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Gene Variants Cut Cholesterol, Protect Heart

      Volume: 48 (19/06/2008)
A joint study by UK and Dutch scientists suggests that one third of the population have genes that could keep them safe from heart disease by increasing their levels of the “good” HDL cholesterol. Findings of the study have been published in the Journal of the American Heart Association.

Studies have already proved that it is possible to protect the heart by cutting down levels of “bad” or LDL cholesterol. Statin drugs that specifically target bad cholesterol are already available and widely in use. However, the link between the levels of “good”, or HDL cholesterol is not clearly established. Some studies have found that raising the levels of this cholesterol is good for the heart.

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The study team from Cambridge and Newcastle Universities, and the University of Groningen in the Netherlands collated the results from nearly 100 studies covering more than 147,000 patients across the world. The researchers studied the effect of having at least one of six different variations of a particular gene – CETP in all the subjects.

They found that the most prominently visible three variations of the gene all seemed to have a modest positive effect on the heart. All these variations raised HDL cholesterol levels by 3% to 5% and people who carried these variations had lesser risk of having a heart attack. The researchers found a 5% reduction in heart attacks for people with these key variations of the CETP gene.

According to study leader Professor John Danesh, their study findings provide weight to the hypothesis that it is possible to prevent heart disease by raising HDL levels, possibly by drugs that block CETP. However, no such drug exists at the moment. A trial on such a drug was abandoned in 2006 as it led to an increase in heart disease and deaths.

Scientists however have not given up on the idea of developing a drug that would target the CETP gene safely and effectively. Professor Peter Weissberg, of the British Heart Foundation said, “Researchers are questioning whether approaches that raise HDL cholesterol could further prevent heart disease. This suggests that it may have benefits, but that more studies are needed to determine how much might be derived.”

Downplaying the findings of the study, Dr. Aroon Hingorani, a lecturer in genetics from University College London expressed the opinion that the decrease in risk due to the CETP gene variant was relatively small. She believes the presence of a particular variant of the CETP gene can not act as an accurate predictor of the heart disease risk faced by an individual. She said, “What it does provide are important insights into the ‘cause and effect’ relationship, and if you understand this better, you can develop drugs which target it.”

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