EATING DISORDERS
To read up on eating disorders, refer to pages 208–227 of Eysenck’s A2 Level
Psychology.
Ask yourself
 What do you think are the characteristics of anorexia?
 What do you think are the characteristics of bulimia?
 What are the clinical characteristics of obesity?
 How can nature and nurture explain these disorders?
What you need to know
ANOREXIA
NERVOSA

Clinical
characteris
tics
according
to DSM-IV
criteria
BULIMIA
NERVOSA

Clinical
characteris
tics
according
to DSM-IV
criteria
BIOLOGICAL
EXPLANATIONS OF
ANOREXIA
NERVOSA AND
BULIMIA
NERVOSA

Biological
explanations,
including
neural and
evolutionary
explanations,
of one eating
disorder: for
example,
anorexia
nervosa,
bulimia
nervosa,
obesity
PSYCHOLOGICAL
EXPLANATIONS OF
ANOREXIA NERVOSA
AND BULIMIA
NERVOSA

Psychological
explanations of
one eating
disorder: for
example,
anorexia
nervosa, bulimia
nervosa, obesity
NOTE: you only need to cover ONE eating disorder. Anorexia and bulimia have been
covered together because many of the research studies and explanations apply to both
eating disorders. So do make sure you decide which disorder you will study. If you
decide you want to study obesity please refer to A2 Level Psychology (pages 218–223)
for details on this.
ANOREXIA NERVOSA
Clinical Characteristics According to DSM-IV Criteria
Weight: Less than 85% of that expected for height and body size.
Amenorrhoea: Menstruation is absent. Absence for three or more consecutive
cycles is sufficient for diagnosis.
Body-image distortion: Anorexics have a distorted idealised body image, and
perception of their own body weight is also distorted as they fail to recognise their
emaciation. Also, they overemphasise its importance to their self-esteem and
minimise the dangers of being underweight.
Anxiety: An intense fear of becoming fat, which is even more irrational given that
they are considerably underweight.
Physiological symptoms: Lowered body temperature, reduced bone mineral
density, low blood pressure, slowed heart rate, irregular heart rhythms, hair loss
and lanugo (soft downy hair on face, back, and arms).
Anorexia is particularly prevalent among certain individuals. Over 90% are female,
onset is usually during adolescence, and it is more common in middle-class than
working-class individuals. It is more common in people from Western cultures, but
is on the increase in populations in which it used to be rare (e.g. Black Americans)
because of the pervasiveness of Westernisation into subcultures and Eastern
cultures.
BULIMIA NERVOSA
Clinical Characteristics According to DSM-IV Criteria:
Binge: When more food is eaten within a 2-hour period than most people would
consume in that time, and the bulimic is not in control of their behaviour.
Purge: Compensatory behaviours, such as vomiting, laxatives, exercise, or skipping
meals to prevent weight being gained from the binge.
Frequency: Binge eating and compensatory behaviour must occur twice a week or
more, over a 3-month period, for diagnosis.
Body image: Bulimics have a distorted idealised body image, and perception of
their own body weight is also distorted as they fail to recognise that their weight
falls within the normal range. Also, they overemphasise the importance of body
image to their self-esteem.
Physiological symptoms: Calluses on fingers due to vomiting, erosion of teeth
enamel, lacerations in the lining of the mouth, and electrolyte imbalance, which can
lead to cardiac arrest.
Bulimia is prevalent in females and onset tends to be in their 20s. It is more
common in people from Western cultures and is more common in middle-class than
working class individuals.
