Anorexia Nervosa

Introduction: history of ideas

Two different approaches may be discerned in the conceptualization of anorexia nervosa.

1.The medico-clinical approach defines the illness in terms of its clinical manifestations; the main landmarks were the descriptions by William Gull in 1874 and Charles Lasègue in 1873.  

2.The socio-cultural approach is unlike the more empirical clinical approach and takes causation into account by viewing the illness as a response to prevailing social and cultural systems. This was best argued by the social historian Joan Jacobs Brumberg who considers anorexia nervosa simply as a control of appetite in women responding to widely differing forces which may change during historical times. This approach allows flexibility in identifying anorexia nervosa in different historical and cultural settings, but it carries the risk of excessive diagnostic latitude.

There is a strong argument for accepting the original descriptions by Gull (1874) and Lasègue (1873) as containing the essence of anorexia nervosa. They both recognized a disorder associated with severe emaciation and loss of menstrual periods, inexplicable in terms of recognized physical causes of wasting. They were both extremely cautious about the nature of the mental disorder. Gull spoke of a morbid mental state or ‘mental perversity', and adopted the more general term anorexia ‘nervosa' which has persisted until today. Lasègue also referred to ‘mental perversity' but was bold enough to call the condition ‘anorexie hystérique, faute de mieux'.

It is probably best to seek a balance between the diagnostic rectitude of the medico-clinical approach and the malleability of anorexia nervosa in response to changing historical and sociocultural settings. Looking back in historical times, it may well be that the self-starvation and asceticism of St Catherine of Siena corresponded to modern anorexia nervosa. In more recent times the preoccupations of the patients have altered so that their disturbed experience with their own body or their ‘morbid fear of fatness' has earned the distinction of becoming one of the diagnostic criteria. Yet this concern with body size was not remarked upon by Gull or Lasègue. This is an argument for concluding that at least the psychological content, and perhaps also the form, of anorexia nervosa are changeable in response to historical times and socio-cultural influences.


Screening instruments The most commonly used screening test in the detection of anorexia nervosa is the Eating Attitudes Test (EAT). Doubt has, however, been expressed about the predictive value of the EAT in the very populations where its use was introduced, as only a small percentage of the EAT-screened positive scores will have an actual eating disorder. Thus, the EAT has limited usefulness in surveys for detecting anorexia nervosa unless it is supplemented by detailed clinical assessments. A survey depending on initial screening by questionnaire also runs the risk of failing to detect cases of anorexia nervosa as it was found that patients currently receiving active treatment were among the non-respondents, presumably because they wished to conceal their disorder.

Populations surveyed

General population surveys

These are often impracticable when the aim is to detect anorexia nervosa, a relatively uncommon disorder.

Surveys of primary care populations

A useful compromise is that of surveying populations of patients who consult their general practitioners. A Netherlands study was successful because a large population was surveyed (over 150 000) and the general practitioners themselves, after suitable training, were responsible for making the diagnoses.

Populations thought to be more at risk

Surveys of ballet and modelling students were conducted because it was thought likely that there would be a high prevalence of anorexia nervosa among them as a result of pressures exerted to sustain a slim figure in keeping with their professional image. Populations of adolescent schoolgirls have also been surveyed as their susceptibility might be raised by virtue of their age, sex, and the frequency of dieting among the school population. The most thorough survey of 15-year-old school-children was that conducted in Göteborg, Sweden.

Surveys based on case registers and hospital records

Data have been obtained on patients referred to inpatient and outpatient psychiatric services, or with the addition of patients who had consulted paediatricians, general medical services, or gynaecologists.  

Results of epidemiological surveys

Incidence of anorexia nervosa

The studies which counted only hospitalized patients tended to yield low estimates of the annual incidence of anorexia nervosa expressed per 100 000 population (e.g. 0.45 in Sweden. Estimates based on case registers of psychiatric patients similarly yielded fairly low incidence rates (e.g. 0.64 in Monroe County, New York. The incidence found in community-based studies was by far the highest (6.3 in The Netherlands and 8.2 in Rochester, Minnesota, presumably because they included the less severe cases.

Prevalence of anorexia nervosa in vulnerable populations

A high prevalence rate was found among Canadian ballet students (6.5 per cent) and modelling students (7 per cent). A similar survey in an English ballet school also showed a high prevalence of ‘possible' cases of anorexia nervosa (7.0 per cent).

Surveys among schoolgirls have shown a fairly wide variation in prevalence rates, ranging from zero to 1.1 per cent. In the English studies a consistent difference in prevalence rate was found between private schools (1 per cent) and state schools (0–0.2 per cent). This social class distinction was not so definite in the Swedish study where the overall prevalence of 0.84 per cent of schoolgirls, up to and including 15 years of age, represents a high rate for anorexia nervosa.

Age and sex

Epidemiological surveys have confirmed clinical opinion that anorexia nervosa commences most frequently in the young, especially within a few years of puberty. The peak age of onset is 18 years. The illness is less common before puberty, but in a series of patients admitted to a children's hospital the age of onset ranged from 7.75 to 14.33 years. The marked predominance of females over males was also confirmed, for example 92 per cent in northeast Scotland and 90 per cent among the children in Göteborg.

Social class and socio-economic status

The view has been widely held that anorexia nervosa occurs predominantly in patients with middle-class backgrounds, since Fenwick's classical observation that anorexia nervosa ‘is much more common in wealthier classes of society than amongst those who have to procure their bread by daily labour'.

Epidemiological surveys aimed at wider populations leave the question of social class distribution somewhat equivocal. Whereas a high percentage of combined social classes 1 and 2 (Registrar General's categories) were found in clinical studies, a high social class predominance was not found in studies utilizing case registers. On the other hand, the schoolgirl studies mentioned above tended to confirm a high social class predominance.

Has the incidence of anorexia nervosa increased since the 1950s?

Hilde Bruch had no doubt about the answer to this question: ‘one might speak of an epidemic illness, only there is no contagious agent; the spread must be attributed to psycho-social factors'. This is an exaggeration as the increase in anorexia nervosa does not merit the term ‘epidemic'. Indeed, such a notion was dismissed in an article ‘The epidemic of anorexia nervosa: another medical myth?'. It was concluded that there had been an increase in first admissions of patients over 10 years (1972–1981) but that this was due to an increase in the number of young women in the population. This rejection of a true increase in the incidence of anorexia nervosa has in its turn been criticized.

The most reliable evidence for changes in the incidence of anorexia nervosa comes from repeated surveys of the same population.This has been achieved with the surveys conducted in southern Sweden, northeast Scotland, Switzerland, Monroe County, New York, and Rochester, Minnesota. The researchers applied the same methodology to a similar population after an interval of several years, thus controlling for many of the variables that make it impossible to compare surveys conducted in different centres. There was a clear trend for an increase in incidence over time. The most thorough study was in Rochester, Minnesota. The researchers separated female patients aged 15 to 24 years (61 per cent) from the remainder and established an increase in these younger patients, but only in hem. They concluded that this increased incidence over time reflected a greater vulnerability of younger female subjects to adverse social factors.

There remains at least one sceptic who has argued that there is no evidence of an increase in anorexia nervosa. He has found statistical imperfections in all epidemiological studies so far, and even questioned the possible significance of changes in diagnostic criteria from DSM-III toDSM-IIIR. He agreed that the Rochester survey had produced robust data, but thought that it still contained unresolved analytic problems.

This issue remains an important one because of its significance in the search for sociocultural factors causing anorexia nervosa. But it is better to pose a different question which renders this controversy unnecessary. We should ask instead whether there has been an increase in the incidence of eating disorders including anorexia nervosa. This is especially relevant in view of the fact that bulimia nervosa is a variant of anorexia nervosa, and inmany patients follows an earlier episode of anorexia nervosa. There is strong evidence that bulimia nervosa is a new disorder and has not simply appeared because of improved medical recognition. Moreover, the incidence of bulimia nervosa has risen sharply during the past 20 years, so that it is now about double that of anorexia nervosa. In conclusion, it is clear that since the 1960s there has been a significant increase in eating disorders, of which the two clearest syndromes are anorexia nervosa and bulimia nervosa.


Aetiological concepts

According to one robust opinion, it is essential to pursue the search for a specific and necessary cause of anorexia nervosa because the currently popular ‘multifactorial' approach has little explanatory power.  Accordingly the failure to identify a necessary causal element is regrettable. Many of the factors within a wide range of psychological, social, and physical causes so far studied may therefore only be relevant in predisposing to anorexia nervosa. The patients ‘become terribly afflicted victims of an often-incurable illness whose causes still elude clarification'. 

The multidimensional approach to anorexia nervosa

It is precisely because we do not know the fundamental (necessary) cause of anorexia nervosa that recourse has to be had to a multidimensional approach, faute de mieux. Although it has its limitations, a multidimensional approach permits one to consider a range of possible causal factors whichnot only act in an additive manner but may combine in a specific manner to bring about the illness: ‘It is the interaction and timing of these phenomena in a given individual which are necessary for the person to become ill'.

It is useful to provide a simple model of the way that two broad sets of factors may interact and augment each other. The outer circle represents the entire population in a developed ‘Westernized' country. Within the circle there is a large sector representing females within an age range of 10 to 50 years who experience prevailing social pressures to acquire a slender body shape through dieting. Evidently only a small proportion of these women develop the illness. It is likely that for anorexia nervosa to develop it is also necessary to possess a genetic predisposition, represented by the small inner circle. The intersection of the inner circle and the large sector produces a small sector of females who have the genetic predisposition and also experience sociocultural pressuresto lose weight, interacting to cause clinical anorexia nervosa.  

Causal factors may not only interact as explained above, but they can also influence the content of the illness, its ‘colouring', and its form. This modelling function is described by the term ‘pathoplastic' which was introduced by Birnbaum. Pathoplastic features are to be distinguished from the more fundamental causes of psychiatric illness, but they do exert a predisposing tendency as well as a modelling role.

Sociocultural causes

The cult of thinness

The pathoplastic sociocultural causes of eating disorders have been subsumed under the term ‘the modern cult of thinness' prevalent in Westernized societies. Vulnerable patients are likely to respond to this pressure by experimenting with weight-reducing diets which carry a degree of risk, and anorexia nervosa is arguably but an extension of determined dieting.

It is proposed that the cult of thinness is responsible for the increase in the incidence of eating disorders since the 1950s. The social pressures which lead to dietary restraint include the publication of books and magazines advising weight-reducing diets, the fashion industry which caters mainly for the slimmer figure, television attaching sexual allure and professional success to the possession of a svelte figure, and the emphasis on physical fitness andathleticism.  

Changes in the psychopathology of anorexia nervosa

At the beginning of this article it was pointed out that the psychological content and the form of anorexia nervosa have changed over historical time and in response to sociocultural influences. Whereas Gull and Lasègue spoke only of ‘anorexia nervosa' and ‘anorexie hystérique' respectively, more recent descriptions of the psychopathology of anorexia nervosa have stressed a disturbed experience of one's own body, a weight ‘phobia', or a morbid dread of fatness. It is precisely the modern anorectic's dread of fatness that is most in keeping with today's cult of thinness. It is arguable therefore that modern societal pressures have determined the patients' preoccupations and contributed to their food avoidance. The beliefs are held obstinately and amount to over valued ideas.

Anorexia nervosa as a culture-bound syndrome  

The proposition that anorexia nervosa is a culture-bound syndrome has much support. An intense fear of becoming obese is as culture bound as the disorder koro (a fear of shrinkage of the genitals) in Malaysia and South China.

A culture-bound syndrome may be defined as a collection of signs and symptoms which is not to be found universally in human populations, but is restricted to a particular culture or group of cultures. Implicit is the view that culture factors play an important role in the genesis of thesymptom cluster ...

Anorexia nervosa meets these criteria, first because it is limited to Westernized or industrialized nations, and secondly because it is clear that the psychosocial pressures on women to become thin constitute a powerful cultural force leading to anorexia nervosa.

In order to allow for exceptions to the rule, when anorexia nervosa occurs in non-Westernized countries, the illness may be understood as arising from cultures undergoing rapid cultural change. Anorexia nervosa is thus a ‘culture-change syndrome', explaining its increased incidence in Japan and Israel. Anorexia nervosa remains rare in Asia (particularly India), the Middle East (with the exception of Israel), and generally in poorly developed countries.

Young female immigrants who move to a new culture may suffer from an increased prevalence of eating disorders. For example, children with anorexia nervosa were found among Asian families living in Britain. This was linked with an exposure to a conflicting set of sociocultural norms in comparison with their parents and grandparents. 

Adverse life events

Anorexia nervosa may be precipitated by adverse life events. Early clinical studies depended solely on the patient's reports ofan adverse life event preceding the onset of the illness. These varied widely in severity and included the death of grandparents, a father's remarriage, a severe physical illness, stress or failure of school examinations, or being teased about being overweight. 

Recent studies have relied on more objective measurements of adverse life events and comparisons with control groups. In one such study, life events were rated according to the Bedford College Life Events and Difficulties Schedule and included the death of a close relative, a poor relationship with parents, or an unhappy marriage. Fairly severe life events and lasting difficulties were found in the majority of patients with a late onset (after 25years), whereas they were only found in a minority of patients with an early onset (before 25 years) or in patients with a ‘chronic' course.

Anorexia nervosa can also be precipitated by sexual experiences and conflicts. In a series of 31 adolescent and young women it was observed that in 14 first sexual intercourse had occurred before the illness.  Sexual problems were seen by 13 patients as major precipitants of their illness; 10 of them had experienced intercourse. The authors concluded that a specific aetiological role of sexual factors seemed unlikely, but there might be a direct relationship between the onset of eating difficulties and concurrent sexual problems.

In a series of 15 patients, anorexia nervosa developed during pregnancy or, more often, during the postnatal period when it wasaccompanied by depression. Risk factors included ambivalence about motherhood, a large weight gain during the pregnancy, physical complications during pregnancy, postnatal depression, and past psychiatric illness.

Childhood sexual abuse

Since it was reported that a high proportion of patients in a treatment programme for anorexia nervosa gave histories of sexualabuse in childhood, it has been supposed that this trauma would be a contributory causal factor. It would be better if this history could be corroborated, but for obvious reasons it is often difficult to do so. Investigators often stress that their patients' accounts are convincing and that they should be believed. Hence this subject raises unusual difficulties in judging the reliability of the data. 

