Causes of Anorexia Nervosa - Essay Example

Table of Contents Word count: 2,165 1 Anorexia nervosa: In the genes or in the mind? 2 Theories about anorexia nervosa 2 Psychodynamic models 2 Psychosocial life stages 3 Dissociation 4 Cognitive theories 4 Sociocultural models 5 Research evidence for the various theories of anorexia nervosa 6 Psychodynamic models 6 Psychosocial life stages 7 Dissociation 7 Cognitive theories 7 Sociocultural models 8 Research evidence for genetic vulnerability 8 Interplay of genetic and psychological factors 10 References 11 Word count: 2,165 Anorexia nervosa: In the genes or in the mind? In this paper I will review the theories and research relevant to anorexia nervosa (AN), and I will attempt to determine whether genetic or psychological factors are more important in the development of this disease, or whether they are equally important. It should be noted that where a patient is referred to as “she”, this could just as well refer to “he” since anorexia is known to occur in men as well as women, although by far the majority of AN patients are female. Theories about anorexia nervosa Psychodynamic models For a long time, AN was explained purely in psychodynamic terms (Sundberg, Taplin & Tyler, 1983), which meant that it was seen as a conflict between the id—with its survival instincts—and the superego, which was the person’s moral conscience (Maddi, 1989). The patient’s relationship with her mother was seen as primary (Farrell, 1995). From a psychodynamic perspective, AN can also be seen as an expression of the death wish, or as a denial of one’s sexual maturity and femininity (Farrell, 1995). It has also been seen as a transfer of conflict from Freud’s “genital stage” to the oral zone, which is more familiar and controllable (Farrell, 1995). Because of the amenorrhoea (lack of menstruation) often seen in AN, the illness is also seen as an expression of unconscious pregnancy fantasies, or of the desire for a penis (Farrell, 1995). Modern psychodynamic theory includes family systems theory. In this model, the family of an anorexic girl is seen as overly controlling or enmeshed, and the girl attempts to reassert her control over her own independence as symbolized by her own body (Minuchin et al., in Spannuth, 2006). Other characteristics of the family may be overprotectiveness, rigidity, lack of conflict resolution and very high expectations for the child’s academic success. Another aspect of an “anorexic family” may be that it appears on the surface of things to be the perfect family, but underneath this façade there is little expression of either true affection or of conflict (Weme & Yalom, in Spannuth, 2006). The empirical evidence for the validity of these theories is discussed later. In object relations theory, eating disorders may be seen as a need to limit the expression of desire and emotion in general (Clinton, 2006). Anorexia is also seen as the patient’s inability to separate from her mother, because her envy of the breast is subjectively felt to be too powerful and destructive to allow for such a separation (Farrell, 1995). Bruch (cited in Farrell) theorized that anorexics receive emotionally inadequate parenting in early childhood, and that they are often overstimulated and learn to become hyperactive to hold themselves together. Psychosocial life stages Erik Erikson’s psychosocial life stage theory would interpret anorexia as a failure of Stage 1, where the child is completely dependent on adults for both her physical and emotional needs. If those needs are met well enough, then she develops a sense of trust in herself as well as trust in the adults caring for her. If parental care is inadequate, however, the child learns that not only are adults untrustworthy, but she is also left with a sense of being flawed within herself and that her own instincts are not to be trusted. This would set the stage for later problems regarding hunger and appetite, thus potentially predisposing her to AN. However, AN itself would only manifest in the adolescent stage of life, Erikson’s Stage 5, which is concerned with establishing one’s identity (Maddi, 1989). Dissociation Torem (cited in Grave, Oliosi, Todisco, & Bartocci, 1996) has suggested that dissociation is responsible for a range of eating disorders. Dissociation results from the person experiencing a traumatic or abusive event or multiple events, including (but not limited to) childhood abuse. In dissociation, part of the person’s consciousness becomes split off from the rest of her awareness, which can lead to a range of problems in terms of impulse control, memory and sense of identity (Grave et al, 1996). Impulse control problems include sexual revictimization or sexual risk-taking, self-mutilation, substance abuse, and eating