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MEBO TMAU TESTING CURRENTLY SUSPENDED INDEFINITELY

MEBO - UBIOME study 2018

'PRESS RELEASE'

NCT03582826
ClinicalTrials.gov

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
& PATM

Started May 2018 - Ongoing

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

NO LONGER RECRUITING

Participation info : LINK English

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TMAU (Dominican)
Metabolomic Profiling Study
NCT02683876

Start : Aug 2016
Stage 1 : 27 Canadian volunteers to test
Latest click here (26 oct) :
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London TMAU meeting with Prof Liz Shephard
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MEBO Research Clinical Trials

Click here to read details of the MEBO Clinical Trials
NCT03582826 - Ongoing not recruiting
Microbial Basis of Systemic Malodor and PATM Conditions (PATM)
United States 2018 - ongoing

NCT02683876 - Completed
Exploratory Study of Relationships Between Malodor and Urine Metabolomics
Canada and United States 2016 - ongoing

NCT03451994 - Completed
Exploratory Study of Volatile Organic Compounds in Alveolar Breath
United Kingdom and United States 2013 - ongoing

NCT02692495 - Completed
Evaluation of Potential Screening Tools for Metabolic Body Odor and Halitosis
United Kingdom 2009 - 2012

Saturday, October 1, 2011

Expert comment on the new paper connecting TMA level with PYROXD2 enzyme

The new paper about trimethylamine and enzyme PYROXD2 has been a lot of new information to take in. How significant the paper will be to people with genetic TMAU due to FMO3 deficiency is yet to unfold.

 An expert in TMAU/FMO research, Dr Ian Phillips of Queen Mary University of London, has kindly given us his first observations of the new paper, which is posted below :

Comment by Dr Ian Phillips
Queen Mary University of London

TMA PYROXD2 paper
The paper describes a so-called metabolite quantitative trait locus (mQTL) study. Basically, the researchers looked for associations between the concentrations of various metabolites (small molecules involved in biochemical processes) in urine and plasma and genetic variation (single-nucleotide polymorphisms (SNPs)) from across the entire human genome. They found that ‘high’ concentrations of trimethylamine (TMA) in urine were associated with a T version of a T/C SNP (rs7072216) present in the PYROXD2 gene, which encodes a probable pyridine nucleotide-disulphide oxidoreductase. The gene is on chromosome 10, whereas the FMO3 gene is on chromosome 1.

The results suggest that common variants of the PYROXD2 gene or of a gene that is close to it can affect the amount of TMA excreted in urine. However, the authors state that the 'high' urinary concentrations of TMA associated with TT homozygotes are within the range found in individuals unaffected by primary genetic TMAuria, which is caused by defects in FMO3. Also, the T version of the SNP is present in Europeans at high frequency (70%), which indicates that a relatively high proportion of individuals will be homozygous for the T version of the SNP. Therefore, the SNP is not relevant to primary genetic TMAuria. However, if a person with primary TMAuria is homozygous for the T version of the SNP, the condition might be worse. In addition, it is possible that mild or transient forms of TMAuria, involving common polymorphisms of FMO3, would be exacerbated in people who are homozygous for the T version of the SNP.

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