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March20 podcast Dr Hazen
anti-TMA pill in a year or 2 ? (scroll 12 mins)

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at UK Findacure conf 2020

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MEBO - UBIOME study 2018



MEBO Gut Microbiome Study
"Microbial Basis of Systemic Malodor and PATM Conditions (PATM)"
Funded by uBiome Research Grant

"Microbial Basis of Systemic Malodor and PATM Conditions (PATM)"

Dynamics of the Gut Microbiota in
Idiopathic Malodor Production

Started May 2018 - Ongoing

Current people sent kits : 100/100
3 kits per person


Participation info : LINK English

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BO Sufferers Podcasts



TMAU Petition world
TMAU UK end total:262
TMAU UK ends 23/01/20
TMAU Petition USA end total 204
USA : Moveon open
TMAU (Dominican)
Metabolomic Profiling Study

Start : Aug 2016
Stage 1 : 27 Canadian volunteers to test
Latest click here (26 oct) :
17 samples returned

Note : Stage 1 is Canada only.
Return cut-off date : passed
Analysis can take 6/8 weeks
Analysis start in/before Nov
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NORD Member Organization
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Denver TMAU Test Lab survey click here
click to Read more/less

USA survey for anyone who wants to improve Denver TMAU test

begun : Dec22
end : no ending for now

A trainee genetic counselor is working at the Denver TMAU test lab. Probably as part of her training. As a project she wishes feedback on any aspect of the Denver TMAU test and process. You can fill in the survey and/or email her (email address is in survey). It's meant for USA people, but perhaps others can give their view too (as we have so few opportunities).

quote from her rareconnect post

"Hello all! I wanted to make you aware of a research study being conducted to better understand the experience and needs of individuals with trimethylaminuria with a goal of being able to create improved patient and healthcare provider education materials. Any participation is completely voluntary and all responses remain confidential. Feel free to use the contact information within the link with any questions or share the survey with others with TMAU."

see this post for more details

Friday, January 20, 2017

Primary TMAU and Secondary TMAU

On this 2016 paper previous mentioned on a post in this blog, 'New Phillips/Shephard TMAU & FMO3 overview paper', the authors give us the definition of Primary TMAU and Secondary TMAU.

"Trimethylamine and Trimethylamine N-Oxide, a Flavin-Containing Monooxygenase 3 (FMO3)-Mediated Host-Microbiome Metabolic Axis Implicated in Health and Disease"
Diede Fennema, Ian R. Phillips and Elizabeth A. Shephard
Drug Metabolism and Disposition November 2016, 44 (11) 1839-1850; DOI:

TMAU, a Deficiency of FMO3

Primary Trimethylaminuria:

In humans, mutations that abolish or severely impair the activity of FMO3 cause the inherited disorder primary TMAU (Dolphin et al., 1997Hernandez et al., 2003). Affected individuals have a severely reduced ability to convert TMA to TMAO and, consequently, excrete large amounts of odorous TMA in their urine, sweat, and breath (Ayesh et al., 1993). Although the disorder has no overt physiologic effects on patient health, it can have profound psychologic and social consequences, resulting in a severe loss of quality of life, in extreme cases giving rise to clinical depression and suicidal tendencies (Mitchell and Smith, 2001Shephard et al., 2015, [Phillips IR and Shephard EA. Primary trimethylaminuria. GeneReviews at GeneTests: Medical Genetics Information Resource (database online): University of Washington, 1997––2015 available at, updated 2015]. In terms of drug metabolism, TMAU individuals have impaired metabolism of the FMO3 drug substrate benzydamine (Mayatepek et al., 2004). Since the first discovery of a mutation known to cause TMAU (Dolphin et al., 1997), many different causative mutations have been identified (Phillips et al., 2007Yamazaki and Shimizu, 2013). A catalog of variants of the FMO3 gene and their effect on the ability of FMO3 to catalyze the oxygenation of TMA and drug substrates of the enzyme can be accessed at the FMO3 locus-specific mutation database (

Secondary Trimethylaminuria:

Production of large amounts of TMA, as a result of gut microbial action, exacerbates the symptoms of primary TMAU. In addition, overproduction of TMA, as a consequence of a dysbiosis of the gut microbiome, can give rise to a nongenetic form of the disorder, known as secondary TMAU (Mitchell and Smith, 2001). Therefore, a better understanding of the bacterial species that produce TMA in the gut may provide insights into why some individuals develop secondary TMAU in the absence of impaired N-oxygenation of TMA (Shimizu et al., 2014) and offers the potential to develop improved strategies for the management and treatment of both primary and secondary forms of the disorder.

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