Eating Behaviour Flashcards

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1
Q

What main factors influence attitudes to food and eating behaviour?

A

Mood, Social Learning and Culture

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2
Q

In what way can mood effect eating behaviour?

A

Through binge eating and comfort eating

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3
Q

In what way does social learning effect eating behaviour?

A

Parental modelling & Media effects

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4
Q

In what way does cultural influences effect eating behaviour?

A

Ethnicity and social class

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5
Q

What did Powell and Khan (1995) find on cultural influence and eating behaviour?

A

They found that body dissatisfaction and related eating concerns were more characteristic of white women than black or Asian women.

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6
Q

What did Downbusch et al (1984) find on cultural influence and eating behaviour?

A

Found that among American adolescents, higher class females had a greater desire to be thin and were more likely to died to achieve this compared to lower class females.

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7
Q

What did Goode et al find on cultural influence and eating behaviour?

A

Found that healthy attitudes to eating were more likely to be found among higher income families.

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8
Q

How can mood affect your eating behaviour?

A

Many people comfort eat in a low mood. Individuals with bulimia nervosa tend to experience anxiety prior to binge eating episode, despite the fact it does not alleviate the low mood; this relationship is also seen in non-clinical populations.

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9
Q

What did Wegner et al find on mood and eating behaviour?

A

Students recorded their eatingpatterns and mood states over 2 weeks. Binge days were lower in mood state than non binge days.

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10
Q

What did Garg et al (2007) find on mood and eating behaviour?

A

They observed the food preferences of 38 participants as they watched a funny movie (sweet home Alabama) or sad movie (love story). They were offered buttered popcorn or grapes. Participants watching the sad film consumed 36% more popcorn than those watching the funny film, who ate more grapes. When given the nutritional information before the consumption of the unhealthy food, snacking dropped dramatically.

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11
Q

What did Davis et al (1988) find on mood and eating behaviour?

A

He studied patients with bulimia nervosa. Patients recorded their food intake and mood every hour for a number of days. The reports showed that negative mood states before a binge episode were higher than before a normal meal.

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12
Q

What is the issue with the relationship between mood and binge eating?

A

It is unclear how a binge eating episode is reinforcing in terms of mood as following a binge there is often a drop in mood.

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13
Q

What did Parker et al (2006) find on mood and eating behaviour?

A

Found that when chocolate was eaten as an emotional eating strategy is it more likely to prolong the negative mood.

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14
Q

What did Brown and Ogden (2004) find on social learning and eating behaviour?

A

Found that there were correlations between parents and their children in terms of snack food intake, eating motivations and body dissatisfaction.

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15
Q

How could parental modelling influence eating behaviour?

A

Children observe the attitudes and eating behaviour of their parents, and parents control the food brought and served at home.

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16
Q

What did Kotler et al (2012) find on social learning and eating behaviour?

A

Conducted two experiments to assess the role of media characters in influencing children’s food choice.

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17
Q

What was the first experiment Kotler et al (2012) did on social learning and eating behaviour?

A

Children were more likely to indicate a preference for one food over another when one was associated with tv characters with whom they were familiar. However, when children were asked to choose between a healthy food with a favoured character and a sugary or salty snack with an unfamiliar one, this effect did not happen.

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18
Q

What was the second experiment Kotler et al (2012) did on social learning and eating behaviour?

A

Children were more likely to try more pieces of a healthy food if a favoured character, in comparison with an unknown character, is promoting that food.

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19
Q

What did Mumford et al (19911) find about culture and eating behaviour?

A

Found that bulimia was greater among Asian school girls than white school girls.

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20
Q

What did Streigel-Moore et al (1996) find on culture and eating behaviour?

A

Found that black girls had more of a drive towards thinness than white girls.

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21
Q

What did Story et al (1995) find on culture and eating behaviour?

A

Found that a sample of American students high social social class was related to greater satisfaction with weight and lower rates of weight control behaviour.

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22
Q

What is homeostatis?

A

The process by which the body maintains a constant internal environment.

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23
Q

What is satiation?

A

The state of being satisfactorily full and unable to take on more.

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24
Q

What is aphagia?

A

Failure to eat when hungry

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25
Q

What is hyperphagia?

A

Abnormally increased appetite for and consumption of food, thought to be associated with a lesion or injury in the hypothalamus

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26
Q

What is leptin?

A

a peptide hormone produced by fat cells and involved in the regulation of appetite and energy metabolism

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27
Q

What is ghrelin?

A

A hormone that is secreted by cells in the stomach and promotes hunger before an expected meal, decreases in amount after eating, and promotes secretion of growth hormone

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28
Q

What is the lateral hypothalamus?

A

It is concerned with hunger. Damage to this area can cause reduced food intake. Stimulating this area causes a desire to eat.

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29
Q

What is the ventromedial hypothalamus?

A

It is concerned with satiation. Stimulating this area causes a reduced desire to eat.

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30
Q

What is Neuropeptide Y (NPY)?

A

A neurotransmitter found in the hypothalamus.

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31
Q

How is homHOMOeostatis maintained?

A

Via a negative feedback loop: this assumes that all body variables have a set point (or range)

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32
Q

What evidence is there that the hypothalamus plays a role in eating and in weight gain and loss?

A

Patients with tumours in the hypothalamus tend to become obsese.

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33
Q

How does the Lateral hypothalamus play a role in eating and weight gain and loss?

A

This area of the hypothalamus contains the feeding centre; it initiates or starts eating behaviour. It responds to decreased blood glucose and, an increase in ghrelin which is a hormone released from the stomach when it is empty.

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34
Q

How does the Ventromedial hypothalamus play a role in eating and weight gain/loss?

A

The VMH contains the satiety centre- it signals when you are full. This inhibits or stops eating behaviour. It responds to an increase in blood glucose, a decrease in ghrelin and CCK (a hormone when food is detected in the duodenum). It also responds to leptin, a long term satiety signal released by fat.

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35
Q

How does the VMH and LH work together to influence eating behaviour?

A

Hunger, leads to eating, which caused an increase in blood glucose, which activates the VMH, which creates a sensation of satiety, so eating stops. After a while there is a decrease in blood glucose, and the LH is activated, which makes us hunger and the cycle continues. P

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36
Q

What did Anad & Brodeck find about the LH and eating behaviour?

A

They found that aphragia (failure to eat when hungry) can be caused by damage to the LH in rats. Rats with these lesions will not eat.

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37
Q

What did Stellar find out about LH and eating behaviour?

A

Stimulation of this area causes eating behaviour in rats.

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38
Q

What did Wickens find out about Neuropeptide Y?

A

When injected into the hypothalamus of rats NPY causes them to immediately begin feeding even when satiated.

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39
Q

What is the PVN?

A

It detects the specific foods our body needs and consequently seems to be responsible for our many ‘craving.

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40
Q

What did Cummings et al (2004) find out about the role of ghrelin in eating behaviour?

