1/ Very cool experiment and thread by @ScepticalDoctor who did a more #PlantBasedKeto and saw low #LDL#Cholesterol given high MUFA/PUFA relative to sat fat, along with high fiber (which supports my prior thread)
If looking to keep LDL low, this might be worth considering...
2/ As per my various tweets before this one on the topic, and not to beat a dead horse, I feel it is too often "low carb vs plant based" is often assumed the latter *must* be high carb -- thus, "low carb, animal-based vs high carb, plant-based"
... This is a false dichotomy...
3/ There are definitely some of us who are, as I like to say, "cautiously optimistic" with regard to higher LDL as appears to be resulting from metabolic fat adaptation in the context of higher sat fat, lower MUFA/PUFA and low to no fiber. But this risk degree is uncertain...
To be sure, resulting LDL levels for those trying a more MUFA/PUFA/fiber-prominent diet does vary, but I can speak from some anecdotal experience that it often *tends * toward lower levels.
5/ Again, this isn't an endorsement of #PlantBasedKeto, what to do with your LDL, etc
But what I do want to endorse -- strongly -- is for everyone to know as many options available as possible, to find what works for them and their goals...
6/ As much as I try to avoid the diet debates, I feel like this specific diet option doesn't get enough attention and that's why I continue to take moments like these to highlight it.
"... But the question then is – how do you actually solve this problem of having discourse and debate that's not in good faith. So we almost need like a third estate..."
2/ "... Like a different place where there's a very smart arbiter who's helping mediate. And it's all done in good faith, and the ideas actually get hashed out more. And the public can watch, right?
But such a thing doesn't really exist right now.
It really doesn't..."
3/ "... Because everybody is so tribalized, and it's very hard to get views on a YouTube or a Facebook doing that.
It's much easier to go 'full tribal'. Much much easier."
1/ Posting here for posterity. In my 2018 LMHR presentation I give a long section near the end where I encourage LMHRs to avoid "echo-chambering", check into different pro-LDL lowering voices (and mention Attia and Dayspring specifically), and extend my personal...
2/ ... promise to with regard to risk discovery and bringing it to attention within the community (and hey, now we're doing the LMHR study -- direct data coming soon).
I follow with a "that said," and posit that I suspect LMHRs will ultimately show low CVD and ACM...
3/ Because YouTube allows for jump-to-current-time links, someone straight up cut to the "that said" portion in order to exclude all the prior emphasis and efforts toward balancing.
2/ But I had no idea there could actually be such a direct pathway to Acetate/Acetoacetate (AcAc) and LPL expression- being crucial for accessing fat stores. While this paper is a mouse model, it’s results are quite impressive when looking to knockout of GRP43 (GRP4-/-) vs normal
3/ and while Nick’s thread importantly mentions the fact these knockout mice *gained* weight on the ketogenic diet — I think a likewise incredible finding is that they also demonstrated far more difficulty in losing weight when eating nothing at all (fasting)
2/ Wow, in the intro Rob mentions Bill having discussed LMHRs with me (and yes, we’ve had many great chats on the topic). Where he agrees, and where he disagrees. To be sure, I have a bit of an advanced preview on what that will likely be. ;) but I’m excited to hear it in the ep.
3/ 28:30 Bill: I think Dave Feldman has probably helped more than any one person in giving disability and how radically our bodies can change [lipid levels] in just days… So yeah, you can actually influence these results quite a bit in a 3 to 5 day period of time…
2/ If it seems like there's a wide spectrum of possibilities between those two endpoints, it's because there is
Sure, I do think this may end up testing if the lipid hypothesis can be taken as "dose-dependent, log-linear" in every context. But that's not testing it categorically
3/ For example, it could well be we observe a very low progression of plaque in LMHRs for reasons none of us are aware of yet, but of which don't apply to those with atherogenic dyslipidema in original sense (thus, mixed outcome, new mechanistic aspects yet to be determined, etc)
Taubes: “One of the defining characteristics of pathological science is — people commit themselves publicly to a result based on premature evidence…”
2/ “…So it’s not ironclad, they haven’t locked it down, there’s still a chance they could be wrong and they don’t understand the likelihood of that chance, no one ever does until you get very good at this when you realize that chance is enormous.”
3/ “And so once you go public, science is supposed to be hypothesis and test, right? You’re supposed to rigorously test your hypotheses and ideally you’re trying to prove that you’re wrong..."