DALLAS, Nov. 10 -- A gene that influences blood cholesterol levels can also predict how much those levels are affected by weight gain, smoking and other lifestyle factors, according to a study presented today at the American Heart Association's 71st Scientific Sessions.
Sathanur R. Srinivasan, Ph.D., and colleagues at the Tulane Center for Cardiovascular Health, New Orleans, showed that the gene called apolipoprotein E, or (apo)E gene, is influenced from childhood to adulthood by environmental factors.
An adult's blood cholesterol level can be influenced by the (apo)E gene -- which is expressed in three forms, or alleles: E-2, E-3 and E-4.
One form, the E-2, is associated with low levels of cholesterol. Cholesterol is a fatty substance in the blood that collects in the walls of blood vessels. If the blood vessels to the heart become narrowed -- a process called atherosclerosis -- a heart attack can result.
However, a new study shows that weight gain and other risk factors for heart disease cause cholesterol levels to rise relatively more in people with the E-2 form of the gene when compared to those with other forms of the gene. "People with E-3 or E-4 still may have elevated cholesterol levels if they gain weight, but the changes in E-2 individuals are greater," says Srinivasan.
"The (apo)E gene influences not only cholesterol levels from childhood to adulthood, but also moderates how an individual's cholesterol levels may interact with the risk factors and behaviors that contribute to heart disease," says Srinivasan. "Although people with the E-2 variant have this beneficial cholesterol profile, smoking, obesity and other cardiovascular risk factors can negate this benefit.
"The study shows that if you know your (apo)E gene type, it is possible to determine your risk status for high cholesterol during life and how great your risk can be influenced by factors such as smoking and decreases or increases in body fat," says Srinivasan.
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Contact: Carole Bullock
caroleb@heart.org
214-706-1279
American Heart Association
10-Nov-1998