Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Psychology 3 > Eating Behaviour > Flashcards

Eating Behaviour Flashcards

You may prefer our related Brainscape-certified flashcards:
Psychology 101 flashcards GRE® Psychology flashcards AP® Psychology flashcards
1
Q

What are the explanations for food preference?

A
  • evolutionary explanation

- role of learning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What 3 areas can the evolutionary explanation of food preference be summarised into?

A
  • early diets
  • taste aversion
  • neophobia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What do early diets suggest about the evolutionary explanation for food preference?

A
  • a preference for high calorie food (due to uncertainty of next meal)
  • preference for meat (nutrients aid brain development, Milton, 2008)
  • preference for sweet food (sugar in fruits give vitamins essential for body growth, Manella, 2014)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does taste aversion suggest about the evolutionary explanation for food preference?

A
  • avoidance of poisonous food (Garcia 1955 found avoidance of bitter foods in rats)
  • taste aversion in pregnancy to protect the infant from harmful substances
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does neophobia suggest about the evolutionary explanation for food preference?

A
  • reluctance to consume new/unfamiliar food (protects ancestors from consuming poison so promotes survival)
  • animals with restricted diets are less likely to display neophobia (e.g. koala) than those with varied diets
  • humans have expectations of food appearance/smell based on culture and reject the unfamiliar
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the strengths of evolutionary explanations for food preference?

A
  • research support for evolved preference for sweet food (early exposure not necessary for children to develop sweet food preference e.g. Inupiat people in Alaska came to contact with cultures that consume sugar and in no cases have rejected the sweet food, newborns showed accepting response the first time they tasted something sweet, Grill and Norgren 1978)
  • real world application (used to understand food avoidance that comes with cancer treatment, radiation and chemotherapy can cause gastrointestinal illness which may cause taste aversion e.g. Bernstein and Webster 1980 gave patients a novel icecream before chemo and found they acquired an aversion to that icecream - resulted in “scapegoat technique” whereby patients are given a novel and familiar food before treatment and develop aversion to the novel food and not the familiar food)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the limitations of evolutionary explanations for food preference?

A
  • food once beneficial to ancestors is now harmful (traits beneficial to ancestors e.g. saturated fats is now harmful to health nowadays so we are likely to avoid them, similarly traits beneficial to us today e.g. consumption of low cholesterol food, has not evolved from ancestors - Krebs 2009 suggests a mismatch between evolved preferences and modern environments e.g. sweet foods cause global health epidemics e.g. diabetes)
  • neophobia may not be adaptive (problematic to those who restrict their diets to inadequate nutrition e.g. Perry 2015 found neophobia to be associated with poor dietary quality in children)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What influences are involved in the role of learning as an explanation for food preference?

A
  • social influences (parental and peer influence)

- cultural influences (media influence and context of meals)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the parental influences in the role of learning in food preference?

A
  • association between parent-child attitudes to food generally (Brown and Ogden found correlations in snack food intake and eating motivations)
  • parents manipulate the availability of certain foods e.g. treat in reward for eating veg - research suggests this makes the distasteful food even less appealing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the peer influences in the role of learning in food preference?

A
  • SLT suggests observation of peers impacts food preference e.g. Greenhalgh found that those shown positive modelling (peers eating novel foods) were more likely to try the food and vice versa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the role of the media in cultural influences for food preference?

A
  • MacIntyre 1998 found media to impact what people ate and their attitudes to food
  • people learn from the media about healthy eating but this influence is dependent on other demographics e.g. age, income - people place info on eating into broader context of their lives
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How does the context of meals culturally influence food preference?

A
  • US societies increasingly rely on “grazing” and desire for convenience food e.g. takeaway
  • Gillman 2000 found eating meals in front of the TV was associated with greater pizza and salt consumption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How can the role of learning in food preference (in terms of social influence) be evaluated?

A
  • parental influence may be limited (studies have been small-scale and on highly selective sample of white Americans so may not be appropriate to generalise findings e.g. Robinson studied 800 children from varying backgrounds and found complex associations between parent-child food preference. Research into methods parents use to influence child food preference has found varied effectiveness e.g. parental modelling was effective but forcing consumption was not)
  • research supports role of peers (when significant others modelled eating “light” yogurt it led to a preference for light products in young children - social facilitation may occur whereby children consume foods demonstrated by others to be safe)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How can the role of learning in food preference (in terms of cultural influence) be evaluated?

