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Anorexia nervosa represents a self-destructive struggle for separate identity, and cultural factors play a part in the present increasing incidence. This paper presents a broad view, which embraces family dynamics and the natural history of the disease, to clarify important issues in its management and prevention. Both family and individual psychotherapy may have a place in the patient's personal rehabilitation.
Anorexia nervosa (AN), a psychosomatic disease mainly affecting young women, is characterized by conscious starvation, periods of excessive carbohydrate intake and often deliberate vomiting. Medical history, dental examination, and saliva tests of 39 patients aged 14 to 42 years, having suffered from AN for periods of 1 to 20 years, showed dental caries, due to excessive carbohydrate consumption, in all subjects, often in a rampant form. In patients with a history of intense vomiting (27 cases) severe lingual-occlusal erosion (perimylolysis) was nearly always present. Buccal erosion, mainly due to high consumption of acid fruits and drinks to relieve thirst caused by dehydration, was more frequent in vomiting than in non-vomiting patients. Subnormal values of saliva properties, owing to dehydration or xerostomia-inducing medication, were present in the majority of cases; the lowest values occurred in those vomiting. The association AN - vomiting - perimylolysis is discussed, as well as prophylactic and therapeutic measures. A medical, psychiatric, and dental survey of AN is presented.
Primary anorexia nervosa (PAN) is an important psychiatric disease with a 7--21% mortality rate. Although altered gastrointestinal function may be an important aspect of its pathophysiology, no information is available concerning gastric emptying and secretion in those patients. During fasting, fractional emptying rates and hydrogen ion (H+) output were decreased twofold in PAN, as compared with healthy controls, and fluid output was slightly but not significantly decreased. Pentagastrin-induced peak stimulation of H+ output in PAN was 64% of that found in controls (P less than 0.05). Peak gastric fluid output was also significantly less in PAN patients, but suppression of fractional emptying produced by pentagastrin was of the same magnitude in both groups. Following a 250-ml water load, the magnitude and the duration of both the emptying and secretory responses were less in PAN patients than in controls. As a result, the initial increase of intragastric volume was greater in PAN patients than in controls, and the gradual return to fasting volume was delayed in those patients. Follow weight gain, fractional emptying tended to return toward control values, but was still significantly less than in controls following the water load. Gastric H+ and fluid output were not significantly modified following weight gain.
Thirty patients were selected for a prospective study according to two criteria: (i) an irresistible urge to overeat (bulimia nervosa), followed by self-induced vomiting or purging; (ii) a morbid fear of becoming fat. The majority of the patients had a previous history of true or cryptic anorexia nervosa. Self-induced vomiting and purging are secondary devices used by the patients to counteract the effects of overeating and prevent a gain in weight. These devices are dangerous for they are habit-forming and lead to potassium loss and other physical complications. In common with true anorexia nervosa, the patients were determined to keep their weight below a self-imposed threshold. Its level was set below the patient's healthy weight, defined as the weight reached before the onset of the eating disorder. In contrast with true anorexia nervosa, the patients tended to be heavier, more active sexually, and more likely to menstruate regularly and remain fertile. Depressive symptoms were often severe and distressing and led to a high risk of suicide. A theoretical model is described to emphasize the interdependence of the various symptoms and the role of self-perpetuating mechanisms in the maintenance of the disorder. The main aims of treatment are (i) to interrupt the vicious circle of overeating and self-induced vomiting (or purging), (ii) to persuade the patients to accept a higher weight. Prognosis appears less favourable than in uncomplicated anorexia nervosa.
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Patients with anorexia nervosa can demonstrate clinical and/or laboratory findings suggestive of reduced thyroid hormone secretion. In this study, the thyroxine (T4) and triiodothyronine (T3) serum concentrations, and thyrotropin (TSH) response to intravenous administration of thyrotropin releasing hormone (TRH) were determined in 6 patients (aged 9 to 15 yr) with anorexia nervosa and the results compared to those found in a group of 15 normal subjects. The mean basal TSH concentration and mean maximum increase in TSH after TRH were comparable to those in the normal subjects. The mean T4 concentration (7.2 mug/100 ml) in the anorexia nerovsa group was slightly but significantly lower than in the normal group (9.5 mug/100 ml). Five of the 6 patients had serum T3 concentrations below the lower limits of normal and the mean T3 concentrations (49.7 ng/100 ml) was significantly lower than in the normal group (106 ng/100 ml). The extremely low serum levels of T3 in these patients with anorexia nervosa suggest that peripheral conversion of T4 to T3 is impaired during chronic starvation.
