Body mass index (BMI) regulates prediction error and food intake control circuitry in the brain, and once altered, the circuitry may activate a response that triggers eating disorder behaviors, according to research results published in JAMA Psychiatry.
In this cross-sectional imaging study, 197 young women with eating disorders were recruited, along with 120 women serving as the healthy control participants at a university imaging facility and eating disorder treatment program. The participants had a mean age of 23.8 (SD, 5.6) years and a mean BMI of 20.8 (SD, 5.4).
The participants in the eating disorder group included a spectrum of eating disorder subtypes: anorexia nervosa (AN) restricting (n=69), binge-eating/purging (n=22), other specified feeding and eating disorders (OSFED) atypical AN (n=17), OSFED purging disorder (n=17), bulimia nervosa (n=56), OSFED binge-eating (n=3), and binge-eating disorder (n=13).
Within the study, participants had to learn to associate 3 taste stimuli (1 molar sucrose solution, no solution, or artificial saliva) with paired visual stimuli. Using probability theory, each conditioned visual stimulus was associated with its unconditioned taste stimulus. The conditioning paradigm evoked the dopamine-related prediction error.
Compared with the healthy control participants and those with bulimia nervosa and binge-eating disorder, the prediction error of participants with anorexia nervosa remained elevated (P =.001). Significant brain response-behavior correlations between BMI and prediction response were found within the eating disorder group.
Investigators found significant correlations between the following and prediction error response: BMI (left nucleus accumbens: r = -0.291; 95% CI, -0.413 to -0.167; P < .001; left ventral anterior insula: r = -0.208; 95% CI, -0.339 to -0.070; P = .004); binge-eating frequency (left nucleus accumbens: r = -0.183; 95% CI, -0.312 to -0.055; P = .01; left ventral anterior insula: r = -0.084; 95% CI, −0.212 to -0.047; P = .26), Eating Disorder Inventory-3 bulimia (left nucleus accumbens: r = -0.207; 95% CI, -0.333 to -0.073; P = .004; left ventral anterior insula: r = -0.143; 95% CI, -0.282 to -0.010; P = .047); and trait anxiety (left nucleus accumbens: r = -0.148; 95% CI, -0.288 to -0.003; P = .04; left ventral anterior insula: r = -0.166; 95% CI, -0.315 to -0.001; P = .02).
The study was limited by the small to moderate effect sizes. The prediction error model is based on dopamine function, but other neurotransmitter systems most likely affect reward processing and behavior control in eating disorders. Dopamine neuronal function was not measured directly within this study. There were no hormonal measures.
The researchers concluded, “Clinically it therefore may be important to implement weight gain in eating disorders in people with underweight and weight loss in eating disorders associated with overweight to normalize brain function and behavior.”
They added, “Furthermore, temperamental traits are biologically oriented behaviors that affect eating disorder behaviors. Treatment modules that specifically target those behaviors may be a key element to promote behavior change and lasting recovery.”