eating behaviour Flashcards

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1
Q

early exposure (SLT)

A
  1. Behaviours are a result of observation (of Role Models) and imitation
  2. We retain the memory of the action/behaviour and when a similar situation arises, we might be motivated to imitate it.
  3. Motivation may be due to vicarious reinforcement (rewarded for +ve behaviour/no consequence of –ve behaviour)
  4. So if peers/parents enjoy a certain food, we will be influenced by this.
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2
Q

early exposure (classical conditioning)

A
  • Associating a neutral stimulus with an unconditioned stimulus
  • Pleasant experiences associated with neutral stimulus (e.g. parents attention on a birthday with birthday cake)
  • But CC can also lead to negative attitude to food (e.g. if we eat something while ill, we might associate it with the ill feeling and ignore it in the future)
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3
Q

early exposure (The Mere Exposure Effect)

A
  • The more exposed we are to something, the more familiar we become with it, which results in a positive attitude towards it.
  • If we are exposed to unfamiliar foods, we are likely to have negative attitudes towards them
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4
Q

research evidence SLT

A

Birch et al. (1980)
Peer Influence to change children’s preference for vegetables
Children sat next to another child who liked different vegetables to them for 4 days (peas vs carrots)
Children showed a definite shift in vegetable preference which was still evident in a follow up study several weeks later.
This supports SLT as a theory because it shows that if children witness their peers eating a different vegetable, they will be likely to imitate them.
It has high validity due to the follow up study (long term)

Ogden (2004):
Parental Influence
Reported consistent correlations between parents and their children in terms of eating habits.
This study shows a correlational link, but there is an issue of causality.
The food preference may be due to availability – i.e. parents buy what they like, so kids eat it because there are no other options.
Self-report issue

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5
Q

research evidence CC

A

Classical Conditioning
Birch et al. (1980):
Food paired with a reward
Gave children food in association with positive adult attention
Found to increase food preference, but it doesn’t prove that it changes attitude, only behaviour.

Garcia et al. (1974):
Food and physiological consequences
Rats in a cage illuminated with red lights (NS)
Given a dose of radiation (UCS) in sweet water (NS) – this caused the sickness (UCR)
Later avoided sweet water (CS for CR)
But didn’t avoid the red lights (no CR) – innately know – not all food preference is learned.
This demonstrates that classical conditioning can shape attitudes to food
CC doesn’t explain why the rat didn’t avoid the red light – not sufficient

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6
Q

research evidence mere exposure effect

A

Birch and Marlin (1982)
Humans create a preference for things merely because they are familiar with them. This arises from exposure on a number of occasions
Introduced 2 year olds to new foods either 20, 10, 5 or 1 time(s)
Found that more exposure led to increased preference
8 – 10 times is usually necessary for a significant shift.
We are generally neophobic (fear of new things)
Show avoidance of new foods
Like familiar foods – once given a few times, it becomes familiar.

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7
Q

early exposure IDA

A

Nature/Nurture Debate
Most factors relating to early exposure are purely environmental and largely work on behaviourist principles. They ignore biological factors; for example, our eating behaviour is also influenced by hormones and neural mechanisms.

The biological theory is reductionist – it reduces a complex human behaviour to a very minimalist and limited theory. This leads to other factors (such as genetics) being ignored.

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8
Q

practical applications of early exposure

A

Influence of parents and peers
Give children food with positive attention

Exposure to new foods
Exposure – introduce children to new foods over a long period of time

Physiological consequences of eating certain foods
Sickness

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9
Q

Stress - individual differences

A
Greeno and Wing, 1994
This suggests that some people are more vulnerable to the effects of stress on food and eating behaviour. There are 4 individual characteristics that explain why some people increase or change food intake when subject to stress.
4 types of eaters: 
External
Emotional 
Restrained
(gender also has an impact)
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10
Q

External eaters

A

Individuals who eat in response to environmental cues
Eat when food is available rather than when hungry
Eat in response to food cues (e.g. sight or smell of food)

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11
Q

Emotional eaters

A

Individuals who fail to distinguish between feelings and hunger
When anxious or emotionally aroused, they misinterpret this emotion as hunger
Could be due to inconsistent parenting

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12
Q

Restrained easters

A

Individuals deliberately try to limit their food intake (e.g. on a diet)
They use willpower to suppress food intake
Will power is undermined by stress

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13
Q

external eaters prediction

A

External eaters are more likely to increase food intake when stressed as long as there is food available. Stress makes them more aware of available food.

