Being born heavier than normal adds to a person’s genetic risk for being overweight or becoming obese during adulthood, a study suggests.
The findings indicate that genes interact with the environment in the uterus to determine the likelihood of becoming obese. As such, a person’s genetic predisposition for obesity may be counteracted by monitoring maternal weight and nutrition during pregnancy, the research stated.
The study, “Are genes destiny? Exploring the role of intrauterine environment in moderating genetic influences on body mass,” was published in the American Journal of Human Biology and was conducted by Jinho Kim, PhD, a professor at The Chinese University of Hong Kong.
Obesity is a major and global public health problem, and while different lines of research have looked at genetic and environmental factors separately, little is known about how much these factors interact to contribute to obesity risk.
The study addressed whether the environment may offset genetic effects on body mass. Specifically, it focused on the influence of the prenatal environment on the genetic risk of excess weight in adulthood.
To do that, Kim studied if pairs of siblings carried genetic risk variants in the obesity-associated FTO gene, while also exploring the environment they had been exposed to in their mother’s uterus, as assessed by their weight at birth. Then, these data were compared with body mass index (BMI) after 50 years of age.
Genetic, BMI, and birth weight data were collected from 876 people (corresponding to 438 pairs of siblings) enrolled in the Wisconsin Longitudinal Study. Of note, analyzing siblings enabled better control of family characteristics that could confound the results. Overall, participants had an average BMI of 26.5 kg/m2 and 20% of them were obese (BMI of 30 kg/m2 or greater).
Results of different models consistently revealed that the association between carrying an obesity risk variant in FTO and having a high BMI is predominantly found among individuals heavier at birth. This means that being born with a higher weight adds to one’s genetic risk for being obese later in life.
One explanation for this environmental effect in utero on obesity, called the fetal origins of obesity hypothesis, suggests that maternal obesity and maternal overeating increase the risk of obesity and type 2 diabetes in the offspring. This may happen through biological programming, a process in which cells and organs are altered to compensate for an oversupply of energy, fat, and sugar during critical periods of development.
“Genes are not destiny and environmental factors may offset the effects of obesity‐promoting genes,” Kim wrote.
The findings suggest that genetic risks for obesity can be counteracted with interventions during pregnancy.
“Monitoring birth weight may help reduce the risk of overweight/obesity later in life by directly addressing the programming effects of the in utero environment and indirectly moderating the obesity-promoting genetic effects,” Kim added.
He also wrote that initiatives to monitor and reduce excessive maternal weight during pregnancy, and to optimize gestational weight gain may be helpful.