Biological Explanations for Anorexia Nervosa (AQA A Level Psychology): Revision Note

Genetic explanations

• Anorexia nervosa (AN) is characterised by restriction of food intake leading to:

  • significantly low body weight

  • an intense fear of gaining weight

  • a distorted perception of body weight or shape

• Candidate gene research has searched for specific genes involved in AN. Scott-Van Zeeland et al. (2014) sequenced 152 candidate genes in 1,205 people with AN and 1,948 controls, and found only one gene significantly associated with AN:

  • epoxide hydrolase 2 (EPHX2) codes for an enzyme involved in cholesterol metabolism

• Twin studies compare concordance rates between MZ twins, who share 100% of their genes, and DZ twins, who share around 50%, so a higher concordance rate for MZ twins is evidence of a genetic component

  • Holland et al. (1988) studied 45 pairs of female twins where one twin had AN, and found a concordance rate of 56% for MZ pairs but only 5% for DZ pairs

  • Treasure & Holland (1995) replicated the study with less dramatic findings; 65% concordance for MZ twins compared with 32% for DZ twins, but this still provides strong evidence of a genetic role

• 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 around an 11 times greater chance of developing AN than relatives of unaffected individuals (Strober et al., 2000)

Neural explanations

• Neural explanations see AN as resulting from abnormally functioning brain mechanisms and functions

• The insula dysfunction hypothesis argues that the insula, a region of the cerebral cortex, develops or functions differently in individuals with AN

  • 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 densely interconnected with these regions

• The neurotransmitter serotonin has been linked to the onset and maintenance of AN, as serotonin is involved in appetite regulation and obsessive behaviours, both features of the disorder

  • Bailer & Kaye (2011) reviewed evidence of low levels of the serotonin metabolite 5-HIAA in people with AN, with levels returning to normal after short-term recovery and increasing beyond normal after long-term recovery, indicating underactivity of the serotonin system during illness

  • Attia et al. (2014) found that AN patients who had not returned to their pre-disorder weight responded less well to drugs that stimulate serotonin activity (serotonin agonists) than AN patients who had restored a healthy weight

• Dopamine has also been linked to AN, with lower levels of the dopamine metabolite homovanillic acid (HVA) found in people with AN compared with controls (Kaye et al., 1991)

  • Bailer et al. (2012) found that when given a drug that increases dopamine release, healthy participants experienced pleasure but participants with AN experienced anxiety, suggesting that restricting food may be a way of reducing dopamine release and therefore anxiety

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

  • They found that relatives of people with AN were 11.3 times more likely than the control group to have AN, supporting the genetic explanation

• Oberndorfer et al (2013) conducted a quasi-experiment using fMRI scans to compare the brains of those with AN with a control group

  • It was 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 people with AN display perfectionist personality characteristics, and three genes associated with AN are also associated with perfectionist personality (Bachner-Melman et al, 2007)

Limitations

• Twin studies of AN depend on the equal environments assumption, that MZ and DZ twins are treated with equal degrees of similarity

  • E.g., Joseph (2002) argues that MZ twins are treated more similarly than DZ twins by parents, teachers and acquaintances, and spend more time together

    • This greater environmental similarity means that heritability estimates may be artificially inflated, so genetic influences on AN may not be as great as twin studies suggest

• 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

Issues & Debates

• Biological explanations reduce a complex mental disorder like AN to biological components such as genes or neurotransmitter imbalances

  • They ignore the role of environmental triggers (e.g., family pressures, media) or psychological factors (e.g., body image distortion, perfectionism)

  • This oversimplified view risks missing out on more holistic treatment strategies

• However, a diathesis-stress explanation resolves this

  • E.g. Abraham (2008) argues that genes create a vulnerability (diathesis) to AN which is only expressed if the individual encounters stressors such as social, cultural or psychological pressures to lose weight

  • Other non-biological risk factors may then act as perpetuating factors, maintaining disordered eating once it has begun

• Biological explanations of AN may reflect beta bias, as they often assume the same biological mechanisms apply equally to males and females

  • However, AN is significantly more prevalent in females, and social/cultural pressures around body image differ greatly by gender, meaning these explanations may overlook important gender-specific influences

  • Minimising these differences may limit the development of gender-sensitive treatment and research