EATING BEHAVIOUR optional 3

Question 1

why have a preference for sweet food?

Answer 1

In evolutionary terms a preference for sweetness would be adaptive for two reasons.

Firstly sweet things contain a large number of calories and are a reliable source of energy, so a sweet taste would act as a readily-detectable signal of nutrients that would provide an easily accessible source of energy.

Secondly sweet things are rarely poisonous, so a sweet taste would signal safety.

Question 2

why have a preference for fatty foods?

Answer 2

Fatty foods
Foods that are high in fat are energy-dense, containing a high number of calories and releasing a lot of energy
Meat is high in fat and calories, allowing humans to survive for the long time there may be between one animal kill and another
Once fire was discovered, meat could be cooked or smoked to preserve it, make it easier to eat and destroy any harmful bacteria

Question 3

why have a preference for salty foods?

Answer 3

Salty foods
Salt is important for conducting nerve impulses, contracting and relaxing muscles, and maintaining the proper balance of water and minerals
The concentration of salt in the blood must remain at a specific level and regularly needs topping up, as small amounts of salt are lost through sweat and the action of the kidneys

Question 4

what is food neophobia

Answer 4

Neophobia is an innate tendency to avoid new or unfamiliar foods

Question 5

when does neophobia usually occur

(Birch, 1998)

Answer 5

Neophobia is found in babies as they move on from milk to solid food and this is when the evolutionary preference for sweet and salty foods can become obvious, as they will usually prefer these (Birch, 1998)

Question 6

How does neophobia get reduced in babies

Answer 6

the neophobic reaction to new food will reduce with repeated exposure to the food and once a child gets used to the taste (Birch, 1998)

Question 7

how does taste aversion occur?

Answer 7

Taste aversion occurs when an individual becomes ill after eating a certain food, resulting in them avoiding that food in the future because they associate it with being ill

Question 8

what is taste aversion, as explained by environmental psychologists

Answer 8

Environmental psychologists explain taste aversion as biological preparedness, which entails being biologically predisposed through evolution to learn through experience to avoid foodstuffs that make us ill, as this has an adaptive survival value

Question 9

Research which investigates explanations for food preferences

taste aversion

Bernstein & Webster (1980)

Answer 9

Bernstein & Webster (1980) investigated taste aversion in humans and found that adults given ice cream before receiving chemotherapy developed a taste aversion to eating ice cream as they had a biological preparedness to associate their nausea with the food they had eaten rather than the chemotherapy that had actually caused the nausea

these findings have 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.

Question 10

Research which investigates evolutionary explanations for food preferences

Steiner (1987)

Answer 10

Steiner (1987) showed that newborn babies’ facial expressions indicate pleasure over a sweet taste and disgust for a bitter taste, suggesting that this preference is innate rather than learned

Question 11

Research which investigates evolutionary explanations for food preferences

Knaapila et al (2007)

Answer 11

Knaapila et al (2007) conducted a twin study and found that, using a standardised questionnaire to measure neophobia, the heritability of this behaviour was 67 per cent, supporting the evolutionary explanation that neophobia evolved from early humans because it protected them from eating harmful foods

Question 12

Strengths of evolutionary explanations for food preferences

(Bell, 1973)

Answer 12

The fact that there are only two taste receptors for sweet tastes but 27 for bitter tastes suggests an evolutionarily determined need to avoid bitter-tasting toxic foods
The idea of an evolutionarily determined preference for sweet tastes is supported by cross-cultural evidence using research on the Inuit people, who, although they had never tasted sweet food before, accepted it immediately (Bell, 1973)

Question 12

Weaknesses of evolutionary explanations for food preference

Answer 12

There are individual differences in taste experience, with some people more/less sensitive to bitterness and also taste for salty and sweet foods can be highly personal, which does not support the evolutionary explanation
Evolutionary explanations for food preferences, neophobia and taste aversion cannot explain cultural differences in food preferences and avoidance

Question 12

how does evolutionary explanations for eating behaviour link to issues and debates

Answer 12

Evolutionary explanations for food preferences are an example of biological determinism. They are also an example of hard determinism, as none of the explanations for preferences, neophobia or taste aversion allow any room for free will.

The evolutionary explanations are an example of biological reductionism, as they reduce the complexity of eating behaviour to an evolutionary adaptation, without considering the meaning of food in different societies and cultures, in a more holistic approach.