A

He monitored PPs ghrelin levels every 5 minutes. PPs had to assess their level of hunger every 30 minutes. 5/6 participants had a significant correlation between ghrelin levels, emptiness of the stomach and hunger.

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41
Q

What does the cognitive aspect of food include?

A

The images, memory, sights and smells of food

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42
Q

Where is it thought the neural control of cognitive factors originates?

A

In the Amygdala and the Inferior frontal cortex.

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43
Q

What does the amygdala do?

A

Primarily used in the selection of foods on the basis of previous experience.

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44
Q

What does the Inferior frontal cortex do?

A

It receives message from the olfactory bulb (smell). Odours influence the taste of foods. Damage to the prefrontal cortex is thought to decrease eating because of diminished sensory responses to food odour and also probably taste. (Kolb and Whishaw)

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45
Q

What is the problem with the neural explanation in terms of it being adaptive?

A

For hunger to be adaptive, it must both anticipate and prevent energy deficit, not just react to them. It should promote levels of consumption that maintain bodily resources well above the optimal level to act as a buffer against future lack of food availability.

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46
Q

What is the limitation to the saying LH has a role in eating behaviour?

A

Damage to the LH also causes deficits in other aspects of behaviour (thirst and sex) not just hunger.

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47
Q

What did Sakuri et al find out about eating behaviour?

A

That it is controlled by neural circuits that run throughout the bran, and not just the hypothalamus.

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48
Q

What did Lutter et al (2008) find out about ghrelin?

A

Shown that the body produces extra quantities of the hormone ghrelin in response to stress. This is part of the bodies natural defence against stress as it reduces the depressive and anxious behaviours. Ghrelin also boosts appetite leading to increased comfort eating.

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49
Q

What are the real world applications of ghrelin research?

A

It suggests that blocking the body’s response to ghrelin may help people with a tendency to comfort eat to control their weight. However, this might reduce ghrelin’s beneficial response to stress.

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50
Q

What are the real world applications of NPY research?

A

Could use drugs to turn off NPY and reduce obesity.

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51
Q

What are the limitations of the Neural approach to eating behaviour?

A
  1. Reductionist, 2. Determinism. 3 Extrapolation of animal research 4. lab experiments may lack ecological validity, 5. physiological drives can be overridden.
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52
Q

What is a preload/taste test?

A

An experimental technique used in the control of eating behaviour where a participant is given a food and then told to ‘taste’ another food to see how much they will eat.

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53
Q

What is disinhibition?

A

Eating more as a result of loosening restraints in response to emotional distress, intoxication or ‘preloading’.

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54
Q

What is restraint?

A

Exerting a cognitive boundary for food intake.

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55
Q

WHo suggested the restraint theory?

A

Herman and Mack

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56
Q

What does the boundary model of the restraint theory say?

A

That our body has a set point which is determined by our biology. We try to maintain this through what we eat. If we go on a diet then we are imposing a cognitive boundary that is below our body weight set point. In restrained eaters the control is undermined by cognitive regulation rather than biological. The gap widens when people change between overating and dieting (Stroebe). Therefore dieters are less sensitive to hunger and satiety cues so the boundary is crossed. Thus the boundary mdoel is a combination of physiological and psychological (cognitive) processes.

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57
Q

What is the boundary model?

A

we have a set biological point which we try to maintain through eating. When we diet we set a cognitive limit which is below our body weight set point. This means that the dieter will try to eat less than is normal and will eat until they reach their self imposed cognitive boundary, whilst trying to ignore their physiological boundary. This causes two boundaries to be working against each other which could cause a diet to fail. Also if a dieter oversteps their cognitive boundary on a day this could lead to disinhibition which means they will eat more and go past their physiological boundary.

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58
Q

What did Herman &Mack (1975) find on restraint and overeating?

A

They gave partipants (dieters and non dieters) a pre-load food, either high or low calorie milshakes. Participants then told they are taking part in a taste preference test. They are left alone to do taste test in own time. The dieters ate more in the taste test if they had the high calorie preload. P

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59
Q

What did Wardle and Beales find on dieting and overeating?

A

They randomly assigned 27 obese women to either a diet group, an exercise group or a control group for 7 weeks. All participants took part in a laboratory procedure to assess their food intake. At week 4 food intake an dappetite were assessed before and after a preload. At week 6 food intake was assessed under stressful conditions. The result indicated the particpants in the diet condition ate more than those in the exercise group and control group.

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60
Q

What does Wardle and Beales study on dieting and overeating support?

A

It supports the idea that simply thinking about restricting food (as associated with the word ‘diet) can cause overeating.

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61
Q

What did Ruderman and Wilson find in regards to restraint theory?

A

They reported that restrained eaters consume significantly more food than the unrestrained eaters, irrespective of the preload. THis suggests that restraint theory is an accurate explanation for the failure of dieting due to disinhibition.

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62
Q

Why has the restraint theory been criticised?

A

The model has been criticised for not specifying the cognitive processes that lead to disinhibition and the ‘what the hell’ effect.

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63
Q

What are the real world applications for restraint theory?

A

Restraint is often recommended as a solution to excessive weight problems. However, if obese people try to diet and fail, this can leave them feeling depressed and like a failure. Therefore overeating could be a consequence of obesity if restraint is recommended as a treatment.

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64
Q

Why does Ogden criticise the restraint theory?

A

He points out that although dieters, bulimics and some anorexics do report episodes of overeating, restraint theory cannot explain the behaviour of a lot of anorexics. If trying not to eat results in overeating, then how do anorexics manage to starve themselves?

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65
Q

What is the theory of ironic processes of mental control?

A

Research in cognitive psychology has shown that attempting to suppress or deny a thought frequently has the opposite effect. Dieting often involves the decision to not eat certain foods or less of them, which results in a state of denial.

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66
Q

What study did Wegner et al (1987) do about the theory of ironic processes of mental control?

A

Asked some participants to NOT think about a white bear and ring the bell when they do. Also asked other participants to think about the bear. THose that were told to not think about the bear rang their bells more often.

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67
Q

What did Wegner admit about the theory of ironic processes of mental control?

A

He admits that the ‘ironic effects’ observed in research are not particularly huge.

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68
Q

What did Soetens et al find out about the theory of ironic processes?

A

PPs were divided into restraints and unrestrained eater and those in the restrained group were subdivided into those with either high or low disinhibition. THe disinhibited restrained group used more suppression than the other groups and also showed a rebound effect afterwards. THis shows that restrained eaters who tend to overeat try to repress thoughts about food more often but then think about it more afterwards.

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69
Q

What does Redden (2008) say about dieting?

A

Suggests that the key to successful dieting is paying attention to what is being eating. He claims that people like experiences less if they repeat them. So we should focus on the specific detail of the meal and reduce boredom.

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70
Q

What study did Redden do on dieting?

A

135 participants. Each given 22 jelly beans one at a time. As jelly beans were dispesned information was flashed into a computer green. Group one had general information (bean number 7), group two had specific information (cherry flaboured bean number 8). Partipants got bored with eating beans faster in group one, whilst group 2 enjoyed the task more.

