AMINO ACIDS, SEROTONIN AND BODY WEIGHT REGULATION

点击翻译按钮获取中文摘要

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Anorexia nervosa (AN) is a serious psychiatric disorder resulting in psychosocial distress for patients and their families, potentially severe medical consequences, and substantial long-term mortality. Occuring most commonly in young women, the disorder is frequently refractory to currently available treatments. Moreover, weight restoration achieved during extended inpatient or outpatient treatment is often followed by recurrence of eating disorder symptoms and relapse to low weight. A major emphasis in current therapeutic research in AN is exploration of new interventions to stabilize recovery and prevent relapse in patients who have achieved weight restoration. This project focuses on stabilization of recovery in AN. Although the etiology of AN is unknown, altered regulation of the neurotransmitter serotonin in the central nervous system (CNS) is thought to contribute to preoccupation with body shape and weight, dysregulated eating patterns, persistent anxiety, and frequent mood fluctuations. Abnormalities in CNS serotonin regulation have also been identified in individuals who have recovered from AN, as reflected in elevated levels of the serotonin metabolite 5-HIAA in cerebrospinal fluid, alterations in serotonin receptor function in PET imaging studies and altered behavioral responses following administration of serotonin-active drugs. This project uses a randomized, placebo-controlled, double-blind crossover design to assess the potential therapeutic effects ofa mixture of branched-chain amino acids in individuals who have recovered from AN. It is hypothesized this intervention, by decreasing serotonin synthesis through lowered CNS tryptophan levels, will diminish residual eating disorder symptoms.