Eating disorders are largely encountered during teenage and young adulthood even though they sometimes appear in childhood or later in adult life. The diagnosis and treatment of eating disorders is a challenge aggravated by the affected individuals aversive tendency to seek treatment. (Becker et al., 1999) (Steiner & Lock, 1998). Eating disorders are veritable medical illnesses and tend to be frequently overlooked in the face of other coexisting diseases like Anxiety, Depression and substance abuse syndrome. The revisions incorporated in the fifth Edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) envisage better classification and characterization of this group of disorders. The objective is to facilitate early detection and develop optimal treatment approaches. (APA, 2013). The purpose of this paper is to review the prevalent therapeutic approaches to eating disorders based on emerging research evidence. It briefly compares the various pharmacological agents in use with respect to their mechanisms of action, side effects and overall therapeutic efficacy.
Under DSM-4, there were only two recognized clinical entities falling under the category of Eating Disorders, namely, Anorexia Nervosa (AN) and Bulimia Nervosa (BN). Patients who did not qualify as AN or BN were, by default, grouped under a heterogeneous group referred to as ‘Eating disorder not otherwise specified’ (EDNOS). Due to the broad clinical spectrum of patients categorized as EDNOS this classification system didn’t help the evolution of targeted therapies and development of clinical guidelines. The rationale for development of DSM-5 was to facilitate accurate diagnosis for people afflicted with eating abnormalities in line with their respective symptoms and behavioral patterns. Under the new system, eating disorders have been classified into 3 categories, namely Binge eating disorders, Anorexia Nervosa and Bulimia Nervosa.
Binge eating disorders are characterized by recurring compulsive episodes of significantly increased food intake even in the absence of hunger. The affected person often feels guilty and embarrassed by his behavior which leads the patient to cover his maladaptive behavior. The qualifying criteria also includes a frequency component (at least one episode a week over a three –month period).
Anorexia nervosa (AN): The condition typically affects adolescent girls and young women and is marked by a distorted perception of one’s own body image leading to severe voluntary diet restriction and resultant weight loss. The fear of weight gain is profound in such patients.
Bulimia Nervosa (BN): A bulimic patient is characterized by frequent instances of binge eating followed by compensatory abnormal behaviors like self-induced vomiting to prevent weight gain. Kessler et al (2003) provided estimates of the prevalence and correlates of BED among adults across a diverse set of countries. The study showed a pre eminence of BED as a public health issue comparable to BN.
Etiopathogenesis of eating disorders
The exact cause of eating disorders is unknown. However, evidence suggests role of biologic, psychological and social factors. Studies have shown a 10-fold increase in risk of developing eating disorders among first degree relatives of patients (APA, 2013). Moreover, serotonin imbalance is understood to play a key role in the pathogenesis. Both these factors suggest strong genetic component in the disease causation. Several personality traits and co existing psychiatric conditions also point towards psychological origins of eating disorders. The most common association of eating disorders is with obsessive-compulsive disorders, anxiety, depression, general emotional lability and often a sense of lack of control. Lastly, social pressures and influences are also thought to precipitate behaviors associated with eating disorders.
Management of eating disorders ideally requires interdisciplinary collaboration between medical doctors, psychiatrists, nutritionists and psychotherapists. The involvement of family members in patient management often makes a key difference in achieving superior outcomes. Cognitive behavioral therapy, interpersonal therapy and family therapy have all been proved effective.
This paper mainly focuses on pharmacological treatment of eating disorders with a brief overview of the available psychotherapeutic modalities.
The lack of efficacy of psychotropic drugs in Anorexia Nervosa has been repeatedly demonstrated. The current clinical guidelines do not support a primary role of drugs in AN. However, drugs can be of value in cases with co-existing disorders like depression and OCDs. Moreover, drugs have been shown to prevent relapses in treated patients. (APA, 1993) In patients symptomatic of anxiety, anxiolytics administered prior to meals has had gratifying results in several instances. Some studies have demonstrated benefit of Olanzipine as appetite stimulants in these patients with frequent weight gain being a common accompaniment of Olanzipine therapy.
