From the Department of Child and Adolescent Psychiatry, Psychotherapy and Psychosomatics, University Hospital, RWTH University Aachen, Germany (Borsdorf, Dahmen, Buehren, Scharke, Herpertz-Dahlmann, Seitz); the kbo-Heckscher Klinikum, Academic Teaching Hospital, Ludwig Maximilian University, Munich, Germany (Buehren); the Institute of Medical Informatics and Statistics, Kiel University, Germany (Dempfle); the Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, University Hospital, Wuerzburg, Germany (Egberts); the Translational Developmental Neuroscience Section, Division of Psychological and Social Medicine and Developmental Neurosciences, Faculty of Medicine, TU Dresden, Germany (Ehrlich); the Eating Disorders Research and Treatment Center, Department of Child and Adolescent Psychiatry, Faculty of Medicine, TU Dresden, Germany (Ehrlich); the Department of Child and Adolescent Psychiatry and Psychotherapy, University Medical Center Freiburg, Germany (Fleischhaker); the Child Neuropsychology Section, Department of Child and Adolescent Psychiatry, Psychotherapy and Psychosomatics, University Hospital, RWTH University Aachen (Konrad); the JARA-Institute Molecular Neuroscience and Neuroimaging (INM-11), Juelich Research Centre, Germany (Konrad); the Oberberg Fachklinik Konraderhof, Cologne-Huerth, Germany (Schwarte); the Institute of Medical Biometry and Epidemiology, Philipps-University Marburg, Germany (Timmesfeld); the Department of Medical Informatics, Biometrics and Epidemiology, Ruhr University Bochum, Germany (Timmesfeld); the Department of Child and Adolescent Psychiatry and Psychotherapy, Cologne City Hospitals, Germany (Wewetzer); the Institute of Laboratory Medicine, Clinical Chemistry and Molecular Diagnostics, University of Leipzig, Germany (Biemann); the Cognitive and Experimental Psychology, Institute of Psychology, RWTH Aachen University, Germany (Scharke).
From the Department of Child and Adolescent Psychiatry, Psychotherapy and Psychosomatics, University Hospital, RWTH University Aachen, Germany (Borsdorf, Dahmen, Buehren, Scharke, Herpertz-Dahlmann, Seitz); the kbo-Heckscher Klinikum, Academic Teaching Hospital, Ludwig Maximilian University, Munich, Germany (Buehren); the Institute of Medical Informatics and Statistics, Kiel University, Germany (Dempfle); the Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, University Hospital, Wuerzburg, Germany (Egberts); the Translational Developmental Neuroscience Section, Division of Psychological and Social Medicine and Developmental Neurosciences, Faculty of Medicine, TU Dresden, Germany (Ehrlich); the Eating Disorders Research and Treatment Center, Department of Child and Adolescent Psychiatry, Faculty of Medicine, TU Dresden, Germany (Ehrlich); the Department of Child and Adolescent Psychiatry and Psychotherapy, University Medical Center Freiburg, Germany (Fleischhaker); the Child Neuropsychology Section, Department of Child and Adolescent Psychiatry, Psychotherapy and Psychosomatics, University Hospital, RWTH University Aachen (Konrad); the JARA-Institute Molecular Neuroscience and Neuroimaging (INM-11), Juelich Research Centre, Germany (Konrad); the Oberberg Fachklinik Konraderhof, Cologne-Huerth, Germany (Schwarte); the Institute of Medical Biometry and Epidemiology, Philipps-University Marburg, Germany (Timmesfeld); the Department of Medical Informatics, Biometrics and Epidemiology, Ruhr University Bochum, Germany (Timmesfeld); the Department of Child and Adolescent Psychiatry and Psychotherapy, Cologne City Hospitals, Germany (Wewetzer); the Institute of Laboratory Medicine, Clinical Chemistry and Molecular Diagnostics, University of Leipzig, Germany (Biemann); the Cognitive and Experimental Psychology, Institute of Psychology, RWTH Aachen University, Germany (Scharke)
J Psychiatry Neurosci. 2021 Sep 1;46(5):E568-E578. doi: 10.1503/jpn.210049. Print 2021 Sep-Oct.
Brain-derived neurotrophic factor (BDNF) influences brain plasticity and feeding behaviour, and it has been linked to anorexia nervosa in numerous studies. Findings in mostly adult patients point to reduced serum BDNF levels in the acute stage of anorexia nervosa and rising levels with weight recovery. However, it is unclear whether this increase leads to normalization or supranormal levels, a difference that is potentially important for the etiology of anorexia nervosa and relapse.
We measured serum BDNF at admission ( = 149), discharge ( = 130), 1-year follow-up ( = 116) and 2.5-year follow-up ( = 76) in adolescent female patients with anorexia nervosa hospitalized for the first time, and in healthy controls ( = 79). We analyzed associations with body mass index, eating disorder psychopathology and comorbidities.
Serum BDNF was only nominally lower at admission in patients with anorexia nervosa compared to healthy controls, but it increased continuously and reached supranormal levels at 2.5-year follow-up. BDNF was inversely associated with eating disorder psychopathology at discharge and positively associated with previous weight gain at 1-year follow-up.
We compensated for attrition and batch effects using statistical measures.
In this largest longitudinal study to date, we found only nonsignificant reductions in BDNF in the acute stage of anorexia nervosa, possibly because of a shorter illness duration in adolescent patients. Supranormal levels of BDNF at 2.5-year follow-up could represent a pre-existing trait or a consequence of the illness. Because of the anorexigenic effect of BDNF, it might play an important predisposing role for relapse and should be explored further in studies that test causality.
脑源性神经营养因子（BDNF）影响大脑的可塑性和进食行为，并且在许多研究中与神经性厌食症有关。在大多数成年患者中的研究结果表明，神经性厌食症急性发作时血清 BDNF 水平降低，随着体重恢复而升高。然而，尚不清楚这种增加是否会导致正常化或超正常化水平，这种差异对于神经性厌食症的病因和复发可能具有重要意义。
我们测量了首次住院的青少年女性神经性厌食症患者入院时（n=149）、出院时（n=130）、1 年随访时（n=116）和 2.5 年随访时（n=76）的血清 BDNF，以及健康对照组（n=79）。我们分析了血清 BDNF 与体重指数、进食障碍心理病理学和合并症之间的关系。
与健康对照组相比，神经性厌食症患者入院时血清 BDNF 仅略低，但连续升高，在 2.5 年随访时达到超正常水平。BDNF 与出院时的进食障碍心理病理学呈负相关，与 1 年随访时的体重增加呈正相关。
我们使用统计措施补偿了损耗和批次效应。
在迄今为止最大的纵向研究中，我们仅发现神经性厌食症急性发作时 BDNF 有轻微降低，这可能是因为青少年患者的疾病持续时间较短。2.5 年随访时 BDNF 的超正常水平可能代表一种预先存在的特征或疾病的结果。由于 BDNF 的厌食作用，它可能在复发的研究中扮演一个重要的易感性角色，并应进一步探索以检验因果关系。
