eating behaviour Flashcards
outline
explanations for food preferences- the role of learning
classical conditioning:
flavour flavour learning (liking anew food because of its association to a food we already like)
due to an innate preference for sweetness, we learn to prefer many new foods by sweetening them.
This association eventually leads to liking the new food on its own.
operant conditioning:
children are often directly reinforced by their food preferences of parents/siblings- rewards/punishment.
However, it’s been found difficult to establish preference in children using rewards, which is why classical conditioning is probably the more powerful form of food preference learning.
social influences:
SLT - modelling + vicarious reinforcement
family influences- parents are ‘gatekeepers’
peer influences- Birch (1980)- preschool lunchroom, placed next to kids with different preference- participant changed preference.
media- encounter adverts for ‘unhealthy’ foods , often with characters/themes children relate to , fun marketing
cultural influences:
Rozin (1984)- cultural influences are the single most significant predictor of food preferences
Hansen (2014)- we learn cultural ‘rules’ around family table.
cultural norms- e.g what constitutes a ‘proper meal’ - roast on Sunday
meat eating- different cultures have different attitudes- e.g France eats whole of animal, kidneys heart etc
culture and learning- associate foods we enjoy as adults to feelings of happiness growing up (classical conditioning)
culture influences food given to children and children see their cultural group enjoying these foods (vicarious reinforcement- acts as reward)
evaluate
explanations for food preferences -the role of learning
-lack of support for classical conditioning
little evidence for the role of classical conditioning
Baeyens (1996)- asked student participants to taste previously untried flavours- in experimental condition, flavours paired with sweet flavour. No differences between two groups in preferences after pairing.
Suggests that classical conditioning via flavour-flavour learning is an incomplete explanation for food preferences.
+support for SLT
Jansen and Tenney (2001)- gave children energy dense or energy dilute drink.
Most preferred energy dense drink (which teacher praised and liked)
Concluded children identified with teacher, so ere more likely to model teacher’s preference (modelling) as they were influenced by teacher’s praise and enjoyment (vicarious reinforcement)
short and long term effects
media can have powerful short term and long term effects on food preferences
Brunn (2011)- studied group of age 8-10 yr old children
Found children who watched most tv, also had the most unhealthy food preferences.
However, this link was much weaker in a follow up study of the same children 6 years later- as other factors (especially friends) influenced preferences more strongly.
outline evolutionary explanations for food preference
PREFERENCES
any preferences must exist because they provided an adaptive advantage (survive, reproduce, pass on)
sweetness - reliable sign of high energy food (in EEA source of sugar was fruit) (EEA is the environment of evolutionary adaptation- environment our species first evolved)
Steiner (1977)- placed sugar cube on newborn’s tongue, positive facial expressions- will consume large amounts of fructose if allowed because it’s ‘fast acting’
salt- desire appears around 4 months old
Harris (1990)- babies prefer salted cereal despite having (unsalted) breastmilk- suggests preference is innate
meat- fossil evidence suggests hunter-gatherers daily diet was mainly derived from animal based products - meat provided nutrients for brain growth
Milton (2008)- without animals, unlikely humans could have secured enough nutrients to survive.
TASTE AVERSION
learned response to eating poisonous/toxic food
animals avoid eating food that makes them ill as they associate them
Discovered by farmers trying to get rid of rats >rats eat a little bit> get ill > don’t eat it again
Garcia (1955)- first study of taste aversion in lab, rats made ill by radiation shortly after eating saccharin> developed an aversion
Research has found odour can also lead to illness> creates aversions
aversions would have helped ancestors survive, would know not to eat that dangerous food again once learned, aversions are hard to shift
NEOPHOBIA
reluctance to try new/unusual foods
reaction is a survival strategy as it protects from poisoning
Prescott (2013)- ‘a world of potential foods whose safety is uncertain’
specialised with specialised diet less likely to get neophobia compared to those with broad diet e.g rats
study rats became ill after familiar and unfamiliar food> would avoid unfamiliar food in future (Rozin,1977)
in humans, neophobia is dependent on culture and current diet
Dovey (2008)- humans have expectations as to what is an ‘acceptable’ food , if the criteria is not met then the food is rejected.
