Detailed course notes along with essay plans for all the topics that can come up on the A-Level Psychology exams. Includes useful tips on exam technique and revision too!
Biological Explanations of Anorexia Nervosa
AO1: AO2:
Genetics: The vulnerability does not necessarily
(Family studies) Lilenfeld et al: looked at the emerge as full blown AN.
family history of 28people diagnosed with AN
and found a family vulnerability for the
disorder. They found that relatives of
anorexics were 7-12x more likely to show
sub-threshold forms of anorexia (not quite
meeting DSM criteria for the disorder).
(Twin studies) Holland et al: found that 56% Genetically similar members of a family tend
of the MZ twins in their study both had AN, to spend more time together, so environment
whereas only 5% of the DZ twins both may be a factor.
suffered. Concordance rate is not 100%, so it can’t be
entirely genetic.
Sample size of twin studies will be small.
Genetic explanations can’t explain the recent
increase in cases of AN.
(Chromosomes) Grice’s et al: found AN is unlikely to b e caused by a single
evidence for susceptibility to AN on gene. It is a complex disorder with a number
chromosomes. They compared DNA sample of genes involved, each contributing a small
from people with AN, with those belonging to effect.
family members. Genetic commonalities
emerged when they looked at families with 2
or more relatives of AN with severe food
restriction.
Neuroanatomy: Davey: It is unlikely that problems associated
Lateral hypothalamus: Damage to the lateral with the lateral hypothalamus are a central
hypothalamus causes loss of appetite causal factor of AN. Animal studies indicate
resulting in a self-starvation syndrome. that damage to this part of the hypothalamus
results in lack of hunger. By contrast, those
who suffer with AN usually report
experiencing intense hunger.
Insula cortex: AN can be accounted for by Difficult to design tests that target the insula
the problems in the neutral circuitry of the cortex without activating the many other
insula cortex structure that helps to areas of the brain to which it is connected
integrate the functions of all the possible and this makes the insula cortex hypothesis
neural centres relevant to the features of AN. very difficult to test.
Neurochemistry: Not clear whether these serotonin levels are
Serotonin: AN often has abnormally high a cause or effect of AN. While animal studies
levels of serotonin and this causes have shown that when serotonin is released
abnormally high levels of anxiety. Serotonin into either VMH or LH animals. Stop eating,
production is stimulated by biological recent research have found lower levels of
components (amino acids) in food. So serotonin activity among people with AN than
starvation may actually make AN’s feel among controls (Kaye et al)
better.
,Sheet,4 08.04.2014
Eating Behaviour
Discuss neural mechanisms involved in controlling eating.
AO1: AO2:
Hunger is the motivation or drive to start Cannon and Washburn: Found that when the
eating and satiety is the feeling of being full. participant was not hungry, there were no
Set point theory- states that we have a contractions and hunger was reported at the
biologically determined standards around height of the contractions, suggesting that
which our body weight is regulated, so if we stomach contractions caused hunger.
eat too much or too little, homeostatic This was a case study so it’s not
mechanisms alter our metabolism and generalisable to the entire population.
appetite to return us close to our original There may be individual differences.
body weight. Lateral hypothalamus; this There is no cause and effect, hunger may
produces hunger, damage to this area have caused the contractions, not the other
results in dramatic reductions in food intake. way around.
Ventro-medial hypothalamus; this triggers Passer et al: showed that feelings of hunger
a sense of feeling full, thereby reducing and satiety are experienced even when all
appetite. the nerves from the stomach to the brain are
Paraventricular nucleus; this is a cluster of cut. This indicates that other neural
neurons with receptors for various mechanisms must play a role in triggering
transmitters that stimulate or reduce hunger e.g. ghrelin.
appetite. Lutter et al: They starved mice for days to
increase the amount of ghrelin in their
systems, they compared these mice to mice
who were allowed to eat freely; the mice with
increased ghrelin levels showed more
anxiety and more signs of depression than
the control group mice. This suggests that
food, hunger, stress and anxiety levels are
all associated.
GLUCOSTATIC THEORY Levels of energy source in the blood don’t
Glucose is a simple sugar that we get from usually drop to anywhere near the threshold
food that gives us energy. The glucose that to trigger eating.
is not used immediately is stored in the liver Studies also indicate that body temperature
and fat cells. Blood glucose levels are increases just prior to spontaneous eating,
constantly monitored by the sensors in the increases still further and then declines as
liver and the hypothalamus – if levels are low eating stops. While some tissues need large
stored glucose is released. amounts of glucose for energy homeostasis,
Changes in supply of glucose available others e.g. the liver use fats. Biology is not
generates signals to the brain that regulate the only initiator of eating.
hunger and appetite.
Strong applications of research for treatment
(e.g. leptin injections)
Non-human animals in research –
generalisability concerns
There are a number of factors that can make
us feel more or less hungry e.g. smell, habits
or mood. Clearly psychological factors as
well as neural mechanisms are at work.
, Sheet 5 08.04.2014
Eating Behaviour
Discuss neural mechanisms involved in controlling satiation (24marks)
AO1: AO2:
Satiety is the unconscious physiological
process that stops you eating. The VMH is
the satiety centre. The VMH provides the
signal to stop eating.
The walls of the stomach and intestinal tract But satiety is not dependent on these
are stretched by the ingestion of food, vagal processes alone. People who have had their
sensory nerves in their muscle layers, which stomachs removed, for medical reasons, still
act as ‘stretch-receptors’, sends signals of experience satiety therefore chemical
satiety to the brain. messengers, must also play an important
role in satiation.
CCK – seems to be the hormone associated with
satiety. It does the opposite of GHRELIN. As food
passes from the stomach to the small intestine
CCK is released. This sends messages to the
brain to inhibit eating.
Leptin – Reduces NPY and high levels of Mayer and Thomas found that trauma to or
increased appetite a decline in leptin is tumours of the VMH can cause hyperphagia
associated with a loss of fat cells & increases our (overeating) and also obesity.
appetite
Insulin is a hormone that helps remove glucose
from the blood. An absence of insulin can lead to
high blood glucose levels which could then lead
to hyperphagia and inhibition of satiety.
Baylis et al: Two symmetrical lesions were made Very small sample which only used one
in the VMH of 8 male and 5female rats. Their breed of rat so it’s not generalisable –also-
body weight was later compared with age they’re rats! Extrapolation issues! Other
matched controls. These rats with lesions in the tissues surrounding the VMH might have
VMH cause hyperphagia and obesity so the VMH
been damaged when the lesions were
must play a role in satisfaction.
created so it might not necessarily just be the
VMH that is involved.
Ethical issues too!
The biological model cannot explain why rats
with damage to their VMH will eat more
provided the food is easily accessible.
Schacter: 20 obese participants were asked
to complete a questionnaire- bowl of nuts
next to them, told to ‘help themselves’
Half the nuts were shelled (no shell) or
unshelled (with shell).
The control group ate similar amounts of
nuts regardless of whether they were shelled
or unshelled but out of the obese group –
only one ate the unshelled nuts (work was
required).
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