A
  • research supports media influence (Boyland and Halford found that exposure to TV food advertising influences food preference/consumption in children, but influences children of different weight profiles differently with high fat/sugar foods having more influence on overweight children, and those who had greatest preference for high carb/fat foods were those that watched the most)
  • this has a real world application as many countries have now developed regulations concerning unhealthy food advertising on TV, either by limiting quantity of advertising or by reducing the effects of this advertising e.g. some govs restrict the use of promotional characters to promote food to children
  • research into food environments through tweets in Columbus (found a significant association between healthy food choices and number of grocery stores around them, but no association between number of fast food outlets and healthy/unhealthy choices - suggests culture to have an effect on learned food habits but that people can resist the development of unhealthy habits if a healthy alternative is available)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the mechanisms involved in the control of eating?

A

neural mechanisms - homeostasis: lateral/ventromedial hypothalamus
hormonal mechanisms - ghrelin and leptin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is homeostasis?

A

homeostasis - the body’s maintenance of a stable internal environment.
in terms of eating: eating - increased glucose - VMH activated - satiety - stop eating - decreased glucose - LH activated - hunger - eating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the lateral hypothalamus?

A
  • part of the brain that causes sensation of hunger
  • deemed the “on” switch to eating -1950s research found damage to the lateral hypothalamus in rats caused “aphagia” (cessation of eating) - when stimulated, the rats started eating again
  • also discovered neurotransmitter NPY to be important in this process - when it was injected into the LH, rats immediately began to eat even if satiated, causing them to become obese in days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the ventromedial hypothalamus?

A
  • part of the brain that causes satiety when blood glucose is high
  • researchers found damage to the VMH caused “hyperphagia” (overeating) - stimulation caused cessation to eating
  • damage to the VMH included damage to the paraventricular nucleus (PVN) which detects specific foods and is responsible for cravings - thought that this alone is responsible for overeating
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What does ghrelin do?

A

“hunger hormone” released into stomach, stimulating the hypothalamus to increase appetite
- levels increase before eating and decrease after

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What does leptin do?

A
  • reduces appetite
  • produced in fat tissue and secreted into the bloodstream where it travels to the brain, binds to receptors in the hypothalamus and counteracts the effects of NPY (which causes eating in the LH), as well as increasing sympathetic nervous system activity which stimulates fatty tissue to burn energy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the strengths of neural and hormonal mechanisms in the control of eating?

A
  • research supports the role of ghrelin (Wen 2001 found significant increase in food consumption when receiving ghrelin (compared to saline infusion) with mean difference of 28% - demonstrates ghrelin to be important signal stimulating food intake in humans)
  • support for the role of the ventromedial hypothalamus (from research finding lesions/damage to VMH led to hyperphagia and obesity, this led researchers to deem the VMH as the “satiety centre” in eating behaviour. compared to lesions in other parts of the brain, those in the VMH caused substantially more eating)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the limitations of neural and hormonal mechanisms in the control of eating?

A
  • homeostatic explanations are limited (theory suggests hunger and eating to be triggered only when energy resources fall below desired levels, which is compatible with how systems must have evolved. But if the mechanisms were truly adaptive, they would promote levels of consumption that maintain body resources well above optimal levels to act against potential lack of food availability)
  • the centrality of LH as the “on” switch to eating may not be the case (research found damage to lateral hypothalamus to cause deficits in other areas e.g. sex, thirst - not just hunger. Recent research found eating is also controlled by neural circuits in the brain and not just the hypothalamus)
23
Q

What are the different explanations for anorexia nervosa?

A
  • biological explanation (genetics/neural)
  • psychological explanation (family systems theory)
  • social learning theory
  • cognitive theory (CBM and transdiagnostic model)
24
Q

What two areas do biological explanations for AN involve?

A
  • genetics (family/twin/adoption studies)

- neural explanations (serotonin, dopamine, limbic system dysfunction)

25
Q

What do genetic studies suggest about AN?

