J Psychiatry Neurosci 2018;43(3):151-160
Laura A. Berner, PhD; Mihaela Stefan, MA; Seonjoo Lee, PhD; Zhishun Wang, PhD; Kate Terranova, BA; Evelyn Attia, MD; Rachel Marsh, PhD
Background: Frontostriatal and frontoparietal abnormalities likely contribute to deficits in control and attentional processes in individuals with bulimia nervosa and to the persistence of dysregulated eating across development. This study assessed these processes and cortical thickness in a large sample of adolescent girls and women with bulimia nervosa compared with healthy controls.
Methods: We collected anatomical MRI data from adolescent girls and women (ages 12–38 yr) with full or subthreshold bulimia nervosa and age-matched healthy controls who also completed the Conners Continuous Performance Test-II (CPT-II). Groups were compared on task performance and cortical thickness. Mediation analyses explored associations among cortical thickness, CPT-II variables, bulimia nervosa symptoms and age.
Results: We included 60 girls and women with bulimia nervosa and 54 controls in the analyses. Compared with healthy participants, those with bulimia nervosa showed increased impulsivity and inattention on the CPT-II, along with reduced thickness of the right pars triangularis, right superior parietal and left dorsal posterior cingulate cortices. In the bulimia nervosa group, exploratory analyses revealed that binge eating frequency correlated inversely with cortical thickness of frontoparietal and insular regions and that reduced frontoparietal thickness mediated the association between age and increased symptom severity and inattention. Binge eating frequency also mediated the association between age and lower prefrontal cortical thickness.
Limitations: These findings are applicable to only girls and women with bulimia nervosa, and our cross-sectional design precludes understanding of whether cortical thickness alterations precede or result from bulimia nervosa symptoms.
Conclusion: Structural abnormalities in the frontoparietal and posterior cingulate regions comprising circuits that support control and attentional processes should be investigated as potential contributors to the maintenance of bulimia nervosa and useful targets for novel interventions.
Submitted Apr. 6, 2017; Revised July 10, 2017; Accepted Aug. 8, 2017; Published online first Jan. 16, 2018
Acknowledgments: This work and preparation of this manuscript were supported in part by grants from the National Institute of Mental Health (R01MH090062 [R. Marsh], K01MH077652 [R. Marsh], F31MH097406 [L. Berner], and F32MH108311 [L. Berner]) and from the Brain and Behavior Research Foundation (NARSAD) [R. Marsh]). The authors thank Kristin Klahr, PhD, and staff in the Eating Disorders Research Unit at the New York State Psychiatric Institute for facilitating recruitment and conducting assessments with participants. The authors also thank the participants for their time.
Affiliations: From the Eating Disorders Center for Treatment and Research, Department of Psychiatry, University of California, San Diego (Berner); the Division of Child and Adolescent Psychiatry, Columbia University Medical Center and the New York State Psychiatric Institute (Stefan, Lee, Wang, Terranova, Marsh); and the Eating Disorders Research Unit, Division of Clinical Therapeutics, Department of Psychiatry, Columbia University Medical Center and the New York State Psychiatric Institute (Attia, Marsh).
Competing interests: None declared.
Contributors: L. Berner and R. Marsh designed the study. L. Berner, K. Terranova and R. Marsh acquired the data, which L. Berner, M. Stefan, S. Lee, Z. Wang, E. Attia and R. Marsh analyzed. L. Berner, S. Lee and R. Marsh wrote the article, which all authors reviewed. All authors approved the final version to be published and can certify that no other individuals not listed as authors have made substantial contributions to the paper.
Correspondence to: L.A. Berner, Eating Disorders Center for Treatment and Research, Department of Psychiatry, University of California, San Diego, San Diego, CA 92121 USA; email@example.com