1/ I'd love to take an opportunity to expand on this important topic, and if I may, suggest something important to watch for with some newly emerging data.

To @MichaelMindrum point, I too believe the #ApoB will demonstrate higher association with #ASCVD than #LDL #Cholesterol..
2/ But to be sure, ApoB can be best represented as:

(1) Non-LDL ApoB lipoproteins
- and -
(2) LDL ApoB lipoproteins

The first category is predominantly chylomicrons, VLDL, and IDL -- which associate very highly with ASCVD.
3/ You can think of category (1) as "Triglyceride Rich Lipoproteins" (TRL, aka "remnants") and category (2) as "Triglyceride Poor Lipoproteins" (TPL)

The population of #LMHRs have extremely high levels of ApoB. But this pattern is a mix of very *low* TRL and very high TPL.
4/ If overall high ApoB alone is atherogenic (whether low in TRL or not), then it stands to reason this should be very concerning for #LMHRs, hence the importance of our #LMHRstudy (currently underway).

Certainly we need these data at a population level to consider further...
5/ But I will say again – I think it's worth understanding the relevance of distinguishing these two categories of remnant, triglyceride-rich ApoB lipoproteins from their triglyceride poor counterparts given what it says about the success and failure of lipid metabolism overall.
6/ Of course, I've touched on this area many times before (#LEM), but this article I wrote a while ago from CC goes into this very specific area in depth:

cholesterolcode.com/thoughts-regar…

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More from @realDaveFeldman

Jun 4
Design a VLC diet that is low in fiber with the goal toward reaching a low respiratory exchange ratio on a cohort of lean, fit athletes (but no other exercise confounding like resistance training or diet confounding like meds/sups, etc).

I’d likewise bet big majority = #LMHRs
Full disclosure - @DrNadolsky and I took to some of this discussion via direct texting. However, it did lead me to a good question that I decided to turn into a poll out of curiosity...
1/2 Another great prop bet @DrNadolsky and I were discussing:

He proposed he could emulate the #LMHR phenotype by consuming a lot of butter and coconut oil while not keto and fat-adapted (thus, high RER). I'd predict the opposite.
Read 4 tweets
Jun 4
1/ Two weeks ago we released our paper on the #LipidEnergyModel (#LEM) along with our video abstract for it. I'm pleased to say it has led to many great connections and expanded discussion.

I'm going to recap on a lot of these in this thread. 🧵 ...

2/ First and foremost, thanks to everyone for their extraordinary support in retweeting our announcement, sharing our paper, and letting researchers know of this model.
3/ As we state many times (including within the video abstract), this model doesn't describe all possible influences on cholesterol levels. For example, other things can impact LDL-C such as M/PUFA-to-saturated fat composition, fiber, genetics, medication, etc.
Read 9 tweets
Jun 3
1/ Cool thread via @DrNadolsky

FWIW, I think I've figured out the perfect experiment via weight loss alone.

If I were to lose, say, 10-15lbs but keep diet composition as identical as possible (thus no increase in sat fat), the LEM would predict increased LDL/ApoB independently
2/ This is a great design given there are now other food items that would change other than possibly a net reduction in overall calories to maintain at the lower weight (but if anything, that would mean less sat fat in the overall, ofc).
3/ Given how strikingly different each model would predict the outcome, it seems like a given I'm going to need to do this experiment.

There's even a chance I line it up before the fiber experiment. (Working out scheduling right now...)
Read 4 tweets
May 25
1/ Listening to @theproof's podcast with @NutritionMadeS3 as I work. I'm really enjoying it thus far and I again commend Gil on his ability for distilling complex scientific discussion effectively in his YouTube videos.
2/ I just got through the part at 47:51 that had me stopping to write a couple thoughts... (the queued spot in the video linked here👇)

@theproof brings up one's individual need to want to feel a "part of a community" (very big deal in the diet space)...
3/ ... And that "...it can challenge our identity if we come across information that is directly challenging one of these very strongly held views from within that community that our fellow community members also hold..."
Read 7 tweets
May 23
1/ I had the debate between @NutritionMadeS3 & @ifixhearts on in the background while working. Really enjoyed it

First and foremost, both gentlemen were very cordial and professional. No ridicule, name-calling, or any other emotive personal attacks, etc..
2/ Which -- as you all know -- I'm a strong advocate for.

@NutritionMadeS3 represented the pro-LDL/ApoB lowering position well. (Note I've linked/tweeted his videos several times)

@ifixhearts brought forward the importance of metabolic health, and fault in it getting ignored...
3/ One important difference I was especially interested in-> do we have enough data in hand to feel confident high LDL/ApoB is a strong independent risk factor regardless of metabolic health. Generally @NutritionMadeS3 appears to favor "yes", @ifixhearts favors "unsure" to "no"
Read 5 tweets
May 23
Yes, @ProfTimNoakes — The study actually gets quite detailed in that area. Note they include LDL-C >= 190 strata across the range of metrics. In fact, they are far and away the largest sample of this with CCTA/CAC of any study I know of.
And of course, I would especially still love to see this stratification in particular…
Read 4 tweets

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