The causes of obesity are complex, but new research suggests that some people are genetically predisposed to be addicted to food. Paul Kenny, professor of pharmacology and systems therapeutics at the Icahn School of Medicine at Mount Sinai, and his lab are studying how genetic variations in one particular brain protein, the dopamine D2 receptor, can cause compulsive overeating
AAASMC's Summer Allen interviewed Kenny about his research exploring the intersection of addiction and obesity. He presented his talk, "Understanding Vulnerability to Obesity" during the 2014 AAAS Annual Meeting as part of the "Addiction: Our Compulsions and Brain Reward Systems" symposium on Friday, Feb. 14.
AAASMC: What are the similarities between overeating and other addictive behaviors?
Paul Kenny, professor of pharmacology and systems therapeutics at the Icahn School of Medicine at Mount Sinai: At the most basic level, overeating and compulsive drug use share the feature that those who suffer from these disorders express a desire to limit their intake, yet continuously "relapse" to destructive patterns of consummatory behavior. The question we seek to answer is whether this similarity is analogous (different mechanisms) or homologous (same mechanisms).
AAASMC: Can you briefly explain your findings about the relationship between dopamine D2 receptor variation and the risk of developing obesity?
Kenny: We find that overweight and obese rats demonstrated reduced levels of D2 receptors in [a part of the brain called the] striatum. Obese humans also show reduced availability of D2 receptors, presumably reflecting their reduced expression at the cell surface. We have investigated the functional significance of this observation by using a virus to knock down D2 receptors in striatum of rats and find that it increases the vulnerability of rats to develop compulsive patterns of eating.
AAASMC: In humans, do D2 receptor variations map to different geographical areas? How are populations with this risk factor affected by the globalization of fast food?
Kenny: I am unaware of the evidence linking D2 receptor polymorphisms to geographic region. Of course, such genetic variation usually occurs independently in discrete populations, so one would presume that there would indeed be geographic concentration, assuming that it was not so long ago that it has been diluted with the passage of time. However, I do not know this literature well.
AAASMC: What can people do to prevent or curb addictive eating behaviors? After all, everyone needs to eat food—unlike, say, smoke cigarettes.
Kenny: I would suggest exerting greater cognitive control—not over if you eat, but over what you eat. Of course, food is essential for survival. But some foods are more pleasant, "dangerous" and presumably habit-forming than others (hamburger versus salad). If you can exert control over your food selections, that helps curb consumption of unhealthy food. Even if you fail in this regard, try again. With practice, hopefully your ability to control food choice increases and you gain control over damaging eating patterns. It is to be hoped that novel medications will emerge that can facilitate this process also.
AAASMC: What are the implications of this research for future drug or behavioral therapies for people struggling with obesity?
Kenny: For me, the most important potential implications of this and similar research is the fact that food is not as innocuous as one would imagine. Highly palatable food, rich in calories, can support the emergence of compulsive-like eating that gradually impacts the ability of the subject to exert control over their food choices. If applicable to humans, this could provide comfort to those who are struggling to control their weight [indicating] that there is indeed a neurobiological mechanism at play, and that with continued effort you may be able to overcome this hurdle. Moreover, understanding the nature of this process could yield new approaches to treat compulsive eating, and perhaps compulsive drug-use and other addictions also.