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14
Q

emotional eaters prediction

A

Emotional eaters will increase food intake when stressed as they experience their anxiety as hunger

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15
Q

restrained eaters prediction

A

Restrained eaters increase their eating while stressed, whereas people who do not have to try hard to control their eating are unaffected by stress.

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16
Q

gender and eating prediction

A

Women are more likely to eat under stress than men, particularly certain foods.
Women are also more likely to be restrained eaters

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17
Q

research evidence for stress and eating

A

Oliver et al (2000)
found that stress didn’t alter overall food intake or appetite.
-Stressed emotional eaters consumed more sweet/high-fat foods than un-stressed non-emotional eaters.
-Women scored higher on emotional eating than men
-Shows support for individual differences for types of food consumed when stressed and a difference between men and women, but not overall intake.

Conner et al (1999)
measured number and severity of daily hassles and number of snacks consumed.
-Pps also asked to complete a questionnaire to assess their eating behaviour: restrained eating, emotional eating and external eating
-Found that external eaters had a strong, positive correlation between hassles and snacking.
-No significant relationship between the same factors for low external eaters, emotional eaters and restrained eaters.

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18
Q

IDA for stress and eating behaviour

A

Deterministic
External eaters may take on a fatalistic approach to dieters – the theory is deterministic and suggests that external eaters will eat food on site and there is little they can do to avoid this.

Nature/Nurture
On the nurture side of the debate – suggests that purely environmental factors influence eating behaviour
Ghrelin and leptin have both been proven to have an impact on eating – as Carlson showed on ‘ob’ mice – missing leptin, and when injected with it, they stopped eating and lost weight

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19
Q

practical applications of stress and eating

A

Dieting could be made more successful if stress is reduced – only if external eaters?

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20
Q

outline the boundary model

A
  • There is a ‘set-point’ that our weight generally stays at – and should return to if we go over or under this weight.
  • If we go under (i.e. during an illness we eat less) hunger is stimulated and we eat more
  • If we go over (i.e. over Christmas we eat more) there in an inhibition of hunger and we eat less.
  • This creates a psychological boundary influencing how much we eat
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21
Q

what is a cognitive boundary? (boundary model)

A

Dieters set cognitive boundaries (lower than the physiological boundary) to lose weight – an unrestrained eater will eat until their body says they are full (physiological boundary), but a dieter will eat until their cognitive boundary – this means they are usually still hungry.

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22
Q

what happens when a dieter passes their ‘cognitive boundary’ ?

A

If for whatever reason (stress or special occasion) a dieter passes their cognitive boundary, they will continue to their physiological boundary due to the ‘what the hell effect’ (or the Cognitive dissonance effect)
The dieter will feel a sense of ‘why bother?’ and continue to eat.
Due to restrained eaters being quite vulnerable to the effects of stress (individual differences model), it happens quite often – this could explain why dieting is often unsuccessful.

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23
Q

boundary model Herman and Mack

A
  • the more unrestrained eaters pre-loaded (given food to see whether consumption of this food affected subsequent food intake – milkshakes, 0, 1 or 2), the less food they subsequently consume (ice cream)
  • restrained eaters that didn’t pre-load, consumed the least food subsequently, but those that did consumed more (those that pre-loaded most subsequently consumed most)
  • found a correlation between higher restrained eating and the more they ate after two milkshakes
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24
Q

how does Herman and Mack support the boundary model

A

Support for boundary model because restrained eaters have their cognitive boundary broken by the milkshake, so the ‘what the hell effect’ kicked in and they ate more ice cream than the no pre-loading group.

