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Feb 6, 2013

Father’s Obesity Connected with Disease in Children

  • Obesity is well known to be a risk factor for a number of health problems, like diabetes and cardiovascular diseases. But can obesity’s risk for disease be passed on to offspring? New research in humans, conducted by Duke Medicine, shows that paternal obesity may alter a genetic mechanism in the next generation, suggesting that a father’s lifestyle factors may be transmitted to his children. This means that a father’s obesity is one factor that may influence his children’s health and potentially raise their risk for diseases like cancer.

    “Understanding the risks of the current Western lifestyle on future generations is important,” says molecular biologist Adelheid Soubry, Ph.D., a postdoctoral associate at Duke Cancer Institute and the study’s lead author. “The aim of this study was to determine potential associations between obesity in parents prior to conception and epigenetic profiles in offspring, particularly at certain gene regulatory regions.”

    It is believed that nutrition and environmental factors during pregnancy can affect children’s health and may raise their risk of chronic diseases. However, few studies have investigated how paternal factors can affect children.

    The Duke research team sought to determine associations between obesity in parents and changes in DNA methylation at the insulin-like growth factor 2 (IGF2) gene among offspring. IGF2 codes for a growth factor that is important mainly during fetal development. Decreased DNA methylation at the IGF2 gene has been associated with an increased risk of developing certain cancers, including colorectal and ovarian cancers. The researchers found that IGF2 was hypomethylated in newborns with obese fathers, but not obese mothers.

    To gather data on newborn health outcomes, the researchers followed families enrolled in the Newborn Epigenetics Study (NEST), a research program that tests the influence of environmental exposures on genetic profiles in newborns.

    Researchers gathered information about the mothers and fathers using questionnaires and medical records. They then examined DNA from the umbilical cords of 79 newborns to determine potential associations between the offspring’s DNA methylation patterns and parental obesity before conception.

    DNA methylation at the IGF2 gene in the offspring of obese fathers was significantly lower than in the children of fathers who were not obese. This suggests that paternal obesity may be associated with an increased risk of children developing certain cancers.

    The researchers noted that the changes in DNA methylation could have been a result of something related to obesity, such as eating a certain diet or having diabetes, that was not measured in this study.

    “During spermatogenesis some regions in the DNA may be sensitive to environmental damage; these effects can be transmitted to the next generation,” says Dr. Soubry. “It is possible that (mal)nutrition or hormone levels in obese fathers leads to incomplete DNA methylation or to unstable genomic imprinting of sperm cells.”

    Additional research is under way to see if these changes in DNA methylation at the IGF2 gene remain as the children grow older. Future studies may also determine if certain interventions can be used prior to or after conception to prevent irregular methylation profiles.

    “Although we cannot define at this point which obesity-related factor may cause an epigenetic effect, we measured in this study a significant association between paternal obesity and aberrant methylation profiles in the offspring,” concludes Dr. Soubry.

    The study appears today in the journal BMC Medicine, in a paper titled “Paternal obesity is associated with IGF2 hypomethylation in newborns: results from a Newborn Epigenetics Study (NEST) cohort”.

    Commentary on this study, also published today in BMC Medicine, suggests that this data does not paint the entire picture. “We must consider the whole genome/epigenome/metabolome in an unbiased way, involving all key genes and networks,” the authors write. “It is also important to critically assess environmental players. It is tempting to over-emphasize the role of a small number of parent-of-origin expressing genes and to speculate about the effects of modest variation in methylation, but we must not be too hasty to blame either parent for their offspring’s health outcomes without being certain that these effects are consequentially robust.” The commentary is titled “Fat dads must not be blamed for their children’s health problems”.


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