Boys Who Smoke In Early Teens Could Pass Harmful Genetics To Future Children

Smoking may not only harm the smoker and those who breathe in the secondhand fumes, but also their future children, UPI News  reported (via Microsoft Start).

New research suggests that boys who smoke in their early teens risk passing on harmful genetic traits to future children. The study probed the genetic profiles of 875 people between 7 and 50 years of age and their father’s smoking behavior.

People whose dads were early-teen smokers had gene markets associated with asthma, obesity, and low lung function. Biomarkers associated with this were different from those associated with maternal or personal smoking, the researchers found.

This is the first human study to reveal the biological mechanism behind the impact of fathers’ early smoking on their children, according to researchers from the University of Southampton in the United Kingdom and the University of Bergen in Norway.

“Changes in epigenetic markers were much more pronounced in children whose fathers started smoking during puberty than those whose fathers had started smoking at any time before conception,” said the study co-author Negusse Kitaba, a research fellow at the University of Southampton. 

“The health of future generations depends on actions and decisions made by young people today – long before they are parents – in particular for boys in early puberty and mothers/grandmothers both pre-pregnancy and during pregnancy,” said co-author Dr. Cecile Svanes of the University of Bergen. “It is really exciting that we have now been able to identify a mechanism that explains our observations.”

The researchers also compared fathers’ preconception smoking profiles with people who smoked and those whose mothers smoked before conception.

“Interestingly, we found that 16 of the 19 markers associated with fathers’ teenage smoking had not previously been linked to maternal or personal smoking,” said co-author Gerd Toril Mørkve Knudsen of the University of Bergen. “This suggests these new methylation biomarkers may be unique to children whose fathers have been exposed to smoking in early puberty.”

While numbers of young smokers in the United Kingdom has fallen, co-author John Holloway from the University of Southampton expressed concern about the growing popularity of vaping. 

“Some animal studies suggest that nicotine may be the substance in cigarette smoke that is driving epigenetic changes in offspring,” Holloway said. “So, it’s deeply worrying that teenagers today, especially teenage boys, are now being exposed to very high levels of nicotine through vaping.”

The evidence in this study comes from people whose fathers smoked in their teens in the 1960s and 1970s when tobacco use was far more common, he noted.

“We can’t definitely be sure vaping will have similar effects across generations, but we shouldn’t wait a couple of generations to prove what impact teenage vaping might have. We need to act now,” Holloway said.

A study titled “Fathers’ preconception of smoking and offspring DNA methylation” was posted on BNC. From the study:

Background: Experimental studies suggest that exposures may impact respiratory health across generations via epigenetic changes transmitted specifically through male germ cells. Studies in humans are, however, limited. We aim to identify epigenetic marks in offspring associated with father’s preconception smoking.

Conclusion: Father’s preconception smoking, particularly in puberty, is associated with offspring DNA methylation, providing evidence that epigenetic mechanisms may underlie epidemiological observations that pubertal paternal smoking increases risk of offspring asthma, low lung function, and obesity.

Introduction: There is growing consensus that perturbations of the epigenome through parental exposures even before their offspring are conceived may explain some of the variation in the heritability of health and disease not captures by genome-wide association studies. 

The period of puberty in future parents, in particular fathers, may represent a critical window of physiological change and epigenetic reprograming events, which may increase the individual’s susceptibility for environmental exposures to be embodied in the developing gametes.

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