A"tudes

to Food and Ea.ng Behaviour

There are two explana.ons into a1tudes towards food and ea.ng behavior; SLT
and cultural inuences.
Banduras Social Learning Theory emphasises the idea that people observe
modeled behaviour from other people. Children may learn a1tudes and
behaviours towards ea.ng from their parents and the parents preferences and
sa.sfac.on. Through this vicarious learning, children will model the behaviour
themselves.
Brown et al found a consistent correla.on between ea.ng habits of parents and
their children in terms of snack food intake and body dissa.sfac.on. Moreover,
parents also mould a childs ea.ng habits as they dictate what kinds of food enter
the household.
The SLT is supported by Gast et al; boys and girls aged 10-12 were surveyed and
they found a +e correla.on between peer inuence and disordered thinking of
food. An important element that determined this correla.on was the likeability by
peers, which is in line with the SLT because the more the child iden.es with the
model the more likely the model will shape their behaviour.
Moreover, Fisher et al found that a good indicator of a daughters ea.ng habits
came from looking at their mothers restrained die.ng and how the mother
perceived the risks of their daughters becoming overweight. This would suggest
that daughters learnt behaviors from their mothers which supports this
explana.on.
SLT is also evident in the impact of TV and magazines as McIntyre found that the
media signicantly impacted what people ate and their a1tudes towards certain
foods e.g. new 5:2 diet fad.

A"tudes to Food and Ea.ng Behaviour

There are two explana.ons into a1tudes towards food and ea.ng behavior; SLT and cultural inuences.
Banduras Social Learning Theory emphasises the idea that people observe modeled behaviour from other
people. Children may learn a1tudes and behaviours towards ea.ng from their parents and the parents
preferences and sa.sfac.on. Through this vicarious learning, children will model the behaviour themselves.
Brown et al found a consistent correla.on between ea.ng habits of parents and their children in terms of
snack food intake and body dissa.sfac.on. Moreover, parents also mould a childs ea.ng habits as they dictate
what kinds of food enter the household.
The SLT is supported by Gast et al; boys and girls aged 10-12 were surveyed and they found a +e correla.on
between peer inuence and disordered thinking of food. An important element that determined this
correla.on was the likeability by peers, which is in line with the SLT because the more the child iden.es with
the model the more likely the model will shape their behaviour.
Moreover, Fisher et al found that a good indicator of a daughters ea.ng habits came from looking at their
mothers restrained die.ng and how the mother perceived the risks of their daughters becoming overweight.
This would suggest that daughters learnt behaviors from their mothers which supports this explana.on.
SLT is also evident in the impact of TV and magazines as McIntyre found that the media signicantly impacted
what people ate and their a1tudes towards certain foods e.g. new 5:2 diet fad.
Another explana.on into a1tudes towards food and ea.ng behaviour is cultural inuences.
Ethnicity seems to play a role in determining ea.ng behaviour; Khan et al found that white women were more
likely to have body dissa.sfac.on and ea.ng disorders such as anorexia nervosa than Asian or black women.
This suggests that ethnicity will impact whether a woman is more likely to develop ea.ng disorders, which may
be because Western cultures tend to promote a beauty standard achieved through thinness.
Moreover, Kennedy et al supports these ndings; over 14,000 women aged 18-23 were studied and they found
that the longer these women lived in Australia, the more likely they were to portray a1tudes and ea.ng
behaviours similar to women born in Australia. This is known as the accultura.on eect.
On the other hand, Mumford et al found completely opposite results; they found that the incidence rates of
bulimia were higher among Asian schoolgirls than their white counterparts. This suggests that ethnicity may
not necessarily play a role in determining ea.ng behaviour.
Similarly, Striegel-Moore found that a drive for thinness was more evidence in black girls than in white girls.
This further emphasises the idea that ethnicity impacts ea.ng behaviour, further weakening this explana.on.

