News & Views on Systemic Body Odor and Halitosis such as trimethylaminuria TMAU. If you have fecal odors or bowel odors it may be metabolic/systemic

1 January 2015

New Hazen paper : Fecal transplant mice get TMAO artherosclerosis

TMAO TMAU research
A recent theory suggests TMA-oxide may cause atherosclerosis. TMA-oxide is oxidized trimethylamine. Hence a therapy is likely to try and reduce or neutralize TMA levels produced in the gut

New paper from Dr Stan Hazen et al re TMA-oxide and CVD  :  Fecal transplants in mice

Dr Stan Hazen research has often been reported here as since around 2011 his lab has suggested a strong connection between TMA-oxide plasma levels in humans and risk of atherosclerosis (CVD). This research may have an added benefit to metabolic malodor sufferers who feel trimethylamine is the sole cause of their malodor, as any resulting therapy may mean neutralizing or blocking TMA production in the gut, thus the person will absorb no TMA into their bloodstream.

Fecal transplant in mice to give them atherosclerosis
In this paper they seemed to use 2 strains of lab mice and gave their fecal transplant microbes to a strain of mouse that was microbe free in the gut. One strain of mouse seems to have a high TMAO 'flora', whereas the other does not. It seems that the transfer of the feces from the high-TMAO producing mouse caused the donor mouse to develop CVD. So they seem to be saying risk of CVD is highly likely to be due to a TMA rich gut flora and when they transfered this flora to a mouse with no gut flora, the mouse then developed CVD.

This seems to be more evidence for the TMAO-CVD connection theory, though I guess it is still a theory to be given a consensus in the CVD research community.

The paper says at the end :
Gut microbes may thus represent a novel therapeutic target for modulating atherosclerosis susceptibility.

So they are suggesting that altering a TMA rich gut flora should reduce the chance of CVD, but also for the TMAU community it should mean reducing or negating or blocking TMA in the gut, possibly by altering the gut flora. This may lead to anti-TMA probiotics, for example. It is also very likely that research will be done to see which microbes generate TMA in the gut.    

     


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