Anorexia Nervosa

• The term 'nervosa' indicates a mental health condition not just physical.
• The DSM-IVR Diagnostic and Statistical Manual for mental disorders identifies 3 categories of eating disorder:

  1. Anorexia Nervosa (AN)
  2. Bulimia Nervosa (BN)- episode of binge eating, self-induced vomiting
  3. Eating disorder not otherwise specified (EDNOS)- mixture of symptoms from other eating disorders
• Symptoms of Anorexia nervosa: (not assessed on this)

  • Body weight 85% or less of normal weight for age/ height
  • Distorted perception of weight/ shape/ size & denial the weight loss is severe
  • Intense fear of becoming fat or gaining weight
  • Loss of 3 consecutive menstrual cycles (women only)
• Two types of Anorexia nervosa:

  1. Restricting- doesn't regularly engage in binge eating
  2. Binge-purge- engages in binge eating, then self-induced vomiting
• Common themes of eating disorders:

  • distorted view of current self
  • fear of weight gain
• Biological explanations of Anorexia nervosa:- AFFH

  • Adapted to flee famine hypothesis
  • In our evolutionary past, the 'hunter-gatherer' humans may have had to regularly migrate when they had exhausted local food supplies.
  • During this time, it would be an advantage to be able to ignore/ deny hunger and be active during times of famine to enable our ancestors to travel to new locations.
• AFFH Evaluation:

  • Strength- does explain denial of hunger & activity
  • Weakness- doesn't explain why eating disorders are mainly found in women, impossible to test scientifically.
• Genetic Theory:

  • In explaining Anorexia Nervosa: suggests there's a gene or group of genes that can cause a person to develop the disorder or at least be more vulnerable to developing the disorder.
  • The gene may have the effect of altering brain chemistry or structure in such a way that leads to the behaviours seen in an AN sufferer. If this was the case, we would expect AN to run in families, as it can be passed from parents to offspring.
  • If genes do play a role, it is likely that they make a person more vulnerable to developing the disorder rather than directly causing it.
• Holland et al 1984 study:

  • Aim: to investigate the genetic contribution to AN using monozygotic & Dyzogotic twins where one of each has AN.
  • If AN was entirely genetic then there would be 100% concordance in MZ twins and around 50% in DZ twins.
  • Method: used 16 MZ female pairs & 14 DZ female pairs.
  • Results: for MZ twins, if one twin had AN, the other has a 55% chance of developing the disorder, compared to a concordance rate of just 7% for DZ twins.
  • Conclusion: there is a significant genetic component to Anorexia nervosa.
• Evaluation of genetic theory- weaknesses:

  • Small sample size in Holland et al's study
  • Nearly all studies are done in Western cultures (cultural bias) as well as using females (gender bias).
  • Twins with Bulimia Nervosa & Anorexia Nervosa are rare, therefore studies usually have low participant numbers or do not measure Anorexia Nervosa.
  • Very inconsistent data- some find high heritability factors and some much lower, making data less reliable.
• Dopamine & Anorexia Nervosa:

  • AN sufferers have over-activity in dopamine receptors of the basal ganglia.
  • Dopamine plays a part in the interpretation of pain & pleasure and it is thought that this altered dopamine activity in AN sufferer means they find it hard to associate pleasure with things most people would, ie food.
  • High dopamine also associated with psychosis (ie inaccurate perception of reality).
• Kaye et al (2005) used PET scans to reveal that recovering AN sufferers had over-activity in the dopamine receptors of the basal ganglia, compared to healthy controls- 10 Anorexia nervosa women & 12 healthy women.
• Evaluation of Dopamine & Anorexia nervosa- weaknesses:

  • Gender bias
  • Small sample
  • We don't know whether the over-activity in dopamine receptors causes anorexia, or if it's perhaps an effect of the disorder rather than the cause. It is possible that the lack of nutrition has caused the changes in the synapses.
• There is support for dopamine & Anorexia nervosa: increased blinking is a known sign of high levels of dopamine in the brain and research has shown a link between anorexia nervosa and increased blinking. Barbato's research also demonstrated a relationship between blink rate & duration of symptoms.
• Serotonin and Eating Disorder:

  • Serotonin= a neurotransmitter in the brain (is a biological explanation)
  • Serotonin is linked to depression & OCD
  • It makes sense to look at serotonin as being implicated in the cause of anorexia, as the symptoms of anorexia have similarities with those of both depression & OCD (feeling low, obsessing about weight & the compulsion to exercise or avoid food etc).
• Serotonin & Eating Disorder:

  • Theory suggests that those who suffer from anorexia have a higher level of serotonin in the brain (although sometimes lower).
  • It may also be that sufferers have fewer serotonin receptors than healthy individuals and that this therefore causes more serotonin to be released to combat this, and that this may be a cause of the eating disorder.
• Serotonin & ED- Bailer (2007): 1

  • Shows strong link between anxiety and binge-purge type of anorexia.
  • Using sophisticated brain scans, they showed significantly higher serotonin activity in several parts of the brain of women who had recovered from the bulimia type form of the disorder.
  • The highest levels in this group were found amongst those women who showed most signs of anxiety.
• Serotonin & ED- Bailer (2007): 2

  • The researchers say their work suggests that persistent disruption of serotonin levels may lead to increased anxiety, which may trigger anorexia.
  • However, they could not rule out the possibility that serotonin levels were altered by the malnutrition associated with the disorder.
• Serotonin & ED- support: 1

  • The use of PET scans & injected chemicals that bind with serotonin receptors in the brain showed that people with ED had reduced numbers of serotonin receptors- shows that anorexia sufferers have lower numbers of serotonin receptors (supporting the theory)
  • This has been shown even in people who have recovered from the disorder- showing that it is not down to low nutrition levels as suggested by some psychologists.
• Serotonin & ED- support: 2

  • However, lack of nutrition can cause chemical changes in the brain and if someone had an ED for long enough, this effect on the brain could last long after recovery.
  • Therefore, this may be a side effect of the illness, not the cause.
  • The only way to really overcome this would be to test someone before the onset of an ED, but this is not possible as the disorders are rare.
• Evaluation of serotonin & ED- :/:

  • Reductionism/ free will vs determinism- these theories suggest that eating disorders are not down to free will, but rather by pre-determined biological factors.
• Evaluation of serotonin & ED- :/:

  • The role of the media is completely ignored despite being known as an important risk factor.
  • Vaughn & Fouts (2003) found for girls whose Anorexia nervosa symptoms severity increased over a 16 month period, also reported an increase in reading fashion magazines over the same period.