greater neophobia towards animal products > likely to have evolved due to the greater risk of illness/threat.
evaluate evolutionary explanations for eating behaviour
- can be maladaptive
poses problems for people who restrict their diet and don’t get sufficient nutrients
Perry (2015) - neophobia is associated with poorer diet quality among children
evolutionary evidence
evidence to suggest neophobia is an evolutionary trait and therefore part of our nature. Knaapila (2007)- measured neophobia in 468 twin pairs and found a heritibility of 67%. This suggests about 2/3rds of variation in food neophobia is genetically determined. Supports view that neophobia developed to protect humans.
RWA from taste aversion
helpful in understanding food avoidance may occur curing cancer treatment.
some treatments (e.g chemo) cause gastrointestinal illness
Bernstein and Webster (1980) - gave icecream to patients before treatment and found they acquired an aversion
- this led to the development of the ‘scapegoat technique’ - give familiar and unfamiliar food to patient so they develop aversion to unfamiliar food
outline neural and hormonal mechanisms in eating and satiation
summary of both:
feel hungry so eat > glucose and leptin increases, ghrelin decreases > VHM activated (satiety) > feel full, stop eating> glucose and leptin decreases, ghrelin increases > LH activated (hunger)
NEURAL
dual centre model - two areas of the hypothalamus provide homeostatic control over glucose levels
lateral hypothalamus (LH) -
‘feeding centre’/’on switch’
contains cells that detect the levels of glucose in the liver and becomes activated when glucose fall beyond a certain point
individual feels hungry, causes motivation to search for and prepare food
also releases neuropeptide Y (NPY) , this is associated with hunger and reduction in physical activity (rats that were injected with NPY directly into hypothalamus eat excessively and eventually become obese)
ventromedial hypothalamus (VMH)-
‘satiety centre’ / ‘off switch’
after eating, glucose levels rise (VMH detects this and is activated) (LH activity inhibited at same time)
individual becomes satiated and stops eating
damage to VMH can cause eating past satiety
Reeves and Plum (1969)- woman’s weight doubled in a two year period, post mortem revealed tumour on VMH (so ‘stop eating’ function failed)
HORMONAL
ghrelin -
is secreted by stomach cells
acts as a hormonal marker of how long it has been since last eaten (more released the longer individual has gone without food)
ghrelin levels detected by receptors in part of hypothalamus called arcuate nucleus
when ghrelin levels rise above set point, arcuate nucleus signals to LH to secrete NPY
ghrelin is an appetite stimulant
leptin-
hormone produced by adipose (fat) cells
level of leptin increases with level of fat cells (detected by VMH)
appetite suppressant and contributes to the satiety mechanism
once levels increase beyond set point, individual feels full and stops eating.
evaluate neural and hormonal mechanisms in eating and satiation
neural:
+research support for dual centre model
Hetherington and Ranson (1942) - lesions in various brain areas of rats > conclusions supporting model , for example lesions in VMH caused them to become hyperphagic (over eat)
- model is too simplistic
only focuses on the neurotransmitter neuropeptide Y (NPY) , however there are other neurotransmitters at play , such as serotonin and dopamine. These interact to either enhance or inhibit each other.
hormonal:
+RWA
Licinio (2004) - studied rare genetic condition where individual does not produce leptin naturally , this is associated with severe obesity.
Treatment is leptin replacement therapy where they are injected with leptin over an 18 month period. Average weight loss of 40% and initial reduction in food intake of 49%.
- model is too simplistic
focuses on hormones ghrelin and leptin.
Valassi (2008)- highlighted the role of hormone cholecystokinin (CKK)
this is produced in intestine and sends signals from gastrointestinal tract to hypothalamus which then indicates satiety.
(for 16 marker combine both ‘simplistic’ points)
Outline Family Systems Theory explanation for anorexia
Minuchin (1978) identified four main features typical of an AN family. He argued these factors CAUSE anorexia.
