A new study from Baylor College of Medicine claims obesity could be linked to a neurodevelopmental disorder fostered while a fetus is still in utero.
The study, published on September 28 in the journal Science Advances, claims that prenatal brain development is likely to contribute significantly to a person’s risk for obesity.
“This is something that is established long before you ever have any say in the matter. This isn’t necessarily because you are weak-willed,” said Dr. Harry MacKay, one of the study’s authors and a behavioral scientist in Canada. “It’s difficult to lose weight because you’re fighting against stuff that was ingrained in your brain’s architecture.”
Dr. Robert A. Waterland, who led the study, argued before publication, “Genetic variation certainly contributes to individual differences in body weight, early environmental influences on the development of body weight regulatory mechanisms (developmental programming) may, in general, play a bigger role in determining individual propensity to obesity.”
Waterland, a professor of pediatrics and nutrition and member of the USDA Children’s Nutrition Research Center at Baylor, said those influences might be ingrained during the late stages of one’s fetal development.
If true, it means a pregnant mother who is obese can cause her child to become predisposed to obesity, according to the findings of this study. Consequently, the study suggested the mother bears responsibility for the health of her child, and her actions before and during her pregnancy can directly influence whether her child becomes overweight.
“What happens over generation after generation is that this is just going to snowball and get increasingly worse,” Waterland suggested.
In the study, Waterland’s team tried to isolate when the developmental programming linked to weight gain occurs by studying mice during the suckling period — the weeks following their birth when developmental programming is still occurring.
“We focused on a brain region called the arcuate nucleus of the hypothalamus, which is a master regulator of food intake, physical activity and metabolism,” said MacKay. “We discovered that the arcuate nucleus undergoes extensive epigenetic maturation during early postnatal life.”
He continued, “This period is also exquisitely sensitive to developmental programming of body weight regulation, suggesting that these effects could be a consequence of dysregulated epigenetic maturation.”
The team compared the epigenetic data they found in mice to human data from large genome-wide association studies that screen for genetic variations associated with obesity. The team claimed it found an overlap between the regions they studied in mice and the human genomic regions associated with body mass index (BMI).
“These associations suggest that obesity risk in humans is determined in part by epigenetic development in the arcuate nucleus,” said MacKay. “Our results provide new evidence that developmental epigenetics is likely involved in both early environmental and genetic influences on obesity risk. Accordingly, prevention efforts targeting these developmental processes could be the key to stopping the worldwide obesity epidemic.”
MacKay estimated that about half of one’s typical body weight is determined by genetics, and brain development likely plays a significant role.
“Whatever it is that establishes your kind of ‘target body weight,’ or your appetite, or whatever you want to call it, it has to be something that happens early, before you really have a lot of control over it,” he said. “Because it’s just so pervasive, it’s so hard to resist once it’s set.”
Both Waterland and MacKay said their study reaffirms the importance of preventing obesity rather than treating it after it manifests, adding they believe public health services could be essential to reducing widespread obesity.
The Dallas Express recently interviewed a local dietitian who said she believes the most important contributors to obesity are a lack of nutritional education and poor eating habits.
