The drive to eat: comparisons and distinctions between mechanisms of food reward and drug addiction

Department of Psychiatry, Yale University School of Medicine, New Haven, Connecticut, USA.
Nature Neuroscience (Impact Factor: 14.98). 09/2012; 15(10):1330-1335. DOI: 10.1038/nn.3202

ABSTRACT The growing rates of obesity have prompted comparisons between the uncontrolled intake of food and drugs; however, an evaluation of the equivalence of food- and drug-related behaviors requires a thorough understanding of the underlying neural circuits driving each behavior. Although it has been attractive to borrow neurobiological concepts from addiction to explore compulsive food seeking, a more integrated model is needed to understand how food and drugs differ in their ability to drive behavior. In this Review, we will examine the commonalities and differences in the systems-level and behavioral responses to food and to drugs of abuse, with the goal of identifying areas of research that would address gaps in our understanding and ultimately identify new treatments for obesity or drug addiction.

  • Source
  • [Show abstract] [Hide abstract]
    ABSTRACT: Fat is a vital macronutrient, and its intake is closely monitored by an array of molecular sensors distributed throughout the alimentary canal. In the mouth, dietary fat constituents such as mono- and diunsaturated fatty acids give rise to taste signals that stimulate food intake, in part by enhancing the production of lipid-derived endocannabinoid messengers in the gut. As fat-containing chyme enters the small intestine, it causes the formation of anorexic lipid mediators, such as oleoylethanolamide, which promote satiety. These anatomically and functionally distinct responses may contribute to the homeostatic control and, possibly, the pathological dysregulation of food intake.
    Journal of Clinical Investigation 02/2015; 125(3):1-8. DOI:10.1172/JCI76302 · 13.77 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Obesity is associated with abnormal brain reactivity in response to palatable food consumption, a factor that may contribute to non-homeostatic eating. However, little is known about how obesity interacts with the reinforcing effects of highly palatable constituents of food (e.g., fat), and if altered reinforcement processes associated with obesity generalize to non-food reinforcers. The current study compared the reinforcing effects of a fat (corn oil) and a drug of abuse (cocaine) in obese and lean Zucker rats. Specifically, obese and lean Zucker rats self-administered corn oil or intravenous cocaine in a behavioral economic demand procedure. For corn oil, maximum demand was higher and demand elasticity was lower in the obese rats compared to their lean counterparts. However, there were no differences in demand for cocaine between the obese and lean rats. These results demonstrate that a fat in the form of corn oil is a more effective reinforcer in obese Zucker rats. However, the fact that demand for cocaine was not different between the obese and lean rats suggests that differences in reward mechanisms may be reinforcer-specific and do not necessarily generalize to non-food reinforcers. Copyright © 2015. Published by Elsevier Inc.
    Physiology & Behavior 03/2015; 143. DOI:10.1016/j.physbeh.2015.03.002 · 3.03 Impact Factor