I really enjoyed this interview with Joeseph of the What I’ve Learned Youtube channel. It has a whopping 850k subscribers and thus many, many new people will be exposed to this research to better understand cholesterol — especially as it relates to the low carb ketogenic diet.
We manage to get into the basics of the energy model and touch on risk as well. If you’re new here and you’d like to learn more, you might want to check out another video interview I had a couple months ago with DietDoctor.com. There’s also an excellent, illustrated Simple Guide to Cholesterol on Low Carb series.
And as always, feel free to plug in your own cholesterol numbers for our risk calculator and/or ask questions at our questions page. Or just comment down below.
Hi Dave and Siobhan,
Have either of you seen this study before? It is entitled “Hepatic secretion of VLDL fatty acids during stimulated lipogenesis in men”. Five healthy men were studied in the basal state, and 1 and 4 days after the start of a hypercaloric carbohydrate-enriched diet (2.5 times energy expenditure). Here is a link to it.
http://www.jlr.org/content/39/6/1280.full.pdf
I would be interested in hearing what you think of it with respect to your energy transport model.
Thanks … Ray
I don’t believe so! Thanks for the excellent link. I have put it on my list to read and discuss with Dave, though so I will get back to you once I’ve done that. 🙂
Sounds good … thanks.
Have you or Dave heard of the theory that that heart disease is really just a case of slow motion scurvy due to inadequate Vitamin C. The last entry on this web site page (https://zonulintightjunction.com/heart-disease-1) has a pdf that summarizes the history of the cholesterol theory of heart disease and then it goes on to discuss the relationship between LPa and Vitamin C. Sounds like a good N=1 experiment for you or Dave … increase your Vitamin C intake to see how it affects your LPa. If you want to try it there is a pharmacokinetics chart in the Vitamin C section of the same web site (zonulintightjunction.com) that can help you decide on the correct oral vitamin C dose.
Yes, I’ve heard of it. I’d imagine any protocol that either directly damages the arteries, or results in impaired ability to heal damage in the arteries would raise lipoprotein(a), as it is an acute phase reactant (inflammation high = lipoprotein(a) higher from baseline) and is involved in wound healing. This would be doable by inducing subclinical scurvy in mice (as I believe was originally done). However, if subclinical scurvy is causing high lp(a) in humans, taking vitamin C should lower it, as you said. But there’s no need for to try it – it has been done already – and it does not work.
Based on that, I haven’t seen good evidence of it being “the” explanation for lp(a). I do however think it’s plausible you could cause higher lp(a) by inducing scurvy, as it would lead to damaged or improperly healed arteries. But, I speculate, so would eating a diet (or doing other things) that causes damaged arteries in other ways. And there does appear to be some good evidence for a genetic baseline, as well, plus other contexts factoring in. Does that make sense? 🙂