QUESTIONS AND ESSAY PLANS
1(a). Outline factors that influence attitudes to food and eating behaviour (9 marks).
Paragraph 1 Introduction
Outline how classical and operant conditioning account for the effect of culture.
Explain how social learning and the learning of schemas also explain the influence of
culture. Use examples of cultural and sub-cultural variations to illustrate the effect
of culture.
Paragraph 2
Use comfort eating to explain the effect of mood on eating behaviour and so explain
that low mood can increase the amount of food consumed and that an anxious or
elated mood can decrease eating. Use chocolate to illustrate how classical and
operant conditioning and social learning theory can explain why this is sought as a
comfort food. Explain how brain biochemicals can account for a link between food
and eating, include tryptophan, and explain that this is a precursor of serotonin.
Explain how levels of serotonin have been linked to the tastiness of food and how
this may explain the over- or under-eating that can characterise depression (Heath
et al., 2006). Describe the effect of caffeine on mood and use Smith et al. (2003) as
evidence.
1(b). Discuss explanations for the success and failure of dieting. (16 marks)
Paragraph 1 Introduction
Explain that learning theory provides an explanation for the success or failure of
dieting. Operant conditioning could positively reinforce dieting behaviour and
weight loss, if the weight loss is successful, and so this would encourage the dieting
behaviour to be repeated. On the other hand, if the diet does not result in weight
loss, this would be seen as punishing and so would stamp out the dieting behaviour.
Evaluate this explanation. A positive is that it has face validity, but key weaknesses
are reductionism and the fact that cognitive factors are not considered.
Paragraph 2
Provide biological factors as a counter-perspective as the reason diets fail may be
less to do with environmental factors and more to do with biological reasons, such
as an imbalance of the hormone leptin. Evaluate that there is strong empirical
support for the role of leptin. The research evidence on the levels of leptin is
objective because such measures are biological and not open to bias. However, the
associated self-report of the levels of hunger are of course subjective and may be
biased by demand characteristics. Also discuss the contradictory evidence that
obese people have high levels of leptin. Then discuss how the leptin explanation has
been expanded on by Laposky et al. (2007) by their suggestion that leptin resistance
may be genetically predisposed. Evaluate the usefulness of such research due to the
potential research applications.
Paragraph 3
Evaluate the reductionism of the biological explanation, and use evidence such as
Truby et al.’s (2006) study to illustrate the importance of psychological factors, such
as the effect of operant conditioning, social support, and media interest. Note that de
Castro and de Castro (1989) provide evidence that dieting is not just biological but
psychological, as the amount of food eaten is strongly influenced by the number of
people present. Also note that it is too simplistic to just focus on dieting, as Miller et
al.’s (1997) research shows that dieting plus exercise is more effective than either
one on its own.
2(a). Describe the neural mechanisms involved in hunger and satiety. (9 marks)
Paragraph 1 Introduction
Introduce the fact that there are key centres in the brain that control hunger and so
these are the neural mechanisms involved in hunger (drive to eat) and satiety
(feeling of fullness that switches off the hunger drive). Describe how de Araujo et al.
(2006) researched the lateral hypothalamus, orbitofrontal cortex, insular cortex,
and amygdala. Then describe why the LH and VMH are known as the “stop/start”
switch of eating. Use the research evidence on animals to illustrate this. Describe the
neural mechanism that links the stomach to the hypothalamus.
Paragraph 2
Describe the role of hormones such as insulin and leptin in eating behaviour. Outline
evidence that shows the effect of lowering blood glucose level. Then outline
research that shows the effect of varying blood insulin levels (Rosenzweig,
Breedlove, & Leiman, 2002). Outline the research evidence into the effect of low
levels of leptin (London, 2007) and how this seems to affect brain structures such as
the insular, parietal, and temporal cortices and prefrontal cortex. Then describe the
role of the hormone PYY in reducing appetite, and outline Batterham et al.’s (2007)
research.
