Abstract
BackgroundTreatments of eating disorders result too often in partial psychological and physical remission, chronicization, dropout, relapse and death, with no fully known explanations for this failure. In order to clarify this problem, we conducted three studies to identify the biochemical background of cognitive-behavioural psychotherapy (CBT), individual psychology brief psychotherapy (IBPP), and psychotherapy-pharmacotherapy with CBT + olanzapine in anorexics (AN) and bulimics (BN) by measuring the levels of plasma homovanillic acid (HVA) for dopamine secretion, plasma 3-methoxy-4-hydroxy-phenylglycol (MHPG) for noradrenalin secretion, and platelet [3H]-Paroxetin-binding Bmax and Kd for serotonin transporter function. The data were then compared with psychopathological and physical alterations.MethodsStudy 1 investigated the effects of 4 months of CBT on plasma HVA, MHPG and [3H]-Par-binding in 14 AN-restricted, 14 AN-bingeing/purging, and 22 BN inpatients. Study 2 investigated the effects of 4 months of IBPP on plasma HVA in 15 AN and 17 BN outpatients. Study 3 investigated the effect of 3 months of CBT + olanzapine (5 mg/day) in 30 AN outpatients. The data were analyzed using one-way ANOVA for repeated measures for the changes between basal and post-treatment biological and psychological parameters, two-way ANOVA for repeated measures for the differences in the psychobiological data in the 3 groups, Spearman’s test for the correlations between basal and final changes in the psychological and biological scores.ResultsStudy 1 revealed significant amelioration of the psychopathology in the AN and BN patients, no effects on HVA, MHPG or Paroxetin binding Kd, and a significant increase in Par-binding Bmax only in the BN patients. Study 2 revealed a significant effect of IBPP on psychopathology in the AN and BN patients, and a significant increase in HVA only in the BN patients. Study 3 revealed a significant positive effect of CBT + olanzapine therapy on the psychopathology and increased HVA values. No correlations were observed in the 3 groups between biological and psychological effects of the three treatments.ConclusionsOur data advance suggestions on the mechanism of action of the three therapies; however, the lack of correlations between biochemical and psychological effects casts doubt on their significance.Clinical Trials.gov. Identifier NCT01990755.
Highlights
Treatments of eating disorders result too often in partial psychological and physical remission, chronicization, dropout, relapse and death, with no fully known explanations for this failure
The treatment of Eating Disorders (ED), including anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorder (BED), is a complex multivariate process which comprises nutritional rehabilitation, psychotherapy, psychopharmacotherapy, and treatment of the medical complications that develop during the course of the disease and that may interfere with its development and prognosis [1,2,3,4,5]
A possible validation of specific therapeutic interventions should first include investigation of the brain’s biochemical impairments that have been reported to consistently occur in ED to see whether and how they correlate with the psychopathology of the disorders, and whether they change or disappear during or after treatment, in parallel with correlated psychopathological aspects, resulting in full contemporary recovery of the psychopathological, behavioural and physical alterations of the diseases. Following this line of reasoning, we conducted three types of experiments in which we looked at the psychopathological, behavioural and physical aspects of ED and, in parallel, at the concentrations of the peripheral metabolites of noradrenalin and dopamine and at serotonin function, as expressed by the serotonin transporter evaluated by platelet paroxetine binding, before and after psychotherapeutic, psychopharmacological and physical treatments
Summary
Treatments of eating disorders result too often in partial psychological and physical remission, chronicization, dropout, relapse and death, with no fully known explanations for this failure. Each treatment is directed at correcting distinct parts of the disorders and each is essential for successful outcome, none being omnivalent or sufficient by itself to induce full recovery, though combined use of multiple therapies is reported to be effective in the treatment of ED. They mostly correct the pathological eating behaviour, often leaving out the psychological background which is the likely cause of the diseases. Each treatment takes into consideration a group of symptoms or specific aspects but not the core of the diseases This may be because the basic cause or the core of ED is still not clear. In spite of extensive of brain imaging studies identifying the areas pathologically involved in ED [6,7,8], the brain’s biochemical background behind the onset and course of these disorders has not been clarified, leaving the question open as to which basic therapy could potentially correct it
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