Eating Disorders Flashcards
Exposure to food…
Birch and Marlin…
Evaluation…
The mere exposure effect suggests that the more exposed we are to something, the more familiar we become with it, resulting in a positive attitude towards it. If we grew up with certain types of food we are likely to have a positive attitude towards them but if we are exposed to new food we are likely to have negative attitudes towards it.
- Introduced 2 year old children to novel food over 6 week period. 1 food was presented 20 x, one 10x and one 5x and one remained novel. The results found a direct relationship between exposure and food preference and found that 9-10 exposures were necessary before preference began to shift
- Doesn’t tell us what happens when kids grow up
- Well operationalised
- practical applications
Social Learning Theory (Peer influence)…
Birch et al…
Evaluation…
SLT proposes that our behaviours are a result of observation and imitation. If role models have our attention we will observe them. A memory of this is retained and when a similar situation arises, we might be motivated to imitate the observed behaviour maybe due to vicarious reinforcement.
- Used peer modelling to change children’s preference of veg. On 4 consecutive days the children were seated next to children who preferred a different tipe of veg at lunch. Resulted in the kid showing a preferred a different veg to the person next to them which was the same in the follow up assessment.
- Generelisability - may not work of other - individual differences
- May be result of conformity
- social desirability.
SLT (parental influence)…
Olivera et al…
Brown and Ogden…
Olivera et al.. Reported a clear relationship between mothers food intake for most nutrients and their pre school children and suggested parents could be targeted for trying to improve children’s diets
Brown and Ogden.. Reported consistent correlations between parents and their children in terms of reported snack food intake and food motivation
Associate learning…
Lepper et al…
Evaluation…
Classical conditioning theory involves learning a new behavior via the process of association. In simple terms two stimuli are linked together to produce a new learned response in a person or animal. If something that we experience as pleasant e.g. our parents’ attention during a birthday party, is paired with a certain neutral stimulus, such as a birthday cake, then we might associate the cake with the pleasant feelings we have previously experienced as a result of our parents’ attention.
Lepper… used imaginary foods called hupe and hule. 28 pre school kids were told a story. The first was non-contingent condition so having 1 kind of food of was NOT contingent on eating the other. The other was the contingent condition so having 1 kind of food was contingent on having the other. Results showed that there was no preference in 1st condition but in the 2nd condition, children preferred food used as a reward claiming it ‘tasted better’
Evaluation
- identifying something as a reward tends to enhance its value
- didn’t get to taste the food so not ecologically valid
- used counterbalancing, half got hupe before hule and half got hule before hupe.
- this may be increasing the child’s preference for pudding even further, as pairing 2 foods in this way can result in the ‘reward’ food more positively.
Early learning effect on eating behaviour IDA
Culture…
Alternative approaches…
Nature-nurture debate…
Culture.. Early experience varies between culture so thus factor highlights cultural differences and can explain why certain foods are more popular in some cultures. However, studies on rating behaviour focus on western cultures and ignore third world countered whose main aim is to avoid starvation rather than deal with food choice.
Alternative approaches.. Food preferences may be due to physiological cravings for certain nutrients e.g. Cravings during pregnancy which are biological
Nature-nuture debate.. ‘Early learning’ suggests that we gradually develop food preferences over time however we may have some innate food preferences e.g. For sweet and fatty foods.
The Garcia effect - blaming food for illness even if the food does. It cause the illness. What did Garcia find?
Garcia gave rats radiation sickness through x rays after they drank saccharine flavoured water, in a red lit room. The rats learnt to avoid saccharine flavoured water but they did not learn to avoid red light.
Also found that when rats were electrically shocked after drinking saccharine flavoured water, they learned to avoid the place they were shocked but no the s flavoured water.
Conclusion: creatures are born ready to learn what makes them sick. This is a stronger ability than the ability to learn an association between two environmental factors meaning there are innate biological constraints on learning.
Evidence for set point theory.
Adopted children’s weight is more similar to that of their biological parents than their adoptive parents. MZ twins, even when reared apart are more similar in terms of weight than DZ twins - this supports the theory that body systems are ultimately genetical.