A"tudes to Food and Ea.ng Behaviour

Social class has found to determine a1tudes towards food. In Dornbusch et als survey of 7000
American adolescents, they found that the upper-class women were more like to strive for thinness
than those of lower social classes. This suggests that social class may inuence body image. To
emphasise this, Goode et al found that such individuals were also more likely to achieve this and a
posi.ve correla.on between income and healthy ea.ng was established.
This is supported by Xie et al who found that teenagers from higher-income background were found to
eat more healthy foods than those from lower-income families. They consume less saturated fats, more
protein and calcium and ate closer to the daily guidelines. This suggests that income impacts ea.ng
behaviour and a1tudes towards certain foods. However, a weakness in this research is that we cannot
infer a cause and eect for certain that higher incomes relates to healthier ea.ng habits. There may be
confounding unknown variables contribu.ng to this correla.on, such as the stress of actually being poor
contribu.ng to poor ea.ng habits.
On the other hand, Story et al found that in a sample of American students, higher social class was
related to greater sa.sfac.on with weight and lower rates of weight control behaviours. This
completely opposes the social class explana.on of cultural inuences, weakening the explana.on.
However, research into cultural inuences on ea.ng behaviour and a1tudes is arguably culturally
biased, as a1tudes towards certain foods may be specic to that culture alone. Thus, what may be valid
for one culture may not necessarily be true for another; for example, the Western ideals of being skinny
may not apply to cultures where the focus is to avoid starva.on.
Most studies have focused purely on women and their a1tudes to ea.ng behaviour, which suggests
that many of these explana.ons suer from beta bias as they a[empt to be generalised to men. This is
an issue because men have dierent body types and dierent metabolic reac.ons so they may not be
prone to cultural inuences or models in the same way as women may be. Therefore, these
explana.ons lack popula.on validity because their applica.on is limited to women solely.
Moreover, there are issues in generalizability as some studies are based on women diagnosed with
ea.ng disorders, some are based on people with subclinical condi.ons and other studies are based on
people who may be experiencing temporary depressed moods. The problem here is that we cannot
generalise ndings from such specic circumstances to other groups or even the wider popula.on itself.
Therefore, the ndings from these studies may lack in external validity because the studies arent
measuring how ea.ng behaviour is aected in a way that can be generalised beyond that niche group of
individuals.

Failures of Die.ng

There are two explana.ons into failures of die.ng; the restraint theory and the role of denial.
One explana.on for the failure of die.ng is the Restraint Theory; this theory suggests that when people
consciously a[empt to eat less and restrain their intake, they actually end up overea.ng. This is o]en
because the dieter has periods of restraint that are very hard to maintain. This then means that the
restraint is followed by periods of dis-inhibi.on. Dis-inhibi.on has been dened as ea.ng more as a
result of loosening restraints in response to emo.onal distress, intoxica.on or preloading.
A study by Wardles and Beales highlighted how die.ng contributed to overea.ng; 27 obese women
were put either into a diet condi.on that focused on restrained ea.ng pa[erns, an exercise condi.on
or a non-treatment condi.on for 7 weeks. Assessments on food intake and appe.te were made before
and a]er they ate a snack at week 4 and 6 (under stressful condi.ons); it was found that women in the
die.ng condi.on ate more than those in the other condi.ons. Thus, this suggests that overea.ng is
caused by peoples a[empts to diet.
Herman and Polivys Boundary Model a[empts to explain why die.ng leads to overra.ng; it suggests
that hunger ensures we dont eat less than the minimum level, whilst sa.ety ensures we dont eat
more than the maximum level. Psychological factors are believed to play a role between these two
levels, with those die.ng believed to have a larger range between sa.a.on and hunger. This could be
because it takes longer for dieters to feel hungry. Once restrained dieters dont eat, they may nd
themselves ea.ng more than they had planned because it takes longer for sa.a.on to begin.
However, one weakness of this theory is that it cannot explain why some people successfully lose
weight through restrained ea.ng or why ea.ng disorders such as anorexia exist. Therefore, this suggests
that other factors may be involved and so the theory is simplis.c in focusing only on people ea.ng less
as the main cause for failures of die.ng when the nature of die.ng is in fact very complex. Thus, this
weakens the restraint theory model.
Moreover, we cannot therefore infer cause and eect between research ndings into restrained ea.ng
resul.ng in overea.ng and diets failing as this is based on correla.onal research. There may be other
extraneous variables like nega.ve cogni.ons that lead to overea.ng.

