Secondary TMAU (precursor overload) and testing

It appears to me that the concept of Secondary TMAU caused by precursor overload and/or bacteria overgrowth seems to be only ever mentioned by people tested in the UK, although I am open to seeing documentation to the contrary opinion. I have looked for articles written by US experts supporting this concept described by UK experts, but have not found any so far.

There are so few researchers in trimethylaminuria, and it seems unclear if there is international agreement as to how the guidelines for the testing results parameters for the urine is determined. This is something we need to clarify as a 'community'. Based on the literature I've come across, it appears that in the UK, the few TMAU experts seem to accept that overgrowth of the bacteria that produce trimethylamine can itself be the problem (saturating the normal fmo3 enzyme), even if the fmo3 enzyme is fully functional. They call this 'secondary TMAU' or 'precursor overload'. There doesn't seem to be reported cases of this in the USA or elsewhere. It's something we as a community need clarification on. Of course people can have both primary and secondary (enzyme function too low, and too much bacteria), but it is interesting that a group of experts are willing to accept 'overload' alone can be a cause, whereas so few (if any) elsewhere seem to mention secondary TMAU.

It appears to me that this means at least some experts accept the principle of 'overgrowth' being a potential cause.

In this case (if the assumption is correct), the patient only seems to be positive for secondary TMAU in the urine test, and consequently they conclude he is positive for primary TMAU from the DNA test.
http://www.ncbi.nlm.nih.gov/pubmed/12653714

The following is a quote from a paper written by experts who accept (perhaps introduced) the concept of Secondary TMAU :

"Substrate overload of FMO3 enzyme activity resulting from either an excess of dietary precursors of TMA or variations in gut fauna, causing increased release of TMA. This type of trimethylaminuria is characterized by a high concentration of TMA in the urine, but a normal urinary TMA/TMA N-oxide ratio."

http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=gene&partid=1103

So it raises the question; has anyone in the USA or anywhere apart from the UK been tested for 'secondary TMAU' ?