Patients with anorexia nervosa have previously been shown to display disturbances in visual self-perception and interoception. In the present investigation we wished to determine the stability of these disturbances and the effects of weight gain on them. We studied 29 females, 16 patients with primary anorexia nervosa and 13 controls, who had also been studied one year previously. Each subject took part in investigations of body image, using a distorting photograph technique, and interoception, using a satiety aversion to sucrose test. We found that some anorexic subjects tend to overestimate body size and have an absence of aversion to repeated sucrose tastes. Moreover, these disturbances were stable over the year and were not affected by weight change.
The literature on anorexia nervosa largely ignores the acid-base and electrolyte disturbances that may accompany this condition. In an attempt to assess the magnitude of these disturbances in anorexia nervosa the authors reviewed the laboratory profiles of 7 patients with the disease who were consecutively admitted to a hospital over a period of 8 years. Several acid-base and electrolyte disturbances were observed; the most frequent was chloride-responsive metabolic alkalosis. The authors suggest that all patients with anorexia nervosa receive diagnostic studies for these disturbances, including ECG and urinary electrolytes when necessary, so that abnormalities can be diagnosed and treated appropriately.
Seven anorexia nervosa (A.N.) patients had reduced urinary excretion values of tetrahydrocortisone (THE), androsterone (A) and 5alpha-tetrahydrocortisol (5alpha-THF). THE to tetrahydrocortisol (THF), A to aetiocholanolone (Ae) and 5alpha-THF to THF ratios were all significantly reduced. Six A.N. patients had oral metyrapone tests with quantitatively normal but delayed urinary 3alpha,17alpha,21-trihydroxy-5beta-pregnan-20-one (THS) response. The steroid determinations were done by capillary gaschromatography, which proves to be of value in the study of the above mentioned metabolic abnormalities.
Patients suffering from anorexia nervosa rarely appear to develop the common cold or influenza. This study examines the immunological response of fifteen female anorexia nervosa patients of both the vomiting and carbohydrate-abstaining type and compares them with a control population matched for age and occupation. Both anorectics and control populations received the admune influenza vaccine. Initially both groups had similar haemagglutination inhibition titres against the three different viral antigens: A/HK; A/PC; A/Eng. However, the anorectics showed over a 2-month period a higher titre of antibody especially to the Hong Kong virus: this was sigignificant. Cellular immune responses were measured using a tuberculin and a macrophage inhibition test, no significant difference between the two groups was obderved. These results which support the clinical findings are discussed.
Four patients with anorexia nervosa were studied by cranial computed tomography (CT). Three of the four demonstrated abnormal enlargement of cortical sulci and subarachnoid spaces as compared with an age-matched control group. The relationship of this finding to established neuropathological changes in anorexia nervosa is discussed.
Four patients with anorexia nervosa were studied. All patients in the acute stage of the illness had low serum luteinizing hormone (LH) levels which were unresponsive to clomiphene. The four women showed almost no LH response on a single iv injection of 100 mug LH-RH; however, the FSH response was similar to that of normal eumenorrheic women. When the patients had regained weight the LH levels were normal, and they responded normally to LH-RH. These results seem to suggest that impaired hypothalamic function is the cause of gonadotropin deficiency in most patients with anorexia nervosa.
Fifteen women with anorexia nervosa were studied before and after weight gain. Basal plasma thyroid stimulating hormone (TSH) and prolactin (PRL), and the responses of both these hormones to thyrotropin releasing hormone (TRH), were normal. Basal plasma luteinizing hormone (LH) and follicle stimulating hormone (FSH) were low in patients who were emaciated, and their responses to gonadotropin releasing hormone (GnRH) were impaired. Both basal and stimulated levels of LH and FSH rose with weight gain, with a linear correlation between gonadotropin levels and body weight expressed as a percentage of standard. The FSH response became greater than normal in patients who had regained weight to more than 70% of standard, while the LH response to GnRH was exaggerated in those who had regained weight to more than 80%. Basal plasma estradiol (E2) levels were low at first, but returned to within the normal range in patients over 80% of standard. Menstruation resumed in some patients after they had regained weight. The relationship between body weight and gonadotropin levels appears to be an important feature of the menstrual disturbance in anorexia nervosa. The restoration of a normal body weight is a prerequisite for the resumption of menstruation in this condition, but other as yet unidentified factors may also be involved.
