Disturbances of neurotransmitter metabolism in anorexia nervosa.

My understanding of anorexia nervosa is that it is ultimately a biological solution to an existential problem for an adolescent female and her family in the classical case. I t is not seen by the individual concerned as an affliction but rather, perhaps, as adaptive and egosyntonic. In order to protect her status the so-called patient will often successfully conceal major aspects of her feelings and behaviour. She shares this propensity with many other similarly-motivated people, for instance many people with neurotic illness, and the alcoholic. One popular construction put upon her syndrome is that she has lost her appetite and that this is the explanation for her reduced food intake. Another view, perhaps bearing in mind such features as her excessive preoccupation with food and involvement in its preparation, is that she is liable to an excessive and premature satiety. In my view neither of these formulations does sufficient justice to the complexity of the experiential aspects including the determinants of this condition. Correspondingly, there are as yet few signs that effective pharmacological manipulation of anorexia nervosa is a near reality. In recent years two principal theoretical contributions have been made in terms of possible disturbances of neurotransmitter metabolism in the condition. Mawson (1974), in a closely-argued thesis, proposed that the syndrome of loss of appetite or excessive satiety or both could be explained on the basis of a subcortical, probably hypothalamic, defect involving progressive depletion of brain noradrenalin or dopamine or both. He suggested that treatment with 1-DOPA might be effective. Mawson’s (1974) grasp of the clinical nature of the condition extended to an understanding that patients often seem purposefully to resist eating. He quotes Russell (1970) as saying that this does not rule out a primary hypothalmic lesion. More recently Redmond, Huang, Baulu, Snyder & Maas (1977) have proposed, again on the basis of animal studies, that the apparently-increased satiety in anorexia nervosa might be due to hyperactivity of postsynaptic noradrenergic receptors. Commenting on Mawson’s (1974) dopamine theory they conclude that the use of 1DOPA is doomed to failure because of the likelihood that it would also increase noradrenalin activity. They suggest that the most effective pharmacological approach would be the exhibition of a-adrenergic blocking agents. At this stage I will make some further comments as a clinician. ( I ) It is in my view likely to continue to be difficult to set up animal models which reflect the complex factors governing behaviour in anorexia nervosa.