Diseased arteries found to be prematurely aged
The results of a study published in the July, 2006 issue of the journal Circulation Research found that heart disease prematurely ages the arteries to the equivalent of up to forty years older than the age of the patient.
In research funded by the British Heart Foundation, Professor Martin Bennett and colleagues at the University of Cambridge studied vascular smooth muscle cells (VSMCs) in normal and diseased arteries derived from heart bypass and transplant patients. The team found an increase in telomere damage in the DNA of cells derived from diseased arteries. Telomeres are caps at the ends of chromosomes that shorten with cell division and cellular aging. Dr Bennett’s team discovered that telomere shortening was significantly associated with increasing atherosclerosis severity. “This is the first study that has mapped the extent of aging in the artery,” Professor Bennett announced. “It's like an archaeological dig. If you take a cross section of the artery, the further you dig down the more aged the cells are.”
Because the artery cells of heart disease patients divide 7-13 times more often than normal cells, the cells rapidly run out of their predetermined division times, resulting in premature arterial aging. This renders the arteries less able to prevent atherosclerotic plaque formation. “In early stages of heart disease, the arteries are between 5-15 years older than the person's real age,” Professor Bennett explained. “If you have mild heart disease and can limit your risk factors by stopping smoking, controlling hypertension and diabetes, and taking statins to lower cholesterol, you will slow this aging process. If you do nothing, the cells can reach extreme old age very prematurely – and once it does that, the process cannot be reversed.”
The researchers found evidence of oxidative DNA damage in vascular smooth muscle cells derived from plaque, which suggests that telomere damage could be caused by oxidative stress. Addition of oxidants to the cells induced premature aging with accelerated telomere shortening. The authors conclude that “Human atherosclerosis is characterized by senescence of VSMCs, accelerated by oxidative stress-induced DNA damage, inhibition of telomerase and marked telomere shortening.”
British Heart Foundation medical director Professor Peter Weissberg stated, “One of the defining features of aging tissues is an inability to repair themselves efficiently: the older the tissue, the less able it is to deal with physical or biochemical injury. This research suggests that if blood vessel cells could be prevented from aging so quickly, then potentially heart attacks could be prevented.”
Interestingly, only about half the people with coronary artery disease have more traditional risk factors, such as elevated cholesterol, smoking, high blood pressure, and obesity. Yet all patients with atherosclerosis suffer from endothelial dysfunction and the damaging effects of oxidized LDL, which provides an important building block for plaque deposits. Antioxidant therapy is therefore important to limit the oxidization of LDL and improve the health of the endothelium by limiting the damage caused by inflammatory cytokines.
Vitamin E is often studied in conjunction with vitamin C for its potent antioxidant powers. It has been shown to decrease lipid peroxidation and inhibit smooth muscle cell proliferation, platelet aggregation, monocyte adhesion, oxidized LDL uptake, and cytokine production—all of which occur during atherosclerosis (Munteanu A et al 2004; Harris A et al 2002). In cultured arterial endothelial cells, vitamin E increased the production of prostacyclin, a potent vasodilator and inhibitor of platelet aggregation (Wu D et al 2004). Most vitamin E supplements come in the form of alpha tocopherol. Life Extension recommends about 400 IU alpha tocopherol a day, along with at least 200 mg gamma tocopherol and 100 mg of coenzyme Q10. There is a concern that taking only the “alpha” form of vitamin E could deplete the body of gamma tocopherol, a critically important antioxidant. Coenzyme Q10 helps regenerate oxidized vitamin E in the body.
September 29, 30 and October 1, 2006
2006 World Health Freedom Assembly will be an historic gathering of health freedom leaders from around the world. National Health Freedom Coalition (NHFC), as host of the Assembly, will invite health freedom non-profit organizations participate in a formal Round. This Assembly will create and endorse a “Declaration of Health Freedom” that reflects the right of all people to access the information, products, and practitioners that they desire when bringing themselves into a state of wellness.
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