Cardiovascular Disease & Oxidative Stress – How Plaques Form

I discussed the mechanisms of oxidative stress & damage in a previous post but how does that effect cardiovascular disease (CVD)?? Atherosclerosis is a buildup of plaque in the walls of arteries that, over time, can build up enough that it closes in on the opening of the artery and blood can no longer flow through in sufficient quantities to supply the tissues. This results in tissue death in the area supplied by the artery. Common examples are heart attacks & ischemic strokes. It is important to have a general understanding of atherogenesis (plaque formation) in order to understand how oxidative stress & damage can lead to these consequences. Atherogenesis is a multifactoral process and can be affected in several ways along the route to its formation.

There are essentially 3 main steps in the formation of plaques in your arteries:

1. Elevated LDL (and/or low HDL)
2. Oxidative Stress & Damage
3. Inflammation

The first risk factor is elevated LDL (Low Density Lipoprotein, aka “bad cholesterol”). We know from years of excellent data that the lower your LDL, the lower your risk for CVD. LDL is a primary component of the plaques within the arteries. We must keep it as low as possible and there are a number of ways to accomplish this goal (diet, exercise, weightloss, medications, supplements, vitamins, alcohol, etc). Cholesterol is an essential component of our cell walls and LDL helps transport that cholesterol to the cells. Too much LDL is bad, builds up, and causes damage. It gets there through a variety of mechanisms. HDL helps to remove the excess LDL – this is why having a healthy amount of HDL is essential! This is merely scratching the surface of the LDL role in atherogenesis. The take home point is that LDL builds up within the arterial wall.

Once the LDL is deposited in the wall of the artery, it is oxidized by hydrogen peroxide, superoxides, or free radicals (see the post on oxidative damage for an explanation). This oxidized LDL (termed oxLDL) is, itself, toxic to the cells and assists with damage and inflammation in the area. Macrophages respond to this damage, recognized the oxLDL as toxic, and engulf it. This causes the macrophages to become “foam cells”. Other forms of damage to LDL, as occurs in diabetes, also exist and lead to the same fate.

The inner wall of the artery, the endothelial cells, retract and expose the foam cells to the circulation which leads to cellular & humoral immunity activation (medical talk explaining the inflammation). Ironically, this is supposed to protect the artery from damage but actually increases it.

Oxidative stress is the primary mechanism for LDL damage, though other forms also exist as mentioned above. If you can reduce the oxidative stress & damage, you will decrease the amount of plaques formed and, therefore, decrease the risk of the effects of cardiovascular disease such as strokes and heart attacks.

There are different types of antioxidants. Your body produces several of them naturally. Exercise increases the activity of these endogenous antioxidants. There are also several that we need from our diet. Vitamin C, Vitamin E, beta-carotene, polyphenols, and a number of other plant phytonutrients are all antioxidants and serve to prevent oxidative stress. Because they all have different affinities for different oxidative stressors, it is important to consume a variety of different types. This is best accomplished by exercise & proper nutrition with whole foods as opposed to supplemental pills.