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)
4/ Or it could be we observe very rapid progression of plaque this data could have a broad impact across the low carb community to take steps in reducing LDL. (Which is why LDL-lowering proponents should want this study most given LMHRs' unique standing to isolate specificity)
5/ But likewise, this will be meaningful data to a lot of people who are LMHR phenotypes, without question.
It shouldn't be taken by anyone as the definitive study (I'm sure my colleague, @DrNadolsky would agree strongly on this).
And feel free to quote me on this as well.
6/ All that said, the research is truly overdue. Before crowdfunding this, I put forth a lot of effort going through typical channels before finally giving up. And I'm proud to say the Low Carb community stepped up to make this a reality (many funders are themselves LMHRs)
7/ In the mean time, should you assume we know the LMHR phenotype is perfectly safe? No -- we don't know that -- it's why we're doing the study.
As always, I want everyone following my work to follow those of opposing opinion as well. Research, learn for yourself.
8/ When I say I'm "cautiously optimistic" regarding lipid changes and the triad (⬆️LDL+⬆️HDL+⬇️TG) as related to metabolic fat-adaptation, the operative word is "cautious" (as opposed to "not cautious")
Here's 13, 14, and 15 of my pinned tweet as a refresher for consideration
9/ Lastly, and perhaps most importantly, if you're pro-lipid hypothesis, please give credit to @DrNadolsky as an investigator for his efforts in helping us craft this study. If you look through his social media, you'll find he's a strong fan of keeping LDL/ApoB substantially low.
10/ And while I can't know/reveal what the details will be until we're through IRB, I can say entire team is quite adamant about releasing as much direct data as we can to everyone, so the ability of any of us on the team to spin it internally is very limited in the first place.
11/ I'm sure they'll still be some on both sides of this issue that have different opinions on what this study means than we do, but for those wanting better clarification -- hopefully this helped.
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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..."
2/ First, I definitely DO NOT want anyone to interpret anything I've said as reflective of analysis with secondary prevention. I'm quite upfront that I prefer looking to lipid research with regard to so called, "primary prevention" (populations without prior heart attacks)...
3/ Second -- and as always -- I want everyone to work with your doctor. Yes, I do think your doctor needs to likewise work with you and your health goals, but this is a given.
If I had a heart attack, I'd definitely be working with my doctor and considering all the options...
2/ For me, this journey started 6 years ago with alarmingly high total and LDL cholesterol following my going on a ketogenic diet. I became obsessed with trying to understand why and begin reading everything I could on lipidology...
3/ I found through a series of experiments there was quite a bit of change I could induce based on dietary patterns. As I developed and executed this "citizen science" research, I turned it around back to the community to hopefully help us in advancing this important topic.
2/ Let's have some fun and use a relatable analogy...
Imagine you had exactly two kinds of stores in the neighborhood: bakeries and butcher shops.
You normally get groceries from both, but recently the bakeries were closed down, so now you just get meat only for meals...
3/ Now that the bakeries are down, there's more demand on the butcher shops, so they are having more inventory sent to them.
But then, the neighborhood increased while the number of butcher shops actually decreased, and this required an even higher rate of shipments to restock.
1/ This would be a good opportunity to clear the air on a few things...
Per @DrNadolsky's tweet, we don't know everything we want to know about #atherosclerosis. Almost everyone would agree it is multifactorial, and most of Med would ascribe the central risk driver to LDL/ApoB..
2/ First, I agree glucose going up and down -- in and of itself -- is not inherently a mechanism of concern.
The key questions of interest are by how much and for how long -- and from this, can we determine if there is a dysregulation?
3/ I was listening earlier in a Clubhouse chat to @Dr__Guess discuss her recent study and how "all over the map" glucose levels were for these T2D patients -- which is unsurprising given the nature of the disease.