2/ Ha! When @IanCramer has me give a little background on how I got into this space, I give one of the clumsier setups I think I've given in an interview. Not the best intro for the energy model either- but you can always check out the general poster here: CholesterolCode.com/model
3/ @IanCramer asks me for a "50,000 foot view of my thesis" where I walk it into the "high LDL where metabolically induced" context.
4/ @IanCramer: "I think if you take someone who is, as you put it, metabolically unhealthy and put them on a ketogenic diet and all of these markers improve -- except for the LDL -- I think this is absolutely a good thing."
5/ "... But I'd caveat that by saying, I think that the LDL cholesterol, LDL particles [being high] is still a risk factor... why not take that additional step and say, 'hey, let's try to bring this down a little bit.'"
6/ About 25 minutes in I give a decent setup for Lipid Profile vs Lipoprotein-centric view points.
But that said, I know I need to do a larger article, video, or both to really unpack it.
7/ At around 41 minutes we get into genetics. I brought up my interest in genetic abnormalities with regard to immune cells, but ironically, I hadn't yet read this paper at the point of recording- which happens to fall in line with what I was discussing pubmed.ncbi.nlm.nih.gov/27680891/
8/ Really, really love the last 20m of this podcast.
@IanCramer and I had some deep discussion on the importance of civility and respectful discourse with people of differing opinions.
Naturally, I have to again applaud his efforts in being such a strong example of this himself
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First, let me say that data on this has been a bit limited. But *IF* we do ultimately confirm there are more ApoB-48 (B48) than ApoB-100 (B100) in ASCVD plaque, it would be a very big deal.
Let's unpack...
2/ First, thanks to @TuckerGoodrich for pinging me on these pubs and pressing the discussion.
But also credit to @CaloriesProper on tweeting this a couple years ago (I missed it then)
To understand why this would be so important if true, some review...
3/ B48 and B100s are the major proteins on chylomicrons (CMs) and VLDLs, respectively.
CMs mostly carry lipids from the small intestine to the bloodstream (lipids consumed), VLDL mostly carry lipids from storage; predominantly from adipose stores.
#Me: Why would triglyceride rich LDL particles be more atherogenic than triglyceride poor LDL particles?
#ChatGPT: Triglyceride-rich LDL (low-density lipoprotein) particles are more atherogenic (i.e., more likely to contribute to the… twitter.com/i/web/status/1…
2/
#Me: Couldn’t it also be possible that triglyceride rich LDL are ultimately the result of metabolic dysfunction and that better explains its association with atherosclerosis?
#Me: Is it possible that almost the entire amount of atherogenesis associated with high triglyceride rich LDL is due to dysfunctional lipid metabolism and the diseases that result in these profiles rather than the LDL particles themselves?
1/🧵 I'm definitely a fan of both @DominicDAgosti2 and @DrRagnar (obviously), so I was excited to see them chatting about #lipids, #LMHRs, and Dom's consideration of increasing carbs to lower his #ApoB
3/ When chatting with Dom in SD last year for dinner, he mentioned focusing less on maintaining such a sizable muscle mass as he typically does, and I predicted he'd likely see his LDL/ApoB as considerably higher with this change if still #keto. This podcast appears to confirm...
But I also know many people in my own family who have struggled their whole lives to lose weight and assume if they don't have this near instant drop to their goal weight like <fill in the blank success story> then they are doing it all wrong...
... I can't tell you how many times I point out truly new, record-setting successes with people I know personally -- but it's their own record, their own health journey.
But they often can't see it because they hear they "won't be hungry anymore on <fill in blank diet>"...