1/6 I'd like to both retweet and add on to @NutritionMadeS3's point here...
Again, and with emphasis, my position is one of cautious optimism. That's an explicit acknowledgement of uncertainty, even if I have a leaning toward the positive in this context...
I'd hope this were self-evident, but if I were completely certain high LDL + high HDL + low TG = low risk in fat-adapted context, there'd be no effort for a study
3/6 I've chatted with @NutritionMadeS3 and others on evidence I consider very compelling regarding the connection of health and illness for lipid metabolism and their impact on lipid profiles. But I likewise stress we'd be better served with prospective data in this context
4/6 That's where LMHRs provide a kind of insight we've never had before. Again, remember the seminal work of Brown and Goldstein re the lipid hypothesis started with homozygous FH, where children with super high LDL (500 mg/dL+) and no other RF observed rapid atherosclerosis.
5/6 This could well be happening with LMHRs and it's why I'm extremely motivated (along with @DrNadolsky and @DrRagnar) to get this study rolling as soon as possible. (Currently in IRB)
Many low carbers aren't waiting for the study to take steps ( see
6/6 And, as always, I don't want anything I say or discuss to be taken as medical advice. Consult your doctor, do your own research, and come to the conclusion that works best for you.
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2/ "Lipoprotein lipase (LPL) is a rate-limiting enzyme for hydrolysing circulating triglycerides (TG) into free fatty acids that are taken up by peripheral tissues."
Translation: LPL is like a key cells use to open lipoprotein boats to offload their fat-fuel cargo (TG)
3/ "Postprandial LPL activity rises in white adipose tissue (WAT), but declines in the heart and skeletal muscle, thereby directing circulating TG to WAT for storage; the reverse is true during fasting"
Sure, post-meal we do more storing in fat via LPL, otherwise we do less.
The tl:dr -> There's more selective control with fatty acid exchange in tissues than we fully understand... but we have a lot more we've learned recently...
2/ "Preferential uptake of FAs into high demand tissues such as the heart, muscle and brown adipose tissue cannot be achieved by non-specific uptake, which would acutely distribute FAs equally into all cells."
- Translation: there's some selective trafficking going on here.
3/ "A second uptake process modulated by activity of capillary lipoprotein lipase (LpL) involves FAs derived from triglyceride (TG) rich lipoproteins (chylomicrons and very low density lipoproteins." (VLDL)
- Yes, lipoproteins + LPL = hydrolysis of TG to cells
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...
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...