Question 12

what is the dual-centre model

Answer 12

In a dual-centre model (also known as dual-control theory) the lateral hypothalamus (LH) was identified as the ‘hunger centre’, initiating eating behaviour, and the ventromedial hypothalamus (VMH), as the ‘satiety centre’, producing a feeling of being full that means a person stops eating

Question 13

Outline the role of the dual-centre model

Answer 13

When the level of glucose (blood sugar) is low, the liver sends signals to the LH, creating a sensation of hunger that motivates an individual to eat
After eating, the blood sugar level rises as glucose is released, activating the VMH, producing a sensation of satiety, which stops further eating
Therefore both the LH and the VMH work together in the dual-centre model to balance hunger and eating

Question 14

What is Ghrelin

Answer 14

Ghrelin is a hormone secreted from the lining of the stomach, whose concentration in the blood falls after each meal and rises progressively until the next meal

Thus the amount of ghrelin in the bloodstream is a marker of how long since the individual last ate and as it rises, so appetite increases

Question 15

How does Ghrelin increase appetite?

Answer 15

Ghrelin is a hormone secreted by the stomach and stimulates the hypothalamus to increase appetite. If a person is undereating their ghrelin levels increase.

It is a hormonal marker of how long since we have last eaten because the amount produced is closely related to how empty your stomach is. The amount of ghrelin in the bloodstream doubles just before a meal, and decreases very quickly after a meal

Question 16

what is leptin?

Answer 16

Leptin is a hormone produced from fat cells and released into the blood to signal to the hypothalamus that calorie storage is high (in the form of fat deposits)

Question 17

Outline how leptin decreases appetite, and therefore inhibits ghrelin.

Answer 17

Leptin is a hormone that is released into the bloodstream from fat cells which acts as a signal to the hypothalamus to stop eating.

Our fat stores are the main indicators of body weight. Fat cells release leptin into the bloodstream, via which it travels to the hypothalamus. The amount of leptin that is released is proportional to the fat content of the cells.

The ventromedial hypothalamus has receptors for leptin, and so it stops food intake as levels of leptin rise. In this way feeding behaviour, the amount of stored fat and body weight are regulated over the long term

Question 18

Research which investigates ​​the role of neural and hormonal mechanisms in eating behaviour

Nakazato et al (2001)

Answer 18

ghrelin injections stimulated feeding and increased weight gain in normal rats and rats genetically deficient in growth hormone, demonstrating the important role of ghrelin in promoting eating and releasing growth hormone

Question 20

Research which investigates ​​the role of neural and hormonal mechanisms in eating behaviour

Licinio et al (2004)

Answer 20

conducted research into a rare genetic condition in severely obese people who were unable to produce leptin naturally, but who, after a four-month period of leptin-replacement therapy, experienced weight loss of more than 40% and a reduction in food intake of almost half

Question 21

role of neural and hormonal mechanisms in eating behaviour

Strengths

Answer 21

Understanding the neural and hormonal mechanisms controlling eating behaviour has real-word application in offering treatment possibilities for obesity, as we better understand the complex interactions between the nervous system and the hormones regulating eating
Research using injections of ghrelin has shown that it stimulates appetite and research using leptin-replacement therapy shows that leptin suppresses appetite, supporting the theory of the role of these hormones in eating behaviour

Question 22

role of neural and hormonal mechanisms in eating behaviour

Weaknesses

Answer 22

other factors such as biological rhythms also affect eating behaviour, shown by the fact that rats become most active and start to eat after dark, regardless of when they last ate (Kraly et al, 1980)

Leptin injections have not been a universally effective treatment for obesity, so this means that research needs to investigate leptin further and identify if it is really useful for weight loss or might be better in preventing weight gain, suggesting there is more to understand about how leptin works

Question 23

role of neural and hormonal mechanisms in eating behaviour

Link to Issues & Debates:

Answer 23

nomothetic approach proposing that because humans share similar physiology then eating behaviours will be universally governed by the hypothalamus, and leptin and ghrelin secretion.

ignores the individual complexity of decisions around food and cannot explain either obesity or eating disorders.

Question 24

role of neural and hormonal mechanisms in eating behaviour

Link to Approaches:

Answer 24

he role of neural and hormonal mechanisms in eating behaviour is a biological approach to behaviour, explaining appetite, eating and satiety through the neural and hormonal mechanisms of the hypothalamus, including the lateral hypothalamus, ventromedial hypothalamus and arcuate nucleus.

Question 25

definition of anorexia nervosa

Answer 25

Anorexia nervosa (AN) is characterised by an obsessive desire to lose weight by refusing to eat

Question 26

Outline the Ephx2 Gene

Answer 26

Scott-Van Zeeland et al. (2014) carried out a candidate-gene association study (CGAS). They compared 1205 AN patients and 1948 control participants by sequencing 153 candidate genes suspected to be linked to features of AN. They discovered that only one gene was significantly associated with AN: epoxide hydrolase 2 (Ephx2). It is a gene that codes for an enzyme involved in cholesterol metabolism. It has been found that many people in the acute phase of AN (when symptoms are particularly severe) have abnormally high levels of cholesterol.