BIOLOGICAL EXPLANATIONS OF ANOREXIA NERVOSA AND BULIMIA NERVOSA
Genetic Factors
RESEARCH EVIDENCE FOR GENETIC FACTORS
 Holland, Sicotte, and Treasure (1988, see A2 Level Psychology page 211)
studied anorexia in monozygotic (MZ, identical) and dizygotic (DZ, fraternal)
twins. A difference was sought between MZ and DZ twins, because MZ are
100% genetically identical whereas DZ have only 50% of their genes in
common. Thus, there should be a higher concordance rate for MZ than DZ
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twins if there is a genetic basis to anorexia nervosa. A significant difference
was found as there was a much higher concordance rate of anorexia for MZ
(56%—9 of 16) than DZ (7%—1 of 14) twins. Further findings were that in
three cases in which the non-diagnosed twin did not have anorexia they were
diagnosed with other psychiatric illnesses and two had minor eating
disorders.
Fairburn and Harrison’s (2003, see A2 Level Psychology page 212) findings
show a concordance rate of about 55% for MZ twins and 5% for DZ twins for
anorexia.
Wade et al.’s (2008, see A2 Level Psychology page 212) research into the link
between temperament and anorexia supports a genetic basis because
temperament is known to be genetically controlled. They found that
perfectionism, a high need for order, and sensitivity to praise and reward
were linked to anorexia. Whilst such traits could be the result of family
experience and culture, the researchers feel these shared risk factors must
be, in part at least, genetic.
Kendler et al.’s (1991, see A2 Level Psychology page 211) study on bulimia
found concordances of 23% for MZ and 9% for DZ twins. This supports a
genetic basis to bulimia.
Monteleone et al.’s (2007, see A2 Level Psychology page 213) findings suggest
that a gene involved in serotonin transmission, whilst not actually causing
bulimia, does seem to be involved in the predisposition to bulimia.
Nisoli et al. (2007, see A2 Level Psychology page 213) established that in a
group of over 100 Italian participants suffering from anorexia, bulimia, or
obesity that a gene previously associated with other psychopathologies such
as alcohol and drug abuse, the TaqA1 allele, is present in those vulnerable to
eating disorders.
RESEARCH EVIDENCE AGAINST GENETIC FACTORS
 The evidence for a genetic basis ignores the role of environmental factors or
nurture in causing anorexia or bulimia. The environment certainly plays a
role, because the concordance rate was for MZ twins are not even close to
100%, which they would be if eating disorders were exclusively due to
genetic factors. Key environmental factors include the fact that MZ twins
often experience a more similar environment and are treated more similarly
than DZ twins because they look and behave more alike (Loehlin & Nichols,
1976, see A2 Level Psychology page 211). However, nurture doesn’t fully
account for the considerable difference found between MZ and DZ twins.
 The recent dramatic increase in sufferers from eating disorders cannot be
explained in genetic terms because there have been no major genetic changes
over the past 20–30 years. Garner and Fairburn (1988, see A2 Level
Psychology page 210) reported figures from an eating disorder centre in
Canada. The number of patients treated for bulimia nervosa increased from
15 in 1979 to over 140 in 1986.




The large differences in the incidence of eating disorders across cultures
(Comer, 2001, see A2 Level Psychology page 211) can also not be accounted
for by genetic factors.
Wade et al.’s (2007 see A2 Level Psychology page 212) research on Australian
female twins showed that the families of anorexics and bulimics made
frequent comments about weight and shape whilst they were growing up;
and higher levels of paternal protection were associated with anorexia than
with bulimia whilst higher levels of parental expectation were associated
with bulimia than with anorexia. Thus, this shows the role of nurture and so
is evidence that anorexia is not just due to genetics.
Research into male anorexics is quite rare but one study into this suggests a
psychological basis and so challenges a purely genetic explanation. Chambry
and Eilles (2006, see A2 Level Psychology page 212) found that there is a
higher frequency of homosexual behaviour than in female anorexics and so
they have linked a vulnerable sexual identity to male anorexia.
Fairburn and Harrison’s (2003, see A2 Level Psychology page 212) findings
show a concordance rate of 35% and 30% for MZ and DZ twins respectively
for bulimia, which does not suggest a strong genetic basis for bulimia, as if
this was the case the concordance for MZ twins with identical genes should
be considerably higher than that for DZ who only share 50% of their genes.
