Smoking Permanently Damages Human DNA, Study Says

By Mary Pascaline Dharshini

September 21, 2016

A study found that smoking can damage the DNA, permanently altering nearly 7,000 genes that can contribute to the development of smoking-related illnesses. Most damage, which can be seen in clear patterns, heals over time but some remains.

The study published online Tuesday in the American Heart Association’s journal Circulation: Cardiovascular Genetics found that smoking leaves its “footprint” on the genome through DNA methylation, the process by which cells control gene expression.

Researchers believe that this process could reveal the individual’s smoking history and help identify potential targets for therapy.

They added that this study is the largest one examining the effects of smoking on DNA methylation.

“These results are important because methylation, as one of the mechanisms of the regulation of gene expression, affects what genes are turned on, which has implications for the development of smoking-related diseases,” Stephanie J. London, last author and deputy chief of the Epidemiology Branch at the National Institute of Environmental Health Sciences, said in a statement.

“Equally important is our finding that even after someone stops smoking, we still see the effects of smoking on their DNA,” she added.

Researchers used blood samples collected from 16,000 people to analyze the DNA methylation sites across the human genome. The participants belonged to 16 groups from the Cohorts for Heart and Aging Research in Genomic Epidemiology Consortium and one group from the Framingham Heart Study.

Researchers compared the methylation sites in current and former smokers to those who had never smoked and found that nearly one-third of known human genes, or 7,000 genes, were altered due to smoking.

Most of the sites in people who quit smoking returned to levels seen in non-smokers within five years of quitting. But some DNA methylation sites remained damaged even after 30 years since quitting.

Researchers added that the affected sites may mark genes that are potentially important to former smokers who are still at an increased risk of developing certain diseases.

“Our study has found compelling evidence that smoking has a long-lasting impact on our molecular machinery, an impact that can last more than 30 years,” Roby Joehanes, first author and an instructor at Harvard Medical School in Boston, said in the statement.

“The encouraging news is that once you stop smoking, the majority of DNA methylation signals return to never smoker levels after five years, which means your body is trying to heal itself of the harmful impacts of tobacco smoking.”

According to the Centers for Disease Control and Prevention, nearly 40 million adults in the country smoked cigarettes.

Cigarette smoking accounts for one in every five deaths or over 480,000 deaths every year in the United States.

Source: Smoking Permanently Damages Human DNA, Study Says

Smoking: Is The Fault In Our Genes?

DNA

A new study finds that people with a particular version of a gene involved in the brain’s reward system are more likely to succeed in quitting smoking.

Compared with people who have other versions of this gene, those with the lucky DNA were also more likely to abstain from cigarettes. The study in Translational Psychiatry was a meta-analysis (a review of other studies) and supports a role for heredity, i.e., genotype, in the likelihood that someone will become a smoker and how difficult it will be, once starting to smoke, to eventually quit.

The primary objective was to determine whether the variant  DRD2/ANKK1 gene Taq1A has any effect on smoking cessation. ANKK1 happens to be next to the DRD2 gene, which helps the brain recognize dopamine, the chemical that’s produced in the brain to reinforce useful behaviors like eating and having sex. Addictive drugs, including nicotine, also cause dopamine levels to spike.

People inherit either an A1 or A2 version of this gene fragment from each of their parents. That means there are three possible genotypes: two A1s, two A2s or one of each. When it comes to quitting smoking, the helpful type is A2/A2. Those with two A2s had better odds of kicking the habit than those with one or two A1s.

Their literature survey consisted of 9,487 Caucasians (an obvious limitation.) Using statistical and epidemiological techniques, they determined that Taq1A A1/ genotypes were significantly associated with smoking cessation. They found an approximately 22 percent higher rate of smoking cessation among the study subjects with the A2A2 variant in the dopamine receptor gene Taq1A.

It is unclear how many smokers, or how many Americans, carry this particular gene variant. Given the fact that even if one carries this trait, the benefit (in the 22 percent better chance of quitting) is not so large as to confer any reliable hope of getting your genes to help you quit. Fortunately, this is a problem going out of existence and we are proud we have helped for 37 years. CDC data show that the smoking rate for both adults and teens in the U.S. is declining but the dire consequences of smoking make me want to remind everyone that it’s better not to rely on lucky genes – the best way to “quit” is to never start! Once addicted to nicotine and smoking, it is very difficult to quit, whatever your genome.

This study is interesting from a “personalized medicine” point of view and for those studying pharmacogenetics but for the rest of us, let me repeat: the fault (smoking) is in ourselves, not in our stars, nor in our genes.

Source: Smoking: Is The Fault In Our Genes? – American Council on Science and Health