Note that 'cholesterol' again shows itself up as the correlational junk science that it is. But let's look at an excerpt of their conclusions (my emphasis included). This is VERY interesting:
“Studies have shown that the administration of inflammatory mediators outside the arterial adventitia leads to immune cell invasion, increases in intimal thickness, and arterial remodeling (40,41) and increased coronary vasa vasorum neovascularization PRECEDES endothelial dysfunction in swine fed a high-cholesterol diet (42,43). These data suggest that local adipokines from EAT could diffuse into interstitial fluid across the adventitia into the vascular wall by paracrine factors or be directly transported into downstream coronary arteries by vasocrine factors (i.e. via the vasa vasorum). This hypothesis supports a notion of outside to inside signaling of atherosclerosis, in which the inflammatory milieu in EAT promotes the development and progression of CAD. Recently, in atherosclerotic swine, McKenney et al11 clearly showed that EAT excision attenuated the progression of CAD, but their observation did not have a clear mechanistic link. Here, we provide critical data on EAT signaling mechanisms underlying CAD.”
Interesting indeedy. Time is brief here so I'll give my top-level takeaways:
1. Vitamin D deficiency seems to has a dramatic effect on Atherosclerosis progression, like a 'root cause' should if it is valid (I have some quibbles that their diets do not seem to be identical outside of the D factor though)
2. They clearly provide support for Subbotin's hypothesis of vasa vasorum being pivotal in atherosclerosis progression - and add other 'outside-in' mechanisms of acceleration from the external surface of the arteries (i.e. NOT the endothelial-ingress concentration gradient stuff that many of us have struggled with)
3. They leave ApoB out of the discussion - fair enough. It's not a 'root cause' that can be changed in magnitude to assess its contribution. In it's native (non-damaged) self It's not really a 'cause' as such by my definition - even though it has mechs in the athero game, and it is supported by much 'correlational' data (although much of this correlation was likely gifted by the insulin resistance which drives both it and athero acceleration up together - sneaky stuff - see: http://www.thefatemperor.com/blog/2015/5/5/hilarious-apob-now-being-used-as-predictor-of-insulin-resistance-cholesterol-lchf).
I'll also direct interested parties to this post, for further ruminations on ApoB as a 'cause'. Real 'causes' stand up to case-control and other scrutiny - but correlational ones don't:
...and of course an overview of Subbotin's atherosclerosis mechanisms paper - I am still waiting for anyone to give a reason or two why Subbotin may be incorrect. After this pig study, the reasons would want to be pretty solid indeed...