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Father’s obesity may increase newborn’s risk for cancer later in life
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The link between maternal obesity and its effect on a newborn’s health status has recently been addressed in the literature. However, preliminary data published in BMC Medicine suggest that paternal obesity could lead to hypomethylation of insulin-like growth factor II, potentially increasing a newborn’s risk for developing cancer.
“During spermatogenesis, some regions in the DNA may be sensitive to environmental damage; these effects can be transmitted to the next generation. It is possible that malnutrition or hormone levels in obese fathers leads to incomplete DNA methylation or to unstable genomic imprinting of sperm cells,” researcher Adelheid Soubry, PhD, of Duke Cancer Institute, said in a press release.
Soubry and colleagues studied DNA from umbilical cord blood leukocytes of 79 newborns born between July 2005 and November 2006 at Duke University Hospital. During their pregnancy, the newborns’ mothers were enrolled in the Newborn Epigenetics Study (NEST). Besides questionnaires and medical records, Soubry and colleagues conducted bisulfite pyrosequencing of DNA methylation patterns at two differentially methylated regions (DMRs); one upstream of IGF-II, and the other upstream of the H19 gene. Further analysis was completed to determine the link between the newborns’ DNA methylation patterns and their parental obesity before conception.
According to data, hypomethylation at the IGF-II DMR was linked to paternal obesity before and after adjustments for several characteristics (P=.003). Furthermore, no significant relationship was found between methylation patterns and paternal obesity at the H19 DMR.
These findings suggest adverse lifestyle factors could have an effect during spermatogenesis. However, further research is needed to confirm the results, researchers said.
Disclosure: The researchers report no relevant financial disclosures.
Perspective
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Angela Ting, PhD
The reprogrammable but heritable nature of epigenetic regulation has made it an attractive molecular mechanism to explain lasting effects on an individual's phenotypes, including disease predisposition, from transient exposures to environmental conditions. This notion has been extended to postulate the impact of parental health conditions on those of the next generation. The correlative results presented in this article certainly add to the growing list of studies that support the hypothesis. Nonetheless, these observations require independent validations and empirical evidence to demonstrate causality before a definitive conclusion can be drawn.
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Harry S. Jacob, MD, FRCPath(Hon)
If the coming obesity-associated epidemic of type 2 diabetes in “developed countries” is not frightening enough, consider this: If these provocative studies prove prescient, we can expect significant increases in cancers in coming generations. The “war on cancer” may now become more difficult if obesity is not tamed rapidly in reproducing adults.
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