Texas A&M Researchers Discover Early Life Exposures Increase Risk of Cancer, Obesity in Adults

 
HOUSTON - July 25, 2013 - PRLog -- Researchers at the Texas A&M Health Science Center Institute of Biosciences and Technology in Houston have discovered long-term health effects from exposures to endocrine disrupting chemicals, or EDCs, early in life.

EDCs exhibit hormone-like properties that attack the endocrine system. They are found in anything from pesticides to water bottles, such as Bisphenol A—more commonly known as BPA—a man-made synthetic compound used to make plastics.

With support by the National Institutes of Health and the Cancer Prevention Research Institute of Texas, Cheryl Walker, Ph.D., director of the institute, and her lab that is part of the Center for Translational Cancer Research in the Texas Medical Center, study cancer at the molecular level. The team focuses specifically on causes of cancer related to the interaction between genes, the epigenome and the environment.

“The DNA we inherit is like computer hardware. What runs the ‘computer’ is the software—the epigenome,” Walker explains. “In early life, as embryos or infants, this epigenetic programming is being ‘installed’ on the genome of developing cells and tissues. Even a short exposure to EDCs early in life can disrupt the ‘install’ of the epigenetic software, altering our genome in a way that increases our risk of disease in adulthood.”

Walker’s team found that animals exposed to EDCs shortly after birth exhibited life-long changes in their epigenome. As a result, in adulthood they demonstrated a much greater susceptibility to diseases—particularly uterine and other cancers—as well as a greater tendency toward obesity. However, lifestyle interventions can potentially reverse the bad “reprogramming” by EDCs to decrease disease risk. Studies showed when calories are restricted by 30 percent, the animals’ risk of uterine cancer returned to normal.

“The good news is that the epigenome is very plastic, meaning that epigenetic markers can be reprogrammed,” Walker said. “This plasticity also provides opportunities for disease prevention and intervention, reducing the risk of disease in at-risk people.”

Expanding upon their findings, Dr. Walker and her team next plan to test other interventions such as exercise or drugs that mimic caloric restriction to determine if they can “correct” defects induced by EDCs during developmental reprogramming.

“Early life development is such a critical time for installation of epigenetic programming,” Walker said. “It is a new and important area of research for understanding environmental causes of disease.”

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Contact: Blair Williamson at bmwilliamson@tamhsc.edu or 979-436-0617.
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