FMO3 malodor syndrome. Best papers as evidence

These 2 papers by SC Mitchell are my favorite 'evidence' of FMO3 Malodor Syndrome and the type that people will have (elusive transient form). I see trimethylamine as only a biomarker of FMO3 function and not a big player in the range of metabolites that people with FMO3 'weakness' will have.

SC Mitchell letter on Trimethylaninuria : the susceptibility of heterozygotes

Quote :

Over the past decade we have encountered many patients who have odour problems on a mild, transient, and periodic basis.3, 4 These otherwise healthy individuals are presumably heterozygotes, or compound heterozygotes, who can cope with the daily burden of trimethylamine, but have little, if any, reserve capacity when stressed by other factors and may fail to metabolically remove trimethylamine.5 To raise the general awareness of this disorder and reiterate that it “is not merely a rare recessive disorder but rather a spectrum of phenotypes of transient or mild malodour” is important,1 but it is also imperative to realise that fish-odour syndrome is not a simple genetic problem and that heterozygotes (carriers) may have to endure a transient and more elusive form of this complaint initiated by various, less obvious, and more ephemeral, factors.

Mitchell & Smith 2003 overcview of Trimethylaminuria (quote below is the main part that I use as evidence that FMO3 malodor seems a possiblity and yet no expert (including in this paper) wishes to go beyond stating TMAU)

Quote :

The intriguing question remains as to whether or not there are other endogenous or dietary substrates whose metabolism is also affected in the fish malodor syndrome. Bearing in mind that many sulfur and basic nitrogenous compounds are substrates for the enzyme system involved, this appears to be highly likely but the question remains unanswered as yet.

By sysbodyodor

fecal body odor, fmo3, gut dysbiosis, systemic body odor

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