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25
Q

boundary model IDA

A

Deterministic
Suggests that eating behaviour is beyond our control and that humans lack free will
Suggests that the diet will fail if cognitive boundary is lower than the set point
When stressed, it suggests that they will overeat

Simplistic
Athletes and anorexics still restrict their diet, but don’t suffer from ‘what the hell effect’.
Anorexics are hungry but won’t eat more if they go over their cognitive boundary
Leads to sections of society being ignored

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26
Q

briefly describe the theory of ironic processes of mental control (denial)

A

thought suppression can have a contradictory effect of making the thoughts that we are meant to be suppressing, more vivid.

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27
Q

research evidence for denial theory

A

Wenger et al (1987)
Asked pps to NOT THINK about a white bear and ring the bell when they do
Asked pps to THINK about a white bear and ring the bell when they do
Those that were asked not to think of the white bear rang their bells more often
This supports the theory because when a dieter is trying not to eat food, they are trying not to think about food either – but because this is a cognitive decision to not think about food, the only thing they think about anyway is food, so they end up eating it anyway.

But it doesn’t explain individual differences

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28
Q

practical applications of denial theory

A

Rather than completely cutting food altogether, we should moderate the amount we eat to feed the temptation but still reduce the amount we eat.

In therapy, you could encourage dieters to think about food – alter the thoughts, don’t suppress them.

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29
Q

cognitive behaviour model and successful dieting

A

in order to diet successfully, the dieter needs to hold certain beliefs, but also behaviour in certain ways

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30
Q

cognitive behavioural model (Cognitive elements-beliefs)

A

Psychological model of obesity – if individuals believe obesity is due to emotional eating, low self-esteem/depression, then dieting can be successful as weight loss is possible
Motivation for weight loss – personal reasons can motivate people to lose weight (e.g. self-esteem or attractiveness)

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31
Q

cognitive behavioural model (behavioural element- operent conditioning)

A

Small successes in weight loss are positively reinforcing (form the self and others) as the individual believes that the weight loss is due to their own behaviour/dieting
Positive reinforcement strengthens behaviours, so dieting is likely to continue and succeed.

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32
Q

cognitive behavioural model research evidence

A

Ogden
investigated the differences between weight loss regainers (WLRs) and weight loss maintainers (WLMs)
WLMs are more likely to endorse a psychological model of obesity in terms of consequences (e.g. depression and low self-esteem) and feel better about themselves.
WLMs are less inclined to endorse a medical model (genes/hormones)
This supports the cognitive elements of model because it shows that those that maintained their weight loss agree with what the model suggests.

Kiernan et al
Found that those more dissatisfied with their body type at baseline were more successful in dieting – the motivation for weight loss may be important
Supports cognitive element (internal motivation)

33
Q

cognitive behavioural model research evidence evaluation

A

Based on interviews and questionnaires
There is an issue of self-report, which creates an issue of validity (individually) and reliability (overall results)
Interviews could have social desirability bias

34
Q

cognitive behavioural model - practical applications

A

Personal motivation in necessary, so may not help those who need to diet for health reasons.

35
Q

cognitive behavioural model IDA

A

On the nurture side of the debate – attitude needs to change for weight loss to be possible
Blames the individual

36
Q

dieting success - paying attention to detail

A
  • People need to pay attention to the individual specific details of the food they’re eating, rather than the food as a whole.
  • This is because humans often find repetition boring, but if we focus on the details it becomes less boring
  • For example, rather than thinking ‘another boring salad’, focus on the ‘crunchy cucumbers’ and the taste of the tomatoes etc.
  • Detail helps maintain a diet
37
Q

dieting success - paying attention to detail

research evidence

A

Redden (2008) –
gave two groups the same jelly beans, but group one had flavour labels (e.g. delicious cherry) and group two just had general labels (e.g. jelly bean 7)
-Found that the group with the flavour labels (more interesting) got less satiated and enjoyed the jelly beans more than the other group at the end of the experiment
-But both groups enjoyed them the same at the start
-This shows that the group with general labels got bored of the jelly beans, but the other group didn’t (or not as much)

