Conceptualizing Bulimia as Addiction: A Resident’s Personal Experience

I became obsessed with staying thin in Junior High. I joined cross-country in high school, principally as a weight-loss strategy. I graduated high school weighing 144 pounds. Thirteen years later, I entered residential treatment for an eating disorder, weighing 115 pounds at 6 feet of height.

Now in recovery, I consider myself well acquainted with eating disorders. I spent 10 years prior to residential treatment bulimic, with intermittent anorexia. The 2 months before treatment I was vomiting three times every day, hours at a time. I was spending more than $100 every day on food. At that point I believe that I was struggling not only with a “feeding and eating disorder” (1), but also with a behavioral addiction, an addiction that involved “poor emotional and behavioral regulation and the development of rewarding, but maladaptive, habitual behaviors” (2). DSM-5 describes addiction as a “problematic pattern” of behavior “leading to clinically significant impairment or distress” (3). I was an impaired, distressed individual suffering from bulimia.

The Director of the National Institute on Drug Abuse, Nora Volkow, along with Roy Wise (1), stated that “choice is initiated in part by means of the prefrontal cortex.” Berner and Marsh (2) implicated the prefrontal cortex in the pathophysiology of bulimia, arguing that “developmental trajectories of self-regulatory and reward-based learning functions, and the overlapping frontostriatal circuits (originating in the PFC) that support these capacities, deviate from normal in bulimia (4).” While there is no clear evidence to date to support this argument, Berner and Marsh used neuroimaging studies to show that the number of binge/purge episodes in individuals with bulimia is inversely associated with prefrontal cortex activity (2). Research is only beginning to characterize the specialized brain circuits of those with eating disorders (4). The interplay of gene expression, neurotransmission, and cortical function in eating-disordered individuals is complex. What has been consistently observed in reviews of the literature and research is that persons with bulimia tend to show enhanced impulsivity and impaired inhibitory control (5, 6). I was very impulsive and felt “out-of-control” in my behaviors.

Analogous to the addicted individual who, by DSM-5 criteria, must dedicate a “great deal of time” in pursuit of his or her addiction, my behaviors consumed a large number of waking hours. My concentration and memory suffered. My focus targeted what would go in and out of my mouth and when and where my next binge/purge could happen. This focus, or anticipation, helped alleviate some of the anxiety and dysphoria I felt between each binge/purge cycle. Kalivas and Volkow (7) stated that when “stimuli predicting drug availability are presented,” there is activation of the nucleus accumbens. Similarly, functional MRI studies using food stimuli in adults with bulimia show activation of the nucleus accumbens. These parallel findings suggest a similarity in the neural circuits involved in anticipating substances in individuals suffering from addiction and from those with bulimia.

Despite “persistent or recurrent social or interpersonal problems caused or exacerbated by the effects” of my eating disorder, I continued to engage in the behaviors (3). My marriage suffered. I lost contact with family members and became a recluse at work. I endured instead of enjoyed relationships. One Christmas morning, I left my family to go indulge in behaviors in a parking lot. I remember the steaming vomit drilling a hole into the snow.

I knew I had persistent physical and psychological problems related to my behaviors, but I continued in them. My parotid glands swelled. My voice was hoarse. I felt sharp, right-sided periscapular pain following purges. I felt heart palpitations. I had bilateral lower extremity edema, was always faint, and felt depressed all the time except when in a binge/purge episode.

Like with any addiction, I developed tolerance for my behaviors. My initial binges consisted of around two thousand calories over 30 minutes. Over the years, I needed to consume more calories for longer periods to achieve the same sense of control, emotional numbness, and euphoria. A 30-minute binge and purge cycle, once satisfying, became a disappointing experience. I needed more time and food. Philip Seymour Hoffman, who died from a drug overdose, explained this phenomenon in an interview on Fresh Air:

Eating just one cookie at a social event was “not a great pleasure.” If I could not binge and purge the whole plate of cookies, I was irritated.

