Public health conversations often focus on a person’s own well-being. But what if our habits in adolescence echo not just through our lives, but through the gene expression and health of our children?
A new study offers sobering evidence of this possibility. It suggests that boys who gain excess weight during puberty may set in motion biological changes that affect the health of their future offspring.
This isn’t just speculation or a sociological observation. The research identifies specific changes in the offspring’s genes linked to asthma, obesity, and low lung function. These are not inherited mutations but rather epigenetic markers – chemical switches that tell genes when to turn on or off.
The study connects lifestyle choices made in early teenage years to real molecular traces in the next generation, offering a sharp reminder of how deep the consequences of obesity may go.
Led by scientists from the University of Southampton and the University of Bergen, the research looked at 339 father-child pairs.
Participants ranged in age from 7 to 51 and came from six different countries. The goal was to understand how changes in a father’s body shape during different life stages might affect their children’s genetic expression.
To estimate fat levels, researchers used a validated silhouette scale showing nine body types. Fathers selected the image that best represented their body shape at age 8, at the time of voice break (a marker for puberty), and at age 30. These responses served as a stand-in for measured body composition.
The researchers then examined DNA methylation – an epigenetic process that affects gene expression – in the offspring. This allowed them to trace whether the father’s earlier body weight left a biological signature in their children’s genes.
The most striking results were tied to weight gain during puberty. Overweight fathers at voice break had children with 2,005 DNA changes in 1,962 genes tied to fat, inflammation, and insulin.
“The overweight status of future fathers during puberty was associated with a strong signal in their children’s DNA which were also related to the likelihood of their children being overweight themselves,” said Dr. Negusse Tadesse Kitaba, Senior Research Fellow at the University of Southampton.
“Early puberty, when boys start their developing sperm, seems to be a key window of vulnerability for lifestyle influences to drive epigenetic changes in future offspring,” noted the authors of the study.
The study identified several genes that may explain the health risks seen in offspring. These include genes that regulate insulin release, fat cell growth, aging, and glucose levels. Many of these genes have been linked in other studies to obesity and metabolic disorders.
For example, one gene affected in the daughters was HIF3A, previously connected to body mass and fat storage.
There was also a gender difference in the results. The biological effects were more pronounced in daughters than sons, though different genes were affected in each. The methylation differences also seemed to carry sex-specific consequences.
Some genes influenced hormone regulation in daughters, while others affected gene-linked fat metabolism in children of both sexes.
Importantly, the changes were not confined to fat-related traits. The study found epigenetic links to asthma and reduced lung function as well.
Nearly 1,000 of the identified methylation changes in offspring were associated with lung performance. This suggests that the impact of a father’s teenage weight gain could extend to breathing ability and respiratory health in children.
“The new findings have significant implications for public health and may be a game-changer in public health intervention strategies,” noted Professor Cecilie Svanes from the University of Bergen.
She stressed that failing to address obesity in young boys today could deepen health inequalities across generations.
“They suggest that a failure to address obesity in young teenagers today could damage the health of future generations, further entrenching health inequalities for decades to come,” said the researchers.
The study found 24 imprinted genes, inherited parent-specifically, linked to obesity, diabetes, and brain development.
These imprinted genes offer a mechanism by which the body might remember environmental exposures from the father’s adolescence.
The genes help explain how temporary factors like teenage weight can have lasting effects without altering the DNA sequence itself. This biological memory adds another layer to how we think about inherited health.
The study also noted that the longer-term body shape trajectory – from puberty to adulthood – was linked to additional methylation effects.
When fathers remained overweight into adulthood, their children showed even more signs of altered gene expression related to asthma and reduced lung capacity.
This finding adds urgency to early intervention. It’s not just a matter of teen boys “growing out of” extra weight.
The effects may stretch well beyond their own lives and into their children’s well-being. The biological signals do not vanish. They accumulate and potentially shape the health trajectory of entire families.
The study comes at a time when childhood and adolescent obesity are rising worldwide. Public health systems often focus on the here and now – on controlling blood pressure, reducing diabetes, and improving lifestyle. But this research asks us to think further ahead.
Study co-author John Holloway is a professor at the University of Southampton and the NIHR Southampton Biomedical Research Centre.
“Childhood obesity is increasing globally,” said Professor Holloway. “The results of this study demonstrate that this is a concern not only for the health of the population now but also for generations to come.”
The study is published in the journal Communications Biology.
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