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

Additional info:
MEBO Karen
at UK Findacure conf 2020

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MEBO Map Testing & Meetups

Full details :
want listed ? contact

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

MEBO Private Facebook Group
to join : go to
or contact
Join/Watch the weekly
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
MEBO Research is a
NORD Member Organization
See RareConnect TMAU

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MEBO Metabolic Malodor Survey (international) for Dr Hazen click here
click to Read more/less

survey for ANYONE who identifies with METABOLIC MALODOR

begun : Oct20
end : no ending for now

Regular readers will know that Dr Stan Hazen et al at Cleveland Clinic are developing a TMA-blocker pill, as they proposed in a 2011 paper that TMAO is a factor in CVD. Recently Dr Hazen and colleagues contacted MEBO as they have always thought they could also help with TMAU. This survey is to give them an idea of the 'state of the community'. It is a "version 1". They may not even look (though they have access permission), but it could be useful to give them an overview of the community

MEBO had a zoom call with Dr Hazen and his team in October. Another zoom call is planned when they have time

This is a GOOGLE FORMS survey

short url for survey :

current participants : 113 (update 18dec20)

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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