New research published in the Lancet medical journal last week shows a potential new way to identify people who have a higher risk of heart disease.
Telomeres are the strands of DNA that cap and protect our chromosomes. They act as a kind of cellular clock, marking the number of times a cell has replicated its genetic material. Each time a cell divides to make two new cells, its telomeres get shorter, until eventually it stops multiplying altogether. Researchers from Leicester and Glasgow Universities have now shown that the erosion of telomeres may play an important role in developing heart disease.
Researchers took blood samples from 484 men aged 45-64 with moderately raised cholesterol levels, as well as 1058 healthy control subjects and compared telomere lengths in their white blood cells both at that time and five years later. People with the shortest telomeres from either the patient or the control group were twice as likely to have developed heart disease.
The study also revealed that cholesterol-lowering drugs called statins appear to reduce the effects of telomere damage and may even guard against telomere shortening in patients with short telomeres. Nilesh Samani, who led the research at Leicester University told New Scientist 'In patients whose telomeres were wearing away at a normal rate, statin treatment didn't make any difference. This suggests that statins were protecting against the worst cases of telomere degradation. Without statins they might have been even shorter'. These discoveries provide important new insights into the causes of heart disease, which is a leading killer in industrialised countries.