Excessive Body Odor May Be Caused By Genetic Disorder


Researchers from Monell Chemical Senses Center in Philadelphia are reporting that people with unexplained body odor issues may be suffering from a metabolic disorder, trimethylaminuria (TMAU) or “fish-odor syndrome”.

TMAU is a genetically-transmitted disease that inhibits the ability of an enzyme to metabolize or transform trimethylamine (TMA) and is not based on lack of hygiene or personal care. Instead, the condition becomes apparent when sufferers digest foods rich in a substance called choline which include saltwater fish, eggs, liver and certain legumes, such as soy and kidney beans, Reuters is reporting.

Giving these people a definitive diagnosis offers relief to these individuals, as symptoms of TMAU can cause social and interpersonal stress. The debilitating symptoms can be lessened primarily with an altering of the diet.

“Health care professionals must arrive at a correct diagnosis to suggest appropriate treatment,” said study lead author Paul M. Wise, Ph.D., a sensory psychologist at Monell. “This research raises awareness of both the disease and also the proper methods of diagnosis and treatment.”

The American Journal of Medicine released the study online and included the testing of 353 patients who had contacted the Monell Center because of unexplained personal odor issues. Underlying causes could not be identified by medical and dental professionals.

Subjects of the study engaged in a choline challenge, in which each patient ingests a set amount of choline, with urinary TMA levels measured over the next 24 hours. A high level of urinary TMA confirmed a diagnosis of TMAU in 118 individuals.

George Preti, Ph.D., an analytical organic chemist at Monell explains, “Although the scientific and popular literature typically describes TMAU sufferers as smelling fishy, our sensory exams demonstrated this not to be so. The odors are diverse and only after a choline challenge do the most severe cases have a fish-like odor.”

Classified as a “rare disease,” meaning that it affects less than 200,000 people in the United States, actual incidence of TMAU remains questionable, due in part to the previously incomplete diagnostic techniques. Discerning the genetic and dietary bases of these differences in the condition will be the subject of future research.

An actual sufferer of the condition must inherit a defective copy of the FMO3 gene from both parents, who themselves would be unaffected “carriers.” If either of the parents had the disorder they would pass it on to their children.

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