Eating behaviour Flashcards

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1
Q

List the factors influencing attitudes to food and eating behaviour

A

1) Early learning and experience

2) Mood, including stress

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2
Q

How does early learning influence attitudes to food and eating behaviour?

A

Early learning shapes eating behaviour and food preferences through exposure to food social learning, operant conditions and classical conditioning.

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3
Q

What is neophobia?

A

Fear of new things

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4
Q

How does exposure and neophobia relate?

A

Exposure to foods helps overcome neophobia, we prefer food we are familiar with

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5
Q

SLT’s explanation for eating behaviour

A

Observing other people’s behaviour
Parental attitudes to food and eating behaviour
Vicarious reinforcement (seeing someone get rewarded)
Vicarious punishment (seeing someone get punished)
Attention, Retention, motivation

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6
Q

Evaluation of SLT and eating behaviour

A

SUPPORT- Birch: gave children food in association with positive adult attention to change food preference.
Lowe: showed children “food dudes” video and shows that food preference can be changed through observation.
PA- SLT can be used to make children eat more healthy

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7
Q

Birch study evaluation for SLT eating behaviour

A

Birch study supports SLT because the children observed their peers behaviour which influenced their own eating behaviour. The children changed their preference for vegetables for example they didn’t like peas at the start but by the end were eating them. This shows how social learning can make a shift in food preference.

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8
Q

Outline Birch’s study

A

Used peer modelling to change children’s preference for vegetables. On 4 consecutive days the children were seated at lunch next to children who preferred a different vegetable to themselves (peas VS carrots). They found a definite shift in their vegetable preference which was evident in a follow up assessment several weeks later. Those who initially didnt like peas at the outset did like them by the end of the study.

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9
Q

Outline Lowe’s study

A

Children were shown videos of “food dudes” (older children who were enthusiastically consuming food that younger kids used to refuse). Results showed that exposure to the “food dudes” significantly changed the children preference and increased their consumption of fruit and veg.

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10
Q

Exposure to food and eating behaviour

A
  • The higher number of exposures to food the more likely -the child’s preferences would shift.
  • Found 8-10 exposures needed to shift preference
  • Prefer food we are most familiar (exposed to regularly)
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11
Q

Outline Birch and Marlin’s study

A

They introduced 2 year old children to novel foods over a 6 week period. One food presented 20 times, one 10 times, one 5 times and one remained new. The results showed a direct relationship between exposure and food preference. Found 8-10 exposures needed. Suggests we like food we are most familiar with.

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12
Q

Evaluation for exposure to food Nature and nurture argument for eating behaviour

A

NURTURE: SLT- learning to like foods e.t.c
can be overcome by parents and caregivers
NATURE: neophobic towards some food so early exposure might make child less neophobic
support :Benton- found that sweet foods are effective in reducing distress in young babies therefore it may be innate.
IDA: EEA- adaptive to avoid new foods incase poisonous
TOO SIMPLISTIC EXPLANATION

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13
Q

Factor that focuses on how much we eat

A

Mood (inc. stress)

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14
Q

Outline research into mood as an influence to our attitudes to food and eating behaviours

A

Garg et al- conducted a study which looked at the amount of popcorn ppts consumed when watching a sad film vs happy film. Ppts consumed more int he sad film than happy which shows how mood can effect the quantity of food we consume. Eat more when sad.

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15
Q

Evaluation of research into mood and eating behaviour

A

Garg et al- repeated measures design accounts for individual differences for example some participants having a greater preference for popcorn or that flavour more than others. They also closely matched the independent variables through rating, running time and genre which allows researches to rule out criticisms of boredom and determine they are measuring participants mood. By isolating the IV this explains how mood enhancement as aa factor of eating.

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16
Q

Biological explanation of eating behaviour and mood

A

One explanation that has been proposed for such mood enhancing effects is the OPIATE hypothesis. Neurotransmitters called ENDORPHINS regulate activity in the brain’s reward pathways. These pathways make us feel good to encourage biologically important behaviours such as eating.

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17
Q

Evaluation for biological explanation of eating behaviour and mood

A

Evidence for this explanation comes from research into naloxone. This drug blocks endorphins receptors; it also reduces food intake, especially sweet foods and suppress’ thoughts about food.

