"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.
4/ They will coincide with many other aspects of metabolic syndrome, and this includes aspects common to atherogenic dyslipidemia bloodwork: Higher CETP activity, VLDL-TG, Lower HDL-C (And to get extra technical, higher % ≤HDL3 vs ≥HDL2 subtypes)
5/ Why?
I'd posit these are all typically consistent with failed delivery of triglycerides to tissues in the periphery, resulting in lipoproteins (both ApoB and ApoA-1) that have higher TG and lower cholesterol content that would be found in healthier metabolisms.
6/ Plainly stated, I believe it's much more likely the case these lipid and lipoprotein levels are generally a reflection of disease state than a driver of it.*
(*As always, I'd caveat we can have exceptions in genetic abnormalities as well)
7/ As it happens, @lluismasana also released the study on HDL and TG association with #Covid19 outcome severity. (Ironically, this was something I was long requesting since the pandemic began)
8/ I'm fortunate to be working with @nicknorwitz and @Ad_SotoMota on the #LipidEnergyModel and how it may better explain these and other phenomena where looking to lipid and lipoprotein patterns such as these.
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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...
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
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?
1/ Okay, finally getting around to this experiment video by @ScepticalDoctor
Naturally, this has many things I'm interested in -->
- N=1
- #Lipids (esp #Cholesterol)
- and not least of all, Anna and I have many respectful, kind debates (more of that plz, #NutritionTwitter)
1/ Yes, my answer to the poll by @nicknorwitz was "Gain 4% body fat". And honestly, it was a pretty easy one when compared to the others.
But to be fair, I also have quite a bit of direct data on this in particular... let's unpack...
2/ First, if you didn't already know this about me, in 2018 I literally gained almost 20lbs of fat for the Weight Gain Experiment. cholesterolcode.com/weight-gain-ex…
(As an aside, I realize now I did presentations on the findings for this experiment, but didn't do a write up. Bad Dave!)
3/ But spoiler alert -- my total and LDL cholesterol did indeed go down where having gained weight and back up where having lost it.
To be sure, I think there are thresholds to "active fat gain/loss" vs standing, stable fat mass, but we'll save that for another thread.
I'm going to provide some updates and answers to frequent questions of the last several days...
2/ "Dave, can you get me in the study?"
No! You have to contact Lundquist directly through the proper channels and they will decide based on the study design whether you qualify as prescribed by existing eligibility criteria we all determined in advance.
3/ While myself, @DrNadolsky and @DrRagnar developed the protocol in collaboration Lundquist, we in no way can (or should) influence any decision making regarding individual considerations -- and that's a good thing. We want this study as fair and objective as possible.
2/ "Lipoprotein lipase (LPL) is a rate-limiting enzyme for hydrolysing circulating triglycerides (TG) into free fatty acids that are taken up by peripheral tissues."
Translation: LPL is like a key cells use to open lipoprotein boats to offload their fat-fuel cargo (TG)
3/ "Postprandial LPL activity rises in white adipose tissue (WAT), but declines in the heart and skeletal muscle, thereby directing circulating TG to WAT for storage; the reverse is true during fasting"
Sure, post-meal we do more storing in fat via LPL, otherwise we do less.