This meta-analytic review of prospective and experimental studies reveals that several accepted risk factors for eating pathology have not received empirical support (e.g., sexual abuse) or have received contradictory support (e.g.. dieting). There was consistent support for less-accepted risk factors(e.g., thin-ideal internalization) as well as emerging evidence for variables that potentiate and mitigate the effects of risk factors(e.g., social support) and factors that predict eating pathology maintenance(e.g., negative affect). In addition, certain multivariate etiologic and maintenance models received preliminary support. However, the predictive power of individual risk and maintenance factors was limited, suggesting it will be important to search for additional risk and maintenance factors, develop more comprehensive multivariate models, and address methodological limitations that attenuate effects.

We examined prevalence, incidence, impairment, duration, and course for the proposed DSM-5 eating disorders in a community sample of 496 adolescent females who completed annual diagnostic interviews over 8 years. Lifetime prevalence by age 20 was 0.8% for anorexia nervosa (AN), 2.6% for bulimia nervosa (BN), 3.0% for binge eating disorder (BED), 2.8% for atypical AN, 4.4% for subthreshold BN, 3.6% for subthreshold BED, 3.4% for purging disorder (PD), and combined prevalence of 13.1% (5.2% had AN, BN, or BED; 11.5% had feeding and eating disorders not elsewhere classified; FED-NEC). Peak onset age was 19-20 for AN, 16-20 for BN, and 18-20 for BED, PD, and FED-NEC. Youth with these eating disorders typically reported greater functional impairment, distress, suicidality, mental health treatment, and unhealthy body mass index, though effect sizes were relatively smaller for atypical AN, subthreshold BN, and PD. Average episode duration in months ranged from 2.9 for BN to 11.2 for atypical AN. One-year remission rates ranged from 71% for atypical AN to 100% for BN, subthreshold BN, and BED. Recurrence rates ranged from 6% for PD to 33% for BED and subthrehold BED. Diagnostic progression from subthreshold to threshold eating disorders was higher for BN and BED (32% and 28%) than for AN (0%), suggesting some sort of escalation mechanism for binge eating. Diagnostic crossover was greatest from BED to BN. Results imply that the new DSM-5 eating disorder criteria capture clinically significant psychopathology and usefully assign eating disordered individuals to homogeneous diagnostic categories.

The dorsal striatum plays a role in consummatory food reward, and striatal dopamine receptors are reduced in obese individuals, relative to lean individuals, which suggests that the striatum and dopaminergic signaling in the striatum may contribute to the development of obesity. Thus, we tested whether striatal activation in response to food intake is related to current and future increases in body mass and whether these relations are moderated by the presence of the A1 allele of the Taq IA restriction fragment length polymorphism, which is associated with dopamine D2 receptor ( DRD2 ) gene binding in the striatum and compromised striatal dopamine signaling. Cross-sectional and prospective data from two functional magnetic resonance imaging studies support these hypotheses, which implies that individuals may overeat to compensate for a hypofunctioning dorsal striatum, particularly those with genetic polymorphisms thought to attenuate dopamine signaling in this region.

The authors tested the hypothesis that obese individuals experience greater reward from food consumption (consummatory food reward) and anticipated consumption (anticipatory food reward) than lean individuals using functional magnetic resonance imaging (fMRI) with 33 adolescent girls (mean age = 15.7, SD = 0.9). Obese relative to lean adolescent girls showed greater activation bilaterally in the gustatory cortex (anterior and mid insula, frontal operculum) and in somatosensory regions (parietal operculum and Rolandic operculum) in response to anticipated intake of chocolate milkshake (vs. a tasteless solution) and to actual consumption of milkshake (vs. a tasteless solution); these brain regions encode the sensory and hedonic aspects of food. However, obese relative to lean adolescent girls also showed decreased activation in the caudate nucleus in response to consumption of milkshake versus a tasteless solution, potentially because they have reduced dopamine receptor availability. Results suggest that individuals who show greater activation in the gustatory cortex and somatosensory regions in response to anticipation and consumption of food, but who show weaker activation in the striatum during food intake, may be at risk for overeating and consequent weight gain.