Example Answers for Section C Eating Behaviour… | tutor2u Psychology
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Example Answers for Section C Eating Behaviour Topic Paper 3 June 2018 (AQA)

  • Levels: A Level
  • Exam boards: AQA

Here are a series of suggested answers for the Eating Behaviour questions in AQA A Level Psychology Paper 3 (Section C) in June 2018.

Question 26: (2 marks)

Restraint theory is a cognitive theory for obesity. It suggests that deliberately limiting the amount of food you eat is counter-productive as it leads to a paradoxical outcome. The person becomes more preoccupied with food and therefore eats more, leading to obesity.

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Question 27: (2 marks)

One strength of restraint theory is that there is evidence to support it. Wardle and Beales randomly allocated obese women to 3 groups (diet, exercise or control) and found that the diet group (restrained eaters) ate more than either of the other two groups. This strongly suggests that restraining what you eat leads to obesity.

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Question 28: (4 marks)

Group A’s scores suggest a normal distributed as the mean, median and mode are all almost the same (22). However, group B’s scores suggest a positively skewed distribution as the mean (26) is higher than both the median (22.5) and the mode (16).

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Question 29: (16 marks)

One biological explanation for anorexia nervosa is that it is passed on through the genes. One candidate-gene association study sequenced 152 suspected candidate genes in a large sample and found only one gene (epoxide hydrolase 2) to be significantly associated with AN. This gene codes for an enzyme involved in the metabolism of cholesterol and abnormally high levels of cholesterol have been found in AN sufferers in the acute phase.

Evidence to support the genetic explanation comes from Holland et al., who found a concordance rate of 56% for MZ and 5% for DZ. MZ twins share 100% of their genes, compared to DZ twins who only share 50% of their genes, so this suggests that genes must have some influence on the development of AN. However, the concordance rate for MZ twins is not 100% which suggests that other factors must also be involved. In addition MZ twins may be treated more similarly than DZ twins and this may help to explain the higher concordance rate.

Neural explanations for AN focus on serotonin and dopamine. For example, Bailer et al. gave amphetamines to participants to increase the release of dopamine. They found that healthy participants reported euphoria (pleasure), but AN patients experienced anxiety. This suggests that individuals with AN might restrict their eating to try to reduce their anxiety levels.

Evidence to support this explanation comes from Kaye et al., who found that levels of homovanillic acid (a dopamine metabolite) are lower in those recovering from AN compared to control participants. These patients were normal weight and not restricting their diets, strongly suggesting that lower levels of dopamine are a causal factor in AN rather than an effect.

An evolutionary explanation for AN is the adapted to flee famine hypothesis which suggests that anorexia is a reflection of behaviours that were once adaptive. When our ancestors were hunter-gathers they needed to move on regularly as food supplies became exhausted. The key characteristics of people with AN are reslessness and high levels of activity and it is hypothesised they would help the individual to migrate in response to famine, thereby increasing the likelihood of survival, reproduction and passing their genes on.

However, while this helps to explain some of the characteristics of AN such as anxiety and denial of hunger, it is not able to explain why AN is found predominantly in women when it would have seemed more sensible for it to affect both men and women. It also leads to questions regarding how the symptoms of AN might be passed on by natural selection, as they decrease fertility and could even kill the individual suffering with it.

Biological explanations for AN can also be criticised for being biologically reductionist. By oversimplifying AN in terms of genes and neurotransmitters, the social context within which it develops has not been considered. For example, the biological approach is not able to explain cultural changes in AN and the way that incidence rates are increasing rapidly in non-Western cultures such as Japan. In order to explain schizophrenia effectively it would be better to take an interactionist approach, such as the diathesis stress model. This suggests that biological factors predispose someone to AN, but this has to be ‘triggered’ by some sort of experience or stressor which could be exposure to media representations of thinness or growing up in an enmeshed family.

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