However, there are limitations to this approach. There are a number of both methodological and ethical objections arising from the use of individual biographies and case studies. Furthermore, patients in therapy are often highly suggestible to the ideas of repressed trauma, therefore making the indications of the approach unreliable. The theory also denies any medical explanation even where strong medical evidence exists. Similarly, alternative forms of psychological therapy are known to be effective in treating some disorders yet these too are dismissed. Finally, there is a small but not substantial body of supporting evidence, which makes many skeptical about the validity of the approach.
Generally, although the validity of the psychodynamic model is still a matter to be discussed, one cannot say that it is absolutely of no value.
“Eating disorders are complicated behaviours with complicated causes.”
Consider whether psychologists have been successful in explaining anorexia nervosa and/or bulimia nervosa using a biological approach. (12 marks)
A physiological aetiology for eating disorders suggests that the following may cause anorexia nervosa: genetics, brain biochemistry, neuroanatomy, and infection.
Anorexia nervosa tends to run in families and there is increasing evidence that genetic factors play some part in the development of eating disorders. Holland, Sicotte, and Treasure (1988) looked studied anorexia in monozygotic (MZ) twins and dizygotic (DZ) twins and found that the concordance rate for MZ twins was 56% compared to 5% for DZ twins. This provides strong support for the genetic hypothesis. However, the fact that not all MZ twins had the disorder means that other factors are important as well as the inherited genes. It may be that genes predispose individuals to develop the disorder, creating a genetic vulnerability. The recent dramatic increase in the number of people suffering from eating disorders also cannot be explained in genetic terms alone, as it is impossible that there have been major genetic changes over the past 20-30 years.
Eating disorders are also often associated with chemical imbalances in the brain. One evidence is the low levels of some neurotransmitters (serotonin and noadrenaline) found in anorexia sufferers. Fava et al (1989) reported links between anorexic behaviour and changes in the levels of serotonin and noadrenaline (related to arousal and stress). In addition, antidepressants (especially SSRIs) have been used successfully on people with eating disorders, which supports the possibility of an underlying neurotransmitter dysfunction. Finally, it is also possible the link between anorexia and amenorrhea is because of an underlying problem with the endocrine system. However, it may be that biochemical imbalances result from the disorder rather than causing it. This is more likely, as menstruation is known to be affected by periods of emotional upset or privation (Russell, 1972).
Another suggestion is that anorexics may have brain abnormalities, specifically in the parts of the hypothalamus that control eating, sexual activity, and menstruation. However, altered hypothalamic activity may well not be a cause, as it is more likely to occur as a result of the weight loss or the anorexic’s emotional distress. In addition, post mortems have not revealed any lesions in this area of the brain.
It is also possible that physical illness may be a cause. Park, Lawrie, and Freeman (1995) studied 4 female anorexics, all of whom had had glandular fever shortly before the onset of the disorder. Park et al argued that the physical disease may have influenced the functioning of the hypothalamus, causing homeostatic imbalances. However, this explanation lacks evidence to back it up.
Although there are still many limitations, biological explanations of anorexia nervosa serve as great references.