Failures of Die.ng

This is cri.cised by another explana.on into the failure of die.ng which is the role of denial. This suggests that
a[emp.ng to suppress thoughts has a counterproduc.ve eect, as it will make the thought even more
prominent in our head. Wegner et als study highlights the basis for this; par.cipants were asked to not think
about a white bear but ring a bell every .me they did whereas a control group were asked to ac.vely think
about the white bear; it was found that those asked not to think about it rang the bell more frequently than
those in the control group. Its referred to as being the theory of ironic process of mental control as denial of
a thought leads to it occurring more o]en. Thus, when dieters a[empt to not eat certain foods or reduce
intake, the foods then become more temp.ng and prominent in their minds, leading to the failure of diets.
Soetens lends experimental support to this theory; par.cipants were divided into two groups: restrained and
unrestrained. The restrained group was further subdivided into those who were either high or low in
disinhibi.on; those in the disinhibited restrained group used more thought suppression than the other groups
and also showed a rebound eect a]erwards. This shows that restrained eaters who tend to overeat try to
suppress thoughts about food more o]en, strengthening the role of denial explana.on.
However, an issue to consider is whether people have the free will to control their weight loss or whether its
biologically determined. For example, lipoprotein lipase (LPL) is an enzyme produced by fat cells to help store
calories as food; a person who produces an overload of LPL will regain lost weight faster than others. This is
supported by Kern et al, whereby 9 people had their LPL levels measured before and a]er losing 90 pounds;
people who were fa[er at the start were found to have higher LPL levels post-weight loss, sugges.ng that the
body was gh.ng harder in those people to retain the lost weight. The weight loss would have ac.vated the
produc.on of LPL, which may explain why some people struggle to lose weight. This weakens both
explana.ons into failures of die.ng as it argues that there is an individualis.c explana.on that exists for each
person.
Moreover, another issue is that research into die.ng has found to be culturally biased as some cultural groups
nd it more dicult to diet successfully due to the natural inclina.on to obesity where they are; for example,
Asian adults are more prone to obesity than European adults. This weakens the explana.ons as they do not
take into account culture and therefore cannot be extrapolated across cultures.
Furthermore, studies into die.ng are based on anecdotal accounts of individuals. These are not 100% accurate,
cannot be replicated nor have controls, which means that the studies suppor.ng the explana.ons are not fully
valid nor reliable, therefore weakening them. This can be xed by using scien.c means of acquiring data.

