Therapeutic approach to eating disorders: the biological background
Authors: PALMIERO MONTELEONE, FRANCESCA BRAMBILLA
Journal: World Psychiatry (2009)

There is a great deal of uncertainty about response of eating disorders to treatment. This is in part due to the fact that not only their etiologic and pathogenetic bases, but also their classification, prevalence, course, comorbidities and prognosis are continually undergoing new appraisal and definition. Eating disorders are the expression of both psychological and physical pathologies, and each of these components has prevailed from time to time and from study to study, orienting toward different diagnoses and supporting different treatments. Today, the psychological component is considered the core of eating disorders, while the physical component is regarded as just the consequence of the aberrant eating behaviours. However, this is to some extent questionable, since some physical impairments are involved in the development of certain psychopathological aspects, contributing to their maintenance, prognosis and response to treatments. Genetic, biological, temperamental and family-social factors have been in turn considered as primary causes for the development of eating disorders, but they are probably effective only when they act all together as a concurrence of causes 1–4. This raises some intriguing questions about treatment of eating disorders: which etiopathogenetic factors must we confront in our treatments? Which should we address as first? Or should we confront all of them simultaneously? Unfortunately, at the moment we have no definitive answer to these questions. K. Halmi describes what can be considered today the optimal approach to the treatment of eating disorders. Why are the results of this approach not predictable and not always satisfactory? One reason could be that we do not know exactly what brain biological impairments are present in patients with eating disorders during the symptomatic phases of their disease, after recovery or when the disorder becomes chronic. Central neurotransmitter alterations have been reported in small groups of patients, with decreased serotonin, noradrenaline and brain-derived neurotrophic factor and increased neuropeptide Y and endocannabinoid production in anorexia nervosa and, in some cases, bulimia nervosa patients 5–7. As for dopamine, data are discordant, revealing either hypo- or hypersecretion of the amine in anorexia nervosa, and hypo- or normosecretion in bulimia nervosa 8,9. However, all these changes reflect mean values of study groups. We do not know whether these alterations occur in every patient or are limited to some of them, being responsible for the prognosis of eating disorders or for some aspects of psychopathology which characterize subgroups of patients. At the moment, we do not have enough data to settle this issue, but the possible biochemical variability from patient to patient or from time to time during the course of the disease may be one reason for the relatively inconsistent and unpredictable responses to treatments 10. Moreover, some of the neurotransmitter alterations are still present long after the recovery of eating disorders, possibly being responsible for relapses and chronicity. Increased 5-HT2A receptors in anorexia and bulimia nervosa, and reduced 5-HT1A receptors as well as increased D2/D3 receptors binding in anorexia nervosa have been observed in specific brain areas one year after recovery, and it has been suggested that a central serotonin and/or dopamine hyperactivity could represent a biological trait of vulnerability to eating disorders, needing correction to prevent relapses and/or recurrences 11–13. At present, no specific psychopharmacological trial has been conducted to verify this hypothesis. As Halmi outlines in a recent editorial 14, “it is unlikely that predictably effective treatment for anorexia nervosa (and, we believe, also for other eating disorders) will be available until we decipher the reinforcing neurobiological mechanisms sustaining the disorder”.