IDA: Doesn’t account for nurture aspect solely nature (biological approach)
Cognitive: override biological factors (losing weight)
Explains comfort eating: Behavioural approach negative reinforcement (comfort eating)

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18
Q

What is naloxone?

A

A drug that blocks endorphins receptors and reduces food intake (especially sweet food) and thoughts about food.

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19
Q

Why don’t we eat much if we take naloxone?

A

Because it blocks endorphins receptors which means you don’t feel any emotion when eating and therefore we eat less. Suppresses thoughts related to food also.

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20
Q

Why does eating cheer us up?

A

Eating stimulates the release of endorphins

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21
Q

Stages of the General effect model (GEM)

A

Stress leads ==> physiological change ==> eating

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22
Q

Theory of General effect model

A

Everybody eats more when stressed

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23
Q

Stages of Individual differences model

A

Differences in learning, attitude or biology

High Vulnerability= stress, physical/psychological change, promotes eating

Low vulnerability= Stress, physical/psychological change, does not promote eating

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24
Q

Theory of individual differences model

A

Only certain people eat more when stressed

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25
Q

Vulnerable groups suggested by IDM

A

Emotional eater: associate hunger + anxiety, response to emotion is eating

External eaters: eating in response (sight and smell) rather than internal (hunger cue)

Restrained eaters: people who have to work to control their eating (dieters) undermining self control

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26
Q

Compare IDM and GEM

A

IDM accounts for nature and nurture and discuss’ differences in vulnerability not generalising to everyone by having 3 categories.

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27
Q

Evaluation for IDM

A

Connor et al weakly supports IDM model as there is a correlation between daily hassles and snacking. Supports external eaters saying they are more vulnerable however doesn’t support restrained and emotional eaters.

Daily hassles (operationalised measure) +

Connor is only one study, other research summarised in a review by Greeno and Wing showed quite a lot of evidence for the importance of restrained eating as a key individual different but (unlike connor) this evidence is lab based.

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28
Q

Outline Garg’s study into mood enhancement and eating behaviour

A

to examine how manipulating happiness and sadness through content of a movie could influence consumption of hedonistic food such as buttered popcorn.

Participants watching full length movies that evoked positive or negative effects (sweet home Alabama vs Love story). Recruited for 2 hour 2 day study. Films matched on key variables running time, genre, critic rating, box office success e.t.c. Viewing rooms like living rooms 5-8 ppts. Given 180g popcorn + calorie free drinks

End of movie ppts asked to give assessment of movie 1= sad 9= happy, rate mood, say what made them happy/sad, popcorn container weighed again.

Results showed that ppts watching the sad filmed consumed 28% more than happy movie.

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29
Q

Outline Connor et al study into stress and eating behaviour

A

33 female and 27 male students asked to keep record of number and severity of daily hassles and number of snacks consumed over a period of 7 days.

PPts asked to complete questionnaire that assessed 3 dimensions of eating behaviour; restrained eating, emotional eating and external eating.

Found that ppts who scored highly on measures of external eating, there was a statistically significant positive correlation between hassles and snacking.

By contrast no significant relationship between these two variable was found for ppts who rated low on external eating.
No significant results found for those who emotional and restrained eaters.

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30
Q

Discuss the role of one factor which influences attitudes to food and/ or eating behaviour (Mood)

A

Mood:
AO1: IDM and GEM models. Explain emotional, restrained and external. Opiate hypothesis (endorphins) reward pathways

AO2: Garg study support for opiate hypothesis
Methodological evaluation- variables accounted for, repeated measures.
Connor et al- stress, daily hassles + snacking support for external
IDA: Behaviourism could also explain comfort eating: eating is negatively reinforced as it removes feelings of sadness. However the opiate hypothesis based on the biological approach goes further than this as it explains the physical mechanism through which this negative reinforcement occurs. it is still not a full explanation though because comfort eating could come about through social learning- for example a child could learn to do this from vicarious reinforcement gained by seeing one of her parents escaping feelings of distress by eating.

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31
Q

Discuss the role of one factor which influences attitudes to food and/or eating behaviour (early learning)

A

Early learning:
AO1: SLT- attention, retention, motivation. Vicarious punishment/reinforcement. Observational. Use of role models (child pays attention to a peer eating peas, identify peer as role model it enhances motivation to eat peas and therefore changing food preference).