A
  • 1st degree relatives have 10x greater lifetime risk (than those without AN in the family) and increased risk of developing other eating disorders (suggesting inherited general vulnerability)
  • Holland et al (1998) found statistically higher concordance in MZ twins (56% compared to 5% in DZ twins) suggesting genetic component to AN
  • comparing MZ and DZ twins as measure of genetic/environmental contributions - suggest moderate/high heritability so some more genetically predisposed than others
  • however twin studies are problematic as MZ twins also share the same environment, and are often treated more similarly so difficult to disentangle influences - therefore adoption studies are used e.g. Klump studied adoptive and biological siblings findong heritability estimates of 59-82% for disordered eating
26
Q

How can the biological explanation of AN be evaluated regarding the role of genetics?

A
  • problematic as actual heritability of AN remains unknown, studies into the area have been inconsistent with estimates and violate the ‘equal environments assumption’ which assumes twins experience similar environments just because they live in the same home (e.g. MZ twins usually treated more similarly)
  • can be applied negatively to the real world - increasing knowledge on the contributions of biology may be manipulated e.g. insurance-based healthcare systems may begin to charge more for genetic vulnerabilities, however US insurance wont pay out for treatment of AN as it is not currently considered a biological problem
27
Q

What does the biological explanation of AN suggest with regards to the role of neural systems?

A
  • neural influences: serotonin, dopamine, limbic system dysfunction
  • some anorexics have over-production of serotonin, causing high anxiety, and eating less food may mean less serotonin is produced, lowering anxiety
  • over-activity in basil ganglia, where dopamine receptors play a role in interpreting harm/pleasure, may cause a lack of interpretation whereby food is not associated with pleasure as it usually is
  • limbic system plays a role in social processing, a dysfunction would mean emotions arent being processed in the usual way, leading to pathological thoughts typical of AN
28
Q

How can the biological explanation be evaluated in terms of the neural influence?

A
  • little evidence for the role of serotonin - study found those with anorexia did not recover when given SSRIs, had little difference with those who didnt receive the drug - however Kaye et al found that they had a use in preventing relapse in recovering patients (therefore it may be that SSRIs only become effective when weight returns, and perhaps the changes in serotonin function caused by AN might negate SSRI action)
  • advantages of biological explanation - if a disorder has a biological component, insurance-based healthcare will be payed out, eliminating stress by removing personal responsibility for the disorder - takes away blame/stigma, more hopeful/treatments more easily developed as biological problems have biological treatments
29
Q

What is the psychological explanation for AN?

A
  • ‘family systems theory’ argues individuals cannot be viewed in isolation but as part of their family as one emotional unit
  • the psychosomatic family model suggests AN to be the result of a dysfunctional family coupled with a physiological vulnerability in the child - therefore aim of treatment involves changing family functions
  • psychosomatic family involves:
    enmeshment (extreme intensity/proximity in family interaction, characterised by family over-involvement, lack of boundaries such that individuals cannot develop autonomy)
    autonomy (failure to develop autonomy during adolescence, retaining accustomed patterns/not allowing for change)
    control (overprotective control/high concern for eachothers welfare, distorting beliefs on extent of control they have on their lives - therefore controlling eating is rebelling against this family control)
    (rigidity - lack of flexibility to new situations, increase rigidity in face of stress, lack of conflict resolution - causes low tolerance for conflict with difficulty acknowledging/resolving conflict)
30
Q

What are the strengths of the family systems theory/psychological explanation of AN?

A
  • enmeshment supported by Manzi - made distinction between family factors that promote/restrict positive emotional development, family cohesion enhanced positive outcomes and psychological wellbeing, where as enmeshment had opposite effect (this was true across cultures)
  • family-based therapies can be successful, showing family as key part of recovery e.g. Carr found evidence for effectiveness of family interventions for AN in adolescents (however…the changes in family functioning caused by family therapy are not necessarily the changes predicted by the psychosomatic family model, and may not happen in all families)
31
Q

What are the limitations of the family systems theory/psychological explanation of AN?

A
  • the changes in family functioning caused by family therapy are not necessarily the changes predicted by the psychosomatic family model, and may not happen in all families
  • Gremillion argues there is a heavy daughter-mother focus in the explanation e.g. enmeshment associated with maternal origin - therefore therapy reducing enmeshment targets ‘dysfunctional mothers’ instead of acknowledging father role - gender bias as role of overcontrolling fathers is often ignored
32
Q

How does the social learning theory explain AN?

