COMMENTS: This study demonstrates sensitization in lean adolescents at risk for obesity (parents are obese). Sensitization means that their reward circuitry releases more dopamine when exposed to food cues than their “normal” counterparts.
Do people overeat because they experience less reward from eating or because they experience more reward from eating? In the March 23, 2011 issue of The Journal of Neuroscience Oregon Research Institute (ORI) senior scientist Eric Stice, Ph.D. and colleagues, including Dana Small, Ph.D. from the J.B. Pierce Laboratory in New Haven Connecticut, provide possible answers to the chicken or egg dilemma of overeating.
Food intake produces dopamine release and the degree of pleasure from eating correlates with the amount of dopamine release. Studies have found that obese relative to lean humans have fewer dopamine (D2) receptors in the brain and it is thought that obese individuals overeat to compensate for this reward deficit.
However, a recent study from Stice and colleagues found that weight gain produced a blunted response to intake of palatable food (chocolate milkshake), suggesting that overeating may lead to reduced reward from food, rather than represent an initial vulnerability factor.
In a novel study using functional Magnetic Resonance Imaging (fMRI) Stice’s team compared the neural response to food and monetary reward in lean adolescents at risk for obesity relative to lean adolescents not at risk for obesity. Results suggest that the initial vulnerability that gives rise to obesity may be elevated rather than blunted sensitivity of the brain’s reward circuitry.
Study participants were 60 lean adolescents. The high-risk teens were children of two obese or overweight parents. The low-risk teens had two lean parents. Adolescent children of obese versus normal-weight parents show a fourfold increase in risk for obesity onset.
Using a brain imaging paradigm, investigators examined the extent to which reward circuitry (e.g., the dorsal striatum) was activated in response to the individual’s consumption and anticipated consumption of chocolate milkshake. The team also used another paradigm to assess brain activation in response to receipt and anticipated receipt of money. Monetary reward is a general reinforcer and has been used frequently to assess reward sensitivity. High-risk youth showed greater activation in reward circuitry to receipt of both food and monetary reward, as well as greater activation in somatosensory regions in response to receipt of food.
“The findings are surprising,” noted Stice. “They suggest that the initial vulnerability for overeating may be hyper-responsivity of reward circuitry to food intake. The fact that the same reward regions showed greater response to monetary reward is novel and implies that individuals at risk for obesity show greater responsivity to reward in general. These findings seem to challenge the widely accepted theory that it is a reward deficit that increases vulnerability to overeating.”
Stice and his team also found that at-risk youth showed hyper-responsivity of somatosentory regions to food intake, which plays a key role in sensing the fat content of food. These results suggest that individuals who are particularly sensitive to detecting high-fat foods may be at unique risk for overeating.
Funded by the National Institutes of Health (NIH), Stice has been studying eating disorders and obesity for 20 years. He has conducted this line of research at Stanford University and the University of Texas, and now continues at the Oregon Research Institute in Eugene, Oregon. This research program has produced several prevention programs that effectively reduce risk for onset of eating disorders and obesity.
Oregon Research Institute is a non-profit, independent behavioral research center with headquarters in Eugene. Founded in 1960, it also has offices in Portland, Oregon and Albuquerque, New Mexico.
Youth at Risk for Obesity Show Greater Activation of Striatal and Somatosensory Regions to Food
The Journal of Neuroscience, 23 March 2011, 31(12): 4360-4366; doi: 10.1523/JNEUROSCI.6604-10.2011
Eric Stice1, Sonja Yokum1, Kyle S. Burger1, Leonard H. Epstein2, and Dana M. Small3,4
+ Author Affiliations
1Oregon Research Institute, Eugene, Oregon 97403,
2University at Buffalo, Behavioral Medicine, Buffalo NY, 14214,
3The John B. Pierce Laboratory, New Haven, Connecticut 06519, and
4Yale University School of Medicine, Department of Psychiatry, New Haven, Connecticut 06511
Obese humans, compared with normal-weight humans, have less striatal D2 receptors and striatal response to food intake; weaker striatal response to food predicts weight gain for individuals at genetic risk for reduced dopamine (DA) signaling, consistent with the reward-deficit theory of obesity. Yet these may not be initial vulnerability factors, as overeating reduces D2 receptor density, D2 sensitivity, reward sensitivity, and striatal response to food. Obese humans also show greater striatal, amygdalar, orbitofrontal cortex, and somatosensory region response to food images than normal-weight humans do, which predicts weight gain for those not at genetic risk for compromised dopamine signaling, consonant with the reward-surfeit theory of obesity. However, after pairings of palatable food intake and predictive cues, DA signaling increases in response to the cues, implying that eating palatable food contributes to increased responsivity. Using fMRI, we tested whether normal-weight adolescents at high- versus low-risk for obesity showed aberrant activation of reward circuitry in response to receipt and anticipated receipt of palatable food and monetary reward. High-risk youth showed greater activation in the caudate, parietal operculum, and frontal operculum in response to food intake and in the caudate, putamen, insula, thalamus, and orbitofrontal cortex in response to monetary reward. No differences emerged in response to anticipated food or monetary reward. Data indicate that youth at risk for obesity show elevated reward circuitry responsivity in general, coupled with elevated somatosensory region responsivity to food, which may lead to overeating that produces blunted dopamine signaling and elevated responsivity to food cues.