The role of neurotransmitter systems in eating and substance use disorders

Abstract

Eating disorders (ED) as well as substance use disorders (SUD) commonly start during adolescence and young adulthood, an important time of brain maturation that includes neurotransmitter receptor expression. Increasing attention should be paid to neurobiological mechanisms and brain circuit alterations that may be shared across those potentially related disorders. Studies in ED suggested lower cerebrospinal fluid (CSF), serotonin (5-HT), and dopamine (DA) metabolite levels, neurotransmitters involved in the regulation of eating, mood, and anxiety, among other functions. Higher 5-HT metabolite levels after recovery suggested that this could be a trait alteration. The body of CSF neurotransmitter research in SUD is small. However, alcoholism may be associated with reduced CSF 5-HT metabolites, and acute substance use may increase 5-HT release but also inhibit 5-HT neuronal activity through auto-inhibition, while withdrawal from most substances is associated with reduced extracellular 5-HT. More recent research in ED using brain imaging implicated neurotransmitter receptors such as the 5-HT 1A receptor, 5-HT 2A receptor, and 5-HT transporter or DA D2/3 receptors, which predicted high anxiety and harm avoidance. Studies in SUD suggested 5-HT and DA receptors may undergo adaptive changes during stages of the illness. Other addictive disorders include tobacco use and gambling behavior, and their neurobiology has been linked to reward and DA pathways. Overall, research suggests that 5-HT and DA are involved in the neurobiology ED and SUD as well as behavioral addictions, and comparative research across disorders should be undertaken to identify underlying mechanisms.