From Brain Mechanisms to Novel Therapies: Understanding and Treating Eating Disorders
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Optimizing and Improving Existing Treatments
Psychosocial interventions, like cognitive behavioral therapy (CBT) and family-based therapy, are the mainstays of treatment for people with eating disorders. For some, anti-anxiety and antidepressant medications also play a role in management of the illness. While these treatments can be helpful, not everyone benefits equally from even the best treatments. For this reason, one area of focus for NIMH is research aimed at improving the efficacy and availability of existing treatments.
CBT, for example, works by teaching individuals with eating disorders to recognize and describe their food-related behaviors, examine their underlying cognitive and emotional motivations, and develop strategies to reduce these motivations and counter maladaptive eating patterns. But CBT can be challenging to deliver and reaching individuals with eating disorders in treatment, especially adolescents, can also be difficult.
One potential solution is to leverage technology to engage individuals in treatment. Three investigators at Washington University in St. Louis, home to a center for eating disorders research, are working hard in this area. Early stage investigator Ellen Fitzsimmons-Craft, Ph.D., is developing and testing an optimized conversational agent, or “Chatbot,” to facilitate mental health service use for individuals with eating disorders. In another project, Patricia Cavazos-Rehg, Ph.D., and Denise Wilfley, Ph.D., are leveraging social media to identify and connect teens who have eating disorders with a low-cost, personalized mobile health intervention to support and motivate recovery. Dr. Wilfley is also testing a similar approach in college-age youth, covering a particularly vulnerable population.
Other efforts are leveraging what we know about how the brain controls behavior to build on existing treatments in order to help more individuals with eating disorders. One approach, being studied by Stephanie Manasse, Ph.D., of Drexel University, takes advantage of the brain’s natural abilities to inhibit habitual behavior, the so-called inhibitory control system. Dr. Manasse is developing and testing a targeted adaptation of CBT for individuals with binge-eating disorder to see if enhancing inhibitory control will help reduce the frequency of binges. Another approach, pioneered by Claire Aarnio-Peterson, Ph.D., of Cincinnati Children’s Hospital, addresses the importance of engaging families in the treatment of adolescents with anorexia nervosa. Dr. Aarnio-Peterson is studying the effectiveness of a family therapy aimed at equipping parents with the skills necessary to effectively support their child through the treatment process. With these studies, researchers hope to expand the reach and effectiveness of current therapies.
From Brain Mechanisms to Novel Therapies
Eating disorders research is also benefiting from advances in neuroscience and the understanding of brain-behavior relationships. A series of studies supported over the past few years has begun to change how we think about eating disorders and potentially how we treat them. Studying the neural mechanism of food choice, a group of investigators—including Joanna Steinglass, M.D., B. Timothy Walsh, M.D., and Daphna Shohamy, Ph.D., of Columbia University—showed that individuals with anorexia had differences in activity in the striatum and prefrontal cortex that accounted for their decisions to avoid high-fat foods and these differences correlated with their restrictive eating behaviors. Around the same time, Guido Frank, M.D., and colleagues at the University of California, San Diego, showed differences in striatal reward-related signals in a separate study of individuals with anorexia.
What do these two NIMH-funded studies have in common? Reward signals in the striatum teach the striatally-based decision-making system how to choose from available options, including food options. Changes in the way these reward signals work (such as the changes discovered by Dr. Frank) could cause the striatum to change how it responds to foods (as shown by the Columbia group), triggering the maladaptive food avoidance behaviors seen in anorexia.
This neuroscience work lays the foundation for novel approaches to treating anorexia. Other NIMH-funded research has shown that striatal reward signals are mediated by the neurotransmitter dopamine. Accordingly, Dr. Frank is studying the potential of drugs that alter dopamine signaling as a way to reverse behaviors associated with anorexia nervosa. He has already published promising preliminary efficacy data from research investigating a currently available dopamine receptor blocker in individuals with anorexia nervosa. Meanwhile, Dr. Steinglass and Jonathan Posner, M.D., also of Columbia University, are studying the time course of striatal dysfunction in anorexia with the goal of developing behavioral treatments that target specific phases of the illness, preventing or reversing maladaptive food choice behaviors.
The burden of eating disorders is substantial for patients, families, and loved ones. At NIMH, we support these and other studies with the aim of reducing this burden and bringing hope to the many who bear it.
Source: National Institute of Mental Health
References
DeGuzman, M., Shott, M. E., Yang, T. T., Riederer, J., & Frank, G. (2017). Association of elevated reward prediction error response with weight gain in adolescent anorexia nervosa. The American Journal of Psychiatry, 174(6), 557–565. https://doi.org/10.1176/appi.ajp.2016.16060671
Foerde, K., Steinglass, J. E., Shohamy, D., & Walsh, B. T. (2015). Neural mechanisms supporting maladaptive food choices in anorexia nervosa. Nature Neuroscience, 18(11), 1571–1573. https://doi.org/10.1038/nn.4136
Frank, G. K., Shott, M. E., Hagman, J. O., Schiel, M. A., DeGuzman, M. C., & Rossi, B. (2017). The partial dopamine D2 receptor agonist aripiprazole is associated with weight gain in adolescent anorexia nervosa. The International Journal of Eating Disorders, 50(4), 447–450. https://doi.org/10.1002/eat.22704