Eating Disorders and Impulse-Control Disorders

By WHITBOURNE, S.K., Halgin, R.P

Edited by Paul Ducham


Clinicians diagnose an individual as having anorexia nervosa (AN) when he or she shows three basic types of symptoms: severely restricted eating, which leads the person to have an abnormally low body weight, intense and unrealistic fear of getting fat or gaining weight, and disturbed self-perception of body shape or weight. In other words, people with this eating disorder restrict their food intake, become preoccupied with gaining weight, and feel that they are already overweight even though they may be seriously underweight. DSM-IV-TR currently requires that the individual “refuse” to eat or maintain body weight. The DSM-5 authors recommend changing this to the more behaviorally oriented term “restriction.” DSM-IV-TR uses “intense fear” of gaining weight as a criterion, but DSM-5 would add the option that emphasizes behavior (“persistent behavior that interferes with weight gain”). DSM-IV-TR also includes amenorrhea (cessation of menses) as a criterion, but the DSM-5 authors suggest removing this because not all women with the disorder experience disturbed menstrual periods—or they may be pre-adolescent or post-menopausal.
        Within the AD category, clinicians may classify individuals as “restricted type,” meaning that they do not engage in binge eating and “binge-eating/purging type,” which means that they do. Currently, the DSM-IV-TR categorizes individuals as one of these two types based on the symptoms that they show while they are undergoing assessment. The DSM-5 authors propose basing the subtype on behavior that an individual has shown over the past 3 months, which is consistent with the subtyping that clinicians use for binge-eating disorders.
         The depletion of nutrients that occurs in people with anorexia nervosa leads them to develop a series of health changes, some of which can be life threatening. Their bones, muscles, hair, and nails become weak and brittle, they develop low blood pressure, slowed breathing and pulse, and they are lethargic, sluggish, and fatigued. Their gastrointestinal system functions abnormally and they may become infertile. Most seriously, their heart and brain suffer damage and they may experience multiple organ failure. These changes can have fatal consequences. A 35-year follow-up of over 500 individuals with AD yielded a mortality estimate of 4.4 percent (Millar et al., 2005). Although the majority of deaths from AD occur in young adults, a Norwegian study of AD–related deaths found that 43 percent of the deaths occurred in women age 65 and older (Reas et al., 2005). Women with AD die not only from the complications of their disorder, but from suicide. The highest rates of suicide attempts (25 percent) occur in women who have comorbid depression and the binging/purging form of the disorder (Forcano et al., 2011).
             People who have AD experience a core disturbance in their body image. They are dissatisfied with their bodies and believe that their bodies are larger than they really are. In one fMRI study, women with anorexia nervosa showed distinct arousal patterns in areas of the brain involved in processing emotion (Mohr et al., 2010). Women with AD also seem to engage in social comparison processes when they view other women’s bodies. An fMRI study compared women’s limbic system activation with AD when seeing their own and other women’s bodies. Their amgydala showed greater activation at viewing other women’s bodies (Vocks et al., 2010). Women with the restrictive form of AD appear not to value thinness so much as they are repelled by the idea of being overweight (Cserjési et al., 2010).
         The lifetime prevalence of AD is 0.9 percent for women and 0.3 percent for men. In addition, people with anorexia nervosa have higher rates of mood, anxiety, impulsecontrol, and substance use disorders. The majority of individuals who develop anorexia nervosa between their early teenage years and their early 20s have the disorder for 1.7 years. Men have 25 percent lower lifetime prevalence than women (Hudson, Hiripi, Pope, & Kessler, 2007).


