Behavioral addictions are psychiatric disorders, in which the object of addiction is not a drug but instead behavior itself, such as gambling or eating. Behavioral addictions share clinical features with substance use disorder, including tolerance against behavior, continued behavior despite negative consequences, withdrawal symptoms and craving. However, little is known about the pathophysiology of these disorders. Behavioral addictions may also serve as a model to investigate the brain reward system at its purest form, without confounding chemical properties of misused drugs. 

The aim of this study was to investigate brain neurotransmitter function in behavioral addictions. Brain dopamine, opioid and serotonin systems were investigated in pathological gambling (PG), in binge eating disorder (BED) and in a control group using positron emission tomography (PET). PET scans were performed using [18F]fluorodopa to target presynaptic dopamine synthesis rate; [11C]carfentanil to label μ-opioid receptors (MORs); and [11C]MADAM to label serotonin transporter. Statistical analyses covered betweengroup comparisons in all three groups, intraregional PET tracer correlations in the PG and the control groups, and correlations between impulsivity and tracer binding in the PG and the control groups. 

BED patients showed decreased nucleus accumbens dopamine synthesis, wide-spread decreases in MOR binding, and regionally selective increases and decreases in SERT binding, whereas PG patients failed to show any changes in relation to controls. The changes were independent from possible confounding factors. Dopamine synthesis rate correlated positively with MOR binding in the basal ganglia in both PG and control groups. Impulsivity correlated inversely with SERT binding in the prefrontal cortex in controls. This association was lost in PG, and instead, midbrain MOR binding was related both with impulsivity and nucleus accumbens dopamine synthesis rate. 

The results of this study indicate that phenotypically distinct behavioral addictions differ also by their neurobiology. Importantly, the findings contrast with previously published results in substance addictions, indicating individual neurobiology in distinct addiction disorders. Whether the observed neurotransmitter alterations in BED and altered relationship between receptor densities and impulsivity in PG reflect predisposing pathophysiology or a neural adaptation remains to be established.