[Pathogenesis of anorexia nervosa. Neurobiological risk factors and possible endophenotypes]. / Az anorexia nervosa kóreredetének újabb megközelítése. Neurobiológiai tényezok és lehetséges endofenotípusok a kutatási eredmények tükrében.

Anorexia nervosa is a serious, chronical state of illness which often starts in childhood or adolescence and has serious consequences on the quality of life. This review focuses on the heterogenity of the disease with emphasis on special diagnostic implications in case of childhood onset. Research findings of the last decade showed that genetic and neurobiological vulnerabilities are at least as potent risk factors as psychological, family constellations and sociocultural preferences. The heritability of eating disorders levels those of diseases predominantly influenced by biological factors. The authors give a summary of the most investigated neurobiologic and neurocognitive factors which could be the fundaments of a biological vulnerablilty. To date, no common risk factor could be identified, but some existing adversities can clearly be related to distinct subgroups with the disorder. The concept of endo- and subphenotypes leads to more specific and more efficient methods of therapy in other somatic and psychiatric diseases.

Anorexia nervosa and the insula.

Anorexia nervosa is a serious illness with major physical and psychological morbidity. It has largely been understood in terms of cultural and environmental explanations. However these are insufficient to explain the diverse clinical features of the illness, nor its rarity given the universality of sociocultural factors. Over the last 20 years, there has been a steady accumulation of neurobiological evidence requiring a re-formulation of current causal models. We now offer a new empirically-derived hypothesis implicating underlying rate-limiting dysfunction of insula cortex as a crucial risk factor for the development of anorexia nervosa. Supporting evidence for this hypothesis is drawn from anatomical and clinical research of insula cortex damage in humans and neuroscientific studies of relevant clinical features including taste, pain perception and reward processing. This hypothesis, if sustainable, would be the first fully to explain the disorder and predicts promising novel treatment possibilities including Cognitive Remediation and Motivation Enhancement Therapies. The knowledge that the challenging behaviours, so characteristic of AN, are the result of underlying cerebral dysfunction, rather than being purely volitional, could help to reduce the stigma patients experience and improve the therapeutic alliance in this poorly understood and difficult to treat disorder.