Question 27

supporting evidence for the genetic explanation of AN

twin studies Holland et el

Answer 27

first degree relatives of individuals with AN have a 10 times greater chance of developing AN than relatives of unaffected individuals

Holland et al (1988) studied 45 pairs of female twins and found a concordance rate of 56% for MZ twins but only 5% for DZ twins. This study was replicated in 1999 with slightly less dramatic findings – 65% MZ, 32% DZ. Both pieces of evidence provide strong evidence for the role of genes.

Question 28

what would neural explanations say about AN

Answer 28

Neural explanations see AN as resulting from abnormally functioning brain mechanisms and functions

Question 29

Dopamine Hypothesis – AO1

Answer 29

Some research suggests high levels of dopamine are associated with AN. Kayee et al. (2005) used a PET scan to compare dopamine activity in the brains of 10 women recovering from AN and 12 healthy woman. In the AN women, they found over activity in dopamine receptors in the basal ganglia where dopamine plays a part in interpretation of harm and pleasure. Increased dopamine activity in this area alters the way people interpret rewards. People with AN find it difficult to associate good feelings with the things that most people find pleasurable e.g. food.

Question 30

outline the Serotonin Hypothesis – AO1

Answer 30

Serotonin is a neurotransmitter involved in the control of feeding behaviour. Nutrients are essential for normal serotonin synthesis and function because without nutrients an essential amino acid (tryptophan) that produces serotonin is prevented from getting into the brain.

Disruption in serotonin (leading to high levels) has been linked to a continual state of stress and anxiety. For someone with anorexia, reducing their intake of calories to starvation level (a consequence of this is reduced serotonin levels) may result in a sense of calmness and temporarily feeling better.
The brain however begins to sense the decreased serotonin production and tries to maintain balance (homeostasis) by increasing the number of serotonin receptors. So the brain is back at ‘square one’, as it is producing less serotonin but is using the decreased amount much more efficiently.

So restricting eating does not feel as good, and the solution (to the person with anorexia) is to eat even less. And so this is where the person with anorexia gets into a negative cycle and they feel they are trapped by their own brain chemistry.

Question 32

Research support for dopamine. Evaluation of neurological explanations of anorexia.

Barbato et al (2006)

Answer 32

Research supports the role of dopamine in AN. Food aversion, weight loss and menstrual dysfunction have been found to be related to increased activity in dopamine pathways. Increased eye blink is indicative of higher levels of dopamine activity in the brain. Barbato et al (2006) found increased eye blinks in AN individuals compared to controls. They also found a significant correlation between blink rate and duration of AN suggesting the relationship between dopamine activity and AN symptoms develop over tim

Question 34

evaluation genetic explanations for anorexia nervosa

Vaughn and Fouts, 2003

Answer 34

Vaughn and Fouts, 2003 carried out a longitudinal study which found adolescent girls whose AN symptom severity increased over a 16month period also reported significantly greater fashion magazine reading over the same period. This can be explained using SLT as children see the models in the media as role models so they would imitate the behaviours of the models.

Polygenic disorder – Many candidate genes have been put forward, but few have found any significant link to AN. It has been argued that searching for a single gene is pointless. It is widely accepted that no one gene can be responsible for a wide variety of physical and psychological symptoms that characterise AN, like appetite loss, body image distortions and fear of weight gain. Instead, it is generally believed now that anorexia is polygenic – many genes make important, but modest contributions to the disorder. These genes may interact with environmental factors to eventually trigger AN (diathesis-stress model)

Question 35

Evaluation of neurological explanation for anorexia nervosa

weaknesses

Answer 35

Neurotransmitters do not work in isolation - It is argued that serotonin may account for some features of AN but not for others. AN can be better explained by considering the interaction between serotonin and another neurotransmitter – noradrenaline. According to researchers, serotonin and dopamine are both secondary to the activity of noradrenaline in AN. They claim that other neurotransmitters, such as GABA are also involved. This demonstrates that neurotransmitter systems do not operate in isolation, but in complex interactions.

Cause and Effect – a problem with the neurochemical explanation links to the issue of research being correlational. Research has only identified a relationship between abnormal neurotransmitter levels and anorexia; it is not clear whether it is excessive serotonin that causes anorexia or whether anorexia causes the high levels of serotonin. Also in ‘normal’ starvation, the pattern of behaviour due to the neuro-chemical change is distinctively different from that in anorexia, which often leads to lethargy and hunger, not hyperactivity and food refusal which is typical for many people with anorexia.

Question 36

Link to Issues & Debates:

biological explanations for AN

Answer 36

The biological explanations for AN are biologically reductionist. They state that the eating disorder has its origins in the genetic make-up of the individual or in an imbalance in the neurochemistry. This is ignoring psychological and environmental explanations that would make explanations for this eating disorder more holistic.