In a careful study of childhood sexual experiences reported by women with anorexia nervosa, the authors classified the events according to the seriousness of the sexual act in childhood and concentrated on sexual experiences with someone at least 5 years older. They found surprisingly high rates (about one-third) of adverse sexual experiences in women with eating disorders, and, unlike other investigators, they did not find that the frequency of these reports was less in anorexia nervosa than bulimia nervosa. They concluded that it was plausible that childhood sexual contact with an adult may in some cases contribute to a later eating disorder.

The complexity of this subject has been increased by a study on the relationship between sexual abuse, disordered personality, and eating disorders. The authors found that 30 per cent of patients referred to an eating disorders clinic (a majority with anorexia nervosa) gave a history of childhood sexual abuse. In addition, they found that 52 per cent of their patients had a personality disorder. A significantly higher proportion of women with a personality disorder had a history of childhood sexual abuse, compared with those without a personality disorder. Surprisingly they still concluded that in patients with eating disorders it was not possible to show a clear causal link between child sexual abuse and personality disorder.

In a review of the subject a number of hypotheses were examined on the relationship between childhood sexual abuse and eating disorders. One hypothesis is that child sexual abuse is more common in bulimia nervosa than in anorexia nervosa. The authors had to concede that the findings remain inconclusive. They also examined the question of whether child sexual abuse is a specific risk factor for eating disorders. They concluded that this was not the case, as the rates of child sexual abuse in eating disorder patients were similar to or less than those in various other psychiatric comparison groups. Finally, they found strong evidence that patients with eating disorders reporting child sexual abuse were more likely to show general psychiatric symptoms including depression, alcohol problems, or suicidal gestures, in addition to the association with personality disorders already mentioned.

Family factors

Two influential groups of family therapists (Minuchin at the Philadelphia Child Guidance Clinic and Selvini Palazzoli in Milan) have devised family models to explain the genesis of anorexia nervosa.

Minuchin et al.identified faulty patterns of interaction between members of the anorexic patient's family; they in turn were thought to lead to the child's attempt to solve the family problems by starving herself:  ‘The sick child plays an important role in the family's pattern of conflict avoidance, and this role is an important source of reinforcement for his symptoms'. Five main characteristics of family interaction were identified as detrimental to the function of the family: enmeshment (a tight web of family relationships with the members appearing to read each other's minds), overprotectiveness, rigidity, involvement of the sick child in parental conflicts, lack of resolution of conflicts.

Selvini Palazzoli also identified abnormal patterns of communication within these families and in addition described abnormal relationships between the family members. She assumed that anorexia nervosa amounted to a logical adjustment to an illogical interpersonal system. But it remains uncertain whether these abnormal interactions are to blame for the illness or develop as a response by parents faced with a starving child. Careful therapists take pains to reassure parents at the commencement of family therapy: ‘...we always find it useful to spend some time discussing the nature of the illness, stressing in particular that we do not see the family as the origin of the problem'.  

Bruch described girls who developed anorexia nervosa as ‘good girls', who previously had a profound desire to please their families to the point of becoming unaware of their own needs. The frequency of broken families in anorexia nervosa is thought to be fairly low. Anorexic families have been found to be closer. They spent most of their spare time together and tended to mix less with people outside the family circle; the patients more often perceived themselves as having happy relationships within the family. 

Personality disorders

A sizeable proportion of patients (30 per cent and 32 per cent were said to have had a ‘normal' personality during childhood before their illness. Nevertheless there is general agreement of a close relationship between obsessional personalities and the later development of anorexia nervosa. In fact Janet, who carefully described obsessions and psychasthenia, was dubious about the validity of the diagnostic concept of anorexia nervosa (anorexie hystérique). He thought that the patient's fear of fatness was an elaborate obsessional idea.

In a study of patients admitted for treatment they were classified into anorexia nervosa, bulimia nervosa, or a combination of the two disorders. Personality disorders were identified through the Structured Clinical Interview for DSM-IIIR personality disorders (SCID-II). Seventy-two per cent of the patients met the criteria for at least one personality disorder. Anorectics were found to have a high rate of obsessive–compulsive personality disorder. On the other hand, bulimic patients with a history of anorexia nervosa showed high rates of borderline (40 per cent) and histrionic (40 per cent) personality disorder.  

There have been attempts to disentangle the features of premorbid personality and illness in order to clarify the personality characteristics predisposing to anorexia nervosa. Women who had recovered from restricting anorexia nervosa were tested at an 8- to 10-year follow-up, using a number ofself-report instruments. They were compared with two control groups: normal women and the sisters of the recovered anorexic patients. The women who had recovered from anorexia nervosa rated higher on risk avoidance and conforming to authority. In comparison with their sisters, the recovered women showed a greater degree of self-control and impulse control, and less enterprise and spontaneity.

In a study examining the close relationships between anorexia nervosa and obsessive–compulsive personality traits and disorder,12 patients who had recovered from anorexia nervosa were examined and compared with normal controls. They continued to exhibit obsessional traits in the weight-restored state and attained significantly higher scores on the Maudsley Obsessive–Compulsive Inventory and the Tridimensional Personality Questionnaire (harm avoidance and reward dependence).

Biomedical factors and pathogenesis

Historical notes

Since the early part of the twentieth century a recurring theme has been the possibility that anorexia nervosa is primarily caused by an endocrine or cerebral disturbance. From 1916 there was much preoccupation with the concept of Simmonds' cachexia, the assumed result of latent disease of the pituitary gland. There was diagnostic confusion between anorexia nervosa and hypopituitarism which was only clarified much later when it became known that in true hypopituitarism weight loss and emaciation are uncommon. Hormonal deficits indicative of impaired pituitary function are indeed common in anorexia nervosa, but are merely a secondary manifestation of prolonged malnutrition.

Interest in the neuroendocrinology of anorexia nervosa led to the formulation of the hypothalamic model. (7,56) From the beginning the model was aimed at explaining pathogenesis rather than aetiology; it was not considered an alternative to the psychological origin for anorexia nervosa, but a means of explaining a constellation of disturbed neural mechanisms, as follows:

  1. a disordered regulation of food intake;
  2. a neuroendocrine disorder affecting mainly the hypothalamic–anterior pituitary–gonadal axis;
  3. a disturbance in the regulation of body temperature.

It was known that these functions all reside within the complex of hypothalamic physiology. A ‘feeding centre' had been described in the lateral hypothalamus because bilateral lesions there induced self-starvation and death in rats. A ‘satiety centre' in the ventromedial hypothalamus whose destruction caused obesity had previously been described. (58)Over the years it has become clearer that many of the disturbances could be attributed to the patients' malnutrition, as demonstrated by experimental studies in healthy young women who were asked to follow a weight reducing diet. It was found that ovarian functionis extremely sensitive to even small restrictions of caloric intake which often lead to impaired menstrual function.  

Cerebral lesions and disturbances

Interest in the hypothalamic model was fuelled early on by clinical reports of patients diagnosed as suffering from anorexia nervosa who were later found to have cerebral lesions, especially tumours of the hypothalamus. More recently, occult intracranial tumours have been detected, masquerading as anorexia nervosa in young children. 

Neuroimaging studies in anorexia nervosa have led to findings suggestive of an atrophy of the brain. CT has disclosed a widening of the cerebral sulci and less frequently an enlargement of the ventricles. The outer cerebrospinal fluid spaces were enlarged markedly in 36 per cent of the patients. When the CT examination was repeated after weight gain 3 months later, the widening of the sulci had disappeared in 42 per cent of the patients who hadpreviously shown this finding. In other patients, however, the widening remained unaltered for 1 year after body weight had returned to normal.

Functional neuroimaging techniques have also been applied to research in anorexia nervosa. Fifteen children with anorexia nervosa were investigated by means of single-photon emission CT which provides a measure of regional cerebral blood flow. In the majority of the children there was an above-critical difference in the regional cerebral blood flow between the temporal lobes. Hypoperfusion was found on the left side in eight children and on the right side in five. Follow-up scans were undertaken in three children after they had returned to normal weight; the reduced regional cerebral blood flow in the temporal lobe persisted on the same side as the initial scan. The authors concluded that there was an underlying primary neurological abnormality—an imbalance of the limbic system which in turn led to a hypothalamic–pituitary abnormality. Caution is advisable when interpreting functional neuroimaging studies as it is extremely difficult to have a control group with children.

Genetic causes

The strongest argument in favour of a biomedical causation of anorexia nervosa is the evidence that genetic factors have a role to play. The evidence is mainly derived through the classical method of comparing the concordance rates for the illness in monozygotic and dizygotic twins. The first sizeable series of twins studied came from the Maudsley Hospital and St George's Hospital in London, and revealed a higher concordance rate for monozygotic than for dizygotic twins. Among the 30 twin pairs the concordance rates were 56 per cent among monozygotic twins compared with 7 per cent among dizygotic twins. The authors concluded that there is a genetic predisposition to anorexia nervosa.

Tentative calculations of the ‘heritability' of anorexia nervosa suggested that it accounts for as much as 80 per cent of the variance. It remains uncertain how the genetic vulnerability to anorexia nervosa expresses itself in terms of the pathogenesis of this disorder. An interesting proposal is that this vulnerability confers a weakness of the homeostatic mechanisms which normally ensure weight restoration after a period of weight loss. This hypothesis would explain why in Western society, where dieting behaviour is common, those who are genetically vulnerable would be likely to develop anorexia nervosa.  

There is also evidence for a familial aggregation of anorexia nervosa. This does not necessarily mean that the origin of the disorder is genetic because environmental factors in common must also be considered. In a series of 387 first-degree relatives of 97 probands with anorexia nervosa it was found that the illness occurred in 4.1 per cent of the first-degree relatives of the anorexic probands, whereas no case was found among relatives of the controls who were probands with a primary major affective disorder or with various non-affective conditions. The authors concluded that anorexia nervosa was familial with intergenerational transmission. It was roughly eight times more common in female first-degree relatives of anorexic probands than in the general population, and absent in the relatives of probands with major affective disorder, thus indicating a specificity in the risk of transmission of anorexia nervosa and an absence of shared familial liability with affective disorders.


Since the early 1970s, the hypothalamic model of anorexia nervosa has been transformed from a consideration of anatomical ‘centres' to ‘systems' involving neurotransmitters. Much evidence has been presented to show that a wide range of neurotransmitters modulate feeding behaviour, and it was only a small conceptual step to suggest that some were involved in the pathophysiology of eating disorders. At first the neurotransmitters considered were mainly the monoamine systems—noradrenaline (norepinephrine), dopamine, and serotonin. In addition, opioids, the peptide cholecystokinin, and the hormones corticotrophin-releasing factor and vasopressin have also been thought to play a part in the pathogenesis of eating disorders. During recent years the main interest has been focused on the role of serotonin (5-hydroxytryptamine, 5-HT) in the control of natural appetite, especially those aspects concerning the phenomenon of satiety, mediated through a range of processes called the ‘satiety cascade'. There is now strong evidence that pharmacological activation of serotonin leads to an inhibition of food consumption. It was also postulated that a defect in serotonin metabolism confers a vulnerability to the development of an eating disorder.  

A boost to the concept of altered serotonin activity in anorexia nervosa has come from research showing that these patients while still underweight had significant reductions in cerebrospinal fluid 5-hydroxyindoleacetic acid (5-HIAA). The levels became normal when the patients were retested 2 months after they reached their target weight. In order to test whether these findings were secondary to malnutrition, the researchers resorted to the ingenious step of studying patients after ‘recovery' when they had reached normal weight. They found elevated levels of cerebrospinal fluid 5-HIAA, possibly indicating increased serotonin activity contributing to the abnormal eating behaviour which often persists in patients who have otherwise recovered. The arguments against this simple model of enhanced serotonin activity as a vulnerability trait in anorexia nervosa should be briefly represented. In two recent studies serotonin function was again assessed in long-term weight-restored anorectics. The investigators used a dynamic neuroendocrine challenge with D-fenfluramine as a specific probe of serotonin function which mediates the release of prolactin. If there were any persistent abnormality in serotonin function, the response to this challenge test should differ from that in normal controls. In fact, the rise in prolactin levels was very similar in former patients and normal controls. Accordingly, these studies failed to support the notion of increased central serotonin function as a vulnerability trait in anorexia nervosa.

Clinical features

Classical anorexia nervosa (postpubertal)

The illness usually occurs in girls within a few years of the menarche so that the most common age of onset is between 14 and 18. Sometimes the onset is later in a woman who has married and had children.

By the time the patient has been referred for psychiatric treatment she is likely to have reduced her food intake and lost weight over the course of several months, and her menstrual periods will have ceased. A regular feature of the illness is its concealment and the avoidance of treatment. Most clinicians are reluctant to express themselves frankly on this subject in case their observations sound derogatory. It is to the credit of one French author, that he has said explicitly: ‘Denial of the illness, lies, cheating, manipulation, are characteristic of the behaviour of anorectics'. Even after having lost 5 to 10 kg inweight and missed several periods, the patient's opening remark is often ‘there is nothing wrong with me, my parents are unduly worried'. It is only when the clinician asks direct questions that she will admit to insomnia, irritability, sensitivity to cold, and a withdrawal from contacts with her friends, including her boyfriend if she has one.

Because of this denial, it is important to enquire from a close relative, as well as the patient, about the most relevant behavioural changes.