AO2- Support for SLT comes from Birch who found that children changed their food preferences (from peas to carrots or vice versa) through watching their peers eat vegetables. This support the idea of observational learning as they changed their preferences after watching the eating behaviour.

Early learning suggests that eating is shaped only by nurture. however the idea of neophobia is rooted in an evolutionary mechanism as avoiding unfamiliar and potentially poisonous foods had an adaptive benefit. This shows that nature is also important to food preferences, a point supported by research such as Desor who showed that babies were born with a preference for sweet foods (innate)

PA- Parents could make sure they eat healthily in front of their children, advertising campaigns designed to encourage healthy eating could use respected celebrities or feature same age role models that children can identify with.

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32
Q

Explanations for the failure and success of dieting

A

Weight set point

Boundary Model

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33
Q

Weight set point model

A

Bennett and Gurin

WSP- largely under genetic control

Body has a range of weight that is comfortable within (5% either side of current weight)

If you go below set point you can plateau and can’t lose anymore as metabolic rate decreases

Internal system regulates % of body fat and weight- optimum weight for mood

Dieting puts us in opposition to WSP

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34
Q

Evidence for WSP

A

Keys et al did a semi-starvation study during World War II. PPts were young men who lost 25% of body weight. Consumed 50% of their normal daily calories. Initially lost weight quickly but weight loss reached a plateau and men became irritable, hungry and obsessed with thoughts about food. Metabollic rates decreased significantly and became lethargic, avoiding physical activity and energy expenditure. Strong urges to overeat.

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35
Q

Support for WSP

A

Keys et al supports the weight set point theory as an explanation for the failure of dieting as the men who consumed 50% of their normal daily calories reached a plateau. This was due to the decrease of their metabolic rate which meant they couldn’t lose anymore weight at the same rate as they were burning calories slower even though they were eating the same amount of calories which leads to them putting on weight. The Men became irritable which supports WSP as our optimum mood is altered by our weight set point. The strong urges to overeat and obsessed thoughts with food meant the men avoided physical activity.

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36
Q

Further support for genetic aspect of WSP

A

Greater similarity of weight in MZ’s (who share 100% of genes) than DZ’s (who share 50%) suggests weight is at least partly under genetic control.

Likewise similarity between weight of children to biological (as opposed to adoptive) parents.

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37
Q

Boundary model

A

Herman and Polivy Boundary model:

explanation for why dieting causes weight gain
-Physiological determined boundries for hunger and satiety
-unpleasant quality of hunger keeps food intake above a minimum level
-unpleasant quality of satiety keeps it below a maximum level
therefore Eating is determined by biofeedback
between boundries there is a zone of biological indifference- eating regulated by social and environmental influences.

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38
Q

Herman and Mack study

A

Herman and Mack gave dieters and non dieters either a high (milkshake) or low (cracker) calorie pre load. They measured how much ppts ate in taste test. Non dieters ate less after high calorie pre load, they behaved according to physiology only (ate less after high pre load as were full). Dieters ate more after high than low calorie pre load. Because once they’ve exceeded cognitive boundary the ‘what the hell effect’ sets in and they keep eating up to satiety boundary .

45ppts women

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39
Q

Evaluation of Herman and Mack study

A

Real world dieting may involve more complicated processs than those studied in lab. Deception (ethical issue) but methodological strength as it overcomes demand characteristics.

Oversimplification- may not apply to men

Research published in peer review journal- good support

Free will/determinism= overeat no choice but to eat more

Beta bias - overlooking gender differences

Independent groups- less likely for demand characteristics

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40
Q

Explanation for success of dieting

A

Ogden’s psychological model

Attention to detail

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41
Q

Ogden’s psychological model

A

Proposes that key psychological factors like:

  • seeing obesity in terms of their own behaviour rather than genetic and hormonal explanations
  • Psychological motives for losing weight as important
  • Psychological techniques such as establishing a new identity as a thinner person
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42
Q

Ogden’s study

A

Questionnaire to explore the factors associated with three groups: stable obese (58), weight loss re gainers (40) and weight loss maintainers (44).