38
Q

outline dual model of feeding

A

Blood glucose levels fall → Sensed by hypothalamus →Hunger is experienced →Lateral hypothalamus is activated →Eating →Leads to an increase in blood glucose → Sensed by hypothalamus → Ventromedial hypothalamus is activated → Stop eating

39
Q

dual model of feeding research evidence

A

Hetherington and Ranson (1942)
Lesions to the ventromedial hypothalamus (VMH) caused rats to overeat and become obese.
VMH acted as a satiety centre (activated when full to inhibit or stop eating)

Anand and Brobeck (1951)
Lesions to the lateral hypothalamus (LH) led to aphagia (loss of eating) in rats.
Suggested that the LH was a feeding centre and stimulated hunger when activated.
Later studies supported this:
Electrical stimulation of the VMH inhibited feeding
Electrical stimulation of the LH produced feeding

40
Q

issues of generalisability in the dual model of feeding

A

While the brain physiology in humans and rats is likely to be similar, humans have the capability to override neural impulses to eat, but rats eat when their brain tells them to.

The lesions/electrical impulses may have also affected other important parts of the brain as well as the VMH/LH. This creates an issue of validity.

41
Q

dual model of feeding IDA

A
  • Focussed purely on Nature side of the debate
  • It cannot explain all eating behaviour in humans as it is too limited
  • Determinism
  • Levels of blood glucose don’t usually drop so low as to trigger feeding
  • Spontaneous eating is usually followed by low glucose levels, but levels are back to normal before eating
  • If prevented from eating when the person craves at the time, glucose returns to normal
  • It is as if the brain deliberately lowers blood glucose momentarily in order to allow yourself to eat.
42
Q

dual model of feeding implications

A

Despite problems, evidence is scientific

Dual centre model itself is likely to be accurate, but it can’t explain all eating behaviours (e.g. Christmas/diets)

43
Q

outline the role of ghrelin in eating

A

Secreted from the stomach to the LH, which creates the sense of hunger, to stimulate feeding.

Encourages eating→
From stomach→
Acts on the Lateral Hypothalamus

44
Q

research evidence for the role of grehlin

A

Cummings et al (2004) –
investigated ghrelin levels between meals (every 5 mins) until pps asked for their evening meals

  • Found that ghrelin levels fell immediately after lunch, then reached their lowest after about 70 mins
  • They then slowly began to rise and peaked when pps asked for the evening meal
  • In 5/6 pps, ghrelin levels correlated with self-assessed hunger levels.
  • This supports the role of ghrelin in eating behaviour because it shows that when least hungry (immediately after a meal) ghrelin is at its lowest. Then as hunger increased, so did ghrelin (peak levels at peak hunger)
45
Q

outline the role of leptin

A

Leptin acts as a satiety signal and is released to the VMH to reduce food intake.

Inhibits eating
From fat cells (adipose cells)
Acts on the Ventromedial Hypothalamus
Acts as a satiety signal

46
Q

research evidence for the role of leptin

A

Carlson (2007) –
studied ‘ob’ mice with the gene that produces leptin missing
The mice didn’t produce leptin, so their VMH doesn’t receive a satiety signal to inhibit eating. This meant that the mice at continuously until they were obese.
They were injected with leptin, and eventually their weight went back to normal.

This may suggest that increasing leptin levels is a potential way of curing obesity
However, this isn’t the case as many obese people have normal, or even high levels of leptin
It seems to be the case that the brain is insensitive to the effects of leptin, or other neural mechanisms override the satiety signals.

47
Q

IDA neural mechanisms

A

Reductionist
Eating is complex, so should not be reduced to the role of an individual brain structure or hormone
This makes it simplistic because it ignores any environmental effects (being an external eater/conditioning/lifestyle/convenience/opportunity etc.)
It also ignores emotional triggers (comfort eating)
It also ignores cognitive (thinking about food triggers neural mechanisms)

Nature/Nurture
Nature side of the debate
It has valid support (dual centre model studies and hormone studies)
But it is simplistic (ignores culture/environment/cognitive/emotional etc.)

Deterministic
The biological approach is deterministic, which could lead to fatalism and people not dieting because they feel that they aren’t in control of their weight, but their hormones are.