EVALUATION OF RESEARCH EVIDENCE INTO GENETIC FACTORS
 Twin studies provide strong genetic evidence. As the MZ twins are
genetically identical whilst DZ twins are no more alike than ordinary siblings,
this supports the involvement of genetic factors. If these were not important,
and instead nurture was the key determinant, then there should be no
difference in the concordance rates between MZ and DZ twins.
 Methodological weaknesses of concordance studies. The evidence from
twin studies must be considered cautiously because diagnosis of the second
twin may be biased by the knowledge that the first twin has been diagnosed.
 Reliability. The concordance rates for anorexia are relatively consistent
across studies, which supports the reliability of the research and
consequently the validity of a genetic basis to anorexia. The concordances for
bulimia are not so reliable given that the difference between MZ and DZ
twins is 14% in Kendler et al.’s (1991) study and yet only 5% in Fairburn and
Harrison’s (2003) study and so the lack of reliability suggests there is not
such a strong genetic basis for bulimia as for anorexia.
 Not 100% concordance rates. Whilst exactly 100% concordances are
unlikely, as even in MZ twins with 100% the same genes there may be some
genetic variation due to epigenetics (i.e. the interaction of nurture in the
switching on or off of the genes), the research shows that the concordances
are not even close to 100%, which we would expect in identical twins if
genes were the main cause of eating disorders. The fact that there are no
100% concordance rates suggests that other factors must be involved.




Small samples. The data on much of the genetics research is from clinic
samples, which are obviously not representative of the general population,
particularly because such samples tend to be quite small (often fewer than
10) because of the difficulty of finding twins where one or both have an
eating disorder, which means that population validity is limited.
Environmental factors. The fact that concordance rates increase with
genetic relatedness may be explained by the fact that this is because they are
also likely to spend more time together, which means environmental factors
may be influential.
Predispose not cause. As the disorder is not wholly genetic this leads to the
conclusion that genes alone do not cause eating disorders; instead they
predispose, i.e. place the individual at a greater risk for developing the
disorder. See the diathesis–stress model in the “So what does this mean?”
concluding section to biological explanations for a more comprehensive
account of how genes predispose, rather than cause, the disorders.
A common genetic basis. Nisoli et al.’s (2007) findings that there is a
common gene associated with a number of psychopathologies has strength in
that a specific gene, the TaqA1 is identified and this may have useful
implications in terms of gene therapy. However, there is a lack of explanatory
power because it does not explain why one person develops a drug abuse
problem and the other an eating disorder.
Biochemical Factors
RESEARCH EVIDENCE FOR BIOCHEMICAL FACTORS
 Bachner-Melman et al. (2007, see A2 Level Psychology page 224) have
established that three genes associated with anorexia are also associated
with the personality trait perfectionism as measured on the Child and
Adolescent Perfectionism Scale (CAPS), and that these genes have neural
effects on dopamine receptors and receptors for other neurochemicals such
as growth factor. Thus, genes and biochemistry may interact.
 Carrasco et al. (2000, see A2 Level Psychology page 211) found that bulimics
tend to have low serotonin activity. Bingeing on starchy foods containing
carbohydrates can increase serotonin levels in the brain and improve mood,
and so may explain why bulimics have the urge to binge eat.
 Research has also linked anorexia to high levels of serotonin. High levels of
serotonin suppress appetite and increase anxiety and obsessive behaviour,
which of course are characteristics of anorexia. Restricting food may be a
form of “self-help” because serotonin levels will drop as a result of less food.
 Molecular genetic research is focusing on serotonin-related genes as
serotonin is known to be important in regulating eating and mood, and so
this suggest that genes and biochemicals interact in the aetiology of eating
disorders.
RESEARCH EVIDENCE AGAINST BIOCHEMICAL FACTORS
Patients with bulimia nervosa do not focus specifically on foods containing
carbohydrates when they binge (Barlow & Durand, 1995, see A2 Level Psychology
page 211).
