1/ I want to take a moment to have a back-and-forth exchange with @MichaelMindrum in a thread, and I’m just gonna keep it to us (Tweet setting) I’m confident we can keep it productive. 👍

First, I think we should get on the same page with where I’m coming from..
2/ I’m not just interested in high LDL for LMHRs. I’m interested in whether it’s meaningful to distinguish high LDL from what appears to be lipid metabolic dysregulation versus high LDL in the context of metabolic fat adaptation.
3/ Much of those following this account know this already from following my work, but often critics do not.

That’s why I’d love to specificity talk to a critic I like, such as yourself, and really unpack this so we can better narrow down where the real disagreements are.
4/ Which brings me back to the two different contexts.

By this point, I hope you‘s agree I rarely discuss LDL risk in isolation – I’m specifically interested in lipid profiles — combination lipid data, like the triad (⬆️LDL+⬆️HDL+⬇️TG)
5/ Or to put it another way, I would consider the following atherogenic dyslipidemic profile as very concerning: ⬆️LDL+⬇️HDL+⬆️TG

… even if high LDL is the common denominator between both profiles.
6/ (⬆️LDL+⬆️HDL+⬇️TG) is understudied, but the limited data we do have shows it has a great deal of relevance toward cardiovascular outcome.

That’s where my focus is – not on LDL alone – much less on data around LDL without context into metabolic health or genetic abnormalities
7/ and that has to be the starting point for any in-depth discussion on what I personally hypothesize regarding ApoB/LDL and its role in this larger puzzle of energy distribution and risk. CholesterolCode.com/model
8/ So before going further – I really do want to be sure that you understand this important point. That I believe lipid profiles are more often a reflection of health or disease than they are drivers of it. But I also acknowledge this is a hypothesis being tested/researched…
9/ Can I confirm you follow me fully up to this point?

It’s important– because I want to avoid further reductionism toward simply LDL in isolation past this.

(if you think most who follow this account believe it’s all about LDL and not about the above, I’m happy to poll again)

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More from @DaveKeto

21 Nov
1/ this one minute clip was released by @chadinabhan an hour ago, and when I watched it I got a bit concerned that it takes a clip out of context and DMed Chadi about it.

He rightly pointed out my reaction was misplaced as this was strictly a teaser.
2/ However, this did provide me an opportunity to expand on the point, given I understand where @ethanjweiss would feel this was “meaningful”.

In our exchange from several months ago (too lazy to link), Ethan pressed as to whether I’d take a statin post heart attack…
3/ I said then (and I’ll say today) – I don’t know, but I feel it would be irresponsible for me to say one way or another.

But what came up in this podcast, is it would be meaningful to Ethan if I pointed out that post MI-research I’d see a scenario where I would.
Read 6 tweets
14 Nov
🚨🚨🚨BREAKING - $20k Analysis Effort🚨🚨🚨
1/2

Since my tweet last night, a donor has now come forward looking to fund 👉👉👉$20,000👈👈👈 toward this effort for publication!!! 🤯🤯🤯

Reaching out to any #DataScientist who is serious about making this happen.

(See next 👇)
2/2
👉👉👉 Here's our newly released post on this project: cholesterolcode.com/announcement-2…

If you're like me and feel this is waaaaay overdue, please help us find the Rockstar(s) who can make this a reality!
Hey #UnitedKingdom docs like @lowcarbGP and @DrScottMurray -- know anyone data scientists on #UKBiobank who'd be interested in this project? 👆👆👆
Read 4 tweets
3 Nov
1/ This is especially important timing.

As many of you know, we're conducting a study on #LMHRs (link later in thread) who not only have extremely high #LDL #Cholesterol, but many (likely most) have diets quite contrary to this advice by the @American_Heart.

Let's unpack...
2/ First, and most importantly, we do not know what the outcome of this prospective study is. So while I'll be outlining commonalities we observe with #LMHRs, this isn't an explicit endorsement of the diet nor any altered lipid levels as a result.

With that said...
3/ We have a lot of data between our standing survey, submissions to CholesterolCode.com, and CC and LMHR Facebook groups (7.7k and 7.5k members, respectively).

Diets are often:
1) Low to no fruits & veg
2) Low to no grains
3) High animal protein
4) Low in plant oils
Read 6 tweets
22 Oct
1/ 👉 "HDL Triglycerides"
or rather HDL-TG
-- As in, triglycerides onboard HDL particles

↗️ Highly associated with: total TG, glycerol, fatty liver index. ↘️Opposite w/ HDL-C/-P

And ofc 👉"Patients with carotid plaques also showed higher HDL-TG."...

pubmed.ncbi.nlm.nih.gov/31252694/
2/ @josefagirona, @lluismasana et al conclude the abstract with:

"HDL-TG should be considered a biomarker of metabolic and cardiovascular risk and could be a marker of HDL dysfunction."

If I can offer a different hypothesis (again, consistent with the #LipidEnergyModel)...
3/ Consider these HDL particles with higher levels of triglycerides aren't really that unique.

They more likely a downstream result of metabolic dysfunction as opposed to a distinct species of particle.
Read 8 tweets
12 Oct
1/ Posting this hypothesis for posterity:

I now suspect #PlantBasedLowCarb (PBLC) isn't as low carb as originally thought.

Before getting started in this thread, I should emphasize I wouldn't consider this a good or bad thing in and of itself, but it is of interest, ofc... Image
2/ Moreover, I've regularly pointed to people following my work who are both (1) very interested in a low carb diet, but (2) would prefer to keep their #LDL low to consider PBLC as a "third option", as I commonly see it associates with this outcome.

Now to my hypothesis...
3/ PBLC generally has two major features separating it from "typical" #keto/#lchf:

1) More fat sourced from mono and polyunsaturated fatty acids (M/PUFA) instead of saturated fatty acids (SFA)

2) A lot more soluble and insoluble fiber via plants
Read 11 tweets
25 Sep
1/ New #LipidEnergyModel video on ANGPTL proteins via @nicknorwitz

And a few added thoughts...

ANGPTLs are *all* inhibitors. They are applying the breaks to the Lipoprotein Lipase (LPL) in particular.

So consider this analogy...
2/ Imagine a room full of people at tables being served with trays of food regularly coming from the kitchen moved around the room by waiters.

No one is particularly famished, but they aren't especially full either, so they are absently taking food off the trays to maintain...
3/ However, a few guests at one table leave to get some exercise and return quit hungry.

And here's the catch: You can't tell specific people to do specific things (including the waiters), but you can say things to the entire room. Is there a way to solve this puzzle?
Read 5 tweets

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