Brain White Matter Abnormalities in Binge Eating Disorder

Abstract

Binge eating disorder (BED) is characterised by loss of control around feeding behaviour. Patients suffer from binge eating episodes, where they consume large amounts of food even to a point of feeling uncomfortable fullness. An important clinical difference between binge eating disorder and bulimia nervosa, is that in binge eating disorder, patients do not use compensatory mechanisms, such as self-induced vomiting or over-exercise. It is a disorder that is associated with significant clinical impairment, but its neurobiological underpinnings remain poorly understood. In this pilot study, diffusion tensor imaging was used to examine white matter organisation in patients with a binge eating disorder by comparing diffusion imaging measures across patients with a binge eating disorder, gambling disorders, and healthy controls. Gambling disorder was chosen as a comparison group as binge eating disorder shares many clinical and symptomatic similarities behavioural addictions. Gambling disorder is currently the only officially recognised behavioural addiction. Diffusion tensor imaging data were analysed to assess fractional anisotropy, mean diffusivity, axial diffusivity, and radial diffusivity. Group comparisons were conducted to identify differences in white matter microstructure and clinical and demographic variables, including symptom severity scores and body mass index. Individuals with BED exhibited significantly higher fractional anisotropy across multiple right- hemispheric white matter regions compared to both healthy controls and the gambling disorder group. BED exhibited increased FA in the retro lenticular part of the internal capsule and the posterior corona radiata compared to the healthy control group. Compared to the gambling group, BED group had increased FA in the anterior, superior, and posterior corona radiata, the body of corpus callosum, the posterior thalamic radiation, and the retro lenticular part of internal capsule. No significant differences in other diffusion measures were observed. Additionally, elevated FA positively correlated with binge eating severity and negatively associated with body mass index. These findings offer an insight into the neurobiology of binge eating disorder and suggest that BED may be associated by altered brain white matter organisation that differs from gambling disorder. Elevated FA in the absence of changes in other diffusion measures may reflect abnormalities in network organisation or there may be constrained efficiency, rather than pure damage to white matter tracts that is typically associated with reduced FA.