bio explanations of AN

AO1

genetic

  • hereditary

    • twin studies suggest that there is a genetic explanation for AN

    • as MZ twins share 100% of their genes but DZ only shares 50%, a higher concordance rate for MZ twins is strong evidence for a genetic component to AN

    • holland et al studied 45 pairs of female twins, they found a concordance rate of 56% for MZ twins but only 5% for DZ twins

  • candidate genes

    • ashley scott-van zeeland carried out a CGAS

    • they compared 1205 people with AN to 1948 control ppt by sequencing 152 candidate genes suspected to be linked with AN. they found that epoxide hydrolase (Ephx2) was significantly associated with it.

    • it codes for an enzyme involved in cholesterol metabolism. surprisingly, many people in the acute phase of AN, when symptoms are particularly sever, do have abnormally high levels of cholesterol

  • genome-wide association studies

    • GWAS offer a different approach because they do not make assumptions about which genes specifically might be involved with AN

    • they look the entire collection of human genes rather than individual ones

    • boraska et al conducted a GWAS with 5551 people with AN and 21080 matched controls. 72 separate genetic variations were identified. scientists argued that their study was not sensitive enough to see if they were significantly related

neural

  • we can learn about neurotransmitters by measuring the level of their metabolites

    • serotonin - 5-HIAA

    • dopamine - HVA

  • serotonin

    • bailer and kaye present evidence of low levels of 5-HIAA in people with AN

    • these levels return to normal after short term weight recovery and increase beyond normal levels after long-term recovery

    • attia et al studied individuals with AN who had not returned to their pre illness weight

    • these individuals did not respond well to drugs that stimulate serotonin activity than people with AN who had restored a healthy weight

    • the pattern of results from these studies clearly indicates underactivity of the serotonin system in AN

  • dopamine

    • kaye et al found lower levels of HVA in recovered AN patients compared with controls. this suggests lowered levels of dopamine are associated with AN

    • another approach was used by bailer et al, injecting ppt with amphetamine, a drug known to increase dopamine. control ppt with no history of EDs experienced euphoria but the ppt w AN experienced anxiety instead

    • eating increases dopamine release, therefore people with AN may restrict food intake to reduce their anxiety levels

AO3

  • one limitation of the genetic explanation is that twin studies may lack validity

  • in every pair, twins share the same environment as each other or at least we believe they do because of the equal environments assumption

  • however, the assumption may be wrong because one aspect of the environment is the way the twins are treated. MZ twins may be treated more similarly because they look similar but DZ twins may be treated differently

  • this means that the genetic influence on AN may not be as great as twin studies suggest

  • one strength of gene studies is that they have highlighted the true genetic nature of AN

  • ironically, this is because studies have been unsuccessful in identifying the genes that contribute to AN. the main contribution of gene studies is to show that looking for one singular gene is futile.

  • therefore, gene studies have shows that AN is polygenic, where multiple genes make significant contributions to the predisposition of AN

  • one strength of the neural explanation is that there is research support

  • many studies have tested cerebrospinal fluid for HVA. kaye et al compared woman diagnosed with AN with women who had no history of EDs. the HVA levels of women with AN were 30% lower than for the non-AN women on averge

  • these findings strongly suggest that a disturbance of dopamine metabolism may contribute to the symptoms of AN

  • one limitation of the neural explanation is that it can be simplistic

  • nunn et al argued that serotonin on its own does not distinguish between people who have AN and those who do not. AN is better explained by considering the interaction between serontonin and noradrenaline. the researcher claims that other neurotransmitters like GABA are also involved

  • this is an important reminder that neurotransmitter systems do not operate in isolation and, like genetics, contribute as a whole to the onset of AN

  • a better approach to explaining AN would be the diathesis stress model

  • genes lay the foundation for AN as seen by research on CG. this creates a diathesis that makes them more predisposed to developing AN. this diathesis is then triggered by a stressor, which could include low self esteem or family stress

  • this means that the diathesis gives rise to AN depending on the stressor. therefore, one way to prevent the development of AN would be to target and control stressor in order to reduce likelihood