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Anorexia and Bulimia: Cognitions, Etiology, Epidemiology, and Treatment

Paper Type: Free Essay Subject: Psychology
Wordcount: 2618 words Published: 18th May 2020

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Q2: Discuss ways that Anorexia Nervosa and Bulimia Nervosa are Similar and are Different. In Addition to Key Symptoms of the Disorders, Refer to Evidence of other Factors (e.g., Cognitions, Etiology, Epidemiology, Treatment) Associated with these Disorders.

Anorexia nervosa (AN) and bulimia nervosa (BN) are two of the four eating disorders within the DSM-5 feeding and eating disorders category (American Psychiatric Association, 2013). Despite this categorization, they may be considered psychosomatic illnesses as the interaction between cultural stressors and underlying biological vulnerabilities can generate the respective symptoms (Gwirtsman, Mitchell, & Ebert, 2008 There are some overlapping behavioural and psychological symptoms, however, there are distinct aspects separating each disorder (Gwirtsman et al., 2008

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The DSM-5 has three main diagnostic criteria for a diagnosis of AN and five main diagnostic criteria for BN (American Psychiatric Association, 2013). For AN these criteria are the restriction of energy intake resulting in a significantly low body weight; an intense fear of weight gain; and a disturbance in self-evaluation (American Psychiatric Association, 2013). For BN the criteria are recurrent binge-eating episodes; recurrent compensatory actions; that both actions occur on average, three times a week;a disturbance in self-evaluation; and that this disturbance is not exclusive to periods of AN (American Psychiatric Association, 2013). A key distinguishing criterion is body weight, which for an AN diagnosis must be a significantly low body weight. This is defined as weight lower than the minimally expected weight at that developmental time period (American Psychiatric Association, 2013). There is no corresponding weight criteria for BN so this diagnosis can occur, irrespective of whether the compensatory actions are resulting in a lower than expected weight.

The disorders are further differentiated symptomatically through the final criteria for a BN diagnosis within the DSM-5 (American Psychiatric Association, 2013). An AN diagnosis can occur with a binge-eating/purging type subtype, wherein the individual has engaged in episodic binge eating followed by self-induced purging behaviour (American Psychiatric Association, 2013). As such, a key distinction between disorders is the intense fear of weight gain (Black & Grant, 2014). This fear often results in a refusal to maintain a normal bodyweight. When this refusal occurs, the appropriate diagnosis is AN with a binge-purge subtype (Black & Grant, 2014).

The cognitions that maintain the symptoms in both AN and BN is a hyper-focus on weight and body shape, with an accompanied body image distortion (Tasca, 2018). There are often cognitive distortions surrounding food and eating as well (Black & Grant, 2014). Within the cognitive-behavioural model these cognitions create a self-schema with bias interpretations of external and internal cues (Williamson, White, York-Crowe, & Stewart, 2004).  Despite the overlap in the cognitions involved, the behaviours performed within this context differs between disorders (Black & Grant, 2014). AN is outlined as a sustained restriction of energy intake, whereas BN is more episodic in nature (Tasca, 2018).

There is immense overlap in the etiology of both disorders (Gwirtsman et al., 2008).  The cultural pressures within industrialized societies have led to an increase in the incidence of eating disorders within the 20th century (Gwirtsman et al., 2008). Sexual or physical abuse are also considered a risk factor for eating disorders, with approximately a third of patients presenting with pre-existing trauma (Gwirtsman et al., 2008). However, childhood sexual abuse, specifically, has been identified as a nonspecific risk factor for the development of BN but not AN(Rorty & Yager, 1996; Wonderlich, Brewerton, Jocic, Dansky, & Abbott, 1997).

Considerable evidence also indicates that underlying neurobiological vulnerabilities, particularly a serotonin disturbance, impact the onset and development of both AN and BN (Kaye, 2008). This disturbance may contribute to dysregulation of the emotional and reward pathways associated with feeding, creating a vulnerability to dysregulated feeding behaviours (Kaye, 2008). However, whether these biological markers are the cause or consequence of the eating disorders is yet to be determined (Gwirtsman et al., 2008).

There is immense overlap in executive functioning deficits within BN and AN (Eichen, Matheson, Appleton-Knapp, & Boutelle, 2017). Recent research indicates that both AN and BN are consistently impaired in most cognitive functioning domains (Weider, Indredavik, Lydersen, & Hestad, 2014). This impairment was most pronounced in individuals with AN, with impairment within BN tending to follow the same trends to a lesser extent (Weider et al., 2014).
Eichen et al. (2017), found that within BN, there is less emphasis placed on future reward, potentially maintaining bingeing behaviour (Eichen et al, 2017). This contrasts with AN as research indicates that individuals are able to delay rewards (Steinglass, Berkowitz, Simpson, Weber, & Walsh, 2012).This research is consistent with the excessive self-control individuals with AN are perceived to have, in contrast to the impulsivity often described within BN (Eichen et al., 2017; Gwirtsman et al., 2008).