The research into AN is gender biased, being conducted mainly on females, as they are many times more likely to suffer from anorexia than males (NIMH, 2017). This means the research has a beta bias, with the results being applied to men, who may have neurotransmission differences when compared to women.

Question 37

What do the family systems theory see An as a result of

Answer 37

anorexia nervosa (AN) as resulting from dysfunctional patterns of family interaction (Minuchin et al, 1978)

Question 38

what do family systems theory focus on and why

Answer 38

More females than males experience AN, and therefore the focus of family systems theory is often on the mother and daughter relationship

Question 39

What is enmeshment

Answer 39

Enmeshment is when the interactions between family members inhibit each family member’s sense of individuality, such as when parents are over-protective of their children, thus preventing any sense of independence developing

Question 40

what is meant by autonomy and control in relation to eating behaviours

Answer 40

Autonomy and control is the ability of an individual to act independently and make choices according to their free will and not the decisions of others

Question 41

what does the family systems theory argues

Answer 41

disturbances in the development of autonomy and control are a defining feature of AN, and show as distortions of body image, misperceptions of internal states and a paralysing sense of ineffectiveness
Weight loss becomes viewed by the adolescent as a visible measure of their autonomy and control

Question 42

Evaluation of Psychological Explanations – AO3

Manzi et al (2006)

research suport

Answer 42

Support for the concept of enmeshment - Manzi et al (2006) demonstrated a distinction between family factors that promote positive emotional development and those that stifle it. Family cohesion for example was indicative of supportive family interaction whereas enmeshment was rooted in manipulation and control. Manzi et al. found that enmeshment between family members was linked to negative outcomes and a range of mental health problems, whereas cohesion had the opposite effect.

Question 43

Evaluation of research investigating family systems theory as an explanation for AN

practical application

Answer 43

Practical application – family based therapy – Although family dysfunction is only one potential cause of AN, the success of family-focused therapies has shown that families are a key part of the recovery process. For example, Carr (2009) concluded that there is compelling evidence for the effectiveness of family interventions for adolescent AN. The therapy aims to identify and modify potentially damaging family behaviour to create a more cohesive, rather than enmeshed family unit.

Question 44

Evaluation of research investigating family systems theory as an explanation for AN
weaknesses

Kog and Vandereycken (1989)

cause and effect

Answer 44

Problems with the family model – Research has tried to establish the characteristics that are specific to families in which a family member has AN and test the predictions of the psychosomatic family model. However, this has produced generally disappointing and inconsistent findings. For example, Kog and Vandereycken (1989) failed to find the characteristics predicted by the family model in families of an individual with AN. There is growing evidence that families in which someone has an eating disorder are a diverse group in terms of nature of family relationships, the emotional climate and patterns of family interaction.

Cause or effect (or both?) - It is argued that enmeshment, rigidity and overprotectiveness and conflict avoidance are consequences of having a son/daughter with AN, and as a result it is impossible to show a cause and effect relationship. The family systems theory argues that this does not actually matter. Regardless of whether the family is the cause of the illness or not, the symptoms become intimately linked to family interactions anyway. Understanding this link can only help in the search for an effective treatment.

Question 45

s

Question 46

what are three ways in which social learning theory suggests that causes AN

Answer 46

Modelling
Social Learning Theory suggests that young people imitate and copy people they admire, this is known as modelling. Young women observe female role models (models may be parents, peers or someone portrayed in the media) being rewarded for being slim and attractive. Today’s western society tends to associate being slim with being successful, fit and healthy. AN can be acquired indirectly through observation of a role model. E.g. a child observing an older sibling constantly restricting her food intake may learn that this behaviour is normal.

Media
According to SLT the media is a major source of influence for the body image attitudes maintained by western adolescents. Over the last 50 years, media images of female role models have become taller and slimmer as demonstrated by the winners of Miss World contests and the images of women in magazines and on TV. This exposure to the media and culturally defined standard of female attractiveness means the ideal is internalised and leads to dissatisfaction with own body weight and shape. As a result young adolescent women may try to copy such models by dieting and striving to achieve this ideal image of attractiveness as a result of vicarious reinforcement.

Reinforcement
If they do manage to lose weight, the reinforcement will be direct, in the form of praise and attention from friends and family. Therefore anorexia becomes a learned behaviour through observation which is maintained by positive reinforcement. E.g. “wow you’ve lost so much weight, you look great”.