  1. A food intake history is obtained by asking the patient to recall what she has eaten on the previous day, commencing with breakfast which is often missed. An avoidance of carbohydrate and fat-containing foods is the rule. It is likely that pastry, puddings, biscuits, and confectionery are entirely omitted, as are fried foods, butter, and full-cream milk. When asked to explain her restricted choice of food, the patient is likely to defend it on the grounds that she wishes to follow a ‘healthy' diet. What remains is an often stereotyped selection of vegetables and fruit. ‘Diet' drinks and unsweetened fruit juice are preferred, although some patients are partial to black coffee. It is the mother who will indicate that her daughter finds ways of avoiding meals, preferring to prepare her own food and withdrawing into her bedroom to eat it.
  2. The patient is usually willing to provide a weight history and has a clear memory of her weight at successive stages of the illness. She may try to conceal her optimum weight before her decision to ‘diet', but she is likely to be objective about her current weight, if only to express pride in the degree of ‘self-control' she has exerted. The clinician then has an opportunity to enquire into her ‘desired' weight by simply asking what weight she would be willing to return to. Her answer will betray a determination to maintain a suboptimal weight.
  3. A history of exercising should be taken. Again, the patient is likely to conceal the fact that she walks long distances to school or to work rather than use public transport. She may also cycle vigorously or attend aerobic classes. A parent may report that his or her daughter is running on the spot or performing press-ups in the privacy of her bedroom, judging from the noise that can be heard. The amount of exercising may be grossly excessive, with the patient indulging in brisk walks or jogging even in the presence of painful knees or ankles due to soft tissue injuries.
  4. Additional harmful behaviours which should be enquired into include self-induced vomiting, purgative abuse, and self-injury. Vomiting and purgative abuse are similar to the behaviours that occur in bulimia nervosa. In anorexia nervosa they may occur without the prelude of overeating and the patient's motive is simply to accelerate weight loss. Even so, vomiting is most likely to occur after the patient's frugal meals, and the laxative abuse is often at the end of the day. The favourite laxatives in the United Kingdom are Nylax, Senokot, and Dulcolax, and the patient is likely to take them in increasing quantities to achieve the wanted effect as tolerance develops. Self-injury should also be enquired into, and the skin of the wrists and forearms inspected for scratches or cuts with sharp instruments.
  5. Menstrual history: the patient may not volunteer the information that her periods ceased, which often occurs soon after commencing the weight-reducing diet. On the other hand she may admit that she is relieved that her periods have stopped as she found them to be a nuisance or unpleasant.

The patient's mental state

Specific psychopathology

Several near-synonyms have been used to describe the specific attitude detectable in the patient who systematically avoids fatness: a ‘disturbance of body image', a ‘weight phobia', or a ‘fear of fatness'.  Magersucht, or seeking after thinness, was a term applied in the older German literature. The patient will express a sensitivity about certain parts of her body, especially her stomach, thighs, and hips. Not only is she likely to assert that fatness makes her unattractive, but she may add that it is a shameful condition betraying greed and social failure. These distorted attitudes generally amount to overvalued ideas rather than delusions. Occasionally, however, a patient may be frankly deluded, such as one young woman who believed that her low weight was due to thin bones and that fatness was still evident on the surface of her body.

Studies have demonstrated that wasted patients, when asked to estimate their body size, see themselves as wider and fatter than they actually are. Since these early observations, numerous perceptual studies have been undertaken using a variety of methods which have been reviewed and the conclusion drawn that anorexic patients overestimate their body width more often than normal controls. These distorted attitudes are often associated with a negative affect, so that the disturbance might be viewed as one of ‘body disparagement'.  

The patient's dread of fatness is so common that it is pathognomonic of anorexia nervosa. There are, however, exceptions. Sometimes a patient may simply deny these faulty attitudes. Another exception is the occurrence of anorexia nervosa in Eastern countries where thinness is not generally admired (e.g. Hong Kong and India). The imposition of fear of fatness as a diagnostic criterion on patients from a different culture, where slimness is not valued, may amount to a contextual fallacy, i.e. a failure to understand the illness in the context of its culture. 


Depression of varying severity, including major depressive disorders, is common. The patients express guilt after eating, adding that they do not deserve to have food. A high rate of depression (42 per cent) was found at presentation in one study and the lifetime history of depression in follow-up studies may be as high as 68 per cent.

Obsessive–compulsive features

The patients frequently eat in a ritualistic way, for example restricting their food intake to a narrow range of foods which experience tells them are ‘safe' because they will not lead to weight gain. There is often a compulsive need to count the daily caloric intake. One patient rejected prescribed vitamin tablets in case they contained ‘calories'. The frequency of obsessive–compulsive disorder in anorexia nervosa was found to be 22 per cent in a clinical series. (24) In studies using structured clinical interviews the frequency ranges from 25 to 70 per cent.

Neuropsychological deficits

These deficits are seldom detected clinically, and an emaciated patient may pursue studies and obtain surprisingly good examination marks. On the other hand, neuropsychological testing has revealed deficits in attention, and impairment of memory and visuospatial function.

The endocrine disorder

The impairment of hypothalamic–pituitary–gonadal function Amenorrhoea is an early symptom of anorexia nervosa and in a minority of patients may even precede the onset of weight loss. Amenorrhoea is an almost necessary criterion for the diagnosis of anorexia nervosa. An exception is when a patient takes a contraceptive pill which in fact replaces some of the hormonal deficit and may lead her to say she still has her periods.

Generally, when the patient is undernourished, levels of gonadotrophins and oestrogens in the blood are found to be low or undetectable. Not only do malnourished patients show low blood levels of luteinizing hormone and follicle-stimulating hormone, but the secretion patternsof these pituitary hormones regress to patterns of earlier development. For example, severely wasted patients display an infantile luteinizing hormone secretory pattern with a lack of major fluctuations over the course of 24 h. With some degree of weight gain a pubertal secretory pattern appears, consisting first of a sleep-dependent increase of luteinizing hormone at night, and later displaying more frequent fluctuations. When a patient is still malnourished the ultrasound pelvic examination will reveal that ovarian volume is much smaller than in normal women.  

Three stages can be discerned in the appearance of the ovaries as the patient gains weight:

  1. small amorphous ovaries;
  2. multifollicular ovaries (with cysts 3–9 mm in diameter);
  3. dominant follicle (10 mm or more in diameter).

At the same time there is a corresponding return of hormonal secretion; follicle-stimulating hormone appears first, followed byluteinizing hormone and finally oestradiol which leads to enlargement of the uterus. (80)

These abnormalities signify that the patient is infertile and remains so until endocrine function recovers. Pregnancy occasionally occurs as the patient is still underweight and improving but before the appearance of the first menstrual period. (81) The pregnancy carries a risk of poor fetal growth during the first trimester, albeit with some ‘catch-up' growth during the neonatal period. (82) Occasionally an underweight anorexic patient may seek treatment at an infertility clinic. Treatment with gonadotrophin-releasing hormone may restore fertility, but this practice has been severely criticized. (83)

Hypothalamic–pituitary–adrenal and hypothalamic–pituitary–thyroid axes

The emaciated anorexic patient shows an increased 24-h plasma cortisol level which returns to normal with a minimal increase inweight, as it is the nutritional intake that is critical.  

Reduced tri-iodothyronine (T3 ) levels are linked to a reduction in energy expenditure during starvation and are adaptive in nature, so that substitution of thyroid hormone is not appropriate in anorexia nervosa.  

Weight loss and malnutrition

Body weight

The severity of weight loss may be recorded as follows.

  1. As a percentage of an ‘average' body weight to be found in tables for normal populations according to age and height (e.g. the Metropolitan Life Insurance Tables).
  2. As a percentage drop from the patient's own weight before the onset of her illness (her ‘healthy' weight).
  3. Using the Quetelet body mass index (BMI)

A BMI between 20 and 25 is regarded as healthy. A BMI of 15 or less indicates a need for hospitalization. A BMI between 10 and 12 represents the lower limit of human survival.

Physical examination

Wasting is variable but may be extremely severe, resulting in a skull-like appearance of the head, stick-like limbs, and flat breasts, buttocks, and abdomen. The hands and feet feel cold and readily turn blue in winter. The skin is dry with an excess of downy hair (lanugo) covering the cheeks, the nape of the neck, the forearms, and the legs. Heartbeat is slow (50–60 beats/min) and the blood pressure is low (e.g. 90/60 mmHg) with orthostatic lability. During the routine physical examination muscle power should be tested to detect proximal myopathy, as explained below.

Differential diagnosis of classical anorexia nervosa

The diagnosis of anorexia nervosa is usually straightforward, especially as the modern diagnostic criteria are objective. Wasting diseases such as inflammatory bowel disease (Crohn's disease or ulcerative colitis), thyrotoxicosis, and diabetes mellitus may sometimes be mistaken for anorexia nervosa, but they can be identified through specific investigations. Occasionally there is an interaction between such a medical illness and anorexia nervosa, whena patient wishes to perpetuate the weight loss caused by the former. Rarely, anorexia nervosa may be mimicked by a cerebral tumour altering the function of the hypothalamus.

In middle-aged or older patients there may be diagnostic difficulty with a major depressive or schizophrenic illness. The weight loss in a severe depressive illness results from loss of appetite and the patient's ideas that she does not deserve food. A schizophrenic patient may avoid food because of paranoid delusions of being poisoned.

Complications of malnutrition

The complications which are part of the illness, such as amenorrhoea due to hypothalamic–pituitary–gonadal axis failure, have already been discussed. The range of medical complications has been extensively reviewed, with recommendations for the investigations needed on presentation of the patient.

Fluid and electrolyte disturbances and cardiovascular complications

Patients who induce vomiting, abuse laxatives, or take diuretics are likely to experience dehydration and various electrolyte disturbances.

Self-induced vomiting

Loss of gastric acid leads to a metabolic alkalosis and hypokalaemia. A low serum level of potassium may lead to cardiac conduction defects and arrhythmias, skeletal muscle weakness, and renal tubular dysfunction.

Laxative abuse

The abuse of laxatives is likely to cause dehydration, metabolic acidosis, hyponatraemia, and hypokalaemia.

The use of diuretics

The use of diuretics such as the thiazide group gives rise to low serum sodium levels which in turn cause fatigue and general weakness. A level below 120 mmol/l may lead to coma. The patient often justifies the use of a diuretic as a treatment for swollen ankles or even ‘bloating' of thestomach, which she misinterprets as being due to fluid retention.

Impaired renal function

This may be caused by different mechanisms: pre-renal failure due to dehydration or hypokalaemic nephropathy.

Peripheral oedema

Fluid retention leading to oedema occurs frequently in patients with anorexia nervosa. It is important to distinguish between ‘benign' oedema, which often occurs during the course of effective refeeding, and oedema from other causes which may have serious consequences.

‘Benign' oedema

‘Benign' oedema may occur during inpatient treatment. If the patient accepts a high caloric intake, fluid retention is the ruleas shown by a steep upward rise in the weight curve. Peripheral oedema is aggravated by venous stasis in patients who walk about the ward or remain standing for long periods.

Famine oedema

If oedema is detected when the patient first presents clinically, or if it develops without a preceding improvement in food intake, the underlying mechanisms should be carefully investigated in order to avoid the risks of congestive cardiac failure and pulmonary oedema. By the time peripheral oedema is detectable, the amount of fluid retained in the body contributes several kilograms to the patient's weight, thereby concealing the true loss of weight. There is a common misconception that peripheral oedema is usually due to a lowering of plasma albumen, but this is uncommon in anorexia nervosa. Therefore the clinician must look for other reasons:

  1. A fall in interstitial fluid pressure has been proposed whereby water seeps from the blood into the interstitial spaces whereas the total exchangeable sodium is likely to remain within the normal range.
  2. ‘Rebound' oedema following hyponatraemia due to abuse of laxatives or diuretics.
  3. Wet beri-beri: vitamin deficiency in anorexia nervosa is uncommon because many patients continue to eat vegetables and fruit. Nevertheless a lack of vitamin B1 (thiamine) may occur in patients who eat a stereotyped diet, and Wernicke's encephalopathy may follow. Vitamin B1 deficiency may also manifest itself in congestive cardiac failure with severe oedema from a nutritional cardiomyopathy, precipitated by refeeding without thiamine.
  4. Congestive heart failure and pulmonary oedema may occur as a result of general undernutrition leading to a decreased cardiac mass, cardiac output, and volume.

Metabolic disturbances


Severe hypoglycaemia with plasma glucose levels as low as 1.0 mmol/l is rare in anorexia nervosa but is recognized as a cause of death. Hypoglycaemia may go unrecognized, as a lack of sympathetic nervous response may mask the classical symptoms and signs.


This is a benign condition causing an orange-yellow coloration of the skin of the palms, soles, forearms, and the region of thenose. It is partly due to the consumption of large amounts of foods rich in carotenoids, especially carrots, tomatoes, and the green outer leaves of vegetables.


Weakness of specific muscle groups is common and is due to severe protein-energy malnutrition. There is a ‘proximal' myopathy, affecting the musculature of the pelvic girdle and the shoulder girdle. The patient first notices an increasing difficulty in climbing stairs. Weakness may also affect the muscles of the head and neck. When the patient is asked to rise from a sitting position, she will tend to push herself up using her hands and arms. She also has difficulty in rising unaided from a squatting position.  

There are no characteristic abnormalities in blood chemistry, although creatine kinase and liver enzymes may be elevated and the activity of enzyme carnosinase may be reduced. Myopathic changes are consistently present in muscle biopsy specimens. Histology reveals the ‘chequerboard' distribution of muscle fibres but with a selective type 2 fibre atrophy. Electron microscopy reveals the presence of strikingly abundant glycogen granules between the myofibrils and under the sarcolemma.  

The detection of myopathy is a clear indication for the patient's admission to hospital and a refeeding programme. After a weight gain of a few kilograms her muscle strength will begin to return and a complete recovery is the rule.


A high proportion of patients with anorexia nervosa risk developing osteoporosis and consequent pathological fractures. Significant reduction in bone mineral density of the femoral neck was found in all 20 patients with anorexia nervosa of 6 years or more duration. The favourite method of measuring bone density in the lumbar spine and hip is by dual-energy X-ray absorptiometry  (DEXA scan). A measurement for all patients with anorexia nervosa of 2 years duration or more is recommended. It is difficult to disentangle the harmful effect of the nutritional deficiency itself from the associated oestrogen deficiency. It is likely that the pathogenesis of osteoporosis in anorexia nervosa differs from that in postmenopausal women. In anorexia nervosa the nutritional deficiency (often including a lack of calcium and vitamin D) leads to a low rate of the recycling of bone through bone formation and resorption, but the balance is disturbed by a relative increase inbone resorption.

