Anorexia Nervosa

Research Paper Writeup

Glenn Booker  PSY101

Summer 2012

The research paper selected is: Attia, Evelyn.  (2010).  Anorexia Nervosa: Current Status and Future Directions.  Annu. Rev. Med. 2010. 61:425–35.  As a review paper, it summarizes many other papers, and does not present an experiment in detail, so the specific questions of interest can’t be addressed.

Anorexia nervosa (AN) is described in terms of its demographics, mortality rate, and history.  The two major types of AN are defined, restricting (R) and binge-purge (BP); the latter is distinguished from bulimia by low patient weight.  The epidemiology of AN is discussed; the lifetime prevalence rate is between 0.3 and 1.0% for men and women, but differences in reporting may be due to better recognition of the disease by physicians.

The phenomenology and course of illness are discussed in detail.  AN tends to be ego-syntonic (consistent with one’s sense of self), so patients don’t recognize symptoms as being anything wrong.  Weight loss or lack of normal weight gain with age is typically accompanied by “food restriction, secretive eating, vomiting or other purging after eating, and excessive exercise.” (all quotes from (Attia, 2010)) They often believe that they are fat, even when normal or underweight.  Females with AN sometimes experience amenorrhea (no period), but that is now less regarded as a meaningful symptom of AN.

Medically, AN slows the metabolism, causing bradycardia, hypotension, and hypothermia (slow pulse rate, low blood pressure, and low body temperature, respectively).  Lower levels of white and red blood cells (leukopenia, anemia) and electrolytes (hypokalemia (potassium), hyponatremia (sodium)) are often present as a result of purging or drinking large amounts of water.  Low levels of hormones (estrogen, testosterone) and low bone density (osteoporosis).  Changes in heart rhythm (prolonged QT interval) increases the chance of sudden death.  Hair loss and skin changes are common.

Psychological symptoms include “distractibility, depression, anxiety, agitation, sleep disturbance, obsessionality, and compulsivity,” but these are mainly a secondary result of severe caloric restriction.  Recovery from AN is too rare – of those seeking clinical treatment, recovery rates from 30% to 67% were reported by various studies, over time periods from 5 years to a median 90 months (7.5 years).  The mortality rate from AN was estimated at 5.6% per decade of illness, significantly higher than bulemia.

“Treatment for AN remains a challenge, as no treatment has clear empirical support.”  Problems with good evidence-based treatment experiments include:  rarity of patients with the illness, reluctance of patients to participate in a study to restore normal weight, and the use of complex and expensive treatment regimens.  The effectiveness of medical treatments is hard to assess, since they are done in conjunction with psychiatric treatments which are already known to be effective.  Antidepressants have not been shown to be effective in AN treatment compared to a placebo.  “Clinical trials of psychotherapies have failed to identify effective interventions for underweight adults with AN.”  For children and adolescents, family-based therapies have been shown effective, based on preliminary data.  Behaviorally oriented treatment programs with strong “psychosocial support and reinforcement” have been offered in many different settings, and there is some evidence of success. [Editorial comment:  they discuss using 3000-4000 cal/day diets in this context.  I can’t imagine a person with AN who could begin to eat that much!]  These programs can result in refeeding syndrome, an uncommon adverse effect that can cause severe fluid and electrolyte imbalances, and result in “congestive heart failure and acute mental status change.”

Relapse prevention is important because relapse rates are high (though not quantified).  One small study (n=32) found that, for patients with the same BMI after weight restoration, those with higher percent body fat were more likely to remain a treatment success.

The biological causes of AN remain unknown.  Twin studies have shown a genetic component to vulnerability to AN.  Studies have shown that “anxiety, obsessionality, and perfectionism appear to be associated with AN.”  Our only conclusion so far is that “the illness probably results from an interaction of genetic, developmental, and environmental factors.”  Other biological factors have been investigated (monoamine neurotransmitters, serotonin (controls appetite, also seen in OCD), dopamine (is dysregulated), norepinephrine) as contributing causes of AN.  The psychological traits of AN have led to study of “behaviors relevant to choosing, learning, and adapting” and have shown that “the ability to move back and forth between tasks or operations” (set shifting) is impaired in patients with AN.

These results have produced a model that integrates the biological and psychological aspects of AN (Figure 1), starting with predisposition to AN from high anxiety, obesessionality and perfectionism, amplified by our culture into rigid dieting practices, producing physical changes that strengthen the predisposition in a vicious cycle.

Figure 1.  A Possible Model for Anorexia Nervosa

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