LESSON FIVE & SIX – ALL YOU NEED TO KNOW ABOUT EATING DISORDERS

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Specification link: You will be able to outline and evaluate:
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Biological, including neural and evolutionary, explanations of anorexia nervosa
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Psychology explanations of anorexia nervosa

Outline and description of theories | Research evidence and commentary | IntroductionThe DSM-IV Rev identifies three categories of eating disorder: * Anorexia nervosa 1. AN -restricting type – refusal to eat 2. AN- binge eating/purging type – episodes of binge eating followed by removal of food from the body by vomiting, laxatives, or enemas.Both of these are associated with significant weight loss and the other symptoms of AN. * Bulimia nervosa – episodes of binging followed by removal of food from the body by vomiting, laxatives, or enemas (no significant weight loss). * Eating disorders not otherwise specified (EDNOS)The four major symptoms of anorexia nervosa are: * The body weight is 85% or less of normal weight for age and height * Distorted perception of body weight/shape, and/or denial that the weight loss is severe * Intense fear of becoming fat * Loss of three consecutive menstrual cycles in women (amenorrhoea)Anorexia nervosa (AN) and Bulimia nervosa (BN) have much in common, particularly a dissatisfaction with body weight and/or shape. AN affects approx 0.3 % of males and 0.9% of females. BN is more common (0.5% of males and 1.5% of females).AN often develops over time into BN although the reverse is less common (Polivy and Herman, 2002).Both conditions affect young women far more than any other group (90% of cases are female) and are extremely resistant to treatment. 30 – 40 % show no improvement after five years.AN is associated with a mortality rate of about 8 % often through suicide.Both AN and BN have a common preoccupation with body weight and shape, which can be associated with distorted perceptions of their actual body weight/shape and body dissatisfaction. This leads to disrupted eating patterns – starvation or binge-purge cycles. | Evolutionary approachesThe adapted to flee famine hypothesis (AFFH)Guisinger (2003) suggested that AN is a reflection of behaviours that were adaptive in the environment of evolutionary adaptation (EEA) (maybe more than one million years ago). When our ancestors were hunter-gatherers they needed to move on regularly as food supplies in the local area were exhausted. Guisinger notes that key characteristics of people with AN are restlessness and high levels of activity. She contrasts this with the usual response to starvation and weight loss, which would be inactivity and depression. She therefore hypothesises that high levels of activity and a denial of hunger would help the individual to migrate in response to famine in their local area. | While the evolutionary explanations makes a good suggestion about why people with AN deny their hunger and often display increased levels of activity it doesn’t provide a reasoned argument for why AN afflicts far more women than men. It would seem more logical for the condition to afflict both men and women as men would be just as involved in gathering up their resources and moving territory as women. Furthermore, it is impossible to test the explanation of AN scientifically as it has to rely on a great deal of speculation. As with all evolutionary explanations of human behaviour, there is no direct evidence for this model and it does not explain why AN is found predominantly in women | Genetics of eating disordersIt is generally agreed now that there is a significant genetic contribution to eating disorders.A better approach than just looking at the occurrence of AN in families and across generations is to compare its occurrence in twins and to compare the concordance rates for identical twins (MZ) with non-identical/fraternal twins (DZ).MZ twins share 100% of their genes so it would be expected that if one twin has AN, the other twin will have AN if it is purely a genetic disorder. DZ twins, on the other hand, are like any other brother/sister and share just 50% of their genes. This would result in a lower concordance rate for AN compared with MZ twins. If MZ twins are more alike for a AN than DZ twins, then the difference between them is likely to be due to genetic factors rather than the environment. Holland et al (1984) found that if on MZ twin had AN, then the concordance rate (the probability of the other twin having AN) was 55%. The concordance rate for DZ twins was 7%.There is a significant difference between the concordance rates and as the only difference between MZ and DZ twins is the greater genetic similarity of MZ twins, the findings point to a significant genetic involvement in AN. | While it is observed that eating disorders can appear regularly across generations in the same family, this could also be because families share similar environments and social learning may occur within them. Therefore AN may afflict several members of a family for reasons other than genetic ones. Holland et al (1984) and Kendler et al (1991)Found that concordance rates for AN were significantly higher for MZ twins than for DZ. Many reviews which have followed of these studies conclude that the genetic contribution to both AN and BN is between 50% and 80%. Therefore, it can now be concluded that genetics play a significant role in eating disorders. However, there are some issues to be considered: * AN and BN are rare conditions. Therefore, studies are based on a very few numbers of participants. This results in a lack of reliability. * In addition, allocation to MZ or DZ twins is usually (as in Holland et al’s study) done on the basis of physical similarity for a few of the twin pairs. This is not a completely reliable method for distinguishing between MZ and DZ twins. MZ twins can look identical but a blood test is needed to be certain that they are monozygotic twins. If results for the twins were counted in the MZ group when they should really have been counted in