Early Learning Effects on eating behaviour (IDA)
- culture
- alternative approaches
- nature-nurture
- the Garcia effect
Culture: early experiences vary between cultures so this factor highlights cultural differences and can explain why certain foods are more common and popular in some cultures. In this sense there is no cultural bias; however, the study of eating behaviour has focused on western societies, ignoring third world countries whose main aim is to avoid starvation rather than deal with food choice.
Alternative approaches: the factor of early learning draws on behaviourist and development approaches; ignoring the idea that food preferences might be due to physiological craving for certain foods.
Nature-nurture: ‘early learning’ suggests that we gradually develop food preferences over time however, we may have some innate food preferences e.g. for sweet and fatty foods (evolutionary approach).
The Garcia Effect: This describes how we blaming food for illness, even if the food does not cause the illness. Garcia did an experiment on rats and found that creatures are born ready to learn what makes them sick. This is a stronger ability than the ability to learn an association between two environmental factors. This means there are innate biological constraints on learning
Stress effects on eating behaviour…
General Effect Model…
Evaluation… Animal studies, Garg and Bellisle.
-Study against GEM
Greeno and Wing 1994..
Stress affects eating via a physiological mechanism. It aims to discover whether stress increases eating generally.
Animal studies- The best evidence for GEM comes from research on housing conditions- rats are aggressive (assumed to be stressed) in isolation whilst Syrian rats are aggressive when housed in groups. Isolated rats put on more weight in isolation and Syrian rats more when it groups.
Garg 2007 - Examined how manipulation happiness and sadness through the content of a movie can influence the consumption of hedonistic foods. Results showed that the movies were successful in manipulating the desired emotions. Second, ppts consumed 28% more while watching a sad movie.
Evaluation…
-Using a full length film enabled researchers to mimic the natural environment in the lab e.g. going to the movies.
-By using lab they could investigate the cause and effect relationship of happy and sad rather than a more global effect.
-Ppts might have known the content of the films therefore the mere anticipation could have influenced consumption.
- Bellisle et al - 12 men reported to hospital for surgery and were asked to choose their lunch from an array of food. Rated anxiety. Returned to hospital one month later and chose lunch again. Anxiety higher on day of surgery but no more calories eaten so evidence against GEM.
-
Individual Difference Model…
IDM predictions…
Evaluation.. Cool, Conner and Wolf.
Greeno and Wing… IDM has been tested on humans and tends to propose psychological mechanisms to explain why stress causes some types of people to eat more or less than they usually do.
- The Individual Difference Model which predicts that stress only causes changes in eating behaviour in vulnerable individuals. It is argued that one particularly vulnerable group are people who have a history of dieting and concerns over their weight and eating.
- Predicts that stress effects eating of some types differently to others e.g. Learning history, attitudes, biology.
- External eating in response to
1) Environmental cues e.g. food availability and food cues such as sight and smell, rather than when they are hungry
2) stress masks hunger - external eaters will eat more when stressed if environmental suggests eating (IDM) - Emotional eating
1) Confusing anxiety with hunger due to childhood starvation worry. This may be due to inconsistent parenting.
2) Emotional eaters will eat more when stressed as they experience anxiety when hungry. (IDM) - Restrained eating i.e. dieting
1) Limiting food intake with will power however this is undermined by stress.
2) Women will eat more than men when stressed esp. certain foods because they are more likely to diet, more emotional and stress effects restrained, emotional eaters more.
(Shacter - people of normal weight eat when they detect cues telling them they are hungry. Stress decreases such cues (e.g. gastric contractions) Obese people fail to learn to identify such internal cues. So stress will decrease eating in hungry people of normal weight but will increase eating in people who are overweight. He did an experiment where obese males did not reduce eating in response to stress,when informed about electric shocks, but normals did eat less.)
Evaluation of stress and the Individual Differences Model
Oliver et al… 68 healthy men and women were randomly allocated to either stress or control group. In the stress condition, participants were asked to prepare a 4 minute speech on a controversial topic and they would be filmed and assessed after lunch. By contrast, the control group listened to a piece of calming music before lunch. A combination of physiological measures and self report measures were used to confirm the effectiveness of stress.
