Aggression: AQA 'A' Psychology A2 textbook by Mike Cardwell and Cara Flanagan, this powerpoint examines social psychology, biological explanations and evolution, more specifically: SLT, deindividuation, institutional aggression, hormones, etc.
2. Attitudes to food and eating behaviour
Explanations:
Social Learning:
• emphasises impact on observation
• Parental Modelling: parents
inevitably affect child’s behaviour →
control over food. Also a general
association: Brown and Ogden:
consistent correlations between
P&C in terms of snack food intake,
eating motivations and body
dissatisfaction.
• Media effects: evident in impact of
TV etc… MacIntyre et al: media has
major impact on what people eat
and attitudes to food → but eating
behaviours are limited by personal
circumstances so even if you learn
from media → placed in boarder
context of circumstances
Cultural Influences:
• Ethnicity: its suggested disorders are
more characteristic of white women
than black or Asian women (Powell
and Khan.) Ball and Kennedy:
+14,000 women between 18-23,
Australia. All ethnic groups : more
time spent there more attitudes +
eating behaviour is similar to native
Australians (acculturation effect.)
• Social Class: body
dissatisfaction/behaviours more
common in higher class. Dornbusch
et al: 7000 US adolescents higher
class = greater desire to be thin +
more likely. Goode et al: Scottish
Health Service: income positively
associated with healthy eating.
Mood and eating behaviour:
• Explanations of some behaviour such
as binge eating see it as a temporary
escape.
• Binge-Eating: people w/ bulimia
nervosa report anxiety prior to a binge.
Davis et al: Self-Monitoring studies: 1
hour before binge more negative mood
than 1 hour before normal snack/meal.
Wegner et al: students record eating
patterns + mood over 2 weeks – Binge
days characterised by low mood, no
difference in mood before/after binge.
• Comfort eating: Garg et al: food
choices of 38 pps – upbeat movie/sad
movie. Popcorn + Grapes: sad film 36%
more popcorn, upbeat far more grapes
than sad.
Eval:
• Meyer and Gast: 10-12 yr. old girls & boys
sign. positive correlation between peer
influence + disordered eating.
• Birch and Fisher: best predictors of
daughters’ eating behaviour was mothers’
dietary restrain and perception of risk of
food on their daughters.
• Social Learning suggests fashion models –
but much more than that → evolution.
• Mumford et al: bulimia more likely
among Asian schoolgirls than white
counterparts.
• Striegel-Moore: more evidence of
drive for thinness among black than
white girls.
• Story et al: sample of US students,
higher social class = greater
satisfaction/lower weight control
behaviours.
• Attitudes towards chocolate: appear to
be influenced by popular claims that it
can lift our mood. But Parker et al:
although chocolate has slight
antidepressant effect on some people
→ when consumed as emotional
strategy more likely to prolong rather
than alleviate.
3. Explanations for success and failure of dieting
Explanations:
Restraint theory:
• Synonymous w/ dieting. 89%of
female population consciously
restrain food intake.
• The boundary model: Herman and
Polivy: hunger keeps food above
minimum and satiety works to keep
food below a certain level.
Restrained eaters have greater
range between the two; when they
go over the dietary restraint they
continue to eat until this level.
The role of denial:
• Attempting to supress/deny thought
tends to have opposite effect.
Wegner: asked some pps not to think
about white bear & some pps to
think about white bear + ring bell
when they did. Those told not to
think about bear rang bell more.
“Theory of ironic processes of
mental control” – paradoxical –
denial often backfires.
• Theory of ironic processes of mental
control: decision to not eat certain
foods – try to supress thoughts.
Increases preoccupation with those
foods, food becomes more attractive
when you deny it.
Detail: key to successful diet:
• Redden 2008 suggests success to
dieting lies in attention we pay to what
is being eaten. People like experiences
less as they repeat them – harder to
stick to 1 regime. To over come this
this instead of “not another salad”
think about contents of the meal such
as tomato or apple → bored less easily.
• Jelly beans experiment: Redden gave
135 pps 22 jelly beans →info of each
one flashed up on the screen. One
group sees general info “jelly bean
number 7” other group sees specific
“cherry flavour number 7” → general =
bored faster.
Eval:
• Wardle and Beales: 27 obese women to 3
groups (diet w/ restraint, exercise group, non-
treatment) assessed at 4 and then 6 weeks. At
4 weeks appetite assessed after a preload. At
6 weeks food intake under stressful conditions
= assessed. Both sessions women in diet
condition ate more than other 2 groups.
• Implications on treatment: don’t restrain
• Limited relevance: how do anorexics starve
themselves?