Results: WLM lighter before dieting, were older and spent longer dieting than members of other groups. No difference between groups in terms of contact with health care professionals but WLM were less likely to endorse medical explanations for obesity. Gave greater endorsement to psychological consequences of obesity (depression, anxiety, low self-esteem) were more likely to report they had been motivated to lose weight for psychological reasons like confidence rather than pressure or medical reasons.

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43
Q

Explanation for success of dieting: Attention to detail

A

Successful dieters are able to pay attention to the details of a healthy diet, people get bored of repetition so should focus on meals details to maintain.

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44
Q

Study for success of dieting: Attention to detail

A

Redden had ppts eat 22 fruit flavoured jelly bean and rated enjoyment.

Ppts asked at end how well they could distinguish flavours, how repetitive the eating task felt, how similar the jelly beans seemed to each other and how much variety they perceived.

People given specific flavour labels become less satiated and kept enjoying jellybeans longer than people given the general jellybean label like number 7.

People given just label jellybean gave lower assessments are the experiment went on compared to the specific flavour labelled jelly beans but both groups rated equally at beginning.

45
Q

Evidence for attention to detail as a success factor for dieting

A

Redden’s study shows how attention to detail is a success factor of dieting as people given labelled jelly beans were less satiated and more satisfied than the non labelling condition. However its weak supporting evidence as only towards the end there seemed to be a difference in rating between the groups whereas at the beginning they were rated equally. This doesn’t support the attention to detail as a success factor for dieting.

46
Q

IDA evaluation for Explanations for failure and success of dieting

A

Determinism- Unsuccessful doctors are more likely to endorse a medical model i.e. genetic and hormonal, ppts more likely to eat if food presented
Weight set point- heavily deterministic
Ogden’s model- more free will overbite more likely to succeed. Advantage over WSP

Gender Bias- Most research involves women
unusual that more women are obese as men carry excess weight on abdomen whereas women it on bum and thighs
men being overweight more dangerous

PA- Dieting books and DVDS
When people need to lose weight effectively
Running local weight watchers
Maintain positive attitude- have goals and reasons why Ogden’s model

Ethnocentric- Park et al suggest that some cultures encounter more difficulties with weightless (due to genetics or cultural factors maybe) Obsession with dieting is westernised.

47
Q

Neural mechanisms AO1

A
Neural= nervous system- brain
Brain regions (Neural mechanisms) control eating
Brain regions= Hypothalamus + neurotransmitters
Hormones = gremlin involved- brain regions sensitive
48
Q

Which brain region is the feeding centre?

A

Lateral Hypothalamus

49
Q

Which brain region is the satiety centre?

A

Ventromedial Hypothalamus

50
Q

What is the Lateral Hypothalamus?

A

A brain region that is known as the feeding centre

51
Q

What is the Ventromedial Hypothalamus

A

A brain region that is known as the satiety centre

52
Q

How are glucose relevant to controlling eating?

A

When blood glucose levels fall its sensed by hypothalamus and hunger is experienced and the lateral hypothalamus is activated leading to feeding behaviour.

Food intake leads to an increase in blood glucose. This picked up by hypothalamus and the VMH is activated and stops feeding

53
Q

What is grehlin?

A

Gremlin is a hormone that is released from the empty stomach that signals the hypothalamus to stimulate feeding.

Amount released is directly proportional to the emptiness of stomach. Longer time from last meal = more grehlin

54
Q

What is CCK?

A

CCK is a hormone released from the duodenum in response to the presence of food- Satiety signal to hypothalamus to stop eating. Suppress’ hunger

55
Q

Neural Mechanisms explanation

A

Satiety signals- increase in blood glucose, decreases gremlin, increase CCK

Activate VMH

Feeling of fullness

Eating stops

Hunger signals- decrease in blood glucose, increase in grehlin, decrease in CCK

Activate LH

Feeling of Hunger

Eating starts

56
Q

Which cells store fat?

A

Adipocytes

57
Q

What are adipocytes?

A

Fat cells

58
Q

What is leptin?

A

Satiety hormone made by adipocytes

59
Q

What determines amount of leptin released by adipocytes?

A

Amount of adipocytes

60
Q

What does leptin do?