Neural Mechanisms into Ea.ng Behaviour

The hypothalamus is a gland in the brain responsible for homeostasis. Homeostasis has two mechanisms: to
detect whether the body has enough nutrients and to correct a situa.on to restore the op.mum environment.
Thus, the hypothalamus is believed to play a role within ea.ng behaviour. There is a large .me lag between the
two mechanisms and the body registering their eects, so the body has evolved two separate systems to
overcome this .me lag; one to turn ea.ng behaviour on and the other, o. Glucose levels play a key role in
producing the feeling of hunger; hunger increases when glucose levels fall, ac.va.ng the lateral hypothalamus.
Once food is consumed, glucose levels rise, ac.va.ng the ventromedial hypothalamus, which causes feelings of
sa.a.on, helping stop further feeding.
However, one weakness for the homeosta.c explana.on is that hunger mechanisms should theore.cally be
adap.ve to an.cipate and prevent decits in energy as opposed reac.ng to them. The idea that hunger and
ea.ng is triggered only due to low glucose levels doesnt t into evolu.onary perspec.ve in which our biology
has evolved.
On the other hand, researchers found that damage to the lateral hypothalamus in rats caused aphagia, the
absence of ea.ng, suppor.ng the lateral hypothalamus explana.on as the LH couldnt be ac.vated.
In contrast however, damage to the LH has shown to cause decits in other aspects too such as sex as opposed
to just hunger. Recent studies have also found that neural circuits running throughout the brain play a role in
ea.ng behaviour too. This suggests that LH does not have an essen.al role in controlling the ea.ng
centre. Therefore, the view that the LH and VMH are alone responsible is simplis.c, as it appears there are
more complex processes occurring, thus weakening the theory.
Yet, Wickens found that s.mula.on to the lateral hypothalamus through injec.on of neuropep.de Y (type of
neurotransmi[er) caused them to begin feeding. This suggests that there is an ON switch and that NPY found
in the hypothalamus plays a role both in s.mula.ng lateral hypothalamus and increasing ea.ng behaviour.
Conversely, Mariah et al manipulated mice to disable them from producing NPY through gene.c modica.on.
They found no subsequent decrease in their ea.ng behaviour. This suggests that hunger s.mulated by NPY
injec.ons may have been an experimental artefact in that NPY ooding causes the opposite behaviour. This
would mean that the research into NPY lacks external validity as they are conducted in laboratory se1ngs. This
suggests that it cannot be generalised to real world ndings.
Addi.onally, another cri.cism is the use of animals as much of the empirical evidence is based on non-human
animals. It can therefore be suggested that the ndings cannot be extrapolated to human beings because our
gene.c makeup and biology are signicantly dierent. This also suggests that such studies may lack internal
validity, as observa.ons made in animal may not apply to human ea.ng behaviour, thus weakening the theory.

Neural Mechanisms into Ea.ng Behaviour

On the other hand, researchers have found that damage to the ventromedial hypothalamus resulted in rats
overea.ng due the lack of a stop signal for sa.a.on onset, leading to hyperphagia which is excessive hunger.
S.mula.on of the VMH was also found to inhibit and stop feeding, again sugges.ng this neural mechanism
controls ea.ng behaviour.
Suppor.ng this, Hetherington and Ranson made lesions on an area of the ventromedial nucleus in rats. This
caused them to over-eat and become drama.cally obese. It was found that this lesion destroyed a centre
thats vital for the control of feeding behaviour; this centre was thought to be the sa.ety centre.
However, damage to nerve bres passing through the VH possibly damages another area in the hypothalamus,
the PVN. Gold suggests that damage to the PVN alone causes hyperphagia and found that lesions to the VMH
alone did not result in hyperphagia, weakening the hypothesis that VMH damage leads to hypoerphagia.
However, the issue with Golds ndings are that no subsequent research has managed to replicate the ndings.
This suggests that the claims are unreliable, as researchers have actually found the contrary; that lesions to the
VMH caused over-ea.ng and weight gain.
Other neural explana.ons suggest that the amygdala and the inferior prefrontal cortex aect ea.ng behaviour
through cogni.ve and neural factors. The amygdala is believed to inuence food choice though previous
experience. Rolls and Rolls ndings conrm this as they found that removing the amygdala in rats would cause
them to consume both familiar and unfamiliar foods. The prefrontal cortex receives messages regarding smell,
which, if damaged, can aect the taste of food.
In contrast, research has found that hunger and ea.ng pa[erns may not be under the control of neural
mechanisms; LuLer et al found the body produced extra ghrelin when stressed, which has been associated
with an increase in appe.te. The view that neural mechanisms alone aects hunger is thus simplis.c because
there may be combina.on of dierent processes involved in hunger management. Yet, research into neutral
mechanisms may be responsible for aec.ng ea.ng behaviour in real life. For example, drugs with Lep.n may
be developed to increase weight loss or drugs that inhibited LH may help people reduce feelings of cravings.
This suggests that there are real world applica.ons that can help people struggling with obesity.
Moreover, cogni.ve factors may play a bigger role in determining sa.ety and when a person is full. People are
aware of when they have eaten and they could therefore conclude that they are full, leading to sa.a.on. This
explana.on accounts for the role of free will because people have the choice to eat or not.

