To what extent does research evidence (theory and/or studies) support the view that anorexia nervosa and/or bulimia nervosa are caused by biological factors?

Thus there is a high indication that there can be a genetic vulnerability to anorexia nervosa, in spite of the experimental validity of Holland’s research being questioned (the independent variable, genetic relatedness, was not able to be manipulated by the experimenter as it occurred naturally, thus the independent variable may be influenced by other factors such as environmental upbringing and twin behaviour imitation through modelling.) However, this research only examines anorexia nervosa and thus it is difficult to apply it to bulimia nervosa due to the fundamental differences between the two disorders. As well as this, genetic factors alone cannot be responsible for the dramatic rate of increase in the occurrence of anorexia nervosa – genetic inheritance as far as researched has remained constant for the past few decades and thus environmental surroundings must also play a part in triggering the disorder.

The biochemical explanation for eating disorders is a plausible one in the context of anorexia nervosa but unfortunately proves unsubstantiated in the case of bulimia by studies into the behaviour of bulimia nervosa sufferers. Fava et. al (1989) studied anorexic behaviour and linked it to changes in serotonin and noradrenaline levels – these hormones are linked to stress and physiological arousal, and this study is supported by the effective use of selective serotonin reuptake inhibitors and other antidepressants on sufferers of eating disorders. As well as this, it was suggested that the theory could be applied to bulimia as eating large amounts of carbohydrate-saturated foods can increase serotoninergic levels and improve mood. However, Barlow and Durand (1995) found that bulimics did not specifically target carbohydrate-saturated foods in their bingeing. It is also argued that endocrine imbalances could be an effect rather than a cause of the eating disorder, supported by the existence of pre-menstrual stress experienced by some female adolescents due to the hormonal imbalances created by menstruation (Russell, 1972) – this would also counteract the argument that amenorrhea and anorexia are linked by endocrine system imbalances.

Finally it has been suggested that anorexia nervosa is triggered by the presence of brain abnormalities such as hypothalamus dysfunction (Garfinkel and Garner, 1982), as the hypothalamus controls eating, sexual activity and menstruation. For example, the lateral and ventromedial hypothalami act as a contrary pair to coordinate weight homeostasis, with the lateral hypothalamus inducing hunger and the ventromedial hypothalamus suppressing hunger. If one or the other fails to function, it could be that an eating disorder is the result. However, like the biochemical theory this explanation is also problematic because the indicated hypothalamus dysfunction may again be a symptom of anorexia, resulting from emotional distress and extreme weight loss, rather than an actual cause. Certainly post-mortems of deceased anorexics have not revealed brain lesions in the hypothalamic area of the brain.

Overall, the main disadvantage of the biological explanations of eating disorders is that they focus mainly on anorexia nervosa, a greatly different disorder to bulimia nervosa – the nature of research such as the twin study by Holland et al make it difficult to translate the findings into the context of bulimia. As well as this there is the difficulty in ascertaining whether physical aspects of the disorder are actually causes or effects of the anorexic/bulimic behaviours. The genetic explanation out of all of the theories put forward has the most evidence to support it, but the genetic theory cannot stand alone as an explanation for the onset of an eating disorder, it can only be one of the factors involved in the development of the condition.