48
Q

3 explanations of eating from evolutionary explaination

A

preference for sweet foods
preference for high calorie foods
preference to avoid food that has made us ill in the past

49
Q

evolutionary explanation - preference for sweet foods

A
  • Sweet foods usually indicate high calorie foods, so it would be adaptive to have this preference for all the same reasons as it is to have a preference for high calorie foods
  • Sweetness also indicates ripeness, which stops us from eating un-ripe berries or foods which can make us ill.
  • These fruits are also generally not poisonous if they are sweet, which makes them valuable.
  • those with this preference were more likely to procreate and their offspring were more likely to survive in the EEA. This means that their genes are more likely to be passed through the generations and the preferences was naturally selected and became widespread.
50
Q

evolutionary explanation - preference for calorie rich foods

A
  • provide energy which increases chances of survival as it will aid in hunting and protecting offspring
  • maximises the fight or flight response which will increase chances of survival
  • Calorific foods also build up fat stores, because food in the EEA (Environment of Evolutionary Adaptedness) was scarce and erratic, this would help in times of food shortage.
  • those with this preference were more likely to procreate and their offspring were more likely to survive in the EEA. This means that their genes are more likely to be passed through the generations and the preferences was naturally selected and became widespread.
51
Q

evolutionary explanation - preference to avoid food that has made us ill in the past

A
  • taste aversion
  • Associating sickness with whatever food was eating (classical conditioning)
  • Adaptive to ancestors because it would have enhanced survival, and made us less vulnerable (as when sick, our ancestors wouldn’t have been able to hunt or protect the family effectively)
  • Avoiding a poisonous food that’s made us ill reduces the chances of death
  • those with this preference were more likely to procreate and their offspring were more likely to survive in the EEA. Therefore their genes are more likely to be passed through the generations and the preferences was naturally selected and became widespread.
52
Q

ao2 preference for high calorie foods

A

Gibson and Wardle (2001) – children told to choose from a range of fruit and vegetables
Found that the best predictor of what food the children would choose was the most calorie dense foods
In particular bananas and potatoes.

53
Q

ao2 preference for sweet foods

A

Meiselman (1977) – found that people of any age were more likely to choose sweet foods over others
Capaldi et al. (1989) – found the same for other species, such as horses, bears and ants.
Logue (1991) – found physiological evidence – the tongue has specific receptors to detect sweetness, but it doesn’t for other tastes, which are detected by non-specific receptors.

54
Q

ao2 preference to avoid food that has made us ill in the past

A

Garcia et al. (1977) – gave wolves a mild poison in lamb wrapped in sheep skin.
When the wolves approached a sheep and sniffed it, they left it alone – they had associated the sickness with the smell of sheep.

55
Q

practical applications from preference to avoid food that has made us ill in the past

A

Cancer patients often suffer from sickness when going through radiotherapy or chemotherapy, and if food in consumed during this time period, food aversion can occur.
Bernstein and Webster (1980) – gave patients going through chemo a novel tasting ice cream and found that they developed an aversion to it because of the association with their sickness.
This led to the development of the ‘scapegoat technique’, which is where a novel tasting food is given alongside a familiar tasting food during chemo, and an aversion is created to the new food, rather than the familiar food

56
Q

Anorexia Nervosa

A

Katzman et al (2004) –
performed a study in Curacao, an island where being overweight is socially desirable, yet the rate of AN is the same as in western cultures (1%)

57
Q

Katzman et al - personality types of AN sufferers

A

Perfectionist
High levels of anxiety
Aspirational
Face challenges when trying to maintain an active professional and personal life
Saw themselves as different from the norm
→ Can cause stress

58
Q

Katzman et al - immediate social groups of AN sufferers

A

Higher-educated
Higher social-class
Generally the white elite
→Can provide pressure

59
Q

Katzman et al -wider island envrionment of AN sufferers

A

Black majority
Lower class
Lesser educated
→Can cause a reaction against the environment