On the whole the evidence favours the likelihood of improvement of bone density with nutritional recovery and resumption of menstruation. There is much uncertainty about the best treatment. Although patients are often automatically prescribed oestrogen replacement, the only controlled trial undertaken so far indicated that oestrogen was only effective in severely underweight anorexic patients. Indeed, it has been argued that oestrogen replacement could be harmful in some patients (children with premenarchal onset) and unnecessary in others with an illness of less than 3 years duration. Instead the emphasis should be on encouraging weight gain, with the possible addition of calcium and vitamin D. There is a wider acceptance that patients with a poor prognosis (e.g. who have been ill over 10 years) might benefit from oestrogen replacement.

Disturbed temperature regulation

Disturbances in the control of temperature are evident from clinical observations; the patients frequently complain of feeling cold, and in the winter they have cold and blue extremities and suffer from chilblains. In the severely malnourished patient hypothermia may be a cause of death. Severe malnutrition is accompanied by a low central body temperature, presumably because of a low metabolic rate. Ingestion of a high-calorie meal can cause a significant increase in the central body temperature which causes some patients to complain of heat in the periphery and sweating after food.

Haematological changes

Anorexic patients may develop a significantly lowered haemoglobin level and a reduced haematocrit and white cell count, with a relative decrease in neutrophil leucocytes and an increase in lymphocytes. The anaemia is usually moderate and is normocytic normochromic in type. The mechanism is that of starvation-induced bone marrow hypoplasia. Only occasionally is there an iron deficiency. The anaemia gradually becomes corrected with weight gain. A low platelet count in the blood has also been observed and there may be an associated thrombocytopenic purpura.

Complications arising during rapid refeeding

Acute dilatation of the stomach.

This complication has also been described in anorexia nervosa during the course of refeeding. The patient develops copious vomiting, upper abdominal pain, distension of the upper abdomen, and rapid dehydration. Treatment is by continuous gastric aspiration, and this complication isone of the rare indications for intravenous infusions of glucose and saline. Gastric dilation is best prevented by avoiding a food intake above 2000 cal daily during the first week of refeeding.


When the illness has been protracted and has led to severe emaciation, the body stores of phosphate become depleted. The fall in serum phosphate is aggravated during refeeding, especially parenteral feeding.  Levels of phosphate may fall as low as 0.2 mmol/l. Clinical features are cardiac irregularities with a prolonged QT interval, impairment of consciousness, and delirium. Treatment is with oral phosphates rather than by intravenous administration.

Anorexic mothers as parents

A patient who is improving may conceive despite having a suboptimal weight and still not menstruating. A mother may also develop the illness after having borne children. In a series of eight mothers, nine out of 13 of their children suffered from food deprivation, identified by reductions in weight for age and in height for age as shown on Tanner–Whitehouse charts. The anorexic mothers had no intention of abusing the children and indeed were affectionate towards them. They adopted different ways to ration their children's food intake according to their age. They might prolong breast feeding, dilute the bottle feeds, reduce the amount of food available in the home, confine eating to meal times, forbid the consumption of sweets, and prevent others giving them food. The privation of the children resulted from the anorexic mothers' abnormal concern with body size being extended to their children. An important part of the management was the recognition of the children at risk through tactful enquiries. A whole-family approach should be adopted, focusing on the children's needs for food. The children should be followed up to ensure that they gain weight and catch-up growth is established.  

Similar findings have been described by other authors. An elegant observational method has been applied to mothers found to have an eating disorder during the postnatal year. They were video recorded while feeding their 1-year-old infants. In comparison with controls, infants of these mothers were found to be lighter, with the weight being inversely related to both the amount of conflict during meal times and the mother's concern about her own shape. The mother's concern about her body shape led her to want a thinner child.

Anorexia nervosa of early onset

It would be too arbitrary to define an early onset by age limits such as an onset from 8 to 16 years. A more meaningful frame of reference is the onset in relation to the stage of puberty which has been reached by the child. Because puberty is a complex developmental process spanning 2 to 3 years, it is best to name as ‘premenarchal' the illness which commences some time after the first signs of puberty and before its completion, as shown by the first menstrual period. In true prepubertal anorexia nervosa the illness begins even earlier, before the very first signs of puberty. Postpubertal anorexia nervosa is when the illness commences after menstruation has been established.

There is much similarity between the clinical features of an illness of early onset and one which is postpubertal. However, there are two important differences. The first is the potential for the illness to interfere with the child's pubertal development. The second is the impact of an early onset with particularly heart-rending consequences for the child's family. It follows that the management of the family is of supreme importance, and the clinician should be prepared for parental reactions which may sometimes detract from a rational plan of treatment.

The clinical presentation is variable. Often there are precipitating events such as a family bereavement or a physical illness leading to weight loss. The onset is likely to be insidious , with the parents noticing nothing amiss except for non-specific features, which are nevertheless important. Symptoms of depression and irritability are common. Some children cannot describe feelings of depression, but tearfulness may be obvious. They withdraw from friends and may refuse to go to school. Others express ideas of being undeserving of love or food. Increasingly these youngsters have been found to injure themselves, especially by scratching with their nails or cutting the skin of the wrists and forearms with sharp objects, and occasionally by knocking and bruising the head. Ina severe depression the child may say she hears voices calling her ‘bad', but further questioning indicates that these are not true hallucinations but vivid expressions of her own thoughts. Another common presentation is with complaints of bodily symptoms, especially headaches, abdominal discomfort, and a wide range of gastrointestinal symptoms, which inevitably elicit physical investigations.

At some stage, however, the parents observe that their child is avoiding food and is reluctant to eat at normal meal times. She resorts to deviousness and secrecy. The omission of school meals often goes undetected. Eventually it is noticed that she has become thinner and may have lost a great deal of weight. Resistance is met when attempts are made to reverse the loss of weight. Even a young child may become preoccupied with the caloric values of foods. Methods of inducing weight loss additional to food avoidance may become evident. The child is likely to exercise excessively—jogging, walking, or cycling long distances. An attempt to reduce the excess activity may lead to solitary exercising in the bedroom, including press-ups or running on the spot. Other patients may induce vomiting or take laxatives even after small meals, but overeating typical of bulimia nervosa is rare in young children. 

Weight loss

Because of the early onset while the child should still be growing in stature, there is a failure to gain the weight which normally accompanies the growth spurt. Later there occurs an actual loss of weight and, because the child has not yet reached her optimum weight, a very low weight indeed may result—25 kg or even less. Symptoms of malnutrition ensue including tiredness, constipation, and sensitivity to cold with cold extremities.

The psychological disorder

Even younger children are likely to disclose that they are fearful of becoming fat, a disturbance similar to the overvalued idea held by older patients. A minority of patients will disclose their reluctance to develop personal, sexual, or social maturity, in a manner which fits into Crisp's model. A few may express reluctance to have menstrual periods. A girl may say she is indifferent whether she menstruates or not, but would like to develop breasts so as not to lag behind other girls in her class. The reluctance to ‘grow up' may be expressed in social terms, with the patient saying that she could not imagine herself ever leaving home or her mother. On the other hand most girls are keen to reach a normal stature. Severe depression was found in 69 per cent of youngsters in the Göteborg study. In the same series one-third of the patients had an obsessive–compulsive personality disorder, and 8 per cent developed hand-washing and other compulsions.

Physical examination

Physical examination will reveal a varying degree of wasting, affecting the limbs, the abdomen, the buttocks, and the facial appearance. The extremities are blue and cold, and ischaemic changes may lead to gangrene affecting the toes. Other physical changes are similar to those in the adult, except for the addition of a delay in puberty.

Delay or arrest of puberty

The illness may adversely affect pubertal development depending on its time of onset. If the onset is truly prepubertal the child will not yet have shown the first signs of puberty, such as the appearance of pubic hair and breast buds. When the illness begins during the course of puberty these early signs may have appeared, but the breasts will show early growth only (Tanner stages 1 or 2), and the child will not yet have menstruated. The effects on pubertal development can be divided into those affecting growth and stature, breast development, and menstrual function.  

  1. Growth in stature may have become arrested. In a series of 20 patients with a premenarchal onset, only two of them had reached the 50th centile in height. With successful treatment and weight gain, catch-up growth of 2 to 5 cm may be achieved, but only in patients aged 17 or less. 
  2. Breast development: in the same series only six patients had normal breasts and as many as 10 had infantile breasts. After prolonged weight gain, eight of the 14 patients showed a considerable response in breast growth.  
  3. Menstrual function: a prepubertal or premenarchal onset of the illness will cause a delay in the onset of menstruation, defined as primary amenorrhoea. In the series already referred to only four of the 20 patients had menstruated by the age of 16 years. A further three began their periods between 16 and 18 years of age, and four at ages ranging from 18 to 25. The remaining patients had prolonged amenorrhoea.

The above series consisted of selected patients in whom pubertal delay was severe, whereas marked pubertal delay has seldom been reported in other series in which only delayed menstruation has been remarked upon.

A young boy who develops anorexia nervosa is also likely to become preoccupied with fatness and accordingly avoids food in order to lose weight. The endocrine disorder in the male similarly consists of a disturbance of the hypothalamic–pituitary–gonadal axis. With a prepubertal onset, the penis and scrotum remain infantile, there is only a scanty growth of pubic and facial hair, and the voice may not break.

Special investigations

Pelvic ultrasound monitoring of the ovaries and uterus is a useful method of ascertaining regression and recovery in children with anorexia nervosa. On first testing, and in the presence of low weight and amenorrhoea, ovarian volume and uterine volume were found to be reduced in comparison with normal pubertal girls. In the latter the normal range of ovarian volume is 3.95 ± 1.7 cm (3) and uterine volume is 14.8 ± 7.6 cm. (3) On retesting the patients 18 months after the first scan those who were menstruating showed significantly larger ovarian and uterine volumes than those with amenorrhoea. The authors concluded that for ovarian and uterine maturity to occur it is necessary to achieve a mean weight of 48 kg and a mean weight-to-height ratio of 96.5 per cent, higher targets than are usually set. They also found that pelvic ultrasound scanning helped to motivate the children to accept a higher body weight.

Differential diagnosis of early-onset anorexia nervosa

Frequent bodily complaints, loss of weight, and abnormalities of growth lead these children to be referred to paediatricians for special investigations. It has been proposed that young anorexic boys should be investigated by means of neuroimaging, so as not to miss occult intracranial tumours masquerading as early anorexia nervosa. The diagnosis of anorexia nervosa should be distinguished from atypical eating disorders in childhood. 

  1. Pervasive refusal syndrome is characterized by a child, usually aged between 11 and 15, refusing to eat, drink, walk, talk, or take care of herself. Anxiety, phobic responses, and depression are also present.
  2. Selective eating is the term applied to a child who restricts food intake to two or three different foods, such as biscuits, crisps, or potatoes, but usually remains in good health.
  3. Food avoidance emotional disorder: this condition is one in which food avoidance is attributable to an emotional disturbance in the absence of a dread of fatness, a necessary criterion for the diagnosis of anorexia nervosa.
  4. Food fads and food refusal: the refusal to eat is usually intermittent and physical health is not compromised.


ICD-10 (including patients with premenarchal onset) 

  1. Body weight is maintained at least 15 per cent below that expected for health. Prepubertal children may fail to gain the weight expected during the growth spurt. Weight loss is caused by avoidance of ‘fattening' foods, possibly with the addition of self-induced vomiting, purgative abuse, excessive exercise, or the use of appetite suppressants.
  2. The patient holds the overvalued idea of a dread of fatness and keeps her weight below a self-imposed threshold.
  3. There is an endocrine failure manifest in women as amenorrhoea and in men as a loss of sexual interest and potency.
  4. If the onset is premenarchal, the sequence of pubertal events is delayed: growth is arrested; in girls the breasts do not develop and there is a primary amenorrhoea; in boys the genitals remain juvenile.


Refusal to maintain body weight above the minimally normal weight for age and height (e.g. weight less than 85 per cent of thatexpected).

2.Intense fear of gaining weight or becoming fat, even though underweight.

3.Disturbance in the way in which one's body weight or shape is experienced.

4.In postmenarchal females, there is amenorrhoea of at least three menstrual cycles.

DSM-IV subdivides anorexia nervosa as follows.

  1. Restricting type, without regular binge-eating or ‘purging' behaviour (in the United States this term includes self-induced vomiting and the misuse of diuretics as well as laxatives).
  2. Binge-eating/purging type.

Anorexia nervosa in males

The relative rarity of anorexia nervosa in the male might lead one to surmise that the disorder is likely to differ between thesexes in its aetiology, clinical manifestations, and prognosis. The first study that examined this premise in a sizeable series of male patients found remarkable similarities between the sexes as regards the age of onset and the specific features of the psychopathology. For example, the male patients tended to select a diet which was low in fattening foods and resorted to subterfuges to dispose of food, such as self-induced vomiting and purging, and strenuous exercising. They expressed a fear of fatness and considered themselves overweight, even when they were thin. Other investigators were also struck by these surprising similarities. 

Of course there are fundamental biological differences which inevitably alter the manifestations of the endocrine disorder in the male and, to a lesser extent, the nutritional disorder. Testicular function, as gauged by the urinary output of testosterone, is disturbed in male patients when they are emaciated. Refeeding leads to at least a partial correction of this abnormality. The body composition of the mature male differs from that in the female; he has a lower reserve of adipose tissue so that protein depletion occurs more rapidly when he loses weight.

The relative resistance of the male against developing anorexia nervosa remains a mystery. It is even unclear whether the sex difference is likely to be due to biomedical factors or psychosocial differences. It has been suggested that young females often become preoccupied with ‘fatness' because of its reproductive, biological, and social significance, whereas young males are more concerned with their musculature and its significance for strength, dominance, and masculinity. These differences are linked with the frequency of dieting among adolescent girls and its rarity in boys. 

In a series of male patients with ‘primary' anorexia nervosa most of the patients reported problems with sexuality. Sexual anxieties had been present with respect to heterosexual as well as homosexual behaviour. One quarter had had homosexual contacts or admitted homosexual tendencies. Almost all were relieved by the loss of libido following weight loss. The authors concluded that males with atypical gender role behaviour had an increased risk fordeveloping anorexia nervosa in adolescence.