Evolu.onary Explana.ons of Food Preferences

Humans evolved from hunter-gatherers and their diet would have consisted of what was available in their
environment e.g. plants and animals.
Preferences for fa[y foods would have been adap.ve because it provides valuable energy resources, which
were vital in an environment where an individuals next meal was never guaranteed. Calories were less
available within the EEA and thus it would have been adap.ve for humans to develop a preference for highly
caloric foods, as these foods would provide them with the longest period of energy.
Moreover, Gibson and Wardle support the idea the importance of caloric foods in an ancestral diet; they
showed that children aged 4-5 preferred fruit and vegetables that were dense in calories, such as bananas and
potatoes, as opposed to foods high in protein or sweetness. This suggests that a fa[y food preference had
evolved, suppor.ng the fa[y food preference explana.on.
To support this, Stanford conducted a study on Tanzanian chimpanzees; when coming close to starva.on, it
was found that the chimpanzees would kill and eat the most fa[y parts of a colobus monkey such as the brain
or bone marrow, leaving tender nutri.ous esh. This emphasises how our own behaviour may have been
shaped in the EEA and thus supports the fa[y food preference explana.on.
Furthermore, humans also developed a preference for sweet foods as its associated with high-energy and not
being toxic so it would be benecial for survival. In contrast, our ability to detect and reject bi[er and sour
tasted also makes evolu.onary sense because these tastes would be indica.ve of poison or toxins that plants
produce to repel predators such as humans. Thus, us having a natural dislike to bi[er and sour taste makes
sense because they would be dangerous if consumed. Humans have 30 genes that code for bi[er taste
receptors so humans have a wider scope to recognise bi[er and possibly toxic foods.
In support of the evolu.onary advantage to bi[er/sour food development, Desor and Steiner found, judging
by facial expressions, that neonates were more sensi.ve to bi[er tastes and preferred sweet foods, which was
an innate preference; these neonates are young and lack environmental experience to know which foods are
safe to eat. This suggests that being more prone to bi[er/sour tastes would have had an evolu.onary
advantage. A strength of this study is that it rules out extraneous variables such as social learning factors
because the neonates are too young to have learnt preferences, making the ndings more valid. On the other
hand, interpre.ng preference using facial expressions is subjec.ve and can easily be misinterpreted and
unreliable. Thus, this methodological aw observed may weaken the study because expressions observed may
not necessarily imply a preference. This can be xed by using quan.ta.ve means of obtaining the results.
Moreover, if sweet preference was determined by evolu.on, it would be found across cultures and would be
universal. However, Stefansson found that Copper Inuits were disgusted by the taste of sugar when they rst
tried it. This undermines the evolu.onary explana.on behind sweet preferences and can instead be explained
by the lack of exposure to sweet foods from their environment instead.