1) enmeshment
family members are overly involved with each other , spending excessive time together and impinging on each other’s privacy. Family is enmeshed and identities become tied up in one and other. Adolescent daughter faces challenge of asserting her independence an differentiating her identity > does this by refusing to eat.
2) overprotectiveness
Family members nurture obsessively to reinforce loyalty, leaving little room for independence. Palazzoli (1974) suggests the mother of the daughter with AN feels all decisions made were for benefit of daughter , therefore it becomes easier to blame daughter. Daughter refuses to eat to gain independence to break away.
3) rigidity
interactions with family are inflexible and deny need for change. Problems arise when circumstances change (internal/external). Adolescent daughter’s seeking of independence can’t be accommodated for. Family (especially mother) squashes self differentiation attempts. Refusing to eat means family has to change.
4) conflict avoidance
suppress/avoid conflict , no discussion of issues where a difference of opinions may arise. Daughter refuses to eat so family has to acknowledge problems.
Minuchin suggests these four factors prevent autonomy and control.
Bruch (1978)- suggests AN is caused by daughter’s desire for autonomy and control, and it is primarily the mother who is domineering, and refuses to accept need for independence. This creates confusion for the daughter, leading to the main symptoms of AN ; distorted body image , inability to identify internal states such as hunger and overwhelmingly feeling of loss of control. The daughter controls her destiny by controlling body weight, with weight loss being a measure of success. Also gains autonomy by disrupting dependent relationship with mother.
Evaluate Family Systems Theory as an explanation for Anorexia.
+support research
Strauss and Ryan (1987) - female anorexic patients demonstrated greater disturbances in autonomy, more controlling style of behaviour regulation , less self differentiation between themselves/family members and perceived poorer communication with families. Shows the four factors are risk factors for AN.
- inconsistent evidence
Aragona (2011) - studied 30 female Portuguese patients with eating disorders. No more enmeshed/rigid than than non-eating disorder families.
Failure to confirm FST may be due to different ways of measuring (questionnaire/observation).
Different outcomes based on methodological variations illustrate wider problem with psychodynamic explanation of AN.
Difficulty confirming predictions derived from vaguely defined concepts such as enmeshment/autonomy.
+treatment applications
evidence that therapies based on FST have some success.
Behavioural Family Systems Therapy (BFST) - attempts to disentangle relationships and reduce parental control
Robin (1995)- 11 anorexic patients , treatment for 16 months - 6 patients recovered- further 3 recovered after 1 year follow up. However, limitation as to what constitutes ‘recovered’ (researcher deeming if they’d recovered knew who had had the therapy)
outline cognitive explanations for anorexia
suggests AN is as a result of faulty/maladaptive thought processes about about the self, body and food/eating.
cognitive distortions are faulty, biased, irrational ways of thinking that mean we perceive ourselves , others and the world inaccurately (usually negatively)
Core psychopathology of AN is cognitive distortions about body shape and weight, these are central to diagnosis of AN in the DSM-5. People with AN are filtering their life experiences through the three factors below
1) disturbed perceptions
Murphy (2010) argues that all other clinical features of AN stem from these distortions, including preoccupation with thought of food, weight, body shape and food restriction/checking.
This causes patients to become more critical of body and misinterpret emotional states as ‘feeling fat’ , also leads to overestimating size and weight.
Williamson (1993)- asked 37 participants to choose silhouette that matches own body shape (Body Image Assessment) - Those with AN were significantly less accurate compared to control group
2) Irrational beliefs
Cognitive errors such as ‘black and white’ thinking , catastrophising and perfectionism.
Perfectionism means AN patients constantly strive to unattainable goals, aiming to meet demanding standards in all areas of life, especially around weight
Hewitt (2003) found when goals were achieved , perfectionism was not satisfied. Forever pursuing goals they cant attain and constantly raising standards. In vicious cycle of raising standards and starvation.
