Gene that enlarges cholesterol particles linked to long life

CHICAGO -- One reason some people live into their 90s and beyond may be a genetic variation that makes the cholesterol particles in their blood really big.

"Supersize it" is not usually associated with good health, but evidence increasingly is showing that bigger is indeed better when it comes to the lipoprotein particles that carry cholesterol through the bloodstream.

Smaller particles, it is believed, can more easily embed themselves in blood vessel walls, contributing to the fatty buildups that lead to heart attacks and strokes.

A study in today's Journal of the American Medical Association suggests that the tendency to have large cholesterol particles can be inborn.

The study, led by Dr. Nir Barzilai, director of the Institute for Aging Research at Albert Einstein College of Medicine, found that people in their late 90s and beyond are more likely to have a gene variation that causes large particles of both HDL cholesterol -- the good variety -- and LDL cholesterol, the bad kind.

"We basically think the size is necessary for longevity," Barzilai said.

The results are intriguing and support the notion that "exceptional longevity may depend, at least in part, on inheriting 'good' genes," said Anna McCormick of the National Institute on Aging, which helped fund the study.

Nevertheless, while genes probably determine particle size, recent research has suggested that exercise can enlarge the particles.

Doctors do not routinely test for HDL and LDL particle size, but a few companies offer such tests commercially. If the findings are confirmed, they could lead to wider testing. Moreover, research is already under way on a cholesterol-lowering drug that also makes the particles bigger.

And Dr. Ronald M. Krauss, director of atherosclerosis research at Children's Hospital Oakland Research Institute, said the findings suggest that large HDL and LDL particles may protect against all sorts of life-shortening ailments, not just heart disease.

The study involved 213 people of Ashkenazi, or Eastern European, Jewish descent, ages 95 to 107, along with 216 of their children. The researchers also used a comparison group made up of 258 of the children's spouses and neighbors.

The gene variation was found in nearly 25 percent of the old people but in just 8.6 percent of the younger comparison group, a threefold difference. The related children were twice as likely to have the mutation as the comparison group.

The Ashkenazi group and their children also had greater levels of HDL cholesterol in their blood and substantially larger HDL and LDL particles than the comparison subjects.