Evolu.onary Explana.ons of Food Preferences

Humans have the ability to learn taste aversion to toxic foods, which can be explana.on through
evolu.onary explana.ons. Taste aversion is when toxic food is ingested and we subsequently develop a
dislike towards it a]er consump.on and illness. This would have been benecial for survival from an
evolu.onary perspec.ve because if we survived the ini.al consump.on, our body would adapt by
learning to avoid the foods and developing a natural dislike for them. The opposite can also occur, with
a preference for foods that enhance health.
One study that supports the evolu.onary explana.on of taste aversion is by Garcia et al. They found
that when a rat with a thiamine (vitamin B) deciency consumed food with a dis.nc.ve taste followed
by a thiamine injec.on, the rat would subsequently develop a preference for this dis.nc.ve-tas.ng
food. This therefore supports the taste aversion explana.on as thiamine enhances health hence why
rats consumed foods that contained thiamine.
Moreover, Sandell and Breslins study supports the evolu.onary explana.on of taste aversion; 35
adults were screened for the hTAS2R38 bi[er taste receptor gene and par.cipants were asked to rate
the bi[erness of various vegetables. Some of these vegetables contained glucosinates, a mild toxic
known to be dangerous in high dosages. It was found that those with the sensi.ve version of hTAS2R38
rated vegetables containing glucosinates as 60% more bi[er than those with the insensi.ve version of
the gene. This suggests an adap.ve ability to detect and avoid toxic foods, which would explain why
such genes are more widespread, suppor.ng the evolu.onary explana.on of taste aversion.
Furthermore, real-world applica.ons can be made by understanding how taste aversion and preference
works; cancer pa.ents have reported developing an aversion to food they consume prior to
chemotherapy, which has resulted in the scapegoat technique to help pa.ents con.nue enjoying their
foods post-treatment. This involves giving cancer pa.ents a novel food along with something theyre
familiar with prior to treatment; results have found that pa.ents form an aversion to the novel food and
not to the familiar food, allowing them to con.nue ea.ng familiar foods.

Psychological Explana.ons for AN

There are two psychological explana.ons into anorexia nervosa: the SLT and the psychodynamic
explana.on.
Within Western society, people learn that beauty is equated to thinness and this ideal of a[rac.on is
thought to be a contributor towards AN. The media is then used to ensure that body ideals are
maintained in adolescents through the inuence of TV, magazines and fashion. All of these consistently
reinforce this cultural ideal within the popula.on as one study found that 16% of all 15-18 year old girls
in the UK were currently on a diet. This could be because girls internalise culturally dened standards
of female beauty, leading to unhappiness over their own body type not matching this ideal and an
obsession with die.ng and food, thus people observe and imitate the model ideal, leading to AN.
One study that supports the impact of learning from the media has on body type was conducted by
Becker et al; it was carried out in Fiji where TV was introduced in 1995; ea.ng disorders were absent
un.l the introduc.on of the TV and inuence of the West as the girls a1tudes began to shi] towards a
desire to lose weight. It was found that a]er 5 years, there was a signicant increase in the number of
girls suering from anorexia and bulimia nervosa. This highlights how the media may contribute to the
onset of AN indirectly, thus strengthening the explana.on. However, one weakness of this study is that
it lacks internal validity because we cannot conclude for certain that the shi] in a1tude towards body
image directly led to AN as there may be other factors that contributed to the onset of AN; this is
emphasised by Jones and Buckingham who argue that not everyone is inuenced by the media in the
same and that its usually those with low self-esteem who are more likely to be inuenced. Therefore
this directly highlights the fact that we dont all learn to be thin because of individual dierences, which
would explain why there are people who dont t into the Western ideals.
On the other hand, Gomeszs meta-analysis of 25 studies found a consistent support for the idea that
slender beauty ideals led to body dissa.sfac.on, which contributed to the development of ea.ng
disorders, primarily under 19s.
Moreover, to support the role of learning AN, Lai et al found that the rate of AN began to increase
amongst people in Hong Kong as the culture become more modernised and therefore westernised,
sugges.ng that learning does inuence AN.

