Naturally, this part of the discussion gets hotly debated in and outside #LowCarb circles. CVD similar, yet higher ACM, however -- harsher environment, less sophisticated healthcare, etc.
Myself, I don't consider Inuit the most ideal corollary..
5/ For better or for worse, with the rise of #Keto/#Carnivore we are now entering a natural experiment with many Vilhjalmur Stefanssons all around us. Very low carb, animal-centric diets with corresponding high #LDL#Cholesterol for a sizable proportion of this population.
6/ The good news is that we're nearing the #LMHRstudy to better understand risk around this diet-induced hypercholesterolemia.
2/ If you've followed me a while, you know I believe it isn't the actual ingestion of cholesterol on #LowCarb that has a big impact on serum levels -- it's predominantly the trafficking of fat. (See CholesterolCode.com/model)
But this is actually a very testable distinction...
3/ All we need is an experiment where I consume a lot of (1) low fat food that still (2) has ample amounts of cholesterol.
Thus, the "processed meat" side of the experiment is key if it has a decent amount of cholesterol -- and it does.
If a drug did many of the same things with one's lipid profile as a #LowCarb diet, particularly decreasing triglycerides while increasing #LDL#Cholesterol:
1) Would it reduce ASCVD risk? 2) And if so, would it be more acceptable than #LowCarb?
2/ If you haven't heard, SGLT2 Inhibitors have recently emerged and have been gaining a lot of popularity. Data thus far shows they typically:
3/ Naturally, that has the attention for those of us interested in how triglyceride trafficking and turnover could be relevant to #LDL increasing for what may turn out to be non-pathogenic reasons (kinda my focus ;) )
2/ FH, particularly HoFH is highly associated with atherosclerosis and is considered a substantial risk.
Cases of HoFH are extremely rare, but are considered a cornerstone of the lipid hypothesis as many with LDL-C levels (comparable to Nick's) demonstrate CVD as children...
3/ Brown and Goldstein have seminal work on this topic.
2/ Per @Lpa_Doc's (2) and (3) in the thread, when we have "normal" TG levels (guidelines would say < 150, I prefer < 100) then most cholesterol in ApoB-containing lipoproteins (ApoB-Lp) are in LDL and there's little VLDL-cholesterol...
3/ But where TG is high, there's more utility in looking at ApoB given it lumps remnants (VLDL/IDL) with LDL.
-- But IMO, that's also the problem. We want to disentangle where remnant association is much more relevant than LDL association...
1/ I’ll be interviewing @KetoCarnivore soon. In preparation, I watched this talk of hers from 2019 that I found very interesting...
2/ She provides some counter opinion analysis regarding both simplified metrics of “nutrient density” and the protein leverage hypothesis (ie @tednaiman). Or more specifically, the challenge in these approaches having potential bias that isn’t easily apparent...
3/ To be sure, I don’t have a very strong opinion myself in this area as I tend to focus more on lipid trafficking (and generally try to avoid the nutrition debates overall).
Moreover, I’m still plotting to do @tednaiman’s P:E diet as an experiment soon along w/bloodwork...