The prime risk factors for heart disease are well known—obesity, smoking, elevated cholesterol, and high blood pressure. Yet many people with these warning signs develop heart problems, while others don’t. This observation indicates that yet-unrecognized factors must also influence risk.
A new study finds that the sequence-repeating sections of DNA called telomeres, which protect the ends of chromosomes, might play a role. Middle-aged men with long telomeres are only half as likely to develop heart disease as are men of the same age with short telomeres, researchers report in the Jan. 13 Lancet.
Telomeres buffer chromosomes’ tips much as plastic caps preserve the ends of shoelaces. But telomeres get shorter with each successive division of a cell, and too-short telomeres ultimately leave a cell unable to replicate.
In the new study, Nilesh J. Samani, a cardiologist at the University of Leicester in England, and his colleagues assessed telomere length in the white blood cells of Scottish men entering a trial of the cholesterol-lowering statin drug pravastatin (Pravachol). The 6,595 participants averaged 55 years old, and all had elevated blood concentrations of low-density lipoprotein (LDL), the bad cholesterol. Researchers randomly assigned them to receive pravastatin or a placebo.
Over the next 5 years, 484 of the men developed heart disease. Samani and his cohorts identified 1,058 other study participants who matched those men in age and smoking status but who remained free of heart problems.
The researchers found that among the men getting the placebo, those with short telomeres were roughly twice as likely to develop heart disease as men with long telomeres were.
The statin drug seemed to remove this distinction. Regardless of their telomeres’ lengths, men taking pravastatin developed heart disease at the same rate.
Among the men with long telomeres, receiving the drug didn’t affect heart disease incidence.
Short telomeres “may provide an explanation for unexplained heart problems,” Samani says. But he cautions that this study offers only an association between telomere length and heart disease, not proof that long telomeres are protective.
Past research has linked chronic inflammation to heart disease (SN: 6/4/05, p. 365: Available to subscribers at Inflammation inhibitor may limit heart attacks). Shortened telomeres in white blood cells might induce those immune cells to trigger inflammation, surmise Ioakim Spyridopoulos and Stefanie Dimmeler of the University of Frankfurt in Germany, also writing in the Jan. 13 Lancet. They suggest that short telomeres might also prevent nascent blood vessel cells from fending off atherosclerosis, a major form of heart disease.
Stress, obesity, and insulin resistance may shorten an individual’s telomeres (SN: 12/4/04, p. 355: Stressed to Death: Mental tension ages cells; 6/11/05, p. 381: Available to subscribers at Obesity and insulin resistance age cells). Other lines of research suggest that shortened telomeres might result from the accumulation of free radicals, which are reactive oxygen or nitrogen molecules that can damage cells.
Heart disease will ultimately involve “more variables than we know, and telomeres may be one of them,” says Kathleen Collins, a molecular biologist at the University of California, Berkeley.