The relevance of the microbe-gut-brain axis to psychopathology is of interest in anorexia nervosa (AN), as the intestinal microbiota plays a critical role in metabolic function and weight regulation.
We characterized the composition and diversity of the intestinal microbiota in AN, using stool samples collected at inpatient admission (T1; n = 16) and discharge (T2; n = 10). At T1, participants completed the Beck Depression and Anxiety Inventories and the Eating Disorder Examination–Questionnaire. Patients with AN were compared with healthy individuals who participated in a previous study (healthy comparison group; HCG). Genomic DNA was isolated from stool samples, and bacterial composition was characterized by 454 pyrosequencing of the 16S rRNA gene. Sequencing results were processed by the Quantitative Insights Into Microbial Ecology pipeline. We compared T1 versus T2 samples, samples from both points were compared with HCG (n = 12), and associations between psychopathology and T1 samples were explored.
In patients with AN, significant changes emerged between T1 and T2 in taxa abundance and beta (between-sample) diversity. Patients with AN had significantly lower alpha (within-sample) diversity than did HCG at both T1 (p = .0001) and T2 (p = .016), and differences in taxa abundance were found between AN patients and HCG. Levels of depression, anxiety, and eating disorder psychopathology at T1 were associated with composition and diversity of the intestinal microbiota.
We provide evidence of an intestinal dysbiosis in AN and an association between mood and the enteric microbiota in this patient population. Future directions include mechanistic investigations of the microbe-gut-brain axis in animal models and association of microbial measures with metabolic changes and recovery indices.
From the Departments of Nutrition (Kleiman, Bulik), Psychiatry (Watson, Tarantino, Bulik), and Medicine (Huh, Carroll), the University of North Carolina at Chapel Hill, Chapel Hill, North Carolina; Eating Disorders Program, Child and Adolescent Health Service, Department of Health in Western Australia (Watson), Australia; School of Psychology and Speech Pathology (Watson), Curtin University, Australia; School of Paediatrics and Child Health (Watson), The University of Western Australia, Australia; Kenyon College, United States (Bulik-Sullivan); and Department of Medical Epidemiology and Biostatistics (Bulik), Karolinska Institutet, Stockholm, Sweden.
Address correspondence and reprint requests to Ian M. Carroll, PhD, University of North Carolina at Chapel Hill, 111 Mason Farm Rd, CB #7032, 7340 MBRB Building, Chapel Hill, NC 27599-7032. E-mail: email@example.com
Received for publication December 30, 2014; revision received July 9, 2015.