Comparing UK trimethylaminuria results with USA results

It has been noted on body odor forums; that in the USA and elsewhere, the person usually understand their result as a percentage, but this % does not seem to be commonly used by British testers giving their results.

The percentage is actually the total amount of TMA that the person managed to metabolize to TMA-oxide, giving an idea of the person's FMO3 metabolic capacity (at least, for that test sample). Trimethylamine is probably the 'best' marker for testing FMO3 function, since unlike most other substrates, it cannot go any alternative route for oxidation. That said, you need to make sure enough TMA is in your system to give it a thorough test of TMA oxidation capacity.

For anyone wishing to calculate their 'FMO3 capacity %', it is based on the TMA/TMAO ratio given in the results.

The calculation is :

TMA-oxide/(TMA + TMA-oxide) x 100

This is the % of TMA present you managed to metabolize into TMA-oxide.

With regards what is the % function of normal people, it does not look as if there is a standard 'cut-off' point which all labs agree. A French paper gave the cut-off point for normals as 95%, whereas others seem to go for around 90% or even a bit lower.
(PDF) Dr Eugene Michel 2002 paper : FMO3 capacity greater than 95%

---

It would seem unlikely that those around 80% would be 'classic' TMAU cases, since the textbooks say a TMAU is someone with 2 mutant copies, which would mean almost no function or a very low % reading. Unfortunately in the case of TMAU, the smell is in the nose of the beholder, and if someone is told they smell and do not have 2 mutant copies, you have to assume that it's not just 'classic' cases that fail the 'smell test'. It would seem more likely that 'mild cases' would be transient. Also, it seems FMO3 may vary at times, such as during menstruation.
2007 TMAU paper : FMO3 and menstruation

With a general glance at genetics, it seems that geneticists class the function of genes into 3 basic groups :
mutant (very poor function. null-alleles etc)
variants/polymorphisms (milder loss of function. Can vary depending on physiological factors)
wild type (milder still ?)

It seems possible that many genetic 'smelly' cases may not be '2 mutant copy' cases, and more a combo of other sub par functioning combinations :
for instance:
1 mutant and a normal copy (? meaning in some cases it may be autosomal dominant)
2 variants
etc

However only the collection of genetic results will be able to clarify this. All of this does not seem to conclusively explain a complaint such as fecal body odor syndrome that most seem to complain of, which seems to imply other factors may be involved with that (either as well, or instead of). MeBO hopes to keep looking for answers to these questions.