A common mutation shortens the life of smokers
A common variant of the CETP gene, which regulates cholesterol metabolism in the body, significantly increases the risk of cardiovascular diseases in smokers. According to American researchers, the presence of this gene in combination with frequent smoking reduces the age of the first heart attack by almost 10 years.
The SETR gene encodes a protein that transports cholesterol esters. The carrier of an unfavorable variant of this gene called TaqIB is from 60 to 70 percent of people. The consequence of this mutation is too rapid cleavage in the body of the so-called "good cholesterol" (high-density lipoproteins). The "usefulness" of this type of cholesterol is explained by the fact that it prevents the formation of atherosclerotic plaques on the walls of arteries, reducing the risk of coronary heart disease and heart attacks.
It is also well known that smoking itself leads to a significant decrease in the level of beneficial cholesterol. As the results of a study by University of Rochester researchers show, the combination of both adverse factors dramatically increases the risk of a heart attack at an early age.
At the disposal of scientists were blood tests of 814 patients who had suffered the first heart attack. 199 of them continued to smoke at the time of hospitalization, 270 had never smoked, and 345 found the strength to break up the bad habit. The average age of patients who smoked more than a pack of cigarettes a day and at the same time were carriers of one or two copies of the unfavorable variant of the gene was 9.4-8.4 years less than those who did not smoke, and averaged 52 years. In people who smoked less than half a pack of cigarettes a day, the age of the first heart attack increased by 6 years, and in patients who quit smoking, the risk of developing a dangerous disease returned to normal within one year after quitting smoking.
There was no such pattern among carriers of other variants of the CETP gene: in these groups, the risk of early development of cardiovascular diseases in smokers and non-smokers was approximately the same.
According to the lead author of the study, Arthur Moss, despite the well-known link between smoking and the risk of cardiovascular diseases, the likelihood of their development in specific patients largely depends on individual genetic characteristics. "I wouldn't be surprised if similar genetic patterns can be identified for other diseases, for example, lung cancer," Moss said.
The research report is published in the journal Annals of Noninvasive Electrocardiology.