For those who've followed my work and know where I'm coming from, WHY would I fully expect LDL-TG (triglyceride content per LDL particle) to closely associate with atherosclerosis?
If it's due to dysfunction in lipid metabolism such that CETP is going up and lipoprotein lipase activity is going down, then it makes a great deal of sense this will change the composition of lipoproteins downstream -- particularly LDL.
And if I can add -- I think LMHRs will show TG/CE ratios in the aggregate at levels never seen before. We'll know this soon with the coming #LMHRstudy data.
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For example, I’ve known many who are into fitness (or just now getting into it) that are seeing better results on PE.
To be sure, that’s anecdotal, and it’s hard to know for sure if they were getting adequate protein in the first place…
… conversely, I’ve also seen a kind of resurgence in people discovering KetoAF after struggling with various versions of keto (high protein or not). Many have health challenges, with many of those preventing their being fitness-centric. (Thus, confounder + cofounder potentially)
2/ "My point is, there is no athero or chronic vascular inflammation without a lipid disorder."
I have a nuanced difference with Sam on this -- but the important point here is that we need to disentangle the disorder/disfunction from the athero to test..
3/ In other words, to confirm/disconfirm the contribution of LDL-P independently to atherosclerosis, we'd want to look to populations without a likely form of disorder or dysfunction (be it genetic or acquired).
Obviously, I think LMHRs provide a unique opportunity on this...
Here are the observations I give my own family members based on what's I've learned in my N=1 experiments.
1) Nothing beats proximity.
The further I'm away from food, the less likely I am to eat it. Not just across town, but in the room.
2) Like many (but probably most), eating something outside my diet commitments on a holiday almost always results in my continually breaking that commitment from then on.
Some things I can "cheat" on (like "normal" pizza). Some I can't (like "normal" chocolate chip cookies).
3) Social cues are way, way, way more powerful than everyone gives them credit for, IMO.
"Mom made us <X>"
"Would you like some <x>?"
"You've been so good lately, try just a bite."
Multiple influences: not wanting to displease/reject, being included, looking to appear moderate
Wow — i’m currently traveling for the holidays and tweeted this out before getting on the road (currently at a stop). I guess this is actually a topic with a lot of interest…
Yes, this was one of the things that got brought up. It’s actually where a lot of the arguing originated because naturally everyone wants to reassure everyone else not to feel insecure. But some chimed in that it isn’t “how the real world works”…
… (shared with her permission) — “I think some guys who are super cut just generally aren’t in long term relationship mode. Even if they think they are.”
2/ Hence the value of stratifying away a period of early deaths for a given population (aka "censoring")
Thus, if you exclude all deaths in a given population that took place during the follow up period up to year X, then this helps to address reverse causality.
3/ I just recently got a chance to relook at the centenarians of NHANES with updated data myself.
And as it happens, they have a built in censoring of 15-20 years due using only ≤85 year olds as they confirm turning 100. 👇
2/ Certainly the biggest impact is bringing this phenotype well into the spotlight.
If you've been following my work from the beginning, you can appreciate just how much energy I've put toward putting this phenotype in front of Lipidologists.
3/ But this is understandably a challenge given how much progress on this research has been accomplished outside typical channels ("Citizen Science").