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.
For example 9/21/18 I ate the following..
4/ 409g Land O' Frost Premium Old World Style Black Forest Ham
- and -
113g Eckrich Chopped Ham
... Come to 265mg of cholesterol.
On the morning of that day my Total and LDL cholesterol were 317 and 233 respectively. So what happened as I continued to eat this way for 7 days?
5/ ...My Total and LDL cholesterol levels were dropping substantially
Again, I think there are many reasons for this I discuss frequently with the #LipidEnergyModel
But the point of this thread is to demonstrate how much (or rather, how little) dietary cholesterol mattered
6/ It's worth adding that there's some biochemistry that helps potentially explaining much of this. Most cholesterol we ingest is in the form of esters which commonly pass through our digestive tract, yet most cholesterol in our blood was actually made by our liver "de novo"
7/ Moreover, I learned early on from Dayspring's lectures the body compensates depending on ingestion. Generally speaking, if you have less coming in from the diet, the body makes more and vice versa.
I should probably tag @lowcarbGP as he's been talking about this lately as well...
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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...