Theory of IPOMC evaluation:
• Soetens et al: pps divided into restrained and
unrestrained group (restrained then split into
high or low disinhibition) Disinhibited restrained
group (tried to eat less but tended to overeat)
used more thought suppression → restrained
eaters who tend to overeat try to supress more
often and think more about food after eating.
• Limited effects: Wegner admits ironic effects
observed are not huge.
Anti-dieting programmes:
Development o programmes aimed at
replacing dieting with conventional
healthy eating. Emphasis on regulation by
hunger and satiety signals and prevention
of inappropriate attitudes to food.
Higgins and Gray meta-analysis:
participation in programmes associated
with improvements in both eating
behaviour and psychological well being.
Also with weight stability rather than
weight change.
9 people w/ average loss of 90 pounds: LPL levels
before and after: rose after weight loss + fatter to start
w/ = higher levels.
Asian adults +
adolescents more
prone to obesity.
4. Neural mechanisms in eating behaviourThe role of
neural
mechanisms:
Homeostasis:
• Involves mechanisms which
detect internal environment and
correct environment to ensure its
in its optimal state.
• Significant time lag between
mechanisms to restore
equilibrium and the body
registering their effect (eating: by
the time sufficient level has been
reached only a small amount has
been digested: insufficient data
to ‘turn off’ eating.)
• Evolved as two separate systems,
one for turning on eating and one
for turning off. Glucose levels
play most important part in
hunger → decrease = hunger
increase → decrease of glucose in
blood = lateral hypothalamus
activation = hunger. Individual
searches for and consumes food.
Rise in glucose levels → activates
ventromedial hypothalamus =
satiation.
The lateral hypothalamus:
• 1950s → damage to lateral hypothalamus
in rats caused a condition called aphagia
(‘absence of eating’)
• Stimulation of LH elicits feeding
behaviour.
• Opposing effects of injury + stimulation →
found the on switch.
• Neurotransmitter in hypothalamus
(neuropeptide Y) =important in ‘turning
on’ eating.
• When injected into rat hypothalamus
causes immediate feeding even when
satiated (Wickens 2000)
• Repeated injections = obesity in a few
days (Stanley et al 1986)
The ventromedial hypothalamus:
• Damage to VMH causes overeating →
hyperphagia.
• Stimulation in this are inhibited feeding.
→ VMH signals ‘turn off’ eating because
of many glucose receptors in this area.
• Damage to nerve fibres in VMH leads to
damage in paraventricular nucleus (PVN)
→ now believed PVN alone causes
hyperphagia (Gold 1973)
• PVN also detects specific food our body
needs.
Neural control of cognitive factors:
• Thinking about food, smells and
food-related sights triggers
feelings of hunger.
• Neural control of these cognitive
factors in hunger probably
originates in two main brain
areas → amygdala and the
inferior prefrontal cortex.
• Amygdala: selection of foods on
the basis of previous experience.
Rolls and Rolls 1973: surgically
removing amygdala in rats
caused them to feed on both
familiar and unfamiliar food
without preference. Where as
rats with the amygdala intact
would initially go for more
familiar foods.
• Inferior frontal cortex: receives
message from olfactory bulb
(responsible for smell.) Odours
influence taste of food so
damage in this area is thought to
decrease eating as there is
diminished sensory response to
food and probably to taste (Kolb
and Wishaw 2006)
5. Neural mechanisms in eating behaviourEvaluation:
Limitations of a homeostatic
explanation:
• For a hunger mechanism to be
adaptive it must both anticipate
and prevent energy deficits not
just react to them.
• The theory that hunger and
subsequently eating are only
triggered when energy resources
fall below their desired level is
incompatible with how such
systems should have evolved →
for such a mechanism to be truly
adaptive it must promote
consumption levels that maintain
bodily resources well above
optimal, to act as a buffer against
future food availability.
The role of the lateral hypothalamus:
• The view that the LH serves as an ‘on
switch’ for eating has a few problems →
damage to the LH also causes deficits in
thirst and sex rather than just hunger.
• Recent research shows that eating
behaviour is caused by neural circuits in
the brain, not just the hypothalamus.
Neuropeptide Y:
• Marie et al: genetic manipulation of mice
so NPY is not produced. They found no
subsequent decrease in feeding
behaviour. They suggest that hunger
stimulated by injections of NPY may
actually be an experimental artefact. The
flood of NPY from injections during
experimental manipulations could cause
behaviour different from normal
amounts.
The role of the ventromedial
hypothalamus:
• Early researches found that
damage to the VMH resulted in
hyperphagia and obesity in a
number of different species
including humans → VMH is
designated the ‘satiety centre’.
• Gold: lesions restricted to VMH
alone did not result in
hyperphagia → overeating only
produced when lesions included
other areas such as the PVN.