A
  • use of modelling: someone (e.g. parents/media figures) models particular attitude/behaviour, providing examples of attitudes to food/dieting which is observed and imitated by the individual
  • use of reinforcement: imitating models behaviour results in positive responses from others, making individual feel good and want to continue losing weight, can also be indirectly reinforced (vicarious learning) e.g. by seeing others being praised
  • role of maternal role models: research suggests mothers model weight concerns to daughters, relationship found between mother and daughter in terms of restraint/dieting behaviours as young as 10
  • peer influences: adolescents susceptible to peer influence on patterns of disordered eating e.g. study found dieting among friends was related to unhealthy weight control behaviours (incl diet pill use), overweight girls most likely to be teased by peers.
  • media influences: major source of body image attitudes in west, those with low self esteem more likely to be influenced/compare themselves to media figures e.g. Button found 11-12 year old girls with low self esteem at greater risk of developing eating disorder later, British Medical Association report found slim models in contrast to body shape of most young women, concluding degree of thinness as unachievable and biologically inappropriate
33
Q

What are the strengths of the social learning theory for AN?

A
  • support for role of peer influence e.g. study found individuals with peers of larger BMIs had lower likelihood of developing eating disorders - suggests that peers with average/higher BMIs ‘protect’ individuals from eating disorders, but those with lower BMIs make AN development more likely
  • support for role of media in shaping body image attitudes from studies of societies where TV has been introduced e.g. after exposure to TV for first time in Fiji, girls stated a desire to lose weight in order to become like western TV characters - however other research shows intervention before media exposure can limit these adverse effects (therefore media is powerful influence in developing eating disorders but that education can prevent this influence)
34
Q

What are the limitations of the social learning theory for AN?

A
  • however influence of media may depend on type of media - studies find magazines as more consistent than TV as a predictor of developing AN e.g. studies of undergrads find association between reading fashion magazines and having preference for lower weight/low body image confidence
  • studies have been inconsistent regarding role of maternal influence e.g. Ogden and Steward found mothers/daughters to have similar BMI but no association in restrained eating/body dissatisfaction, they suggest contribution of mother to developing disordered eating is more than simply acting as role model and instead may be nature of mother-daughter relationship itself that is important (incl the degree of enmeshment)
35
Q

How does the cognitive theory explain AN development?

A
  • emphasises existence of irrational beliefs (e.g. must be thin to be liked) and cognitive distortions (errors in thinking that cause negative body image, perhaps resulting from comparisons) that lead to misperception, self-disgust and attempt at weight loss
  • two models used to explain development of AN:
  • Cognitive Behavioural Model (CBM)
  • Transdiagnostic Model
36
Q

What does the Cognitive Behavioural Model suggest?

A

AN patients have characteristics in common e.g. perfectionist/introvert, and exposure to cultural ideals leads to increased importance of body weight, leading to irrational belief that weight loss will reduce distress/make them more attractive - weight loss then provides sense of achievement, positive comments about weight lead to anxiety about eating that develops into food avoidance

37
Q

What does the Transdiagnostic Model suggest?

A

underlying cause of all eating disorders is same set of cognitive distortions incl overestimation of weight, overemphasis on self-control/appearance, self-esteem becomes determined by appearance and ability to control weight leads to increased monitoring of weight. increased self-control increases self-esteem, consequences of food restriction perceived as failure so food restriction increases

38
Q

What are the strengths of the cognitive explanation of AN?

A
  • in Ben-Tovim’s ‘food stroop’ test, AN patients found it harder to colour-name words related to weight concerns than those without AN - suggests selective preoccupation with such stimuli, as predicted by the CBM and TM which suggest AN patients’ attention will be directed towards body-related stimuli
  • CBT-E treatment is specifically designed to address cognitive problems that underlie AN - study found that following treatments, 2/3 of CBT-E patients met criteria for remission, compared to 1/3 of those receiving psychtherapy - reinforces view that cognitive issues are root cause of AN (as cognitivie treatments successful)
39
Q

What are the limitations of the cognitive explanation of AN?

