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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)

Sunday, October 6, 2013

FMO3 gene : E158K and E308G

There are a few ways that people can have 'faults' in their DNA that cause them an inability to develop a fully functioning protein of some sort (eg FMO3 protein). Most errors will only affect function by a certain %, say meaning 90% function etc. It's 'null mutants' and deletions that are probably the worst type of errors, that can cause almost total inability to create the protein (usually people have maybe 20% function even if severe). Currently with TMAU, the severe genetic type is associated with having 2 copies of null mutants.

However the most common type of 'errors' are 'Single Nucleotide Polymoprhisms', 'variants' that are missense changes which mean the wrong amino acid is inserted in the 532 amino acids track that go to make a full FMO3 protein. Usually there are many of these missense changes in a gene pool and often do not have any 'clinical' effect on protein formation. However sometimes a missense copy here and there in your FMO3 DNA can compound to possibly affect function to some degree.

2 common polymorphisms for the FMO3 protein are what are known as E158K and E308G. This means that on the 532 amino acid 'DNA railtrack', at codons ('track') 158 and 308 there are missense amino acids. At both 158 and 308 they should be E (Glutamic acid) but instead it is :
158 : should be glutamic acid : instead is lysine
308 : should be glutamic acid : instead is glycine

Apparently, it is estimated that around 50% of the white population carry a copy of the E158K error, and about 20% carry a copy of the E308G error

What researchers do is in the lab use FMO3 DNA and check to see how the 'faults' may affect total formation of the (FMO3) protein. Currently it is thought that carrying a copy of E158K and E308G on the same allelle (i.e. from the same parent) may affect FMO3 function to some degree (say meaning 70%-90% function)

Whether later it will be thought carrying them on either allelle is enough to cause some deficiency is unknown. However it does seem that these little 'SNPs' (not just at 158 and 308) compounded may in the future be predicted to cause problems in the FMO3 DNA 532-track railtrack. To have a copy of one 'null-mutant' as well as these little SNP faults may be enough to put people in the 'risk zone' at times. We will need to wait and see the full picture

Link: amino acid symbols
Link: letter to editor about compound heterozygosity and FMO3 function

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Anonymous said...

mój problem nieświeży oddech już 7 lat , jedyne po czym jest gorzej to amfetamina, gdy zażyje amfetaminę pogarsza się bardzo

przeczytałem ten artykuł

i pytam- czy jeśli pogarsza się po amfetaminie to mogę mieć tmau1?

Dec 27, 2016, 11:00:00 AM
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