Gerald Russell

Evaluation of family treatments in adolescent anorexia nervosa: A pilot study

In the search for more effective methods of psychological treatment in anorexia nervosa, there are a number of controlled trials evaluating the efficacy of different forms of treatment. Previous studies have shown that family therapy is the superior treatment for patients with an early onset and short duration of illness. In order to assess the impact and the effective components of family therapy, we conducted a pilot trial in which consecutive referrals of anorexia nervosa patients were randomly assigned to one of two forms of family treatment: family therapy (conjoint family sessions) or family counselling (separate supportive sessions for the patient and counselling for the parents). Changes taking place within the patient and the family were evaluated at regular intervals, while within and between group comparisons were made. Although tentative, it was found that, in the short term, there were few differences in terms of symptomatic relief between the two treatment groups.

Structural and functional changes in skeletal muscle in anorexia nervosa.

Abstract Protein-energy malnutrition in anorexia nervosa is an under-recognised cause of muscle dysfunction. To characterise the skeletal myopathy that occurs in patients with severe anorexia nervosa, muscle function and structure were comprehensively examined in eight young adult female patients with severe (40%) self-induced weight loss. All of the patients showed impaired muscle function on strength and exercise measurement. The maximum voluntary contraction force for the patient group was significantly less than predicted values. Electromyography revealed myopathy in five of the patients, four of whom also had electro-physiological evidence of neuropathy. However, muscle biopsy specimens consistently showed myopathic changes with severe type 2 fibre atrophy but with no evidence of neuropathic changes. Ultrastructurally, there was separation and segmental loss of myofibrils and most biopsy samples contained abundant glycogen granules; we have previously reported that one of the most consistent biochemical abnormalities in these patients is impaired ischaemic lactate responses to forearm exercise. The result of severe protein-energy malnutrition on the musculo-skeletal system is a metabolic myopathy. Although the patients admitted to a variety of abnormal dieting behaviours, such as over-exercising and self-induced vomiting, no association was found between any of these and quantitative histological changes in the muscle biopsy samples. It is recommended that myopathy in anorexia nervosa be treated by instituting an appropriate refeeding programme.

Mothers with anorexia nervosa who underfeed their children: their recognition and management

BACKGROUND Women with anorexia nervosa have a reduced fertility but they may have borne children before the onset of their illness or after partial recovery. Little is known on how to identify the anorexic mothers who underfeed their children and how to manage them. This article aims to remedy these gaps. METHODS The clinical scientific method is the only means of identifying the children of anorexic mothers who are at risk. Eight such mothers were identified as a result of obtaining serial measurements of the childrens weights and heights over time. Tanner-Whitehouse charts were used to plot weight for age and height for age. A simple rating scale was devised to measure the acceptance of treatment involving both mother and child. RESULTS Nine children (eight boys and one girl) were found to have suffered food deprivation: with severe reduction in weight-for-age in six and in height-for-age in eight. Five siblings were not affected. Catch-up growth was correlated with the degree of engagement in treatment of both mother and child. Long-term treatment of one mother, combining family therapy with admissions to hospital, resulted in catch-up growth in her two sons. CONCLUSIONS The mechanisms underlying the privation of the children stem from the anorexic mothers abnormal concerns with body size extending to her children. The children may become unduly accepting of the underfeeding. It is essential to obtain the confidence of anorexic mothers suspected of underfeeding their children and to adopt a whole family approach to treatment.

WEIGHT GAIN AND REPRODUCTIVE FUNCTION: ULTRASONOGRAPHIC AND ENDOCRINE FEATURES IN ANOREXIA NERVOSA

Pelvic ultrasonographic measurements and reproductive hormone levels in 36 patients with anorexia nervosa were followed as they gained weight during inpatient treatment. In 24 patients who were severely malnourished (69% of premorbid weight) the ovaries were small and amorphous and the levels of LH, FSH and oestfadiol were very low. Weight gain led to the appearance of multifollicular ovaries when levels of LH and oestradiol remained low but FSH levels had increased resulting in an LH: FSH ratio of less than 1. The emergence of a dominant follicle in 19 patients after weight gain (to 97% of premorbid weight) was accompanied by an increase in uterine area and associated with increased levels of LH and oestradiol and an LH: FSH ratio greater than 2. Among these patients with a dominant follicle at peak weight, 11 menstruated within a month of discharge.

Eating disorders: psyche or soma?

Speculation about the etiology of eating disorders has gone through different phases, variously favoring familial, organic, and psychosocial factors. Recent evidence has particularly contributed to our understanding of the organic view. We review the evidence for an organic contribution to the illness and present a series of cases in which organic factors were present. The cases illustrate the complex interaction between biological and psychological factors. In particular, a growth hormone-producing pituitary adenoma was discovered in a patient following successful treatment of her bulimia by psychological means alone. Etiological theories of eating disorders need to encompass both organic and psychosocial factors, allowed to interact in complex ways. Focusing exclusively on either aspect is a disservice to our patients.

The Modern History of Anorexia Nervosa An Interpretation of Why the Illness Has Changed

1. To examine the changes undergone by anorexia nervosa during recent decades; 2. To set these changes within the broader historical context of the fasting behavior in women since the 14th century; 3. To assess the role of sociocultural factors in causing anorexia nervosa, shaping the clinical form of the illness, or influencing the content of the patient’s psychological concerns; 4. To attempt to integrate sociocultural influences with disturbed biological mechanisms so as to facilitate a multidimensional view of anorexia nervosa.