A
  • cognitive explanations over-rely on self-report data - assumes that pre-occupations with thoughts of weight is accessible through verbal measures. but most scientists reject self-report measures in faovur of performance-based measures that directly sample cognitive-processing - therefore understanding of cognitive disrotions are limited due to problems with methods used to access them
  • some claim cognitive models are the result of clinical observation, rather than empirical research - little research done to test the hypothesis derived from cognitive models, thus the approach has lagged behind a cognitive approach to other disorders e.g. depression
40
Q

What are the different explanations for obesity?

A
  • psychological explanation (restraint theory, boundary model, disinhibition)
  • biological explanation (genetics/neural explanation)
41
Q

What does the psychological explanation for obesity involve?

A
  • restraint theory (dieting/restraining eating paradoxically results in overeating, and therefore increases obesity risk. 2 types of restrained eating: rigid or flexible - rigid restraint found to be less effective in reducing fat intake)
  • boundary model (explains restraint theory)
  • disinhibition (overeating in response to stimuli, 3 types: habitual, emotional, situational - habitual most common and found to strongly associate with weight gain as daily life presents eating opportunities e.g. coffee shops)
42
Q

What does the boundary model suggest with regards to obesity?

A
  • explains why restraint theory occurs:
  • food intake is regulated on a continuum with hunger and satiation at either end, biological processes drive hunger/satiation but in between these, in the ‘zone of biological indifference’, it is down to psychological factors
  • this zone is larger for restrained eaters as they have lower hunger threshold and higher satiation threshold (so are less sensitive to feelings of hunger/satiation)
  • the cognitively-set diet boundary is lower than the satiation threshold, and exceeding this boundary leads to the ‘what the hell effect’
  • Herman and Mack’s ‘milkshake study’ involved 3 groups given 0, 1 or 2 milkshakes, then asked to taste 3 flavours of icecream - found that those not on a diet ate less if they had had a milkshake (acted as preload), those without a preload who were on a diet were restrained, but those who had 2 milkshakes ate the most icecream (had exceeded self-imposed boundary leading to ‘what the hell effect’)
43
Q

What are the strengths of psychological explanations of obesity?

A

Wardle and Beatles (1988) supports restraint theory - assigned obese women to either a diet group, exercise group or non-treatment group for 7 weeks, assessments at 4 and 6 sweeps showed those in the diet condition ate more than those in other conditions

  • disinhibited eating may be related to insecure attachment e.g. Wilkinson (2010) found attachment anxiety to be linked to disinhibited eating and BMI (suggesting tendency to deal with anxiety through overeating), this is consistent with research that significant life events lead to shifts in BMI - anxiously attached may be more sensitive to these events so more likely to engage in disinhibited eating to cope
44
Q

What are the limitations of psychological explanations of obesity?

A
  • most research into the theory is based on lab researchers (out of the lab dieters would be able to control their eating more) - Tomiyama et al (2009) found dieters that tracked their intake over a few days didnt overeat following diet violations (questions boundary model - do violations lead to overeating?)
  • most research restricted to white women - conclusions drawn specifically to this group and not applicable to others - e.g. Atlas (2002) reported lower restraint and disinhibition in Afro-American students than white
45
Q

How does the biological explanation explain obesity in terms of genetics?

A
  • emphasis on genetic inheritance of obesity:
  • twin studies: average heritability estimates at 40-75%, meta-analysis involving 75,000 found heritability for BMI at 74% for MZ and 32% for DZ twins - even when raised apart BMI was more similar between MZ twins
  • adoption studies: allow researchers to look separately at influence of genetic/environmental factors e.g. Stunkard found strong relationship between weight categories of adopted individuals and biological parents, but no relationship with adoptive parents
46
Q

How does the biological explanation explain obesity in terms of neural influences?

A
  • hypothalamus plays key role in regulating metabolism
  • within this the arcuate nucleus (collection of neurons) plays role in appetite and obesity: monitors sugar levels and acts when energy levels are low by sending messages to other body parts, producing desire to eat and coordinating this with energy utilisation - therefore responsible for maintenance of body weight and adjusting food intake to physical activity - malfunction may lead to overeating
  • leptin - hormone secreted by fat cells that decreases feeding behaviour and promotes energy expenditure, acts on leptin receptors in the brain which inhibit food intake e.g. by stimulating neuropeptide y in arcuate nucleus - study found leptin signalling dysfunction in hypothalamus results in obesity
  • ‘thrifty gene hypothesis’ suggests that ‘thrifty’ genes have been positively selected ie genes that were efficient in food intake made people fat and so provided energy necessary for survival during famine - such genes once provided a survival advantages but are now disadvantageous as they promote fat storage in preparation for a famine that never comes, resulting in widespread obesity
47
Q

What are the strengths of the biological explanation for obesity?