The onset of both AN and BN tends to occur in early adulthood (17-21 years) however, recent research is indicating that the age of onset is decreasing (Smink, Hoeken, & Hoek, 2012). The incidence rates, expressed per 100 000 persons per year, for AN within primary care was 4.2 and 12.2 for BN (Turnbull, Ward, Treasure, Jick, & Derby, 1996). However, the disparity between incidence rates is thought to be caused by increased recognition rather than increased incidence (Turnbull et al., 1996).  A longitudinal study of the prevalence and course of eating disorders found that AN had a lifetime prevalence rate of 1.9%, whereas BN had a lifetime prevalence of 2.2% (Wade, Bergin, Tiggerman, Bulik, & Fairburn, 2006)

There are many different psychological treatment options for eating disorders, with remarkable progress being made over the past 25 years (Wilson, Grilo, &Vitousek, 2007). Within BN, a cognitive behavioural therapy (CBT) approach is the most evidence-based treatment option, eliminating binge-purge behaviour in roughly 30-50% of cases (Wilson et al., 2007). Within AN, a multidisciplinary approach with focus being paced on weight restoration for seriously underweight patients is essential (Gwirtsman et al., 2008). A longitudinal study found that young AN patients that were treated within speciality units appeared to have better outcomes than diagnosis and treatment as adults (Fitcher, Quadfleig, & Hedlund, 2006). Family therapy, especially for adolescent patients, is the most researched treatment method for AN (Wilson et al., 2007).

As a key criteria for AN is a refusal to maintain a normal bodyweight, treatment can be somewhat limited, with research showing that of anorexics that come to medical attention, fewer than half complete all treatment (Steiner, Mazer, & Litt, 1990). This is in strong contrast to research indicating that self-directed treatment in BN may be effective (Troop et al., 1996).

All classes of antidepressants have also demonstrated short-term efficacy in reducing BN symptoms (Gwirtsman et al., 2008). However, any long-term treatment benefit has only been demonstrated for psychotherapy and not medication alone (Zhu & Walsh, 2002). This is in contrast to AN, where no class of psychopharmacological medication has demonstrated efficacy outside of a structured, behaviour-focused program (Gwirtsman et al., 2008).

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Fitcher et al., (2006), conducted a longitudinal study of the course and outcome of AN. They found that 12 years after the beginning of therapy, 30% of their sample had received a diagnosis of AN again, or were currently diagnosed with AN. The study also had a mortality rate of 8.8% after the 12 year follow up (Fitcher et al., 2006). These statistics vary greatly from a similar longitudinal study conducted by Fitcher and Quadfleig (2004) into the course and outcome of BN. Within that study there was a mortality rate of 2% and 10% had a BN diagnosis at the 12 year follow up. In contrast to AN, BN remission rates increased between follow up interviews, whereas within AN, the mortality rate rose between follow up interviews (Fitcher et al., 2006; Fitcher & Quadfleig, 2004). These results are congruent with the opinion that AN is more a more chronic disorder than BN (Gwirtsman et al, 2008).


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  • Kaye, W. (2008). Neurobiology of anorexia and bulimia nervosa. Physiology & Behavior, 94, 121-135
  • Rorty, M., & Yager, J. (1996). Histories of Childhood Trauma and Complex Post-Traumatic Sequelae in Women with Eating Disorders. Psychiatric Clinics of North America, 19(4), 773-791.
  • Smink, F. R., Hoeken, D. V., & Hoek, H. W. (2012). Epidemiology of Eating Disorders: Incidence, Prevalence and Mortality Rates. Current Psychiatry Reports, 14(4), 406-414. doi:10.1007/s11920-012-0282-y
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  • Steinglass, J. E., Figner, B., Berkowitz, S., Simpson, H. B., Weber, E. U., & Walsh, B. T. (2012). Increased Capacity to Delay Reward in Anorexia Nervosa. Journal of the International Neuropsychological Society, 18(4), 773-780. doi:10.1017/s1355617712000446
  • Turnbull, S., Ward, A., Treasure, J., Jick, H., & Derby, L. (1996). The Demand for Eating Disorder Care. British Journal of Psychiatry, 169(6), 705-712. doi:10.1192/bjp.169.6.705
  • Troop, N., Schmidt, U., Tiller, J., Todd, G., Keilen, M., & Treasure, J. (1996). Compliance with a self-care manual for bulimia nervosa: Predictors and outcome. British Journal of Clinical Psychology, 35(3), 435-438. doi:10.1111/j.2044-8260.1996.tb01197.x
  • Tasca, G. A. (2018). Attachment and eating disorders: A research update. Current Opinion in Psychology,25, 59-64. doi:10.1016/j.copsyc.2018.03.003
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Personal Reflection:

I had originally decided to cover personality disorders as we had already covered these in lectures. However, after researching, I realised that I was more interested in eating disorders and changed topics. As we haven’t covered eating disorders in class, I had to do slightly more contextual research so I could understand the disorders before I started properly researching for the essay.

In comparison to the lab reports, I found researching this essay more difficult but having a longer page limit made it easier to include all key points. As all the information for the lab reports was discussed in class, any further research was a bonus. For the essay however, the research component was integral as we weren’t given a baseline understanding during lectures. Having a page limit of 5 pages was easier than the single page limit we had in labs. It felt like there was enough to go in depth about each important aspect of the essay.

I found researching the epidemiology difficult as many of the papers I found were either reviews or meta-analyses of epidemiology rather than individual research papers. I was unsure whether to include the statistics I found in these analyses or the statistics from individual longitudinal studies.

I found it difficult to find more recent research into eating disorders. Much of the recent research I found was on obesity and binge-eating disorder or eating disorder not otherwise specified. This made finding primary sources more difficult than I anticipated as a large portion of the research is older and now being included in meta-analyses and reviews. Some of the more fundamental research wasn’t available online and so in those cases I used meta-analyses and reviews of past research so I could still comment on the research.


  1. Wonderlch, Brewerton, Jocic, Dansky & Abott
  2. Rorty and Yager 


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