Regulating Satiety in Bulimia Nervosa: The Role of Cholecystokinin

Bulimia nervosa (BN) is a chronic and debilitating illness that is characterized by extreme alterations in eating patterns, including an irresistible urge to overeat followed most often by self-induced vomiting. BN’s core defining feature, repeated binge-eating episodes and the associated compensatory behavior, has a serious impact on the psychological and physiological well-being of this vulnerable and often chronic population. The fourth edition, text revision of the Diagnostic and Statistical Manual of Mental Disorders (American Psychiatric Association, 2000) identifies the cardinal feature of BN as binge eating, characterized as a “loss of control” during repeated episodes of eating excessively large amounts of food (American Psychiatric Association, 2000, p. 594). This is followed by inappropriate purging or nonpurging compensatory behaviors. Purging behaviors include self-induced vomiting, laxative abuse, diuretic abuse, and misuse of enemas. Nonpurging behaviors include fasting, strict dieting, or excessive exercising in an effort to maintain or lose weight. To meet diagnostic criteria, binge-eating and purging behaviors must occur at a minimum frequency of two times per week over the course of 3 months. This disorder often begins in adolescence and can persist through adulthood. Research suggests that BN is more common in young women than men, and is genetically linked (Bulik et al., 2003), with an estimated 1% lifetime prevalence (Hudson, Hiripi, Pope, & Kessler, 2007). Commonly, depression, anxiety, and substance use disorders co-occur with bulimia (Steinhausen & Weber, 2009) and can result in significant role impairment (Hudson et al., 2007) and a substantial economic burden (Simon, Schmidt, & Pilling, 2005). A pervasive devalued self-worth (including loathing of body weight and shape) is characteristic of BN. Common premorbid characteristics of impulsivity (Wolfe, Jimerson,& Levine, 1994), dysregulated emotions (Kaye, Bulik, Thornton, Barbarich, & Masters, 2004), low self-esteem, early menarche, dieting, and being criticized by others concerning their eating habits (Fairburn, Welch, Doll, Davies, & O’Connor, 1997) may contribute to the vulnerability and expression of this disorder. Individual risk factors can include genetic and familial vulnerabilities to dieting, obesity, psychiatric disorders, and substance misuse disorders (Fairburn & Harrison, 2003). Affected individuals are likely to maintain normal weight despite fluctuations and a decreased metabolic rate (Birketvedt et al., 2006). Food restriction and dieting generally precede episodes of binge eating; however, these attempts are generally futile against the cycle of repeated binge purge episodes (Beumont, 2002). Comorbid medical conditions ensue with persistent illness. Teeth can become eroded secondary to the direct repeated exposure to gastric acids following a vomiting episode (Milosevic, 1999). The most frequent compensatory behavior, self-induced vomiting (Reba et al., 2005), can further compromise electrolyte status, requiring careful monitoring of specific laboratory values to avert complications (Wolfe, Metzger, Levine, & Jimerson, 2001). Surprisingly, even when individuals affected by BN present for routine medical care and/or eating disorder-related symptomatology, this illness often goes undetected (Johnson, Spitzer, & Williams, 2001) as patients may underreport symptoms secondary to shame, guilt, and/or a desire to retain this aberrant eating behavior. Less than half of those affected by BN seek treatment (Hoek & Van Hoeken, 2003) and less than 50% of those in treatment achieve a full and lasting response (Fairburn, 2002; Steinhausen & Weber, 2009). For example, cognitive–behavioral therapy (the most widely accepted and studied) results in less than 50% of individuals achieving full remission, and the only one Federal Drug Administration-approved medication, fluoxetine, merits a 40% success rate (American Psychiatric Association Workgroup on Eating Disorders, 2006). Finally, outcome studies show that at least one third of individuals who previously recovered were likely to relapse and over two thirds maintain eating disorder symptoms of clinical severity (Fairburn, Cooper, Doll, Norman, & O’Connor, 2000).