2(b). Discuss the evolutionary explanations of food preference. (16 marks)
Paragraph 1 Introduction
Introduce the universal human preference for foods rich in protein, fat, oils, and
sugar as evidence that we have evolved these preferences and so they are genetic
and hard-wired into us. Explain why such foods were adaptive in terms of energy
and growth and repair and use Eaton and Konner’s (1985) research into the
“paleolithic diet” as evidence for. Explain how the evolution of human brain size
may have driven our need for energy-rich foods. Provide evidence for this as it is
claimed that modern hunter-gatherers obtained an average of 40–60% of their
dietary energy from animal foods and these ancestral types were already obtaining
almost all of their dietary protein from animals.
Paragraph 2
Provide evidence against the “paleolithic diet” as it has been suggested humans have
evolved to be flexible eaters (Leonard, 2002). Rather than humans evolving for very
specific diets, it may be the other way round: that particular diets have driven
evolution, use Perry et al. (2007) as evidence. However, Perry et al.’s suggestion that
diet drove brain size can be criticised due to the timing of man’s ability to make fire.
Evaluate that there is a range of evidence from which we know about our ancestors’
diet, such as cave drawings and paintings, tooth-wear patterns from skulls, and
radioactive isotope analysis from buried refuse heaps. However, discuss the
limitations of evolutionary theory, such as the fact the theory is post hoc and how
this means there is a lack of scientific validity. The evolutionary explanations have
high face validity, and may explain the obesity epidemic of today’s society because
now more than ever we lead sedentary lives and so many of us eat more than our
energy requirements with the unnecessary calories being stored as body fat.
Paragraph 3
Criticise the explanations as deterministic and reductionist. Eating is not just about
survival and so the explanations focus solely on nature and ignore the role of
nurture. Explain how learning will also shape food preferences, such as particular
foods being enjoyed because they have been classically conditioned with positive
emotions, parents may have used certain foods as reward, and so evolution alone
cannot account for food preferences. Explain why a multi-perspective is needed.
3. Outline and evaluate biological explanations of one eating disorder. (25 marks)
This essay plan is based on anorexia nervosa but of course you do have a choice and so
could cover bulimia nervosa or obesity instead.
Paragraph 1 Introduction
Introduce genetic factors as the possible cause of anorexia nervosa and explain why
twin studies such as Holland, Sicotte, and Treasure’s (1988) have been used to test
the genetic explanation. Explain the difference between MZ and DZ twins and
summarise Holland et al.’s findings. Note that the similarity of Fairburn and
Harrison’s (2003) findings to Holland et al.’s shows reliability, and so supports the
validity of a genetic basis to anorexia nervosa. Outline Wade et al.’s (2008) findings
on the relationship between genetically predisposed temperament and anorexia.
Also note further support for a genetic basis is provided by Nisoli et al.’s (2007)
research, which found a common genetic basis across a number of
psychopathologies.
Paragraph 2
Provide evidence against the genetic basis, such as Loehlin and Nichols (1976) who
point to the role of nurture, given that MZ twins are treated more similarly than DZ
twins. There is also the fact that genetic factors cannot account for the rise in
anorexia in recent years nor the large differences in the incidence of eating
disorders across cultures (Comer, 2001). Note how contradicting genetic factors and
supporting the role of nurture is covered in research such as Wade et al.’s (2008),
which suggests the role of the family, and Chambry and Eilles’ (2006) research into
male anorexia, which linked this to sexual identity.
Paragraph 3
Evaluate the genetics research, including the positives such as the strong genetic
research, for example a specific gene was identified in Nisoli et al.’s (2007) research,
and consider that the concordance rates for anorexia are relatively consistent across
studies. However, there are issues with the twin research such as the
methodological weaknesses of concordance studies. For example, the concordance
rates are not even close to 100% and research is based on small samples due to the
nature of such clinical research (i.e. finding twins where one has anorexia). Thus,
explain why the genetics research provides evidence of predisposition, not cause.