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71
Q

What are anti-dieting programmes?

A

Replacing dieting with healthy eating programmes. Emphasise regulation of body hunger and satiety signals and prevention of inappropriate attitudes to food.

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72
Q

What sort of environment did our ancestors live in?

A

An environment of evolutionary adaptation

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73
Q

What would the evolutionary explanation be for the preference of meat?

A

Caused by decline in plant foods by receding forests 2 million years ago. Fossil based evidence shows daily diet derived mainly from animal based foods such as animal organs etc. high energy sources and thought to be the catalyst for brain development

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74
Q

What did Abrams show about early humans?

A

Through anthropological evidence he showed that all societies showed preference for animal foods and fats. Early humans would not have been able to survive on plant sources alone

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75
Q

What did Davis study about innate preferences for food?

A

Observed choices of children living in a paediatric unit. Found that young children had an innate, regulatory mechanism and make healthy food choices, but could only do so if healthy food choices were available, so food choice changed over time based on the environment

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76
Q

What did Desor et al show about innate preferences for food?

A

Investigated babies food and preferences based on facial expressions and sucking behaviour. Newborn babies demonstrate innate preference for sweet tasting food, and reject bitter tasting substances

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77
Q

What could be the evolutionary basis for food preferences?

A

Sweet food=fruit=natural fructose content-= energy
Bitter food=poison
Neophobia=fear of new foods (unknown =possibly dangerous)

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78
Q

What did Sandell and Breslin do in innate preferences for food?

A

Screened 35 adults for the hTAS2R38 bitter taste receptor. PPs rated the bitterness of various vegetables, some of which contained glucosinolates (toxic at high doses) and others that did not. Those with the sensitive gene rated the glucosinolate-containing vegetables as 60% more bitter than those with the insensitive form of the gene.

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79
Q

What did Gibson and Wardle do on innate food preferences?

A

Showed that the best way to predict which fruit and veg would be preferred by 4-5 year old was not how sweet they were but how calorie dense, hence the preference for bananas and potatoes. Demonstrates the evolved preference for calorie rich food.

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80
Q

How was bait shyness (taste aversion) discovered?

A

Discovered by farmers who would put poison in rats food, but rats would only eat a small portion and if they became ill they learned to avoid it.

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81
Q

What did Garcia et al find about taste aversion?

A

Rats made ill through radiation shorty after eating saccharin developed an aversion to it and associated their illness with saccharin.

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82
Q

What is the medicine effect?

A

Animals can learn preference for food that make them healthier, with any food eaten just before recovery from illness being preferred in the future

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83
Q

What did Garcia fine about the medicine effect?

A

That when a distinctive flavour is presented to a thiamine deficient rat and then followed by an injection of thiamine the animal would acquire a preference for that flavour

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84
Q

What are the limitations of research for the evolutionary theory?

A

Lab observations- controlled but may lack ecological validity
Food diaries may change eating behaviour
Self-report may inaccurate
Naturalistic observations may have risk of Hawthorne effect
Reductionist and deterministic
Has human evolution stopped or are we still evolving?
Difficult to falsify, so questionable validity

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85
Q

What are the strengths of the evolutionary explanation?

A

Lab experiments are controlled
Questionnaires and food diaries give insight into PPs real life
Can explain innate food preferences
Accounts for both nature and nurture
Focus in ultimate rather than proximate causes could provide more effective intervention strategies

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86
Q

What are the clinical characteristics of anorexia?

A

Weight loss below 85% normal BMI
Anxiety about being overweight
Cessation of menstruated period for 3 months- Amenorrhea
Body image distortion

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87
Q

What could be the cultural influence of anorexia?

A

Western standards of attractiveness are important in the development of AN. In western societies it is generally thought that ‘thinness’ is attractive also portray of thin models in media is thought to be a significant contributory factor especially to those with low self esteem.

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88
Q

What study did Hoek et al do on cultural influences of anorexia?

A

Examined records of 44, 192 people admitted to hospital between 1987-89 in Curaçao, a non-westernised Caribbean where it is acceptable to be overweight. They found six cases, a rate they claim is within the range of anorexia reported in Western counties

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89
Q

What study did Becker et al do on cultural influences of anorexia?

A

Studied eating behaviour among Fijian girls following he introduction of tv in 1995. Found the girls desire to lose weight became more like Western TV characters.

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90
Q

What did Yamamiya et al find on cultural for anorexia?

A

That if instructional intervention is given prior to media exposure this limits the adverse effects

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91
Q

What did Grabe and Hyde find on cultural influences to anorexia?

A

Found a difference between African-Americans and White and Hispanic females. African-Americans reported significantly less body dissatisfaction than other two groups

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92
Q

What did Pollack find about cultural difference?

A

That positive attitudes towards large body sizes in non-western cultures such as Fiji and Caribbean are associated with attractiveness, fertility and nurturance

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93
Q

What did Cachelin and Regan find about cultural differences in anorexia?

A

Found no significant differences in prevalence of disordered eating between African Americans and white participants.

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94
Q

What did Roberts et al find on cultural influences to anorexia?

A

Report that it is only in older adolescents that white populations have a higher incidence of anorexia than black populations

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95
Q

How can peer influence affect eating behaviour?

A

Peer acceptance during adolescence is particularly important. May be susceptible to peers influence in disordered patterns of eating

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96
Q

What did Eisenberg et al find about peer influence and anorexia?

A

In US dieting among friends was significantly related to unhealthy weight control behaviours such as diet pills or purging

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97
Q

What did Jones and Crawford find about peer influence and anorexia?

A

Teasing on overweight girls and overweight boys most likely enforce gender based ideals

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98
Q

What did Shroff and Thompson find on peer influence and anorexia?

A

Found no correlation among friends on measures if disordered eating in an adolescent sample.

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99
Q

What did Lunde et al find on peer influence to eating behaviour?

A

A study of 10 year olds found positive correlation between BMI and teasing for both boys and girls

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100
Q

How does Hilde Bruch explain anorexia? (Psychodynamic)

A

Originates in early childhood. Effective parents respond to child’s needs when hungry vs ineffective parents who fail to correctly respond, so children may grow up confused about their internal needs and become overly reliant on their parents. During adolescence they try to exert control and autonomy but often can’t, so may take excessive control over body shape by developing abnormal eating habits

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101
Q

What is the support for Bruch’s explantation for anorexia?

A
  • observations in parents of adolescents with anorexia define their children physical needs rated than letting the child define their own (Steiner et al)
  • people with AN rely excessively on the opinions of others, worry how others view then as feel lack of control over their lives (Button and Warren)
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102
Q

How could perfectionism in anorexia suggest a genetic vulnerability?

A

Perfectionism appears to run in families

103
Q

What did Strober et al find about perfectionism and anorexia?

A

Retrospectively evaluated personality traits in teenagers receiving treatment for AN. Found high levels of perfection in 73% of girls and 50% of boys

104
Q

What did Nilsson et al find about perfectionism in anorexia?