• Not very reliable: other
researches fail to replicate his
findings → most studies show
that VMH lesions ate
substantially more than those
with PVN lesions and
subsequently gained more
weight.Neural control of cognitive factors:
• Klüver-Bucy Syndrome: Patients with this syndrome typically show increased appetite, indiscriminate eating
and even attempts to eat non-food items. Research suggests that damage to the amygdala and inferior
prefrontal cortex suggests that food cues no longer accurately represent their real reward value to the
individual.
• Research support: Zald and Pardo 1997 → physiological evidence that amygdala participates in emotional
processing of olfactory stimuli. Exposed healthy adult pps to aversive olfactory stimuli while measuring blood
flow to amygdala using a PET scan. Exposure to unpleasant odours showed sign. Blood flow increases to the
amygdala where as non-aversive smells did not cause an increase. Increased blood flow also associated with
subjective ratings of the perceived unpleasantness of the stimuli.
Theorists
suggest
motivation for
eating comes
from positive
incentive value,
relish for foods
which promote
survival.
Yang et al: Canada, NPY produced by
abdominal fat, vicious cycle, targeting
high NPY individuals, drug therapy.
6. Evolutionary Explanations of Food Preferences
Explanations:
Environment of Evolutionary
Adaption:
• Environment where species
first evolved.
Early Diets:
• Energy resources were vital in
order to stay alive and find
the next meal – developed
preference for fatty foods.
• High calorie foods not as
plentiful, developed a
preference for them.
Preferences for meat:
• Meat began to be included
in human diet due to decline
in quality of plant foods.
• Milton suggests that without
animals it is unlikely we
would have secured enough
nutrition from a vegetarian
diet in order to evolve so
intelligently.
• Meat supplied amino acids,
minerals and nutrients.
Taste aversion:
• Bait shyness: farmers trying to rid
themselves of rats – difficult to kill as they
would only take small amount of any new
food (poisoned) and rapidly learn to avoid it.
Garcia et al; rats made ill through radiation
shortly after eating saccharin, developed an
aversion to it, associated illness with
saccharin.
• Adaptive advantages: Once learned,
aversions were hard to shift – adaptive
quality designed to keep ancestors alive.
• Medicine effect: preferable food eaten when
ill in the future; Garcia et al: when a
distinctive flavour is presented to a thiamine
deficient rat followed by thiamine injection
they will acquire a preference for that
flavour.
Eval:
• Importance of calories in early diets:
Gibson and Wardle: best way to predict
which fruit + veg would be preferred by
4/5 yr. olds was how dense in calories they
were. Bananas + Potatoes are calorie rich
more likely to be chosen.
• Could early humans have been
vegetarian: Cordain et al: argued humans
could’ve mostly got calories from sources
other than animal fat. Suggestion of
vegetarian. BUT Abrams shows that from
anthropological evidence we can see that
all societies display preference for animal
foods and fats. Nor would it have been
possible for early humans to get sufficient
calories from plants and grains available.
• Explaining taste aversion: Seligman claimed
different species evolve different learning abilities,
something he called biological preparedness.
• Support for evolutionary theory: Detecting toxins:
bitter taste evolved as a defence mechanism for
potentially harmful in plants. Sandell and Breslin:
screened 35 adults for bitter taste receptor gene.
Rated bitterness of vegetables, some containing
glusinolates and some not, well known for toxic
effects at high doses. Those w/ sensitive gene form
rated glusinolate containing vegetables as 60% more
bitter.
• Evidence from other primates:
Craig Sanford observed
Chimpanzees in Tanzania’s
national park showed same
problems we used to face. After
coming close to starvation for
much of the year, when they
finally manage a kill, they go
straight for the fattiest parts such
as the brain and bone marrow,
rather than tender, nutritious
flesh.
Doesn’t include ‘nurture’
side of food preferences,
such as religion.
Based on a time
period from
which we can no
longer test,
reliability
reduced.
7. Psychological explanations of Anorexia Nervosa
Explanations:
Cultural Ideals and the Media:
• Cultural ideals: western standards
of attractiveness widely believed to
contribute to AN development.
Gregory et al: 16% of 15-18 year old
girls in the UK were currently on a
diet.
• Media influences: Major source of
influence for body image attitudes.
Individuals with low-self esteem
more likely to compare themselves.
Ethnicity and peer influence:
• Incidence of AN in non-western and
Black cultures is much lower. Grabe
and Hyde, meta-analysis, 98 studies,
African Americans reported
significantly less body dissatisfaction.
• Peer influence: particularly
important to an adolescent, so they
may be susceptible to peer influence
over disordered eating. Eisenberg:
dieting among friends significantly
related to unhealthy weight control
behaviours such as pills or purging.
