Although there is no specific evidence linking the VMH/LH to eating disorders there is evidence to support the dual-centre theory including research that found that damage to the LH may cause Aphagia- failure to eat when hungry. Rats whose VMH had been damaged developed binge eating and became obese. The behaviours of other animals may not be affected by the same factors as humans e.g. social context, cognitive factors and emotions.
Cummings et al (2004) found a strong correlation between ghrelin levels and hunger. The problem with the study was that it used a fairly small sample of PPs, limiting the generalisability of the study. Cultural factors may have played a large role in the findings as the PPs judgments of hunger may have been influenced by expectations of food based on meal times. As it was a laboratory experiment it was highly controlled which is good because other variables were controlled but it does lack ecological validity. However, other evidence does support Cumming’s findings for example ghrelin injections result in increased food intake in animals and even real-life evidence gastric bands used to treat obesity, reduce ghrelin secretion.
Although many studies have showed biochemical changes in individuals with eating disorders, it’s difficult to decide whether these changes are the cause or the consequence of the eating disorder e.g. starvation may eventually cause an imbalance in biochemical functioning.
Genetic origin: Eating disorders especially AN has been found to be an increased risk in the 1st-degree relatives of AN sufferer. (Holland et al. 1988). Twin studies carried out on identical twins and non-identical twins, have shown a 55% concordance rate in identical twins for anorexia nervosa, whereas only a 7% concordance rate in non-identical twins. This suggests a possible genetic factor. However, identical twins have 100% same genes, so why is there still 45% who were discordant. This discordance has been explained by Hsu who suggests that the genetic link may relate to personality traits e.g. mood or personality disorders. If the person is more susceptible to stressful life events because of the genetic link then the stress could manifest as an eating disorder or another mental disorder.
The link is less clear for bulimia nervosa as studies of identical twins have shown concordance rates of 23% and non-identical 9%. It was also a longitudinal which gives it more validity. Furthermore, about 25% of the non-bulimic twins reported anorexia, a phobic disorder, or an anxiety disorder. Both studies were natural experiments, hence they have high external validity. But it may be that other extraneous variables were not controlled e.g. personality traits which could affect the reliability of the results.
Genetic factors and social, environmental influences within a family are hard to separate. Some studies have shown evidence that family tensions may trigger eating disorders, hence it may have been the environment that increased the risk of developing anorexia, as the majority of the twins shared the same environment. Also the sample of twins used was very small, so it was not an accurate representation of the population and cannot be generalised without limitations.
Anorexia and bulimia nervosa are most common in white people in western societies. However, it is difficult to distinguish the influence of genetic factors and social/cultural pressures.
A sudden increase in eating disorders about young women was noticed in a study in Fiji since the arrival of TV, (Fearn, 1999). This suggests a strong social and cultural component as TV seems to have influenced and pressurised these young women.
Conclusion: A significant factor in the biological explanation of eating disorders is that it ignores the underlying cognitive problems and depression behind these disorders. The distorted image that more often than not accompanies eating disorders has not been explained by the biological explanation. The cause & progression of any eating disorder is unlikely to be singular, but more likely a combination of factors including: Biological, Psychological, Environmental and Socio-cultural. For example the diathesis model which believes that there must be genetic predisposition as well as an environmental trigger which cause a disorder.
