2/ At 25:20, @LisaRosenbaum17 makes some fantastic observations about medical professionals and empathy— and how it illustrates problems with our existing system and how it changes them.
3/ at 34:27 @LisaRosenbaum17 expresses her deeper curiosity on understanding people‘s behaviors and motives on their decision-making beyond the quantifiable (like money). This has been an obsessive subject for me as well, particularly with challenge cases within my family.
4/ So ironic — i’m on a walk in the Vegas sun today so I was able to continue the @ethanjweiss and @LisaRosenbaum17 podcast which I didn’t finish yesterday. They are now talking about problems in the system, many relevant points to my discussion with @ethanjweiss yesterday...
5/ Fav quote from @LisaRosenbaum17, 56:53 “I’d rather have a heart attack today then 50 years ago, but I’d rather be cared for by doctor 50 years ago.” (They were discussing the degree of admin tasks required by doctors in the modern age and how this impacts joy of medicine.)
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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>"...