A Question of Time? :

When it comes to cholesterol, how long it’s under control — and how early that control starts — is as important as how low it goes.

For the last few years, “How low can you go?” has been the big question driving cholesterol researchers. Elbowed to the sidelines is an equally important question: When should you start thinking about cholesterol?

New work on simple mutations that influence blood levels of low-density lipoprotein (LDL), the so-called bad cholesterol, may turn the spotlight on this topic. The upshot of this work may be that we pay more attention to cholesterol levels before middle age, when damage to arteries is already under way. It may also lead to new strategies for keeping cholesterol in check.

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It’s in the genes
Back in 1999, French researchers found that a specific stretch along human chromosome 1 was linked with naturally high levels of LDL in some people. Further work pinpointed the source of the problem, a mutation in a gene for proprotein convertase subtilisin/kexin 9, blessedly shortened to PCSK9. That prompted a team from the University of Texas Southwestern Medical Center to search for other PCSK9 variations. They found three that cause naturally low levels of LDL. Two of them are more common in African Americans, the other in European Americans. These gene variants probably work by increasing the number of LDL receptors in the liver, making the liver better able to pull excess LDL out of the bloodstream.

To look at the impact of these gene variations, the researchers turned to a landmark long-term, multicultural study of heart disease risks, the Atherosclerosis Risk in Communities (ARIC) study. They tested blood samples the volunteers had given at the beginning of the study for PCSK9, and tallied up who did, and did not, develop heart disease over the course of the 15-year study.

Blacks with one of the unusual genes had a whopping 88-percent lower risk of having a heart attack, needing bypass surgery or artery-opening angioplasty, or dying of heart disease over a 15-year period than those with the normal PCSK9 gene. Among whites, the reduction was 47 percent. And these reductions were in spite of the fact that many of the PCSK9 carriers were overweight, had high blood pressure, smoked, or had diabetes — all potent risk factors for heart disease. The results were reported in the March 23, 2006, New England Journal of Medicine.

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