A

Controls long term food intake

61
Q

Neural Mechanisms AO2

A

Importance of VMH in regulatory food intake supported by Heatherington and Ranson study

VMH lesioned rats became obese- support as undamaged stops rat eating too much

Importance of LH in suppressing food intake supported by Anand and Brubeck

LH lesioned, rats ate less- support as undamaged LH signals to rat that its hungry

Leptin- Carlson study supports

Obese mice had no leptin and were obese, lost weight when petit injected- suggests leptin is a satiety signal

May not apply to humans- NM may be different

Oversimplification

Differences in brain structure but similar mammalian bain so ED may be similar

Unethical to do on humans

Cause and effect established- lab exp, high control
IV= before + after damage
DV = eating behav

Not whole story- Schacter - time of day obese ate more when clock showed dinner time, external vs internal

IDA- combo of approaches; social, emotional, cognitive, behavioural with Neural mechanisms approach.
Diets= decision= cognitive

62
Q

Methodological evaluation for Neural mechanisms

A

May not apply to humans- NM may be different

Oversimplification

Differences in brain structure but similar mammalian bain so ED may be similar

Unethical to do on humans

Cause and effect established- lab exp, high control
IV= before + after damage
DV = eating behav

Not whole story- Schacter - time of day obese ate more when clock showed dinner time, external vs internal

63
Q

IDA evaluation for Neural mechanisms

A

IDA- combo of approaches; social, emotional, cognitive, behavioural with Neural mechanisms approach.
Diets= decision= cognitive

64
Q

Schacter study for NM

A

Experiment measuring the amount of cracker eaten when the real time was manipulated by a faster or slower clock. Obese people ate more when clock falsely showed it was close to dinner time (classically conditioned to eat)

65
Q

Anand and Brubeck study for NM

A

Made a lesion in another area of hypothalamus- lateral hypothalamus led to a loss of feeding This supports the its part of the feeding centre which tells you you’re hungry

66
Q

Hetherington and Ranson study for NM

A

Made a lesion in brain in the VMH which caused rat to combine eating and become obese. This supports the idea that the VMH tells you when you’re full.

67
Q

Evolutionary explanations of food preferences

A
  • Genes make certain preferences
  • Hunter gather communities; men hun mean women fruit
  • Natural selection of food, adaptive
68
Q

Evolutionary food preferences

A
  • Preference for sweet foods; energy to fight or flee
  • Salt is essential to maintain sodium balance- meat salty
  • Prefer fatty foods
  • Eat impulsively adaptive- harsh conditions less food
  • Prefer familiar food, NEOPHOBIA
  • Prefer not to eat foods that make us sick (taste aversion learning)
69
Q

Why do Humans prefer certain foods?

A

Humans prefer high fat foods due to our ancestors eating high calorie foods to gain energy and these fatty foods give an individual more energy fast than protein and carbohydrates. The tendency to eat impulsively became adaptive as during migration millions of years ago people would come across places of harsher weather conditions and less availability of food.

70
Q

Evaluation for evolutionary explanations

A

Desor and Bell studies- sweet foods innate, lack of exposure

Garcia + Koelling= rats + flavoured water= nausea
-taste aversion learning

Bernstein + Webster- chemo and novel ice cream (PA)

  • Food preferences for survival not NS- PA spices in hot countries (Sherman and hash)
  • IDA difficult to falsify, adaptive EEA, Reductionist, causes not problem, observation
71
Q

Desor study for food preferences

A

Desire found using facial expressions and sucking behaviour as indicators of food preference that 1-3 day od infants prefer sweet over non-sweet fluid. - innate, biological drive, haven’t been exposed.

72
Q

Bell Study for food preferences

A

Bell gave sweet, sugar foods to Eskimos in Alaska who lacked sweet foods and drink they found that they didnt reject the sugar containing foods

73
Q

Garcia + Koelling study for food preferences

A

Rat study:

Rats avoid drinking flavoured water when followed by illness than electric shock
Supports taste aversion learning

74
Q

Bernstein and Webster study for food preferences

A

Gave patients novel-tasting ice cream before they received chemotherapy and the patients developed aversion to that ice cream. This led to the idea to give a novel food along with some familiar food before their chemo and then the patient develops an aversion to the novel food but not to the familiar food so comfortable eating the food during and after treatment.

