Every time a cell in the body replicates, the DNA string (the telomere) at one end of the chromosome gets shorter. When it gets too short, the cell dies.
Current scientific thought holds that this process is directly related to aging. Telomere shortening happens at different rates for different people. This suggests that our chronological age (the number of years since our birth) is different from our biological age (as measured by telomere shortening).
Does our "biological age" really predict death and disease? Scott W. Brouilette, Ph.D., and colleagues have previously shown that telomere length in people who have heart attacks before age 50 and in people who are candidates for triple bypass surgery tends to be shorter than telomere length in healthy people of the same age and sex.
In their current study, the researchers looked at people enrolled in a clinical trial of the cholesterol-lowering drug Pravachol. Over five years, 484 patients developed heart disease. The researchers compared their telomere length in white blood cell DNA to that of 1,058 matched people who remained free of heart disease.
Sure enough, those who got heart disease had telomere lengths similar to those in the comparison group who were six years older. Study participants in the top third of telomere length were about 50 percent less likely to have heart disease as those in the middle or lower third in telomere length.
"Our findings lend support to the hypothesis that premature biological aging might contribute to the risk of coronary heart disease," Brouilette and colleagues suggest in the Jan. 13 issue of The Lancet.
Oddly, the heart risk seen with shorter telomere length did not increase beyond a certain point.
"This finding suggests that, especially with increasing age, there could be a threshold beyond which further shortening of telomeres does not confer additional risk," the researchers theorize.
Interestingly, Pravachol — one of the statin family of cholesterol-lowering drugs — dramatically lowered the heart disease risk of people with shorter telomeres. But the drug seemed to have little effect on heart disease risk in people with the longest telomeres.
Brouilette and colleagues suggest that statin drugs may slow biological aging not by lowering cholesterol but by increasing blood levels of a molecule that stabilizes telomeres.
The researchers suggest that by measuring telomere length, doctors could identify those patients most likely to benefit from statin treatment.
However, a Lancet editorial appearing alongside the study casts doubt on this idea.
Ioakim Spyridopoulos, M.D., and Stefanie Dimmeler, Ph.D., of the University of Frankfurt, Germany, agree with Brouilette and colleagues that biological aging could contribute to heart disease risk. But they note that different people start out life with different-length telomeres. An individual's telomere length, they suggest, says nothing about how fast that person is aging.
Looking at telomere length in a large number of people may provide insight into the relationship between biological aging and disease. But they flatly reject the idea that telomere length could predict an individual's risk of heart disease.
SOURCES: Brouilette, S.W. The Lancet, Jan. 13, 2007; Vol. 369: pp. 107-114. Spyridopoulos, I. and Dimmeler, S. The Lancet, Jan. 13, 2007; Vol. 369: pp. 81-82.
By Daniel DeNoon
Reviewed by Louise Chang, M.D