Eating Behaviour

1. Eating Behaviour Anorexia Nervosa Unit PSYA3

2. AQA A Specification Where we are now What we have covered

3. Biological explanations • Genetic basis? • Serotonin • Dopamine • Lateral hypothalamus • Neurodevelopmental factors Evolutionary explanations • Reproductive success hypothesis • Adapted to flee famine hypothesis What will we cover today?

4. Twin studies (Holland et al, 1984)Looked at the concordance of AN between: - • Identical twins – monozygotic (MZ), 100% of genes in common. • 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… Does AN have a genetic basis?

5. 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. Evaluation

6. 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. Neural explanationsChanges in the nervous system

7. 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… Evaluation of serotonin

8. 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 individual’s weight returns to a normal level (i.e. when in recovery/remission to prevent a relapse). Evaluation of serotonin

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? Evaluation of serotonin

10. 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. Dopamine and AN

11. 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. Dopamine and AN

12. + 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? Evaluation of dopamine and AN

13. 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… Brain areas

14. Complete the gap fill exercise on neurodevelopment explanations of AN. You have 10 minutes. Independent task

15. 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 individual’s 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. Treatment implications (IDA)

16. 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. Real-world application

17. 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!!! IDA

18. 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 A summary so far…

19. Read the page in your booklets on evolutionary explanations of AN: - • The reproductive suppression hypothesis • The ‘adapted to flee famine’ hypothesis (AFFH) • Essay structure for EDs Q. Over Easter…