EVALUATION OF RESEARCH INTO BIOCHEMICAL FACTORS
 Cause, effect, or correlate? The biochemical imbalances are difficult to
interpret, as it is difficult to determine if they are a cause or a consequence of
having the disorder. For example, low levels of serotonin in anorexia may be
due to insufficient food, or a consequence of the binge–purge cycle in
bulimics, and so biochemical imbalance may be an effect rather than a cause
of the disorder. It is only possible to conclude that biochemical imbalances
are associated with eating disorders rather than a being a cause.
Brain Structural Abnormality
RESEARCH EVIDENCE FOR BRAIN STRUCTURAL ABNORMALITY
 Hypothalamus dysfunction may be an explanation as this part of the brain is
involved in the control of hunger. In fact the ventromedial hypothalamus
(VMH) and the lateral hypothalamus (LH) are known as the “stop/start”
mechanisms for hunger. They maintain weight homeostasis because the LH
or “start switch” produces feelings of hunger and the VMH or “stop switch”
suppresses feelings of hunger. Anorexics may have an abnormality in the LH,
which produces feelings of hunger, and bulimics and obese individuals may
have an abnormality in the VMH, which suppresses hunger.
EVALUATION OF RESEARCH INTO BRAIN STRUCTURAL ABNORMALITY
 Cause, effect, or correlate? Causation is also an issue with the brain
structural abnormality explanation because we cannot be sure if the
abnormality is a cause or consequence of the disorder. This means causation
cannot be established and so it is only possible to conclude that brain
structural abnormalities are associated with eating disorders rather than
being a cause.
OVERALL EVALUATION OF BIOLOGICAL EXPLANATIONS
 Scientific and objective evidence. The biochemical levels and brain
structural abnormality provide objective evidence because such measures
are not very open to opinion or bias. Thus, the evidence for the biological
explanations has scientific validity, which means we can have more
confidence in the findings.
 Deterministic. The biological explanations can be criticised as biologically
deterministic because they ignore the free will and ability of individuals to
control their own behaviour. The explanations suggest that if someone has
particular genes or biochemical imbalances they will inevitably have an
eating disorder, which ignores the individual’s motivation to resist or
overcome eating disorder.


Reductionist. The biological explanations try to explain behaviour using
only one factor (biology) and so they are reductionist, which means they are
too simplistic and as a consequence the explanations lack conviction. For
example, the explanation that hypothalamus dysfunction may explain eating
disorders is oversimplified as motivation and cognition can override this to
some extent.
Do not account for social and psychological factors. The biological
explanations cannot account for the psychological aspects of eating
disorders, such as the distorted body image and intense fear of weight gain.
This is because the explanations ignore nurture, i.e. psychological and social
factors. For example, eating may be due to motivational rather than physical
factors. Similarly, biological explanations cannot explain the recent rapid rise
in eating disorders. Social and cultural factors are more likely to explain this
rise.
Evolutionary Explanations
Evolution predicts that if a behaviour exists over time then it must in some way be
adaptive (i.e. increase chances of survival) to have stayed in the gene pool. If it was
not adaptive it would have been weeded out through natural selection (the process
by which genes advantageous to survival are selected into the gene pool. This
suggests that anorexia nervosa, bulimia nervosa, and obesity are in some way
adaptive. Evolutionary explanations of food preferences have been covered above so
do refer back to this section as it provides insight into the evolutionary explanations
of eating disorder.
EVIDENCE FOR EVOLUTIONARY EXPLANATIONS OF ANOREXIA NERVOSA
 Inclusive fitness refers to the idea that behaviour may have evolved because
it benefits the group rather than the individual. The group members would
be related and so relatives would thrive at the expense of the individual. The
individual would be less likely to reproduce and so instead would achieve
reproductive fitness because the genes shared with the relatives would be
more likely to survive. This may explain anorexia as if one member of the
group ate very little then this would leave more food available for other
group members and this would be advantageous, particularly in hard times
when food became scarce.
