The Psychology of Eating: From Healthy to Disordered Behavior

236 Eating Disorders

these neurotransmitters). Third, subjective reports from people with AN,
both during and after their illness, suggest that they are hungry but choose
not to eat. In fact, the term anorexia nervosa (meaning “nervous loss of
appetite”) is probably a misnomer because they may not have a loss of
appetite. It is possible that self-imposed starvation causes changes in
neurotransmitters which may not be the cause of AN but may perpetuate
it because the individual no longer recognizes that their bodily signals are
indicating hunger and that they are deprived of food.

Problems with a physiological model
There are several problems with a physiological model of eating disorders
which need to be considered:

• Eating disorders remain a problem of the West. A genetic model cannot
  explain why eating disorders do not occur in developing countries.


• Over the past few decades there has been an increase in the occurrence
  of eating disorders. This increase far outweighs any possible changes to
  the gene pool. A genetic model cannot explain this increase.


• The environmental differences for identical and non-identical twins is
  a problem for a genetic model.


• The environmental similarities for adoptee families and biological
  families is a problem for a genetic model.


• Eating disorders can be life-threatening problems. A genetic basis to a
  problem which can result in death does not fit in with the survival drive
  of either the individual or the gene which is central to genetics.


• A genetic model cannot explain how a genetic tendency is expressed.


• A model emphasizing the role of neurotransmitters cannot separate out
  cause and effect. Further, it neglects the obvious social and cultural
  patterning of eating disorders.

A psychoanalytic model of eating disorders

There are many different psychoanalytic models of eating disorders. In
general, such models do not aim to offer an all-encompassing model of
causality to predict who will or will not develop an eating disorder, but
offer a way of understanding the patient’s experiences. Such models have
two factors in common. First, they emphasize the meanings attached to
the individual’s symptoms and the function and need for such symptoms.
Second, they emphasize the role of infancy and subsequent experiences in