Medical Management Of Anorexia Nervosa And Bulimia Nervosa - Medical Management of Eating Disorders

Written by HealthyPlace.com Staff Writer

Treatment options. Numerous therapeutic interventions are possible, even though there is not yet enough evidence to prove that bone mineral density deficiency resulting from anorexia nervosa can be reversed.

• One easy intervention is for patients to take 1,500 mg of calcium per day for restoration. (The current RDA is 1,200 mg per day.)

• Weight-bearing exercise is helpful but avoid high-impact cardio exercise, which burns too many calories (interfering with weight gain) and may lead to fractures.

• The administration of oral contraceptives or HRT is controversial, as many professionals prefer to wait until the individual gains enough weight for menses to return naturally, particularly for young teens with amenorrhea.

According to researchers at Massachusetts General Hospital in Boston, weight was highly correlated with bone density while estrogen supplementation was not. Dr. David Herzog and his colleagues used bone density screening by dual-energy X-ray aborptiometry (DEXA) and correlates of low bone density among ninety-four women with anorexia nervosa ("Weight, Not Estrogen Use, Correlates with Bone Density" 1999). Bone density was no different in patients who had used estrogen than in those who hadn't been prescribed estrogen. In contrast, a highly significant correlation was established between bone density and body mass index (BMI). Thus, weight, a measure of overall nutritional status, was highly correlated with bone density. This study is indicative of the important and independent effect of malnutrition on bone loss among these patients. It was also noted in this study that more than half of all women with anorexia nervosa have bone loss greater than two standard deviations below normal.

In the January/February 1997 issue of Eating Disorders Review, British researcher Dr. Janet Treasure and her colleagues reported that "anorexia nervosa seems to be associated with a high level of bone resorption that is dissociated from bone formation" (Treasure et al. 1997). Weight gain seemed to reverse this pattern, resulting in increased bone formation and decreased bone resorption. The results also suggested that sufficient intake of calcium and vitamin D (vitamin D stimulates osteoblast activity) may be a component of treatment for osteoporosis caused by anorexia nervosa. See Table 15.1 for steps in managing osteoporosis in patients with chronic anorexia nervosa.

Table 15.1 makes it clear that these researchers do not recommend HRT unless the individual has suffered from anorexia nervosa for more than ten years.

A study on the resumption of menses in teens with anorexia nervosa showed that "(1) return of menses (ROM) does not depend on a patient's percent body fat, and (2) measuring serum estradiol levels may help predict ROM. . . . Neville H. Golden, M.D., and his colleagues at Albert Einstein College of Medicine studied factors associated with ROM. In contrast to the theory that ROM depends on a fixed critical weight, these researchers hypothesized that ROM depends upon restoration of hypothalamic-pituitary-ovarian function. The latter would require nutritional rehabilitation and weight gain, but could occur independently of percent of body weight as fat" (Lyon 1998).

In this study, subjects who regained menses and those who remained amenorrheic also gained weight and increased their BMI. However, "when the authors compared those with ROM and those without, the estradiol levels of the ROM group increased from baseline to follow-up and were significantly related to ROM. The estradiol levels of the subjects who remained amenorrheic did not change. Estradiol levels at or above 110 mmol/1 correctly identified 90 percent of the individuals with ROM and 81 percent of those who remained amenorrheic. The authors point out that these results support the use of serum estradiol levels to assess ROM in adolescents with anorexia" (Lyon 1998). The results of this study suggest that ROM requires restoration of hypothalamic-pituitary-ovarian function and is not dependent on achieving a specific level of body fat. The researchers concluded that the low estradiol levels in anorexia nervosa were due to decreased ovarian production secondary to hypothalamic-pituitary suppression, not to reduced body fat.

TABLE 15.1 TREATMENT RECOMMENDATIONS FOR OSTEOPOROSIS IN ANOREXIA NERVOSA

Source: Used with permission from Lucy Serpell and Janet Treasure, Eating Disorders Review 9, no. 1 (January/February 1998).