Question 47

Evaluation of social learning theory – AO3

Support for role of peers

Costa-Font and Jofre Bonet (2013)

Answer 47

Support for role of peers – Costa-Font and Jofre Bonet (2013) investigated the effect of peer weight on the likelihood of an individual developing anorexia. They found that individuals who had peers with a larger BMI (Body mass index) had a lower likelihood of subsequently developing an eating disorder such as AN. This association between BMI and the likelihood of becoming anorexic was even more marked in younger women.
This suggests that having peers with an average or higher than average BMI protects individuals from eating disorders, whereas having peers with lower than average BMI makes the development of AN more likely.

Question 48

Evaluation of social learning theory – AO3

Research for the role of the media

Answer 48

Research for the role of the media - Evidence for the role of the media in shaping perceptions of body image comes from studies of societies where television has been introduced. Eating attitudes and behaviours were studied among adolescent Fijian girls, following the introduction of TV in 1995 (Becker).
The girls stated a desire to lose weight to become more like western television characters. After five years there were significant numbers of girls with anorexia, even though the disorder was absent before the introduction of TV. This supports the social learning explanation as it suggests that girls were influenced by what they deemed to be ‘role models’.

Question 49

Evaluation of social learning theory – AO3

Limitations

Answer 49

Vulnerability – A limitation of the SLT explanation of anorexia nervosa is that it cannot explain why only some people develop anorexia. Everybody in western societies is exposed to the same media images, but it is only a minority of individuals who develop eating disorders, this suggests that there are other factors that make some individuals vulnerable. Vulnerability factors identified include perfectionism, high social anxiety and low self-esteem. It is clear that the media is not directly responsible for disordered eating and so the social learning theory alone cannot explain the development of anorexia.

Cultural and Gender Bias – The external validity of the social learning explanation is limited as the focus is still on a predominantly western female population indicating a cultural and gender bias in research. Although there is an increasing number of cross cultural studies into eating disorders, most research still takes place in the west. As the samples studied are mainly female, this may mean yet again the understanding of anorexia may be limited for men, as what contributes to their disorder may be very different from women. This means that SLT is better at explaining the development of anorexia in females and the increase of the disorder in the West and further work needs to be carried out to gain a full understanding of the complexities of anorexia for all sufferers.

Question 50

Cognitive Theory – AO1

Answer 50

Distortions
Cognitive distortions are errors in thinking that cause the individual to develop a negative body image. In most cases AN sufferers have a disturbed perception of their own body image. Murphy et al 2010 argue that all other clinical features of AN stems from these distortions. People with AN become more and more critical of their own body. They mis interpret their emotional state as feeling fat even as they get thinner and thinner.
Irrational belief
Individuals often develop self-defeating habits because of faulty beliefs about themselves and the world around them. Irrational beliefs are not based on facts, and tend to be unrealistic. A typical irrational belief in an individual suffering from AN is that “If I’m not thin then I must be fat” – all or nothing thinking. These irrational beliefs become second nature and give rise to automatic negative thoughts.
A key irrational belief in AN is perfectionism, the view that the individual has to meet their most demanding standards all the time, and failure to do so is judged severely. This applies to all aspects of the AN sufferer’s life – academic success, relationships, career aims- but especially to eating and body shape. Often perfectionists are not satisfied when they reach their targets, but merely raise their standards higher – so they are forever pursuing an unrealistic goal they can never attain.

Question 52

list the three most common cognitive distortions related to AN

Answer 52

Connecting self-worth to physical appearance only
Perceiving the body as overweight when it is underweight
Having faulty beliefs about eating and dieting

Question 53

name 3 examples of irrational beliefs

Answer 53

All or nothing thinking - the individual has eaten one chip or one piece of chocolate and this immediately leads them to believe that they will put on lots of weight
Magnification and minimisation - the individual believes that they are a complete failure if they cannot restrict their eating - but they also believe their weight loss is minimal and is not harmful
Magical thinking - the individual believes that if they could just reach their (usually totally unreasonable) target weight then they would be happy and popular

Question 54

Research support for cognitive theory as an explanation for AN

Answer 54

Support from food stroop test studies – Garner and Bemis and Fairburn et al. predict that an AN individual’s attention will be biased toward stimuli that are related to body fatness and to fattening food because such stimuli are perceived as more threatening to people with an eating disorder. Ben-Tovim et al. (1989) used a version of the Stroop test (the food stroop test) and discovered that compared to normal controls, patients with AN found it harder to colour-name words that were relevant to their weight concerns suggesting a selective preoccupation with those stimuli and words related to them

Question 55

Evaluation of cognitive theory as an explanation for AN
practical applications.

