A* AQA A-Level Psychology Eating Behaviour 16 Mark Model Essays
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Course
Eating
Institution
AQA
9 comprehensive, fully-developed exemplar essays (16 / 16 marks) covering questions that have appeared in past papers, as well as 6 predicted essays that haven't yet been asked in an exam, increasing the likelihood that they will appear as questions in the 2025 examination series. As well as featur...
1. Outline and evaluate Social Learning Theory of anorexia nervosa (16 marks)
Social learning theory suggests that a person may be more likely to develop anorexia nervosa (AN) if
they have restricted eating behaviours modelled to them. For example, an older sibling who limits
their food intake and is then praised by other members of the family for their slim figure. The sibling
acts as a role model with whom the child identifies, making imitation of their behaviour more likely.
Seeing the sibling being praised for their disordered eating behaviour serves to vicariously reinforce
that this behaviour is aspirational to the child. Alternatively, social learning theory suggests that
someone may develop AN from role models in the media who advocate for extreme diets or who
have an unrealistically thin body shape. The child may experience direct reinforcement for weight
loss from friends and family. Research from Dittmar et al. supports the idea that young girls who are
exposed to images of Barbie dolls - whose thinness they associate with glamour and popularity -
report higher body shape dissatisfaction and lower self-esteem.
One strength of social learning theory (SLT) as an explanation for AN is that it has been supported by
the findings of Becker et al. The researchers aimed to measure whether the introduction of Western
media - in the form of television broadcasts - to the island of Fiji changed the way that girls living
there perceived their bodies. In 1995, 63 girls completed a questionnaire, of which 13% gained a
high score, indicating a high risk of developing AN. In 1998, after TV broadcasts were made available,
a different sample of 65 girls completed the questionnaire; 29% scored highly. This suggests that the
media plays a significant role in creating risk factors for AN. However, the study was flawed because
it used a different sample of girls in 1995 and 1998, which means that it may have been confounded
by participant variables.
Further research support for SLT as an explanation for AN comes from Chisuwa and O’Dea. They
investigated the increase in incidences of AN amongst Japanese populations over the last 40 years
and found that it was mostly young women who read Western fashion magazines who had become
more likely to develop AN. Whereas the ideal body shape in Japan had traditionally been that of
‘plumpness’, indicating wealth and fertility, this had been supplanted in recent years with the
Western ‘thinness’ ideal. Again, this provides evidence that the globalisation of media has an impact
on how likely people are to develop AN.
However, one limitation of using SLT to explain the development of AN is that it does not offer
effective treatment. Simply showing people with AN images of a more realistic body shape does not
help them to recover from the disorder. In contrast, biological explanations for AN have helped to
develop drugs that represent convenient, cost-effective and proven treatments, helping patients to
return to some form of normality. Some would therefore argue that it is more beneficial to explain
AN in terms of its neurochemical causes, rather than in terms of observation and imitation, because
this has a more positive impact on recovery options.
2. Outline and evaluate the genetic explanation for obesity (16 marks)
The genetic explanation for obesity considers obesity to be a product of heritable genes and
therefore its main mode of investigation is twin studies and genome sequencing. Chaput et al. found
a 20 - 50% concordance rate for obesity among first-degree relatives, indicating a moderate degree
of heritability. However, Nan et al. carried out a meta-analysis of 12 studies and found a 60 - 80%
concordance rate among both DZ and MZ twins, suggesting a much more substantial genetic
, component. Meanwhile, Locke et al. studied the genomes of over 300,000 people and found 97
genes associated with variations in BMI. These accounted for just 2.7% of BMI variation, which is a
small fraction of the heritability of obesity. This suggests that obesity may have a genetic cause, but
it is polygenic. The neural explanation, on the other hand, focuses on the role of neurotransmitters
such as serotonin and dopamine. Obese people may have lower levels of serotonin, resulting in
accurate satiety signals being sent to the brain. Serotonin usually activates the VMH, inhibiting the
LH, and causes us to stop eating. Without this mechanism, obese people are prone to overeating,
weight gain and craving fatty, high-calorie foods. Low levels of serotonin linked to disinhibited
eating. Wang et al. found that obesity is also associated with having fewer dopamine receptors
(called D2 receptors) in an area of the brain called the striatum. Dopamine levels increase when we
eat food, stimulating a pleasure response. If someone has fewer D2 receptors, they have to eat more
in order to activate their reward systems, leading to obesity
One limitation of the genetic explanation for obesity is that it is most appropriate in the context of
the diathesis-stress model. Arguably, someone does not inherit their obesity, but a predisposition to
it. It is dependent on an environmental trigger whether obesity is expressed or not in their
phenotype. For example, a stressful situation such as exam week may cause a person with a
vulnerability to obesity to eat more, leading them to gain weight. Therefore, the genetic explanation
is not a complete one and should be viewed more as a contributing factor to a variety of others.
One strength of the neural explanation derives from research support by Ohia et al. The researchers
bred ‘knockout’ mice, enabling them to eliminate the gene for the serotonin (2C) receptor. These
mice therefore lacked serotonin and went on to develop late-onset obesity, suggesting a link
between low levels of neurotransmitter and weight gain. Research on the role of dopamine in
obesity has also been carried out. Spitz et al. found that one version of the DRD2 gene on the B1
allele (which is involved in coding for the D2 receptor) was twice as prevalent in people with obesity.
These participants were likely to have fewer D2 receptors, predisposing them to over-eat in order to
gain satisfaction.
One strength of the genetic explanation for obesity is that it is a plausible biological mechanism.
O’Rahilly and Farooqi have suggested that we may inherit a vulnerability to the sensory properties of
food which makes us more likely to be tempted to overeat. For example, some people may be
genetically more sensitive to the sights and smells of food, which makes it harder for them to resist.
This is a good example of how the genetic explanation can be applied in the context of our real-
world environment.
3. Discuss one or more explanations for food preferences (16 marks)
Food preferences can be explained by both evolutionary and learning theory. Evolutionary theory,
which includes Martin Seligman’s theory of biological preparedness, states that we have a
preference for foods that are high in salt (because it contains essential mineral ions), sugar and fat
(both of which indicate high-calorie foods. Eating these would have represented a survival
advantage to our ancestors by providing them with energy needed to reproduce, hunt prey and
escape from predators. This explains why Arya’s son only likes to eat sweet things, like ‘biscuits’.
Garcia and Koelling classically conditioned an aversion to sweetened water when it was paired with
poison in rats. We also acquired taste aversions to foods that are high in toxins, signalled by a sour
or bitter taste, because these would have threatened our ancestors’ survival. Neophobia - the fear of
eating new foods - arises around the age that infants are weaned off their mother’s milk and is an
adaptive response that would have ensured children did not eat foods that were not pre-approved
by their parents. Historically, many foods would have been unsafe to eat and babies who did not
have an innate aversion to trying them could have become ill and died.
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