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

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.^(9,10)

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.^(11,12)

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.⁽¹³⁾ The most thorough survey of 15-year-old schoolchildren was that conducted in Göteborg, Sweden.⁽¹⁴⁾

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.^(15,16)

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⁽¹⁵⁾). Estimates based on case registers of psychiatric patients similarly yielded fairly low incidence rates (e.g. 0.64 in Monroe County, New York⁽¹⁵⁾). The incidence found in community-based studies was by far the highest (7.7 in The Netherlands⁽¹⁰⁾ and 8.2 in Rochester, Minnesota⁽¹⁷⁾), presumably because they included the less severe cases.

A high prevalence rate was found among Canadian ballet students (6.5 per cent) and modelling students (7 per cent).⁽¹¹⁾ A similar survey in an English ballet school also showed a high prevalence of ‘possible’ cases of anorexia nervosa (7.0 per cent).⁽¹²⁾

Surveys among schoolgirls have shown a fairly wide variation in prevalence rates, ranging from 0 per cent 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).⁽¹³⁾ 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.⁽¹⁴⁾

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.⁽¹³⁾ 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.⁽¹⁸⁾ A prevalence of 2.0 per cent in females aged 18 to 25 was found in a community survey in Padua, Italy.⁽¹⁹⁾

A marked predominance of females over males is usually reported in surveys, for example 92 per cent in North-east Scotland⁽¹⁵⁾ and 90 per cent among the children in Göteborg.⁽¹⁴⁾ On the other hand a community survey in the province of Ontario gave rise to a more balanced female to male ratio (2:1) when cases of partial anorexia nervosa were included.⁽²⁰⁾

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’.⁽¹⁵⁾

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,⁽²¹⁾ a high social class predominance was not found in studies utilizing case registers.⁽¹⁵⁾ On the other hand, the schoolgirl studies mentioned above tended to confirm a high social class predominance.

The pathoplastic sociocultural causes of eating disorders have been subsumed under the term ‘the modern cult of thinness’ prevalent in westernized societies.⁽¹⁵⁾ 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.⁽²⁸⁾

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 and athleticism.⁽³⁾

At the beginning of this chapter 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,⁽⁵⁾ a weight ‘phobia’,⁽²⁹⁾ or a morbid dread of fatness.⁽⁶⁾ 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. These beliefs are held obstinately and amount to overvalued ideas.

The proposition that anorexia nervosa is a culture-bound syndrome has much support.^(30,31) 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 the symptom cluster … ⁽³⁰⁾

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.⁽³¹⁾ 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.⁽³²⁾

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,⁽⁴⁷⁾ 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.^(6,48) 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:

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.⁽⁴⁹⁾ 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 function is extremely sensitive to even small restrictions of caloric intake which often lead to impaired menstrual function.⁽⁵⁰⁾

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.⁽⁵¹⁾

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.⁽⁵²⁾ 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 had previously 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. Regional cerebral blood flow was measured in three series of children.⁽⁵³⁾ In the majority of the children there was an above-critical difference in the regional cerebral blood flow most often between the temporal lobes but sometimes affecting other brain regions. Hypoperfusion was found on the left side in about two-thirds of the children. Follow-up scans were undertaken in 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 found that there was a significant association between reduced blood flow and impaired visuospatial ability, impaired complex visual memory, and enhanced information processing.

As with general psychiatric disorders, genetic and environmental factors are no longer viewed as opposing causes of anorexia nervosa, but rather as interacting with one another. Thus there may be groups of genes that determine risk of the illness and specific environmental situations that elicit or prevent the expression of these genes. There is evidence for a family aggregation of anorexia nervosa. This does not necessarily mean that the origin of the disorder is genetic because environmental factors common to the family 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 disorders.⁽⁵⁴⁾ 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. The absence in the relatives of probands with major affective disorder indicated the specificity in the risk of transmission of anorexia nervosa and the absence of shared familial liability with affective disorders.

The strongest argument favouring a part-genetic causation of anorexia nervosa is derived from the classical method of comparing the concordance rate of the illness in monozygotic and dyzygotic twins. Underlying the method of twin studies is the supposition that the environment for MZ twins and DZ twins is the same, or at least it does not differ in such a way as to cause greater concordance for MZ twins. Although it is known that the environments shared by MZ twins are more often similar than those shared by DZ twins, these similarities are thought not to be of aetiological relevance to anorexia nervosa.⁽⁵⁵⁾ The first sizeable series of twins came from the Maudsley Hospital and St George’s Hospital in London and showed higher concordance rate for MZ than for DZ twins.⁽⁵⁶⁾ Since then the findings have been replicated and the analysis of the twin data has suggested that the liability can be broken down into three sources of variability:

The individual-specific environmental effects are those which contribute to differences between the members of the twin pair. This would happen if only one member of the twin pair had suffered from an adverse effect. It is perhaps surprising that the unique environmental effects contribute to the disorder but not the twins’ common environment.

Bulik has found the concept of heritability and its estimation prone to misinterpretation. There is not just one heritability estimate because this statistic varies across the population sampled and the time of the study. One estimate of heritability of anorexia nervosa gave it as 0.74 in 17-year-old female twins.⁽⁵⁵⁾

It remains uncertain how the genetic vulnerability to anorexia nervosa expresses itself in terms of the pathogenesis of this disorder. One view is that this vulnerability confers instability of the homeostatic mechanisms, which normally ensure the restoration of weight after a period of weight loss. This hypothesis would explain why in western societies, where dieting behaviour is common, those who are genetically vulnerable would be more likely to develop anorexia nervosa.⁽⁵⁷⁾ It has also been found that MZ twins have a higher correlation for the trait of ‘body dissatisfaction’ than DZ twins.⁽⁵⁵⁾

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’.⁽⁵⁸⁾ 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.⁽⁵⁹⁾

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.⁽⁶⁰⁾ 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.⁽⁶¹⁾ The arguments against this simple model of enhanced serotonin activity as a vulnerability trait in anorexia nervosa should be briefly presented. Serotonin function was again assessed in long-term weight-restored anorectics.⁽⁶²⁾ 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, this study failed to support the notion of increased central serotonin function as a vulnerability trait in anorexia nervosa.⁽⁶²⁾