1/ Initial #Lipid thoughts...
(@KevinH_PhD's new study - osf.io/preprints/nutr…)
Of course, the panels follow the pattern I'd speculate given the Lipid Energy Model (see CholesterolCode.com/model), but per the model, body fat/metb status is very relevant context, so note bf%...
(@KevinH_PhD's new study - osf.io/preprints/nutr…)
Of course, the panels follow the pattern I'd speculate given the Lipid Energy Model (see CholesterolCode.com/model), but per the model, body fat/metb status is very relevant context, so note bf%...
2/ This isn't a critique on their study design or its population. But I'd bet if this same study were performed on average or leaner/athletic types, we'd see a more pronounced shift in lipid values for each diet. (ie. See Volek and Phinney typical study population for comparison)
3/ Now, what I *do* want to highlight is the Free Fatty Acids going up much more with ABLC Diet vs the PBLF diet
Baseline 328±48
ABLC 760±48
PBLF 508±48
Yet Triglycerides fell for ABLC, increased for PBLF
Baseline 75±4.5
ABLC 63.4±4.5
PBLF 93.3±4.5
Why is this so important?...
Baseline 328±48
ABLC 760±48
PBLF 508±48
Yet Triglycerides fell for ABLC, increased for PBLF
Baseline 75±4.5
ABLC 63.4±4.5
PBLF 93.3±4.5
Why is this so important?...
4/ Free Fatty Acids (FFA or NEFA) are a key driver of Very Low Density Lipoprotein (VLDL) synthesis and secretion. It's a supply-driven process on this side of the ledger.
Much of the FFA are esterified into triglycerides at the liver and loaded as cargo on to the VLDLs...
Much of the FFA are esterified into triglycerides at the liver and loaded as cargo on to the VLDLs...
5/ Now some of those FFAs will be shuttled toward ketogenesis, of course. But is it 100% of the new excess? I certainly don't think so.
6/ Rather (as per the model) I think there's greater VLDL-TG synthesis+secretion in the liver, and greater *turnover* in delivery to peripheral tissue, resulting in higher LDL cholesterol and particle count as they are the downstream of this process.
7/ I've been on several podcasts and interviews trying to explain this and find it is the toughest part for many people to get since it takes thinking of this turnover rate as dynamic, not static.
Most people assume TG level reflect VLDL secretion, full stop. I definitely don't.
Most people assume TG level reflect VLDL secretion, full stop. I definitely don't.
8/ Usually higher TG is likewise coupled with higher FFA in metabolically unhealthy individuals. Yet we see this pattern of low TG + high FFA commonly in low carbers, and it's particularly pronounced in very fit and lean low carbers (like LMHRs).
9/ Now again, this model doesn't account for all influences on LDL that can alter it's balance as well (such as PUFAs, fiber, etc -- see )
But all else being equal, do I think most metabolically healthy subjects would see these results? Yes.
But all else being equal, do I think most metabolically healthy subjects would see these results? Yes.
10/ In case you haven't already watched it, I go into all this in depth with my recent presentation to @Stanford here --
11/ And this is what is so awesome about crossover experiments. We can test this hypothesis more at a per-person level...
Hey @KevinH_PhD -- how many of the subjects *didn't* see their LDL/ApoB levels higher on the ABLC diet relative to PBLF diet?
Hey @KevinH_PhD -- how many of the subjects *didn't* see their LDL/ApoB levels higher on the ABLC diet relative to PBLF diet?