A

In a longitudinal study showed the importance of perfectionism in the duration of AN. Individuals who had short illness duration had lower levels of perfectionism, and those with high levels were more at risk for long illness duration

105
Q

What did Halmi et al find on perfectionism and anorexia?

A

Studied 322 women with a history of AN across Europe and US. They scored significantly higher on the multidimensional perfectionism scale compared to control group. Extent of perfectionism directly related to severity of AN.

106
Q

What did Butler and Montgomery find about anorexia and impulsiveness?

A

Found that compared to a control group patients with AN responded quickly but inaccurately to a performance task. Although they themselves through self report gave low scores for impulsiveness

107
Q

How can serotonin be linked to anorexia?

A

Increase in serotonin (which suppressed appetite) linked to AN and also anxiety which may trigger AN

108
Q

What did Bailer et al find about serotonin and anorexia?

A

Found high levels of serotonin in AN with binge/purge patients compared to healthy control

109
Q

What did Kaye et al find on serotonin and anorexia?

A

Found SSRIs were effective in preventing relapse of recovering patients but were ineffective in AN patients

110
Q

How is dopamine linked to anorexia?

A

Increase in dopamine levels linked to AN. Dopamine is linked to the interpretation of harm and pleasure those with AN find it difficult to associate good feelings with things usually found pleasurable- food!

111
Q

What did Kaye et al find about dopamine and anorexia?

A

Used PET scans of 10 recovering AN sufferers and 12 healthy people and found an overactivity if dopamine in the basal ganglia of AN sample

112
Q

What did Wang find about dopamine and anorexia?

A

Lower dopamine levels in obese

113
Q

What did Castro-Fornieles et al find about dopamine and anorexia?

A

Adolescents with AN had higher levels if Homovanillic acid (a waste produce of dopamine) than a control group

114
Q

What did Lindberg and Hjem find on anorexia and neurodevlopment?

A

Significant association between premature birth and development of AN

115
Q

How are birth complications linked to anorexia?

A

They can lead to brain damage caused by hypoxia (lack of oxygen) impairing the neurodevlopment of the child

116
Q

What did Favaro et al find on neurodevlopment and anorexia?

A

Found that perinatal (immediately before or after birth) complications significantly associated with the risk of developing AN were placental infarction (obstructed blood supply in the placenta), early eating difficulties and a low birth weight

117
Q

How can the season of birth influence anorexia?

A

More common in spring months; caused by intrauterine infections during pregnant and temperature at time d conception

118
Q

What did Eagles find about anorexia and neurodevlopment?

A

Individuals with anorexia are more likely to be Ben during spring months

119
Q

What did Willoighby et al find about anorexia and neurodevlopment?

A

Found no season effect of AN for season of birth in equatorial regions if the world

120
Q

What did Eagles et al find on anorexia and neurodevlopment?

A

Anorexic individuals tended to be born later in birth order than healthy, the more elder siblings the child had whilst in the womb the more infections they are exposed to and maybe passed onto the unborn child. Critical period for brain development is the second trimester of pregnancy, so for a sprig birth the second trimester would occur at the time of year when infections are more likely

121
Q

What are the two evolutionary theories of anorexia?

A
  1. Reproductive suppression hypothesis

2. ‘Adapted to flee’ hypothesis

122
Q

Who created the reproductive suppression hypothesis?

A

Survey (1987)

123
Q

What is the reproductive suppression hypothesis?

A

Evolution delays the onset of sexual maturation in response to cues in the environment about the probability of poor reproductive success. It enables the female to avoid giving birth at a tike when conditions are not conductive to the survival of her offspring. Anorexia is a ‘disordered variant’ if te adaptive ability- when many feel unable to cope with biological, emotional and social responsibility of womanhood

124
Q

What is the evaluation of reproductive suppression hypothesis?

A

+amenorrhea & onset of puberty delayed
+ based upon the observation of species
- how are the symptoms passed on when it can decrease fertility and kill?

125
Q

Who created the ‘adapted to flee’ hypothesis?

A

Guisinger (2003)

126
Q

What is the adapted to flee hypothesis?

A

Symptoms reflect adaptive mechanisms that caused migration when local famine conditions occurred. Food restriction is a common feature when competition for food, and migration behaviour. Therefor for modern-day individuals, those with a genetic pre-disposition to anorexia, losing too much weight may trigger ancestral mechanisms

127
Q

What is the evidence to support the adapted to flee hypothesis?

A

+treatment implications- Guisinger claims AFHH ‘relieves therapists of the need to search for familial reasons for anorexia.’ Awareness f this causal influence can help treatment and encourage parents to be more compassionate towards their child

128
Q

What are the limitations if the evolutionary approach to anorexia?

A
  • AN decreases fertility so how do genes pass on?
  • reductionist; not search for more complex explanaion
  • deterministic
  • cultural influence; why doesn’t it happen equally in all cultures?
129
Q

What did Doenbusch et al find on social class and eating?

A

Higher class Females had a greater desire to be thin and were more likely to diet than their lower class counterparts

130
Q

What did Kolb and Whishaw find about the inferior frontal cortex and eating behaviour?

A

That damage to the prefrontal cortex is thought to decrease eating behaviour because of diminished sensory responses to food odour and also probably taste

131
Q

What is the restraint theory?

A

Attempting not to eat actually increases the probability of overrating

132
Q

Who developed the boundary model?

A

Herman and Polivy

133
Q

According to the boundary model why are dieters more likely to overeat?

A

Stroebe showed that the gap between the hunger boundary and the satiety boundary widens wen people change between overrating and dieting. Therefore dieters are less sensitive to hunger and satiety cues, so the boundary is crossed

134
Q

What did Macintyre et al find about media effects?

A

Found that the media have a major impact both on what people eat and also their attitudes to certain foods. Also stated that many eating behaviours are limited by personal circumstances such as age, income and family circumstances. Thus people learn from the media but must place this information within the broader context of their own lives.

135
Q

What explanation did Garg et al suggest for his findings in his study on attitudes to food and eating behaviours?

A

Claimed that people who feel sad/depressed want to ‘jolt themselves out of the dumps’, therefore they are more likely to go for a snack that tastes good to give them a sudden rush of euphoria. Happy people want to extend their upbeat mood and so choose healthy foods.

136
Q

What does research suggest about ethnicity and attitudes to food and eating behaviour?

A

Suggests that body dissatisfaction and related eating concerns and disorders are more characteristic of white women than black or asian women.

137
Q

What did Ball and Kenardy find about ethnicity and eating?

A

Studied over 14,000 women between 18-23 in Australia. Results showed that for all ethnic groups, the longer the time spent in Australia, the more the women reported attitudes and eating behaviours similar to women born in Australia (known as the Acculturation effect)

138
Q

What does research suggest about attitudes to food and eating behaviour?

A

Found that body dissatisfaction, dieting behaviour, and eating disorders are more common in higher-class individuals.

139
Q

What did Goode et al find about attitudes to food and eating behaviour?

