On the basis of clinical research, a broad range of clinical correlates have been identified as precursors to eating disorders. Their influence on the individual and the disease process operates through environmental, biological and psychological domains. Socioculturally determined precursors are shared between AN and BN, yet others seem to be disease specific. In AN, especially the restricting form, a drive for activity and a personality tending towards cognitive, emotional and behavioural inhibition, rigidity and perfectionism seem to be of importance [27]. The antecedent conditions for BN include a tendency towards familial overweight, a familial tendency towards affective and substance abuse disorders and an environment that increases the risk of dieting, none of which are typically associated with AN.

One of the key questions is whether a particular precursor is a risk factor, given that several studies have used the latter term [24,51,53]. The answer requires well-designed prospective studies. The factor in question and any other factor possibly interacting with it would need to be measured prospectively in the population at risk and in control populations throughout the ages of risk - throughout adolescence for AN and into young adulthood for BN - to prove a main or interactive effect on disease development. Clearly, this type of study has not been done and is unlikely to be done soon, considering the enormity of the task.

Although each precursor alone is unlikely to bring about AN or BN, each in combination with others contributes to a permissive environment in which a genetic or physiological predisposition is more likely to be expressed. In this sense precursor conditions expose dispositions. For example, a persistent negative energy balance induced by dieting appears to enhance a drive for activity in individuals who may be genetically susceptible to AN [77]. Since the energizing effect of increased activity levels counteracts the fatigue brought about by the starvation state, this predisposition would permit the weight loss to proceed to dangerously low levels without causing alarm. In BN, food restriction occurs against a background of a healthy appetite and emotional lability, making dieting a stressful proposition. In this model, then, severe caloric restriction resulting in weight loss would represent a specific antecedent variable for AN and so would disordered restrictive eating for BN.

Some precursor conditions may be preventable; others might be modifiable through treatment. Among the preventable precursors and prodromes, prolonged food restriction or abstinence from food for whichever reason stand out. Cultural expectations are subject to change. For example, fasting for religious reasons now infrequently provides the incentive for chronic food restriction resulting in AN [43]. It is conceivable, even if it seems improbable, as long as food is abundantly available in the Western and increasingly in the Eastern world [15], leading to excess consumption, that women might adopt aesthetic principles favouring a fuller feminine body, obviating the need for dieting.

Quite apart from these sociocultural forces, childhood personality traits of introversion, excessive control, caution, perfectionism and rigidity, which likely follow a pattern of familial transmission, need to be considered as predisposing factors for the development of AN, in particular the restricting type, albeit a certain proportion of patients with the bulimic type of AN seem to share caution, perfectionism and rigidity in childhood, along with greater emotional instability [26]. Even if the transmission of personality traits is believed to be partly genetic [78], the environment, including treatment, can mitigate or reinforce personality trends [79].

If the primary motivation underlying the caloric restriction is not reasonable dieting, but the wish for control over one's life and/or the need for social approval through achieving thinness, it would be more effective to help young girls who feel ineffective and ignored to achieve control over their lives and attain recognition through developing better and more rewarding relationships with people instead of focusing on body weight control. It must be recognized that negative affectivity is a nonspecific risk factor for AN, implicated also in panic attacks and major depression, whereas anxiety sensitivity, so far not described in AN, appears to be a specific factor that increases the risk for serious panic attacks in adolescents [80].

Furthermore, the effect of any of the precursors must be understood in the context of other precursor variables contributing to the development of the disorder. The ''risk factor'' literature, for instance, provides no information regarding the relative weight or severity of the antecedent condition necessary to increase the likelihood of an eating disorder, yet a certain amount of weight loss seems to be necessary to consolidate the anorectic attitude [42].

How, then, can the knowledge about precursors be applied to prevent eating disorders? Most of the screens differ widely with regard to their objective, their psychometric properties and the validation methodology used. The majority of available screens identify current diagnostic categories of eating disorders; only a few are appropriate for the identification of at-risk behaviours or to predict future eating disorders. The EAT-40 remains an instrument with standardized properties and a high sensitivity [74]. An item-by-item analysis can identify individuals at risk for AN or BN. It is less well known how truthfully survey questions are being answered by individuals with eating disorders. College admission surveys and the students' subsequent health records could provide data to test this question. Since unhealthy eating behaviours have been found to increase the risk for depression, screening surveys and preventive intervention programmes need to incorporate questions about mood disorders symptoms. So far, intervention programmes primarily directed at reducing body dissatisfaction as one of the reasons for dieting have been successful at improving knowledge about good nutrition, the perils of dieting and weight loss, yet they have failed at changing behaviour, such as reducing the dieting frequency or unhealthy eating patterns.

Without knowing more about the aetiological processes, in particular the biological and genetic structure underlying the eating disorders, the mechanisms through which precursors work together remain elusive. The literature on antecedents reviewed here suggests that eating disorders are conditions in which the expression of the genotype - e.g. certain personality dimensions and a drive for activity for AN, and familial tendencies towards overweight, affective disorders and substance abuse disorders for BN - occurs in the presence of a particular environmental exposure, severe or repeated dietary restriction, sanctioned by contemporary Western society.

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