I’m giving the reddit link which has the article link, because one of the comments has a good chunk of text posted in
Interesting. I’m going to have to sit down and read the entire paper. While it’s clear the authors haven’t yet got it completely right, they do seem to be on to something.
Full paper appears to be pay/subscription walled. However, there are these comments, the first from Dave Feldman:
SFAs play the leading role in 1 of the greatest controversies in nutrition science. Relative to PUFAs, SFAs generally increase circulating concentrations of LDL cholesterol, a risk factor for atherosclerotic cardiovascular disease (ASCVD). However, the purpose of regulatory mechanisms that control the diet-induced lipoprotein cholesterol dynamics is rarely discussed in the context of human adaptive biology. We argue that better mechanistic explanations can help resolve lingering controversies, with the potential to redefine aspects of research, clinical practice, dietary advice, public health management, and food policy. In this paper we propose a novel model, the homeoviscous adaptation to dietary lipids (HADL) model, which explains changes in lipoprotein cholesterol as adaptive homeostatic adjustments that serve to maintain cell membrane fluidity and hence optimal cell function. Due to the highly variable intake of fatty acids in humans and other omnivore species, we propose that circulating lipoproteins serve as a buffer to enable the rapid redistribution of cholesterol molecules between specific cells and tissues that is necessary with changes in dietary fatty acid supply. Hence, circulating levels of LDL cholesterol may change for nonpathological reasons. Accordingly, an SFA-induced raise in LDL cholesterol in healthy individuals could represent a normal rather than a pathologic response. These regulatory mechanisms may become disrupted secondarily to pathogenic processes in association with insulin resistance and the presence of other ASCVD risk factors, as supported by evidence showing diverging lipoprotein responses in healthy individuals as opposed to those with metabolic disorders such as insulin resistance and obesity. Corresponding with the model, we suggest alternative contributing factors to the association between elevated LDL cholesterol concentrations and ASCVD, involving dietary factors beyond SFAs, such as an increased endotoxin load from diet–gut microbiome interactions and subsequent chronic low-grade inflammation that interferes with fine-tuned signaling pathways.
Everyone repeat after me: saturated fats DO NOT cause heart disease.
I haven’t been able to get the article, the normal source did not work. Not sure how Dave got the article.
George Hendersen filed a “rapid response”, too. (@puddleg on Twitter)
However, George often cites to studies where overweight people don’t get an increase in LDL from saturated fat and also no increase in LDL if fasting multiple days. He says that an increase in LDL is a normal response to saturated fat, and no increase is an aberrant response.
For me, I don’t seem to get an increase in LDL with saturated fat, but I DO get an increase in LDL when I fast. So, my results don’t agree with the studies he cites.
I don’t think it’s possible to get everything right. It’s like trying to find one theory covering Einstein’s general theory of relatively (large objects like planets) and quantum theory (atoms and smaller). Maybe there is no single theory able to cover both?
I think Dave’s theory of the energy lipid model is correct. But lipids are also involved in the immune system, and potentially numerable other body processes. And even within Dave’s theory, where there are lean mass hyper-responders, why don’t all lean people who are exercising a lot get the same response?
My theory for a while now is not that saturated fat causes “cholesterol” to go up, but that polyunsaturated fat causes “cholesterol” to go down. And that’s what they say.
Unfortunately, It doesn’t segue well with Dave’s theories.