A

Used data from 2003 Scottish Health Survey and established that, in general, income was positively associated with healthy eating.

140
Q

What did Rozin et al claim about cultural differences with attitudes to food and eating behaviour?

A

Claimed that food functions differently in the minds and lives of people from different cultures.

141
Q

What did Rozin et al find about cultural differences and attitudes to food and eating behaviour?

A

Adults and college students from Belgium, France, USA, and Japan completed a survey dealing with food-related issues, including beliefs about the diet-health link, consumption of ‘healthy’ food, and satisfaction with the healthiness of their own diets. In all areas except beliefs about the importance of diet for health, they found substantial cultural (and usually gender) differences. In all four contries, females, more than males, showed a pattern of attitudes that was more like the American and less like the French (i.e. food associated with health rather than pleasure). Argued it may partially account for national differences in rates of cardiovascular disease.

142
Q

What did Meyer and Gast find about attitudes to food and eating behaviour?

A

They surveyed 10-12 year old girls and boys and found a significant positive correlation between peer influence and disordered eating. The ‘likeability’ of peers was considered the most important factor in this relationship.

143
Q

What did Birch and Fisher find about attitudes to food and eating behaviour?

A

Found that the best predictors of the daughters’ eating behaviour were the mothers’ dietary restraint and their perception of the risks of the daughters becoming overweight.

144
Q

What did Siever find about attitudes to food and eating behaviour?

A

that in men, homosexuality is a risk factor in the developement of disordered eating attitudes and behaviour, including body dissatisfaction and higher levels of dieting. Suggests studies concentrating only on women offer a limited view.

145
Q

What are the three basic forms of dieting?

A
  1. Restricting the total amount of food eaten
    2 Refraining from eating certain types of food
  2. Avoiding eating for long periods of time
146
Q

Who developed the restraint theory?

A

Herman and Mack

147
Q

What does the restraint theory suggest?

A

Herman and Mack suggest that attempting not to eat actually increases the probability of overeating.

148
Q

Who developed the boundary model?

A

Herman and Polivy

149
Q

What does the boundary model state?

A

That hunger keeps intake of food above a certain minimum, and satiety works to keep intake below some maximum. Between these two levels, psychological factors have the greatest impact on consumption. Dieters tend to have a larger range between hunger and satiety levels as it takes them longer to feel hungry and more food to satisfy them. Restrained eaters also have a self-imposed desired intake. once they have gone over this boundary they continue to eat until they reach satiety, i.e. beyond the maximum level imposed as part of their diet.

150
Q

How does the role of denial effect the success and failure of dieting?

A

Research in cognitive psychology has shown that attempting to suppress or deny a thought frequently has the opposite effect, making it even more prominent.

151
Q

What does the theory of ironic processes of mental control suggest?

A

Attempts to suppress thoughts of food only serve to increase the dieters’ preoccupation with the very foods they are trying to deny themselves. As soon as a food is denied, therefore, it simultaneously becomes more attractive.

152
Q

How does Lipoprotein lipase affect the success or failure of dieting?

A

Lipoprotein lipase (LPL) is an enzyme produced by fat cells to help store calories as fat. If too much LPL is produced, the body will be especially efficient at storing calories. LPL also makes it easier to regain lost weight- suggests that success/failure of dieting may be determined by genetic mechanisms as well.

153
Q

What did Kern et al find about the success and failure of dieting?

A

Nine people who lost an average of 90lbs had their lipoprotein lipase (LPL) levels measured before dieting and again three months later. Levels of LPL rose after weight loss, and the fatter the person was to start with, the higher the LPL levels were, as though the body was fighting to regain the weight. Believed that weight loss activated the gene producing the enzyme, which may explain why it is easier for a dieter to regain lost weight than for someone who has never been obese to put weight on.

154
Q

What does Ogden suggest about obesity treatment?

A

Argues that although obesity may not necessarily be caused by overeating, overeating may be a consequence of obesity if restraint is recommended as a treatment.

155
Q

What are anti-dieting programmes?

A

Emphasize regulation by body hunger and satiety signals and the prevention of inappropriate attitudes to food (e.g. comfort eating or food avoidance)

156
Q

What did Higgins and Gray find about anti-dieting programmes?

A

Did a meta analysis of the effectiveness of anti-dieting programmes and found that participation in these programmes was associated with improvements in both eating behaviour and psychological wellbeing and with weight stability rather than weight change.

157
Q

What did Green find about dieting?

A

Studied 55 women between 18-40, some on weight loss diets, some not. The two groups were given a task involving recognising and responding to sequences of numbers. Compared to the non-dieting women, those on the very low-calorie diets processed this information more slowly and took longer to react. Green suggests that preoccupation with body shape, food restriction, and the dieting experience typical of someone on a ‘crash diet’ may in some way overload the dieter’s metal capacity.

158
Q

Why is research into the success and failure of dieting culturally bias?

A

Because some cultural groups find it harder to diet successfully because of a nautral inclination to obesity.

159
Q

What did Park et al find about obesity research?

A

That Asian adults are more prone to obesity than Europeans.

160
Q

What did Misra et al find about obesity research?

A

That Asian children and adolescents have a greater central fat mass when compared with Europeans and other ethnic groups.

161
Q

How does glucose work in eating behaviour?

A

Hunger increases as glucose levels decrease

162
Q

How do the Lateral hypothalamus and vetromedial hypothalamus work in eating behaviour?

A

A decline in glucose levels in the bood activate a part of the brain called the lateral hypothalamus, resulting in feelings of hunger. This causes the individual to search for and consume food, which causes glucose levels to rise again. This rise in glucose levels activates the ventromedial hypothalamus, which leads to feelings of satiation, which in turn inhibits furhter feeding.

163
Q

What did Wickins find about neural mechanisms in eating behaviour?

A

When neuropeptide Y (NPY) is injected into the hypothalamus of rats, NPY causes them to immediately begin feeding, even when satiated.

164
Q

What did Stanley et al find about neural mechanisms in eating behaviour?

A

Repeated injections of NPY into the hypothalamus of rats produces obesity in just a few days.

165
Q

What is neuropeptide Y (NPY)?

A

A neuortransmiter found in the hypothalamus, which is particularly important in turning on eating.

166
Q

What are ob/ob mice?

A

Some mice receive two copies of the gene for obesity (abbreviated ob). These mice have a tendency to overeat, especially foods high in fat or sugar.

167
Q

What role does leptin play in eating behaviour?

A

Leptin is normally produced by fat tissue and secreted into the bloodstream where it travels to the brain and other tissues, causing fat loss and decreased appetite.

168
Q

What did Zhang et al find about neural mechanisms in eating behaviour?

A

Discovered that ob/ob mice have defective genes for the protein leptin, which causes fat loss and decreased appetite. In ob/ob mice, this process does not happen. Injecting ob/ob mice with leptin causes them to lose weight dramatically.

169
Q

What role could the paraventricular nucleas (PVN) play in eating behaviour?