Results: Although stress did not alter overall intake of food or measures of appetite, stressed eaters in this study consumed more sweet, high- fat foods and ate more ‘energy-dense’ meal that unstressed eaters. Women also scored more highly on emotional eating that men. He also found that stressed/emotional eaters in this study consumed more sweet high, energy-dense foods that non-emotional eaters.
However, Conner et al (1999) students were asked to keep a daily record of the number and severity of daily hassles and the number of snacks consumed over a period of 7 days. Ppts were also asked to complete a questionnaire that assessed three dimensions of eating behaviour: restrained eating, emotional eating and external eating. For participants who scored highly on measures of external eating , there was a statistically significant positive relationship between hassles and snacking. No significant results were found between the two variables for ppts who were rated low on external eating.
Evidence against the influence of stress comes the study of ‘binge-eating disorder’. This disorder can be seen as comfort eating taken to the extreme. Wolff et al (2000) investigated differences between 20 female binge eaters and 20 female normal eaters focusing on daily, self-reported measures of mood, coping and eating behaviour over a three week period. It was found that the binge group reported more stress and negative moods but that their stress levels were similar on binge and non-binge days, whereas negative mood states were more apparent on binge days. This suggests that negative mood is more influential to our eating behaviour than stress.
But…..how can this research be criticised?
A great deal of research into mood and eating focuses on studying women. However, women are more likely to be dieters, have a greater incidence of eating disorders and often have a pre-occupation with food because of these things. This is a problem because such research and the theories related to it will have a female oriented view of eating because women are pre-dominantly studied. This gives an unrepresentative view of eating behaviour across both genders.
Set-point theory…..
- This theory explains why repeated dieting is unsuccessful in producing long term change in body weight. Going on a diet is an attempt to overpower the set point - the the set point is a seemingly tireless opponent to the dieter.
- The set point is a control system built into every person dictating how much fat he or she should carry - a kind of thermostat for body fat. Body fat percentage and body weight are matters of internal biological controls that are set differently in different people. Studies show that a persons weight at the set point is optimal for efficient activity and a stable optimistic mood.
- The set point is very good at supervising fat storage but cannot tell the difference between starvation and dieting. The dieter who begins a diet with a high set point experiences constant hunger, as part of their body’s attempt to restore the status quo.
- After an initial, relatively quick loss, dieters become stuck in a plateau and lose weight at a much slower rate despite feeling very hungry. Long-term caloric deprivation, in a way that is not clear, acts as a signal for the body to turn down its metabolic rate. Calories are burned more slowly so that even a meager diet almost suffices to maintain weight loss. The body reacts to stringent dieting as though famine has set in and consequently the metabolic machinery shifts to a cautious regime designed to conserve calories it already has.
- MZ twins are more similar in body weight, even when reared apart. and adopted children are more similar in body weight to their parents than their adopted parents This supports the theory by sugggesting that body systems are ultimately genetical.
- Keys et al - in WW11 4 men agreed to loose 25 percent of their body weight as a way of working out how to re-feed starving people in Europe. They began eating 50 percent of their usually calorie intake. Initially they lost a lot of weight however they then reached a point where they stopped loosing weight quickly, were lathargic and avoided physical activites and had cravings to over eat. When they were allowed to eat again, they did overeat and ate high sugar foods that would fill up their fat tissues faster.
Evidence as to why diets fail…
THE BOUNDARY MODEL OF DIETARY CONSTRAINT -
Everyone has a biological set-point which acts as a physiological boundary for food intake. Restrained eaters consciously lower their food intake to a cognitive boundary.
If this is overcome, perhaps through stress or on a special occasion, the ‘what the hell’ effects takes over and eating is disinhibited. The individual eats past the physiological model, consequently eating more than they would off the diet, allowing the diet to fail.
