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Kidney Function: The Missing Link In The TMAO-Health And Disease Story?

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Animal products, including meat, cheese, and eggs contain carnitine and choline, metabolites that are converted by gut bacteria into TMA, which is then converted by the liver into TMAO. Plasma levels of TMAO are associated with an increased risk of disease and death, so should we limit intake of these animal products?

Separately, fish contains relatively high levels of TMAO, and blood levels of TMAO spike after fish consumption, but there is a decreased all-cause mortality risk for fish consumers. To explain these disparate findings, other factors may be involved in the TMAO-health and disease story. In the video, I discuss the impact of kidney function on plasma levels of TMAO, disease and mortality risk.


Edited by Mike Lustgarten
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The TMAO story continues to be confusing, and this video does not shed as much light on it as may seem on the surface.

The problem is that the kidney angle does not explain the fish paradox at all. In fact, I was disappointed to see such poor followup.

If kidney function declines with age (which it does), and past about 40 it declines below the magical cutoff of EGFR 90, then you would expect the advantages of fish consumption to decline past 40 with the massive TMAO spike. 

It raises the questions: is there evidence that consuming animal protein dramatically raises TMAO related morbidities past the age of 40? And importantly to the fish paradox, is there evidence that consuming fish past 40 raises those morbidities dramatically in tandem with the dramatic impact of TMAO from fish? I am unaware of any research that shows fish consumption to be dramatically worse for you than meat/eggs past age 40.

In other words, this whole thing doesn’t hold water.

This video does NOT explain or account for the fish paradox in the TMAO story. I recommend going back to the drawing board.

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Well my take is that we try to simplify these things and they ain’t simple. One study in rats showed heart benefits for Tmao compared to controls. Like LDL cholesterol and particle size, triglycerides hdl, lp(a) etc which can explain why some folks with high ldl levels do not develop atherosclerosis while many with lower levels do. We are still trying to figure all the interactions of lipids and how they effect our arteries and so my guess is it will be a long time before we understand the dynamics of this new card in the game. 


for anyone interested in the deep complexity of lipids and atherosclerosis I thought Dr. Krauss was quite compelling

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I agree Mike. We know extremely little about lipids and the whole story of atherosclerosis, CVD and so on. And TMAO is a poster child for how we actually know next to nothing - isolated effects, and no big picture. Re: Peter Attia, in general he's very good wrt. lipids and CVD, with super illuminating podcasts, especially with Tom Dayspring. 

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On 11/20/2020 at 5:29 PM, Saul said:

Hi Tom!

My view:  whenever an "expert" decides to prove something by showing you a video, rather than presenting in writing, skip it.

Too many video "experts".

  --  Saul

Most people don't want to read, it's easier to watch. Also, I don't pretend to know it all, and one reason I make videos is for the feedback, which helps me learn, too.

Edited by Mike Lustgarten
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