There are only a few follow-up studies of anorexia nervosa in males. In the best study available, 27 patients were followed up for a minimum of 2 years and a mean of 8 years. Expressed in the terms of the Morgan–Russell categories of general outcome, a good outcome was found in 44 per cent, an intermediate outcome in 26 per cent, a poor outcome in 30 per cent, and no deaths. Only a few predictors of outcome were identified: disturbed relationships with a parent in childhood led to a poor outcome, and the occurrence of previous sexual activity was associated with a good outcome. The outcome in males was remarkably similar to that in females. 

Course and prognosis

The natural outcome is defined as the long-term results of the illness or disease process. The clinical prognosis is the difficult task of forecasting the future course and final outcome of the illness in an individual patient.

Outcomes from follow-up studies in anorexia nervosa

There have been comprehensive appraisals of follow-up studies in anorexia nervosa which have put forward criteria for the near-perfect follow-up study, which in practice are seldom fully met. Among the easier criteria are precision in the diagnostic features, the use of standardized interviews, 100 per cent success in tracing the patients, and a sufficiently long follow-up to determine eventual outcome. An arbitrary interval of at least 4 years was previously set and most recent studies have adhered to this recommendation. Several groups of investigators have adopted the same measures of outcome based on the Morgan–Russell scales. Their use gives rise to three possible categories of general outcome based on body weight and menstrual function: ‘good', ‘medium', and ‘poor'.

In a review comparing three British studies and one Swedish study, each with a mean follow-up of 5 to 6 years, it was found that the patients treated in Bristol had a better outcome than those treated at the Maudsley Hospital in London. The explanation is one of selection bias already mentioned: the Maudsley patients had all required inpatient treatment, whereas in the Bristol series the majority were outpatients. The third British study, from St George's Hospital, London, showed a quality of outcome intermediate between the other two.

The Swedish study was extended by two later follow-ups at 15 and 33 years, and showed a trend in two directions. On the one hand, the percentage of good outcomes gradually increased, while the percentage of poor outcomes diminished. On the other hand, the death rates increased with time; after 33 years the total mortality from anorexia nervosa or suicide was 18 per cent. Slow recovery was the rule: only 29 per cent of patients recovered in less than 3 years of illness, another 35 per cent within 3 to 6 years, and the remainder took much longer with recovery after 12 years being rare. The Maudsley series of patients was also extended to a mean follow-up of 20 years. There was a reduction in the percentage of patients with a poor outcome, but an increase in the mortality rate close to that of the Swedish study.  

Prognostic predictors of outcome In the long-term

In the Maudsley study a poorer outcome was predicted by an older age of onset, a longer duration of illness, the presence of neurotic traits in childhood, personality problems, and the occurrence of relationship difficulties within the family.

Comparison of mortality rates

In a review of 42 studies the aggregate annual mortality rate from anorexia nervosa was found to reach 0.56 per cent on average. Complications of anorexia nervosa accounted for 54 per cent of deaths, suicide for 27 per cent, and other causes for 19 per cent. When the death rate is expressed as a percentage per annum a fair measure of consistency has been found in different parts of the world, especially when allowance is made for selection biases: in Denmark 0.5 per cent per annum (younger patients), in Sweden 0.75 per cent per annum, in the United States 0.66 per cent per annum, and in the United Kingdom 0.75 per cent per annum.  

Follow-up studies in early-onset anorexia nervosa

In a series of 34 children with a mean age of onset of 11.7 years treated at Great Ormond Street Hospital, London, a good outcome was obtained in 60 per cent, but there was a mortality rate of 7 per cent over a mean follow-up of 7.2 years. In a series of 60 patients in Berlin with a mean age of onset of 14.7, followed up for at least 4 years, recovery occurred in 68 per cent of patients but there was a 6.6 per cent mortality over a mean of 4.8 years. In both studies a somewhat higher mortality rate was found than in the Danish study already mentioned.


Theander has provided good advice and useful definitions:

  • "Clinical experience has repeatedly shown that patients with anorexia nervosa can recover after a period of illness amounting to more than ten years."

A distinction should be made between a ‘chronic' illness and a long-standing illness. The word ‘chronic' should be restricted to a continuous illness of more than 15 years' duration because up to then the patient is still capable of a full recovery. The term ‘protracted' is preferable for an illness of prolonged duration but not as long as 15 years.


Review of evidence

There have been regrettably few controlled trials evaluating the effectiveness of treatment in anorexia nervosa. This contrasts with a much larger number of controlled studies in bulimia nervosa. The reasons are not surprising. Most controlled trials in anorexia nervosa encounter serious practical and ethical difficulties arising from the severity and prolonged nature of the illness, and a variable compliance on the part of patients.

Inpatient treatment

Treatment as an inpatient in a specialized eating disorder unit is most likely to restore the patient's weight to a near-normallevel within 3 months or less. There have been no controlled studies comparing different treatment programmes. A possible exception is a study comparing a strict operant conditioning programme while refeeding the patients with a ‘lenient' programme which was introduced later. No significant difference was found in the rate of weight gain between the two treatments. The value of a specialized eating disorder unit in inducing weight gain has been demonstrated from a series of 17 patients admitted to the Maudsley Unit in 1990. They had previously been admitted elsewhere and information on their previous weights was obtained. In the case of theMaudsley admissions the mean weight rose from 65.8 per cent average body weight (ABW) to 90.4 per cent ABW; in comparison the admissions elsewhere only led to a mean weight rise from 64.4 to 75 per cent ABW.

Day hospital treatment

Once again there is a paucity of controlled trials of day programmes. An exception is the comparison of inpatient and day treatment carried out in Edinburgh. A traditional inpatient programme, aimed strictly at weight gain, was compared with a more permissive day programme stressing open communication and patient autonomy. The day programme consisted of intensive psychological treatments and was available on 4 days each week. Thirty-two patients who would have merited admission to hospital were randomly allocated to the day programme or the inpatient programme. Although statistically significant differences were not found between the two methods of treatment, the author reported interesting trends as gauged by the categories of outcome using the Morgan–Russell scales. The only advantage conferred by inpatient treatment was a slightly greater weight gain. In contrast, the day programme was more popular with the patients who preferred to have a greater say in the rate of weight gain. There was also an impression of a greater return of personal autonomy in the day-patients. A criticism of this study is that the two programmes were imperfectly matched in terms of the therapeutic input and enthusiasm of the two teams.

Comparison of outpatient treatments and hospital admission

An ambitious study, conducted at St George's Hospital, London, aimed at evaluating the advantages of different treatment settings. There were three treatment groups and one control group:

  1. inpatient treatment on average lasting 4 months, followed by 12 sessions of outpatient psychotherapy;
  2. outpatient treatment combining individual and family therapy over the course of 12 sessions spanning several months;
  3. outpatient group therapy consisting of 10 group meetings for the patients and 10 group meetings for the parents separately at monthly intervals;
  4. a control group who were given only a ‘one-off' but detailed evaluation.

The two outpatient treatment groups received in addition four sessions of dietary counselling.

Ninety patients were randomly allocated to one or other of the four treatment options above. The authors have stressed the serious methodological difficulties. Patients might drop out of the treatment when it did not conform with what they wanted; for example, out of 30 patients offeredinpatient treatment, only 18 accepted it. Among the 20 patients allocated to a one-off evaluation, the majority sought treatment elsewhere.

The patients' progress was re-evaluated at the end of 1 year. The clearest finding was that patients allocated to any one of the three active treatment options fared better than those allocated to the one-off evaluation session. There were fewer clear-cut differences between the patients in the three different treatment groups. The inpatients tended to achieve a more rapid and higher weight gain towards the end of their admission, but at the 1-year follow-up the weights were similar in all three treatment groups. The patients' improvement in their socio-economic status was greatest in the individual–family therapy group.

Family therapy

Family therapy is the main treatment which has been evaluated in anorexia nervosa. A controlled trial of family therapy was undertaken at the Maudsley Hospital on a series of 57 patients. The principles of the family therapy have been incorporated in the Maudsley model. One assumption is that the family is ineffective in helping the patient eliminate her symptoms, or might contribute to their maintenance. It was also considered essential to correct the patient's starvation by assisting the parents to take control jointly of their child's eating until her weight had returned to normal. The effects of the family therapy were compared with a control individual therapy. In order to reduce any ethical objections to the random allocation to two different treatments, the risks were minimized by first ensuring that the patients' weight loss had been corrected by admission to the Eating Disorders Unit. The trial was of outpatient family therapy administered for 1 year. The patients were assessed after treatment for 1 year and 5 years later by a researcher who was not involved in the treatment.  

In order to increase the homogeneity of the groups undergoing treatment, the patients were subdivided into three groups according to recognized prognostic criteria.

  • Group 1: age of onset less than 19 years, duration of illness less than 3 years.
  • Group 2: age of onset less than 19 years, duration more than 3 years.
  • Group 3: age of onset 19 years or older.

After entry into the appropriate subgroup the patients were randomly allocated to one or other therapy.

The control treatment was a supportive and problem-centred individual therapy with elements of cognitive, interpretative, and strategic therapies. Body weight was recorded daily during inpatient treatment and at each subsequent outpatient attendance and during follow-up. The Morgan–Russellscales were utilized to obtain categories of general outcome and measures of adjustment along five dimensions: nutritional status, menstrual function, mental state, psychosexual adjustment, and socio-economic status. An ‘average outcome score' was calculated as the mean of the scores on the five scales.

  1. Group 1 (early age of onset, short history): a tendency for the patients to lose weight on discharge from hospital was reversedmore readily in those who had been allocated to family therapy, and the superiority of family therapy was demonstrated by a higher weight at the end of treatment (p< 0.02). The superiority of family therapy was also demonstrated on the Morgan–Russell scales in terms of more good outcome categories and ahigher average outcome score. 
  2. Group 2 (early age of onset with long duration of illness): the effect of the two therapies did not differ significantly among these patients.
  3. Group 3 (late age of onset): in this group of patients the effect of the two therapies was reversed. Individual therapy led to a significantly greater weight gain when comparing levels at the 6-month follow-up. 

From this study it can be concluded that family therapy was more effective than individual therapy in patients whose illness had begun before the age of 19 years and had lasted less than 3 years. A more tentative finding was the greater value of individual supportive therapy in older patients.

Enduring benefits from family therapy

The patients who took part in the original controlled trial of family therapy were followed up 5 years after the end of treatment, in order to determine the levels of improvement from the illness and any evidence of long-term benefit from family therapy. Follow-up information was obtained on all 57 patients, but three had died.

The patients' clinical status was ascertained, as before, by their weight and their status on the Morgan–Russell scales. A good or intermediate outcome was found in 34 out of 54 patients at the 5-year follow-up compared with 22 out of 54 at the end of treatment. This overall improvement was mainly attributable to the natural outcome of anorexia nervosa. Within two of the patient groups, however, significant benefits attributable to the previous psychological treatments were still evident.

  • Early-onset/short-history group: within this group the patients who had received family therapy achieved a mean weight of 103 per cent ABW, whereas those who had had individual therapy reached a mean weight of 94 per cent ABW. However, this difference was no longer statistically significant. On the Morgan– Russell scales a significant improvement after family therapy was still discernible in terms of the higher proportion of patients who had achieved a ‘good' outcome and a higher average outcome score.
  • Late-onset group: the late outcome of this group was better than expected, with almost three-quarters having a ‘good' or ‘intermediate' outcome. When comparing the effects of family and individual therapy, the results were similar to those found at the end of treatment. On theMorgan–Russell dimensional scales the patients who had been in individual therapy obtained a higher average outcome score.

In conclusion, the patients in the early-onset/short-history group showed the best outcome at the end of 5 years, as was predictable from these prognostic indicators. The more important finding was that the benefits of family therapy endured until the 5-year follow-up. Most of the patients with a late onset of illness progressed reasonably well and it was confirmed that the individual supportive therapy had conferred benefits still detectable at 5 years.

Components of family therapy found to the beneficial in adolescent patients

The finding that family therapy is effective in younger patients with anorexia nervosa has led to a search for the effective components of this therapy. Most family therapists consider that it is important to understand the way the family functions; however, some prefer a symptom-oriented approach with an emphasis on helping the parents to manage their child's problem.  

The relative importance of the two components of family therapy was investigated by comparing conjoint family therapy with family counselling. In conjoint family therapy the whole family was seen together in the treatment sessions. In family counselling the parents were seen together and given advice on how best to manage their daughter's eating problem; the same therapist also saw the patient for counselling and support. In conjoint family therapy it is possible to observe and interpret family transactions. In family counselling, however, the therapist can only discuss ways in which the family might modify its behaviour but cannot intervene directly in the ‘whole' family system. The two treatments share the therapeutic advice to sustain a united parental approach aimed at establishing control of their child's eating pattern. The design was that of an outpatient controlled clinical trial with random allocation between conjoint family therapy and family counselling.

It emerged that the benefits of conjoint family therapy and family counselling were similar, with considerable gains in weight. The family counselling actually produced a somewhat better weight gain, but the differences were not statistically significant. With both treatments there were considerable improvements in the Morgan–Russell average outcome scores when assessed at the end of 32 weeks' treatment. When separated according to the form of treatment the differences were not statistically significant. This finding suggests that the simpler family treatment—family counselling—is as effective as family therapy, at least as far as weight gain is concerned.

Advice on management

It is not possible for the clinician to confine his treatment of anorexia nervosa to those methods which have been proved to beeffective.

Main obstacle to treatment: the patient's avoidance of treatment

The avoidance of treatment by the patient is part and parcel of anorexia nervosa. There have been attempts to predict the likely level of the patient's compliance with treatment. For example, a ‘transtheoretical model of change' is aimed at improving the patient's motivation by overcoming ambivalence while at the same time avoiding confrontation. Different stages in the patient's approach to treatment have been recognized: precontemplation, contemplation, preparation, action, maintenance, and relapse. Motivational enhancement therapy is at an early stage of development but a practical guide is available. 