the DZ group, the study will be invalid. * Furthermore, such studies assume that environmental influences are the same for both types of twin and that the only difference is in their genetics. However, it is possible that MZ twins are treated more similarly than DZ twins while growing up (for instance they are always the same sex, they look the same and are often dressed the same and confused for each other). This extra similarity may result in them being treated more similarly than DZ twins which may contribute to the higher concordance rates. * By far the majority of studies have been carried out in Europe and America. It is not certain that the same results would be found in non-Western cultures such as Africa and Asia. * While a genetic contribution has been identified, it is not clear what exactly is inherited. For example, AN is accompanied by body image dissatisfaction. It is difficult to see how this aspect of AN could be inherited. * Genes cannot provide a complete answer as concordance rates in MZ twins, while higher than in DZ twins, are never 100%. They would be if genes were the only component involved. As it is, there must be other factors to take into account. For this reason, it is more accurate to say that there is genetic predisposition for AN which may be triggered by environmental and psychological factors. A key question for researchers today is how any genetic tendencies interact with environmental factors. | Neural factors Serotonin, is a brain neurotransmitter that is involved in many behavioural functions including depression and obsessive-compulsive disorder. Early studies (Kaye et al, 2005) found a reduction in levels of the important serotonin metabolite 5-HIAA in people with eating disorders. This would suggest that brain serotonin pathways were underactive. Background info However, the introduction of brain scanning techniques has transformed the study of eating disorders. In PET scans a drug that combines with serotonin receptors is injected and travels to the brain and binds to serotonin receptors. A brain scan is taken and the drug shows up as a brightly lit area. These can be measured and this gives an estimate of the number of serotonin receptors in different parts of the brain. This is far more direct than measuring serotonin levels. PET scans have shown that there are fewer serotonin receptors in the brains of people with eating disorders (Kaye et al, 2005). A reduction in receptors suggests a dysfunction of the serotonin system in eating disorders. The brain serotonin system has been implicated in personality traits associated with eating disorders, such as obsessionality perfectionism, anxiety and depression. It is also part of the neurotransmitter system of the hypothalamus that controls feeding behaviour. Therefore, it is likely to be involved in the causes of eating disorders. | However, most of these early studies were done on people with ongoing AN and BN and it is possible that the illness had produced the changes in serotonin activity rather than the other way round. In AN, the loss of body weight produces many hormonal and brain changes as the body tries to cope. For this reason, it is not possible to conclude that serotonin abnormalities caused the eating disorder as they may have been the result of it.More importantly PET scans show that these changes are found in people who have recovered from eating disorders, i.e. they are not due to loss of body weight or other physiological changes associated with AN and BN (Kaye et al , 2005)However, this still does not show conclusively that changes in the serotonin system cause eating disorders. The loss of weight in SN produces alterations in the body’s physiological systems. These alterations may be so profound that they persist even after the person has recovered, that they are still secondary to the illness and not the cause. The only convincing way to show that dysfunction of the serotonin system causes eating disorders would be to show that the changes were there before the onset of AN. This is very difficult to do because it would mean testing a huge amount of people and following them in a longitudinal study to see which of them developed AN and as it only affects a small proportion of the population, this is impractical. | An integrated approach to AN Research evidence shows that there must be an interaction between biological and psychological factors in eating disorders, but studies usually focus on one or the other. The simplest model would be a genetic vulnerability interacts with environmental factors, such as media influence or family dynamics to produce ANConnan et al (2003) have suggested a more detailed model of AN based on the characteristics of the disorder for example, ‘maternal anxiety’ in a pregnant mother has a biological effect on the hypothalamic-pituitary (HPA) stress response in the developing child. This can lead to the child having an over-reactive stress system. AN, typically, has its onset in adolescence which is a time when the young person has a lot of changes to cope with and is, therefore, a very stressful time. AN may be a reaction to the stress of coping with these changes. Furthermore, at puberty there is a surge of oestrogens (female hormones) in girls which has been shown to have a direct effect on brain serotonin and to affect a number of brain systems including those related to the control of mood, appetite and the HPA system. | There is some evidence for an integrated model (Connan et al, 2003) especially the early developmental problems associated with AN. There is also evidence for disturbances of brain function. Additionally, levels of the stress hormone cortisol are raised in AN. However, much of the model is speculative, with little reliable research evidence but, it is an important attempt to show how the biological and psychological approaches might be combined. There is no doubt that the eventual understanding of eating disorders will require this type of combination. Currently, while there are a number of increasing cross-cultural studies into eating disorders, it is fair to say that that the focus is still