Reprinted from Eating Disorders Review
November/December Volume 25, Number 6
Obesity is highly heritable, and researchers are currently identifying specific obesity-related genes. But the fact that obesity has grown markedly more common in the last half century poses a conundrum: Why wasn’t obesity a problem 200 years ago? Change in the gene pool occurs very gradually and so the idea that obesity is substantially heritable, and yet has recently become much more common, would seem to be in conflict. In a presentation at the American Psychological Association meeting in Washington, DC, last August, Jane Wardle, PhD, of University College, London, offered a hypothesis: satiety responsiveness is associated with genetic risk for obesity, and thus may be “an intermediate neurobehavioral process” that explains genetic risk for obesity and that causes weight gain. Dr. Wardle described her research team’s cross-sectional observational study of a population-based cohort of twins born between January 1, 1994 and December 31, 1996 (the Twins Early Development Study).
The study included 2258 unrelated 10-year-olds; one twin was randomly selected from each twin pair (JAMA Pediatr 2014; 168:338). The scientists measured satiety responsiveness with the Child Eating Behavior Questionnaire. BMI and waist circumference were calculated from parent reports. The results suggest that low satiety responsiveness is a mechanism that does partially explain how genetic risk for obesity actually leads to weight gain in the current environment where food is generally plentiful and palatable. People who do not sense or react to satiety as clearly as others may be more likely to eat to excess when the opportunity presents. Processed, high-fat, and high-calorie fast foods have become abundant. Fast food also has an appealing taste and is widely available to most people worldwide. The researchers also suggest further work to identify ways to increase satiety responsiveness as an approach to obesity prevention.