Hydraulic stress in thrust fittings and accelerating curves of arterial system generate inflammatory gene expression

Normal mice just don't get atherosclerosis.  Just never.  In every lab on Planet Earth, these hardy beasts must be genetically handicapped in ways that humans never are, and then poisoned with massive doses of lard or high blood pressure hormone to induce a similar pathology to that which develops in humans over decades (not overnight).  When the LDL cholesterol receptor is ablated, and then these mice insulted with the lard or AngII, they exhibit a pattern of inflammation in their arteries at the high pressure regions, the branches or "thrust fitting" joints as a master plumber would call them or in high acceleration curves.  At these points, white blood cells stick to the intimal surface, forming the first lesions of atherosclerosis called foam cell lesions that look like butter from afar, but under the microscope are distinctly living white blood cells.  As things progress further, these cells may die leaving a trash dump of necrotic debris including the accumulated cholesterol delivered via lipoproteins.

The NF-κB signal transduction pathway in aortic endothelial cells is primed for activation in regions predisposed to atherosclerotic lesion formation

The lesions don't happen haphazardly and randomly, but predictably in mechanical stress sites where inflammatory gene expression is activated, consequently drawing the ire of our own immune system cells and acute phase reactants.

The first barrier to the living wall of muscle cells of the artery are the endothelial cells that sit happily on top of their collagen basement membrane, in tight formation with not much that can slip through their cell junctions bigger than small organic molecules.  When there is damage, either directly to an endothelial cell, causing endothelial denudation, or by well meaning white blood cells causing collateral damage, the collagen membrane floor is revealed, which is sticky to many problematic things including the infamous Lp(a) which sticks to exposed lysyl residues of collagen strands.  The wall is then vulnerable to insudation by clotting systems as they should or activated platelets that stick to collagen.

To prevent all this from occurring, the thing to do would be to dial down the inflammatory signals that turn on NF-Kappa Beta, a ubiquitous nexus and hub for many inflammatory processes both useful and malignant.

As you might have guessed, there are nutritional means to do this without relying on hazardous, poisonous, expensive, and annoying prescription drugs, none of which are designated as specific NF-kappa B inhibitors anyways.

For example,
Antioxidants like Vitamin C can turn this switch off
Molecules from herb extracts can turn this switch off.
simple amino acids can halt this stress signal.
Resveratrol can turn this switch off.

and many other functional foods...