Cigarette after Valentine snuggle deadlier for some

Bad gene, not Cupid, puts arrow through some smokers' hearts

The proverbial cigarette after a Valentine’s Day snuggle can prematurely end a love affair, as new evidence emerges that a common defect in a gene significantly increases a smoker’s risk of an early heart attack. Researchers say that as much as 60 to 70 percent of the population has a gene defect that delivers a one-two punch to smokers: In a recent published study, heavy smokers with this common gene variant experienced a heart attack around the age of 52.

“We’ve all heard the stories: Someone’s great-uncle has smoked three packs of cigarettes since he was 14, and now, at the age of 88, he’s living a fine, healthy life,” said Arthur Moss, M.D., director of the Heart Research Follow-up Program at the University of Rochester Medical Center. “Contrast that with the 52-year old neighbor, who also was a heavy smoker, and just last week, dropped dead from a heart attack. Why is it that some smokers seem unaffected by their habit and even outlive the healthiest individuals, while many other smokers suffer significant cardiac events at a relatively young age? We think we now know why.”

According to Moss, the answer lies is a common deviation of the gene CETP (cholesteryl ester transfer protein), a protein found in all people that controls cholesterol metabolism. Smokers with a common form of this gene are likely to suffer a heart attack 12 years earlier than a non-smoker, while smokers who do not carry this variant appear to be “protected” and have the same risk of heart attack as non-smokers.

While genes have long been linked to diseases, it’s only been recently that researchers have been able to begin unraveling the intricate interplay between genes and the environment. By understanding how certain environmental factors such as diet, chemicals and even smoking can influence how well – or not – a particular gene works, scientists hope to provide new approaches to help decrease a person’s risk of disease.

In this case, researchers zeroed in on CETP, which manages a person’s level of high-density lipoproteins (HDL), the “good cholesterol.” Unlike low-density lipoproteins (LDL), which build up plaque on artery walls and predispose a person to heart attacks or strokes, HDL helps filter LDL out of the blood and chips away at the plaque lining artery walls.

When CETP has a common defect, it makes the protein controlling HDL work on overdrive. This overactive protein more furiously “attacks” HDL, breaking it into smaller particles that are more easily cleared from the blood, leading to decreased HDL levels – and less good cholesterol.