1/ So allow me to get engineer-y for a moment -- I was really happy with how the structure of this debate played out.
To recap:
- We worked out having 5 minutes uninterrupted from each for opening statements to the featured questions...
2/ - After that, we moved into the "unstructured, conversational" portion of the debate on that question.
Since I said I'd give a polite warning whenever either participant ran over 5m, it seemed both took around 5m each in a back-and-forth during this phase...
3/ To be sure, both participants might have the other interject for clarifications or to make a point briefly, but it was almost never abused.
And my general rule was to give the one being interrupted some extra time to complete their point. And overall, this worked very well.
4/ When both participants know the moderator is keeping a close eye on the time and seeking to enforce equal parity, I think it makes them feel more comfortable waiting for the other to finish and less of a need to interrupt and talk over them to get enough time in.
5/ And well... I know I'm biased in this case, but I think this overall format really delivered a lot of substance from both of them. I felt by the end that there was quite a bit of ground covered, yet each managed to challenge each other on the areas we were expecting anyway.
6/ Of course, I again have to credit both @BioLayne and @DoctorTro for being professionals. Structure is pretty useless if each participant isn't already onboard with having a productive debate in the first place.
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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>"...