 Another evolutionary hypothesis relates to rank theory, which is the idea
that the human struggle for survival results in a great deal of conflict. The
anorectic behaviour is a sign of accepting defeat after some sort of conflict
and so assuming a low position in the rank (Gatward, 2007, see A2 Level
Psychology page 214). The anorexia signals that the individual is weak and no
longer a threat.
EVIDENCE AGAINST EVOLUTIONARY EXPLANATIONS OF ANOREXIA NERVOSA
 It seems highly implausible that anorexia is adaptive. It seems more
maladaptive now so surely it would have been even more so in the more
harsh conditions of our hunter-gatherer world? The anorexic would be weak

and so a liability to the group. It seems unlikely that the gain in food to the
group would outweigh the time and care needed to support the anorexic
when very close to death.
Similarly, starving oneself seems an extreme way of showing submission,
which again suggests the hypothesis lacks validity.
EVIDENCE FOR EVOLUTIONARY EXPLANATIONS OF BULIMIA NERVOSA
 The binge aspect of bulimia can be explained as adaptive because our huntergatherer ancestors could not be sure when they would next eat as this
depended on the success of the hunt, and foods gathered would perish very
quickly. Individuals that could feast when food was plentiful and store this as
body fat would be better able to survive in times of famine. Clearly this would
increase chances of survival and, particularly in the case of females, it would
increase chances of reproduction as pregnancy and lactation require fat
reserves.
 Then a mutation could have linked the gene for bingeing with one that causes
the stomach to empty quickly if it became very full, thus producing the
purging behaviours.
EVIDENCE AGAINST EVOLUTIONARY EXPLANATIONS OF BULIMIA NERVOSA
 Bulimia like anorexia seems more maladaptive than adaptive. The purging
aspect could never be a healthy behaviour and so could not be called
successful.
 If genetic mutation caused the purging behaviour then it is not due to
evolution, which only accounts for behaviour evolving because it is adaptive.
Maybe all aspects of bulimia are due to genetic mutation rather than
evolution of the disorder as an adaptive behaviour.
EVALUATION OF EVOLUTIONARY EXPLANATIONS
 Maladaptive rather than adaptive. Evolutionary explanations seem highly
implausible. The idea that eating disorders are somehow beneficial in some
way is counter-intuitive to the extremely maladaptive nature of them. Mental
disorders are often very disturbing to the patient and may severely disrupt
their everyday functioning, thus we shouldn’t exaggerate any adaptive value
they may have.Why should a disorder be adaptive? It seems a real
contradiction in terms. The eating disorders would limit survival and
reproduction.
 Conjecture—evolutionary stories? Deciding what was adaptive in our
evolutionary past is highly speculative. Consequently, they have been
criticised as evolutionary stories because we have no way of establishing if
they are true or not.
 Post hoc and so lack scientific validity. We cannot research our
evolutionary past and so the evolutionary explanations are post-hoc (made
up after the event) hypotheses. The evidence we do have from fossils is very
limited especially in terms of human behaviour. They cannot tell us if bulimia




or anorexia were adaptive for our evolutionary ancestors. Thus, whilst
evolution itself is fact, the evolutionary explanations of human behaviour are
not, they are just speculation and cannot be verified or falsified. Karl Popper
identifies falsification as a key criterion of science and so on this basis the
explanations lack scientific validity.
Reductionist and deterministic. Evolutionary theories are reductionist as
they focus on one factor only (the gene) when other emotional, social,
cognitive, behavioural, and developmental factors are highly relevant to the
aetiology of eating disorders. They are oversimplified accounts at best. They
are also deterministic as they suggest that the genes control behaviour,
which ignores the free will of the individual. See the overall evaluation of
biological explanations for further elaboration of these criticisms.
Psychological explanations. The psychological explanations of eating
disorders are counter-perspectives and are ignored by evolution. Moreover,
they may account for why adaptive behaviours have become distorted. For
example, bingeing may have evolved as an adaptive response but
sociopsychological factors may explain why today such food consumption
creates anxiety and so is followed by purging.
