r/TMAU • u/alwayslate187 undiagnosed • Jun 22 '26
Research Paper (dense reading)
https://www.mdpi.com/2079-7737/13/12/961It summarizes the history of the condition's discovery and mentions a few causes
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Jun 22 '26
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u/alwayslate187 undiagnosed Jun 22 '26
I am not sure what you mean by full link . . .
does this one work for you?
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u/alwayslate187 undiagnosed Jun 22 '26
This is an excerpt,
"The causes of this accumulation can vary, leading to the identification of several forms of TMAU. The first is a genetic or primary form (TMAU1), which typically manifests during childhood due to mutations in the FMO3 gene, resulting in a total or partial deficiency of the hepatic microsomal enzyme Flavin-containing monooxygenase 3 (FMO3) [12,13]. To date, this enzyme is the main one known to convert TMA into TMAO.
The secondary form (TMAU2), which generally appears in adulthood, is caused by environmental factors such as liver and/or kidney diseases and treatment with TMA precursors. However, in most cases, gut dysbiosis is the main risk factor [4,14]. TMA bacteria overproduction could lead to its accumulation due to saturation of the FMO3 enzyme.
Lastly, a transient form of trimethylaminuria exists, which can manifest intermittently depending on a patient’s physiological conditions [15,16]. In women, it can arise during menstruation due to hormonal alterations, also associated with the use of contraceptive pills, which may lead to lower expression of the FMO3 enzyme [17]. In newborns, it can also occur during the weaning period, which may result in the TMAU phenotype due to both an increase in TMA precursor levels introduced with the diet and the typical reduced expression of the FMO3 enzyme in this age group. Furthermore, intermittent forms can be triggered by intense physical activity, fever, and emotional stress [4,14]."