Binge eating is characterized by recurrent episodes of eating, in a discrete period of time, an amount of food that is much larger than most people would eat in a similar time period under similar circumstances. There is a sense of lack of control over eating during the episode. Eating is much more rapid than normal and one eats until feeling uncomfortably full. After overeating one feels disgusted, depressed or guilty. Binge eating disorder is included in eating disorders not elsewhere specified in the DSM-IV and is a symptom of bulimia nervosa and anorexia nervosa.
Research has shown that patients with eating disorders have high rates of co-occuring substance use disorders. The substance of abuse and food appear to compete for sites in the brain and abstinence from substance use causes craving for the substance and also for food. Addictions involving food and substances share similar etiologies and behavioral symptoms. Individuals suffering from binge eating disorder are more likely to have first degree relatives with a substance abuse disorder. According to retrospective reports of patients, the initiation of disordered eating usually began before substance abuse. The general reward pathway includes the ventral tegmental area and basal forebrain. Substance abuse has been shown to change the neural processes around these connections. The mesolimbic dopamine system connects the ventral tegmental area to the basal forebrain and is critical for the self-administration of psychomotor stimulants. Dopamine deficiency has been suggested to be a common characteristic of individuals who are prone to substance or food addiction. Striatal dopamine receptor (DRD2) availability is significantly lower in obese individuals than in controls. Body mass index is shown to correlate inversely with measures of D2 receptors.
Functional neuroimaging studies have revealed that pleasant smelling, looking, and tasting food has reinforcing characteristics similar to drugs of abuse. Many of the brain changes reported for hedonistic eating are also seen in various types of addiction. Overeating may have an acquired drive similar to drug addiction with respect to motivation and incentive craving. In both cases, the desire and continued satisfaction occur after early and repeated exposure to stimuli.
Addictive behavior manifests itself in permanent preoccupation with food and eating, withdrawal symptoms, continuation of disturbed eating behavior in spite of negative consequences, loss of control, and frequent relapse.
Human and animal studies have demonstrated that in some brains the consumption of sugar-rich foods or drinks primes the release of euphoric endorphins and dopamine within the nucleus accumbens, in a manner similar to some drugs of abuse. The neurobiological pathways of drug and "sugar addiction" involve similar neural receptors, neurotransmitters, and hedonistic regions in the brain. Craving, tolerance, withdrawal, and sensitization have been documented in both human and animal studies. In addition, there appears to be cross sensitization between sugar addiction and narcotic dependence in some individuals There also appears to be some common genetic markers between alcohol dependence, bulimia, and obesity, such as the A1 allele gene and the dopamine 2 receptor gene.