Fri, Feb-19-16, 22:16
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Senior Member
Posts: 15,075
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Plan: mostly milkfat
Stats: 190/152.4/154
BF:
Progress: 104%
Location: Ontario
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Quote:
Originally Posted by RawNut
My question is why are they always using TMAO to dis red meat when fish and other seafood contain so much more of it, PREFORMED at that?
It would stand to reason that fish eaters would have higher TMAO levels yet fish is inversely associated with heart disease. WTF?
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Maybe because the Walt Willetts of the world are too powerful and well respected. There's good grant money to be had, as long as the business you're at is giving even remotely plausible mechanisms to back up spurious correlations.
I'm sure if they look hard enough, next they can find some substance in fish that, at ridiculous doses, protects mice from the increase in atherosclerosis that can be caused by ridiculous doses of TMAO.
Every plant and every animal is a virtual pharmacopeia, there's no end to the substances with drug-like effects to be found. In plants they look for things that might protect from disease, so they find them--even though the amount of something like resveratrol you'd need to get from a food is unrealistic, that didn't keep people from claiming for a while that it might be behind the French paradox. With animal foods, the assumption going in is that it's deadly--and you'll always find something that's deadly, at some dose.
http://www.ncbi.nlm.nih.gov/pubmed/25686243
Quote:
Fish oil ameliorates trimethylamine N-oxide-exacerbated glucose intolerance in high-fat diet-fed mice.
Gao X1, Xu J, Jiang C, Zhang Y, Xue Y, Li Z, Wang J, Xue C, Wang Y.
Author information
Abstract
Trimethylamine N-oxide (TMAO), a component commonly present in seafood, has been found to have a harmful impact on glucose tolerance in high-fat diet (HFD)-fed mice. However, seafood also contains fish oil (FO), which has been shown to have beneficial effects on metabolism. Here, we investigated the effect of FO on TMAO-induced impaired glucose tolerance in HFD-fed mice. Male C57BL/6 mice were randomly assigned to the high fat (HF), TMAO, and fish oil groups. The HF group was fed a diet containing 25% fat, the TMAO group was fed the HFD plus 0.2% TMAO, and the FO group was fed the HFD plus 0.2% TMAO and 2% fish oil for 12 weeks. After 10 weeks of feeding, oral glucose tolerance tests were performed. Dietary FO improved the fasting glucose level, the fasting insulin level, HOMA-IR value, QUICKI score and ameliorated TMAO-induced exacerbated impaired glucose tolerance in HFD-fed mice. These effects were associated with the expression of genes related to the insulin signalling pathway, glycogen synthesis, gluconeogenesis, and glucose transport in peripheral tissues. Dietary fish oil also decreased TMAO-aggravated adipose tissue inflammation. Our results suggested that dietary FO ameliorated TMAO-induced impaired glucose tolerance, insulin signal transduction in peripheral tissue, and adipose tissue inflammation in HFD-fed mice.
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Looks like omega 3's have already been proposed as a protective factor vs. TMAO.
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