Anorexia Nervosa: Causes, Treatments, and Prevention

Introduction

Anorexia nervosa (AN) is attributed to many factors, including media images of ultra-thin models and actresses, family conflicts, and genetics. The first recorded case dates to 1689, suggesting that genetics and family dynamics have long played a role in the disorder (DeAngelis, 2002). Symptoms can include distorted body image, very low body weight, obsession with losing weight, fear of food and weight gain, excessive exercise, purging, and amenorrhea (Hatch et al., 2010). Anorexia is, of course, just one form of eating disorder; experts from the National Association of Eating Disorders claim that as many as 10 million Americans are suffering from some form of eating disorder "at any given time" (Novotney, 2009), and today it is estimated that up to 13% of patients are male. Anorexia often worsens over time or develops into bulimia, and its consequences can include osteoporosis, infertility, dental erosion, and death (Novotney, 2009).

This life-threatening illness is often difficult to treat, and much research has been devoted to determining its root causes and possible treatments. However, as Lock and Fitzpatrick (2009) have noted, until recently most psychological research has focused on adult patients rather than children or adolescents — a significant problem, because eating disorders most often develop during childhood and adolescence. Finding the best treatment for anorexia will likely require more intensive research on younger populations (Lock & Fitzpatrick, 2009). Moreover, this approach will likely yield a much higher treatment success rate, since the disorder can become highly resistant to improvement by the time a patient reaches adulthood (Lock & Fitzpatrick, 2009). "Nipping it in the bud" will likely require early intervention.

Etiology

Very recent research suggests that AN may be more genetically determined than previously thought (Hatch et al., 2010). One 2010 study found a link between AN and dysfunctions in emotional processing that are likely genetic in origin (Hatch et al., 2010). Other researchers believe the disorder has a genetic basis because the incidence rate is actually low given societal pressures to be thin, because it often runs in families, because it is resistant to treatment, and because it has a "typical age of onset" (Hatch et al., 2010).

There are also biological reasons why the habits involved in the day-to-day life of someone with AN are difficult to break. As Kanarek et al. found in a 2009 study on rats, food restriction leads to the need for increased exercise in order for the brain to produce sufficient endogenous opioids for feelings of well-being; in turn, this increased exercise becomes an addiction that leads to severe withdrawal upon discontinuation (Kanarek et al., 2009). In addition, self-starvation can produce addictive feelings of euphoria as the body "gives up" on receiving adequate nutrition and hunger decreases as a result of the release of internal opiates (Lucas, 2004).

In a study of over 2,100 female twins that hypothesized a link between AN, heredity, and a predisposition for depression, researchers found a 58% heritability estimate for comorbid depression with AN (Wade et al., 2000). However, regardless of the degree of genetic basis, the fact that AN so often begins in childhood or adolescence lends credence to therapeutic approaches that focus on family dynamics and the challenges of growing up. Researchers already know that family dynamics associated with AN include "enmeshment, rigidity, and lack of conflict resolution" (Rhodes et al., 2009).

Therapy

Family therapy has a consistently higher success rate among patients who have had symptoms of AN for less than three years, compared to individual therapy (Rhodes et al., 2009). Researchers first began studying family dysfunction as a cause of AN in the 1970s, and in the 1980s the Maudsley Hospital developed an integrative family therapy approach based on evidence from randomized control trials (Rhodes et al., 2009). This particularly effective approach was developed in the United Kingdom and promotes long-term success despite being a short-term, outpatient program (DeAngelis, 2002). In general, the Maudsley treatment approach calls for parents and siblings to take an active role in the patient's day-to-day eating habits and emotional support (Rhodes et al., 2009). Food intake must be increased gradually until menstruation returns; this step is followed by a reintroduction to normal adolescent activities such as socializing and dating (Rhodes et al., 2009).

Other forms of family therapy used to treat AN include structural, systemic, narrative, and multi-family approaches (Lock & Fitzpatrick, 2009). Individual psychotherapies utilized in the treatment of AN include psychodynamic, interpersonal, cognitive behavioral, developmentally oriented, cognitive remedial, and dialectical approaches (Lock & Fitzpatrick, 2009). In addition, nutritional therapy is often necessary to restore body and brain chemistry before meaningful improvement can take place (Lock & Fitzpatrick, 2009).

Conclusion

AN has proved a perplexing condition to treat successfully. This is likely due to a complex interplay between genetic, physiological, emotional, and social etiological factors. Fortunately, researchers are finding that prevention interventions are helpful for young girls at risk of developing the disorder, and the Maudsley family therapy approach is highly effective for teenagers after onset (DeAngelis, 2002). For adults with AN — estimated to constitute 35% of all cases — the prognosis is not as bright.

However, if prevention programs are successfully implemented as part of elementary, middle, and high school curricula, the number of new cases may decrease dramatically. Moreover, even when prevention does not succeed, successful application of the well-tested Maudsley family therapy method should keep many cases from progressing to the resistant adult phase. For existing adult cases, couples therapy may prove the most effective approach, since it takes advantage of day-to-day relationship dynamics in much the same way the Maudsley method does within families.

References

DeAngelis, T. (2002). Promising treatments for anorexia and bulimia. Monitor, 33(3), 38.

Hatch, A., et al. (2010). Emotion brain alterations in anorexia nervosa: A candidate biological marker and implications for treatment. Journal of Psychiatry & Neuroscience: JPN, 35(4), 267+.

Kanarek, R., et al. (2009). Running and addiction: Precipitated withdrawal in a rat model of anorexia. Behavioral Neuroscience, 123(4), 905–912.

Lock, J., & Fitzpatrick, K. (2009). Advances in psychotherapy for children and adolescents with eating disorders. American Journal of Psychotherapy, 63(4), 287+.

Lucas, A. (2004). Demystifying anorexia nervosa: An optimistic guide to understanding and healing. Oxford University Press.

Novotney, A. (2009). New solutions. Monitor, 40(4), 46.

Rhodes, P., et al. (2009). The Maudsley model of family-based treatment for anorexia nervosa: A qualitative evaluation of parent-to-parent consultation. Journal of Marital and Family Therapy, 35(2), 181+.

Wade, T., et al. (2000). Anorexia nervosa and major depression: Shared genetic and environmental risk factors. American Journal of Psychiatry, 157, 469–471.