High shear stress. wait wait wait, no. Low shear stress. Wait wait. Low then high shear stress. Oh, okay high shear stress too.

The problem is that you don't have high shear stress WITHOUT high tensile strain, all while disregarding oscillatory tensile strain, pulsatile acceleration between peak systole and diastole, as well as vortice formation.

In my own opinion after carefully digesting all viewpoints, it seems that tensile stress and vortice formation are the most important damaging forces upon an artery.  Shear stress is most contradictory if you disregard vortical turbulence/stagnation, and once again, tensile strain.

Shear stress is basically "drag."  Like a hand in the wind palm forward, the drag on it is higher than when the hand is held parallel to the wind, creating less drag.  How high drag is better for the artery than low drag is explained by the high drag drawing the endothelium tight, like a comb over a dogs' fur in a straight, undeviating stroke.  Low drag is supposedly bad for an artery because it doesn't pull the cells tight.  To me that doesn't make a lot of sense, but when pulsatile flow (a slight backwards flow on diastole with a majority forward flow on systole) is taken account, that makes sense.  Also, vortical formation, is important, but these things are never mentioned in one sentence, causing major confusion.  It is not that hard to understand together, it makes it more confusing and ambiguous not to talk about all these things at once.  Low shear stress + pulsatile flow caused by a local pressure differential + vortices (tornados of the blood) cause the endothelium to become dissheveled.  Like taking your hand and making random circles in your pet's fur, this will cause the once linearly oriented cells to become haphazardly arranged rather than in the direction of the laminar flow.

It is counterintuitive.  LOW SHEAR STRESS causes atherosclerosis not high shear stress.  Studies in coronary arteries show a precise opposition between high shear areas free of plaque and the low shear area laden with plaque.  The problem most have is to confuse shear stress with tensile stress (combined radial, circumferential, longitudinal).  Like the thumb and the toe, they are absolutely different things.  But more confusing, when there is a big plaque, there is high shear stress in the throat it makes with lumenal occlusion. Then, high shear stress may rip open the plaque, causing thrombosis and downstream ischemia.  All the while, tensile stress is proportional to shear stress, and higher tensile stress causes more load on the force bearing elements of the arterial ECM, which invariably only causes one thing:  wear and tear (literally).

With venous systolic pressure up to ten times lower than arterial systolic pressure, it is not difficult to understand why arteries always endure more tensile strain.  Whatever the shear stress condition, tensile strain in the artery is always higher than in a vein, partially explaining why only thrombosis is found in veins but no plaque.  It is interesting to note that a vein placed in the coronary bed for bypass does then suffer plaque stenosis when it never did before.  What is the sudden difference?  Systolic pressure and tensile strain is much higher in the arterial bed.

Yet there are instances when high shear stress contributes to arterial damage, such as a biscupid aortic valve.

You'll see above, that the high shear stress area (which is invariably a zone of high tensile strain) coincides perfectly with proximal aortic dissection, the Stanford Type A, Debakey Type II dissection, as well as a frequent site of aortic root (not sinus) plaques.

Valve-Related Hemodynamics Mediate Human Bicuspid Aortopathy

Superb Blog of Blog: "Ancient Transporters: HDL and LDL Lipoproteins Carry Precious Cargo "

This is a scientific island of common sense worth visiting.  Extremely insightful and ties together things far apart for an understanding with "range."

http://drbganimalpharm.blogspot.com/2013/03/ancient-transporters-hdl-and-ldl.html

Bathe your insides with green plant juice.

Why would you do that???

TNF-alpha shreds your arteries and causes plaque to start forming

Chlorophyll prevents TNF-a from doing its business to you.

Therefore, green plant juice may prevent atherosclerosis.

Cholesterol does not cause atherosclerosis. Oxidized cholesterol byproducts do.

Here are a few things to keep in mind:  1) Cholesterol is not soluble in water or blood.  A derivative of cholesterol that is soluble in blood or water is not cholesterol.  2) The only way cholesterol is moved around either in the blood or as an adduct is by the action of adding a hydrophilic protein or converting free cholesterol enzymatically to a soluble form.  3) The only way cholesterol gets to an artery wall is through a lipoprotein or the soluble form made first by a cell's action upon ingested cholesterol.  4) It has already been proven that native LDL is harmless to endothelial layers even in very high concentrations of the particle and that the oxLDL particle is the one that causes havoc to the endothelial layer.

That being said, even in the most severely diseased coronary artery disease (CAD) patient with acute coronary syndrome (ACS) presenting as angina, respiratory problems, and/or MI, the level of oxLDL is 4-5mg/dL maximally.  Normally, they are half this value to none.  This value of 4-5 doesn't occur until after the coronary artery disease, so how could it be that oxLDL caused the CAD?  Temporally, and logically, oxLDL could not have caused CAD if it was absent beforehand.

There is no question that toxic adducts of cholesterol DO cause arteriosclerosis and the consequence is atherosclerosis.  Is it an inevitable event that cholesterol becomes 25-hydroxycholesterol and cholestane-3beta, 5alpha, 6beta-triol, the culprits of endothelial aggravation?  No.

It is not cholesterol, it is OXIDATION that causes these culprit oxidized cholesterol molecules to arise and cause harm.  By having administered pure non-oxidized cholesterol to the artery cells with no harm, scientists made sure of the fact as early as 1976.  Extending the first post, here are younger studies confirming the first.

Effect of auto-oxidation products from cholesterol on aortic smooth muscle cells: an in vitro study.

Cytotoxicity of oxidation derivatives of cholesterol on cultured aortic smooth muscle cells and their effect on cholesterol biosynthesis.

Ironically, the hydroxycholesterol and other oxygen adducts shut off cellular cholesterol synthesis, making the matter worse as your cells, especially the fastest dividing ones, make it for a mission critical reason.  As the repeat, "Purified cholesterol showed no cytotoxic effect and minimal inhibition of cholesterol biosynthesis"

Inhibitory effect of cholesterol oxides on low density lipoprotein receptor gene expression.

Again, after two decades, the groups repeat that ". Pure cholesterol showed only minimal inhibition."

The question of importance is how much of the toxic oxygenated cholesterol is there in food?  Who would know for something boiling around in hot oil and open air for weeks?  My guess is a significant amount of cholesterol has turned to ox-cholesterol and probably stuff like that should be avoided.  Minimally cooked foods, or fresh foods would have a minimum of this toxic cholesterol derivative.  So indeed, the way meat is cooked may be a significant way to introduce these cholesterol-oxygen problem compounds in the blood, and these are indeed soluble.
 
However, like most everything, there is a reason for this artery aggravating 25-hydroxycholesterol (immune response against viruses) to exist:

Armand-Frappier Outstanding Student Award--The emerging role of 25-hydroxycholesterol in innate immunity.

25-Hydroxycholesterols in innate and adaptive immunity.

There is an enzyme that responds to interferon by hydroxylating cholesterol.  25HC is antiviral.

Given that your blood levels of ApoB bound cholesterol are from your liver and not from a vat of oil boiling around for weeks, it would not cause any arterial injury.  This is dependent on antioxidant functions preventing oxidation.  These are enzymatic, such as PON and glutathione, and enteral/parenteral such as Vitamin C, E, and A.