Requiescat in pace Ray Peat

Dr. Ray Peat

Ray Peat, a legendary figure in nutrition science, died on Thanksgiving. We don't know any details beyond that single fact, but he will continue to have an impact for years.

I didn't agree with all of his positions, but his cautionary work about dietary PUFAs was trail-breaking, even though he didn't do the research. There's a huge role in science for people who actually read the papers and connect the dots, to get a coherent picture out of the rubbish bin that medical science all too often is. He did an impressive job of that.

He'll be missed.

Thanks to David Gornoski for reaching out to Dr. Peat and making these two podcasts happen, I was honored to have the chance to speak to him, and to have learned from him.

Interview: Ray Peat, with David Gornoski on A Neighbor's Choice

"My Big Fat Panel: How Seed Oils Cause Obesity" on A Neighbor's Choice with David Gornoski

David put together a retrospective of some of our discussions with Dr. Peat:

Peat's kind of a niche, but he's also kind of a genius.

— Tucker Goodrich (@TuckerGoodrich) August 10, 2017

Yep. Peat is a bit of a genius, as is Skulachev. Add @DrPhilMaffetone to the list of guys decades ahead of their time...

@PeatDon

— Tucker Goodrich (@TuckerGoodrich) January 1, 2019

Thoughts on "Sugar on Your Coconut Oil?"

 Peter posted some interesting thoughts on obesity/NAFLD in a low-linoleic context. I posted the following as a comment over there, but wanted to surface it here. So read this first:

"Sugar on your coconut oil?"

Comment:

Thanks for Parekh 1998, hadn't seen that one.

It raises a couple of thoughts.

Igarashi et al., 2015 (10.1016/j.bbalip.2015.05.006) found that sugar stimulated the endocannabinoid system, but to a less extent than LA, but via the same mechanism:

"Additionally, we report the unexpected finding that 7-day maintenance on a diet high in sucrose can also disable feeding-dependent OEA and LEA mobilization. The results suggest that FAE-mediated satiety signaling is suppressed by high fat or high sucrose in the diet, and that this suppression might contribute to hyperphagia and the development of obesity."

So if you have a high fat diet that's too low in LA, sucrose might substitute for it, in part.

Second, the other extra-mitochondrial LA obesity pathway is generation of the obesogen HNE, which of course only comes from LA and other n-6 fats. Cannizzaro et al., 2017 (10.1186/s12986-016-0149-z) measured the harm of a HFD (for maximal confusion, this is a High FRUCTOSE Diet):

“The level of HNE-modified proteins in plasma was increased almost 2-fold by HFD treatment, while RGZ completely normalized the level of HNE adducts (Fig. 6a).”

Which gets us back to Surwit. If you want to reduce the obesogenic effect of the Surwit diet, Chang et al., 2020 (10.21203/rs.3.rs-104384/v1) block the proliferation of HNE by stimulating the HNE detox pathway in the form of aldehyde dehydrogenase (ALDH):

“Importantly, the ALDH2 activator AD-9308 increased both the catalytic activity of WT and mutant enzyme, reduce serum 4-HNE levels, and effectively alleviated diet-induced obesity, fatty liver, insulin resistance, and glucose intolerance in both Aldh2-KI and WT mice in a dose-dependent manner.”

So sucrose/fructose is required to reduce the production of anti-obesogen OEA and stimulate production of obesogen HNE, in a low-LA environment?

The first and third of those posts are from my Obesity post.