Biological Explanations of AN

It is debated whether biological explanations of Anorexia Nervosa (AN) are sufficient in themselves.

One biological theory regarding the development of Anorexia Nervosa is the limited, reproductive suppression hypothesis. This evolutionary theory argues that anorexia has evolved as its symptoms are adaptive during times of famine. In our evolutionary past, amenorrhea (the loss of menstruation) stopped women from having a child during periods of food scarcity, when a child was unlikely to survive. In this way, 'reproductive suppression' (Wesser and Barash) stopped women wasting their care on a child who was unlikely to survive, allowing them to invest in exsiting chilren or children born later when conditions improved. Therefore ancient women would have been more likely to successfully pass on her 'selfish genes' (Dawkins). Although AN is no longer adaptive in modern, western society, the evolved mechanism still exists, meaning some women are genetically predisposed to suffer from the condition.

Another biological explanations for the development of AN is genetics, which argues that AN can be explained by faulty genes, as demonstrated by the higher concordance for AN in monozygotic twins (who are 100% genetically identical) compared to dizygotic twins (who only share 50% of their genes). 

Compelling evidence for biological explanations of AN comes from Holland who studied 30 pairs on Mz and Dz twins and found a 56% concordance rate for AN in Mz twins and only a 7% concordance rate for Dz twins developing AN. As there are strong social pressures to treat identical twins similarly and non- identical twins differently, this may explain the high concordance rate for AN in Mz twins compared to Dz twins.  However, that means that 44% of Mz twins did not show a concordance rate in developing AN, and if it was purely due to genetic factors there would be a 100% concordance rate show, therefore other factors e.g. the environment, must play a role in the development of AN. Therefore, genetic factors can be criticised for difficulty establishing cause and effect; which is where it is impossible to establish a causal relationship between two variables as there is no direct control over the independent variable. This is because it is impossible to separate the influence of genes and environment on behaviour.

Further strong evidence to support biological explanations of AN comes from Klump who performed meta-analysis of twin studies and concluded that concordance rates in Mz twins for AN are between 50-80%. Similarly Lilenfeld found that relatives of anorexics were 7-12 times more likely to show 'sub-threshold' symptoms of AN (some criteria of the DSM-IV list met). Both pieces of research show that genetic explanations may in part explain the development of AN.

A final biological explanation of AN is neurological. Hypothalamic damages argues that a link has been found between damage in the lateral hypothalamus (LH)- the hunger centre of the brain and loss of appretite. Non-clinical participants with damage to the LH report a general loss of appetite and display 'self-starving syndrome' which is similar to anorexia. However, this can be criticised for being simplistic as if AN was caused by damage to the LH it would not be able to be cured, yet AN sufferers have shown recovery rates. Furthermore, reduced serotonin activity levels have been linked to AN, as anorexics are known to have lower levels of serotonin and fewer serotonin receptor sites- as seen in the brains of non-clinical participants. 

Scientific evidence to support biological explanations of AN come from Frank, who used PET scans to show a reduced number of serotonin receptor sites in individuals with personality traits such as anxiety and depression. As these are key symptoms in anorexia, this shows that low levels of serotonin may be linked with AN.

Finally, compelling evidence to support biological explanations of AN comes from animal studies, which have shown that damage to the hypothalamus causes a reduction in hunger. This shows that hypothalamic damage is linked to loss of appetite.

Suggesting the sufficiency of biological explanation of AN they can be praised for being parsimonious as they are justifiable simplistic, this is because genetic explanations are fully support by research evidence (Holland). 

However, undermining the sufficiency of biological explanations in explaining AN, some psychologists may argue that genetic explanations are simplistic as they ignore other important factors, for example concordance rates are not 100% in Mz twins even though they share 100% of their DNA meaning other factors such as the environment must play a role in the development of AN. 

Further undermining the sufficiency of biological explanations of AN they can be criticised for being alpha biased. By unfairly exaggerating the difference between men and women, this is because theories are is only based upon female participants, this is especially true for evolutionary explanations of AN as it claims to only be in the evolutionary history of women because men do not experience amenorrhea.

Therefore, due to the wealth of evidence against, biological explanations of AN are not sufficient in explaining eating behaviour (e.g. environmental factors also play a role).