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Letters to the Editor |
Metametrix Clinical Laboratory, Norcross, GA
aAddress correspondence to this author at: Metametrix Clinical Laboratory, 4855 Peachtree Industrial Blvd, Norcross, GA 30092. Fax 770-441-2237; rslord{at}metametrix.com.
To the Editor:
In 1995, Shaw et al. (1) reported the gas chromatographic–mass spectrometric identification and quantification of various compounds in the urine of two autistic brothers. In that report (1) and a subsequent one (2), the authors concluded that the presence of several compounds, including tartaric acid (excreted as tartarate), may be causally related to the autistic symptoms and that their origin is an overgrowth of intestinal yeast. The practice of analyzing urine for these compounds to detect intestinal yeast continues, although several lines of evidence contradict these conclusions.
Dietary intake is usually the major contributor to urinary tartarate. The US Food and Drug Administration considers it a generally recognized as safe (GRAS) human food ingredient (3). Gram quantities of tartaric acid are commonly consumed in grapes and grape products, and many prepared foods contain large quantities of the acid or its salts (4)(5). Dietary intake of tartaric acid by the two individuals in the study by Shaw et al. (1) was not evaluated.
To demonstrate the magnitude of dietary impact from grape juice, we measured urinary tartarate concentrations in 23 individuals on 2 consecutive days. On day 1, participants restricted their diets by avoiding any products that contained tartaric acid on their labels. Each participant collected an overnight urine. On day 2, participants followed no restrictions, but drank 28 mL (10 oz) of grape juice with a tartaric acid content of 2.0 g/L between 1900 and 2200 and again collected an overnight urine. Urinary tartarate was measured by a liquid chromatographic–electrospray tandem mass spectrometric method similar to that reported by Pitt et al. (6). The results, normalized to creatinine, are presented in Fig. 1
. Ingestion of 28 mL of grape juice containing 590 mg of tartarate increased mean urinary tartarate concentrations from 7.4 to 282 µg/mg of creatinine, with the lowest concentration measured on day 2 being 131 µg/mg of creatinine. Shaw et al. (1) reported that the two brothers had a mean urinary tartaric acid of 69.2 mmol/mol of creatinine, equivalent to 91.9 µg/mg of creatinine. Thus, ingestion of moderate amounts of grape juice produces urinary tartarate concentrations above those suggested by Shaw et al. (1) to produce toxic effects.
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Regarding the production of tartarate by intestinal yeast, the evidence supports the opposite conclusion: that it is destroyed by fungi and bacteria. At least 23 varieties of bacteria are able to degrade tartaric acid (7), and there is no evidence that any type of yeast or fungus can produce tartaric acid as a metabolic end product.
Even when urinary tartaric acid is greatly increased, there is no evidence of physiologic harm. The majority of tartaric acid is destroyed in the intestinal tract by microbial action (8)(9). The presence of tartaric acid in human urine is not associated with any toxic consequences at doses up to 20 g. Long-term studies in rats demonstrated that a diet containing up to 1.2% tartaric acid for 2 years produced no significant toxic effect (10).
We conclude that dietary sources strongly influence the concentration of urinary tartarate and that its production by intestinal yeast or bacteria is insignificant. Ingestion of 28 mL of grape juice frequently produces urinary tartarate concentrations >300 µg/mg of creatinine. Furthermore, tartaric acid in human urine specimens provides no evidence regarding yeast overgrowth or toxic consequences. At this time, there is no justification for routine clinical measurement of tartaric acid in human urine.
References
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