3) cognitive inflexibility
Treasure and Schmidt (2013) - proposed ‘cognitive interpersonal maintenance model’ of AN , suggesting AN patients struggle with set shifting. This means they find it hard to move fluently between tasks which require a different set of cognitive skills in a changed situation.. Once weight loss process begins, they rigidly persist , finding it difficult tot think healthily about body. Weight loss is a solution to a problem that no longer exists.
evaluate cognitive explanation for anorexia.
+research support for perfectionism
Halmi (2012) - studied 728 women over age 16 with EATATE diagnostic interview
measured AN symptoms and indicators of childhood perfectionism.
found this was a significant predictor of later development of AN, and therefore is a risk factor
(however limitation of this is that the method sued to assess childhood perfectionism was retrospective ,decreases validity)
+research support for disturbed perceptions
Sachder (2008)- used fMRI scans on AN and control , showing images of other bodies and own bodies.
Same brain area for both groups activated in non-self images.
When self images shown, those with AN showed very little activation (compared to control) in part of brain associated with attention.
This lack of attention is a form of cognitive distortion because they are not reacting normally, suggesting disturbed perceptions exist in AN- did not attend to own body images.
+Treatment Applications
Different forms of cognitive behaviour therapy (CBT) , attempt to change distorted cognitions and irrational beliefs.
Grave (2014)- study of enhanced CBT shows significant increase in weight and decreased concerns about body image amongst 26 hospitalised AN patients. Shows that tending to cognitive distortions improves anorexia.
Outline biological explanations for anorexia
GENETIC:
anorexia runs in families
evidence for genetic explanation comes from twin studies. Concordance rate indicates proportion of twin pairs in which both individuals have AN.
As MZ twins share 100% of DNA and DZ only 50% , a higher concordance rate for MZ twins supports genetic explanation.
Holland (1998)- studied 45 female twin pairs and one set of triplets , finding 56% concordance for MZ and only 5% for DZ
candidate genes
Zeeland (2014)- carried out candidate gene association study (CGAS)- compared control to those with AN by sequencing 152 genes. Discovered only one gene significantly associated with AN- epoxide hydrolase 2 (Ephx 2) - this codes for an enzyme involved in cholesterol metabolism- AN patients found to have significantly high cholesterol during AN phase
genome wide association studies
these do not make assumptions about what genes may be involved, look at entire collection of human genes
Boraska (2014)- used matched controls to identify 72 genetic variations between AN and control. However, none were significantly associated to AN (researchers suggest this is not because they don’t exist, but because the study was not sensitive enough to detect them)
BIOLOGICAL
serotonin (metabolite 5-HIAA)
research has established involvement of serotonin in behaviours that are features of AN. (appetite reduction and obsessiveness)
Bailer and Kaye (2007)- evidence of low levels of metabolite 5-HIAA (chemical by product of serotonin)
Attia (2014)- studied individuals with AN who had not returned to pre-illness weight, finding they responded less well tod rugs that stimulate serotonin activity (serotonin antagonists) compared to people who had restored a healthy weight. Pattern of results indicates underactivity of the serotonin system in AN.
dopamine (metabolite HVA)
Kaye (1991)- lower HVA levels in recovered AN patients compared to control group.
Bailer (2012)- injected patients with amphetamine (increases dopamine) - control pps experienced euphoria whilst AN pps experienced anxiety - may suggest why AN patients avoid food in order to reduce anxiety levels.
Evaluate biological explanations for anorexia
GENETIC:
- polygenic
It is widely accepted that no one gene can be responsible for the wide range of physical and psychological symptoms of AN. The illness is polygenic meaning it is most likely many genes contributing to symptoms of AN. Pinerio (2010) , therefore the search for one single gene is futile.
-diathesis stress model
Model makes widely accepted point that AN can only be understood by considering interaction between genetic and non-genetic factors. Genes may create a vulnerability (a diathesis), that is only expressed when individuals experience a stressor, such as trying to lose weight.
NEURAL
- over simplistic
Nunn (2012)- serotonin alone does not distinguish between those who have AN and those who do not.
