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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

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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
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, March 5, 2010

A common FMO3 polymorphism may amplify the effect of nicotine exposure in sudden infant death syndrome (SIDS)

A common FMO3 polymorphism may amplify the effect of nicotine exposure in sudden infant death syndrome (SIDS)

Poetsch M, Czerwinski M, Wingenfeld L, Vennemann M, Bajanowski T.
Institute of Legal Medicine, University Hospital Essen, Hufelandstr. 55, 45122, Essen, Germany

Smoking during pregnancy has been identified as one of the major modifiable risk factors of sudden infant death syndrome (SIDS). It has been demonstrated that the risk of SIDS increases with increasing cigarette consumption. A variety of hypotheses have been proposed for explanation, including a genetic predisposition. The flavin-monooxygenase 3 (FMO3) is one of the enzymes metabolising nicotine, and several polymorphisms have already been described in this gene. Here, we studied variations in the exons and introns of the FMO3 gene by direct sequencing analysis and minisequencing in 159 SIDS cases and 170 controls. The three common variants G472A (E158K), G769A (V257M) and A923G (E308G) in the exons of the FMO3 gene were identified. The homozygote 472AA genotype occurred more frequently in SIDS cases than in controls (p = 0.0054) and was more frequent in those SIDS cases for which the mothers reported heavy smoking (p = 0.0084). This study is the first to demonstrate a gene-environment interaction in SIDS. The findings suggest that the common polymorphism G472A of FMO3 could act as an additional genetic SIDS risk factor in children whose mothers smoke. Parents who could pass on the 472A allele should be informed of the increased risk associated with smoking. Smoking mothers should be strongly advised to give up smoking during pregnancy and for at least the first year of the child's life.
As previously mentioned in this blog, FMO3 enzyme deals with 1,000's of substrates, probably mostly oxidizing them for detoxification. Considering the amount of substrates it deals with, it is surprising that the pharmaceutical industry probably neglect the enzyme when testing new drugs for bad reactions. As well as many drugs, FMO3 will deal with many other sulfides, amines and phosphorous containing compounds. Dr Cashman has mentioned previously that FMO3 plays a minor but very important role in detoxifying nicotine.

These German researchers have been involved at looking at the possible cuases of Sudden Infant Death (SID) Syndrome. Apparently one hypothesis was that pregnant women who smoke heavily may be genetically predisposed to SID, with the FMO3 enzyme being investigated for a possible genetic connection in this study.

They checked the mothers of SID cases for common polymorphs (variants) of the FMO3 enzyme. They found that there was a higher rate of those homozygote (i.e. 2 copies) of the 472AA polymorph, especially among some of the heaviest smokers, and regard it as statistically significant. They also say it is the first study to show a genetic-environmental relation to SID.

Hopefully this will interest other researchers around the world to investigate FMO3, which seems to be the 'neglected' xenobiotic enzyme, despite possibly being the busiest of them. Any research into FMO3 is likely to be beneficial to TMAU sufferers, and possibly other systemic odor sufferers, given the range of sulfides and amines it deals with.


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