A02:
Herman and Mack - investigated the effect of pre-loading on eating behaviour in restrained and unrestrained eaters. 3 groups, the first had no pre-load (control group), the second given 1 milkshake as a pre-load and asked to rate the test qualities of the milkshake. The third group were given two milkshakes as a pre-load and asked to rate the taste qualities of the milkshakes. All groups were given three tubs of ice cream and 10 minutes to eat as much as they want to rate their taste quality. Finally all ppts were given a questionnaire to assess their degree of dietary restraint. Each group was divided into 2 subgroups -restrained and non-restrained eaters. The unrestrained eaters in groups 1 ate the most, in group two ate less and in group 3 ate even less. The restrained eaters in group 3 at the most, then group 2 ate a bit less then group 1, significantly less then both the other groups.
Conclusion: the results show a boundary model of dietary restraint. Restrained eaters have a cognitive dieting boundary for food intake. Once this is overcome (by the milkshakes), the ‘what the hell’ effects takes over and eating is disinhibited. So they eat more in the pre-load condition than in the zero preload condition.
Evaluation:
- No account was taken for individual differences. Group sizes were quite small. Some participants may have liked ice cream more or less than others despite three different varities being provided.
- Participants recieved course credits for taking part, which implies some degree of coercion e.g. they were not purely volunteers. However the study was not unethical as they could eat as little or as much as they lied. There was elelment of deception , essential of the experiment was to be valid, but ppts were given full debrief.
- The restrained questionnaire was given post-hoc to avoid ppts guessing the aim of the study. However this meant the the distribution of restrained and non-restrained ppts in each group was uneven which may of cause bias within the results, reducing the reliability of the research.
(- Masking hypothesis - diets fail when distress about an uncontrollable aspect of life is relieved by shifting into a diet, the perceived cause of the low mood. So long as the diet fails, this masks the source of the distress. It is better to feel that you could have succeeded than to feel a victim.)
Another explanation for the failure of dieting is the role of denial which suggests that attempting to suppress thoughts of foods is counterproductive and has the opposite effect. This theory illustrates the ironic processes of mental control because it represents a paradoxical effect of thought control. Diets often fail because when a restricted food becomes forbidden, the denied food becomes more attractive making attempts to suppress it difficult.For example
- Wegner (1987) asked half a sample of participants to not think about a white bear, but to ring a bell if they did. Those instructed not to rung the bell significantly more than those who were not instructed to. Therefore as soon as a food is denied, it becomes more attractive and likely to be eaten which ruins the diet.
What factors are there that potentially lead to the success of dieting…
Ogden 2000 - This model suggest that in order to diet successfully, the dieter needs to hold certain beliefs and also needs to engage in certain behaviours.
Cognitive elements: - Pyschoogical model of obesity - if individuals believe obesity is due to emotional eating, and causes depression and low self esteem then dieting can be successful as the individual believes weight loss is possible as they will be motivated to fix these problems
- Motivation for weight loss - if individuals are motivated to lost weight for personal reasons e.g. attractiveness.. dieting can then be successful.
Behavioural elements: - Small successes in weight loss are positively reinforcing as the individual believes weight loss is due to their own behaviour/dieting.
- Positive reinforcement strengthens behaviour, so dieting is likely to be continued.
2) Kieman et al found that individuals who were more dissatisfied at baseline with their bodies were more successful - motivation for weight loss is underpinned by a high value on attractiveness. Your behaviour will, as a consequence, the more motivated you become, resulting in success.
3) In Odgens and odgen and hills 2008 research - weightless was triggered by a key life event, such as divorce or illness. This initial behaviour was translated into longer term behaviour change if a number of conditions were not met including… a reduction in the choice over when and what you eat… and a reduction in the benefits and function of eating…. a belief in the behavioural model of obesity… a process of re-invention.
4) HOWEVER, there is a large problem of social desirability when using self-reort methods. In addition much of the research as an beta bias as it involves mostly women.
IDA: Important cause it stresses the importance of free will and the need to disbelieve the determinstic biological approach. However, it may ignore individuals are may have biological limitations to their weight loss.