Paragraph 4
Introduce biochemical imbalances as another biological explanation, which may
inter-link with genetics as they may be genetically predisposed. Use BachnerMelman et al.’s (2007) research as evidence as they have linked particular genes to
anorexia and neurochemical receptors. Also, describe how molecular genetics
research is focusing on serotonin-related genes. Research has linked anorexia to
high levels of serotonin. Explain how anorexia may be a “self-cure” for this anxiety.
Comment that the key weakness of this research is that we cannot establish if
biochemicals are a cause, effect, or correlate.
Paragraph 5
Another biological explanation is brain structural abnormality, so explain how
hypothalamus dysfunction may explain anorexia nervosa. Then evaluate that the
limitation is the same as the biochemical explanation, as we cannot establish if
biochemicals are a cause, effect, or correlate.
Paragraph 6
Give an overall evaluation of the biological explanations and come to a conclusion.
Consider the fact that the explanations are scientific and objective, deterministic,
and reductionist, and so do not account for social and psychological factors, the
difficulty of separating nature and nurture as influences, and the compromise
position of the diathesis–stress model.
4. Outline and evaluate psychological explanations of one eating disorder. (25 marks)
This essay plan is based on anorexia nervosa but of course you do have a choice and so
could cover bulimia nervosa or obesity instead.
Paragraph 1 Introduction
Introduce the psychodynamic approach by explaining it looks to unconscious
conflicts from childhood as the basis of the eating disorder. For example, anorexia
nervosa may be due to fear of increasing sexual desires and eating being seen as a
form of oral impregnation. Another psychodynamic explanation suggests anorexia is
a way to arrest sexual development. Family systems theory also looks to childhood
experience as the cause and suggests anorexia develops in response to an enmeshed
family (Minuchin et al, 1978). In a similar vein, explain how Bruch (1991) links
anorexia to a struggle for identity and autonomy. Thus, a high level of conflict
characterises the interactions of families with an anorexic child.
Paragraph 2
Introduce Hsu (1990) as evidence against, and explain how this raises the issue of
cause and effect. Then comment on the generalisability of some of the explanations.
This is an issue because some of them only relate to adolescent girls. Discuss the
issues of scientific validity because the evidence lacks objectivity and the concepts
are difficult to test because they cannot be operationalised.
Paragraph 3
Outline the cognitive explanation: that eating disorders are due to cognitive
distortion of body image. Give evidence for, including McKenzie et al. (1993). Then
describe how obsessive thinking and perfectionism may explain the disorder (Pike
& Rodin, 1991). Evaluate the cognitive explanations. Comment on the positive as the
evidence for is scientific. However, on the other hand, explain there is the problem
of cause and effect.
Paragraph 4
Introduce cultural explanations by explaining social learning theory, in particular
the processes of vicarious reinforcement and direct reinforcement through operant
conditioning. Cite evidence for, such as Barlow and Durand (1995), Nasser (1986),
and the fact that anorexia is a culture-bound syndrome, as shown by Sing (1994).
Paragraph 5
Consider the evidence against by Cooper (1994), who points to the fact that the
distorted beliefs held by anorexics are merely exaggerated versions of the beliefs
held by society at large. Explain why this means the cultural explanation lacks
explanatory power and how this links to the fact that operant conditioning does not
account for differences in the perception of reinforcement. Discuss how social
learning theory does account for cognition and so has greater validity than operant
conditioning. Also comment on the determinism and reductionism of behavioural
explanations.
Paragraph 6
Give an overall evaluation of the psychological factors, such as they consider a
number of causes. However, any one explanation can only partly explain anorexia.
Use the biological evidence as a counter-perspective because of course there is
strong evidence for biological factors in anorexia. Conclude that the diathesis–stress
model offers a more comprehensive account, and that an idiographic rather than a
nomothetic approach is needed.