Aetiology of anorexia nervosa: from a “psychosomatic family model” to a neuropsychiatric disorder?

Abstract

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 25 years 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.