Attitudes to Food and Eating Behaviour

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A02-Attitudes to Food and Eating Behaviour


  • Research isnt straight foward. Story et al (1995) contrasted Dornbusch et al, found higher social class related to satisfaction with weight+ less weight control behaviours

Cultural Differences

  • Rozin et al (1999) suggested food functions differently between cultures. Studied people from France, USA + Japan and found cultural differences. Mumford et al (1991) found Bulimia was greater among Asian schoolgirls than white schoolgirls. 


  • Garg et al found nutritional info was important in food consumtion while watching a sad film. Suggests when poeple comfort eat they should check the nutritional information. 

IDA  Gender Bias- focuses on womens attitudes

        Culture Bias- Dornbusch (American adolescents)

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A01-Explanations for the Success+Failure of dietin

A01: Forms of Dieting

  • Higgins+Gray (1999) dieting is assocaited with a mentality over concern with body, size, shape and weight.

Restraint Theory

  • Herman+Mack (1975) explains causes+concequences with cognitive dieting

The Role of Denial

  • Wegner et al (1987) asked participnts not to think about a white bear. Results showed those told not to think about a bear rang the bell more often. Theory is called 'Theory of ironic processes of mental control'. 

Detail-key to a successful diet

  • Redden (2008) successful diet is due to attention. dieting is hard to stick to, so you must focus on specifics e.g Rocket, tomato, lettuce instead of salad (jelly bean experiment)
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A02-Explanations for the Success+Failure of dietin

A02-Restraint Theory-Implications for obesity treatment

  • Ogden (1994) obesity traetment is restraint. Failed dieting lead to depression. Obesity may not be caused by overeating, overeating may be a consequence of obesity if restraint is used as a treatment. How do anorexis starve themselves if restraint leads to overeating?

Anti dieting programmes

  • Replace dieting with healthy eating-Higgins+Gray (1999) meta analysis of effectiveness of dieting programmes. Found participants had improved eating behaviour with weight stability

IDA-Free will/Determinism 

  • Dieting S/F due to genetics (deterministic) Kern et al (1990) found LPL levels rose after weight loss. Easier for a dieter to put back on weight than someone who has never been obese due to gene production

Culture Bias

  • Park et al (2001)- Asian adults more prone to obesity
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A01-Evolutionary Explanations of food preference

AO1-EEA-Environment of Evolutionary Adaptation-how the world was when our ancestors lived

Preference for meat

  • High nutrience foods helped survival, compensation for decline in plants in EEA
  • Buss (2008) women divorced men who didnt provide food-meat made males more desirable 
  • Milton (2008) without meat humans wouldnt have evolved as they have 

Early Diets

  • Fatty/high calorie foods are adaptive, provides vital energy for hunting

Taste Aversion

  • Only eat in small ammounts to avoid poisonous foods 
  • Garcia et al (1955) studied taste aversion by adding bitter flavours to food, rats developed an aversion to food which made them ill, this helps their survival 
  • Foods eaten before recovery from illnesses are prefered in the future 'medicine effect'
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A02-Evolutionary Explanations of food preference


  • Gibson+Wardle (2001)-supports importance of calories (bananas+potatoes are most liked)


  • Cordain et al (2006) ancestors ate plants which suggests they were vegetarians however...
  • Abrams (1987) showed a preference for meat and would be impossible to recieve enough calories from plants alone

Real World Application

  • taste aversion can be found in cancer patients recieving treatment
  • Bernstein+Webster (1980) gave patients new flavoured ice cream prior to treatment, created the 'scapegoat technique' patients given familiar and new flavours. They had an aversion to new foods but not familiar ones. This is an adaptive avoidance know as neophobia.
  • Cultural differences- what we are used to e.g spicy food is accepted more in asian countries.
  • Animal Studies (Primates) 
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A01-Biological Explanations for Anorexia Nervosa


SERETONIN- levels change when individual has an eating disorder

  • Bailer et al (2007)-compared seretonin in women with AN/BE/Normal. Found higher seretonin in Binge-eating women. Suggests unstable seretonin levels may cause anxiety+trigger AN.


  • Kaye et al (2005)- used PET scans on 10 women with AN and 12 normal women. Results showed dopamine receptors were overactive in AN women. Increased dopamine alters how people interpret rewards , those with AN find it hard to associate food with pleasure

NEURODEVELOPMENT- Eagles (2001) AN more likely if born in spring months/youngest sibling

EVOLUTIONARY EXPLANATIONS- Adapted to flee hypothesis (AFFH)

  • Giusinger (2003)- symptoms of AN are restriction+denial of starvation shows adaptive mechanisms which causes migration when food is low (when food is low you restrict)
  • When a person loses weight they conserve energy as an adaption to help survival
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A02-Biological Explanations for Anorexia Nervosa


SERETONIN- SSRI which alters brain seretonin is not effective on AN patients 

  • kaye et al (2001) found drugs were effective in preventing a relapse in recovering AN patients 

DOPAMINE- Supportive evidence

  • Castro-Fomieles et al (2006) found adolescent girls with AN had higher levels of homovanillic acid (waste product of dopamine)
  • Wang et al (2001) low dopamine levels are associated with obesity
  • Real World Application- Research allows insurance companies to consider AN as a psychiatric condition
  • Gender Bias- Research is concentrated on women but 25% of adults with an eating disorder are men.
  • Treatment implications- Bulik et al (2006) suggested if there were genetic profiles to show risk levels it wuld develop treatment methods for AN. Treatment reduces guilt for parents.
  • Reductionist/ Deterministic 
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A01-Neural Mechanisms in Eating Behaviour


  • A mechanism which restores the internal environment to its optimum state.
  • The body has developed 2 one which turn eating on the other off. Glucose produces feelings of hunger which triggers the lateral hypotthalamus to seek food, After a rise in glucose due to eating the ventromedial hypothalamus is activated which leads to feelings of satiation. 


  • Damage in rats causes aphagia and stimulation of LH elicits feeding behaviour
  • 'ON' switch for feeding, Neuropeptide Y is important in turning on eating (Wickens)
  • Stanley et al found repeated injections of NPY caused rats to become obese in a few days 


  • Damage causes rats to overeat leading to hyperphagia
  • Stops eating+causes damage to paraventricular nucleus which is the cause of hyperphagia
  • Gold found lesions restricted to VMH alone didnt result in hyperphagia, only when included other areas such as paraventricular nerves
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