Better explained by considering interaction between serotonin and other neurotransmitters such as noradrenaline.
Oher neurotransmitters such as GABBA are also involved. These do not operate in isolation, but rather in complex interactions between one and other.
+drug treatments
drug treatments targeting dopamine/serotonin may help reduce symptoms of AN. For example, SSRIs (also used in treatment of depression) may be effective and help avoid relapse. Kayne (2001) found 63% on SSRIs didn’t relapse compared to 16% who weren’t on SSRIs.
outline social learning theory as an explanation for anorexia
social learning is learning through observation, imitation and modelling
Bandura (1977) argued there are four mediational processes in social learning: attention/retention/motor reproduction/motivation
modelling in AN:
An can be acquired indirectly through observation of a model , an individual forms a ‘template’ for behaviour that the observer can imitate. The model can exist in real life such as a family member, or they can be symbolic such as a cartoon character. Models are influential because they provide an example of behaviour to follow and can also modify social norms by establishing what is acceptable/unacceptable behaviour in a situation.
vicarious reinforcement in AN:
Observing the consequences of a behaviour. Can be vicarious reinforcement or vicarious punishment. Family members are a major source pf vicarious reinforcement because they spend a lot of time together- observation of a behaviour is not a one off occurrence, it is repeated frequently over time. If behaviour such as food restriction is rewarded, an observing younger child will experience many instances of vicarious reinforcement that make imitation much more likely. Also, if a model is praised for losing weight, this makes it more likely observer will imitate model.
role of media:
Media provides symbolic symbols and is a powerful transmitter of cultural ideas about body shape and size. There is a danger that young women who identify with the glamour of female celebrities who overwhelmingly conform to ‘thin ideal’ will be motivated to lose weight. extreme dieting an exercising may occur, vicariously reinforced by the rewarding fame, success, wealth and respect they observe in female role models from the media.
key study:
Ditmarr (2006) - studied the influence of one common model of the thin ideal - Barbie.
A Barbie doll’s waist is 39% smaller than that of all AN patients and it is estimated that 42% of UK women owned a Barbie as children and 99% of age 3-10 US girls own one.
procedure:
162 girls age 5-8
three different groups
1) exposed to barbie
2)exposed to Emme doll which had more realistic body
3) control group exposed to images of flowers/balloons/clothes
asked to rate statements about body self esteem and also body dissatisfaction accessed by asking them to colour in two body silhouettes (what they look like , and what they would like to look like)
findings:
girls who saw barbie images were significantly more dissatisfied with their body shape and had lower self esteem.
researchers concluded the barbie is a ‘powerful aspirational role model’ for young girls. Girls identify with barbie because of the glamour associated with her body shape. They internalise the thin ideal barbie represents and this initiates body dissatisfaction, possibly leading to eating disorder such as AN.
Evaluate Social learning theory as an explanation for Anorexia.
+research support
Becker carried out a natural experiment of the effects of television on eating disorder is Fiji, where television only became available in 1990s.
1995 - 63 females completed questionnaire, 13% had high score , indicating eating disorder risk.
1998- 65 females completed questionnaire, 29% had high score
suggests girls may have been influenced by female body shape transmitted through the media. This shows that eating disorders can be the outcome of social learning process.
- Diathesis stress explanation
There may be stressors that trigger AN such as the media. However, if media influence is a major cause of AN then we would expect to see a larger number of cases, as most young women are exposed to role models of thinness in the media. The fact that there aren’t large numbers on AN suggests other factors may be involved. This would explain why some young women develop AN and others don’t when exposed to the same media influences. The missing factor could be a diathesis, an underlying vulnerability to develop AN.
-no effective treatment applications
unlike other explanations, the SLT explanation has not lead to effective treatments for AN. SLT could be used by showing patients images of healthy eating/body shape - however would have to accompany with other therapies such as CBT or SSRIs as this alone is not as effective. The lack of treatments from SLT alone raises a question of validity, explanation of helping people with AN is limited.