disorders. Cognitive theories People with AN tend to think that they are much fatter than they really are, and/or to feel that they are unattractive physically. The way that they think about themselves drives them to try and becoming more attractive by losing weight (Rosen, Reiter, & Orosan, 1995). Other cognitive characteristics of these patients are that they tend to be perfectionists, and may keep standards that are pathologically high, and they may be compulsive or obsessive (Wonderlich, Lilenfeld, Riso, Engel, & Mitchell, 2005). Fairburn, Cooper and Shaffran (2003) propose a “transdiagnostic” model which relies on a cognitive-behavioral approach to anorexia and bulimia. They propose that there are four processes which maintain severe eating disorders, namely the person’s perfectionism, her low self-esteem, her inability to manage or tolerate her own moods (also in Grave et al., 1996), and problems in interpersonal relations (Fairburn et al., 2003). Sociocultural models About 90% of AN patients are female (Lask & Bryant-Waugh, 2000). Feminist writers, in particular, adopt a socio-cultural approach towards AN. They believe that all women—in the westernized world at least—are subjected to undue pressure to be thin, and the problem thus lies at the sociocultural level rather than being a fault or vulnerability within the individual or her family. Slenderness is seen as an ideal for the female body, and thin women are glamorized in the media far more than women of normal weight or overweight (Tiggermann & Pickering, 1996). Young girls are easily impressed by these cultural models of beauty, and may aspire to become similar to them. Until recently, it was thought that AN occurred only or mostly in whites and in middle to upper income groups, and that girls and women from other cultural or economic groups did not experience the same pressures towards being thin, or did not internalize such high levels of self-criticism and perfectionism. However, this perception may be due to the fact that most studies have focused on whites and on more wealthy subjects. These days AN is certainly found in members of minority groups, as well as among people from less economically privileged backgrounds (PBS website). Research evidence for the various theories of anorexia nervosa Psychodynamic models Psychodynamic models of AN are difficult to research empirically, and tend to be based on in-depth case studies (Maddi, 1989). The systems theory of family dysfunction has sometimes been supported by empirical research and at other times not (Spannuth, 2006). According to several researchers, in general it does appear that most families of anorexic patients are quite dysfunctional, and tend to be enmeshed (i.e. family members are overly involved with each other), perfectionistic, and unable to express warmth or to resolve conflicts (Spannuth, 2006; Newsome & Schettler, 2004). Parents of girls who develop anorexia may be insecure, tend to feel victimized, may have poor impulse management, show poor styles of communication, and may have weak interpersonal boundaries (Spannuth, 2006). However, there is the problem of establishing causality: does having an anorexic child in the family somehow increase these familial and parental problems, or do these tendencies predate the anorexia and give rise to it? This question has not been answered satisfactorily through empirical research. According to Spannuth, an additional problem is that studies involving families of anorexics tend to have small sample sizes, and the operationalization of the variables is often complex or inconsistent (for example, asking the patients’ viewpoints versus the parents’ viewpoints). There is scope for far more empirical research into anorexics’ family characteristics in the future. Psychosocial life stages Some empirical support exists for Erikson’s stage theory, although it is indirectly related to the theory itself. Grave et al. (1996) state that one of the main problems which their anorexic subjects reported concerned issues of identity and a sense of being fragmented. This supports Erikson’s conceptualization of Stage 5, adolescence, during which a person either manages to create a stable and coherent sense of personal identity or fails to do so. It appears that people with AN and other eating disorders struggle with the tasks of this stage, and this is may be why AN often manifests in adolescence or early adulthood. Dissociation In terms of Torem’s theory of dissociation as a psychological cause of anorexia, people with AN do, as a group, report higher levels of childhood abuse than do members of non-clinical populations (Grave et al., 1996). However, a traumatic childhood or childhood sexual abuse was reported more often in patients with binge-eating or purging-type