on Western industrialised societies, indicating a cultural bias in research. | Psychological explanations for anorexia nervosa | IntroductionIf AN is a biological disease we would expect to see examples of it throughout time and across cultures. The first formal description of anorexia nervosa was in the 19th century (Gull, 1874) and much later for bulimia nervosa (1970s). However, there are references to AN in literature going back to the 12th century (Keel and Klump, 2003) so AN has been acknowledged for some time. However, there is clear evidence that it has significantly increased between the 1970s and 1990s and many studies have tried to explain this increase. | Eating disorders have been identified in all of the cultures which have been studied but it has been noted that the frequency of its occurrence is affected by media influence such as television. TV portrays Western lifestyles and values and this often involves idealised images of women.In a major review of cross-cultural studies of eating disorders, Keel and Klump (2003) drew some important conclusions. Anorexia nervosa is found in all of the cultures studied, even in those not exposed to Western influences. However, the frequency is proportional to the degree of the influence of Western ideals. The more Westernised the society, the more AN is found. One reason for this could be that girls internalise culturally defined standards of female beauty, including slimness. In some girls, this creates a tension between the real self and the ideal self. This leads to dissatisfaction with their own body weight and shape, which in turn leads to dieting and an obsession with food. In some vulnerable girls, this can lead to a fully fledged eating disorder. The process may be helped by imitation of role models (social learning) and vicarious reinforcement (seeing others rewarded for being thin) which leads to direct reinforcement by praise from family and friends for losing weight (operant conditioning). | Hock et al, 1998 found that the black inhabitants of the Caribbean island of Curacao had a much lower rate of AN than the white population. They concluded that this was because the white population aspired to more Western lifestyles, especially the representation of the ideal woman while the black population still valued larger female body sizes. It is interesting to note that Bulimia nervosa is not found across cultures in the same way as AN is. This deserves some consideration.Media images of the idealised woman have become taller and slimmer over the last 50 years, as demonstrated by the winners of the Miss World contests and images of woman in newspapers, magazines, films and on TV. There is a general agreement that this is an important factor in the development of eating disorders (Striegal-Moore and Bulik, 2007). There is much evidence to support the role of the media in the development of body dissatisfaction in females. For example, Groesz, Levne and Murnen (2002) did a meta-review of 25 studies and concluded that body dissatisfaction significantly increased after exposure to media images of thin women. The increase in dissatisfaction was greatest in those with most dissatisfaction before exposure. Becker et al (2002) carried out a study which has become well known in Fiji. They found that eating disorders were absent in Fiji before the introduction of TV and exposure to Western influences. After five years there were significant numbers of women with AN and BN. However, everyone is exposed to these influences and images but only a few develop an eating disorder so there must be some factors that make some people more vulnerable than others. | Women who develop eating disorders tend to: * have low self-esteem, * to be perfectionists (eating disorders often occur together with obsessive-compulsive tendencies) * have high social anxiety.Studies of their families show that parents are often high achievers with high expectations of their children and a tendency to be over controlling. The concept of ‘enmeshment’ refers to the over-involvement of parents with the child, so it is difficult for the child to feel autonomous (independent). | | Psychodynamic interpretations of ANBruch (1973) proposed that AN was an attempt by the individual to exert some sort of control. They felt used and exploited and were struggling for autonomy – to feel independent from their parents. Eating behaviour was one area that they felt they could control and this control makes them feel good about themselves. Crisp (1980) developed similar ideas based on the fact that self starvation and the loss of body weight in AN leads to a postponement of menstruation in pre-pubertal girls and loss of menstruation (amenorrhoea) in post-pubertal girls. He proposed that this was an attempt by the girl to remain a child and to postpone the onset of adulthood and the responsibilities this brings. Crisp suggested that this was stressful to them. Minuchin, Rosman and Baker (1978) took a family systems approach. They suggested that a child develops AN as a means of diverting attention away from other family problems. It is a misguided attempt to keep the family together, for example in cases where the parents are having relationship problems. | While there is no doubt that most cases of eating disorders involve complex interactions between children and parents. However, it can be difficult to identify family problems that come before the eating disorder and those that are caused by it. Living with someone with AN can be very stressful and often brings about much tension within the family. Although psychodynamic interpretations seem to fit descriptions of some cases, they are difficult to test scientifically. Evidence comes mainly from case studies and these always have issues of reliability as they are unique in their detail and cannot be replicated. Findings cannot, therefore, be generalised to all people with AN. However, various forms of psychotherapy and family therapy have been used successfully in the treatment of AN, which suggests that there may be some valuable aspects of the psychodynamic and family systems explanations. |

