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March20 podcast Dr Hazen
anti-TMA pill in a year or 2 ? (scroll 12 mins)

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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

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Blog Archive

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, December 3, 2008

Can TMA producing bacteria cause a choline deficiency in the host ?

Obviously someone on a low choline diet has to think about the concern of giving themselves a choline deficiency; but ironically, in theory, it must seem possible that someone with a lot of trimethylamine-producing bacteria in their gut may also end up with a choline deficiency due to the bacteria 'eating' the choline and giving the host lots of trimethylamine instead. Choline has been associated with fatty liver (it's a very common ingredient in liver detox supplements, since it's 'lipotropic' quality is thought to make it a good liver 'decongestor'). It wasn't classified as an essential nutrient by the National Academy of Sciences until 1998. The gut ecology can play a big role in what we end up 'absorbing' (both good and bad). for example, many of the B vitamins are produced by good bacteria in our gut. Conversely, as in this case, factors in the gut can mean you end up deficient in certain nutrients, either through the altered gut flora 'eating' the nutrient themselves, or the 'friendly' bacteria which produce good nutrients being depleted (and probably other reasons).

Recent metagenomic studies have also shown a strong interaction between gut flora and detoxification of xenobiotics
In this 2006 study, which involved Dr Stephen Mitchell who is an FMO3 expert in London, they found that mice with too much trimethylamine-producing bacteria in their gut did in effect have a blood 'choline deficiency' despite choline being in their diet, when they tested the plasma phospatidylcholine levels.

Testing B vitamin status (or associated nutrients) in metabolic body odor and halitosis cases would seem a sensible 'checklist' option for individuals and in metabolic body odor and halitosis studies (for instance, by a BO & halitosis research center).

Pubmed paper 2006: Abstract : Metabolic profiling reveals a contribution of gut microbiota to fatty liver phenotype in insulin-resistant mice.
Full paper on site

related links and info:
Linus Pauling Institute entry for Choline
Healthworld Online article on Choline by Elson Haas
test used in the study: plasma phosphatidylcholine levels

Choline properties:
Is a methyl donor in methylation
Is a fat 'emulsifier/decongestant'
Important part of the neurotransmitter acetylcholine

Blog suggestion: group get an idea of choline plasma blood levels, whether on the TMAU diet or think they may have TMAU.

Gut Microbiota Mimic Choline-Deficient Diets.

Choline-deficient diets have been consistently associated with hepatic steatosis, which is reversible by choline i.v. infusion (12). We have also shown that quantitative variation in dietary choline induces an inverse quantitative variation in liver fat content (see Fig. 9). We show here that lower plasma PC levels in strain 129S6 on HFD compared with BALB/c mice can be explained by reduced bioavailability of choline (see Fig. 8) because of conversion of choline into methylamines by gut microbiota, with subsequent urinary excretion. This mechanism thus mimics a choline-deficient diet. This microbiota-related reduced choline bioavailability may result in the inability to synthesize PC necessary for the assembly and secretion of very-low-density lipoprotein (VLDL) (37) and subsequent accumulation of TG in liver. Methylamines also induce hepatotoxicity and hepatocarcinogenicity in rats (38). Indeed, microsomal FMO-detoxification enzymatic systems have been evolutionarily coselected toward the assimilation of biologically active natural compounds involved in biological defense signaling (39). This enzymatic system detoxifies soft nucleophilic functional groups of natural origin, such as alkaloids, with basic side chains, and organic sulfur xenobiotics. Microbiota-derived methylamines, predominantly excreted in urine, share the same metabolic detoxification process and may also share the same toxicity as other soft nucleophiles. Recent metagenomic studies have also shown a strong interaction between gut flora and detoxification of xenobiotics


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