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Mothers have often – unfortunately and unfairly – had to carry the burden of being “to blame” for any of their child’s health-related shortcomings. When pregnant women are advised: eat more of this but nottoo much of that, drink this but definitely none of that… why does dad get off scot-free amid these typically well-intentioned suggestions? Previous studies have, for example, epigenetically linked dad’s drinking to his son’s sensitivity and preference for alcohol and connected a father’s diet to negative pregnancy outcomes. Research has even hinted that stressed-out fathers could epigenetically set-up his son for high blood sugar later in life. A review article conducted at Georgetown University Medical Center and published in the American Journal of Stem Cell shows that both mothers and fathers contribute to their offspring’s health via epigenetic alterations. It seems like common sense that both parents contribute to their child’s health, but science has only just begun to demonstrate it, according to Joanna Kitlinska, PhD, an associate professor in biochemistry, and molecular and cellular biology at Georgetown University.
“We know the nutritional, hormonal and psychological environment provided by the mother permanently alters organ structure, cellular response and gene expression in her offspring,” she said. “But our study shows the same thing to be true with fathers – his lifestyle, and how old he is, can be reflected in molecules that control gene function. In this way, a father can affect not only his immediate offspring, but future generations as well.”
The review takes into consideration a wide range of evidence, looking at the effects of paternal preconception exposures – such as paternal diet, exposure to toxins, and psychosocial stress – on the child’s health via epigenetic mechanisms. This collection of animal and human studies investigating epigenetic marks of interest, including DNA methylation, histone modification and miRNA expression, provides evidence of the link between fathers’ experiences and heritable epigenetic programming.
For instance, a child can have fetal alcohol spectrum disorder (FASD) even if the mother never drank alcohol. Kitlinska explained, “Up to 75 percent of children with FASD have biological fathers who are alcoholics, suggesting that preconceptual paternal alcohol consumption negatively impacts their offspring.”
Among the numerous studies assessed, investigators found evidence associating increased paternal age with abnormal social interaction in mice offspring. In another, they found that a lack of food at a young age was associated with marked epigenetic changes. Specifically, “low amounts of dietary resources during the father’s pre-adolescence was correlated with a lower chance of cardiovascular mortality in his offspring,” hinting that a father’s diet while he’s young may epigenetically impact his child’s and grandchild’s risk of cardiovascular disease and death later in life.
Other studies reported an epigenetic connection between a father’s exposure to toxicants, like smoking and irradiation, and his child’s genome. Irradiation has previously been “correlated with decreased viability in murine offspring.” They discovered that male mice exposed to irradiation had less de novomethyltransferase, DNA methyltransferase 3a (DNMT3a), and hypomethylation of long and short nuclear elements. They indicated that “these epigenetic changes lead to detrimental effects on somatic thymus tissue in the progeny of exposed mice.”Additional studies suggest a father’s obesity can impact his child’s likelihood for developing diseases like diabetes or experiencing abnormal metabolic regulation. They found that “paternal obesity is linked with hypomethylation at the differentially methylated regions (DMR) of the IGF2 gene.” This epigenetic modification leads to an increase in IGF2 proteins, which are, in turn, linked to obesity. Children of obese fathers were shown to have “hypomethylation in their MEST, PEG3, and NNAT DMRs,” which can result in “enlargement of adipocytes, changes in metabolic regulation, diabetes, rhabdomyosarcoma, glioma, and obesity,” the researchers reported. DNA methylation is a common, well-known epigenetic mechanism defined by the addition of a methyl group to DNA, predominantly attaching to cytosine residues. This epigenetic modification restricts the expression of genes. However, hypomethylation is characterized by a lack of methylation, thereby increasing the expression of genes.
Additional evidence investigating a father’s alcohol consumption on his child’s health suggests that this behavior could epigenetically decrease newborn birth weight, reduce brain size, and impair cognitive function. This evidence contributes to the growing body of evidence on epigenetic mechanisms that may play a role in fetal alcohol spectrum disorders (FASDs). Researchers are still investigating the specific modifications that can lead to these changes, but they have found that epigenetic marks in sperm DNA can be transferred to the offspring.
Overall, numerous experiments indicate that a father’s early exposures and habits, such as smoking, drinking, or diet, may epigenetically impact his child’s health. Perhaps this new scientific revelation will ease society’s pressures on mothers and take into consideration the effect both parents’ lifestyles may have on their children, among many other factors.
“This new field of inherited paternal epigenetics needs to be organized into clinically applicable recommendations and lifestyle alternations,” Kitlinska said. “And to really understand the epigenetic influences of a child, we need to study the interplay between maternal and paternal effects, as opposed to considering each in isolation.”
Source: Day, J., Savani, S., Krempley, B.D., Nguyen, M., Kitlinska, J.B. (2016). Influence of paternal preconception exposures on their offspring: through epigenetics to phenotype. Am J Stem Cells, 5(1):11-18. (pdf)
Reference: Georgetown University Medical Center. Review finds fathers’ age, lifestyle associated with birth defects. EurekAlert. 15 May 2016. Web.