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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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Full details : https://goo.gl/TMw8xu
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TMAU Petition world
TMAU UK end total:262
TMAU UK ends 23/01/20
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USA : Moveon open
TMAU (Dominican)
Metabolomic Profiling Study
NCT02683876

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
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London TMAU meeting with Prof Liz Shephard
19th Oct 11am - 1pm
St Mary's Hospital
Praed St, Paddington
London W2 1NY
click to read more
more details : karen.james@meboresearch.org

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

Wednesday, April 8, 2009

Transient trimethylaminuria related to menstruation

Herein, we describe data to support the proposal that menses can be an additional factor causing transient trimethylaminuria in self-reported subjects suffering from malodor and even in healthy women harboring functionally active flavin-containing monooxygenase 3 (FMO3)Only a handful of sources worldwide seem to be publishing new papers on FMO3 or trimethlymainuria over the last 5 years, one of them being Dr John Cashman et al (either with fellow staff or collaborating with others worldwide), based at HBRI Institute in San Diego (from a genetic perspective). In this case 2 Japanese researchers were the lead researchers. They have done previous work on FMO3 genetics.

If medical students were ever taught about TMAU, it would likely say the problem is autosomal recessive with the person having to have 2 mutant copies to be affected. However, over the last decade or so, the evidence seems to be growing that it may be autosomal dominant in certain circumstances. This paper from 2007 was strong evidence towards this, indicating that menstruation can inhibit the FMO3 enzyme in some women with only one bad copy (a polymorphism ... usually regarded as mildly suboptimal) of the FMO3 enzyme around the time of menstruation. Perhaps some women who have 'unexpectedly passed' the TMAU urine test may be vulnerable around menstruation, although this is not a recommendation for testing. There still seems too many puzzles regarding the FMO3 enzyme and body odor. Another genetic aspect is that it doesn't seem to be as simple as perfect functioning copies and mutant copies. There seems to be gray areas of genetic function, known as polymorph or variant copies. Also there are such questions as: is having one 'null-allelle' (very poor functioning copy) worse than having 2 variants ? We will need to investigate this further to clearly classify the different categories. Below is the abstract of the paper, with possible interesting points highlighted in bold.

BACKGROUND: Trimethylaminuria, or fish odor syndrome, includes a transient or mild malodor caused by an excessive amount of malodorous trimethylamine as a result of body secretions. Herein, we describe data to support the proposal that menses can be an additional factor causing transient trimethylaminuria in self-reported subjects suffering from malodor and even in healthy women harboring functionally active flavin-containing monooxygenase 3 (FMO3). METHODS: FMO3 metabolic capacity (conversion of trimethylamine to trimethylamine N-oxide) was defined as the urinary ratio of trimethylamine N-oxide to total trimethylamine. RESULTS: Self-reported Case (A) that was homozygous for inactive Arg500stop FMO3, showed decreased metabolic capacity of FMO3 (i.e., approximately 10% the unaffected metabolic capacity) during 120 days of observation. For Case (B) that was homozygous for common [Glu158Lys; Glu308Gly] FMO3 polymorphisms, metabolic capacity of FMO3 was almost approximately 90%, except for a few days surrounding menstruation showing <>. In comparison, three healthy control subjects that harbored heterozygous polymorphisms for [Glu158Lys; Glu308Gly] FMO3 or homozygous for wild FMO3 showed normal (> 90%) metabolic capacity, however, on days around menstruation the FMO3 metabolic capacity was decreased to ~60-70%. CONCLUSION: Together, these results indicate that abnormal FMO3 capacity is caused by menstruation particularly in the presence, in homozygous form, of mild genetic variants such as [Glu158Lys; Glu308Gly] that cause a reduced FMO3 function.

Full paper
Transient trimethylaminuria related to menstruation : 2007


Related links:
Pubmed abstract : Transient trimethylaminuria related to menstruation

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