A
  • research support for role of leptin - evidence to suggest some people do not produce leptin and so are predisposed to obesity e.g. Montague (1997) found 2 severely obese cousins had v low leptin levels, Gibson found that an obese child after 4 years of leptin injections became less obese (supports role of leptin in regulating appetite and its deficiency acts as risk factor for obesity)
  • biological explanations offer a view that obesity is out of personal control, therefore less stigmatising - where as psychological explanations highlight personal failings, simplicity of biological influence makes it more appealing and ‘scientific nature’ means biological treatments offer hope to combatting the disorder e.g. leptin injections
48
Q

What are the limitations of the biological explanation for obesity?

A
  • increasing obesity rates in the UK ove past 20 years, but nature of the gene pool remains the same - this increase can therefore not be explained by genetics alone - obesity rates vary within the same culture geographically, if it was genetic influences there would be little variation, therefore psychological factors may be at play
  • if the thrifty gene hypothesis was true, the majority would have inherited the successful ‘thrifty’ gene and so the majority would be obese - the obesity epidemic in the west is only recent and restricted to cultures where cultural habits include consumption of fatty foods e.g. it was found that 50% of the world’s obese live in 10 countries, therefore obesity may be better explained by cultural influences
49
Q

What are the explanations for the success and failure of dieting?

A
  • attention to detail
  • theory of hedonic eating
  • role of denial
50
Q

How does attention to detail cause dieting to succeed/fail?

A
  • people like experiences less as they repeat them, and focusing on details can make them more interesting
  • Redden’s ‘jelly beans experiment’ involved two groups: one with general info on jelly beans (e.g. no. 3), other with specific flavour details (e.g. no. 3 is raspberry) - group with general info got bored
  • therefore dieting more likely to be successful if focusing on detail of the food and make it more interesting
51
Q

How does the theory of hedonic eating cause dieting to succeed/fail?

A
  • dieters particularly sensitive to pleasures of food
  • therefore presence of attractive food triggers a desire to eat due to its perceived pleasures
  • pleasure thoughts (hedonic thinking) dominates thinking of dieter - so attention is diverted away from diet and allocated to food/its pleasures - resulting in eating
52
Q

How does the role of denial cause dieting to succeed/fail?

A
  • attempts to suppress thoughts actually increase them
  • Wegner’s white bear study - one group told not to think about the bear, the other told to think of anything including the bear - suppression was difficult for the first group compared to the other, and had more white bear thoughts
  • known as theory of ironic processes of mental control - the more you suppress a thought the more you think of it
  • therefore suppressing food thoughts increases them and leads to failure to diet
53
Q

What are the strengths of explanations for success/failure of dieting?

A
  • real world application - highlighting concerns over the ineffectiveness/damage of diet programmes has led to development of programmes emphasising conventional healthy eating rather than dieting - stressing regulation by body hunger and satiety signals, and preventing inappropriate attitudes to dieting - found to be better associated with improvements in eating behaviour and wellbeing
  • research support for hedonic theory by Brunstorm who found dieting Ps showed greater salivary response to pizza than those who were not dieting - suggests difference in perception of food between restrained/unrestrained eaters
54
Q

What are the limitations of explanations for success/failure of dieting?

A
  • many studies rely on anecdotal evidence, limited as recall not accurate, assessment of success of diets is not objective - creates problems for reliability of personal account evidence - also causal connections between dieting and weight loss are made too easily and without control of extraneous variables
  • may be that genetic mechanisms exert influence on weight, so success of dieting may be determined by factors other than lifestyle choice - e.g. has been found that the fatter the person was initially, the higher the LPL levels, (enzyme that stores calories in bodies, making it easier to regain lost weight) - weight loss may activate gene that produces LPL - may suggest why it is easier for dieters to regain weight than for someone never fat to gain weight (therefore people will struggle to lose weight due to genetics regardless of intentions)

Psychology 3 (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions