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By Shane Young | October 23, 2012 |
A recent study published in the American Journal of Pathology adds to the already considerable body of evidence which suggests that inflammation is a primary cause of heart attacks and strokes.
In an article I wrote last year, Preventing Heart Disease Without Drugs, I reviewed the current scientific understanding of what causes heart disease. If you’ve been following this blog, you know that inflammation and oxidative damage – not saturated fat and cholesterol – are the primary causes of heart disease.
Inflammation is the body’s response to noxious substances. Those substances can be foreign, like bacteria, or found within our body, as in autoimmune diseases like rheumatoid arthritis. In the case of heart disease, inflammatory reactions within atherosclerotic plaques can induce clot formation.
When the lining of the artery is damaged, white blood cells flock to the site, resulting in inflammation. Inflammation not only further damages the artery walls, leaving them stiffer and more prone to plaque buildup, but it also makes any plaque that’s already there more fragile and more likely to burst.
Oxidative damage is a natural process of energy production and storage in the body. Oxidation produces free radicals, which are molecules missing an electron in their outer shell. Highly unstable and reactive, these molecules “attack” other molecules attempting to “steal” electrons from their outer shells in order to gain stability. Free radicals damage other cells and DNA, creating more free radicals in the process and a chain reaction of oxidative damage.
Normally oxidation is kept in check, but when oxidative stress is high or the body’s level of antioxidants is low, oxidative damage occurs. Oxidative damage is strongly correlated to heart disease. Studies have shown that oxidated LDL cholesterol is 8x greater stronger a risk factor for heart disease than normal LDL.
The data from this study provide further support for the “oxidative response to inflammation” hypothesis described above. The researchers found that inflammation leads to a reduction of mature collagen in atherosclerotic plaques, leading to thinner caps that are more likely to rupture. This is important because other studies have shown that it is not atherosclerosis alone, but the rupture of the atherosclerotic plaques, that causes heart attacks and strokes.
It follows, then, that if we want to prevent heart disease we need to do everything we can to minimize inflammation and oxidative damage.
By focusing on reducing or completely eliminating, when possible, the factors in our life that contribute to oxidative stress and inflammation, we can drastically lower our risk for heart disease.
For more in-depth information about each of these factors and how to minimize your risk of heart disease without drugs, please refer to Preventing Heart Disease Without Drugs.
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