A

Researchers have discovered that damage to the ventromedial hypothalamus (VMH) causes hyperphagia, but damage to the nerve fibres passing through the VMH tends to also damage another area of the hypothalamus. It is now believed that damage to the PVN alone causes hyperphagia.

170
Q

What does the paraventricular nucleus (PVN) do?

A

It detects the specific foods out body needs and consequently seems to be responsible for many of our ‘cravings’.

171
Q

Where does the neural control of cognitive factors of hunger originate?

A

Probably in two main brain areas, the amygdala and the inferior prefrontal cortex.

172
Q

What is the role of the amygdala thought to be?

A

To be primarily in the selection of foods on the basis of previous experience.

173
Q

What did Rolls and Rolls find about neural mechanisms in eating behaviour?

A

Found that surgically removing the amygdala in rats would cause the animals to consume both familiar and novel foods indiscriminately, whereas amygdala-intact rats would initially avoid novel foods and consume only the more palatable familiar foods instead.

174
Q

What did Kolb and Whishaw find about neural mechanisms in eating behaviour?

A

Because odours influence the taste of foods, damage to the inferior prefrontal cortex is thought to decrease eating because of diminished sensory responses to food odour, and also probably taste.

175
Q

What does the inferior frontal cortex do?

A

Receives messages from the olfactory bulb (part of the brain responsible for smell).

176
Q

What is the problem with the view of the lateral hypothalamus as the ‘on switch’ for eating?

A

Damage to the LH caused deficits in other aspects of behaviour (e.g. thirst and sex) rather than just hunger. Also, more recent research has shown that eating behaviour is controlled by neural circuits that run throughout the rbain, and not just by the hypothalamus.

177
Q

What did Marie et al find about neural mechanisms in eating behaviour?

A

Genetically manipulated mice so that they did not make NPY. They found no subseuqnet decrease in their feeding behaviour. The researchers suggest that the hunger stimulated by injects of NPY may actually be an experimental artfact, in that the flood of NPY during experimental manpulations could cause behaviour not like that caused by normal amounts of the neuotransmitter.

178
Q

What did Yang et al find about neural mechanisms in eating behaviour?

A

Showed that NPY is also prodcued by abdominal fat. The researchers suggest that this leads to a vicious cycle where NPY produced in the brain leads to more eating and the production of more fat cells, which in turn produce more NPY and more fat cells and so on. By targeting indiviudals at risk of icnreased levels of NPY, they believe it should be possible to treat them with drugs that turn off NPY and thus prevent obesity.

179
Q

What role does ghrelin play in eating behavhiour?

A

THe hormone ghrelin plays a role in the bodies response to stress but also boosts appetite, leading to increased comfort-eating.

180
Q

What did Gold find about neural mechanisms in eating behaviour?

A

Found that lesions restricted to the VMH alone did not result in hyperphagia and only produced overeating when they included other areas, such as the paraventricular nucleus (PVN).

181
Q

What is the problem with Gold’s findings about neural mechanisms in eating behaviour?

A

Subsequent research has failed to replicate Gold’s findings, with most studies showing that compared to lesions in other brain areas such as the PVN, animals with VMH lesions ate substantially more and gained substantially more weight.

182
Q

What is Kluver-Bucy syndrome?

A

Patients with this syndrome typically show increased appetite, indiscriminate eating, and even attempts to eat non-food items.

183
Q

How could the neural control of cognitive factors explain Kluver-Bucy syndrome?

A

Damage to the amygdala and inferior prefrontal cortex could explain the feeding abnormalities observed in Kulver-Bucy syndrome. Research ont he effects of damage to these brain areas suggests that food cues no longer accurately represent the real reward value to the individual.

184
Q

What did Zald and Pardo find about neural mechanisms in eating behaviour?

A

Provided physiological evidence to support the claim that amygdala partipates in the emotional processing of olfactory stimuli. They exposed healthy adult participants to aversive olfactory (smell) stimuli whilst measuring blood flow to the amygdala by means of a PET scan. Exposure to unpleasant odours produced significant blood flow increases to the amygdala whereas non-aversive odours did not cause increased blood flow. Increased blood flow tot he amygdala was also associated with subjective ratings of the perceived unpleasantness of the stimuli.

185
Q

Why would preferences for fatty foods been adaptive?

A

Because conditions in the environment of evolutionary adaption meant that energy resources were vital in order to stay alive and also to find the next meal.

186
Q

When did human ancestors begin to include meat in their diets?

A

To compensate for a decline in the quality of plant foods caused by receding forests two million years ago.

187
Q

What did Milton argue about the preference for meat?

A

Claimed that without animals it is unlikely that early humans could have secured enough nutrition from a vegetarian diet to evolve into the active and intelligent creatures t hey became. It supplied essential amino acids, minerals and nutrients required, supplemented with plant based food.

188
Q

What did Garcia et al find about taste aversion?

A

Rats who had been made ill through radiation shortly after eating saccharin, developed an aversion to it and very quickly associated their illness with the saccharin.

189
Q

What is the medicine effect?

A

Learning a prefermnce for food that makes them healthier, with any food eaten just before recovery from illness being preferred int he future.

190
Q

What did Garcia et al find about the medicine effect?

A

Found that when a distinctive flavour is presented to a thiamine-deficient rat and then followed by an injection of thiamine, the animal will acquire a preference for that flavour.

191
Q

What is neophobia?

A

The adaptive avoidance of novel foods.

192
Q

What did Bernstien and Webster find about real world applications of taste aversion?

A

Gave patients a novel-tasting ice cream prior to thir chemotherapy and the patients acquired an aversion to that ice cream. These findings hve resulted in the development of the ‘scapegoat technique’ which involves giving cancer patients a novel food along with some familiar food just prior to their chemotherapy. The patient forms an aversion to the novel food and not to the familiar, usual food.

193
Q

What is a common way of testing evolutionary hypothesis?

A

Through comparison with a different species.

194
Q

What did Gibson and Wardle find about evolutionary explanations for food preferences?

A

They showed that the best way to predict which fruit and vegetables would be prefrred by 4-5 year old was about how dense they were in calories. Bananas and potatoes are particularly calorie-rich, and were more likely to be chosen by the children, demonstrating an evolved preference for calorie-rich food.

195
Q

What did Cordain et al argue about early humans?

A

That early humans consumed most of their calories from sources other than saturated animal fats. They were vegetarian.

196
Q

Why is it unlikely that early humans could have been vegetarian

A

Anthropological evidence (e.g. Abrams) shows that all societies display a preference for animal foods and fats. Nor would it have been possible for early humans to be completely vegetarian because they would not hae been able to get sufficient calories from the plants and grains available.

197
Q

What is a major problem with evolutionary explanations of food preferences?

A

Many things that were important to our ancestors (such as saturated animal fats) are harmful in modern environemnts, so we are more likely to avoid them in order to survive and lead a healthy life. Also, vast majority of specific foo likes and dislikes appear not to be predetermined. Innate responses cannot account for the broad range of food likes and dislikes that develop beyond infancy

198
Q

How did Seligman explain taste aversion in humans?