Twenty women with anorexia nervosa were investigated at varying stages during weight gain. Basal prolactin and TSH and prolactin responses to TRH were normal and unrelated to body weight. LH, FSH and 17 beta oestradiol were low in emaciated patients and rose with weight gain. There was no correlation between serum gonadotrophin and prolactin concentrations. T3 and T4 concentrations were low but T3 rose with weight gain during refeeding over 4-6 weeks, whereas T4 remained low. A positive correlation was found between the TSH response to TRH and body weight. The abnormalities in the hypothalamic-pituitary-thyroid axis were similar to those seen in a variety of chronic illnesses and appear to be unrelated to the amenorrhoea. The failure of restoration of normal function at least after short-term refeeding requires further investigation. It was concluded that the amenorrhoea in anorexia nervosa is not associated with changes in prolactin secretion but is determined primarily by changes in the hypothalamic-pituitary-gonadal axis. These changes are induced largely by nutritional factors but psychological factors may also be involved.
Although large series studies of anorexia nervosa families have found a greater than expected occurrence of anorexia nervosa in family members, there are no reports of the anorectic's parents' weights during the time of the patient's illness. An unusual degree of weight aberrations present in the parents at the time of the patient's illness could represent both a genetic and noxious environmental influence for the development of anorexia nervosa. In order to examine the possibility that weight aberrations may be more frequent in anorectic patients' parents, we obtained height and weight measurements from the parents of 30 anorexia nervosa patients. The parents were compared with 30 control families in which the father was matched for age, level of education, occupation, and salary to the patient's father. Matching the control group for socioeconomic status was necessary since previous studies have shown a relationship between socioeconomic status and weight. An analysis of covariance showed no difference between the weight of the patient and control parents, although a significant relationship between educational level and weight was present.
Nine female patients with anorexia nervosa were studied, three of them at different stages of weight gain. Basal plasma LH (luteinising hormone) was depressed in emaciated patients, but basal plasma FSH (follicle stimulating hormone) was normal. LH was significantly lower in patients who had been amenorrhoeic for less than 24 months than in those whose amenorrhoea was of longer duration. LH and FSH levels were stimulated by LHRH (luteinizing hormone releasing hormone), infused at a rate of 0.5 microgram/min for four hours. One patient, tested at 60% of standard weight, had no LH response. In all other patients below 70% of standard, the maximal LH response occurred within the first hour of infusion. In patients at higher weights, the LH response was biphasic, and the maximal level was reached during the last hour of the infusion. The FSH response, similarly, approached maximal during the first hour in patients below 70% of standard, but continued to rise throughout the infusion in patients at higher weights. Body weight expressed as a percentage of standard correlated significantly with both phases of the LH response, but not with the FSH response. Most previous authors have found an association between low body weight and depressed pituitary gonadotrophins in anorexia nervosa. The present findings further elucidate this relationship.
In 18 patients with anorexia nervosa, plasma cholesterol and triglyceride concentral concentrations were repeatedly determined over a period of 14 mo. In 11 patients elevated cholesterol concentrations were found which were due to an increase of low-density lipoprotein cholesterol, whereas high-density lipoprotein and very low density lipoprotein cholesterol levels were in the normal range. The elevated cholesterol values did not correlate with clinical and laboratory parameters such as the degree of weight loss and thyroid function tests. In follow-up studies it could be shown that in patients who regained their original weight, elevated plasma cholesterol concentrations fell to normal levels parallel to weight increase. In patients who showed no change in weight, however, cholesterol levels remained high. The cause for this secondary type II hyperlipoproteinemia in anorexia nervosa is not known. Hepatic triglyceride lipase and lipoprotein lipase activities in post-heparin plasma were found to be low despite normal triglyceride concentrations.
100 females with anorexia nervosa were followed up 4-8 years after first presentation. All but 12 had had refeeding and/or psychotherapy. 48 had a good outcome (weight at least near normal, regular menstruation, largely satisfactory mental state and psychosexual and psychosocial adjustments) but outcome was intermediate in 30, and poor in 20 patients. 2 had died. Poor outcome could be positively associated with clinical data such as longer duration of illness, older age of onset and presentation, lower weight during illness and at presentation, presence of symptoms such as bulimia, vomiting, and anxiety when eating with others, poor childhood social adjustment, and poor parental relationships.