Medical Management Of Anorexia Nervosa And Bulimia Nervosa

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HEMATOLOGICAL SYSTEM

Not infrequently, the hematological (blood) system is also affected by anorexia. Approximately one-third of individuals with anorexia nervosa have anemia and leukopenia (low white blood cell count). The relevance of this low white blood cell count for the functioning of the immune system of the patient with anorexia nervosa is controversial. Some studies have indeed found an increased risk of infection due to impaired cellular immune function.

In addition to the low white cell count, anorexic patients typically have low body temperature. Thus, the two traditional markers of infection, namely fever and a high white cell count, are often lacking in these patients. Therefore, there has to be heightened vigilance toward the possibility of an infectious process when these patients report some unusual symptom.

The hematological system is thus similar to other body systems that can be ravaged by anorexia nervosa. However, nutritional rehabilitation, if done in a timely and well-planned fashion, in concert with competent medical supervision, promotes a return to normal in all these systems.

ENDOCRINE SYSTEM

Anorexia nervosa can have profound negative effects on the endocrine system. Two major effects are the cessation of menstrual periods and osteoporosis, both of which are physiologically interrelated. While the exact cause of amenorrhea (lack of menstruation) is not known, low levels of the hormones involved in menstruation and ovulation are present in the setting of an inadequate body fat content or insufficient weight. Clearly, there is also an important contribution from the tenuous emotional state of these patients. Reversion to the age-appropriate secretion of these hormones requires both weight gain and remission of the disorder.

Due to the increased risk of osteoporosis seen in eating disordered patients who have amenorhea and to the fact that some studies suggest that the lost bone density may be irreversible, hormone replacement therapy (HRT) has often been suggested for these individuals. In the past, the traditional line of thinking has been that if the amenorrhea persists for longer than six months, HRT should be used empirically if there are no contraindications for such treatment. However, the results of recent research are unclear as to whether (and, if so, when) HRT should take place; consequently there has been much controversy over this issue. For further discussion of this important topic, see "Bone Density" below.

BONE DENSITY

Since the first edition of this book was published, there has been continued research in the area of bone mineral density (bone density) and hormone replacement therapy for eating disordered individuals with amenorrhea. Results have been conflicting. Bone loss or insufficient bone density is an important and possibly irreversible medical consequence of anorexia nervosa and, although less often, of bulimia nervosa as well. Therefore a thorough discussion of the current information is warranted.

There is increasing evidence that peak bone density is reached fairly early in life, at about age fifteen. After this, bone density increases very slightly until about the mid-thirties, when it begins to decline. This means that a teenager who suffers anorexia nervosa for as little as six months may develop a long-lasting bone deficiency. Bone density tests have shown that many twenty- to twenty-five-year-olds with anorexia nervosa have the bone densities of seventy- to eighty-year-old women. Whether bone density deficiency is permanent or whether it can be restored remains unknown.

Postmenopausal versus anorexia-caused bone deficiency. "Results of recent studies from London, Harvard, and other teaching centers are showing that the bone deficiency caused by anorexia is not identical to that of postmenopausal women. The major deficiency in postmenopausal osteoporosis is of estrogen and, to some extent, calcium. In contrast, in anorexia nervosa, chronic low weight and malnutrition often make estrogen ineffective, even when it is present through oral contraceptives" (Anderson and Holman 1997). Other factors that likely contribute to bone density problems in anorexia include inadequate dietary calcium; diminished body fat, which is necessary for the metabolism of estrogen; low body weight; and elevated serum cortisol levels from weight loss and comorbid depression.

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.

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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).

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