60
Q

which factors put people at high risk of developing AN

A
Hard working/high achieving
High need for control/low tolerance of change
Perfectionist
Compliant, high need for approval
Competitive environment
Occupation associated with low weight
61
Q

socio-cultural explanation of AN

A
Western standards of attractiveness is held as an important contributory factor
The media (e.g. magazines, films, toys etc.) creates the social norm that ‘thin is good’
This creates a drive for thinness among western adolescent girls.
But the media doesn’t influence everyone in the same way – those with low self-esteem are more likely to compare themselves to the idealised images in the media
62
Q

how does SLT play a role in socio-cultural explanation of AN

A

Social learning takes place while these individuals observe thin models receiving admiration, attention and praise (vicarious reinforcement) and are therefore motivated to imitate their behaviour.
If they lose weight are become more like their idols, self-efficacy increases and whatever they did to induce weight loss continues.
This could be influenced by other people praising the individual and the positive reinforcement could influence them to continue losing weight.

63
Q

A02 socio-cultural explanation of AN

A

Becker et al. (2000) -
studied the effects on adolescent girls and AN that TV has when it is introduced to Fiji
Findings:
% of girls who reported to vomit to control their weight increased by 12% (3% in 1995 to 15% in 1998)
% with a high score on the eating questionnaire, indicating a risk of disordered eating increased by 16% (13% ’95 to 29% ’98)
Those who reported to watch more TV, were more likely to be at risk
Conclusions:
Overall, this indicates a strong link between exposure to western ideals of thinness (TV/media) and changed attitudes towards eating.
The fact that girls’ desire to be slim increased when they were exposed to western media, is a sign that young Fijians are striving to conform to western standards.
These changed attitudes are likely to lead to the development of eating disorders.

64
Q

Evaluation of Becker et al

A

The findings don’t demonstrate a cause – the IV wasn’t manipulated (due to it being a natural experiment), so we cannot make causal assumptions.
The changes could be due to the strains of the traditional culture attempting to keep up with the more technologically advanced cultures.
The assumption that changing attitudes leads to eating disorders may be wrong
Eating disorders may be at least related to biological reasons, then the cultural explanation alone isn’t sufficient.

65
Q

socio-cultural explanation of AN IDA

A

Gender differences – female stereotypes are more associated with dieting and thinness – we are also more likely to imitate role models who are similar to us (same sex)
More anorexics in general (including males) – there is an increasing emphasis on thinness due to the media being more widespread

Cultural differences – different attitudes to eating and different social norms
But it cannot explain individual differences. Everyone is exposed to the media in the west, but only 1% develop AN. Furthermore, many people try to diet, but again, very few develop AN from it.

The socio-cultural model is insufficient on its own, and may need another biological or psychological explanation to explain individual differences.
Katzman answers this as it’s the more aspirational/anxious/perfectionist people that tend to suffer more.

66
Q

outline cognitive explanations of AN

A
  • Suggests that AN is a mental illness caused by faulty cognitive processing and fault schemas
  • AN sufferers may have faulty processes because they perceive themselves as unattractive or overweight and have a distorted body image.
  • This could be due to their perception of cultural ideals of thinness.
  • leads to increasingly anxious and obsessive thoughts which are linked to future consequences.
  • One way of dealing with this is to increase the desire for control – one area which is perceived as being easy to control is food intake.
  • When individuals restrict food intake, they get an increased sense of control which increases the sense of self-worth which positively reinforces restricted eating and weight loss.
  • As hunger is seen as a threat to control, it negatively reinforces restricted eating.
  • The individual’s anxiety is reduced when not eating, so AN may develop.
67
Q

cognitive explanation of AN Slade and Russel

A

tested people with and without AN to see if there was a difference in the way they perceive their own body width and the height and width of some objects.
Found that people with AN, overestimated the width of their own bodies by 25-55%
The control group estimated their body with accurately
No difference between AN sufferers and control group for estimations of objects
Concluded that there was a strong difference between distorted body image and AN

BUT there were methodological issues with this study: generally we overestimate out own body width, and we get better at estimating with age. The control group was significant older than the AN group, so we would presume that the control group would overestimate less.