A

Claimed that different species evolved different learning avilities, something he called biological preparedness. THis natural selection of differential learning has occured so that each species has the ability to learn certain associations more easily than others, particularly those associations that help individuals survive.

199
Q

What is believed to be the evolutionary explanation for bitter taste?

A

Scientists have long assumed that bitter taste evolved as a defense mechanism to detect potentially harmful toxins in plants.

200
Q

What did Sandell and Breslin find about taste aversion?

A

Screened 35 adults for the hTAS2R38 bitter taste receptor gene. Participants rated the bitterness of various vegetables, some of which contained glucoinolates and others that did not. Glucosinolates are well known for their toxic effects at high doses. Those with the sensitive form of the gene rated the glucosinolate-containing vegetables as 60% more bitter than those with the insensitive form of the gene. The ability to detect and avoid naturally-occuring glucosinolates would confer a selective advantage on our ancestors, which would explain why such genes are widespread today.

201
Q

What did Standford find about evolutionary explanations of food preferences?

A

that after coming close to starvation for much of the year, when chimpanzees manage a kill (usually a colobus monkey) they go straight for the fattiest parts (e.g. the brain and bone marrow) rather than the tender, more nutritious flesh.

202
Q

What are the clinical characteristics of anorexia nervosa?

A
  1. Anxiety: excessive fear of being fat
  2. Weight: Dropping below 85% of the individuals normal BMI
  3. Body image distortion
  4. Amenorrhea: Cessation of menstrual periods for three months.
203
Q

What are the psychological explanations for anorexia nervosa?

A
  1. Cultural ideals
  2. Media influence
  3. Ethnicity
  4. Peer influences
  5. Personality
204
Q

What did Jones and Buckingham find about media influence?

A

The media does not influence everyone in the same way, for example, individuals with low self-esteem are more likely to compare themselves to idealised images portrayed in the media.

205
Q

How is ethnicity thought to influence anorexia nervosa?

A

ther cultural groups do not place the same value on thinness as an ideal for women> The incidence of AN in non-western culturals and in black populations in Western cultures is much lower than within a white western population.

206
Q

What did Grabe and Hyde find about ethnicity and anorexia nervosa?

A

In a meta-analysis of 98 studies, found a difference between African-Americans, Causcasions and Hispanic females. African-Americans reported significantly less body dissatisfaction than the other two groups.

207
Q

What did Pollack find about ethnicity and anorexia nervosa?

A

In many non-Western cultures (e.g. Fiji and the Caribben) there are more positive attitudes toward large body sizes, which are associated with attractiveness, fertility and nurturance.

208
Q

What did Eisenberg et al find about peer influence and anorexia Nervosa?

A

A US Study, found that dieting among friends was significantly related to unhealthy weight control behaviours, such as the use of diet pills or purging.

209
Q

What did Jones and Crawford find about peer influence and anorexia Nervosa?

A

Found that overweight girls and underweight boys were most likely to be teased by their peers, suggesting that through teasing, peers serve to enforce gender-based ideals.

210
Q

What did Hilde Bruch claim was the origin of anorexia nervosa?

A

Claimed that it is in early childhood. She distinguished between effective parents who respond appropriately to their child’s needs (e.g. feeding them when hungry) and ineffective parents who fail to respond to their child’s internal needs. If a child cries because they are anxious, an ineffective parent may feed them, or may comfort them when actually they are hungry. Children of ineffective parents may grow up confused about their internal needs, becoming overly reliant on their parents. Adolescence increases a desire to establish autonomy, but adolescents are often unable to do so, feeling that they do not own their own bodies. To overcome their sense of helplessness, they can take excessive control over their body shape and size by developing abnormal eating habits.

211
Q

What personality traits are thought to increase the risk of anorexia nervosa?

A

Perfectionism and impulsiveness.

212
Q

What did Strober et al find about personality and anorexia Nervosa?

A

Retrospectively evaluated personality traits in teenage boys and girls receiving treatment for AN. They found high levels of perfection in 73% of the girls and 50% of the boys.

213
Q

What did Butler and Montgomery find about personality and anorexia nervosa?

A

Found that compared to a control group, patients with AN responded rapidly (but inaccurately) to a performance task, indicating behaviour impulsiveness, despite their low self-reported impulsiveness.

214
Q

What did Hoek et al find about anorexia nervosa and cultural ideals?

A

Examined the records of 44,192 people admitted to hospital between 1987-1989 in Curacao, a non-westernised Carribean island where it is acceptable to be overweight> They found six cases, a rate that they claim is within the range of rates of AN reported in Western countries.

215
Q

What did Becker et al find about media influences and Anorexia nervosa?

A

Studied eating attitudes and behaviours among adolescent Fijian girls following the introduction of tv in 1995. The girls stated a desire to lose weight to become more like Western TV characters.

216
Q

What did Yamamiya et al find about media influences and anorexia nervosa?

A

Showed that instructional intervention prior to media exposure to idealized female images prevents the adverse effects of exposure

217
Q

What did Cachelin and Regan find about ethnicity and anorexia nervosa?

A

Found no significant differences in prevalence of disordered eating between African-American and White caucasian participants.

218
Q

What did Roberts et al find about ethnicity and anorexia nervosa?

A

Found that the stereotypical view that white populations have a higher incidence of AN than black populations appears to be true only in older adolescents.

219
Q

What did Shroff and Thompson find about peer influence and anorexia nervosa?

A

Found no correlation among friends on measures of disordered eating in an adolescent sample.

220
Q

What did Lunde et al find about peer influence and anorexia nervosa?

A

A study of 10 year olds found a positive correlation between BMI and teasing for both boys and girls.

221
Q

What did Steiner et al find about anorexia nervosa?

A

Observed that parents of adolescents with AN have a tendency to define their children’s physical needs rather than allowing their childrent o define their own (supports Bruch’s theory)

222
Q

What did Button and Warren find about anorexia nervosa?

A

Supports Bruch’s claim that people with AN rely excessively on the opinions of others, worry about how others view them and feel a lack of control over their lives.

223
Q

What did Nilsson et al find about personality and anorexia nervosa?

A

A longitudinal study which showed the important of perfectionism in the duration of AN. INdividualswho had short illness duration had lower levels of perfectionism, and those with high levels were more at risk for long illness duration.

224
Q

What ist he difficulty with studying personality factors related to anorexia nervosa?

A

methodological problems with the need to seperate out lasting personality traits from short-lived states that may be caused by starvation.

225
Q

What did Halmi et al find about personality and anorexia nervosa?

A

Investigated the relationship between perfectinoism and anorexia nervosa in 322 women with a history of AN across Europe and the US.Those individuals who had a history of AN scored significantly higher on the multidimensional perfectionism scale when compared to a comparison group of healthy women. in addition the extent of perfectionism was directly related to the severty of AN experienced. Researches icluded pateitns with relatives who also suffered from AN, and found that perfectionism appears to run in families and therefore represents a genetic vulnerability for AN.

