If you haven’t already tuned in to the recent sit down between Dave and Ivor Cummins, here’s your reminder to do so! They share their thoughts during the aftermath of Dave’s recent appearance on Peter Attia’s podcast, including their thoughts on mass balance, root causes, and more.
Very good! That clarified the main leftovers from the Attia podcast.
It makes perfect sense to me that persons who have an easy time mobilizing their fat stores would establish homeostasis at a higher level of cholesterol recycle due to the higher perceived demand for fat as fuel. The higher fraction of cholesterol recycled is then, as you say, ‘along for the ride’. It also makes sense, strictly from a conservation standpoint, for homeostasis to be maintained at a level where there is a larger pool of cellular repair material available (i.e., cholesterol) because, when energy demand goes up, it’s a good bet more cell repair is necessary.
This is a great companion piece to the Attia podcast and an excellent discussion on its own merits. It’s interesting getting to hear the discussion with someone hostile to it (to “stress-test” the lipid energy model) and with someone agreeable to it (to help explain it). It certainly helped a biochemical novice like me have a better understanding of the whole cholesterol discussion.
In my review of the Attia podcast, I mentioned that Attia’s strongest point was about the phenotypic FH cases with low triglycerides, high-HDL, and high-LDL, and how those should be counted in assessing the risk of high LDL in LMHRs. Now that it appears that Attia likely misspoke (there are likely not 2000 known genetic mutations showing low-trig, high-HDL, high-LDL– Attia has not responded to you nor to multiple people reaching out for clarification on Twitter), it certainly detracts from his point and from his criticisms of the lipid energy model.
Your charitable demeanor is commendable, as always.
Thank you both for using your engineering mindsets toward the meaning of these lipid values and toward health.
Why don’t we get an anti-LDL group of Dave, Ivor, Dr. Malcolm Kendrick and a pro-LDL group of Attia, and maybe 1-2 more people together? Give them a moderator and let them each have 1 minute or so to respond, like a debate. I would like to see that. (And by “anti-LDL, I do not necessary mean they believe LDL is meaningless for heart disease, just that they have different ideas as to what the significance is for LDL.)
I have listened to this, but not to the Attia/Feldman podcast (3 hours is a bit long). I will listen to that one day, though.
Two root-causes of endothelial and epithelial damage are retinol and retinoic acid. These likely underlie the other root-causes mentioned. Grant Genereux, an engineer in Alberta Canada has much to say on the subject. Appreciate all of your work. Very nice interview. One mini-review I was reading today may provide some insight if you can decode the use of “RBP4”. The key question to ask is: Why does a macrophage create RBP4 in the first place?
Hi, thanks for sharing! While I’ve heard of Genereux I’ve not looked into his work in-depth. Luckily he’ll be speaking at CarnivoryCon in May (which I’m also speaking at) so I should get a general overview there (lucky me!). I will have to read the paper you linked and try to see if I can find the answer (unless it’s already answered there – ha). It does sound interesting. 🙂