13.3.1 Biological Explanations for Anorexia Nervosa

• Anorexia nervosa (AN) is characterised by an obsessive desire to lose weight by refusing to eat
• Genetic explanations for AN were first developed after research published in 2003, identifying candidate genes involving appetite, anxiety, and depression that were all unusual in people with anorexia (Bergen et al, 2003)
• Evidence from twin, adoption and family studies indicates an increased risk for individuals with close relatives with AN, which suggests that the disorder is in part genetically transmitted.
• first degree relatives of individuals with AN have a 10 times greater chance of developing AN than relatives of unaffected individuals (Strober et al, 2000)

Sisters are an example of first degree relatives.

• Neural explanations see AN as resulting from abnormally functioning brain mechanisms and functions
• The insula dysfunction hypothesis argues that  the insula brain area, which is  part of the cerebral cortex, develops differently in individuals with anorexia
• The insula dysfunction hypothesis arose from the observation that many symptoms of AN are associated with dysfunction in several brain areas, all connected to the insula, which is responsible for more neural connections than any other part of the brain
• The neurotransmitter serotonin has also been linked with the onset and maintenance of AN, because of its link to anxiety, as reducing eating also reduces serotonin levels  (Bailer et al, 2007) 
• Those with high levels of serotonin may feel compelled not to eat as they realise it makes them feel better emotionally because of the reduction of serotonin and consequently the reduction in anxiety
• Dopamine has been shown to have a role in AN, as increased dopamine activity in the Basal ganglia appears to alter the way that individuals interpret rewards (Kaye et al, 2005)

Serotonin can trigger anxiety over eating.

Research which investigates biological explanations for anorexia nervosa

• Strober et al. (2000) used clinical interviews and family history to compare rates of AN in first-degree relatives of those with AN with first-degree relatives of individuals who were not experiencing AN, and found that those related to AN sufferers were 11.3 times more likely than the control group to have AN, supporting the genetic explanation for AN
• Oberndorfer et al (2013) conducted a quasi-experiment using fMRI scans to compare the brains of those with AN with a control group and found that participants with anorexia had reduced responses to sweet tastes in the right anterior insula brain area, supporting the neural explanation for AN

Evaluation of  biological explanations for anorexia nervosa

Strengths

• There are practical applications of neural explanations for anorexia as an imbalance in neurotransmitters could be treated using drug therapy
• The genetic argument is strong, because genes may also exert an indirect influence upon the development of AN, as many sufferers display perfectionist personality characteristics and three genes associated with AN are also associated with perfectionist personality (Bachner-Melman et al, 2007)

Weaknesses

• Although research indicates that genes are a factor in the development of anorexia, the fact that multiple genes are involved makes it difficult to identify and quantify the role of individual genes
• The research is correlational and it may be that the levels of serotonin and dopamine found in people with anorexia are an effect of the malnutrition associated with AN, rather than a cause of the disorder

Link to Issues & Debates: 

The biological explanations for AN are biologically reductionist. They state that the eating disorder has its origins in the genetic make-up of the individual or in an imbalance in the neurochemistry. This is ignoring psychological and environmental explanations that would make explanations for this eating disorder more holistic.

The research into AN is gender biased, being conducted mainly on females, as they are many times more likely to suffer from anorexia than males (NIMH, 2017). This means the research has a beta bias, with the results being applied to men, who may have neurotransmission differences when compared to women.