75
Q

Study for taste aversion learning

A

Bernstein and Webster, Garcia and Koelling

76
Q

Sherman and Hash study for food preferences

A

Some widespread food preferences useful of survival did not evolve through natural selection. Example is spices which are effective at killing bacteria and to preserve food.

77
Q

Anorexia definition

A

Anorexia nervosa literally means nervous loss of appetite. Suffered do feel hungry but do not respond to hunger by eating.

78
Q

Symptoms (DSM 5) of anorexia

A

Persistent restriction of energy intake leading to significantly low body weight
An intense fear of gaining weight or of becoming fat
Disturbance in the way ones body shape is experienced, undue influence of body shape and weight on self-evaluation or persistent lack of recognition of their low body weight

79
Q

What are the 2 types of anorexia?

A

Restricting type: self starvation not associated with purging
Binge purging: involves losing weight through self induced vomiting. Bulimia same but doesn’t involve symptoms of excessive weight loss

80
Q

General background for anorexia

A

90% of sufferers are female, increasing in males. Typical age is between 13 and 18.

According to DSM the incidence of the disorder among young females is between 0.5 and 1%

Davey (2008) found between 5 and 8% of people diagnosed die from disorder due to the physical problems it causes.

81
Q

Hoek’s research

A

Fat is considered beautiful in Curaco (near venezuela) and only 8 cases of anorexia found
more biological than social

82
Q

keyes explanation for anorexia

A

A variation in a serotonin receptor gene is more common in anorectics than among the general population.

Serotonin system is involved both in eating and in obsessional behaviour.

For eating disorder sufferers high levels of serotonin cause high anxiety. Often sufferers say they feel better when they don’t eat.

Serotonin is made from tryptophan which comes from food. Starvation reduces the amount of tryptophan and therefore amount of serotonin.

83
Q

How is serotonin made?

A

Tryptophan

84
Q

What does the serotonin system do?

A

Involved both in eating and in obsessional behaviour

85
Q

What is tryptophan ?

A

Amino acid

86
Q

Holland study for anorexia

A

Opportunity sample of 34 twin pairs and a set of triplets because one of the pair was diagnosed. Physical resemblance questionnaire established genetic resemblance. blood test carried out if unsure. Longitudinal study researchers checking over time.

Supports genetic explanation for anorexia as there was a higher concordance rate found for anorexia for MZ twins (56%) compared to DZ twins (7%). Mz’s share 100% of genes which shows how genes play a key role however as the concordance rate isn’t 100% it shows genes are not solely responsible but a genetic vulnerability and an environmental trigger is needed.

87
Q

Bailer study anorexia

A

Bailer et al did a PET scan. Chemical tracer which combines with serotonin receptors is injected. travels to brain and drugs shows up bright on scan. Bailer found that highest levels of serotonin activity in those who showed most anxiety.

More anxiety= more serotonin

however doesn’t show than AN reduces serotonin activity

88
Q

Kaye study for anorexia

A

3 groups (14/5 in each condition); healthy controls, revered anorexics, ill anorexics

All go through acute tryptophan depletion procedure one day (reducing serotonin) then placebo day.

Measure how much their anxiety increases or decreases

Significant reduction in levels of tryptophan in ill anorexic and recovered anorexics

Significant reduction in levels of anxiety

89
Q

Evaluation of Kaye’s study

A

Causality- association between excess dopamine and AN. Something else could cause disorder then disorder cause changes to bodys system.

However this is overcome by using recovered anorexics as they are recovered AN cannot still be causing change in dopamine receptors. Dopamine is a risk factor and possible that AN has had a long term effect that changed the body to persist even after the recovery.

90
Q

Evaluation of neural explanations of anorexia

A

Neural explanations offer the possibility of drug treatments to normalise neurotransmitter levels .
Kaye says theres a link between genetic and neural explanations and therefore it may be possible to use an individual’s genetic profile to indicate risk level. then specifically tailored prevention programme could be developed for the most susceptible people.

Further implication is that these explanations reduce the guilt caused by psychodynamic explanations which suggest that parents are to blame for their children anorexia.