68
Q

cognitive explanation of AN Cooper and Turner

A

used a questionnaire to assess the emotional aspects of body self-perception
AN patients reported more negative beliefs about themselves than dieters and a control group (no unusual eating behaviour)
AN patients were more likely to believe that their acceptance from other people was reliant on their body type.
They were more likely to base their own self-esteem on their body type.

69
Q

IDA for cognitive explanation of AN

A

-Good explanatory power
Can explain why only some dieters develop AN – all exposed to ideals of thinness, but only those with faulty processes are affected.
-Practical applications
Therapy, in particular CBT
But Wilson (2005) found that while CBT was the most effective therapy for AN, it was also limited in its effectiveness and didn’t help all sufferers.
-Cause or effect
It’s difficult to say whether cognitive biases exist before the onset of AN, or after.

70
Q

outline the evolution of eating disorders

A
  • Binge-eating would have been adaptive as food resources would have been scarce and erratic in the EEA.
  • It would have been adaptive because it would help to make the most of the sweet/calorific foods when they do become available.
  • Almost everyone would have been better off with more fat, sugar and salt so it would be adaptive to constantly crave more of them.
71
Q

The reproduction suppression hypothesis

A

Surbey (1987)
suggests that adolescent girls’ desire to control weight comes from the adaptation to control sexual maturity. This is because women in the EEA wouldn’t have wanted to fall pregnant when the conditions weren’t favourable as chance of death in childbirth was extremely high.
Surbey suggests that AN is a ‘disordered variant’ of the adaptive ability of females who wish to alter the timing of reproduction because they feel unable to cope with the biological, emotional and social responsibilities of womanhood.
Stress triggers this evolutionary adaptation in today’s adolescent girls.

72
Q

The ‘adapted to flee’ hypothesis (AFFH)

A

Guisinger (2003)
suggested that the symptoms of AN, such as food restriction, hyperactivity and denial of starvation all reflect the adaptive mechanisms that once caused migration if there was a local famine.
it would have been adaptive to migrate, especially during a local famine, because it would be possible to find food in other places. If they do find food, it means they are more likely to survive and pass on their genes.

73
Q

evolutionary explanation of AN research evidence

A

Holland et al (1988)

34 twin pairs, where one of the twins has AN
The concordance rate for MZs =56% and DZs = 7%
This suggests a genetic basis for AN
Yet, genes are not completely responsible, they create a predisposition to the illness.
Environmental triggers may interact with genetic predisposing = Diathesis Stress Model

If AN evolved with is, it must be in our genes
MZs had a higher concordance rate than DZs. This shows that there must be a genetic link when it comes to AN

74
Q

explanatory power of evolutionary explanation of AN

A

The evolutionary explanation doesn’t explain:
The increased incidence in higher socio-economic classes
The increased incidence in immigrants to western cultures compared with those who stay at home.
The recent increase in prevalence
Gender differences (90% of AN sufferers are female) – could be the reproductive suppression hypothesis?

75
Q

IDA for evolutionary explanation of AN

A

reductionist:
Reducing AN down to simply evolution leads to other factors (e.g. environmental/stress) to be ignored

Diathesis Stress Model – we evolved the genes but need the environmental trigger (e.g. stress)
People may stop fighting the illness as it is in their genes – fatalistic

76
Q

Neural explanations – the role of the hypothalamus in AN

A

Garfinkel and Garner (1992) suggested that AN sufferers may have disturbed functioning of the hypothalamus. If the LH is damaged, under-eating will occur because there are no feelings of hunger. It is also possible that the hypothalamus is undamaged but there is a malfunction of ghrelin getting to the brain.

77
Q

Neural explanations – the role of the hypothalamus in AN research evidence

A

Anand and Brobeck (1951) found that lesions to the LH led to a loss of eating behaviour in rats.
There is an issue when trying to apply this to AN sufferers because some people with AN do feel hungry – it is part of the disorder. Therefore, the illness cannot be purely explained by lesions to the LH because if it was, then all AN sufferers wouldn’t feel hungry.
In addition, some factors may impact humans, but not rats (e.g. socio-cultural/media/why we eat – emotional etc.)

78
Q

IDA of neural explanations - the role of the hypothalamus in AN

A

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