A new study has revealed that smoking cigarettes can alter more than 7,000 human DNA genes which may be a contributory factor in the development of smoking-related diseases. This is about one-third of all known human genes. The study reviewed results from nearly 16,000 people who were part of both the Cohorts for Heart and Aging Research in Genetic Epidemiology (CHARGE) Consortium and also subjects from the Framington Heart Study. One of the conclusions that arose from it was that most of the genes returned to normalcy within five years of quitting smoking.
Dr. Stephanie London, deputy of the epidemiology branch of the U.S. National Institute of Environmental Health Sciences, found however that some genetic changes were permanent even 30 years after quitting smoking. Her team focussed on DNA methylation – a process that records changes that do not alter genetic code but rather how they are expressed or switched on. Dr. London was quoted as saying that, while the process “emphasizes the long-term residual effects of smoking, the good news is the sooner you can stop smoking, the better off you are.”
Dr. Norman Edelman, a senior scientific advisor for the American Lung Association, expressed the effects of smoking on genes in grimmer terms. He said that smoking had “an enormous widespread impact on your genes. Most of it is reversible but some is not. So if you smoke, you’re going to alter your genetic makeup in a way that’s not totally reversible.”
Smoking is linked to a number of illnesses including cancer, heart disease and strokes and is responsible for nearly 6 million deaths annually. While giving up smoking may significant lower the chances of contracting any of these illnesses, it is not a guarantee that ex-smokers are completely immune from them. And it has been suggested that DNA methylane changes are the reason for this risk.
Dr. London expressed the view that DNA changes could lead to the development of diagnostic tests that might help to more precisely determine a patient’s smoking history as well as possibly lead to new ways of repairing DNA methylation sites. She explained that having good biomarkers of smoking was always useful and that “it allows you to pinpoint the effects of other exposures in a more rigorous way.” The study was published on Sept 20 in a journal called ‘Circulation: Cardiovascular Genetics’.