IDA- Eating disorder becomes worse due to child feeling guilty or border to family

Psychodynamic- free will, family influence

Biological- genetic profile for those most vulnerable may ignore other factor like behavioural and media aspects SLT

Deterministic- focus on biological chemicals undermines individuals choice to eat, free will

Gender bias- focussing on women as participants problematic as claims to be entirely biological but there may be a difference

If focused on biological patient may feel recovery is down to biological not psychological (PA)

91
Q

Evolutionary explanations of anorexia

A

The reproductive suppression hypothesis

The adapted to flee famine hypothesis

92
Q

Reproductive hypothesis AO1

A

Amenorrhea, body realises women is not able to carry healthy baby and thus causes infertility.

Wasser and Barast suggest this is an adaptive mechanism and give birth when their environmental conditions are favourable and think of resources nd survival of offspring. Controlling food intake meant that ancestors couldn’t produce children only at optimum time.

Surbey sees anorexia as a disordered variant of females adaptive ability to alter the timing of reproduction to best fit the demands of the environment, Delaying onset of fertility may enable woman to provide better for offspring,

93
Q

The adapted to flee famine hypothesis AO1

A

Guisinger proposes that some features of anorexia are restriction of food intake, denial of starvation and hyperactivity are evolved adaptive mechanisms.

When a person loses wait usually physiological mechanisms conserve energy and increase desire for food these adaptations facilitate survival in hard times.

However in EEA ancestors migrated to more favourable environments and they did this efficiently by switching off normal responses to starvation. Instead they were energetic and restless and denied their thinness to successfully migrate. Although this is no longer an adaptive responses as she proses that a very low body weight causes some individuals bodies to respond as though they must migrate from famine.

94
Q

Evaluation for reproductive suppression hypothesis

A

Explains amenorrhea and delayed onset of puberty

Monarch supports amenorrhoea aspect

IF theory correct then anorexia would never appear in males though

Fertility in men

Though no evolutionary benefit for a man not to reproduce

Keel and kulmp not only in western culture but study shows it isn’t the whole explanation and that other approaches should be considered like socio-cultural, nature vs nurture

Guisenger: PA understand causes and treatment. Ethical strength of evolutionary explanation

95
Q

Evaluation of adapted to flee famine hypothesis

A

Delusion of appearance

Explains denial of starvation, distorted body image and hyperactivity

applies to both- both have to migrate

Mrovosky- support but only may apply to women

Ealing and pierce, menarche

Holland- preparedness

Support evolutionary theories as based on genetic basis

AN effects minority- individuals difference on this behaviour

Limited- doesn’t specify which explanation.

96
Q

Menarche study for anorexia

A

found the onset of puberty is delayed in pre-pubertal girls with AN

97
Q

Mrosovsky and Sherry study for anorexia

A

Food refusal found in many species is common and that species stop eating even though food is available when they migrate

98
Q

Epling and Pierce study for anorexia

A

Found rats which were starved in lab would then ignore their food and exercise excessively

99
Q

Keel and Klump study

A

Meta analysis of cross cultural studies of ED. Concluded that AN is not culture bound and found in all cultures even those not exposed to western influences.

More western= more anorexia

100
Q

Bell study for anorexia

A

Middle ages women fasted excessively leading to what is now known as holy anorexia. Church canonised over 85 very thing saints who were recognised in part for their miraculous ability to live with very little food.

101
Q

Guisenger for anorexia

A

claims that AFFH relives therapists of the need to search for familiar reason for AN. A struggle for control between patients and those who want to get better. This struggle is explained in terms of the worried family and the anorexics biological org etc avoid food. Awareness of this casual influence can help treatment and encourage parents to be more compassionate towards an anorexic child.

102
Q

Name the two psychological explanations for anorexia

A

Sociocultural

Psychodynamic

103
Q

Sociocultural explanation for anorexia

A

Western cultures slim=attractive

Media propagate slim body type with thin models on TV

We internalise these standards through SLT

SLT role models or slim models and encouraged to copy through vicarious reinforcement. Glamorous lifestyle of model who is thin

Tension between actual and ideal self leading to dissatisfaction with own body weight and being thin

Leads to dieting and obsessions with food strengthened by Operant conditioning

Dieters lose weight they may receive praise and attention for weight loss. Positive reinforcement for weightloss maintaining dieting

104
Q

Evidence and evaluation for Sociocultural explanation for anorexia

A

Becker study - fiji tv 13% increase of girls vomitting
Keel and Klump- meta analysis finding not cultural bound
Groesz- meta review and found body dissatisfaction increased after exposure to media
Beta bias- only women, underestimate importance of gender
accounts for cultural differences
ignores biological influences
PA- media use larger healthier models
Frequency of AN directly proportional to western exposure

105
Q

Psychodynamic explanation for anorexia AO1

A

Freud: REFUSAL OF ADULT SEXUALITY- fear of growing up going through puberty. eating substitute for sexual expression so ED way of suppressing sexual impulses. Fear of pregnancy

Crisp: postponing menstruation girls attempting to remain in prepubertal state and postpone onset of adulthood as scared they cannot cope.

