Outline and Evaluate the biological explanation of one eating disorder (24 Marks)
Anorexia Nervosa (AN) seems to be associated with the role of serotonin dysfunction. Abnormalities in serotonin levels are already known to be linked to depression and anxiety. Bailer et al found higher serotonin activity in recovered binge-purge anorexics. All the participants had slightly higher serotonin activity. But the highest levels of serotonin in those showing the most anxiety. One suggestion is that higher serotonin levels lead to more anxiety and actually starving oneself leads to those serotonin levels lowering. AN then could be seen as almost a form of serotonin. This may explain SSRIs that heighten the serotonin levels don’t actually work for many anorexics. However, they do work for some. Therefore, the exact relationship between serotonin and anorexia is not understood. Malnutrition in any case causes changes in levels and it is not cert ain whether serotonin imbalance comes first or is actually the result of AN.
The role of genetics has also been examined by Holland et al (1984) who used a sample of 40. They researched the genetic link by comparing MZ and DZ twins, where one twin of each pair was suffering from AN. They hypothesized that as MZ twins are genetically identical, if AN characterised entirely genetic, it should be a shared trait. Holland et al. found a concordance rate of 55% for MZ twins and of only 7% for DZ twins. The significantly higher concordance rate for MZ twins suggests a genetic involvement in AN, but clearly it is not the only component in place. If it was entirely genetic, the concordance rate would surely have been 100%. Environmental factors also are an implicating factor on whether an individual suffers from AN as MZ twins are more likely to be treated similarly than DZ twins which in turn increases the chances of both twins suffering from AN. However, Holland et al’s research has been supported by other research. Kendler et al. (1991) found similar results in their twin study which in turn increases the reliability of Holland et al’s study as a suitable explanation for why people may develop AN.
There are also evolutionary explanations of AN that suggest some of the symptoms and characteristics of AN are in our hard-wiring. The ‘Reproduction Suppression Hypothesis’ suggest that adolescent girls’ desire to control their weight represents an evolutionary adaptation in which ancestral girls delayed the onset of sexual malnutrition in response to cues about the probability of poor reproductive success. The ability to delay reproduction is adaptive because it enabled females to avoid giving birth at a time when conditions aren’t conductive to survival (e.g. famine).
In the ‘Adapted to Flee Hypothesis’ Guisinger proposes that the typical AN symptoms of food restriction and hyperactivity reflect the operation of adaptive mechanisms that once caused migration in response to local famine. Normally when a person begins to lose weight the body naturally conserves energy (becomes tired) and hunger ensues. However, our ancestors who were nomadic foragers may have needed to turn this mechanism off and be energetic despite the lack of food as this would have increased their chance of survival. Having energy would have meant that they could flee to another more favourable environment. In the EEA those starving foragers who deceived themselves about their physical condition would have been more confident about moving on to a more favourable environment and therefore more likely to survive.
Such ultimate approaches can be beneficial as it can help treatments be developed and encourage parents to be more compassionate and less defensive. However, it is problematic that AN could be passed on through natural selection when it ultimately doesn’t lead to survival but actually could lead to death. Also, the ‘Reproductive Suppression Hypothesis’ is gender biased in that it offers only an explanation of how girls could develop AN when in fact boys develop it too.
Both the biological and evolutionary explanations of AN are reductionist. Reducing complex causes for AN down to neurotransmitter imbalance is simplistic. A problem with it is it ignores all of the other causes such as the media and environment. Modern Western society has to be implicated in some way as AN is so much more common in the Western world where media images idealise thinness. A benefit of such reductionism however is of course that treatments for AN can be developed as indeed SSRIs do work for some anorexics.
The biological explanation of AN is also determinist as we have free will and don’t have to develop AN just because of genes or hormones or even evolutionary hard wiring. Most people don’t have this illness. There is also a danger in suggesting that there is nothing anyone can do about it. In fact such a view might discount the importance of psychological therapies in treating AN. This view seems to suggest that nature is more important than nurture in the development of AN when in fact there is plenty of evidence that AN is caused by an interaction of both the environment and genes. AN is linked to the psychological trait of perfectionism and this trait is often found in the family of anorexics. Perfectionism may be a genetic vulnerability (diathesis) and/or perfectionists may create an environment in which anorexics can thrive. An important implication of this would be that the families of anorexic sufferers could be targeted in order to help promote a healthy diet and make sure that all family members are aware of the dangers that AN can cause to.
19/24 Grade A AQA A