Answer 55

Practical application; CBT-E - Cognitive behavioural therapy for eating disorder is a form of treatment specifically designed to address the cognitive problems that underlie eating disorders such as AN. A study by Fairburn et al (2015) compared CBT-E with interpersonal psychotherapy (IPT) a leading alternative treatment that has no cognitive element. 130 patients with an eating disorder were randomly assigned to either CBT-E or IPT. At the end of 20 weeks treatment, two thirds of the CBT-E participants met the criteria for remission compared to just one third of the IPT participants. The findings indicate that CBT-E is an effective treatment for the majority of individuals with an eating disorder and reinforces the view that cognitive issues are a root cause of AN

Question 56

Evaluation of cognitive theory as an explanation for AN
weaknesses, causation

Answer 56

Causation – Although research shows that distortions and irrational beliefs are features of AN, it is not all clear that they cause the disorder. There is very little research to show that these cognitive factors exist before the onset of AN. E.g. Shott et al (2012) found that younger AN patients were no worse at set-shifting than non-anorexic controls, but older patients were. This suggests that cognitive inflexibility does not make an individual vulnerable to developing AN, but is instead a consequence of the disorder.

Question 57

Evaluation of cognitive theory as an explanation for AN. Contradictory research

Answer 57

Contradictory research – Cornelissen et al. (2013) compared AN patients with non AN patients on a morphing task. Participants had to adjust a computerised image of themselves until it matched their estimated body size.
The researchers found no significant differences between the groups of women in the accuracy of their estimates. As it is not possible to distinguish between the body size estimates of healthy and AN women, this suggests that over estimation is not pathological. This finding challenges the central role of body image distortion in cognitive theories of AN.

Question 58

Neural Explanation – AO1 for obesity, seratonin and dopamine.

Answer 58

Serotonin explanation
Serotonin is a neurotransmitter involved in the control of feeding behaviour. Research studies of both humans and non-human animals show that obesity is associated with abnormally low levels of serotonin.
Normal levels of serotonin regulate feeding behaviour by triggering activity of the Ventromedial Hypothalamus (VMH) to reduce food intake. Serotonin is part of the system that signals to the hypothalamus that we have eaten to satiety (fullness). Low serotonin levels lead to cravings for carbohydrates and energy-dense foods (including sugars) leading to weight gain through too many calories.
Dopamine
Dopamine activity is associated with the pleasure we derive from eating and cues associated with eating e.g. smell of food. However, obesity has been linked with a dysfunctional dopamine system in many research studies. Wang et al. (2001) found that obese individuals had significantly fewer dopamine D2 receptors than normal weight controls.

Because dopamine levels are so low in some people, the neurotransmitter cannot perform its usual pleasurable reward function in response to eating, i.e. a person does not feel good after eating. Overeating can therefore be seen as an attempt to activate reward centres in the brain that provide feelings of pleasure by increasing dopamine levels.

Question 59

Bonus AO1 neural content (stuff you already know), on obesity.

Answer 59

The Ventromedial hypothalamus
This rise in glucose levels activates the ventromedial hypothalamus, which leads to feelings of satiation (fullness), which in turn stops further feeding. The ventromedial hypothalamus is the signal to stop eating and its stimulation inhibits (stops) feeding. One suggestion is that damage to the VMH is linked with continued eating past the point of satiety and eventually obesity.

Leptin
Leptin is a hormone that is released into the bloodstream from fat cells which acts as a signal to the hypothalamus to stop eating. Our fat stores are the main indicators of body weight. Fat cells release leptin into the bloodstream, via which it travels to the hypothalamus. The amount of leptin that is released is proportional to the fat content of the cells. If there is an underproduction of leptin this means the VMH may not be triggered to stop eating, eventually leading to obesity.

Question 60

Evaluation of Biological Explanation – AO3

genetic explanations of obesity.

limitations

Answer 60

The problem of time and geography – a 2015 UK government report described a sharp increase in obesity rates in the UK over the last 20 years. For example in 1993, 13% of males were classified as obese, but this figure has risen to 26% by 2013. However, the nature of the gene pool has remained constant over the same period. An explanation based on genetics alone, therefore could not explain this sudden increase in obesity rates.

Problems with comorbidity. People with obesity are at an increased risk for developing many medical problems, including psychological disorders such as binge-eating, insomnia and depression. One of the difficulties with trying to identify specific genes responsible for obesity is that is may actually be the result of a different psychological disorder (e.g. depression may have caused obesity, which means we should be looking for a gene for depression, not obesity). This means it may not be simply a case of identifying one gene that is responsible for such a complex disorder.

Question 61

Evaluation of Biological Explanation – AO3

Neural explanation

limitations

Answer 61

Research support for dopamine – Low dopamine levels are often due to D2 receptors so research has focused on the DRD2 gene which codes for the D2 receptor. Ritchie and Noble (2003) conducted a PET scan study and found that people who inherited one version of the DRD2 gene had 30-40% fewer D2 receptors compared to those with other versions. This supports the claim that people with low dopamine levels (due to fewer D2 receptors) experience less dopamine-activated pleasurable reward from eating which makes them more likely to overeat.

