caa a22 4500 44534427X CHVBK 20180317142824.0 cr unu---uuuuu 170323e20111101xx s 000 0 eng 10.1007/s00406-011-0246-y doi (NATIONALLICENCE)springer-10.1007/s00406-011-0246-y Aetiology of anorexia nervosa: from a "psychosomatic family model” to a neuropsychiatric disorder? [Elektronische Daten] [Beate Herpertz-Dahlmann, Jochen Seitz, Kerstin Konrad] Eating disorders and, in particular, anorexia nervosa (AN) have morbidity and mortality rates that are among the highest of any mental disorders and are associated with significant functional impairment. More than 25years ago, several researchers hypothesised that the prerequisite for the development of AN was a family process characterised by an overprotective and conflict-avoiding parent-child interaction. Family studies, however, suggest that AN is a complex genetic disorder that is likely expressed primarily by temperament and specific traits during childhood, including inhibition, perfectionism and harm avoidance. Recent studies have described an impaired flexibility and deficits in social cognition that are independent of body weight and the current state of the eating disorder, providing further evidence for a genetic component of AN. The physiological and psychological alterations and the increasing societal demands that occur during puberty may trigger onset. The starvation process itself is associated with severe alterations of central and peripheral metabolism, especially neuroendocrine and neurotransmitter changes, which are thought to affect the adolescent brain during the vulnerable period of neural restructuring. Long-standing malnutrition during adolescence and young adulthood associated with hormonal and neuropeptide dysfunctions may produce "biological scars” that maintain and accelerate the disorder and likely result in chronic mental disorders in adulthood as well as poor social functioning. Springer-Verlag, 2011 Anorexia nervosa nationallicence Adolescence nationallicence Genetic liability nationallicence Personality nationallicence Starvation nationallicence Brain function nationallicence Neuroendocrine changes nationallicence Herpertz-Dahlmann Beate Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, RWTH Aachen University, Neuenhofer Weg 21, 52074, Aachen, Germany aut Seitz Jochen Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, RWTH Aachen University, Neuenhofer Weg 21, 52074, Aachen, Germany aut Konrad Kerstin Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, Child Neuropsychology section, RWTH Aachen University, Neuenhofer Weg 21, 52074, Aachen, Germany aut European Archives of Psychiatry and Clinical Neuroscience Springer-Verlag 261(2011-11-01), 177-181 0940-1334 261<177 2011 261 406 https://doi.org/10.1007/s00406-011-0246-y text/html Onlinezugriff via DOI 1 review-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s00406-011-0246-y text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Herpertz-Dahlmann Beate Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, RWTH Aachen University, Neuenhofer Weg 21, 52074, Aachen, Germany aut NATIONALLICENCE 700 1- Seitz Jochen Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, RWTH Aachen University, Neuenhofer Weg 21, 52074, Aachen, Germany aut NATIONALLICENCE 700 1- Konrad Kerstin Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, Child Neuropsychology section, RWTH Aachen University, Neuenhofer Weg 21, 52074, Aachen, Germany aut NATIONALLICENCE 773 0- European Archives of Psychiatry and Clinical Neuroscience Springer-Verlag 261(2011-11-01), 177-181 0940-1334 261<177 2011 261 406 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer