Anorexia Nervosa: Treatment of Low Bone Mass

Abstract & Commentary

By Leon Speroff, MD, Editor, Professor of Obstetrics and Gynecology, Oregon Health & Science University, Portland, is Editor for OB/GYN Clinical Alert

Synopsis: Body weight is the major determinant of changes in bone density in adolescents with anorexia nervosa.

Source: Golden NH, et al. J Clin Endocrinol Metab. 2005:90:3179-3185.

Golden and colleagues compared alendronate treatment (10 mg daily) with placebo in a randomized clinical trial, in 32 female adolescents with anorexia nervosa. In addition, every participant was supplemented with calcium and vitamin D. Every individual was malnourished and had either primary or secondary amenorrhea. After one year of treatment, bone density in the spine and femoral neck as measured by DEXA increased in the alendronate group compared with no increase in the placebo group, although the difference achieved statistical significance only in the femoral neck. However, both groups gained weight and the bone density response was influenced by individual response in body weight. Those individuals who gained weight had the greatest increases in bone density; however, even though two-thirds of the patients resumed menses, less than a third restored bone mass to the normal range, and 3 experienced fractures.

Commentary

It is well recognized that young women with anorexia nervosa have reduced bone mass. This loss of bone is the result of 2 forces: 1) GnRH suppression resulting in amenorrhea and hypoestrogenism with increased bone resorption, and 2) The deprivation of adequate nutrition and its support of normal physiology such as the dynamic process of bone remodeling, resulting in both increased resorption and decreased bone formation. Although not well documented, there is every reason to believe that the loss of bone at a young age impairs the attainment of normal bone mass, placing anorexic individuals at risk of osteoporosis and fractures. Therefore, bone mass in an anorexic adolescent is an important concern, and it is worthwhile to provide treatment to increase bone accumulation.

Golden et al were encouraged by the response to alendronate, and compared their results to reports in the literature indicating no response to estrogen or oral contraceptives. But the key is not the treatment with alendronate. The important factor is response in body weight because of an improvement in the anorexia. Even the control group in this report gained bone—because most of the individuals, both in the treatment group and the control group, responded to active management of their primary problem, anorexia nervosa.

There is a simple clinical lesson in these results that has been apparent to me for many years from my own experience. Unless there is an improvement in the eating disorder and better nutrition, the bone responds poorly or not at all to antiresorptive agents such as estrogen or bisphosphonates. In patients with eating disorders, the bone response to hormone therapy will be impaired as long as an abnormal weight is maintained. I have taught for many years that a lack of response indicated by repeated bone density measurements is an excellent method to detect an on-going eating disorder that may have been camouflaged by the patient. Because the pubertal gain in bone density is so significant, individuals who fail to experience this adolescent increase may continue to have a deficit in bone mass despite hormone treatment. Reduced menstrual function for any reason early in life (even beyond adolescence) may leave a residual deficit in bone density that cannot be totally retrieved with resumption of menses or with hormone treatment. This is just one of the reasons to focus on the cause of the problem, the eating disorder. Until good nutrition is restored and body weight returns to normal, adjuvant bone treatments don’t do much good.