Nature/nurture. The evolutionary explanations overemphasise the role of
nature and ignore nurture. It is not a question of nature or nurture, as
indisputably an interactionist perspective must be taken. However, as the
evolutionary explanations ignore nurture this is a key weakness.
Genetic transmission may not be adaptive. Eating disorders may not have
been weeded out because they are recessive, i.e. a person may carry the gene
but not exhibit the disorder, which only manifests when both parents carry
recessive alleles. Thus, it is naturally selected not because of increased fitness
but because it is difficult to eliminate, as recessive genes do not affect the
individual’s reproductive fitness. Another explanation is that nature did not
create perfect organisms. “Bottlenecks” in human evolution (when the
population was very small) meant genetic mutations could not be weeded
out in the usual way. Both of these possibilities, recessive alleles and
“bottlenecks”, suggest the disorders have been transmitted in spite of being
maladaptive and so challenge the evolutionary explanation that eating
disorders are adaptive.
SO WHAT DOES THIS MEAN?
It is hard to separate out the influence of nature and nurture or environment in the
development of eating disorders. It is oversimplified and reductionist to consider
only one factor, biology, as a basis for anorexia or bulimia.
The compromise position of the diathesis–stress model is more convincing than
biological explanations alone. According to this, the genes (nature) load the gun, but
it is the environment (nurture) that pulls the trigger. This means an individual may
inherit a vulnerability to a disorder (particular genes that cause biochemical and
brain structural abnormality: the diathesis), which places the individual at greater
risk of developing the disorder. But it is not inevitable that the disorder will develop
because it depends on the interaction of the diathesis with psycho-social stressors.
Thus, psychological and biological explanations, (i.e. a multi-perspective) are
needed to fully explain eating disorders.
OVER TO YOU
1. Outline and evaluate biological explanations of one eating disorder. (25 marks)
2(a). Outline the clinical characteristics of one eating disorder. (5 marks)
2(b). Critically consider the biological explanations of one eating disorder. (20
marks)
PSYCHOLOGICAL EXPLANATIONS OF ANOREXIA NERVOSA AND BULIMIA NERVOSA
Psychodynamic Explanations
RESEARCH/THEORY
 The psychodynamic approach suggests unconscious conflicts from childhood
may be the basis of eating disorder. The fact that the disorder is mostly found
in adolescent girls suggests that anorexia might be due to fear of increasing
sexual desires; denying oneself food is a way of repressing these sexual
desires. Another fear may be pregnancy, where eating may be seen as a form
of oral impregnation. Starvation is a way to avoid becoming pregnant
because one of the symptoms of anorexia nervosa is amenorrhoea (the
absence of menstruation).
 Another psychodynamic explanation suggests anorexia is a way to arrest
sexual development because the anorexic has an unconscious desire to
remain pre-pubescent. Their weight loss prevents them from developing the
body shape associated with adult females, and thus allows them to preserve
the illusion that they are still children.
 Family systems theory (Minuchin et al., 1978, see A2 Level Psychology page
215) suggests that the families of anorexics are characterised by conflict,
overprotectiveness, rigidity, and enmeshment, meaning that none of the
members of the family has a clear identity because everything is done
together. The enmeshed family is smothering and can lead to a lack of
identity. The child rebels against the family by refusing to eat. It is an attempt
to gain independence and take control.
 Family conflicts have also been identified in families with a child showing
signs of bulimia or anorexia. The number of negative interactions outweighs
the positive interactions. It is also suggested that the anorexia is a result of
parental conflicts because these are reduced by the need to attend to the
anorexic child.
 Bruch (1991, see A2 Level Psychology page 215) proposed that eating
disorders are due to the individual’s struggle for identity and autonomy.