Cause and Effect – A problem with the neurochemical explanation links to the issue of research being correlational. Research has only identified a relationship between abnormal neurotransmitter levels and Obesity, it is not clear whether it is a lack of serotonin that causes obesity or whether obesity causes the low levels of serotonin.

Bonus neural evaluation – if you have outlined the VMH and leptin explanations then you can use the research by Hetherington and Ranson (1942) study (damage to VMH in rats) and Zhang et. al. (leptin deficiency) to support your explanation.

Question 62

Evaluation of Biological Explanation – AO3

general evaluation of biological explanations

Answer 62

General AO3 for the biological explanation

Less stigmatising – an advantage of biological explanations of obesity is that they offer explanations of obesity that are perceived as being out of the individual’s control and therefore less stigmatising. This is in sharp contrast to many psychological explanations of obesity that highlight the personal failing of the individual. Because of the ‘scientific’ nature of biological explanations, treatments may offer individuals some hope of dealing with their disorder.

Question 63

Restraint Theory – AO1

Answer 63

Lack of restraint is synonymous with obesity. Herman and Mack (1975) developed the restraint theory suggesting that attempting not to eat actually increases the probability of overeating. They claim that in the majority of cases, rather than restraint leading to weight-loss, it leads to overeating and weight gain and therefore increases the risk of becoming obese. Herman and Polivy argued restrained eating is counter-productive and ultimately self defeating.

Provencher et al. (2003) reported that rigid restraint tends to be positively associated with amount of body fat, waist circumference and BMI.

Question 64

Different types of disinhibition as identified by Bond et al. (2001):

Answer 64

Habitual Disinhibition (overeating in response to daily life situations),
Emotional Disinhibition (overeating in response to emotional state e.g. anxiety/depression)
Situational Disinhibition (overeating in response to environmental cues e.g. wedding party).

Question 65

what are the different types of restraints –

Answer 65

Flexible restraints - flexible restraint eaters attempt to limited their intake of fatty foods without actually giving them up completely.
Rigid restraints - rigid restraint eaters are more likely to take an ‘all or nothing’ approach to eating. This means attempting to completely cut out fatty foods. Such rigid thinking and denial of foods (‘I must not eat anything fatty’) can lead to constantly thinking about the food, and subsequently experiencing cognitive conflict (a form of stress) in which over time can mean they eat the foods they are trying to avoid to reduce this conflict.

Question 66

The Boundary Model – AO1

Answer 66

Food intake exists on a continuum from hungry to feeling full. In between these two areas is the zone of biological indifference where biological processes have minimal impact on if we eat. Instead, cognitive and social factors have their greatest influence on food intake – when we are neither particularly hungry nor full.
Restrained eaters have a lower hunger boundary so are less responsive to feelings of hunger. They also have a higher satiety boundary, so they need more food before they consider themselves full. This means more of their eating will come under cognitive rather than physiological control.
Restrained eaters have a self-imposed ‘cognitive boundary’, which represents their diet. If this is set too low, they will break the boundary and continue to eat up and beyond the satiety boundary. This is known as the ‘what the hell effect’.
The Boundary Model:

Question 67

Disinhibition – AO1

Answer 67

Disinhibition is the tendency to overeat in response to different stimuli and can occur in a variety of circumstances. In these circumstances, normal inhibitions which prevent us from eating too much are removed and so people respond less to feelings of satiation and are more likely to overeat. The explanation suggests that those who have a lower threshold at which disinhibition occurs are more prone to overeating and subsequent obesity.

Question 68

Restraint Theory - AO3

Answer 68

Research Evidence for Restraint theory – Wardle and Beales (1988) randomly assigned 27 obese women to either a restrained diet group, an exercise group or a non-treatment group over 7 weeks. At weeks four and six, all participants were assessed under laboratory conditions, and at both times, women in the restrained diet group ate more than women in the exercise and non-treatment group. This supports the theory that rigid restrained diet will actually lead to increase in food consumption and eventually weight gain.

Question 69

Boundary Model - AO3

Answer 69

Research Evidence for the Boundary Model - Herman and Mack gave a group of non-dieters and a group of dieters either a high or low calorie preload (high- two milkshakes, low – one milkshake). The participants were then given access to a unlimited buffet and the amount eaten was recorded.

The dieters/restraint eaters ate more in the taste test if they had the high calorie preload than when they had the low calorie preload:
Herman and Mack conclude the results support a boundary model of dietary restraint. Dieters have a cognitive boundary for food intake; once this is overcome by the preloads the ‘what the hell effect’ takes over and they eat more.

