Premature Aging of Cells
Linked to Artery Disease
Excerpt By Merritt McKinney, Reuters Health Writer

NEW YORK (Reuters Health) - The artery disease atherosclerosis could be linked to premature aging, a report from the UK suggests.

Researchers at the University of Leicester have found that people with coronary artery disease tend to have shorter telomeres--bits of DNA at the end of chromosomes that shorten as cells age--compared with people with healthy arteries. Eventually, telomeres become so short that cells can no longer divide, which leads to cell death.

Compared with 20 healthy patients, 10 patients with severe atherosclerosis had telomeres in white blood cells that looked like telomeres belonging to people nearly 9 years older than they were, Dr. Nilesh J. Samani and colleagues report in the August 11th issue of The Lancet.

``The question our observation raises is, why should circulating white cells of patients with disease in their coronary arteries have shorter telomeres making them 'look' like normal people almost 9 years older?'' Samani said in an interview with Reuters Health.

One possibility, according to Samani, is that telomeres are shortened by risk factors for coronary artery disease, such as diabetes or high blood pressure.

``If this is the case, then it can be regarded simply as a bystander consequence of the disease process,'' Samani said.

On the other hand, the UK researcher pointed out, it is possible that people with diseased arteries have pre-existing shortened telomeres, either as a result of genetics or from an excessive turnover of cells in early life.

There are two pieces of evidence that support this idea, Samani suggested. The first is that there is an ``unexplained genetic tendency to coronary artery disease'' in some people. The second is that people who weigh less than average at birth and go through ``catch-up growth'' in childhood--which increases body cell turnover--are more likely to develop coronary artery disease than people of normal birth weight.

``Since telomeres affect cellular function, could our observation bring together a number of different strands of the pathogenesis of coronary artery disease under a unifying...mechanism?'' Samani asked.

``This is, of course,'' he continued, ``all speculative at this stage, but this is the reason for our excitement regarding the finding.''

SOURCE: The Lancet 2001;358:472-473.

Reference Source 89

For more information on how to prevent other diseases, use
PreventDisease.com's "Quick Prevention Resources".