There is conflict with the mother because she has never been able to identify
and successfully meet the needs of the sufferer. This is linked to food being
used as a comfort. Anorexia is a rejection of food as a reward as it is not used
for comfort, whereas bulimia involves using food as a reward to oneself. This
also suggests that the eating disorder is a way to take control.
RESEARCH EVIDENCE AGAINST PSYCHODYNAMIC THEORY
 Hsu (1990, see A2 Level Psychology page 215) reported that families with an
anorexic child tend to deny or ignore conflicts and to blame other people for
their problems. The problem is that these parental conflicts may be more a
result of having an anorexic child than a cause of anorexia.
EVALUATION OF PSYCHDYNAMIC EXPLANATIONS
 Conflict—cause or consequence? Family conflicts may be more a result of
having a family member suffering with an eating disorder, and so may be an
effect rather than a cause. Furthermore, many families have conflicts but this
does not necessarily result in abnormality, nor does it explain why the
disorders occur in women more than men.
 Generalisability. This is an issue because the psychodynamic explanations
based on sexual development only relate to adolescent girls. Anorexia is
more common in adolescent girls is not exclusive to them, so explanations
cannot explain anorexia in boys or adults.
 Psychodynamic explanations are subjective (not objective). They are
based on clinical interviews and case studies, which are vulnerable to
researcher bias. Because they are theory rather than evidence, this means
they are opinion rather than fact: they have not been tested rigorously and
objectively.
 Psychodynamic concepts are vague and hard to define so they cannot be
operationalised. This means they cannot be tested empirically and so can
neither be falsified nor verified. Nobody can prove they are right, but they
also cannot be proven to be wrong. This means the explanations lack
scientific validity because Popper identified falsifiability as an important
criterion of science.
Cognitive Explanations
RESEARCH EVIDENCE FOR COGNITIVE EXPLANATIONS
 People with eating disorders have a distorted view of their own body image
and what an ideal body image should look like. They place too much
importance on their weight and its role in their well being. They usually
overestimate their body size. Cooper and Taylor (1988, see A2 Level
Psychology page 216) reported an overestimation in patients with bulimia.
People with eating disorder also have a desired body size that is smaller than
it is for healthy women.
 Bulimics perceive their body size to be larger than do control individuals of
the same size, and they also mistakenly believe that eating a small snack has
a noticeable effect on their body size (McKenzie, Williamson, & Cubic, 1993,
see A2 Level Psychology page 216).
 Eating disorders are characterised by obsessive thinking about food and
weight gain. Recent research has also linked the disorder to perfectionism,
which involves the individual having impossibly high standards for
themselves. Individuals high in perfectionism may strive to achieve an
unrealistically slim body shape. The mothers of girls with disordered eating
often have perfectionist tendencies (Pike & Rodin, 1991, see A2 Level
Psychology page 216).
EVALUATION OF COGNITIVE EXPLANATIONS
 Scientific evidence. The research evidence on cognitive factors is scientific
as it is based on the experimental method. For example, the research on body
size distortion has been tested experimentally because eating disorder
patients are compared against control groups and their body image
distortion is measurable. This means the research has scientific validity.
 Cognitive dysfunction—cause or consequence? The cognitive
explanations can only explain eating disorders so far, as they do not explain
what caused the breakdown in information processing in the first place.
Moreover, they may be an effect rather than a cause of the disorder, in which
case they are a characteristic, rather than a causal factor.
Cultural Explanations
RESEARCH EVIDENCE FOR CULTURAL EXPLANATIONS
 Social learning theory explains that eating disorders develop as a result of
observation and imitation of role models. Such role models are seen as
successful and so the observer experiences vicarious reinforcement (i.e.
observes others experiencing rewards) and desires the same rewards for
themselves so that they can experience direct reinforcement through operant
conditioning.
 Evidence to support this is Barlow and Durand’s (1995, see A2 Level
Psychology page 217) findings that more than half of Miss America
contestants are 15% or more below their expected body weight, which of
course is one of the diagnostic criteria for anorexia.
