#321: Dave Feldman & Alan Flanagan – Debating LDL Causality & the “Lipid Triad”

Sigma Nutrition Radio

Danny Lennon

Sigma, Dietetics, Evidencebased, Nutrition, Training, Health & Fitness, Science, Diet, Fitness, Evidence, Bodybuilding, Health

4.8 • 626 Ratings

🗓️ 25 February 2020

⏱️ 118 minutes

🔗️ Recording | iTunes | RSS

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Summary

Dave Feldman is a software engineer and runs the Cholesterol Code website. In 2015 Dave adopted a low-carb high-fat diet, which improved his overall health. However, upon seeing his LDL-cholesterol skyrocket, he set out learn all he could about blood lipids and health.

Dave has gained prominence as a “LDL-skeptic” and promoter of his “lipid triad” hypothesis. This lipid triad relates to a situation where one sees high LDL-C, high HDL-C and low triglycerides. Dave hypothesises that in such a context, the high LDL-C does not confer high risk of cardiovascular disease. This is counter to the current consensus position of the lipid hypothesis, where LDL plays a causal role in atherosclerosis development.

Alan Flanagan is the Research Communication Officer here at Sigma Nutrition. Alan is currently pursuing his PhD in nutrition at the University of Surrey, UK, with a research focus in chrononutrition. Alan previuosly completed a Masters in Nutritional Medicine at the same institution.

SHOW NOTES: https://sigmanutrition.com/episode321

Transcript

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0:00.0	Hello, you are listening to Sigma Nutrition Radio. I am your host, Danny Lennon,
0:05.7	and we're at episode 321 of the podcast. And for anyone who is a new listener of the show,
0:12.6	this is the place where you get discussions about nutritional and health science every week.
0:18.7	Now, today's episode, we're going to be delving back into a topic that is
0:23.8	rooted its head on several occasions over the past while, both with the release of the Sigma
0:30.3	Statements series of posts on cardiovascular disease risk and the influence of diet. Within that series, we looked at the influence of blood lipids and lipoproteins on cardiovascular disease risk.
0:44.3	And then recently we've also had a couple of podcast episodes, one with Samia Mora, where we got into lipids and lipoproteins.
0:52.3	And we also had a discussion where I brought on
0:56.6	Sigma's research communication officer, Alan Flanagan, who authored our cardiovascular disease
1:03.1	risk series to discuss that series of statements and to go through some of the common questions that would come up afterwards,
1:12.6	some potential counterpoints, or just to go into some of the nuances of things that we concluded,
1:18.6	but maybe didn't explain completely within that written post that there's some little nuanced
1:23.6	side discussions to. So just really to kind of flesh out more of what were in those statements and to kind of
1:31.7	round off that series by recapping it and to give some further information.
1:37.8	Now within that podcast episode, myself and Alan talked about one of the common objections some people have
1:48.2	when discussing the causality of LDL in atherosclerosis development.
1:54.0	And that is the hypothesis that in the context of high HDL cholesterol and low triglycerides, within that context then a high LDL, and typically
2:05.8	we're talking with LDL cholesterol, but as we'll discuss later, this will extend LDL particle
2:10.6	number as well. But the high LDL isn't cause for concern or doesn't confer that high risk for cardiovascular disease that would be
2:21.7	part of what we concluded in the statements, but is also a cornerstone of the lipid hypothesis
2:27.8	in terms of the role that LDL plays in atherosclerosis and therefore risk of cardiovascular disease and that
2:35.2	hypothesis has been mainly championed at least I can see online by Dave Feldman
	...

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