The conventional CVD/lipid hypothesis: challenged

The conventional mainstream lipid hypothesis suggests high cholesterol is directly associated with elevated CVD risk. High plasma cholesterol diffuses into the endothelial space via the LUMEN, and initiates atherosclerosis.

https://en.wikipedia.org/wiki/Lipid_hypothesis

There are many fallacies of this mainstream theory.

A very LITTLE known paper from 2012 actually proves that CVD initiates from the INSIDE, namely, the adventitial vasa vasorum, and NOT the interior lumen side!
 

Neovascularization of coronary tunica intima (DIT) is the cause of coronary atherosclerosis. Lipoproteins invade coronary intima via neovascularization from adventitial vasa vasorum, but not from the arterial lumen: a hypothesis

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3492120/pdf/1742-4682-9-11.pdf

Summary

(1) A hypotheses underlining our efforts to approach coronary atherosclerosis must

be consistent with undisputed facts concerning the subject. Furthermore, a hypothesis

should incorporate logical evaluation, and not contradict established and proven

concepts in biology and medicine without well-grounded reasons.

(2) Atherosclerosis occurs in arteries with normal DIT, while sparing the rest of

arterial bed. However, while normal DIT exists in numerous arteries [120,194], some

of these are never affected by atherosclerosis; coronary arteries are almost always the

target. On logical grounds, an arterial disease that never affects some arteries but

usually affects certain others is not systemic.

(3) Coronary atherosclerosis is not an inflammatory disease, as multiple clinical trials

demonstrate no correlation between anti-inflammatory therapies and risk of disease.

(4) High LDL levels are not a fundamental cause of coronary atherosclerosis, as

lowering such levels protects only 30-40% of those at risk. Furthermore, humans and

animals with normal LDL levels can suffer from coronary atherosclerosis.

(5) Neovascularization of the normally avascular DIT is the obligatory condition for

coronary atherosclerosis development. This neovascularization originates from

adventitial vasa vasorum and vascularizes the outer part of the coronary DIT, where

LDL deposition initially occurs.

(6) It is suggested that excessive cell replication in DIT is a cause of DIT

enlargement. Participation of enhanced matrix deposition is also plausible. An increase

in DIT dimension impairs nutrient diffusion from the coronary lumen, causing

ischemia of cells in the outer part of coronary DIT.

(7) Ischemia of the outer DIT induces angiogenesis and neovascularization from

adventitial vasa vasorum. The newly formed vascular bed terminates in the outer part

of the coronary DIT, above the internal elastic membrane, and consists of permeable

vasculature.

(8) The outer part of the coronary DIT is rich in proteoglycan biglycan, which has a

high binding capacity for LDL-C. While in avascular DIT, biglycan has very limited

access to LDL-C due to diffusion distance and LDL-C properties; after

neovascularization of the outer DIT, proteoglycan biglycan acquires access to LDL-C

particles, and extracts and retains them.

(9) Initial lipoprotein influx and deposition occurs from the neovasculature

originating from adventitial vasa vasorum - and not from the arterial lumen.

(10) Although lipoprotein deposition in the outer part of the coronary DIT is the

earliest pathological manifestation of coronary atherosclerosis, intimal

neovascularization from adventitial vasa vasorum must precede it.

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I will posit that it's INSULIN RESISTANCE that is the core initiation of this neovascularization. 

https://high-fat-nutrition.blogspot.com/search?q=subbotin

"There are several things which spring to mind about DIT, insulin and oxygenation. If, as I think likely, a general thickening occurs under the effect of chronic hyperinsulinaemia acting on the ILGF-1 receptors which are on the lookout for platelets, we have a reason why insulin, not glucose, drives CVD. Anything which hastens thickening of the tunica intima hastens CVD. Insulin"