At our present level of knowledge it is simplest to ascertain the patient's attitude to treatment through the mental state examination. A revealing question is to ask her at the initial interview what weight she would be willing to reach. At this stage it is best to refrain from challenging the patient's weight threshold, even though it will be well below a reasonable therapeutic goal. Having ascertained the limited degree of compliance on the patient's part, the clinician needs to develop a strategy to improve it gradually as treatment proceeds. It is poor clinical practice to place all the onus on the patient herself for accepting or rejecting a package of treatment at the first interview, or even at a later stage. ‘Engaging' the patient in treatment is an essential part of most psychotherapeutic methods including cognitive-behavioural therapy.  Another tactic for improving the patient's co-operation is to enlist the help of close members of the family. In the case of young patients it is essential to form a therapeutic alliance with the parents. Young patients are likely in any case to require a form of family treatment.

The stepped-care approach

The principle of stepped-care is that with an early presentation of anorexia nervosa the clinician should first apply relatively simple remedies. Only if they fail should more vigorous and time-consuming treatments be provided. In practice, however, the patient who has avoided treatment as long aspossible may first be seen when weight loss is already substantial and abnormal attitudes entrenched. If this happens it is not possible to follow a graduated sequence and a short cut may be needed to a more vigorous method including admission to hospital. Admission is also indicated in the presence of ‘famine' oedema or proximal myopathy.

In the event of a truly early presentation it will be appropriate for the patient's treatment to be overseen by her general practitioner. A minimal approach should still include dietary education as to the value of nutritious (high-caloric) foods and forging an alliance with the patient's family.The patient should be asked to attend once a week to be weighed with the clear message that she must arrest the weight loss and gradually return to a healthy weight determined by the clinician and not by her.

Outpatient psychotherapies

In the event of a patient's weight loss not exceeding 20 per cent of her healthy weight, it may be possible to obtain a therapeutic response by outpatient treatment including attendance at non-specialist clinics in general psychiatry or child/adolescent psychiatry. The feasibility of this approach will depend on the availability of appropriate psychotherapeutic resources. The clinician should not imagine any conflict between the psychotherapeutic approach and weighing the patient. It is never justified to accept apparent compliance with psychotherapy if the patient's weight continues to decline.

Models of psychotherapy

Hilde Bruch: ‘a sparrow in a golden cage'

Bruch developed her aetiological model of anorexia nervosa as the child becoming involved with her family in such a way that she fails to achieve a sense of independence. Thus a paralysing sense of ineffectiveness pervades all her thinking and activities. Bruch used this model to provide an entry into the psychotherapy. She engaged her patient in a dialogue which became central for the resolution of her conflicts. Patients are often receptive and reassured when the therapist does not criticize them for behaviours associated with their illness. They may even obtain a relief from the implication that in some way the families are to blame for the anorexia nervosa. Using this model the therapist will engage his patient in the therapeutic metaphor in which she is seen as ‘a sparrow in a golden cage'. She is then encouraged to think of ways of fulfilling her own needs and desires, rather than relying on others, and seek an autonomy that frees her from the tyranny of anorexia nervosa. 

Crisp's model of anorexia nervosa as a flight from growth

Crisp has explained in detail how the programme of treatment is based on his model of anorexia nervosa as a refuge from puberty which the patient has found overwhelming. The youngster reverses her pubertal development by limiting her intake of food. His treatment initially involves an intensive inpatient programme lasting 10 to 12 weeks followed by outpatient treatment for up to 6 years. The advantage of this extensive programme is that itenables the patient to accept gradually an increase in weight while facing up to the feelings of panic and helplessness that originally led her to arrest her puberty through self-starvation. This interpretation is presented to the patient and to her family so that they come to see the psychotherapy as a way of solving the problems.

The model is a useful one even within a more limited outpatient psychotherapeutic setting. Some patients will readily identify their distress when overwhelmed by powerful sexual feelings or when confronted with personal and social responsibilities perceived as the result of growing up. The aims of the psychotherapy are to support the patient while she is beginning to abandon the psychobiological regression of anorexia nervosa. In addition she is encouraged to broaden her perception of herself in ways that are no longer wholly dependent on her physical appearance but include an improved sense of competence and self-esteem. She is helped to tackle personal and social problems from which she had previously escaped so that she can address her own and her parents' concerns about sexuality.

Cognitive-behavioural therapy

Although a strictly cognitive-behavioural model for the aetiology of anorexia nervosa has not yet been recognized, a theory for faulty cognitions maintaining the illness has been put forward by Fairburn et al. The argument for examining the role of faulty cognitions in anorexia nervosa is inescapable. The original description of perceptual and conceptual disturbances in anorexia nervosa was put forward by Bruch in 1962. It was appreciated that faulty attitudes to body size contributed in part to the patient's determination to reduce her food intake and lose weight. These observations led to the first development of a cognitive-behavioural therapy for anorexia nervosa. Despite the appeal of a therapy based on a cognitive-behavioural approach, there have been virtually no controlled clinical trials of this therapy. The current evidence of its benefit relies therefore on clinical impressions and case reports.  

Cognitive-behavioural therapy has much in common with other methods of treatment including the refeeding programme which will be described under inpatient treatment. It relies on building a positive therapeutic alliance between therapist and patient.

The patient's weight and food intake is monitored at each session and she is told her weight at each session. She is encouraged to think of food as medication and to follow a meal plan. She is encouraged to keep a daily written record of all food and liquid consumed. The patient is educated in the disturbances of bodily and psychological function consequent on the state of starvation. The content of the therapy may be divided into two ‘tracks'. The first track includes an examination of the behaviours adopted by the patient in order to reduce her weight or maintain it at a low level. The second track is more concerned with psychological themes such as self-esteem, perfectionism, interpersonal functioning, and family conflicts. By asking the patient to give her reasons for specific behaviours, the therapist discovers faulty beliefs and assumptions on her part. For example, the ‘anorexic wish' is the patient's wish to recover from her disorder without gaining weight. She is gently persuaded that this is an impossible aim because her real psychological difficulties will remain inaccessible so long as her experiences are clouded by starvation and dieting. The patient also expresses a fear of ‘losing control'. By ‘losing control' she means that she will run the risk of overeating and become fat. It is explained to the patient that her rigid ‘control' over eating deprives her completely of choice, and that far from being in control the reality is the converse. It is also useful for the therapist to analyse the pros and cons of maintaining the disorder of anorexia nervosa. She often feels more uncomfortable at confronting the hidden rewards of remaining thin, for example succeeding in losing weight when everyone else fails.

Having ascertained the particular meanings of attitudes and behaviours for the patient, she is helped to find more adaptive ways of achieving healthier goals, including more relaxed normal eating and weight gain.

Family treatments

Family therapy and family counselling have already been discussed, but additional practical advice will now be given.

Family therapy

The frequency of the sessions is determined by clinical need; it averaged 10.5 over the course of 1 year in the Maudsley trial. There are three stages to the therapy.

  1. The first phase begins with a family meal. The parents are urged to identify their future joint attitude to the feeding pattern that should be adopted by their daughter. With a younger patient the therapist assumes that the parents would initially need to take control of their child's eating. With an older patient a preliminary discussion should lead to a decision either to control her eating or to adopt the attitude that her eating was noneof their business.
  2. During the second phase the parents are urged to be present together at each meal so that they can reinforce each other's efforts in the practical task of ensuring an improved food intake and a steady weight gain.
  3. When the patient's weight is under control, responsibility for continued weight gain is handed back to her. Discussions can then commence on more normal family concerns. With an adolescent patient the main focus is on achieving increased autonomy. With an older patient the central theme is how to establish healthy relationships with her parents without the eating disorder as a medium for communication.

Family counselling

As in family therapy the parents are given direct advice on how to manage their daughter's eating problem. The patient herself is provided with individual educative therapy. The therapist provides counselling about abnormal attitudes to weight and emphasizes the weight issue until steady progress has been made. This method is often preferred by the patient and her parents, largely because it is almost devoid of overt confrontation. It is also easier to gain access to the patient's fears and conflicts.

Day treatment

The Edinburgh controlled trial of a day-patient programme has already been discussed. At the Toronto Hospital a day-hospital programme for eating disorders utilizing group treatment has been established since 1985. The programme originally operated on 5 days each week, but since 1994 it has been reduced to 4 days per week. The goals are as follows:

  1. a normalization of disturbed eating behaviour and weight gain;
  2. the identification of psychological and familial processes that serve to perpetuate the eating disorder.

Two meals (lunch and dinner) and a snack are provided during the treatment hours. The staff take turns in supervising the patients during meal times. The psychological treatment consists of intensive group therapy divided between disturbed behaviours around eating and weight, and more general conflicts.

The clinical advantages of day treatment are a reduction in the dependence of patients who still have to maintain themselves in a functioning state outside the hospital. The group treatments carry the advantage of providing an atmosphere of mutual support while permitting interventions through group pressures. There are few contraindications to this treatment, but patients with medical or suicidal risks are admitted instead to inpatient care. For some patients day treatment does not provide as strong a sense of containment as might be found on an inpatient unit. When patients succeed in reducing their disturbed eating behaviours they may ‘act out' by self-harm. The clinical staff may find their skills severely taxed by the continuous staff–patient interaction.

Inpatient treatment

At one time inpatient programmes were run on behavioural principles, but in recent years ‘lenient' programmes have found favour. The great advantage of treating a patient in a specialist eating disorders unit programme is the certainty that considerable benefit will accrue, including a substantial gain in weight, if the patient can be persuaded to remain in hospital.  

Nursing care

Inpatient treatment will include a wide range of psychotherapeutic interventions (individual, group, and family) as well as occupational therapy and an educational programme. But the sheet anchor of successful treatment is a well-trained nursing staff working as a team. The role of the medical staff is subsidiary and consists of maintaining a high level of expectation that the patient's weight will be restored to a normal (or healthy) level. It is necessary to give the nursing staff moral support so that they can develop their confidence and skills. There are two main components to the nurses' treatment: their psychotherapeutic input and their supervisory role. The latter is less important and should never be draconian. The nursing team establish a relationship of trust with the patient. They get to know each patient as an individual with her own personal needs and concerns. The nurses should also be acutely aware of the anorexic patient's tendency to avoid food and to exercise excessively. It is preferable for the treatment programme to stress the supportive aspects of the nurse's relationship with her patient rather than the undoubted need for careful supervision. The nurse will come to rely on the daily weight record to monitor the success of her treatment as the weight chart should show a smoothly rising curve. All meals are taken in the ward; thus the anorexic patients constitute a group in which peer interactions take place. The meal is taken in the presence of one or more nurses also seated at the table. From the beginning of the treatment the patient learns that she is expected to consume all the food placed before her.

Dietary care

It is not only the patient who tends to underestimate the food requirements to restore her weight to normal. Metabolic studies have demonstrated that for each kilogram of weight gain a surplus calorie balance of 7500 cal is needed. It is prudent to begin with a modest calorie intake of 1200 to 1500 cal daily during the first 7 days in order to avoid the rare but dangerous complication of acute gastric dilatation. Thereafter the caloric intake is gradually increased and may rise to 4000 cal daily. The best diet is that consisting of a wide range of foods avoiding any preferences for ‘safe' foods and including carbohydrate and fat-containing foods. Concentrated foods (e.g. Build-up, Complan, Carnation Breakfast Food) added to milk may be used to achieve a high caloric intake. The aim is to achieve a positive energy balance of 1500 to 2250 cal daily, leading to a daily weight gain of 200 to 300 g.

Assessment of progress

Weighing should be a standardized daily procedure before breakfast after the patient has emptied her bladder and while she wears light night clothes. A paradoxical psychological improvement, with a diminution in concern with body size and shape, occurs with weight gain. The improvement is partly through the correction of malnutrition and partly the result of the ‘exposure treatment' whereby the patient gradually accepts a higher body weight.

Drug treatment

Exceptionally the patient's tension and depression do not improve and there is a continued resistance to food. It may then be helpful to prescribe moderate doses of chlorpromazine (not more than 300 mg daily), carefully avoiding a fall in blood pressure which is a risk in the emaciated patient. In the case of persistent depression, treatment with an antidepressant may be indicated. However, antidepressants are often ineffective in the presence of malnutrition, and by themselves do not assist the patient to gain weight.

General measures

Inevitably the patient will find it irksome to forego home visits for the whole period of weight gain. Therefore interesting and therapeutic activities should be provided through group meetings, occupational therapy, and social interactions. Visiting is generally encouraged unless the patient's restlessness is such that visiting parents are subjected to emotional appeals to be taken home. They may then be asked to postpone their visits or reduce their duration. The aim is to restore body weight to a healthy level within 8 to10 weeks; a further period (usually 2 weeks) in hospital is needed to allow the patient to test her ability to maintain her weight by eating in the general dining room or at home on leave days. It is important to effect a smooth transition to further treatment as a day patient or outpatient.

Compulsory treatment in anorexia nervosa

The management of patients reluctant to accept essential therapeutic goals requires that they should be gradually engaged in a genuine alliance. However, there remains a minority of patients with whom this strategy fails and whose health becomes endangered. For them, compulsory treatment should be considered. A compulsory admission to hospital is indicated not only when patients threaten suicide or suffer from a life-threatening malnutrition, but also when they fail to respond to simpler measures such as outpatient treatment or day care, or in the event of avoiding treatment altogether. Ill health persisting over the course of several months or the development of serious physical complications (e.g. water and electrolyte imbalance, hypoglycaemia, and myopathy) should also elicit compulsory admission if the patient cannot be persuaded to accept inpatient treatment.

In the United Kingdom the Mental Health Act Commission has recently (1997) clarified many of the doubts in the minds of clinicians and social workers called upon to consider a compulsory admission under the Mental Health Act 1983. It recognized that anorexia nervosa is a mental disorder within the meaning of the Act and that in some patients their ability to consent may be compromised by fears of obesity or denial of the consequences of their actions. The Mental Health Act Commission concluded that when the patient's health is seriously threatened by food refusal she may be detained in hospital so as to treat the self-imposed starvation. The Commission went as far as to state that nasogastric feeding can be a medical process forming an integral part of the treatment for anorexia nervosa, notwithstanding that nasogastric feeding is seldom required even in patients who are compulsorily admitted.

