A new study has unearthed evidence that a common genetic defect significantly increases a smoker's risk of an early heart attack.
Dr. Arthur Moss, director of the Heart Research Follow-up Program at the University of Rochester Medical Center, says that as much as 60 to 70 per cent of the population has a gene defect that makes smokers vulnerable to a heart attack.
Among the study participants, said the researcher, heavy smokers with the same common gene variant experienced a heart attack when they were around 52 years old.
"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 Dr. Moss.
"Contrast that with the 52-year old neighbour, 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," he added.
The gene central to such a heavy susceptibility of smokers is called cholesteryl ester transfer protein (CETP). Found in all people, this protein controls cholesterol metabolism.
According to the researchers, smokers with a common form of this gene are likely to suffer a heart attack 12 years earlier than a non-smoker, whereas smokers without this variant appear to have the same risk of heart attack as non-smokers.
Dr. Moss has revealed that CETP manages a person's level of high-density lipoproteins (HDL), also known as the "good cholesterol". When the gene has a common defect, it leads to a decrease in the good cholesterol's levels.
"It's this efficient removal of HDL caused by the CETP gene defect that puts people at higher risk of an early onset of heart disease. The problem only gets worse for smokers who have this form of CETP, because smoking is known to also lower HDL levels. The cumulative effect is a dramatic drop in the age such smokers are likely to experience a heart attack - about a dozen years earlier than someone who also has the variant but does not smoke," said Dr. Moss.
He further said that the study, published in the Annals of Noninvasive Electrocardiology, also gave an insight into why some heavy smokers appeared to beat the odds when it came to heart disease.
"If you're a smoker and you don't carry the CETP variation, you have the same risk for heart disease as a non-smoker carrying the same gene. These smokers can thank their lucky genes for not suffering heart attacks at a young age," he said.
Dr. Moss insisted that people who smoked more than one pack a day were likely to suffer heart attacks about 12 years earlier than non-smokers, and that the gae difference was only six years for those who smoked less than one pack a day.
He also suggested that smokers could recover lost ground within one year of quitting. According to him, people who had smoked more than one pack a day gained about four years within one year of quitting, while those who had smoked less than one pack a day gained about six years.
The researcher believes that the understanding of how certain environmental factors ó like diet, chemicals and even smoking ó influence any particular gene's work may pave the way for new approaches to axe a person's risk of disease.
"When we were younger, we learned how genes gave us a certain hair or eye colour. But we are increasingly finding that our ability to untangle a person's genes can help us understand why some get certain diseases and some don't. I wouldn't be surprised if there's a similar gene variation that predisposes some smokers to other diseases, such as lung cancer," he added.