Explicating the role of amygdala substructure alterations in the link between hypoleptinemia and rumination in anorexia nervosa

Author:

Wronski Marie‐Louis12ORCID,Hohnemann Charlotte3,Bernardoni Fabio1ORCID,Bahnsen Klaas1,Doose Arne1,Arold Dominic1,Borucki Katrin4,Holsen Laura M.5ORCID,Lawson Elizabeth A.2ORCID,Plessow Franziska2ORCID,Weidner Kerstin6,Roessner Veit7,Diestel Stefan3,King Joseph A.1ORCID,Seidel Maria1ORCID,Ehrlich Stefan18ORCID

Affiliation:

1. Translational Developmental Neuroscience Section, Division of Psychological and Social Medicine and Developmental Neurosciences, Faculty of Medicine Technische Universität Dresden Dresden Germany

2. Neuroendocrine Unit, Department of Medicine Massachusetts General Hospital and Harvard Medical School Boston Massachusetts USA

3. Schumpeter School of Business and Economics, Faculty of Economy University of Wuppertal Wuppertal Germany

4. Department of Clinical Chemistry and Pathobiochemistry Otto‐von‐Guericke University Magdeburg Magdeburg Germany

5. Division of Women's Health, Department of Medicine/Department of Psychiatry Brigham and Women's Hospital and Harvard Medical School Boston Massachusetts USA

6. Department of Psychotherapy and Psychosomatic Medicine, Faculty of Medicine Technische Universität Dresden Dresden Germany

7. Department of Child and Adolescent Psychiatry, Faculty of Medicine Technische Universität Dresden Dresden Germany

8. Eating Disorder Treatment and Research Center, Department of Child and Adolescent Psychiatry, Faculty of Medicine Technische Universität Dresden Dresden Germany

Abstract

AbstractObjectiveThe amygdaloid complex plays a pivotal role in emotion processing and has been associated with rumination transdiagnostically. In anorexia nervosa (AN), we previously observed differential reductions of amygdala nuclei volumes (rostral‐medial cluster substantially affected) and, in another study, elevated food−/weight‐related rumination. Both amygdala volumes and rumination frequency correlated with characteristically suppressed leptin levels in AN. Thus, we hypothesized that amygdala nuclei alterations might be associated with AN‐related rumination and potentially mediate the leptin‐rumination relationship in AN.MethodsRumination (food−/weight‐related) was assessed using ecological momentary assessment for a 14‐day period. We employed frequentist and Bayesian linear mixed effects models in females with AN (n = 51, 12–29 years, majority admitted to inpatient treatment) and age‐matched healthy females (n = 51) to investigate associations between rostral‐medial amygdala nuclei volume alterations (accessory basal, cortical, medial nuclei, corticoamygdaloid transitions) and rumination. We analyzed mediation effects using multi‐level structural equation models.ResultsReduced right accessory basal and cortical nuclei volumes predicted more frequent weight‐related rumination in AN; both nuclei fully mediated the effect of leptin on weight‐related rumination. In contrast, we found robust evidence for the absence of amygdala nuclei volume effects on rumination in healthy females.ConclusionThis study provides first evidence for the relevance of specific amygdala substructure reductions regarding cognitive symptom severity in AN and points toward novel mechanistic insight into the relationship between hypoleptinemia and rumination, which might involve the amygdaloid complex. Our findings in AN may have important clinical value with respect to understanding the beneficial neuropsychiatric effects of leptin (treatment) in AN and potentially other psychiatric conditions such as depression.

Funder

Deutsche Forschungsgemeinschaft

Schweizerische Anorexia Nervosa Stiftung

B. Braun-Stiftung

Publisher

Wiley

Subject

Psychiatry and Mental health

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