LONGECITY

Low-density lipoproteins (LDL cholesterol) are involved in the progressive damage to blood vessel walls that leads to atherosclerosis. The initial presence of oxidatively damaged LDL can cause a cascade of inflammation responses and further retention of LDL in the inflamed area. Macrophage cells arrive to clean up, some of which are overwhelmed by the amount of LDL to deal with and die. Their debris attracts more macrophages and changes local cell behavior, and all of this leads to a dysfunctional remodeling of the blood vessel wall and eventual growth of fatty plaques that can block the blood vessel or break off to cause a blockage elsewhere.

One source of damaged LDL is the small population of cells with dysfunctional, damaged mitochondria that exist in older people. Getting rid of those through some form of repair treatment yet to be developed would help the issue. The authors of this open access review paper propose interfering elsewhere in the process, targeting the molecular biochemistry involved in other aspects of damaged LDL behavior in the blood vessel wall:

An early sign of atherosclerosis is the accumulation of LDL-derived lipid droplets in the arterial wall. According to the widely accepted 'response-to-retention hypothesis', LDL binding to the extracellular matrix proteoglycans in the arterial intima induces hydrolytic and oxidative modifications that promote LDL aggregation and fusion. This enhances LDL uptake by the arterial macrophages and triggers a cascade of pathogenic responses that culminate in the development of atherosclerotic lesions. Hence, LDL aggregation, fusion, and lipid droplet formation are important early steps in atherogenesis.

Although the molecular mechanism of LDL retention and lipid droplet formation in the arterial subendothelium is not fully understood, it is increasingly clear that aggregation and fusion of modified LDLs prevent their exit from the arterial wall and contribute to atherogenesis. In contrast to modified LDLs, native LDLs do not readily aggregate or fuse under physiological conditions, suggesting that lipoprotein modifications drive these transitions. Many aspects of these reactions remain unclear, e.g., how do the apparently disparate chemical or physical modifications exert similar structural responses in LDL? Is there a synergy among numerous factors that influence LDL fusion? Which enzymatic or nonenzymatic modifications are particularly important in promoting or preventing LDL fusion in vivo? What are specific steps in LDL aggregation, fusion, and lipid droplet formation, and what therapeutic agents can block these pathogenic processes? These and other unanswered questions reflect the fact that atherosclerosis is a very complex chronic disease that can be influenced by an immense number of factors, many of which are not well understood.

Link: http://www.ncbi.nlm....les/PMC4154560/

What about preventing the oxidation of LDL?

Vit E, (I think getting all 8 forms is important?) Vit A, Vit K seem to be what nature intended to do the job, but  they could use some help I think:

Astaxanthin, cell membrane nutrient with diverse clinical benefits and anti-aging potential.
"...This molecule neutralizes free radicals or other oxidants by either accepting or donating electrons, and without being destroyed or becoming a pro-oxidant in the process. Its linear, polar-nonpolar-polar molecular layout equips it to precisely insert into the membrane and span its entire width. In this position, astaxanthin can intercept reactive molecular species within the membrane's hydrophobic interior and along its hydrophilic boundaries...
...In double-blind, randomized controlled trials (RCTs), astaxanthin lowered oxidative stress in overweight and obese subjects and in smokers. It blocked oxidative DNA damage, lowered C-reactive protein (CRP) and other inflammation biomarkers... Astaxanthin lowered triglycerides and raised HDL-cholesterol in another trial and improved blood flow in an experimental microcirculation model. It improved cognition in a small clinical trial and boosted proliferation and differentiation of cultured nerve stem cells. In several Japanese RCTs, astaxanthin improved visual acuity and eye accommodation. It improved reproductive performance in men and reflux symptoms in H. pylori patients. In preliminary trials it showed promise for sports performance (soccer). In cultured cells, astaxanthin protected the mitochondria against endogenous oxygen radicals, conserved their redox (antioxidant) capacity, and enhanced their energy production efficiency. The concentrations used in these cells would be attainable in humans by modest dietary intakes. Astaxanthin's clinical success extends beyond protection against oxidative stress and inflammation, to demonstrable promise for slowing age-related functional decline.
http://www.ncbi.nlm....pubmed/22214255

Astaxanthin: a novel potential treatment for oxidative stress and inflammation in cardiovascular disease.
"...Results from multiple species support the antioxidant/anti-inflammatory properties of the prototype compound, astaxanthin, establishing it as an appropriate candidate for development as a therapeutic agent for cardiovascular oxidative stress and inflammation..."
http://www.ncbi.nlm....pubmed/18474276

Astaxanthin in cardiovascular health and disease.
"...Experimental investigations in a range of species using a cardiac ischaemia-reperfusion model demonstrated cardiac muscle preservation..."
http://www.ncbi.nlm....pubmed/22349894

Reversing arterial plaque
http://www.longecity...rterial-plaque/

I cant help thinking C60oo may be an even more effective cell membrane antioxidant and wondering again about a synergy with Astaxanthin?

http://www.longecity...ndpost&p=548381
http://www.longecity...ndpost&p=549575
http://www.longecity...ndpost&p=549745

http://www.longecity...burn-yesterday/


Then there is the controversial BHT and BHA (no it wont cause cancer)
http://www.ncbi.nlm....pubmed/11156442
http://www.sciencedi...014579389804569
http://augmentinforc...ALTH EFFECT.htm