1/2 Example 1:
🚬 Imagine if the average person from the moment they're born were taught to be 2 pack a day smoker.

⛔️ Now imagine a fraction were born into families that were 0 pack a day smokers.

Would we expect that latter group to have greater longevity than the former?
2/2 Example 2:
Now imagine most people averaged 100 #LDL cholesterol over their lifetime.

But a fraction were born with a genetic mutation that kept their average at 20.

Would we expect that latter group to have greater longevity?
If genetically low LDL/ApoB had universally a net benefit -- this would be strong evidence that indeed this particle is pathogenic -- which is to say, disease-causing overall (not just atherogenic)

But does existing genetic data support this hypothesis? Is there clear longevity?
Hence my interest whenever it comes up (ie @theproof's podcast re centenarians)

Genetically low LDL associating w/ longevity benefit against the avg population would meet with the expectation of LDL/ApoB being truly pathogenic (no CVD to non-CVD tradeoff)
When I get back more bandwidth soon, I'm hoping to get in more time to set up study on these kinds of questions.

For example, do we find those born with PCSK9 loss of function (LOF) have an average lifespan that exceeds the general population?

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More from @realDaveFeldman

Feb 1
1/4 Interesting study regarding #LDL-C vs all cause mortality*

✅NHANES -- so it's #OpenScience 👏
✅Lowest LDL-C associates with highest ACM
⚠️ No short term censoring (more on this below)

(*had in my reading list, but forgot until ht
@BobJohnson462) nature.com/articles/s4159…
2/4
A couple notes...

1️⃣ Many assume the higher ACM associated with LDL-C is due to "reverse causality". It's a hypothesis, to be sure, but one I think worth exploring.

Thus, it would have been ideal of the authors tried at least one or more analyses censoring 2-3 years.
3/4
2️⃣ As always, be aware these data are observational.

And as I say often👇

(Always worth a mention of Bradford Hill and his criteria, btw)
Read 4 tweets
Jan 30
Yes, read it when it came out.

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?

(By now this should be a very easy question.)
2/ Let's start with causal directionality.

Which of the following are possible?

1) High LDL-TG is causing higher atherosclerosis

2) One or more things are causing both higher LDL-TG and higher atherosclerosis
Answer is: Both are possible.

Now that said, it is way more common for people to only consider (1) and not (2)

I regularly do my best to get folks to consider (2) as well -- and have been doing so for several years now.
Read 7 tweets
Jan 26
I don’t want to bias the results, but I’ll concede my answer would depend on the population criteria.
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)
Read 4 tweets
Jan 9
Great comments today via @Lpa_Doc -- please note his precise language. 👇

I'm going to thread 🧵 this and his other comments and then add some of my own...

/1
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...
Read 5 tweets
Dec 25, 2022
🎄My Holiday N=1 Overeating Survival 🧵

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
Read 8 tweets
Dec 19, 2022
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…

some quick answers to questions…
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.”
Read 4 tweets

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