3/6 If you read nothing else, check out this section from the article, and why I'm so vocal about *not* looking only at #ApoB (which lumps non-LDL and LDL) together.
Again -- and with emphasis -- this is part of the larger hypothesis. But all the more reason to research it...
4/6 More recently, there's greater focus on Remnant Cholesterol, which I consider very encouraging -- particularly where stratifying out against LDL in particular. (HT @shashiiyengar)
5/6 But ideally, we'd look to populations with very high LDL, yet low RC (such as #LMHRs) to better determine if this is indeed more systemic to lipid metabolism vs inherent atherogenicity of the lipoprotein (and yes, per @raphaels7's mention, I think it's much more the former)
6/6 And of course, we're in the process of putting together a study on #LMHRs right now via the CitizenScienceFoundation.org -- so hopefully we'll have some very relevant data on that soon.
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1/ I have a new favorite term: "unadjusted hypothesis-naïve exploratory linear regression"-- and it comes from @Ad_SotoMota, who @nicknorwitz and I are honored to be working with in this new project (news on that soon...)
I don't typically see the term as it's rarely employed...
2/ My layperson explanation is that this is explicitly letting the data speak for itself. Literally starting from scratch and seeing what patterns machine learning tells us are emerging. No adjusting the data at the beginning of the process which can bias the outcome (of course)
3/ I'm much more used to methodology sections describing several steps of adjustment selection by the researchers. This isn't to imply any wrongdoing by any means, but understandably, this can be problematic if one or more underlying assumptions for adjustments are incorrect...
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...
"... 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)