Unhealthy lifestyle accelerates cellular aging, resulting in heart attacks

Robin Wulffson MD's picture
aging, heat attack, coronary heart disease, telomeres, smoking, obesity
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COPENHAGEN, DENMARK - All individuals age; however, some age more rapidly than others. Although this is partly due to genetics, environmental factors and lifestyle choices, such as smoking and obesity, play a role. In addition, poor lifestyle choices increase the risk of heart attacks and early death.

Chromosomes, which are contained in the cell nucleus, contain telomeres, which are a sequence of DNA material at the end of the chromosome. Telomeres protect the end of the chromosome from deterioration or from fusion with neighboring chromosomes. These telomeres shorten over time; however, smoking, obesity, and other poor lifestyle choices accelerate the process.

For decades, scientists have theorized that the shortening of telomeres increases the risk of heart attack and early death. According to a large new study, a direct link exists between these poor lifestyle choices and cellular health. In addition, the study provides methodology to evaluate an individual’s cellular health.

A research team led by Professor of Genetic Epidemiology Borge Nordestgaard at the University of Copenhagen used data from the Copenhagen General Population Study, which comprised 19,838 Danes; some were followed for almost 19 years. The researchers isolated each individual’s DNA and analyzed their specific telomere length.

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"The risk of heart attack or early death is present whether your telomeres are shortened due to lifestyle or due to high age," noted Professor Nordestgaard. He added, "That smoking and obesity increases the risk of heart disease has been known for a while. We have now shown, as has been speculated, that the increased risk is directly related to the shortening of the protective telomeres––so you can say that smoking and obesity ages the body on a cellular level, just as surely as the passing of time."

The researcher found that 25% of the subjects had telomeres of such a short length that not only would they statistically die prematurely but also have an almost 50% increase in the risk of a heart attack. Professor Nordestgaard said, "Future studies will have to reveal the actual molecular mechanism by which the short telomere length causes heart attacks." He posed the question, "Does one cause the other or is the telomere length and the coronary event both indicative of a third–– yet unknown ––mechanism?"

A possible major benefit of the study is that the blood tests used by the researchers could be conducted in the clinical situation. Physicians could order simple blood tests, which would reveal the patient’s telomere length; thus, determining cellular wear and age.

The study "Short Telomere Length, Myocardial Infarction, Ischemic Heart Disease, and Early Death ” is currently available online at this link. It is scheduled for publication in the March issue of the journal Arteriosclerosis, Thrombosis and Vascular Biology published by the American Heart Association.

Coronary heart disease is responsible for almost 25% of deaths in the United States and is the leading cause of death for both men and women. Every year about 785,000 Americans suffer their first heart attack. Another 470,000 who have already suffered one or more heart attacks have another attack.

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