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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
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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)

Wednesday, September 24, 2008

Some may be genetically in need of more choline than normal

Re: A paper written by experts at the University of North Carolina, Chapel Hill, NC
Common genetic polymorphisms affect the human requirement for the nutrient choline

Since low-choline is so important to the presently advised 'TMAU diet', this paper is of interest for 2 reasons: Partly because it goes into detail of what choline is needed for, and also it raises awareness that some people may need more choline than the RDA because of a weakness in an enzyme that deals with choline metabolism.

While crippling mutant genes are (supposedly) in the minority (supposed to be around 10% of genetic weaknesses), single nucleotide polymorphisms (SNP) are very common. Generally they are what make us different. In the case of cell enzymes, they are what make some people have enzyme weaknesses. Rather than having a crippling 'null-allele' type chromosome pairing that hardly functions (say down in the 0-30% range), SNPs make it more of a % game depending on the chromosome combination. Usually only a minor weakness, depending on the 2 chromosomes. For instance a null-allele chromosome coupled with a normal chromosome is likely to make things awkward. Coupled with a known SNP weakness, it may be the most common type of bad formation. Or 2 known 'weak' SNP pairings. This may explain why the TMAU testers seem to have gone from a 50% hurdle originally, to around 85%-90% now (depending on the tester. In the UK they even diagnose 'secondary tmau' where the enzyme output was regarded normal but too much tma was in the urine)

This intro was written so as to give the paper some context. The intro should not be regarded as being wholly accurate.

Humans eating diets deficient in the essential nutrient choline can develop organ dysfunction...

CHOLINE IS AN essential nutrient needed for structural integrity and signaling functions of cell membranes, methyl group metabolism, and neurotransmitter synthesis. Humans eating diets deficient in choline develop fatty liver, liver damage, and muscle damage. These effects occur, in part, because a specific lack of phosphatidylcholine limits the export of excess triglyceride from liver and induces apoptosis and subsequent leakage of enzymes (e.g., AST, ALT, and CPK) from tissues of liver and muscle. Women’s dietary requirements for choline are of special interest because deficient maternal dietary intake of choline during pregnancy in humans was associated with a 4-fold increased risk of having a baby with a neural tube defect...

Of the 57 participants, 68% developed organ dysfunction when fed the low choline diet and this resolved when choline was added back to their diets...

Common genetic polymorphisms have been reported to influence human requirements for nutrients. For example, a common SNP in the methyltetrahydrofolate reductase gene increases dietary requirements for the vitamin folic acid...

Common genetic polymorphisms affect the human requirement for the nutrient choline


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