Trimethylaminuria (TMAU) is a metabolic condition in which the body is unable to break down an offensively pungent alkaline chemical called trimethylamine (TMA). TMA, which can produce a faecal rotten egg or fishy smell, is therefore emitted through bodily orifices and secretions (hence, why the condition used to be called fish-odour syndrome).
TMAU1 is a genetically inherited disorder, which is very uncommon. TMAU2, however, is an acquired disorder (perhaps triggered by an infection, small intestinal bacterial overgrowth or emotional trauma) and is part of a group of systemic breath/body odour conditions some of which are, as yet, unnamed.
TMA is the product of eating normal nutritious foods containing choline. This essential nutrient, however, needs an enzyme (FMO3) to break it down. In the inherited condition (TMAU1), the gene that produced FMO3 is faulty. In some cases, the liver cannot produce FMO3 or the enzyme is dysfunctional. TMA is also excreted by dysbiotic bacteria present in the gut. However, these pathogenic bacteria are yet to be identified and, at least in my case, are extremely resistant to antibiotics. Figure 1 shows the production of TMA in a normal gut and the conversion of TMA to TMA N-Oxide in the liver by the FMO3 enzyme.
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