The range of health problems in BN patients and their general aversion to seek care is an ongoing challenge in treatment of these patients. e.g., research has shown that a vast majority of bulimic women do not receive specific treatment and the symptoms are usually masked by co-existing psychiatric abnormalities. (Mond et al, 2007) A systematic review of randomized controlled trials provided evidence in favor of both pharmacotherapy and behavioral therapy for BN. (Shapiro et al., 2007). Drugs are also useful in containing co-existing conditions with their use being particularly of value in chronic refractory cases and in patients not responding to psychotherapy.
Selective serotonin reuptake inhibitors (SSRIs): As their name indicates, the SSRI’s act by physiochemical modulation of neurotransmitter Serotonin in central nervous system. More specifically, they prevent reuptake of serotonin by neurons, the net effect of which is mood elevation. SSRIs have no effect on other neurotransmitters. A wide body of evidence points to the superior efficacy and safety profile of SSRIs. (Mayor &Walsh, 1998) Fluoxetine and Sertraline are most commonly used antidepressants. Of these, Fluoxetine is the sole drug approved by US FDA for treatment of BN. The therapeutic dose of Fluoxetine is between 20 to 80 mg per day depending on severity of symptoms and individual tolerance. Sertraline at 100 mg has also been shown to be effective. Use of other drugs like Citalopram and Fluvoxamine is generally restricted, owing, in large part, to their side effects.
The mechanism of action of antidepressants in BN is unclear but appears to be linked to its effect in prolonging intercellular concentration of Serotonin Higher doses of SSRIs require more vigilance regarding side effects, though they appear to be well tolerated in this population.
Some of the other classes of drugs like Tricyclic antidepressants (TCAs) and monoamine oxidase inhibitors (MAOIs) have been successfully used to treat BN. However, their toxicity is a major oncern preempting their use only in chronic or refractory cases of BN. (Walsh, Sysko and Parides, 2006).
Mood stabilizing agents
The anti epileptic drug Topiramate has shown promise in cases of binge eating disorders. Conclusive evidence of their efficacy, however, is still awaited. (Arbaizar, Gomez-Acebo, Llorca, 2008). Moreover Topibromate is also associated with weight loss, rendering it redundant in treatment of underweight patients.
Lithium and Valproate are similarly not suitable in BN because of their propensity to cause major fluid disturbances and toxicity at relatively lower doses.
Evaluation of other drugs like, ondansetron, baclofen and antiandrogenic oral contraceptives is still an unresolved issue as most of these agents were tested in rather small scale studies. Overall, there is a consensus that pharmacotherapy with antidepressants in BN should be preceded by detailed patient evaluation, counseling and written consent.
Non pharmacological therapy
Cognitive behavioral psychotherapy is perhaps the most important therapeutic modality for BN. While exact treatment needs careful consideration of the patient’s condition, behavioral approaches are usually the most effective in these patients. Goals of therapy include avoidance of undesirable eating habits by a combination of efforts aimed at behavioral and environmental modification. In particular, psychotherapists focus on factors that precipitate the abnormal behavior as also the results of the peculiar habits like binge eating and purging episodes. Identification of the patient’s thought processes that result in the patient’s disordered perception are key targets of intervention in behavioral therapy.
The symptoms of BN often have their origins in the patient’s interpersonal sphere that often provide contextual priming for the patient's symptoms. Individual roles and processes associated with processes like conflicts, transitions, emotional intensity, grief, etc. play a major role in the disease pathogenesis. Targeted therapy often alleviates mood disorders and improves self esteem thus preventing the chain of events that eventually trigger the bulimic tendency. The efficacy of IPT has been found comparable to CBT in reducing binge eating. The evidence of their effect on behaviors like purging, however, has been less forthcoming.
Diet modification and Counseling
Proper compliance with structured dietary modification help prevent the compulsive urge for binge eating and self purging by patients. Moreover, a responsive meal plan has obvious advantages like better health and satiety. Therefore nutritional assessment is a quintessential component of treatment of BN.
Disruption of congenial relationships, abnormal attitudes and communication within the familial sphere often lie at the root of BN. This phenomenon particularly manifests itself during adolescence and more so in adolescents still cohabiting with their parents. Nonetheless, conclusive evidence of therapeutic benefit of family therapy in BN has not been forthcoming.