Psychological Explana.ons for AN

However, another explana.on that directly cri.cises the idea of learning AN is the psychodynamic
theory by Bruch. The principles of the psychodynamic theory is that adolescents do not want to grow up
and separate from their parents so they become xated at the oral stage where they are completely
dependent on their parents. Those with AN will want to lose weight so that they lose secondary sexual
characteris.cs to remain childlike and asexual, enabling them to return to the safety of their families.
Bruch argued that AN is ac.vated in early childhood, sugges.ng that it is caused by how parents
respond to their childs needs; eec.ve parents recognise their needs and feed them when theyre
hungry whereas ineec.ve parents fail to respond to their childs needs by feeding the child when they
are not hungry or vice versa. Children with ineec.ve parents grow up confused about their internal
needs, becoming more reliant on them. Therefore, they may nd it dicult to establish autonomy when
they become adolescent, as they dont feel control over their own bodies. Thus, to overcome their
sense of helplessness, they develop abnormal ea.ng habits and take excessive control over their body
shape and size. As a result, anorexia nervosa is an a[empt to control ones life and strive for autonomy.
Moreover, Crisp developed the idea of remaining pre-pubescent through starva.on, leading to
amenorrhoea, underdeveloped hips and breasts.
Steiner supports Bruchs psychodynamic explana.on of AN, as they found that parents of AN pa.ents
have a tendency of dening their childs physical needs than allowing the child to be autonomous in
dening their own. Thus, this suggests that AN enables teenagers with AN to strive for the autonomy
they have been deprived of, strengthening the theory.
However, Minuchin disagrees and suggests that the onset of AN is actually related to family problems
and developed the family system approach. Anorexia diverts a[en.on from family problems so its a
misguided a[empt at keeping the family together as they will start to worry about the child and ignore
other issues.
Furthermore, the psychodynamic approach has been cri.cised for being unscien.c because it is based
on small case studies, for example Bruchs studies are based on qualita.ve case studies. This means that
it cannot be replicated so it lacks validity and cannot be tested using the scien.c method.

Psychological Explana.ons for AN

On the other hand, the explana.on into AN is personality, which is a gene.c characteris.c,
directly cri.cizes both the SLT and the psychodynamic theory. Personality traits are thought
to play an important causal role on the onset and maintenance of AN. Those with a
perfec.onist personality are more likely to have AN as Strober et al retrospec.vely studied
boys and girls receiving treatment of AN and found high levels of perfec.onism amongst
them.
To emphasise the link between perfec.onism and AN, Nilsson et als longitudinal study
found that those with a short period of AN were less perfec.onist, strengthening the
personality explana.on.
Halmi et al supports this explana.on. They inves.gated the rela.onship between AN and
perfec.onism in 322 women in the US and Europe. They found that women with a history of
AN scored higher on the Mul.dimensional Perfec.onism Scale when compared to a control
group. Moreover, they found that the extent of perfec.onism was directly related to the
severity of AN.
As part of this study, Halmi et al also included rela.ves of those with AN and found that
perfec.onism as a personality traits appears to be passed on from rela.ves and thus
represents a gene.c vulnerability for the onset of AN. Therefore, this suggests that biological
explana.ons can cause the onset of AN. This means that a diathesis-stress model may be[er
explain how both nature and nurture play a role, with perfec.onism being gene.c but
inuenced by the environment.
However, most of the research is also based on females so all the explana.ons into AN may
suer from beta (gender) bias; the same psychological factors impac.ng women may not
necessarily explain the onset of AN in men as they may perceive the world dierently, thus
weakening the psychological explana.ons into AN.

