Oh, and tfor. Apparently seafood increases TMAO more then meat and eggs.
http://www.ncbi.nlm....pubmed/10456680 Dietary precursors of trimethylamine in man: a pilot study.
Of 46 different foods investigated, only fish and other sea-products gave rise to significant increases in urinary trimethylamine and N-oxide. Ingestion of fruits, vegetables, cereal and dairy produce, and meats had no measurable effects
Theres also this http://www.ncbi.nlm..../pubmed/6842395 Formation of methylamines from ingested choline and lecithin.
"Twenty-seven millimoles of choline chloride, choline stearate or lecithin were administered to healthy human subjects. It was found that these treatments markedly increased the urinary excretion of TMA, DMA and MMA, with choline chloride having the greatest effect."
"Rats were treated with 2 mmol/kg b.wt. of choline chloride or lecithin, and it was found that these treatments significantly increased urinary TMA excretion and did not alter DMA or MMA excretion. Our choline chloride preparation contained no MMA, DMA or TMA; however, it was found that our choline stearate and all the commercially available lecithins tested were contaminated with methylamines. Prior removal of methylamines from our lecithin preparation minimized the effect of oral administration of this compound on methylamine excretion in urine of rats and humans."
Correct me if im wrong, but i think this means that uncontaminated lecithin in eggs could have a much smaller effect on TMAO then supplimented choline chloride
Chris masterjohn has an interesting statement about blood levels of choline here.
http://www.westonapr...-heart-disease/
"In order to even begin supporting such a hypothesis, we would have to first see to what degree eating seafood leads to the accumulation of TMAO in the blood, and here we only have urinary data. If the kidneys efficiently dispose of TMAO into the urine after eating seafood, TMAO may be unlikely to accumulate in the blood for any length of time.
Indeed, the massive increases in urinary trimethylamine and TMAO following meals rich in seafood suggests that our kidneys excrete these compounds very efficiently.
So how, then, should we interpret the correlation between heart disease risk and plasma concentrations of choline, betaine and TMAO in humans?
Blood levels of choline are currently considered an emerging marker for destabilization of coronary plaques or ischemia in acute coronary syndrome, as reviewed here. During the process of blood clotting, inflammatory enzymes release choline from membrane phospholipids in order to also generate phosphatidic acid, which is used as an important signaling molecule. Elevated blood levels of choline, then, and perhaps its metabolite betaine, could simply reflect an inflammatory or pro-clotting environment."
The study he links to is this one http://www.ncbi.nlm....pubmed/20214535 Choline in acute coronary syndrome: an emerging biomarker with implications for the integrated assessment of plaque vulnerability.
I have also heard that gut bacteria plays a role.