The need for individual psychotherapy is often felt in patients with personality disorders or developmental abnormalities. Psychodynamic approaches in individual or group format are usually successful in developing coping skills after remission of bingeing and purging behaviors. Supportive-expressive psychotherapy (SEP) in individual or group therapy formats may also be helpful for patients with bulimia.
Binge eating disorders
SSRI’s, appetite suppressing agents and some antiepileptic drugs have been known to offer value in Binge eating disorders. These include SSRIs, antiepileptics, and appetite suppressants. (Arnold, McElroy, Hudson et al., 2002) (McElroy et al., 2003), (Appolinario, Morgan, Zanella, & Coutinho, 2003), Among these topiramate has been widely researched and found to offer considerable therapeutic advantage in Binge eating disorders.
Eating Disorders are often associated with iceberg phenomenon wherein the exact prevalence and the extent of the problem often remains hidden due to poor reporting and aversive behavior on the part of patients. Pharmacological therapy is of benefit in these disorders and is usually employed in conjunction with psychotherapeutic and behavioral interventions. While Anorexia Nervosa is notorious for being resistant to drug therapy alone, treatment of Bulimia Nervosa with antidepressants appears to accrue several therapeutic advantages. Several drugs like anti epileptics and appetite suppressants have from time to time shown to be effective in a certain subset of patients with Eating Disorders. Most commonly such patients include, resistant/refractory cases and patients with co-existing psychiatric disorders. The newly revised classification system for eating disorders will help facilitate diagnosis and development of better treatment options.
American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Arlington, VA: American Psychiatric Publishing. Available online at http://dsm.psychiatryonline.org/doi/book/10.1176/appi.books.9780890425596.
American Psychiatric Association (1993). Practice guidelines for eating disorders. American Journal of Psychiatry;150: 212
Appolinario, J. C., Morgan, C., Zanella, M. T., & Coutinho, W. (2003). A Randomized, Double-blind, Placebo-Controlled Study of Sibutramine in the Treatment of Binge-Eating Disorder. Archives of General Psychiatry, 60(11), 1109-16. doi:10.1001/archpsyc.60.11.1109.
Arnold LM, McElroy SL, Hudson JI, Welge JA, Bennett AJ, Keck PE (2002). A placebo-controlled, randomized trial of fluoxetine in the treatment of binge-eating disorder. The Journal of Clinical Psychology; 63(11):1028-33.
Arbaizar, B, Gomez-Acebo, I, Llorca, J. Efficacy of Topiramate in bulimia nervosa an binge-eating disorder: a systematic review. General Hospital Psychiatry. 2008;30:471-475.
Becker AE, Grinspoon SK, Klibanski A, Herzog DB. Eating disorders. New England Journal of Medicine, 1999; 340(14):1092–1098.
Mayer LE, Walsh BT. The use of selective serotonin reuptake inhibitors in eating disorders. Journal of Clinical Psychiatry. 1998;59 Suppl 15:28-34.
McElroy, S. L., Arnold, L. M., Shapira, N. A., Keck, P. E., Rosenthal, N. R., Karim, M. R., . . . Kamin, M. (2003). Topiramate in the Treatment of Binge Eating Disorder Associated With Obesity: A Randomized, Placebo-Controlled Trial. American Journal of Psychiatry, 160(2), 255-261. doi:10.1176/appi.ajp.160.2.255
Mond JM, Hay PJ, Rodgers B, Owen C (2007). Health service utilization for eating disorders: findings from a community-based study. International Journal of Eating Disorders. 2007; 40:399.
Ronald C. Kessler, Patricia A. Berglund, .Miguel Xavier (2013). The prevalence and correlates of binge eating disorder in the WHO World Mental Health Surveys. Biological Psychiatry; 73(9): 904–914. doi: 10.1016/j.biopsych.2012.11.020.
Shapiro JR, Berkman ND, Brownley KA, et al. Bulimia nervosa treatment: a systematic review of randomized controlled trials. Int J Eat Disord. 2007; 40:321.
Steiner H, Lock J. Anorexia nervosa and bulimia nervosa in children and adolescents: a review of the past ten years. Journal of the American Academy of Child and Adolescent Psychiatry, 1998; 37:352–359.
Walsh BT, Sysko R, Parides MK (2006). Early response to desipramine among women with bulimia nervosa. International Journal of Eating Disorders; 39(1):72-5.