5) One more factor is the attention paid to food. Many people get bored of repetition so should focus on the details of the meal e.g. crunchy cucumber and juicy tomatoes in a boring salad. - This was investigated by REDDEN - ppts are 22 fruit flavoured jelly beans while rating their enjoyment. At the end ppts wet asked to indicate how well they could distinguish the flavours and how similar the jelly beans seemed to each other and hoe repetitive the eating task felt. People who were given specific flavour labels became less satiated ad kept enjoying the jellybeans longer than people given the general label of jellybean number 7; Everyone ate the same variety of jellybeans, people who were just given ‘jellybeans’ to eat as opposed to ‘cherry jellybeans’ gave lower assessments as the experiments wore on.
What signals are there for starting a meal? A01/2
Dual centre model - A decline in glucose levels in the blood, leads to the stimulation of the lateral hypothalamus. The lateral hypothalamus is part of the hypothalamus that functions as feeding centre, stimulating feeding in response to signals of the body. The lateral hypothalamus therefore detects the decline in glucose and triggers feelings of hunger. The individual then consumes food and glucose levels begin to rise activating the VMH. The ventromedical hypothalamus is part of the hypothalamus that functions as a satiety centre to inhibit feeding. Therefore when the VMH detects the rise in glucose levels this leads to feelings of satiation which inhibits further feeding.
1) ANAND and BROBECK A and B found a lesion in another area of the hypothalamus, the lateral hypothalamus, led to a loss of feeding beahviour in rats, also known as aphagia - failure to eat when hungry.
2) Hetherington and Ranson. A02: H and R demonstrated that lesion in the Ventromedical hypothalamus of the brain caused rates to overeat and become dramatically obese.
2) It has been known for many years that an empty stomach sends signals to the brain to start eating. These sginals may include direct neural pathways from the stomach to the brain, animportant role i played by a hormane GRHELIN - released from the stomach that signals the hypothalamus to stimulate feeding. The amount released is proportional to the emptiness of the stomach. There is evidence that ghrelin acts directly on the brain mechanisms of feeding behaviour, including the hypothalamus
Cummings et al - investigated changes in blood ghrelin levels over time between meals. 6 ppts ate lunch then ghrelin levels were measured from blood samples taken every 5 minutes until the pps requested their evening meal. Pps assessed their degree of hunger every 30 minutes. Findings were that ghrelin levels fell immediately after eating lunch, reaching their lowest level at about 70 minutes. They then slowly began to rise, peaking as pps requested their evening meals. Importantly, in five out of six correlated closely with levels of hunger reported.
Conclusion: The authors conlcuded that ghrelin levels directly reflect stomach emptiness and are closely related to subjective feelings of hunger. Ghrelin is a key appetite signal in humans.
4) Mechanisms controlling feeding in the hypothalamus and related structures must receive a signal indicating the bodys fat reserves… - leptin. This hormone is released from adipocytes into the blood stream and travels to the hypothalamus where it acts as a satiety signal. As more fat is stored in adipocytes so more leptin is released and the hypothalamus is stimulated to reduce food intake.
Body weight is determined by muscle mass and more importantly body fat. Fat is sorted in specialised cells called adipocytes and fatty tissues is made up of these adipocytes. During early development, the number of adipocytes can be affected by diet but after this period, the number is set and the only way our fat stores can vary is through how much is stored in each cell.
CARLSON: Looked a obese mice and found that they did not produce lepton and so they ate continuously and became obese. Also found that injections of lepton into on mice stops them eating as much and their weight eventually returned to normal .
HOWEVER There are some rare individuals where people are obese because of a leptin defficiency but the majority have normal or higher than normal levels. The problem in theses cases seems to be that the brain mechanisms controlling feeding behaviour are insensitive to the effects of leptin.
IDA - Neural mechanisms involved in eating…
There is no doubt that we are biological organisms and our eating relied on complex biological systems therefore an understanding of these systems plays a key role in explaining the regulation of human eating behaviour. It is relevant to normal regulation, but also disorders such as anorexia and obesity.
HOWEVER, the biological approach is reductionist focusing only on the biological systems regulating food intake and body weight. It does not consider cultural or social factors.
- Practical applications - knowledge of what causes obesity can help prevent. We can reduce ghrelin secretion from the stomach by using Gastric bands on those with obesity. This will decrease the amount of ghrelin being sent to the LHM. Because the method has shown to reduce obesity, this increases the validity of the theory
