Eating behaviour Flashcards
List the factors influencing attitudes to food and eating behaviour
1) Early learning and experience
2) Mood, including stress
How does early learning influence attitudes to food and eating behaviour?
Early learning shapes eating behaviour and food preferences through exposure to food social learning, operant conditions and classical conditioning.
What is neophobia?
Fear of new things
How does exposure and neophobia relate?
Exposure to foods helps overcome neophobia, we prefer food we are familiar with
SLT’s explanation for eating behaviour
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
Evaluation of SLT and eating behaviour
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
Birch study evaluation for SLT eating behaviour
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.
Outline Birch’s study
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.
Outline Lowe’s study
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.
Exposure to food and eating behaviour
- 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)
Outline Birch and Marlin’s study
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.
Evaluation for exposure to food Nature and nurture argument for eating behaviour
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
Factor that focuses on how much we eat
Mood (inc. stress)
Outline research into mood as an influence to our attitudes to food and eating behaviours
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.
Evaluation of research into mood and eating behaviour
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.
Biological explanation of eating behaviour and mood
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.
Evaluation for biological explanation of eating behaviour and mood
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)
What is naloxone?
A drug that blocks endorphins receptors and reduces food intake (especially sweet food) and thoughts about food.
Why don’t we eat much if we take naloxone?
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.
Why does eating cheer us up?
Eating stimulates the release of endorphins
Stages of the General effect model (GEM)
Stress leads ==> physiological change ==> eating
Theory of General effect model
Everybody eats more when stressed
Stages of Individual differences model
Differences in learning, attitude or biology
High Vulnerability= stress, physical/psychological change, promotes eating
Low vulnerability= Stress, physical/psychological change, does not promote eating
Theory of individual differences model
Only certain people eat more when stressed
Vulnerable groups suggested by IDM
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
Compare IDM and GEM
IDM accounts for nature and nurture and discuss’ differences in vulnerability not generalising to everyone by having 3 categories.
Evaluation for IDM
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.
Outline Garg’s study into mood enhancement and eating behaviour
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.
Outline Connor et al study into stress and eating behaviour
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.
Discuss the role of one factor which influences attitudes to food and/ or eating behaviour (Mood)
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.
Discuss the role of one factor which influences attitudes to food and/or eating behaviour (early learning)
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.
Explanations for the failure and success of dieting
Weight set point
Boundary Model
Weight set point model
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
Evidence for WSP
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.
Support for WSP
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.
Further support for genetic aspect of WSP
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.
Boundary model
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.
Herman and Mack study
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
Evaluation of Herman and Mack study
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
Explanation for success of dieting
Ogden’s psychological model
Attention to detail
Ogden’s psychological model
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
Ogden’s study
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.
Explanation for success of dieting: Attention to detail
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.
Study for success of dieting: Attention to detail
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.
Evidence for attention to detail as a success factor for dieting
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.
IDA evaluation for Explanations for failure and success of dieting
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.
Neural mechanisms AO1
Neural= nervous system- brain Brain regions (Neural mechanisms) control eating Brain regions= Hypothalamus + neurotransmitters Hormones = gremlin involved- brain regions sensitive
Which brain region is the feeding centre?
Lateral Hypothalamus
Which brain region is the satiety centre?
Ventromedial Hypothalamus
What is the Lateral Hypothalamus?
A brain region that is known as the feeding centre
What is the Ventromedial Hypothalamus
A brain region that is known as the satiety centre
How are glucose relevant to controlling eating?
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
What is grehlin?
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
What is CCK?
CCK is a hormone released from the duodenum in response to the presence of food- Satiety signal to hypothalamus to stop eating. Suppress’ hunger
Neural Mechanisms explanation
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
Which cells store fat?
Adipocytes
What are adipocytes?
Fat cells
What is leptin?
Satiety hormone made by adipocytes
What determines amount of leptin released by adipocytes?
Amount of adipocytes
What does leptin do?
Controls long term food intake
Neural Mechanisms AO2
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
Methodological evaluation for Neural mechanisms
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 evaluation for Neural mechanisms
IDA- combo of approaches; social, emotional, cognitive, behavioural with Neural mechanisms approach.
Diets= decision= cognitive
Schacter study for NM
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)
Anand and Brubeck study for NM
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
Hetherington and Ranson study for NM
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.
Evolutionary explanations of food preferences
- Genes make certain preferences
- Hunter gather communities; men hun mean women fruit
- Natural selection of food, adaptive
Evolutionary food preferences
- 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)
Why do Humans prefer certain foods?
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.
Evaluation for evolutionary explanations
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
Desor study for food preferences
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.
Bell Study for food preferences
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
Garcia + Koelling study for food preferences
Rat study:
Rats avoid drinking flavoured water when followed by illness than electric shock
Supports taste aversion learning
Bernstein and Webster study for food preferences
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.
Study for taste aversion learning
Bernstein and Webster, Garcia and Koelling
Sherman and Hash study for food preferences
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.
Anorexia definition
Anorexia nervosa literally means nervous loss of appetite. Suffered do feel hungry but do not respond to hunger by eating.
Symptoms (DSM 5) of anorexia
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
What are the 2 types of anorexia?
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
General background for anorexia
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.
Hoek’s research
Fat is considered beautiful in Curaco (near venezuela) and only 8 cases of anorexia found
more biological than social
keyes explanation for anorexia
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.
How is serotonin made?
Tryptophan
What does the serotonin system do?
Involved both in eating and in obsessional behaviour
What is tryptophan ?
Amino acid
Holland study for anorexia
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.
Bailer study anorexia
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
Kaye study for anorexia
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
Evaluation of Kaye’s study
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.
Evaluation of neural explanations of anorexia
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)
Evolutionary explanations of anorexia
The reproductive suppression hypothesis
The adapted to flee famine hypothesis
Reproductive hypothesis AO1
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,
The adapted to flee famine hypothesis AO1
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.
Evaluation for reproductive suppression hypothesis
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
Evaluation of adapted to flee famine hypothesis
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.
Menarche study for anorexia
found the onset of puberty is delayed in pre-pubertal girls with AN
Mrosovsky and Sherry study for anorexia
Food refusal found in many species is common and that species stop eating even though food is available when they migrate
Epling and Pierce study for anorexia
Found rats which were starved in lab would then ignore their food and exercise excessively
Keel and Klump study
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
Bell study for anorexia
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.
Guisenger for anorexia
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.
Name the two psychological explanations for anorexia
Sociocultural
Psychodynamic
Sociocultural explanation for anorexia
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
Evidence and evaluation for Sociocultural explanation for anorexia
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
Psychodynamic explanation for anorexia AO1
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
Evaluation of Psychodynamic explanation for anorexia
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.
Outline and evaluate one or more explanations for the success and failure of dieting (4+8)
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
Outline and evaluate neural mechanisms involved in the control of eating behaviour (4+12)
-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