Avoiding development of adult body by restricting food intake

ASSERTING CONTROL:

Hilde Bruch claimed that origins of anorexia aren childhood. Parenting not being effective and ineffectively responding to childs needs for example feeing when child is anxious. Child grows up confused and becomes over reliant on parents and then adolescent want to have control. Take excessive control of body by developing abnormal eating habits

106
Q

Evaluation of Psychodynamic explanation for anorexia

A

Button and Warren found anorexics report lack of feeling control in lives

Steiner notes that parents of adolescents with anorexia have a tendency to define their childs psychical needs rather than allowing children to define their own. Bruch found that many of these parents claimed to anticipate their children needs rather than ever letting them feel hungry.

Carter et al found that 48% of the 77 female anorectics they studied reported childhood sexual abuse. Similarly in a study of gay and bisexual men. Feldman and Meyer found that those who reported childhood sexual abuse were more likely to be anorexic.

Psychodynamic explanation are mainly case studies. Policy and Herman pointed out case studies investigating family influences are correlational and carried out after diagnosis. Therefore is is difficult to determine whether dysfunctional family relationships contribute to development of anorexia to if anorexia leads to dysfunctional family or if there is another factor influencing both.

Denial people have with anorexia might be defensive mechanism

Personality structure- superego may be too strong to listen to causing the ID to be suppressed, stopping any satisfaction could increasing the superego.

Doesn’t explain how adults get anorexia and ignores biological factors.

107
Q

Outline and evaluate one or more explanations for the success and failure of dieting (4+8)

A

SUCCESS:

WSP: control system dictating how much fat person should carry.
- Twin&adoption studies largely under genetic control due to sharing 100% genes
Ogden’s: own study supporting theory WLM were more likely than the stable obese or WLRG to report psychological motivation for dieting such as enhancing self confidence rather than for medial reasons

FAILURE:
Boundary model- dieting may actually cause weight gain
- Herman and Mack non dieters ate more when no preload but for dieters other way round

AO2:

WSP: twin + adoption studies

IDA: Free will/ determinism- unsuccessful dieters more likely to endorse a medical model i.e. genetic and normal
ppts more likely to eat food if presented
WSP- heavily deterministic
Ogden’s model- more free will over diet more likely to succeed.
Gender bias: Most research dieting involves women
inherent gender bias in research into dieting and obesity
Unusual that more women are obsess as men carry excess weight on abdomen whereas women carry it on bum and thighs- even though men being overweight is more dangerous
PA- Dieting books and DVDS. local weight watchers
maintain positive attitude- have goals and reasons- ogden’s model.
Ethnocentric: Park et al suggest that some cultures encounter more difficulties with weight loss maybe due to genetics or cultural factors relating to diet) Obsession with dieting is a western concern

108
Q

Outline and evaluate neural mechanisms involved in the control of eating behaviour (4+12)

A

-LH- feeding centre detects low glucose and high grehlin
-VMH- satiety centre detects high glucose and CCK
-Blood glucose levels
Grehlin (not NM but hormone detected by LH secreted from empty stomach)
CCK
Leptin

AO2:
Biological approach - overlooks role of learning (Schacter) responding to environmental rather than internal cues

If brain abnormality causes disorder or other way round
-Lesioning byt H&R overcomes this can infer cause and effect strengthens idea that VMH is responsible for feelings of satiety

Biological differences between rat and human brains
Human cortex reflects psychological differences and how Humans eating is governed by conscious thought processes emotional and social consideration rather than just biological factors like NMs

Becker- influence of SLT on prevalence of anorexia suggests that NM alone doesn’t say enough
Determinist - Ogdens model shows that people believe the do have influence over eating rather than jus bio influence