Back in my early blogging days, one of my soapbox issues was that dietary saturated fat is probably harmless.
My views on that have evolved over the years and it's time for me to share the update.
At the time I wrote about saturated fat, it was the halcyon days of the ancestral health movement.
There was a lot of good in the movement but it had more than a little anti-establishment animus, and that bled into my writing.
I had read books by Anthony Colpo and Gary Taubes, and observational studies by and large hadn't found a link between saturated fat intake and adverse health outcomes.
It was exciting to help tear down a wrong old paradigm.
I now think the position I held back then was partially wrong, and overconfident.
To the extent that certain types of saturated fat-containing foods increase LDL (particle number and/or cholesterol), they're likely to increase cardiovascular risk.
One nuance is that some of the largest sources of saturated fat in typical diets have little impact on LDL-c relative to a typical diet without those foods.
In particular, most types of dairy: milk, cream, yogurt, and cheese. Chocolate also falls into this category.
Dairy is a major source of saturated fat in American and most European diets.
I suspect this is a key reason why observational studies typically find little or no link between saturated fat intake, LDL-c, and cardiovascular risk.
I think there are probably other reasons for the lack of association as well, but I won't get into them here.
So which saturated fat-containing foods do increase LDL, relative to typical mixed diets?
Butter, lard, the fat in red meats, and tropical fats like coconut and palm oils. These show up in some processed foods as well.
At the time I was writing about this topic, I had a high intake of butter and tropical fats. My LDL-c was high, HDL-c was very high, with a favorable ratio.
I thought this was a good situation, but I no longer do.
The evidence has gotten even stronger that LDL causes CVD, and the evidence has collapsed that raising HLD-c prevents CVD (it does *correlate* inversely w risk).
At this point I wouldn't bet my life that raising HDL-c via saturated fat is protective against the increase in LDL
Today, I don't eat much saturated fat, and what I do eat comes mostly from yogurt, poultry, and nuts. My LDL-c is low-ish, my HDL-c is high-ish, and my triglycerides are low.
I think this is a better situation and I intend to maintain it.
What lessons did I learn here?
I think the main one is that diet subcultures are extremely seductive and it's easy to get swept up in a narrative, especially if you're saying something that appeals to people.
Mainstream/establishment positions aren't always correct so it's a tough situation, but if we're going to critically evaluate them, we should apply the same level of skepticism to alternative positions.
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Folks, nutrition research has an insanely big problem, detailed in a new piece by @cremieuxrecueil.
If you make a histogram of p-values from a body of research, if there are no shenanigans the curve should fall between the two below. cremieux.substack.com/p/ranking-fiel…
This is what the curve looks like for nutrition research.
In lieu of a string of curse words, I'm going to go with YIKES.
What this suggests is that there is a massive amount of p-hacking and/or publication bias in nutrition research.
57% of published results in nutrition research fall in the range of p = 0.05 and 0.01.
@patrickc There's another RCT of psychological treatment for chronic back pain that is more rigorous and found larger effect sizes jamanetwork.com/journals/jamap…
@patrickc I don't think anyone can claim the concept is woo at this point
@patrickc I had an exchange with @mdonnino and revisited his group's paper. The effect size is actually similar to the paper above (uncertainty intervals overlap).
The @mdonnino study is rigorous for a pilot study, quite promising, and I look forward to the follow-up.
Leptin is the primary hormone that has been implicated in the regulation of body fatness in mammals.
This is a quick thread covering some of the evidence that its primary site of action is the brain.
Jeff Friedman's group was the first to provide evidence in this 2001 paper. They showed that partially deleting the leptin receptor in neurons specifically caused mice to develop obesity. doi.org/10.1172%2FJCI1…
In 2004, Streamson Chua and colleagues went further. They started with mice completely lacking the leptin receptor, and added them back only in neurons.
A recent study examines what happens when the new weight loss drug semaglutide (Wegovy) is withdrawn after 68 weeks of treatment. Some interesting things to chew on in this paper.