Biological Explanations of Anorexia Nervosa Flashcards
What are the two biological explanations of AN?
- Genetic
- Neural
Genetic explanation:
According to the genetic explanation: Anorexia Nervosa is an inheritable disorder passed through DNA.
- Twin studies
- Candidate genes
Twin studies are used to investigate the role of genes in AN
E.g. Holland et al looked at 45 pairs of twins and found a concordance rate for anorexia of 56% of MZ twins and 5% for DZ twins. - Due to the significantly higher CR for MZ twins compared to DZ regarding anorexia, we can conclude that anorexia is heavily genetically based.
Candidate genes:
Scott-Van Zeeland identified the main candidate gene for anorexia. He identified that variants of the EPHX2 gene have an association with AN.
Since the gene is involved in cholesterol function, it explains why anorexics have an abnormal level of cholesterol.
What are the two neurotransmitters involved in neural explanation of AN:
- dopamine
- serotonin
Dopamine:
Dopamine abnormalities may also play a part in anorexia. Kaye et al. (2005) found overactivity in dopamine receptors in the basal ganglia of anorexics where dopamine plays a part in the interpretation of harm and pleasure.
Abnormal dopamine activity in BG alters the way we interpret rewards/ pleasure.
This explains why people with AN find it difficult to feel pleasurable feelings with food. This further contributes to their avoidance of meals.
Serotonin:
Bailer and Kaye 2011 – found that individuals with AN report high levels of anxiety prior to developing the disorder – believed this to be linked to high serotonin.
As high serotonin leads to anxiety in anorexics, if they are able to disrupt serotonin synthesis, they are granted temporary relief from anxiety.
Serotonin synthesis requires adequate levels of tryptophan, which is an amino acid.
When anorexics skip meals, they lack the nutrients to create tryptophan and thus serotonin.
As a result of not producing enough serotonin, their anxiety decreases.
Therefore, skipping meals acts as a way to regulate overactivity of serotonin and be able to improve their mood.
What did Kaye et al find for serotonin:
Kaye et al found that reduced tryptophan was linked to reduced anxiety in people with AN.
This suggests that self-starvation and eventual AN is caused by the desire to re-balance serotonin activity in order to avoid anxiety.
Evals:
- A weakness of genetic explanation of AN: reductionist.
- A weakness of genetic explanation: relies on twin studies which have a methodological flaw.
+ A strength of neural explanation: supporting evidence for the role of dopamine. - A weakness of the neural explanation; evidence it relies on is correlational.
A weakness of genetic explanation of AN: reductionist. This is bc it oversimplifies the complex beh of anorexia down to just the role of genes. In doing so, it ignores other factors that can contribute to development of anorexia, such as observation, imitation and vicarious reinforcement.
Vaughn and Fouts: carried out longitudinal study - found adolescent girls whose AN sympto severity increased over 16-month period also reported significantly greater fashion magazine reading over the same period.
WB: shows that you can in fact develop AN through SLT concepts like VR. E.g. The girls may see the models in the magazine receive praise and thus engage in anorexic behaviours in an attempt to imitate the models for the same reward.
Thus genetic explanation of AN is incomplete, thus reducing in validity.
A weakness of genetic explanation: relies on twin studies which have a methodological flaw.
Twin studies assume that the higher CR for beg in MZ than Dz twins is bc they share more genes (100% compared to 50%). This overlooks the possibility that the real reason behind the higher CR is due to MZ twins being treated the same (due to looking identical to each other)
The twin studies make the “equal environment assumption” when they assume that the environment that MZ and DZ twins share are equal in influence, when in reality, the env that MZ twins have, influence them greatly.
Thus the validity og twin studies is undermined, as a result the genetic explanation is undermined in validity.
A strength of neural explanation: supporting evidence for the role of dopamine.
Previous research has found that high levels of dopamine can lead to increased eye blink rate in people.
Barbato found increased eye blink rate in people with AN compared to control group (the longer duration of having AN - higher the blink rate)
SB: shows that it is plausible that increased dopamine may infact be responsible for anorectic tendencies such as avoidance of food and thus, subsequent weight loss. As the neural explanation assumes this, it increases in validity.
A weakness of the neural epxlanation; evidence it relies on is correlational.
The explanation argues that abnormal levels of dopamine and serotonin cause anorexia. However we do not know whether abnormal dopamine causes anoreixa or if it is simply a symptom.
If the former is true - explanation is validated. If the latter is true - cause of anorexia lies in another explanation.
E.g. AN may actually be caused by cognitive distortions (Fairburn et al who found that CBT-E is effective in treating anorexia symptoms in 2/3 of ppts - indicating that there is a cognitive element to anorexia which neural explanation doesnt account for.)
As neural explanation relies on correlational/ weak evidence, the neural explanation decreases in validity.