Question 70

Disinhibition - AO3

Answer 70

Gender and culture bias in disinhibition research – Research on disinhibition is often restricted to white women making it difficult to generalise conclusions to men and other racial groups. Atlas et al. (2002) suggested that African American women are less prone to the effects of disinhibition, meaning such eating behaviours may be less prevalent among African American women. Similarly, several studies have reported that men are less prone to the effects of disinhibition than women. All of this suggests that while the disinhibition theory may be able to explain eating behaviour in some members of the population, it cannot be generalised to all.

Question 71

General AO3 practical application point (relevant for all three theories)

Answer 71

Real World Application: Anti dieting programmes – Concerns about the ineffectiveness and potentially damaging effects of many diet programmes has led to the development of programmes aimed at replacing dieting with conventional healthy eating. These programmes emphasise regulation by body hunger and satiety signals and the prevention of inappropriate attitudes to food (e.g. comfort eating or food avoidance).
This suggests that eating only when hungry and stopping when satiated is more likely to be successful than trying to restrict or restrain food intake.

Question 72

Failure of Dieting – AO1

Answer 72

You can use the Restraint Theory and the Boundary Model from the Psychological explanations of obesity hand-out to explain the failure of dieting:

Restraint Theory: rather than rigid restraint leading to weight-loss, it leads to overeating and weight gain.
Boundary Model: Restrained eaters set a ‘cognitive boundary’ to reduce food intake – this is often set too low. If the boundary is broken (they eat past the self-imposed limit, they will continue to eat until satiety (which is often higher than non-restrained eaters).

Question 73

Evaluation of Success and Failure of Dieting – AO3

real world applications

Answer 73

Real World Application: Anti dieting programmes – Concerns about the ineffectiveness and potentially damaging effects of many diet programmes has led to the development of programmes aimed at replacing dieting with conventional healthy eating. These programmes emphasise regulation by body hunger and satiety signals and the prevention of inappropriate attitudes to food (e.g. comfort eating or food avoidance)

This suggests that eating only when hungry and stopping when satiated is more likely to be successful than trying to restrict or restrain food intake.

Question 74

success of Dieting – AO1

Answer 74

Mindful eating
Research by Redden (2008) suggests that the secret of successful dieting lies in the attention we pay to what is being eaten. People usually like experiences less as they repeat them. That’s why when it comes to dieting it is harder to stick to a particular regime.

To overcome this, Redden suggests instead of thinking ‘not another salad’, we should focus on the details of the meal (e.g. the taste, texture, smell, country of origin). By focusing on the specific details of each meal, not only do people get bored less easily with the food they are eating, they actually slow down. This gives the ventromedial hypothalamus time to recognise the increase in blood glucose, and so we eat less.

Self-monitoring
Self-monitoring involves dieters keeping daily records of their food consumption, including type of food consumed, and quantity. Dieter’s progress should be assessed regularly which can enable the dieter to make adjustments to targets if necessary (e.g. increase calorie allowance on specific days). These records can be kept through the use of food diaries which are objectively measured and increase the sense of control the dieter has over the diet.

Question 75

Evaluation of success of dieting, alternative approach

Answer 75

Alternative Approach - Cognitive models such as the boundary model are limited as they ignore the role of important biological factors such as body weight set point. Dieting to reduce weight below the body weight set point is difficult because the body tries to restore the set point in any way it can.

In order to do this the body will increase feelings of hunger and will reduce the BMR (basal metabolic rate – the rate at which cells burn up energy). A lower BMR reduces energy expenditure making weight loss difficult even on a diet. This evidence on set point emphasises that body weight set point is a valid alternative explanation for the complex nature of dieting and that one explanation alone cannot account for its failure.

Question 76

Limitations of success of dieting, AO3

Answer 76

Limitations of anecdotal evidence - Many studies of dieting success or failure rely on the personal accounts of individuals (i.e., anecdotal evidence). Such evidence is often used to justify claims concerning particular dieting strategies. However, anecdotal evidence has a number of problems that properly controlled scientific studies do not have.

The main limitation is that memory is not 100% accurate as it often relies on the subjective accounts of dieters (who may lie, or forget about calorie intake). This which creates problems for the validity and reliability of the evidence provided by personal accounts and anecdotes.

Question 77

free-will and determinism. issues and debates, success and failure of dieting AO3.

Answer 77

Freewill or determinism – It is likely that a number of genetic mechanisms exert an influence on weight, suggesting that the success or failure of dieting may be determined by factors other than an individual’s choice of lifestyle.

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. Researchers believe that the weight loss activates the gene producing the enzyme which might explain why a dieter (who was obese) is more likely to regain lost weight compared to someone who has never been obese to put on weight.

This suggests that some people will struggle to lose weight because of their genetics regardless of their intentions to do so. This suggests that whilst we may want to believe we have the free will to lose weight, this may actually be determined by our genes.