Jones and Crawford found that peers
serve to enforce gender based
ideals; over weight girls and
underweight boys tend to be most
teased.
Personality:
• Perfectionism: often found in
individuals with AN. Strober: compared
to normal control group –
retrospectively evaluated personality
traits in teenage boys and girls. Boys:
50% perfectionism, Girls: 73%
perfectionism.
• Impulsiveness: Individuals with AN act
more impulsively than they self-report.
Butler and Montgomery: compared to
normal control, patients with AN
responded rapidly but inaccurately to a
performance task.Eval:
• Hoek: set out to test if AN was rare among
non-western cultures. Curacao (island
where it is acceptable to be overweight)
hospital records over two year period,
approx. 44,000 people, found 6 cases,
within range of results reported in Western
countries.
• Becker et al: Fijian girls, introduction of a
television in 1995, girls stated desire to be
thin like the Western television characters.
Bruch’s psychodynamic explanation:
Observation that parents who have children with AN tend to define their children’s needs rather than
allowing them to define their own. Bruch found many of these parents claimed to anticipate their
children’s needs rather than letting them ‘feel’ hungry. Research by Button and Warren also supports
Bruch's claim that people with AN rely excessively on the opinions of others.
• Cachelin and Regan: no sign. Differences in
occurrence of disordered eating between
African Americans and white counterparts.
• Shroff and Thompson: found no
correlation between friends and measures
of disordered eating.
• Halmi: 322 women, with history of AN
across Europe and US. Individuals with
AN history scored high on multi-
dimensional perfectionism scale when
compared to a group of healthy
women.
• Methodological questions: difficult
separating personality traits from
short-lived states which may be
caused by starvation. Relies on sample
of diagnosed patients, based view of
relationship between personality and
disordered eating.
8. Biological explanations of Anorexia Nervosa
Neurotransmitters:
• Serotonin: disturbance of S levels
characteristic of eating disorders.
Bailer et al: women recovering from
restricting type AN and purging type
+ healthy controls, sign. Higher S
levels in those recovering from
purging type. Highest S levels also in
those w/ most anxiety, consistent
disruption may lead to anxiety +
trigger AN.
• Dopamine: Kaye et al: PET scan, 10
AN recovery, 12 healthy, AN women
= over activity in dopamine
receptors in basal ganglia where
dopamine plays role in perception
of harm and pleasure. People with
AN find it hard to associate good
feelings with food.
Neurodevelopment:
• Pregnancy and birth complications:
Lindberg and Hjern- sign. Association
between premature birth and AN.
Birth complications may lead to brain
damage caused by hypoxia –
impairing neurodevelopment.
Nutritional factors may be implicated
if mothers have an eating disorder.
Bulik et al: mothers with AN expose
their child to ‘double disadvantage’:
genetic vulnerability transmission
and inadequate nutrition.
• Season of Birth: Eagles: people with
AN more likely to be born in spring.
Wilhoughby: among equatorial
regions of the world, no seasonal
effect. Other places are subject to
cooler temp and infections.
Adapted to flee hypothesis:
• Adaptive response to famine
conditions: symptoms of AN such as
food restriction, hyperactivity and
denial of starvation reflect operation of
adaptive mechanisms that used to
cause migration in response to famine.
When someone loses weight,
physiological mechanisms conserve
energy and increase desire for food.
These must be turned off when
extreme weight loss is due to food
depletion, so that individuals can
increase survival rate by migrating.
• Migratory restlessness: Hyperactivity
found in Anorexics may be a form of
‘migratory restlessness’. In the EEA
starving foragers who deceived
themselves about their physical
condition would’ve had more
confidence about moving on to a more
favourable environment and would’ve
been more likely to survive.
• SSRIs: SSRIs alter levels of brain serotonin, but
are ineffective when used on patients with AN.
But Kaye et al, found that when used on
recovering patients, the drugs were effective in
preventing relapse.
• Castro-Fornieles: found adolescent girls with AN
had higher homovanillic acid (dopamine waste
product) than control group. Improvement in
weight levels associated with normalisation of
acid levels.
• Favro et al: Found the perinatal
complications significantly associated
with risk of developing AN, were
placenta blood supply obstruction, early
eating difficulties and low birth weight.
• Eagles et al: Found individuals with AN
tend to be born later in birth order.
More elder siblings had while in the
womb – more infections exposed to.
Critical period = 2nd trimester, spring
birth – infections during critical time.
• Evolution: Why AN symptoms passed on, as
they decrease fertility /fatal, AN would serve
function in ancestral setting, not modern.
• Treatment implications for AFHH: this
biological reason can help families;
awareness of causal reason can make them
more compassionate towards anorexic child.