Metabolic abnormalities associated with skeletal myopathy in severe anorexia nervosa

The aim of this study was to characterize the metabolic disturbance associated with the skeletal myopathy resulting from extreme weight loss in anorexia nervosa. Muscle function was examined in eight female patients with severe (40%) weight loss due to anorexia nervosa and histologically confirmed myopathy. A wide range of biochemical and hematologic investigations were carried out, including serum enzymes and the response of plasma lactate to ischemic exercise of forearm muscles. All patients showed proximal muscular weakness. A diminished lactate response to ischemic exercise was a consistent finding, and a reduction of serum carnosinase activity was also found. There were no other consistent biochemical or hematologic abnormalities apart from lymphopenia of no clinical consequence. These findings contribute to our understanding of severe protein-energy malnutrition on the musculoskeletal system. The resulting disorder is a metabolic myopathy from which the patients recover rapidly as their nutrition improves. Although the patients admitted to a variety of abnormal eating behaviors, no correlation was found between a specific type of abnormal eating behavior and subsequent biochemical abnormalities. Reinstating appropriate eating behavior will treat the myopathy.

Steroid metabolism and excretion in severe anorexia nervosa: effects of refeeding,

BACKGROUND To our knowledge, changes in steroid metabolism in subjects with anorexia nervosa (AN) after weight gain have not been elucidated. OBJECTIVE We characterized urinary steroid excretion and metabolism in AN patients and investigated the effects of refeeding. DESIGN In an intervention study, we recruited 7 women with life-threatening weight loss upon admission and after a median [interquartile range (IQR)] of 95 d (88-125 d) of intensive refeeding; 15 age-matched women were recruited as control subjects. The major urinary metabolites were quantified in 24-h collections by capillary gas chromatography. A single examiner measured weights, heights, and skinfold thicknesses. RESULTS The median (IQR) age of patients was 24 y (21-26 y), and the duration of AN was 4.0 y (3.3-8.0 y). Body mass index (BMI; in kg/m(2)) increased from 12.8 (12.7-13.1) to 18.6 (18.0-19.6) after refeeding (P < 0.0001). Steroid values [median pre-, post-refeeding (P value)] were as follows: androgen metabolites [472, 1017 μg/24 h (0.93)], cortisol metabolites [1960, 3912 μg/24 h (0.60)], and ratios of androsterone (5α)/etiocholanolone (5β) [0.28, 0.63 (<0.001)], 5α-/5β-tetrahydrocortisol [0.20, 0.48 (0.02)], tetrahydrocortisols/tetrahydrocortisone [0.87, 0.61 (0.09)], 20-hydroxy-/20-oxocortisol metabolites [0.29, 0.47 (0.01)], and 20α-/20β-reduced cortisol metabolites [1.18, 1.89 (≥1.00)]. BMI change was positively correlated with 5α-/5β-tetrahydrocortisol (r = 0.95, P < 0.001). Before refeeding, the following metabolites were lower in patients than in control subjects: androsterone, 5α-tetrahydrocortisol, α-cortolone and α-cortol, 5α-/5β-tetrahydrocortisol, androsterone/etiocholanolone, and 20-hydroxy/20-oxocortisol (all P < 0.05). After refeeding, all steroid metabolites in patients were at concentrations that were comparable with those in control subjects. CONCLUSIONS Significant changes in urine steroid-metabolite excretion occurred upon starvation, which were reversed upon refeeding. For cortisol, there were decreases in 5α-/5β-tetrahydrocortisol and 20-hydroxy-/20-oxometabolites; for androgen, there was a decrease in androsterone/etiocholanolone.

Follow-up mortality study of compulsorily treated patients with anorexia nervosa

OBJECTIVE In a previous study we found that compulsory inpatient treatment was associated with an increase in the number of deaths over the following 5 years when compared to non-compulsory admission. This study aimed to examine the longer term mortality of patients admitted compulsorily. METHOD The mortality outcome of patients with a compulsory admission (n = 81) and a comparison group (n = 81) of patients admitted to the specialized eating disorder unit at the Maudsley Hospital in the period 1983-95 was traced over two decades through the National Register held by the National Health Service (NHS) Central Register. RESULTS Approximately 20 years following admission there were 27 deaths in the series. The standardized mortality rate in the compulsory treatment group no longer differed significantly from that of the non-compulsory group. The suicides were not particularly linked with compulsory admission. DISCUSSION Although the mortality in the 5 years following a compulsory admission is higher than that seen in the non-compulsory patients, this difference is attenuated over time. The overall standardized mortality rate remains elevated.

Neuromyopathic complications in a patient with anorexia nervosa and vitamin C deficiency

A 19-year-old female patient with anorexia nervosa developed profound weight loss over 1 year associated with vegetarianism and excessive exercise. There was severe wasting and proximal muscle weakness in the legs and bilateral weakness of eye closure. A purpuric rash developed due to vitamin C deficiency. This case demonstrates a new neurological sign in anorexia nervosa indicating a weakness of the orbicularis oculi muscles as part of a more general myopathy. The myopathic and scorbutic features may have a common pathogenesis.