Eating Behaviour Anorexia Nervosa Unit PSYA3. AQA A Specification Eating behaviour Factors...

Click here to load reader

  • date post

  • Category


  • view

  • download


Embed Size (px)

Transcript of Eating Behaviour Anorexia Nervosa Unit PSYA3. AQA A Specification Eating behaviour Factors...

  • Slide 1
  • Eating Behaviour Anorexia Nervosa Unit PSYA3
  • Slide 2
  • AQA A Specification Eating behaviour Factors influencing attitudes to food and eating behaviour. For example: cultural influences; psychological influences (mood); and social influences (health concerns/media). Explanations for the success and failure of dieting. Biological explanations of eating behaviour Neural mechanisms involved in controlling eating behaviour. Evolutionary explanations of food preference. Eating disorders In relation to either anorexia nervosa or bulimia nervosa: Psychological explanations. Biological explanations, including neural and evolutionary explanations. What we have covered Where we are now
  • Slide 3
  • What will we cover today? Biological explanations Genetic basis? Serotonin Dopamine Lateral hypothalamus Neurodevelopmental factors Evolutionary explanations Reproductive success hypothesis Adapted to flee famine hypothesis
  • Slide 4
  • Does AN have a genetic basis? Twin studies (Holland et al, 1984) Looked at the concordance of AN between: - 1)Identical twins monozygotic (MZ), 100% of genes in common. 2)Non-identical twins dizygotic (DZ), 50% of genes in common. If the underlying cause of AN is genetic, then there should be a higher concordance in MZ twins than in DZ twins (due to genes). 56% of MZ twins both had AN compared to only 5% of DZ twins. This suggests
  • Slide 5
  • Evaluation Twin studies (Holland et al, 1984) Reductionist only takes one factor (genes) into account. The concordance rate for MZ twins was well below 100%. This suggests For example, MZ twins may be treated more similarly than DZ twins as they look more alike and therefore they may display similar behaviours (environmental explanation). Could be that genetics provide a predisposition to AN but other factors also contribute and trigger the onset of AN.
  • Slide 6
  • Neural explanations Changes in the nervous system The role of serotonin in the development of AN Read the two studies in your booklet and answer the associated questions. You have 10 minutes.
  • Slide 7
  • Evaluation of serotonin -Selective serotonin re-uptake inhibitors (SSRIs drugs), which alter the levels of serotonin in the brain, are ineffective when used with AN patients. -I.e. using SSRIs to maintain/decrease the level of serotonin does not aid the recovery of AN patients. -This suggests
  • Slide 8
  • Evaluation of serotonin However, Kaye et al (2001) found that SSRIs were effective in preventing relapse and maintaining remission in recovering AN patients. This suggests that malnutrition-related changes in serotonin function may block the action of SSRIs, and that these drugs only become effective when the individuals weight returns to a normal level (i.e. when in recovery/remission to prevent a relapse).
  • Slide 9
  • Evaluation of serotonin Difficult to establish cause and effect. Is this dysfunction in serotonin levels a cause of AN OR is it a result of AN?
  • Slide 10
  • Dopamine and AN Kaye et al (2005) 10 women recovering from AN and 12 healthy women. Compared activity of dopamine receptors in the Basal Ganglia using a PET scan of the brain. In this part of the brain, dopamine receptors plays a role in the interpretation of rewards and pleasure, as well as weight and feeding behaviours. FINDINGS: AN women increased activity of dopamine receptors in the Basal Ganglia.
  • Slide 11
  • Dopamine and AN Kaye et al (2005) This suggests that alteration in dopamine function (i.e. increased dopamine activity) in this brain area appears to alter the way AN patients interpret rewards. For example, it suggests that AN patients may have difficulty associating good feelings with things that most people find rewarding and pleasurable, i.e. food.
  • Slide 12
  • Evaluation of dopamine and AN + Research has found that adolescents with AN had higher levels of homovanillic acid (a waste product of dopamine) than a control group. Improvement in weight levels was associated with normalisation of homovanillic levels. This supports and suggests - Difficult to establish cause and effect. - Is this increase in dopamine activity a cause of AN OR is it a result of AN?
  • Slide 13
  • Brain areas The development of AN can be linked to the hypothalamus. Which part of the hypothalamus is linked to hunger? Lateral hypothalamus. If this area is damaged, what happens? Loss of appetite, no feelings of hunger. How can we relate this to AN? If the LH is damaged in AN patients this could partially explain why they starve themselves as they do not experience feelings of hunger. However, it is much more likely that the development of AN is due to many factors, not just damage to the LH which results in undereating. For example
  • Slide 14
  • Independent task Complete the gap fill exercise on neurodevelopment explanations of AN. You have 10 minutes.
  • Slide 15
  • Treatment implications (IDA) Biological explanations of AN offer the promise of a range of treatment possibilities including: - Drug therapies to normalise NT levels (serotonin and dopamine). If we could use an individuals genetic profile to indicate the level of risk of AN, we could develop a specifically tailored intervention programme for those susceptible to developing AN. + Dealing with dysfunctional biology which is treatable using drugs.
  • Slide 16
  • Real-world application Implication of insurance pay-outs for psychiatric conditions. E.g. In the USA, treatment for AN is restricted under many insurance plans as it is not considered to be biologically-based. This research (serotonin/dopamine/lateral hypothalamus) creates a case for insurance companies to consider AN in the same way as other psychiatric conditions (e.g. schizophrenia) that are considered to be biologically based.
  • Slide 17
  • IDA Gender bias Most studies on eating disorders have studied females. However recent statistics indicate that 25% of the cases reported are male. Has AN increased in males? Or did they just escape attention/diagnosis before? Clearly it is not exclusively a female problem. Can the findings be generalised if most studies are on females? Could be different causes of AN for the different genders. Now, write your own!!!
  • Slide 18
  • A summary so far The development and maintenance of AN Dysfunction of Serotonin levels Increased Dopamine activity in the Basal Ganglia Role of the Lateral Hypothalamus Neurodevelopment pregnancy, birth complications and season of birth
  • Slide 19
  • Over Easter Read the page in your booklets on evolutionary explanations of AN: - 1)The reproductive suppression hypothesis 2)The adapted to flee famine hypothesis (AFFH) Essay structure for EDs Q.