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Depression: Treatment, Causes and Diagnosis |
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Binge Eating DisorderBinge Eating Disorder Introduction:This eating disorder affects both men and women equally and occurs in mainly obese patients. About 20% of obese patients belong into this category. These patients take excessive calories in by binging, but unlike bulimia nervosa patients they do not purge. This means that the excessive calories are stored as body fat. Symptoms: The symptom of obesity is easily measurable, but the history of binge eating may be concealed, although a relative who accompanies the patient may volunteer this, if the patient does not. There are elaborate questionnaires that can be used to quantitate the symptoms of overeating and binging. It also helps in assessing the severity of the binge eating disorder. In Ref.12 such questionnaires have been used as a predictor to the outcome of treatment. This study shows that testing criteria at the outset were effective in evaluating the severity of the binge eating disorder and the tests also predicted the success rate of the treatment program. This way the physician can predict whether a combination of treatment modalities should be employed or whether a simple cognitive behavior therapy would suffice.
Treatment: We know from literature reviews what the natural history of the disease would be. For instance, Ref. 14 describes an Oxford University study by Fairburn et al., where 150 patients with either bulimia nervosa or binge eating disorder were followed over a 5-year period without intervention. Patients with bulimia nervosa were shown to have a poor prognosis with about 40% still having an eating disorder or obesity after 5 years. In contrast the binge eating disorder group showed a much better prognosis with a spontaneous cure rate of 80%. A New York study (Ref. 15)showed that the success rate is higher when a combination therapy program is chosen where fluoxetine (brand name: Prozac) is used to treat depression and a psychiatric counseling program is employed to change the long-term attitude towards food and life in general. This holistic approach appeals both to the patient and the treating physician and when combined with methods as mentioned in Ref. 12 it is possible to monitor the treatment success on an ongoing basis. Another method, namely the use of self hypnosis, can be incorporated with such a combination treatment approach. Ref. 15 makes the point that an open ended approach is better for the long-term success, which is the ultimate goal. The physician hopes that a high percentage of the patients will gradually change their behavior pattern towards food, become physically more active and change emotionally by conquering depression and low self esteem. This is a slow process, and it takes a period of trials and errors coupled with determination and the human factor to truly change body image and eating patterns. There are new approaches and new weight loss medications, which will become part of a comprehensive treatment program such as outlined above. One such newer agent is outlined in Ref.16. This paper shows that the anticonvulsant medication topiramate (brand name: Topamax) was effective in reducing weight in a group of patients with binge eating disorder at a dosage of 400 to 600 mg daily. You may want to discuss this with your doctor. If this medication is used, one has to slowly start the dose and work up to the above mentioned maintenance dose and at the end of treatment slowly wean the medication to avoid seizures. There are a number of neurological side-effects, which your doctor could explain to you. However, any treatment decisions are strictly between you and your doctor. Just because one study says that a new treatment modality is effective does not mean that this would be the best treatment in your case. Here is more info on binge eating disorder. References: 1. Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, (DSM-IV), American Psychiatric Association, Washington, DC,1994. 2. Wonderlich et al. J Am Acad Child Adolesc Psychiatry 2000 Oct(10):1277-1283. 3. Ivarsson et al. Compr Psychiatry 2000 Sept/0ct(5): 398-403. 4. Exner et al. Mol Psychiatry 2000 Sept(5): 476-481. 5. Nakai et al. Clin Endocrinol (Oxf)2000 Sept53(3):383-388. 6. Frank et al. Biol Psychiatry 2000 Aug 48(4):315-318. 7. Sheppard-Sawyer et al. Int J Eat Disord 2000; 28(2):215-220. 8. Cotrufo et al. Neuropsychobiology 2000;42 (2): 58-61. 9. Steel et al. Int J Eat Disord 2000 Sept 28(2):209-214. 10. Walsh et al. Am J Psychiatry 2000 Aug 157(8):1332-1334. 11. Agras et al. Am J Psychiatry 2000 Aug 157(8):1302-1308. 12. Peterson et al. Int J Eat Disord 2000 Sep28(2):131-138. 13. Karhunen et al. Psychiatry Res 2000 Jul 99(1):29-42. 14. Fairburn et al. Arch Gen Psychiatry 2000 Jul 57(7):659-665. 15. Devlin et al. Int J Eat Disord 2000 Nov28(3):325-332. 16. Shapira et al. J Clin Psychiatry 2000 May61(5):368-372. |
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