 Nasser (1986, see A2 Level Psychology page 217) compared Egyptian women
studying in Cairo and London; none of those studying in Cairo developed
eating disorders, but 12% of those studying in London did. This shows the
influence of Western standards of idealised body images and that eating
disorders are linked to cultural norms and role models.
 The fact that eating disorders are considerably more common in Western
than Eastern cultures has led to them being classed as a culture-bound
syndrome. For example, about one woman in 200 suffers from anorexia
nervosa in Western Europe and the United States. In Hong Kong, in contrast,
only one person out of more than 2000 Chinese people sampled had anorexia
(Sing, 1994, see A2 Level Psychology page 217).
RESEARCH EVIDENCE AGAINST CULTURAL EXPALNATIONS
 Most of the distorted beliefs held by anorexic and bulimic patients are merely
exaggerated versions of the beliefs held by society at large (Cooper, 1994, see
A2 Level Psychology< pages 217–218). This means that the cultural
explanation fails to clearly discriminate between those who go on to develop
an eating disorder and those who do not, despite sharing similar concerns
about weight and body size.
EVALUATION OF CULTURAL EXPLANATIONS
 Cultural factors do not account for variations in vulnerability to eating
disorder. The great majority of young women are exposed to cultural
pressures towards slimness yet do not develop eating disorders, and so these
factors lack explanatory power as they do not explain why some people are
more influenced by these factors than others.
 Operant conditioning does not account for differences in the perception
of reinforcement. This can of course account for why some find weight loss
more rewarding than others. Operant conditioning does not account for such
differences because it ignores cognitive factors, which are considered
unscientific and not worthy of study as they are not observable or
measurable. Yet cognitive factors seem to be a causal factor, given the
cognitive distortions shown and the obsessive thinking many people with
eating disorders display.
 Social learning theory accounts for cognition and appears to be valid
(correct). Social learning theory is more sophisticated than the traditional
learning theories because it accounts for cognition in its explanation that we
can learn through vicarious reinforcement and imitation, as this involves
expectations and thought about which role model should be imitated and
what rewards can be expected. Moreover, it accounts for eating disorders as
a cultural phenomenon, as role models and social learning differ across
cultures. Research on cultural variations provides support for the validity of
social learning theory, as do patients’ accounts of their susceptibility to the
idealised body images shown in magazines.
 Deterministic. The behavioural explanations can be criticised as
environmentally deterministic because they imply that the environment
shapes behaviour, which ignores the free will of the individual to reject the
influence of the environment.
 Reductionism. The behavioural explanations are also reductionist because
they only consider nurture. They are too simplistic as they do not consider
other explanations for eating disorders such as biological and cognitive
factors.
SO WHAT DOES THIS MEAN?
The strength of the psychological explanations is that they cover a number of
factors. However, any one of these explanations on their own is reductionist as they
only consider one level of explanation. The strong evidence for a genetic basis
shows that psychological factors alone cannot account for eating disorders and so a
multi-dimensional approach is needed to fully account for eating disorders.
The compromise position of the diathesis–stress model best accounts for the
influence of nature (genes) and nurture (environment) and so is the most
comprehensive account of anorexia or bulimia. This means an individual may
inherit a vulnerability to disorder, (particular genes that cause biochemical and
brain structural abnormality: the diathesis), which places the individual at greater
risk of developing the disorder. But it is not inevitable that the disorder will develop
because it depends on the interaction of the diathesis with psycho-social stressors.
Thus, an interactionist and idiographic (individual) approach is needed, which
means that the factors may interact in different ways to explain the development of
the disorders in different individuals rather than there being one multi-factorial
explanation that accounts for development in all anorexics and bulimics. Such a
nomothetic approach, i.e. trying to provide a universal explanation, is
oversimplified.
OVER TO YOU
1. Outline and evaluate psychological explanations of one eating disorder. (25
marks)
2(a). Outline the clinical characteristics of one eating disorder. (5 marks)
2(b). Critically consider the psychological explanations of one eating disorder. (20
marks)