Biological Explana.ons for AN

There are two biological explana.ons into the onset of AN: neurotransmi[ers, the reproduc.ve
suppression hypothesis and the hypothalamus dysfunc.on theory.
Neurotransmi[ers are thought to cause the AN. Neurotransmi[ers involved include serotonin &
dopamine.
Kaye et al found that drugs such as SSRIs that alter serotonin levels were eec.ve in recovering
AN pa.ents as they prevented relapse. SSRIs alter serotonin levels by blocking uptake of serotonin
from the synap.c cle]s, which maintains higher serotonin levels. This suggests that there is a link
between serotonin levels and the onset of AN, suppor.ng the explana.on.
Although it ahs been suggested that serotonin is involved its the dopamine, the second
neurotransmi[er, that is the most responsible for the onset of AN is dopamine. Kaye et als PET
scan compared dopamine ac.vity in the brains of 10 women recovering from AN and 12 healthy
controls. They found that in the AN women, there was an over ac.vity in dopamine receptors in
the basal ganglia where dopamine plays a part in interpreta.on of harm and pleasure. Increase
dopamine ac.vity in the basal ganglia seems to alter the way people interpret rewards so those
with AN nd it harder to associate good feelings with things that people nd pleasurable such as
food. However, one weakness of this study is that it has a small sample size that only uses
women; therefore, we cannot be certain that the imbalances in dopamine would be the same in
men with AN and the small sample size means that we cannot generalise the ndings to men, let
alone the general popula.on. As a result, it lacks external validity and thus weakens the
explana.on of dopamines eect on AN.
Furthermore, Castro-Fornieles et al found that AN teenage girls had higher levels of homovanilic
acid (waste product of dopamine) than a control group and they also found that improvement in
weight levels normalised homovanilic acid. This suggests weight gain decreased the ac.vity of
dopamine levels hence the decreased homovanilic acid, strengthening the theory.

Biological Explana.ons for AN

Another biological explana.on is the hypothalamus dysfunc.on theory, which suggests that people have a set
weight for their bodies; as weight increases or decreases, the body adapts to make adjustments in food
regula.on to return the individual to their set weight. The hypothalamus is believed to have a role in hunger
and sa.a.on as the lateral hypothalamus turns ea.ng behaviour on whilst the ventromedial hypothalamus
turns sa.a.on on to decrease feeding. Thus, Garfunkel et al argued that a disturbed hypothalamus causes AN
through the LH as it stops sending signals to eat or the VMH being overac.ve with the individual receiving
signals telling them they are full.
Brobeck supports this theory, as they found that damaged LH in rats lead to aphagia which is the failure to eat
when hungry. This provides support for the idea that damage of the hypothalamus could lead to reduced
ea.ng, suppor.ng this theory. Moreover, Stellar et al found that s.mula.ng VMH inhibited feeding, which
again support the idea that possible over-ac.va.on of the VMH could lead to the onset of AN.
However, biological explana.ons e.g. hypothalamus dysfunc.on theory can be cri.cised as biologically
determinis.c as they ignore the free will and ability of individuals to control their own behaviour. They suggest
that if someone has par.cular genes or biochemical imbalances they will inevitably have an ea.ng disorder,
which ignores the individuals mo.va.on to resist or overcome ea.ng disorder, thus weakening the theory.
Evolu.onary explana.ons involve the reproduc.ve suppression hypothesis. The reproduc.ve suppression
hypothesis assumes that weight loss was a strategy for suppressing reproduc.ve capability when food was in
limited supply as pregnancy would have been risky for the mother and survival changes for the infant would
have been reduced. Reproduc.on is costly to females so when a female faces condi.ons that are unfavourable
to reproduc.on she can increase her life.me reproduc.ve success by delaying reproduc.on un.l condi.ons
improve. Because a minimum amount of fat is needed before menstrua.on begins and for regular ovula.on to
be maintained, Frisch et al argues that this could have been an eec.ve mechanism for controlling sexual
matura.on and fer.lity in ancestral females.
However, a major cri.cism of this explana.on is that AN appears more maladap.ve overall than adap.ve,
especially during harsh condi.ons in the EEA. AN causes an individual to be weak, frail and vulnerable as well
as a liability to the group and it seems unlikely any benet could be achieved from such a weak person. Also,
the basics for survival also become dicult, e.g. hun.ng for food which is necessary for all animals. This further
undermines the evolu.onary explana.on.
Moreover, a further cri.cism is that AN cannot be evolu.onary because it cannot be passed down gene.cally
as those with AN would die out of malnutri.on. AN kills which therefore contradicts with the idea that it helps
us survive.