccharomyces cerevisiae triggers morphogenic transition, a virulence trait of pathogenic fungi. Genetics. 2010;185(1):211-220.
- Evenepoel P, Meijers BKI, Bammens BRM, Verbeke K. Uremic toxins originating from colonic microbial metabolism. Kidney Int.76:S12-S19.
- Karu N, McKercher C, Nichols DS, et al. Tryptophan metabolism, its relation to inflammation and stress markers and association with psychological and cognitive functioning: Tasmanian Chronic Kidney Disease pilot study. BMC Nephrol. 2016;17(1):171.
- Sallée M, Dou L, Cerini C, Poitevin S, Brunet P, Burtey S. The Aryl Hydrocarbon Receptor-Activating Effect of Uremic Toxins from Tryptophan Metabolism: A New Concept to Understand Cardiovascular Complications of Chronic Kidney Disease. Toxins. 2014;6(3):934-949.
- Gevi F, Zolla L, Gabriele S, Persico AM. Urinary metabolomics of young Italian autistic children supports abnormal tryptophan and purine metabolism. Mol Autism. 2016;7:47.
- Wong PW, Lambert AM, Pillai PM, Jones PM. Observations on nicotinic acid therapy in Hartnup disease. Arch Dis Child. 1967;42(226):642-646.
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- If elevated, decrease protein intake and address digestion and GI issues. Bacteroides, Clostridia, and E. coli ferment tryptophan to produced indoleacetic acid.
- It has been found elevated in liver disease, ASD, and cancer, and has been noted as a marker of microbial activity.
- Indoleacetic acid can be degraded by Bacillus subtilis, or Pseudomonas aeruginosa.
- Elevated IAA in the urine suggests incomplete digestion and absorption of tryptophan in the intestine, allowing colonic bacteria to convert tryptophan to IAA.
- Elevations may also reflect an overgrowth of bacteria acting on tryptophan.
Clinical Associations: IAA elevations and altered tryptophan metabolism have been associated with systemic inflammation, psychologic and cognitive function, autism, and chronic diseases such as cardiovascular disease. Hartnup’s disease, a genetically-linked dysfunction in the transport of freeform amino acids across the intestinal mucosa, can cause severe elevations of urinary IAA.
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1-Methylhistidine, 1-Methylhistidine (Plasma), 2-,3-, and 4-Methylhippuric acid, 2-Methylhippuric Acid, 2-Methylsuccinic Acid, 3,4-Dihydroxyhydrocinnamic Acid, 3,5-Dihydroxybenzoic Acid, 3-Methylhistidine (Plasma), 3-Phenylpropionylglycine, 4-Hydroxybenzoic Acid, 4-Hydroxyphenylacetic Acid, 4-Hydroxyphenylpyruvic Acid, 5-Hydroxyindoleacetic Acid, 8-Hydroxy-2'-deoxyguanosine, a-Hydroxybutyric Acid, a-Keto-b-methylvaleric Acid, a-Ketobutyric Acid, a-Ketoglutaric Acid, a-Ketoisocaproic Acid, a-Ketoisovaleric Acid, a-Aminoadipic Acid (Plasma), Adipic Acid, Alanine, Alanine (Plasma), Aldosterone, Anserine (Plasma), Anthranilic Acid, Arabinitol, Arginine (Plasma), Arginosuccinic Acid, Arginosuccinic Acid (Plasma), Asparagine (Plasma), Aspartic Acid (Plasma), b-Hydroxybutyric Acid, b-Hydroxyisovaleric Acid, b-Alanine (Plasma), Benzoic Acid, Benzoylform, Branched Chain Alpha-Keto Organic Acids, Carnosine, Carnosine (Plasma), cis-Aconitic Acid, Citric Acid, Citrulline (Plasma), Cortisol, Cortisone, Creatinine, Cystathionine (Plasma), Cystine (Plasma), D-Lactic Acid, Equol, Ethanolamine (Plasma), Ethylmalonic Acid, Formiminoglutamic Acid, Fructose, Fumaric Acid, g-Aminobutyric Acid (Plasma), Glucaric Acid, Glucose, Glutamic Acid (Plasma), Glutamine (Plasma), Glutamine / Glutamate Ratio (Plasma), Glutaric Acid, Glycine (Plasma), Glycylproline (Plasma), Hexanoylglycine, Hippuric Acid, Histidine (Plasma), Homocitrulline (Plasma), Homocystine (Plasma), Homogentisic Acid, Homovanillic Acid, Hydroxykynurenine, Hydroxyproline, Hydroxyproline (Plasma), Indoleacetic Acid, Isocitric Acid, Isoleucine/allo-Isoleucine (Plasma), KT Ratio, KT Ratio (Plasma), Kynurenic Acid, Kynurenine, Kynurenine (Plasma), Lactic Acid, Leucine (Plasma), Lysine (Plasma), Malic Acid, Mandelic Acid, Methionine (Plasma), Methylmalonic Acid, Microalbumin, Ornithine, Ornithine (Plasma), Orotic Acid, Oxalic Acid, pH, Phenylacetic Acid, Phenylalanine (Plasma), Phosphate, Phosphoethanolamine (Plasma), Picolinic Acid, Pimelic Acid, Proline (Plasma), Pyridoxic Acid, Pyroglutamic Acid, Pyruvic Acid, Quercetin, Quinolinic Acid, Sarcosine (Plasma), Sebacic Acid, Serine (Plasma), Suberic Acid, Suberylglycine, Succinic Acid, Sulfocysteine (Plasma), Tartaric Acid, Taurine (Plasma), Threonine (Plasma), Total Branched Chain Amino Acids (Plasma), Tryptophan, Tryptophan (Plasma), Tyrosine, Tyrosine (Plasma), Valine (Plasma), Vannilylmandelic Acid, Xanthurenic Acid
