Eric Stice, Ph.D.Senior Research Scientist at Oregon Research Institute
Dr. Stice completed a Ph.D. in clinical psychology at Arizona State University, a clinical internship at the University of California San Diego, and a postdoctoral research fellowship at Stanford University in behavioral medicine. He then accepted a position at the University of Texas at Austin as an Assistant Professor, and was later promoted to Associate Professor. More recently, he accepted a position as a Senior Research Scientist at Oregon Research Institute.
His program of research has primarily focused on elucidating factors that increase risk for onset of eating disorders and obesity, as well as the development and evaluation of prevention programs for these conditions. To date he has conducted four large prospective risk factor studies and eight randomized prevention trials. He developed a cognitive dissonance-based eating disorder prevention program that reduces the extent to which adolescent girls and young women pursue the thin-ideal espoused for women in our culture. This brief intervention produced a 60% reduction in risk for onset of eating disorders over a 3-year follow-up, which is a first for an eating disorder prevention program. Of note, this intervention has produced positive effects in evaluations conducted by several independent labs. He also developed a brief healthy weight control obesity prevention program that produced a 55% reduction in risk for obesity onset over a 3-year follow-up. This also appears to be a novel finding. He is currently focusing on dissemination of these prevention programs, with the hope of affecting a reduction in the prevalence of these two serious health problems in the US.
More recently, Dr. Stice has begun using brain-imaging procedures (functional magnetic resonance imaging [fMRI]) to test whether obese individuals experience abnormal reward from food intake and anticipated food intake relative to lean individuals. Several studies that we have completed indicate that obese versus lean individuals show greater activation in the gustatory cortex and the somatosensory cortex in response to receipt of chocolate milkshake and anticipated receipt of milkshake, which are regions that encode the sensory and hedonic aspects of food reward. Yet, obese individuals also show blunted activation of the dorsal striatum in response to intake of milkshake in the scanner relative to lean individuals in several studies, potentially because obese individuals have fewer dopamine receptors in this brain region. This brain region mediates reward from food intake. We are also trying to extend the literature by conducting prospective tests of whether abnormal activation of food reward circuitry increase risk for future weight gain, as virtually all brain imaging studies are cross-sectional making it impossible to know whether the abnormalities are a precursor or consequence of obesity. These studies are revealing that abnormal activation in these brain regions do predict increased risk for future weight gain and that these effects explain much more variance in weight gain than do typical self-report measures studied previously. We have also begun genotyping participants on dopamine-related genes and find that individuals with abnormal responses in reward circuitry in response to food are at greatest risk for future weight gain if they have genotypes associated with compromised dopamine signaling. We hope to continue this line of research to better characterize abnormalities in brain reward circuitry that may increase vulnerability to weight gain.
There are several research and intervention programs that could benefit from additional financial support. I think there is a pressing need for prospective brain imaging studies that determine whether abnormal responses of brain reward circuitry to food actually predate unhealthy weight gain and or are a consequence of unhealthy weight gain. We also need to more fully characterize these abnormalities using novel procedures such as Positron Emission Tomography to map abnormal responses to receptor density and neurotransmitter levels. Amazing advances have been made in the addictions field that should be tested with regard to food addition. These studies should include a strong focus on genetic risk factors that make people more vulnerable to obesity and addiction to food. Again, much of what we have learned in the addictions literature seems germane to obesity, but has not yet been fully studied.
Equally important, it would be beneficial if there were greater financial support for evaluation of obesity prevention programs that are based on the notion that high-fat and high-sugar foods are addicting and create brain changes that increase risk for escalations in caloric intake and unhealthy weight gain. For instance, it would be very informative to evaluate an intervention that encourages parents to either reduce the amount of high-fat and high-sugar foods they feed their children or feed them as usual, to see if those in the former condition show less unhealthy weight gain and a more normal response to food intake in brain imaging studies. To my knowledge, no one has ever used fMRI in a trail evaluating of an obesity prevention program. More generally, it would also be important to disseminate obesity prevention programs on a large-scale basis to see if we can achieve a true reduction in the prevalence or incidence of obesity. At present, we know little regarding how to identify and train interventionists to deliver empirically supported obesity prevention programs on a large-scale basis.
- Relation Between Obesity and Blunted Striatal Response to Food Is Moderated by TaqIA A1 Allele
- Dissonance and Healthy Weight Eating Disorder Prevention Programs: Long-Term Effects From a Randomized Efficacy Trial
- Relation of Reward From Food Intake and Anticipated Food Intake to Obesity: A Functional Magnetic Resonance Imaging Study
- A Meta-Analytic Review of Obesity Prevention Programs for Children and Adolescents: The Skinny on Interventions That Work