Stress-induced anorexia: implications for anorexia nervosa

Recent studies have suggested that stress may be a precipitating factor in the etiology of anorexia nervosa. The present paper examines the possible mechanisms involved in stress-induced anorexia and suggests how stress-induced changes in opiate systems, the hypothalamic-pituitary-adrenal axis and serotonergic systems may provide an explanation of many of the physiological and behavioral responses observed in anorexia nervosa. The present paper suggests that certain psychosocial and endocrinological factors may interact to provide the setting conditions for the syndrome. Finally, it is suggested that a dual therapeutic approach is required in that the syndrome needs to be treated both physiologically and psychologically to prevent relapse.     

Angiotensin-converting enzyme and anorexia nervosa

Angiotensin-converting enzyme (ACE) activity was measured in 10 patients with anorexia nervosa, 6 with hyperthyroid Graves' disease, and 7 with primary hypothyroidism. Patients with anorexia nervosa had a low serum ACE activity (9.8 +/- 2.2 IU/l), as compared to findings in normal subjects (13.4 +/- 3.5 IU/l) (P less than 0.05). Patients with hyperthyroid Graves' disease had high serum ACE activity (23.7 +/- 5.8 IU/l), as compared to levels in normal subjects (P less than 0.01), and patients with primary hypothyroidism tended to have low serum ACE activity (10.1 +/- 1.8 IU/l), compared to the normal subjects (P less than 0.1). Following weight gain (before; 71.3 +/- 10.2% of ideal body weight, after; 88.7 +/- 5.6% of ideal body weight), serum ACE activity in patients with anorexia nervosa reverted to within the normal range (13.8 +/- 3.5 IU/l), and serum T3 concentration was restored to the normal range (before; 0.7 +/- 0.2 ng/ml, after; 1.1 +/- 0.3 ng/ml). In these patients, ACE activity correlated with the per cent of ideal body weight (P less than 0.05). These data suggest that, in underweight subjects with anorexia nervosa, decreased serum ACE activities may relate to emaciation.     

Steroids and neuroendocrine function in anorexia nervosa

Anorexia nervosa is a primarily psychiatric syndrome of self-induced weight loss due to an intense fear of becoming obese. Numerous endocrine abnormalities occur in anorexia nervosa patients, and in many respects these alterations reflects the endocrinology of reduced energy intake. However, the basic mechanisms of those alterations are far from being understood. In an attempt to understand the disrupted mechanisms of the hypogonadotropic hypogonadism of the anorectic state, we studied 10 anorectic women in the acute phase of their illness; all met the DSM III criteria. On each patient, two tests were performed with either saline as control or infusion of the opioid antagonist naloxone, and both LH and FSH levels were measured. Four mg of naloxone as bolus was used, followed by a naloxone infusion of 2 mg/h for 4 h. Compared with the pattern of normal women, naloxone did not increase in the anorectic patients either LH or FSH levels nor pulsatility. This result suggests that endogenous opioid peptides are not implicated in the low gonadotropic situation of anorexia nervosa. An alternative explanation could be that the low estrogenic "milieu" of these patients could mask the opioid action. To test this second possibility, another group of 7 anorectic women after partial weight recovery were challenged with estrogen administration. Compared with the pattern of normal women volunteers, all the anorectic patients but one presented an abnormal response in both LH and FSH levels after estrogen administration. In fact, the negative feedback and the delayed positive feedback of LH after estrogen were absent in these patients. Interestingly enough, the only patient with near-normal LH response to estrogen was considered fully recovered by the Psychiatric Unit. Several alterations in the hypothalamic-pituitary-adrenal axis has been reported in anorexia nervosa. Seven anorectic patients and 7 aged-matched women were challenged by ACTH 1-24, 250 micrograms (i.v.) and the ratio of increments in adrenal steroid products to precursors monitored. ACTH-induced increments in cortisol with respect to increments in 17-OH-progesterone was similar in anorectics and controls. On the contrary, the ratio of increments of androstenedione with respect to increments in 17-OH-progesterone were greater in anorexia nervosa than controls. These results suggest that in anorexia nervosa the 11-beta-21-alpha-hydroxylase system is normal but a deficient 17-20 desmolase system is present. Finally, the altered pattern of GH secretion in anorexia was studied using GHRH (1 microgram/kg) as stimulus of pituitary GH secretion.(ABSTRACT TRUNCATED AT 400 WORDS)     

Compliance and outcome in anorexia nervosa.

Anorexia nervosa is notoriously difficult to treat, but little is known regarding the relationship of compliance to treatment outcome. We investigated in 41 adolescents who fulfilled DSM-III-R criteria for anorexia nervosa, the relationship between the completion of a standard psychosocial treatment program, subtypes of anorexia nervosa, and outcome as determined by standardized measurements. These adolescents were observed for an average of 32.4 months. Overall, 29 patients (70%) improved considerably, but 10 (24%) were symptomatic, and 2 (5%) remained in poor condition. There were no deaths. Of the 41 patients, 14 (34%) completed our entire treatment program, 15 (37%) received major treatment and failed in the outpatient follow-up phase only, 7 (17%) dropped out of inpatient treatment before its completion, and 5 (12%) refused treatment in our system altogether. Of all the dropouts, 10 received no further treatment. One patient was admitted to hospital elsewhere but again dropped out in the outpatient phase of that program. Seven patients (17%) received further outpatient treatment only, and 9 (22%) received inpatient and outpatient care and seemingly completed their treatment. Treatment completion significantly affected the measures of global clinical functioning and specific psychopathologic features, but only for those patients who completed the initial program. Bulimic patients did considerably worse on follow-up and were less likely to complete treatment. Patients with restricted anorexia nervosa were more likely to complete treatment than those with a bulimic subtype (P = .03). Differential compliance rates in the two subtypes confound the effects of treatment completion and need to be controlled for in future studies. Depression was not associated with noncompliance but, if present, was associated with poor outcome on follow-up and abated in only a third of those in whom it was initially present.