It is now a well-known fact that obesity is largely influenced by genetics, and obesity-related genes are being identified. Based on numerous twin, family, and adoption studies, our weight is heritable by more than 50 percent. However, if that’s the case, why is the world fatter now than ever before, and why has obesity not been so widespread 200 years ago?
The answer may lie in the way that our current environment, sense of satiety and obesity genes interact through a satiety responsiveness mechanism.
In a recent study discussed at a session yesterday, Jane Wardle, PhD, and colleagues tested the hypothesis that satiety responsiveness is associated with polygenic obesity risk, and may thus be an intermediate neurobehavioral process that links genetic risk of obesity with weight gain. They observed a population-based cohort of twin children and found that low satiety responsiveness is one of the mechanisms through which genetic predisposition leads to weight gain in a food-rich environment.
Evolutionarily, it makes sense and explains why so many more children and adults are obese now than at any point in the past. Food, and specifically processed, high-fat, high-sugar and high-calorie fast food has been at the peak of its abundance for years. It is also highly appealing because of its taste, and is available to the vast majority of people worldwide due to low cost. Individuals who are genetically predisposed to low satiety and who choose to eat these (and other energy-dense) foods are at higher risk for obesity than those who do not have the genetic predisposition. The latter ones will feel a satiety response kick in after consuming an adequate number of calories, whereas the former group will continue eating as the satiety response will be weak, or not kick in until much later in the eating process. When such energy-dense foods were not available in the past, individuals genetically predisposed to low satiety were at a lower risk for obesity than they are now, simply because of the unavailability of caloric overabundance in the environment.
Knowing that this is one way in which our genes predispose us to overeating and obesity, can we take certain practical steps to lower the obesity pandemic? Could enhancing the satiety response help prevent weight gain in the genetically at-risk individuals? If so, should they all just sprinkle Sensa on everything they eat throughout their lifetime, or is that not enough? Is it possible that after enhancing the satiety response, the brains and bodies of the predisposed individuals will find other strategies to increase caloric intake and maintain obesity?
While the science may not have all the answers yet, these are all important questions to ask as the large-scale research on understanding, preventing, and treating obesity continues. It is a complex and multi-faceted disease and even though tackling it via satiety enhancement may not solve all obesity cases, it may nevertheless put us one step closer to lowering obesity rates worldwide.
Nicole Avena, PhD studies appetite and addiction at the NY Obesity Research Center, at Columbia University. You can learn more about her work at DrNicoleAvena.com. She can also be found on Twitter and Facebook, or on her Psychology Today blog.