AN, and in bulimia nervosa patients, than in patients with restricting-type (“starvation”) AN (Grave et al., 1996). Cognitive theories Jansen, Smeets, Martijn and Nederkoorn (2006) examined the hypothesis that people with eating disorders have a distorted body image or internalized picture of themselves. Surprisingly, they found that in fact it appears that people with eating disorders perceive themselves quite objectively, since their self-perceptions tend to agree with the ratings of their bodies as given by neutral judges or raters. In contrast, control or normal participants perceived themselves as being far more attractive than the judges or raters perceived them as being. Thus, although it is true that people with eating disorders rate their own appearance very harshly, it cannot be said that they suffer from cognitive bias. It is non-eating-disordered people who appear to suffer from such bias, but in an overly positive direction which allows them to feel good about themselves (Jansen et al., 2006), which means that they see no need to alter their body weight. Sociocultural models Toro, Salamero, and Martinez (1994) found evidence that anorexic girls were more involved in, or exposed to, sociocultural influences that emphasize thinness than were non-anorexic girls. Garner and Garfinkel (1980) studied girls and women who were involved in dancing or modeling and determined that women in these professions—in which slenderness is stressed—were far more likely to develop AN at some point. Research evidence for genetic vulnerability Bulik, Sullivan et al. (2006) state that the development of AN is linked with a predisposition towards neuroticism, which in turn has genetic influences. Bulik, Reba, Siega-Riz and Reichborn-Kjennerud (2005) state that there is a genetic risk for AN, but that this needs to be “activated” by environmental events or factors after birth. Wade, Bulik, Neale and Kendler (2000) carried out a study of more than 2,000 female twins, and concluded that the heritability of AN is around 58%. However, they were not able to completely control for the effect of shared environmental influences on the twins, and the number of participants who were actually anorexic in the study was small. Furthermore, they concluded that the high rate of comorbidity between depression and AN may be partly due to the same genetic factors. Klump, Kay and Strober (2001) report that research has clearly indicated a genetic vulnerability to AN, and that at least 50% of the variance in eating disorders is accounted for by genetic influences. They state that anxiety disorders, as well as depression, are often comorbid with AH, and that these problems may all share a common genetic base. Klump et al. pinpoint certain specific genes, as well as ovarian hormones, as worthy of further investigation in AN studies. Further genetic research might examine the role of neurotransmitters, especially serotonin, in the development and maintenance of AN, and try to discover if the serotonin imbalances that that appear to be associated with AN (Kaye, Frank, et al., 2005; Kaye, Bailer, Frank, Wagner, & Henry, 2005) have a genetic basis. Studies have found that serotonin levels are abnormal in people with AN and that the abnormality persists after the illness has gone into remission. This suggests that brain function may be disturbed in people who are prone to developing AN. Serotonin is involved in many behaviors which are affected in AN, such as hunger, impulse control, mood regulation, depression and anxiety, and harm avoidance (Kaye, Bailer, et al., 2005). The presence of stress indicators such as the hormone cortisol might also be examined in terms of genetic risk. Interplay of genetic and psychological factors It is clear from the above review that there is no single or simple cause of AN. Individuals differ in their genetic vulnerability to the disease, while those who are vulnerable are exposed to varying degrees of risk. For example, involvement in careers such as dancing or modeling implies a higher exposure to glamorized underweight models, and might result in a vulnerable individual developing AN in an attempt to emulate those models. Thus it is probably true that not all genetically vulnerable people will become anorexic. By the same token, about half of people who do become anorexic do not appear to have a genetic vulnerability to the illness. In these cases, other influences, such as personality, emotional, cognitive-behavioral, familial, social, cultural, religious or other variables (including, for some, childhood sexual abuse or trauma) will play a more important role in the development of the illness. References Bulik, C.M., Reba, L., Siega-Riz, A.M., & Reichborn-Kjennerud. 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