The “withdrawal” I experienced following behaviors aligns with addiction literature that details signs of withdrawal common to every abused substance, for example, signs of anxiety, irritability, dysphoria, malaise, hyperkatifeia (hypersensitivity to emotional distress), and alexithymia (9). My wife witnessed these signs in me first-hand.

In-vivo microdialysis reveals decreases in dopaminergic and serotonergic transmission in the nucleus accumbens during substance withdrawal (9). Research with rats using analogous protocols demonstrates increased dopamine levels in the nucleus accumbens compared to controls during sucrose binges (6). Additionally, underweight rats showed enhanced dopamine release with sucrose binges (10). Such findings could implicate neurochemical reward systems in bulimic persons that act to drive behaviors. I remember feeling abnormally euphoric, to the point of laughter, when eating food after prolonged fasting. Perhaps I experienced enhanced dopamine surges during these episodes.

I experienced psychosomatic relief when bingeing. My physical weakness abated, my parotid glands decompressed, my gastrointestinal pain dissolved, and my anxiety and depression subsided. Volkow and Wise (1) suggested that just as there are “neuroadaptations … documented in the opioid system on the cocaine abuser and in alcoholics ….[P]reclinical studies show adaptations in the opioid system after administration of palatable foods.” The opioid system may explain the analgesic effect of my binges on such “palatable foods.”

The constant eating calmed and soothed me. I felt excited when I saw a whole cake in front of me, ready for consumption. I felt many times a sense of “well-being, confidence and euphoria,” especially when eating 20 consecutive Big-Macs (3). I felt that I could accomplish great things and that everything would be okay. Dysphoria almost always followed my binge/purge episodes, along with physical exhaustion.

I required inpatient treatment to break a tortuous cycle of preoccupations, binges, negative affective states, and more preoccupations—the addicted person’s cycle (3). I needed 24-hour supervision, locked bathrooms, and weight restoration before I could engage in therapy.

In recovery, I met with other substance abusers in 12-step groups. The thoughts driving my disordered behaviors closely resembled the thoughts driving the behavior of a substance abuser.

My binges/purges eased my psychological pain the same way substances ease the pain of an individual with a substance use disorder. Those with eating disorders can find meetings with a 12-step focus across the country.

Relapse is a real part of substance abuse and eating disorders. The high relapse rates may relate to long-standing brain changes resulting from chronic substance use or feeding behaviors (11). Interestingly, studies show that substance abuse in fathers of persons with bulimia is associated with poorer outcomes (11, 12). Perhaps the same neurocircuitry that genetically predisposes to addiction underlies the development of bulimia nervosa.

Treatment Implications

When treating a patient with bulimia, it is important to remember that cognitive-behavioral therapy (CBT) remains the first-line approach (13). Pharmacotherapy can be a powerful second-line adjunct. Selective serotonin reuptake inhibitors are the first-line agents of choice. Fluoxetine at 60 mg/day is the most studied of all SSRIs and has shown efficacy in reduction of symptoms compared to placebo in two large randomized control trials (13). It is well tolerated and demonstrates efficacy in maintenance past one year of treatment. Fluoxetine is the only Food and Drug Administration-approved agent for treatment of bulimia.

SSRIs have been shown to decrease impulsivity. In my own experience, I felt less impulsive during CBT while on fluoxetine. I felt more able to overcome urges and instead attend weekly 12-step groups, such as Eating Disorders Anonymous, or call my sponsor. For treatment of substance abuse, the emphasis is on psychodynamic psychotherapy, CBT, motivational enhancement, and 12-step facilitation, all of which are considered more efficacious in the long-run than pharmacotherapy alone (11). The same approach is most efficacious for treatment of eating disorders.

The American Society of Addiction Medicine (14) describes addiction as “reflected in an individual pathologically pursuing reward and/or relief by substance use and other behaviors.” I offer this review of the literature and my personal experience to support the idea that an eating disorder, specifically bulimia, may be conceptualized as an addiction when considering the patient and proposed treatment modalities.

Key Points/Clinical Pearls