Previous exam question
June 2010
Discuss explanations of one eating disorder. (25 marks) Mark scheme

AO1 = 9 marks Outline of explanations of one eating disorder
Candidates are able to choose from anorexia nervosa, bulimia nervosa, or obesity.
Psychological explanations may include self-image and body dissatisfaction, combined with the role of family, peer groups, and the media. Psychodynamic explanations would also be relevant. Biological explanations may include the genetic factors or the role of brain mechanisms (eg neurotransmitters, hypothalamic feeding centres). Evolutionary theories for eg anorexia nervosa or obesity would also be directly relevant to this question. Examiners should be alert to candidates presenting creditworthy material not on the Specification.
Given the Specification, candidates must be clear on what disorder they are discussing, although explicit application of an explanation to more than one disorder may earn AO2 credit. Answers outlining only one explanation are showing partial performance and can receive a maximum of 6 marks for AO1. However candidates may focus on psychological or biological explanations, or draw from both areas.

AO2/AO3 = 16 marks Analysis and evaluation of explanations of one eating disorder
Candidates must be explicit on which eating disorder is being evaluated. Given the availability of relevant studies research evidence would be an effective route to AO2 credit. Another key feature of this area is the complexity of the conditions, and the comparison with alternative explanations, or commentary on the range of explanations, would be directly relevant and creditworthy. Candidates may also comment on individual vulnerability to e.g. media influences, or the difficulty of showing that changes in the brain are primary and not secondary to e.g. weight loss.
General evaluation of broad approaches, such as the psychodynamic or biological, can receive some AO2/AO3 credit if clearly linked to the issue of eating disorders.
Indicative issues/debates/approaches in the context of psychological and biological explanations of one eating disorder: approaches – biological, cognitive, behavioural, psychodynamic; gender and cultural differences and biases; use of non-human animals; nature/nurture; free will and determinism; reductionism.
Further sources of AO2/AO3 credit might include methodological evaluation of relevant research evidence; other material relevant to How Science Works might include: communication of scientific ideas using appropriate terminology; applications of scientific ideas and findings e.g. to treatments; role of science in social decision making. Any material must be used effectively to earn marks.
Note that commentary and evaluation in this area is often generic, with issues common to more than one explanation. Therefore there are no partial performance criteria for AO2/AO3 credit, although marks will vary according to the focus of the answer and the effective use of material.

Examiners’ report
Although anorexia nervosa was the most popular focus for this question, there were a substantial number of answers on obesity, and rather less on bulimia nervosa. A common weakness was to begin the answer with detailed descriptions of clinical characteristics and symptoms which were not linked to explanations. However, in general candidates showed impressive awareness of a range of explanations for their chosen disorder. These included evolutionary/genetic factors through neurotransmitters and brain systems underlying feeding behaviour, to psychodynamic, social and cultural factors. AO1 marks were often in the top two bands. Evaluation in the higher bands used research evidence effectively, although some candidates still fail to fully understand the use of MZ/DZ twin studies; it is critical that findings from studies are effectively linked to specific explanations. As all disorders have a variety of alternative explanations this is an excellent area for issues and debates. However these were often presented in rudimentary fashion with no evidence of clear understanding; this was particularly evident for reductionism and determinism.
June 2011
Outline one psychological explanation of one eating disorder. (5 marks)

Outline of one psychological explanation of one eating disorder
Examples of eating disorders given in the Specification are anorexia nervosa, bulimia nervosa and obesity. Each of these has a range of psychological explanations, such as social/cultural influences (e.g. social learning theory and other conditioning explanations) and psychodynamic approaches (e.g. Bruch, Minuchin).

Explanations of obesity are likely to focus on a range of cultural and environmental factors. These should be considered as one psychological explanation.

Answers should be assessed on their accuracy and coherence, and focus on a single disorder. Where a single disorder cannot be identified, such generic answers eg on the role of social learning on eating disorders in general, can earn a maximum of 3 marks. Studies can be credited to the extent to which they illustrate the explanation.

Examiners’ report
Anorexia nervosa was the most popular disorder considered and the media/social learning approach was the most popular explanation. The question was answered moderately well though many answers lacked sufficient detail of the psychological processes involved to move into the top bands. Technical terms such as observational learning, modelling, vicarious reinforcement etc should all form part of an outline of the role of SLT in any behaviour. Psychodynamic explanations were usually more impressive, with the roles of enmeshment and over control accurately outlined. Obesity and bulimia nervosa were less popular, but the socio-cultural explanation of obesity was used effectively by some candidates. A significant minority of answers were either too long or too short for the marks available, and in some cases presented AO2/AO3 material that did not earn marks.