Discuss biological explainations for AN

DIsturbances in the levels of neurotransmitters such as Serotonin have been linked to the onset of Anorexia Nervosa. Early studies looking into the role of serotonin found underactive serotonin pathways in the brain, indicating that sufferes had a reduction in levels of seotonin, which shows there is a correlation between low levels of serotonin and the development of eating disorder AN.

Supporting this claim, Bailer et al (2007) compared serotonin activity in women recovering from restricting-type anorexia (restricted food intake) and binge-eating/purging with healthy controls. He found significantly higher serotonin activity in women who showed the most anxiety. This therefore, implies that persistent disruption of serotonin levels could lead to increased anxiety and this could trigger AN, as typically one of the symptoms of AN is suffering from heightened anxiety in relation to food.

However, explainations using the biological approach are extremely deterministic, as they state that from your biological makeup, that you are predisposed to certain conditions which you have no control over. This study states that if you have low levels of serotonin, it is likely that you will develop AN, however it provides no explaination to why certain people have low levels of serotonin, this limits our overall understanding of why certain people develop AN by low levels of serotonin as the root cause has not been resolved. Therefore making it unclear serotonin is the cause.

In fact some researchers have found that SSRI's are not effective when used with AN patients. As a result of this, the theory seems to be incorrect as these drugs will help balance our the Serotonin levels, meaning the AN patients experience less anxiety but research has shown that this does not seem to work, therefore, implying that AN cannot just be down to Serotonin levels.

Supporting this, Kaye et al (2005) used PET scans and found that there are fewer serotonin receptors in the brains of people with eating disorders. Such changes are also evident in people who have recovered from eating disorders. This suggests an explaination why SSRI treatment has been ineffective, as AN could be the cause of insensitive receptors not low levels of the chemical itself.

On the other hand, Kaye (2001) found that if you use serotonin drugs with recovering anorexics, they were good for stopping relapses. Therefore, there is evidence towards the explaination for serotonin activity being a key factor as well. Consequently, this suggests that serotonin does play a role in AN, but it is not the underlying factor. However, there is a postive from this research as although they do not work with AN patients, they do seem to prevent relapses.

Another neurotrasmitter which has been found to be linked with anorexic's behaviour consequently negatively impacting on their views of food, is dopamine. Kaye et al (2005) looked at PET scans and compared Dopamine levels of activity in the brains of ten women recovering from AN and a control group of twelve healthy women. In the anorexics, he discovered overactivty in the dopamine receptors. Dopamine is a key factor in the interpretation of harm and pleasure. These increased levels seem to change the way in which we think about rewards. Therefore this research suggests that anorexics may find it challenging to link good feelings with food, as high levels of the rewarding chemical dopamine would postively reinforce their actions of avoiding food. As a result their behaviour would continue as long as they are being rewarded from dopamine.

There is strong evidence to support the theory about dopamine levels influencing onset of AN. Wang (2001) found lower levels of dopamine receptors in the brains of obese individuals. This evidence consequently, proves the explaination is useful and high in ecoglogical validity as it is relevant to real cases. Therefore as high dopamine levels have been associated with anorexic patients this theory could be applicable to treatment as you can control these levels by the use of drug therapy.

And as a result, the role of neurotransmitters has good real life applications for it. Drug therapies are used to normalise neurotrasmitter levels ans even gene-replacement therapy. Another advantage of biological explainations is that people realise they are dealing with dysfunctional biology, which is treatable, as opposed to a dysfunctional family, which often is not. Although, the most important impliaction of this is that it reduces the guilt generated by the view that it is parents who cause the development of eating disorders in their childern.

However, reductionism is a significant issue to consider here as simplifying the onset of AN down to just neurotransmitters levels and neurodevelopment is an example of oversimplification. The process are a lot more complex than just balance the levels out and no one will get AN anymore. There are many other factors to consider, for example the patients attitude to food and the underlying problems they have such as body dismorphia which is where the individual has a distorted perception of body image, this is a psychological issue where there has been no evidence to suggest it is related to biology of AN suffers.   

If certain genes or neuroanatomical features can predispose individuals to AN, evoluationary psychologists would argue that AN must have some adaptive advantage which would have been useful in the EEA. This is a useful way of looking at AN, as if it wasnt adaptive to our ancestors, they would have not reproduced or survived.

The reproductive suppression hypothesis proposed by Surbey (1987) believed that adolesecent girls desire to control their weight represents an evoluationary adaption in which ancestral girls delayed the onset of sexual maturation in response to cues about the probabiltiy of poor reproductive success. It is adaptive because it enables a female to avoid giving birth at a time when conditions are not favourable to her offsprings survivial.

However, the reproduction supression account of AN does not explain why AN would develop in men, therefore can be criticised for being gender bias. According to recent statistics, 25% of adults with eating disorders are male, suggesting that AN is not solely a female disorder. Therefore, males cannot be explained just in terms of the suppression of reproduction. COnsequently if just this theory only was used to explain the causes of AN, there would be treatment implications for men suffering from AN as giving birth does not apply to men.

Another evoluationary explaination, the adapted to flee hypothesis suggests that anorexics hyperactiivety and denial of starvation would have been a useful strategy as a response to famine. This would enable them to remain active and migrate to other areas with heigher food availabliitiy in order to aid survival.

However even though this may have been the case with our ancestors, we cannot go back in time to test if this speculation si true therefore this theory lacks in validity as there is no direct supporting empirical evidence.

Also, it is questionable how the symptoms of AN would have been passed on through generations by natural selection, particulary as AN decreases fertility and makes reproduction more difficult, and may even kills the individual. These traits would reduce the individuals's survivability therefore in the long term, AN seems to be a disadvantage.

Additionally, if the causes of AN was to just be based on speculation from the EEA, there may be an issue of temporal validity. Modern day humans differ in many ways to our ancestors, one of which is that food is not scarce. Therefore by stating the cause of AN is due to famine would not be applicable; as there are many modern day cases of AN when food is plentiful. AN may have been effective in the harsh conditions of the EEA, outside these condtions the development of AN would not be favourable to the individual. This suggests that the development of modern day AN traits is a consequence of factors that are not assoicated with evolution.