In a study of the use of compulsory treatment in patients admitted to the Eating Disorders Unit of the Bethlem Royal and Maudsley Hospital, as many as 81 patients (16 per cent) were detained. Section 3 of the Mental Health Act, valid for up to 6 months, was the most frequently applied section. The compulsorily admitted patients were compared with a population of voluntary patients. The need for a compulsory admission was found to have two dimensions—the presence of a severe illness and a rejection of treatment, the latter in part due to abnormal personality traits. The compulsory patients gained at least as much weight as the voluntary patients but required a longer admission for them to return to a near-normal weight. It was thought likely that the compulsory patients presented a selected group by virtue of a more entrenched reluctance to accept treatment. Accordingly it was predicted that in the long term they would fare less well than voluntary patients. It was possible to determine the mortality rate of these patients through the National Register which provided the data at a mean of 5.7 years after the index admission. Ten out of 79 detained patients had died in comparison with two out of 78 voluntary patients, a statistically significant difference. The deaths among the compulsory patients were all due to anorexia nervosa or one of its nutritional complications. Thus the mortality rate among compulsory patients was extremely high at 2.17 per cent per annum. It was concluded that this high mortality was due to the selection factors. Therefore the evidence points to the usefulness of a compulsory admission in appropriate circumstances in so far as the patients responded well in the short term.

Nevertheless, a patient who has required a compulsory admission carries a higher risk, so that it is essential to safeguard her through a long period of observation.