226
Q

What are the neural explanations for anorexia nervosa?

A

Neurotranmitters: Serotonin and Dopamine
Neurodevelopment: Pregnancy and birth complications and season of birth

227
Q

What are the evolutionary explanation for anorexia nervosa?

A

The reproductive suppression hypothesis

The ‘Adapted to flee’ hypothesis

228
Q

What did Bailer et al find about neural explanations for Anorexia Nervosa?

A

Compared serotonin activity in women recovering from restricting-type anorexia (restricted food intake) and binge-eating/purging type (periods of restrictie eating and binge-eating/purging with healthy controls. They found significantly higher serotonin activity in the women recovering from the binge-eating/purging tpe. In addition they found the highest levels of serotonin activity in women who showed the most anxiety, suggesting that persistent disruption of serotonin levels may lead to increased anxiety, which may trigger AN.

229
Q

What did Kaye et al find about neural explanations for anorexia nervosa?

A

Used a PET scan to compare dopamine activity in the brains of 10 women recovering from AN and 12 healthy women. In the AN women they found overactivity in dopamine receptors in a part f the brain known as the basal ganglia, where dopamine plays a part in the interpretation of harm and pleasure. Increased dopamine activity in this area appears to alter the ways people interpret rewards. Individuals with AN find it difficult to associate good feelings with the things that most people find pleasurable (such as food)

230
Q

How may pregnancy and birth complications explain anorexia nervosa?

A

Birth complications may lead to brain damage caused by hypnoxia (Lack of oxygen) imparing the neurodevelopment of the child> Nutritional factors may be implicated if mothers have an eating disorder.

231
Q

What did Lingberg and Hjern find about neural explanations for anorexia nervosa?

A

Found a significant association between premature and development of AN.

232
Q

What did Bulik et al suggest about neural explanations for anorexia nervosa?

A

Suggest that mothers with AN expose their offspring to a ‘doube disadvantage’-transmission of genetic vulnerability to AN, and inadequate nutrition during pregnancy.

233
Q

What did Eagles et al find about neural explanations for anorexia nervosa?

A

That individuals with AN are more likely to have been born during the spring months.

234
Q

How is season of birth thought to influence anorexia nervosa?

A

Explanations include intrauterine infections during pregnancy and temperature at time of conception

235
Q

What did Willoughby et al find about neural explanations for anorexia nervosa?

A

Found that among patients with AN in equatorial regions fot he world (where it is constantly hot) there was no seasonality effect in the development of AN.

236
Q

Who developed the reproductive suppression hypothesis?

A

Surbey

237
Q

How does the reproductive suppression hypothesis explain anorexia nervosa?

A

Survey suggests that adolescent girls’ desire to control their weight represents and evolutionary adaption in which ancestral girls delayed the onset of sexual maturation in response to cues about the probability or poor reproductive success. SUrbey argues that AN is a ‘disordered variant’ of the adaptive ability of females to alter the timing of reproduction at at ime when they feel unable to cope with the biolgoical, emotional and social responsibilities of womanhood.

238
Q

Why would the ability to delay reproduction be adaptive according to the reproductive suppression hypothesis?

A

It is adaptive because it enables a female to avoid giving birth at a time when conditions are not conducive to her offspring’s sruvival

239
Q

What is the reproductive suppression hypothesis based on?

A

On the observation that in a number of species pubery is delayed or reproduction suppressed in females when they are subjected to stress or are in poor physical condition.

240
Q

WHo developed the ‘adapted to flee’ hypothesis (AFFH)?

A

Guisiger

241
Q

How does the ‘adapted to flee’ hypothesis explain anorexia nervosa?

A

Proposes that the typical AN symptoms of food restriction, hyperactivity and denial of starvation, reflect the operation of adaptive mechanism that once caused migration in response to local famine conditions. Normally, when a person begins to lose weight, physiological mechanisms conserve energy and increase desire for food. However, among nomadic forages, when extreme weight loss was due to a severe depletion of local food resources, this adaption must be turned off so that individuals can increase their chances of survival by migrating to a more favorable environment. Thus, for modern day individuals, among those who are genetically vulnerable to AN, losing too much weight may trigger these ancestral mechanisms.

242
Q

How does the adapted to flee hypothesis explain the hyperactivity typically found in anorexics?

A

Argues that this ‘hyperactivity’ may be a form of ‘migratory restlessness’ as many species increase activity in times of food shortage and prior to migration.

243
Q

How is the ‘adapted to flee’ hypothesis adaptive?

A

In the EEA those starving forages who deceved themselves about their physical condition would have been more confident about moving on to a more fabourable (in terms of food avalability) environemnt, and so would have been more likely to survive. Also, food restriction is a common feature of many species when feeding competes with other activities, such as migration or breeding.

244
Q

What is the significant real world application for biological explanations for anorexia nervosa?

A

Cretes a case for insurance companies to consider AN in the same way as other psychiatric conditions that are considered to be biological base, and offer a range of treatment possibilities.

245
Q

WHat is the problem with linking serotonin to anorexia?

A

That SSRIs, which alter levels of available brain serotonin, are ineffective when used with AN patients. However, malnutrition related changes in serotonin function may negate the action of SSRIs, which only become effective when weight returns to a more normal level.

246
Q

What did Kaye et al find about neural explanations for anorexia nervosa?

A

Found that when SSRIs are used with recovering AN patients, these drugs were effective in preventing relapse.

247
Q

What did Castro-Fornieles et al find about neural explanations for anorexia nervosa?

A

Found that adolescent girls with AN had higher levels of homovanillic acid (a waste product of dopamine) than a control group. Improvement in weight levels was associated with normalisation of homovanilic levels.

248
Q

What did Wang et al find about neural explanations for anorexia?

A

Showed that lower than normal levels of dopamine receptors in the brains of obese individuals.

249
Q

What is levels of dopamine thought to be linked to with anorexia?

A

Levels of dopamine appear to be inversely related to body weight, although whether this is a cause of a consequence is not yet clear.

250
Q

What did Bulik et al suggest about anorexia nervosa?

A

Suggests that if we could use an individual’s genetic profile to indicate level of risk, it would be possible to develop specially tailored prevention programmes for those most susceptible to developing AN.

251
Q

What did Favaro et al find about neural explanations for anorexia nervosa?

A

Found that perinatal (i.e. immediately before or after birth) complications significantly associated with risk of developing AN were placental infarction (obstructed blood supply in the placenta), early eating difficulties, and a low birth weight.

252
Q

What are the problems associated with evolutionary explanations for anorexia nervosa?

A

How can the symptoms of AN be passed on by natural selection, as they decrease fertility and can be fatal? AN would have functioned more effectively in ancestral conditions, yet outside the ecological setting in which it evolved disoders such as AN can be deadly.

253
Q

What is the problem with studies of eating disorders concentrating on women?

A

Recent statitions suggest that 25% of adults with eating disorders are men. Thus, eating disorders such as AN are not exclusively a female problem.