Shedding unwanted pounds may not be as simple as changing your diet and increasing your physical activity, according to new research.
Researchers from the Texas A&M Health Science Center's Institute of Biosciences and Technology found that the likelihood of adults developing obesity go beyond obvious contributing factors such as inactivity and healthy eating habits. The chances of becoming obese may be determined before birth.
"The DNA we inherit is like computer hardware. What runs the 'computer' is the software - the epigenome. In early life, as embryos or infants, this epigenetic programming is being 'installed' on the genome of developing cells and tissues," Cheryl Walker, Ph.D., director of the Texas A&M IBT, said in a statement. "Just like a computer, if the epigenetics - or software - isn't installed correctly, the computer - or DNA - doesn't work optimally."
While the embryos or infants are developing, "Mother Nature" steps in and prepares the growing fetus to adapt and survive in its future environment, according to the university press release.
"If while a woman is pregnant, her environment is nutrient-poor, there are cues given to the developing fetus and the epigenetic software modifies slightly so that after the child is born, he or she is able to survive in an environment where food is in short supply," Walker said.
However, when there is a disconnect between the cues given to the fetus and the environment they end up living in , the child's risk of metabolic diseases such as diabetes, obesity, cardiovascular disease and cancer increase.
For example, if the infant is prepared for a nutrient-poor environment, but is born into a nutrient-rich environment, that causes a disconnect and can result in a greater risk for disease, according to Walker.
A second area of the study, researchers focused on environmental chemicals, specifically endocrine disrupting chemicals (EDCs), which are found in many everyday products, including plastic bottles, metal food cans, detergents, flame-retardants and pesticides. This study is the first to look at the effect EDCs have on the liver, the most central organ in total body nutrition.
"Results show even a short exposure to EDCs early in life can disrupt the 'install' of the epigenetic software, causing a 'reprogramming' of the epigenome and increasing susceptibility to disease in adulthood," Walker says.
In a complementing study, researchers used a rodent model to study the long-term effects of exposure to EDCs early in life. They found that animals exposed to EDCs shortly after birth exhibited life-long changes in their epigenome and as a result, they were at much greater risk for uterine cancer as adults and also became obese.
They found that if these animals' calories were restricted by 30 percent, the risk of cancer decreased dramatically. The findings illustrate that lifestyle interventions can potentially reverse the bad "reprogramming" by EDCs to decrease the risk of disease in adulthood.
Researchers plan to test subjects and focus on how the endocrine disrupters are "talking" to the epigenetic software that causes those animals to become obese.
According to the press release, researchers believe the findings may have greater implications for the future of obesity research. They hope to build on the research to test lifestyle interventions, such as diet and exercise, to determine the possibility of resetting the epigenetic programming back to normal, ultimately decreasing the risk of disease.
"Research can move toward pinpointing specific genes that are the target for this programming and consequently develop biomarkers to identify individuals that are at a potential higher risk for disease," Walker said.
