Arteriosclerosis refers to stiffening or hardening of the arteries where atherosclerosis, on the other hand, is a specific type of arteriosclerosis (although the terms are sometimes used interchangeably). Atherosclerosis refers to the buildup of fats and cholesterol in and on your artery walls (plaques), which can restrict blood flow. Then there is peripheral arterial disease (P.A.D.). Similarly, P.A.D. is a disease in which plaque builds up in the arteries but it also can affect the arteries that carry blood from your heart to your head, arms, kidneys, and stomach.
The etiology that sets in motion the processes that initiate the creation of arteriosclerosis may vary but there are particular pathways involved in its progression that have been solidly indentified. Inflammation is one of these processes.
Inflammation is defined as a response to injury from infectious, physical, or chemical agents. It is now widely accepted that inflammation plays a major role in the development and progression of atherosclerosis, where the initial injury is damage to the endothelial cells lining the blood vessels. Some of the factors leading to this injury include increased levels of oxidized low density lipoproteins (for instance, free radicals formed by cigarette smoking), possible infectious agents, and the shearing stress placed on endothelial cells due to hypertension.
Injury to the endothelial cell wall triggers a cascade of events and the secretion of mediators that modulates the inflammatory response. This includes the release of a variety of cytokines including TNF-α, NFκβ and chemokines such as monocyte chemoattractant protein-1 (MCP-1) and the vascular cell adhesion molecule-1 (VCAM-1). This causes an influx of leukocytes, monocytes and platelets to adhere to the cell wall, where the monocytes are then able to migrate across the endothelial barrier into the intima layer and differentiate into macrophages. The macrophages then phagocytize the increased amount of lipoproteins from the LDLs and transform into foam cells. The newly formed foam cells secrete pro-inflammatory molecules such as interleukin-1 (IL-1), interleukin-6 (IL-6), and TNF-α; all of which can contribute to additional leukocyte accumulation and induce smooth muscle proliferation and migration from the medial layer into the intima. The arterial wall begins to thicken as more LDLs are taken up by macrophages and an atheroma is formed.
Addressing endothelial damage and dysfunction in newly diagnosed cases may be the first order of business when attending to the systemic inflammation and subsequent oxidation. Something as simple as vitamin C and folic acid supplementation has been shown to reverse endothelial dysfunction in patients with coronary artery disease, probably due to its powerful antioxidative properties in the case of vitamin C and the possible modulation of homocysteine in the case of folic acid, as high homocysteine is associated with the progression of the condition.
Obviously, incorporating a more comprehensive dietary regimen which focuses on healthy anti-inflammatory fats, plenty of vegetables and a reduction in processed food such as the Mediterranean diet, can also help reverse endothelial damage while facilitating the healing process.
Astaxanthin, a pigment found in krill and some species of algae, is a powerful antioxidant that helps regulate blood lipid metabolism and prevents lipid peroxidation while also mitigating endothelial damage due to excessive oxidative stress.
Finally, in animal models, curcumin, my favorite Ayurvedic herb, has been shown be a potential therapeutic tool for its potent antioxidative and anti-inflammatory characteristics. These include the down-regulation of inflammatory cytokines, thus modulating the inflammatory pathway discussed earlier.
While prevention is always preferable to treatment, enough tools exist to help at least reduce the progression of what could well turn out to be a deadly process.
Michael Fuhrman, D.C.