1.Gull, W.W. (1874). Anorexia nervosa (apepsia hysterica, anorexia hysterica). Transactions of the Clinical Society of London, 7, 22–8.
2.Lasègue, C. (1873). De l'anorexie hystérique. Archives Générales de Médicine, 21, 385–403.
3.Brumberg, J.J. (1988). Fasting girls: the emergence of anorexia nervosa as a modern disease. Harvard University Press, Cambridge, MA.
4.Bell, R.M. (1985). Holy anorexia. University of Chicago Press.
5.Rampling, D. (1985). Ascetic ideals and anorexia nervosa. Journal of Psychiatric Research, 19, 89–94.
6.Bruch, H. (1962). Perceptual and conceptual disturbances in anorexia nervosa. Psychosomatic Medicine, 24, 187–94.
7.Russell, G.F.M. (1970). Anorexia nervosa: its identity as an illness and its treatment. In Modern trends in psychological medicine(ed. J. Harding Price), pp. 131–64. Butterworths, Norwich.
8.Garner, D.M. and Garfinkel, P.E. (1979). The Eating Attitudes Test: an index of the symptoms of anorexia nervosa. Psychological Medicine, 9, 273–9.
9.Williams, P., Hand, D., and Tarnopolsky, A. (1982). The problem of screening for uncommon disorders—a comment on the Eating Attitudes Test.  Psychological Medicine, 12, 431–4.
10.Johnson-Sabine, E., Wood, K., Patton, G., Mann, A., and Wakeling, A. (1988). Abnormal eating attitudes in London schoolgirls—a prospective epidemiological study: factors associated with 
abnormal response on screening questionnaires. Psychological Medicine, 18, 615–22.
11.Hoek, H.W. (1991). The incidence and prevalence of anorexia nervosa and bulimia nervosa in primary care. Psychological Medicine, 21, 455–60.
12.Garner, D.M. and Garfinkel, P.E. (1980). Socio-cultural factors in the development of anorexia nervosa. Psychological Medicine, 10, 647–56.
13.Szmukler, G.I., Eisler, I., Gillies, C., and Heyward, M.E. (1985). The implications of anorexia nervosa in a ballet school. Journal of Psychiatric Research, 19, 177–82.
14.Crisp, A.H., Palmer, R.R.L., and Kalucy, R.S. (1976). How common is anorexia nervosa? A prevalence study. British Journal of Psychiatry, 128, 549–54.
15.Mann, A.H., Wakeling, A., Wood, K., Monck, E., Dobbs, R., and Szmukler, G.I. (1983). Screening for abnormal attitudes and psychiatric morbidity in an unselected population of 15-year-old 
schoolgirls. Psychological Medicine, 13, 573–80.
16.Råstam, M., Gillberg, C., and Garton, M. (1989). Anorexia nervosa in a Swedish urban region. A population based study. British Journal of Psychiatry, 155, 642–6.
17.Theander, S. (1970). Anorexia nervosa: a psychiatric investigation of 94 female patients. Acta Psychiatrica Scandinavica, Supplement 214.
18.Jones, D.L., Fox, M.M., Babigian, H.M., and Hutton, H.E. (1980). Epidemiology of anorexia nervosa in Monroe County, New York: 1960–1976. Psychological Medicine, 42, 551–8.
19.Szmukler, G.I., McCance, C., McCrone, L., and Hunter, D. (1986). Anorexia nervosa: a psychiatric case register study from Aberdeen. Psychological Medicine, 16, 49–58.
20.Willi, J., Giacometti, G., and Limacher, B. (1990). Update on the epidemiology of anorexia nervosa in a defined region of Switzerland.  American Journal of Psychiatry, 147, 1514–17.
21.Lucas, A.R., Beard, C.M., O'Fallen, W.M., and Kurland, L.T. (1991). 50-year trends in the incidence of anorexia nervosa in Rochester, Minn: a population-based survey.  American Journal of 
Psychiatry, 148, 917–22.
22.Fosson, A., Knibbs, J., Bryant-Waugh, R., and Lask, B. (1987). Early onset anorexia nervosa. Archives of Disease in Childhood, 62, 114–18.
23.Fenwick, S. (1880). On atrophy of the stomach and on the nervous affections of the digestive organs. p. 107. Churchill, London.
24.Morgan, H.G. and Russell, G.F.M. (1975). Value of family background and clinical features as predictors of long-term outcome inanorexia nervosa: four-year follow-up study of 41 patients. 
Psychological Medicine, 5, 355–71.
25.Bruch, H. (1978). The golden cage: the enigma of anorexia nervosa. Open Books, London.
26.Williams, P. and King, M. (1987). The ‘epidemic' of anorexia nervosa: another medical myth? Lancet, i, 205–7.
27.Russell, G.F.M. (1993). Social psychiatry of eating disorders. In Principles of social psychiatry(ed. D. Bhugra and J. Leff), pp. 273–97. Blackwell Science, Oxford.
28.Fombonne, E. (1995). Anorexia nervosa, no evidence of an increase. British Journal of Psychiatry 166, 462–71.
29.Russell, G.F.M. (1979). Bulimia nervosa: an ominous variant of anorexia nervosa. Psychological Medicine, 9, 429–48.
30.Russell, G.F.M. (1995). Anorexia nervosa through time. In Handbook of eating disorders: theory, treatment and research(ed. G. Szmukler, C. Dare, and J. Treasure), pp. 5–17. Wiley, 
31.Campbell, P.G. (1995) What would a causal explanation of the eating disorders look like? In Handbook of eating disorders: theory, treatment and research(ed. G. Szmukler, C. Dare, and J. 
Treasure), pp. 49–64. Wiley, Chichester.
32.Garfinkel, P.E. and Garner, D.M. (1982). Anorexia nervosa: a multi-dimensional perspective. Brunner–Mazel, New York.
33.Birnbaum, K. (1923). Der Aufbau der Psychose, pp. 6–7. Springer, Berlin.
34.Patton, G.C., Johnson-Sabine, E., Wood, K., Mann, A., and Wakeling, A. (1990). Abnormal eating attitudes in London schoolgirls—a prospective epidemiological study: outcome at 
twelve-month follow-up. Psychological Medicine, 20, 383–94.
35.Crisp, A.H. (1970). Premorbid factors in adult disorders of weight, with particular reference to primary anorexia nervosa (weight phobia). A literature review.  Journal of Psychosomatic Research, 
14, 1–22.
36.Wig, N.N. (1983). DSM-III: a perspective from the Third World. In International perspectives on DSM-III: diagnostic and statistical manual of mental disorders(ed. R.L. Spitzer, J.B.W. Williams, 
and A.E. Skodol), pp. 79–89. American Psychiatric Press, Washington, DC.
37.Prince, R. (1985). The concept of culture-bound syndromes: anorexia nervosa and brain-fag. Transcultural Psychiatric Research Review, 22, 117–21.
38.DiNicola, V.F. (1990). Anorexia multiforme: self-starvation in historical and cultural context. Transcultural Psychiatric Research Review, 27, 165–96, 245–86.
39.Bryant-Waugh, R. and Lask, B. (1991). Anorexia nervosa in a group of Asian children living in Britain. British Journal of Psychiatry, 158, 229–33.
40.Mynors-Wallis, L., Treasure, J., and Chee, D. (1992). Life events and anorexia nervosa: differences between early and late onset cases.  International Journal of Eating Disorders, 4, 369–75.
41.Beumont, P.J.V., Abraham, S.F., and Simson, K.G. (1981). The psychosexual histories of adolescent girls and young women with anorexia nervosa. Psychological Medicine, 11, 131–40.
42.Tiller, J. and Treasure, J. (1998). Eating disorders precipitated by pregnancy. European Eating Disorders Review, 6, 178–87.
43.Sloan, G. and Leichner, P. (1986). Is there a relationship between sexual abuse or incest and eating disorders? Canadian Journal of Psychiatry, 31, 656–60.
44.Palmer, R.L., Oppenheimer, R., Dignon, A., Chaloner, D.A., and Howells, K. (1990). Childhood sexual experiences with adults reported by women with eating disorders: an extended series. 
British Journal of Psychiatry, 156, 699–703.
45.McClelland, L., Mynors-Wallis, L., Fahy, T., and Treasure, J. (1991). Sexual abuse, disordered personality and eating disorders.  British Journal of Psychiatry, 158(Supplement 10), 63–8.
46.Wonderlich, S.A., Brewerton, T.D., Jocic, Z., Dansky, B.S., and Abbott, D.W. (1997). Relationship of childhood sexual abuse andeating disorders. Journal of the American Academy of Child 
and Adolescent Psychiatry, 36, 1107–15.
47.Minuchin, S., Baker, L., Rosman, B.L., Liebman, R., Milman, L., and Todd, T.C. (1975). A conceptual model of psychosomatic illness in children: family organization and family therapy. 
Archives of General Psychiatry, 32, 1031–8.
48.Selvini Palazzoli, M. (1974). Self-starvation. From the intrapsychic to the transpersonal approach to anorexia nervosa(trans. A. Pomerans), pp. 202–16. Human Context Books, London.
49.Dare, C. and Eisler, I. (1997). Family therapy for anorexia nervosa. In Handbook of treatment for eating disorders(2nd edn) (ed. D.M. Garner and P.E. Garfinkel), pp. 307–24. Guilford Press, 
New York.
50.Heron, J.M. and Leheup, R.F. (1984). Happy families? British Journal of Psychiatry, 145, 136–8.
51.Janet, P. (1903). L'obsession de la honte du corps. In Les obsessions et la psychasthénie, Vol. 1, Section 5. Germer Gaillière, Paris.
52.Wonderlich, S.A., Swift, W.H., Slotnick, H.B., and Goodman, S. (1990). DSM-III-R personality disorders in eating disorder subtypes. International Journal of Eating Disorders, 9, 607–16.
53.Casper, R.C. (1990). Personality features of women with good outcome from restricting anorexia nervosa. Psychosomatic Medicine, 52, 156–70.
54.O'Dwyer, A.-M. (1999). Studies of the relationship between obsessive–compulsive disorder and anorexia nervosa. MD Thesis, Trinity College, Dublin.
55.Simmonds, K. (1916). Über kachexie hypophysaren ursprungs. Deutsche Medizinische. Wochenschrift, 42, 190–1.
56.Russell, G.F.M. (1977). The present status of anorexia nervosa. Psychological Medicine, 7, 363–7.
57.Anand, B.K. and Brobeck, J.R. (1951). Localization of a ‘feeding center' in the hypothalamus of the rat. Proceedings of the Society for Experimental Biology and Medicine, 77, 323–4.
58.Hetherington, A.W. and Ranson, S.W. (1940). Adiposity in the rat. Anatomical Record, 78, 149–72.
59.Schweiger, U., Tuschl, R.J., Laessle, R.G., Broocks, A., and Pirke, K.M. (1989). Consequences of dieting and exercise on menstrual function in normal weight young women. In The menstrual 
cycle and its disorders(ed. K.M. Pirke et al.), pp. 142–9. Springer Verlag, Berlin.
60.Diamond, E.F. and Averick, N. (1966). Marasmus and the diencephalic syndrome. Archives of Neurology, 14, 270–2.
61.DeVile, C.H., Sufraz, R., Lask, B., and Stanhope, R. (1995) Occult intracranial tumours masquerading as early onset anorexia nervosa.  British Medical Journal, 311, 1359–60.
62.Ploog, D.W. and Pirke, K.M. (1987) Psychobiology of anorexia nervosa. Psychological Medicine, 17, 843–59.
63.Gordon, I., Lask, B., Bryant-Waugh, R., Christie, D., and Timimi, S. (1997). Childhood-onset anorexia nervosa: towards identifying a biological substrate.  International Journal of Eating 
Disorders, 22, 159–65.
64.Holland, A.J., Hall, A., Murray, R., Russell, G.F.M., and Crisp, A.H. (1984). Anorexia nervosa: a study of 34 twin pairs and one set of triplets.  British Journal of Psychiatry, 145, 414–19.
65.Holland, A.J., Sicotte, N., and Treasure, J. (1988). Anorexia nervosa: evidence for a genetic basis. Journal of Psychosomatic Research, 32, 561–71.
66.Strober, M., Lampert, C., Morrell, W., Burroughs, J., and Jacobs, C. (1990). A controlled family study of anorexia nervosa: evidence of familial aggregation and lack of shared transmission with 
affective disorders. International Journal of Eating Disorders, 9, 239–53.
67.Blundell, J.E. and Bill, A.J. (1991). Serotonin, eating disorders and the satiety cascade. In Serotonin-related psychiatric syndromes: clinical and therapeutic links(ed. G.B. Cassano and H.S. 
Asikal), pp. 125–9. Royal Society of Medicine Services, London.
68.Kaye, W.H., Gwirtsman, J.E., George, D.T., Jimerson, D.C., and Ebert, M.H. (1988). CSF-5HIAA concentrations in anorexia nervosa: reduced values in underweight subjects normalize after 
weight gain. Biological Psychiatry, 23, 102–5.
69.Kaye, W.H., Gwirtsman, H.E., George, D.T., and Ebert, M.H. (1991). Altered serotonin activity in anorexia nervosa after long-term weight restoration: does elevated CSF-5HIAA correlate with 
rigid and obsessive behavior? Archives of General Psychiatry, 48, 556–62.
70.O'Dwyer, A.-M., Lucey, J.V., and Russell, G.F.M. (1996). Serotonin activity in anorexia nervosa after long-term weight restoration: response to D-fenfluramine challenge.  Psychological 
Medicine, 26, 353–9.
71.Ward, A., Brown, N., Lightman, S., Campbell, I.C., and Treasure, J. (1998). Neuroendocrine, appetitive and behavioural responses to D-fenfluramine in women recovered from anorexia 
nervosa. British Journal of Psychiatry, 172, 351–8.
72.Samuel-Lajeunesse, B. (1994). Troubles du comportement alimentaire: aspects sémiologiques. In Les conduites alimentaires(ed. B. Samuel-Lajeunesse and C. Foulon), pp. 83–109. Masson, 
73.Slade, P.D. and Russell, G.F.M. (1973). Awareness of body dimensions in anorexia nervosa: cross-sectional and longitudinal studies.  Psychological Medicine, 3, 188–99.
74.Hsu, L.K.G. and Sobkiewicz, T.A. (1989). Body image disturbance: time to abandon the concept for eating disorders? International Journal of Eating Disorders, 10, 15–30.
75.Hsu, L.K.G. and Lee, S. (1993). Is weight phobia always necessary for a diagnosis of anorexia nervosa? American Journal of Psychiatry, 150, 1466–71.
76.Szmukler, G.I., Andrewes, D., Kingston, K., Chen, L., Stargatt, R., and Stanley, R. (1992). Neuropsychological impairment in anorexia nervosa before and after refeeding.  Journal of Clinical and 
Experimental Neuropsychology, 14, 347–52.
77.Crisp, A.H., Chen, C., Mackinnon, P.C.B., and Corker, C. (1973). Observations of gonadotrophic and ovarian hormone activity during recovery from anorexia nervosa.  Postgraduate Medical 
Journal, 49, 584–90.
78.Fichter, M.M. and Pirke, K.M. (1995). Starvation models and eating disorders. In Handbook of eating disorders: theory, treatment and research(ed. G. Szmukler, C. Dare, and J. Treasure), pp. 
83–107. Wiley, Chichester.
79.Treasure, J.L., Gordon, P.A.L., King, E.A., Wheeler, M., and Russell, G.F.M. (1985). Cystic ovaries: a phase of anorexia nervosa.  Lancet, ii, 1379–82.
80.Russell, G.F.M. and Treasure, J. (1989). The modern history of anorexia nervosa: an interpretation of why the illness has changed. Annals of the New York Academy of Sciences, 575, 13–30.
81.Namir, S., Melman, K.N., and Yager, J. (1986). Pregnancy in restrictor-type anorexia nervosa: a study of six women. International Journal of Eating Disorders, 5, 837–45.
82.Treasure, J.L. and Russell, G.F.M. (1988). Intrauterine growth and neonatal weight gain in babies of women with anorexia nervosa. British Medical Journal, 296, 1038.
83.Van Wezel-Meijler, G. and Wit, J.M. (1989). The offspring of mothers with anorexia nervosa: a high-risk group for undernutrition and stunting?  European Journal of Pediatrics, 49, 130–5.
84.Sharp, C.W. and Freeman, C.P.L. (1993). The medical complications of anorexia nervosa. British Journal of Psychiatry, 162, 452–62.
85.Treasure, J. and Szmukler, G. (1995). Medical complications of chronic anorexia nervosa. In Handbook of eating disorders: theory, treatment and research(ed. G. Szmukler, C. Dare, and J. 
Treasure), pp. 197–220. Wiley, Chichester.
86.Passmore, R. and Eastwood, M.A. (1986). Human nutrition and dietetics. Churchill Livingstone, Edinburgh.
87.Handler, C.E. and Pirkin, G.D. (1982). Anorexia nervosa and Wernicke's encephalopathy: an undiagnosed association. Lancet, ii, 771–2.
88.McLoughlin, D.M., Spargo, E., Wassif, W.S., et al.(1998). Structural and functional changes in skeletal muscle in anorexia nervosa. Acta Neuropathologica, 95, 632–40.
89.Treasure, J.L., Fogelman, I., Russell, G.F.M., and Murby, B. (1987). Reversible bone loss in anorexia nervosa. British Medical Journal, 295, 474–5.
90.Serpell, L. and Treasure, J. (1997). Osteoporosis—a serious health risk in chronic anorexia nervosa. European Eating Disorders Review, 5, 149–57.
91.Klibanski, A., Biller, B.M.K., Schoenfeld, D.A., Herzog, D.B., and Saxe, V.C. (1995). The effects of oestrogen administration on trabecular bone loss in young women with anorexia nervosa. 
Journal of Clinical Endocrinology and Metabolism, 80, 898–904.
92.Wakeling, A. and Russell, G.F.M. (1970). Disturbances in the regulation of body temperature in anorexia nervosa. Psychological Medicine, 1, 30–9.
93.Rieger, W., Brady, J.P., and Weisberg, E. (1978). Hematologic changes in anorexia nervosa. American Journal of Psychiatry, 135, 984–5.
94.Russell, G.F.M. (1966). Acute dilation of the stomach in a patient with anorexia nervosa. British Journal of Psychiatry, 112, 203–7.
95.Beumont, P.J.V. and Large, M. (1991). Hypophosphataemia, delirium and cardiac arrhythmia in anorexia nervosa. Medical Journal of Australia, 155, 519–22.
96.Russell, G.F.M., Treasure, J., and Eisler, I. (1998). Mothers with anorexia nervosa who underfeed their children: their recognition and management.  Psychological Medicine, 28, 93–108.
97.Stein, A., Woolley, H.P., Cooper, S.D., and Fairburn, C.G. (1994). An observational study of mothers with eating disorders and their infants.  Journal of Child Psychology and Psychiatry, 35, 
98.Russell, G.F.M. (1985). Premenarchal anorexia nervosa and its sequelae. Journal of Psychiatric Research, 19, 363–9.
99.Lask, B. and Bryant-Waugh, R. (1992). Early onset anorexia nervosa and related eating disorders. Journal of Child Psychology and Psychiatry, 33, 281–300.
100.Lask, B. and Bryant-Waugh, R. (1986). Childhood onset anorexia nervosa. In Recent advances in paediatrics(ed. R. Meadow), Vol. 8, pp. 21–31. Churchill Livingstone, Edinburgh.
101.Lai, K., de Bruyn, R., Lask, B., Bryant-Waugh, R., and Hankins, M. (1994). Use of pelvic ultrasound in childhood onset anorexianervosa. Archives of Disease in Childhood, 71, 228–31.
102.World Health Organization (1992). International statistical classification of diseases and related health problems, 10th revision. WHO, Geneva.
103.American Psychiatric Association (1994). Diagnostic and statistical manual of mental disorders(4th edn). American Psychiatric Association, Washington, DC.
104.Beumont, P.J.V., Beardwood, C.J., and Russell, G.F.M. (1972). The occurrence of the syndrome of anorexia nervosa in male subjects.  Psychological Medicine, 2, 216–31.
105.Crisp, A.H. and Burns, T. (1990). Primary anorexia nervosa in the male and female: a comparison of clinical features and prognosis. In  Males with eating disorders(ed. A.E. Andersen), pp. 
77–99. Brunner–Mazel, New York.
106.Burns, T. and Crisp, A.H. (1990). Outcome of anorexia nervosa in males. In Males with eating disorders(ed. A.E. Andersen), pp. 163–86. Brunner–Mazel, New York.
107.Fichter, M.M. and Daser, C. (1987). Symptomatology, psychosexual development and gender identity in 42 anorexic males. Psychological Medicine, 17, 409–18.
108.Steinhausen, H.-C., Rauss-Mason, C., and Seidel, R. (1991). Follow-up studies of anorexia nervosa. A review of four decades of outcome research. Psychological Medicine, 21, 447–54.
109.Morgan, H.G. and Hayward, A.E. (1988). Clinical assessment of anorexia nervosa. British Journal of Psychiatry, 152, 367–71.
110.Theander, S. (1985). Outcome and prognosis in anorexia nervosa and bulimia: some results of previous investigations, compared with a Swedish long-term study.  Journal of Psychosomatic 
Research, 19, 493–508.
111.Ratnasuriya, R.H., Eisler, I., Szmukler, G.I., and Russell, G.F.M. (1991). Anorexia nervosa: outcome and prognostic factors after 20 years. British Journal of Psychiatry, 158, 495–502.
112.Sullivan, P.F. (1995). Mortality in anorexia nervosa. American Journal of Psychiatry, 152, 1073–4.
113.Tolstrup, K., Brinch, M., Isager, T., Nielsen, S., Nystrup, J., and Severin, B. (1985). Long-term outcome of 151 cases of anorexia nervosa. The Copenhagen anorexia nervosa follow-up study. 
Acta Psychiatrica Scandinavica, 71, 380–7.
114.Eckert, E.D., Halmi, K.A., Marchi, P., Grove, W., and Crosby, R. (1995). Ten-year follow-up of anorexia nervosa: clinical course and outcome.  Psychological Medicine, 25, 143–56.
115.Bryant-Waugh, R., Knibbs, J., Fosson, A., Kaminski, Z., and Lask, B. (1988). Long-term follow-up of patients with early onset anorexia nervosa. Archives of Disease in Childhood, 63, 5–9.
116.Steinhausen, H.-C. and Seidel, R. (1993). Outcome in adolescent eating disorders. International Journal of Eating Disorders, 14, 487–96.
117.Theander, S. (1992). Chronicity in anorexia nervosa: results from the Swedish long-term study. In The course of eating disorders(ed. W. Herzog, H.-C. Deter, and W. Vandereycken), pp. 
198–213. Springer-Verlag, Berlin.
118.Touyz, S.Q., Beumont, P.J.V., Glaun, D., Phillips, T., and Cowie, I. (1984). A comparison of lenient and strict operant conditioning programmes in refeeding patients with anorexia nervosa. 
British Journal of Psychiatry, 144, 517–20.
119.Freeman, C. (1992). Day patient treatment for anorexia nervosa. British Review of Bulimia and Anorexia Nervosa, 6, 3–9.
120.Crisp, A.H., Norton, K., Gowers, S., et al.(1991). A controlled study of the effect of therapies aimed at adolescent and family psychopathology in anorexia nervosa.  British Journal of Psychiatry, 
159, 325–33.
121.Russell, G.F.M., Szmukler, G.I., Dare, C., and Eisler, I. (1987). An evaluation of family therapy in anorexia nervosa and bulimia nervosa.  Archives of General Psychiatry, 44, 1047–56.
122.Eisler, I., Dare, C., Russell, G.F.M., Szmukler, G., le Grange, D., and Dodge, E. (1997). Family and individual therapy in anorexia nervosa—a 5-year follow-up.  Archives of General Psychiatry, 
54, 1025–30.
123.Le Grange, D., Eisler, I., Dare, C., and Russell, G.F.M. (1992). Evaluation of family treatments in adolescent anorexia nervosa: a pilot study.  International Journal of Eating Disorders, 12, 
124.Prochaska, J.O. and Di Clemente, C.C. (1992). The transtheoretical approach. In Handbook of psychotherapy integration(ed. J.C. Norcross and M.R. Goldfried), pp. 300–34. Basic Books, New 
125.Treasure, J. and Ward. A. (1997). A practical guide to the use of motivational interviewing in anorexia nervosa. European Eating Disorders Review, 5, 102–14.
126.Garner, D.M., Vitousek, K.M., and Pike, K.M. (1997). Cognitive–behavioural therapy for anorexia nervosa. In Handbook of treatment for eating disorders(2nd edn) (ed. D.M. Garner and P.E. 
Garfinkel), pp. 94–144. Guilford Press, New York.
127.Crisp, A.H. (1980). Anorexia nervosa: let me be. Academic Press, London.
128.Crisp, A.H. (1997). Anorexia nervosa as flight from growth: assessment and treatment based on model. In Handbook of treatment for eating disorders(2nd edn) (ed. D.M. Garner and P.E. 
Garfinkel), pp. 248–77. Guilford Press, New York.
129.Fairburn, C.G., Shafran, R., and Cooper, Z. (1999). A cognitive-behavioural theory of anorexia nervosa. Behaviour Research and Therapy, 37, 1–13.
130.Garner, D.M. and Bemis, K.M. (1982). A cognitive-behavioural approach to anorexia nervosa. Cognitive Therapy and Research, 6, 123–50.
131.Kaplan, A.S. and Olmsted, M.P. (1997). Partial hospitalisation. In Handbook of treatment for eating disorders(2nd edn) (ed. D.M. Garner and P.E. Garfinkel), pp. 354–60. Guilford Press, New 
132.Andersen, A.E., Bowers, W., and Evans, K. (1997). In-patient treatment of anorexia nervosa. In Handbook of treatment for eating disorders(2nd edn) (ed. D.M. Garner and P.E. Garfinkel), pp. 
327–53. Guilford Press, New York.
133.Russell, G.F.M. and Mezey, A.G. (1962). An analysis of weight gain in patients with anorexia nervosa treated with high calorie diets. Clinical Science, 23, 449–61.
134.Goldner, E.M., Birmingham, C.L., and Smye, V. (1997). Addressing treatment refusal in anorexia nervosa: clinical, ethical, and legal considerations. In  Handbook of treatment for eating 
disorders(2nd edn) (ed. D.M. Garner and P.E. Garfinkel), pp. 450–61. Guilford Press, New York.
135.Mental Health Act Commission (1997). Guidance on the treatment of anorexia nervosa under the Mental Health Act 1983, pp. 1–6. Mental Health Act Commission, Nottingham.
136.Ramsay, R., Ward, A., Treasure, J., and Russell, G.F.M. (1999). Compulsory treatment in anorexia nervosa: short-term benefits and long-term mortality.  British Journal of Psychiatry, 175,