People with the eating disorder bulimia nervosa engage in binge eating during which they eat an excessive amount of food during a short (e.g., 2 hours) period. During these episodes, they feel a lack of control, which makes them feel that they cannot stop eating or regulate how much they eat. In order to avoid gaining weight, they then engage in purging, during which they compensate for the added calories through inappropriate methods such as self-induced vomiting, misuse of laxatives, diuretics or other medications, and fasting or excessive exercise. In addition to engaging in these behaviors, they base their self-evaluation on how much they weigh and their body’s shape. To receive a bulimia nervosa diagnosis, these episodes must not occur exclusively during episodes of anorexia nervosa.
     DSM-IV-TR specifies that the binge eating and purging must occur at least two times a week for 3 months. However, based on evidence that people close to the diagnosis of bulimia nervosa engage in fewer episodes per week (Wilson & Sysko, 2009), the DSM-5 authors are recommending changing the frequency criterion to once per week. Currently, clinicians assigning a diagnosis of bulimia nervosa distinguish between subtypes called “purging” or “nonpurging.” In DSM-IV-TR, people who have the purging type are the ones who induce vomiting, administer an enema, or take laxatives or diuretics. Those who receive the nonpurging diagnosis try to compensate for what they eat by fasting or engaging in excessive exercise. Again, though, the DSM-5 authors found evidence that this was not a valid distinction and are recommending its removal (van Hoeken, Veling, Sinke, Mitchell, & Hoek, 2009).
          Individuals with bulimia nervosa develop a number of medical problems. The most serious of these problems are those that occur with purging. For example, ipecac syrup, the medication that people use to induce vomiting, has severe toxic effects when one takes it regularly and in large doses. People who induce vomiting frequently also suffer from dental decay because the regurgitated material is highly acidic. The laxatives, diuretics, and diet pills that people with bulimia use can have toxic effects. Some with bulimia nervosa also engage in harmful behaviors, such as using enemas, regurgitating and then rechewing their food, or overusing saunas in efforts to lose weight. In addition to the effects of dehydration that binging and purging cause, the bulimic individual runs the risk of permanent gastrointestinal damage, fluid retention in the hands and feet, and heart muscle destruction or heart valve collapse.
           The lifetime prevalence of bulimia nervosa is 1.5 percent among women and 0.5 percent among men. Researchers estimate the prevalence of bulimia nervosa at any one time at 1.3 percent among college women, but binge eating (8.5 percent), fasting (8.1 percent), and excessive exercise (14.9 percent) are far more common. The majority (59.7 percent) of college women have concerns about their weight or body shape. These estimates have remained relatively stable over the 15-year period from 1990 to 2004 (Crowther, Armey, Luce, Dalton, & Leahey, 2008). Disordered eating patterns in college tend to improve over time. A 20-year follow-up of a college student sample of men and women showed that 75 percent no longer had symptoms in early midlife. However, 4.5 percent still had a clinically significant eating disorder (Keel, Gravener, Joiner Jr, & Haedt, 2010).
              Although bulimia nervosa is more prevalent in women, symptoms of the disorder are, nevertheless, present in men. An online survey of over 6,500 members of a health maintenance organization revealed that substantial percentages of men engaged in periods of uncontrolled eating (20 percent), binge eating at least once a week (8 percent), fasting (4 percent), laxatives (3 percent), exercise (6 percent) and body checking (9 percent). Women were more likely than men to show almost all of these behaviors, but there were no significant sex differences in the use of laxatives and exercise to avoid weight gain after a period of binge eating (Striegel-Moore et al., 2009).


Eating disorders reflect a complex set of interactions among an individual’s genetic vulnerability, experiences with eating, body image, and exposure to sociocultural influences. From a biological point of view, researchers are particularly interested in the role of dopamine, which plays a role in feelings of reward and pleasure including those feelings related to eating. According to this view, binge eaters feel relief from depression and anxiety, which, in turn, reinforces the binge-eating behavior. Like people who are dependent on substances, binge eaters experience withdrawal symptoms in between bingeing, continue to binge even though they know it is harmful, feel compelled to engage in the behavior, and feel deprived when they cannot binge. Purging, in turn, would also have positively rewarding properties to these individuals who regard their own ability to stay thin with pride and pleasure (Broft, Berner, Martinez, & Walsh, 2011).
          Researchers have conducted studies of a mouse strain with a lethal recessive mutation that relates to immune functioning that leads to reduced food intake. This mutation may have a link to altered immune functioning in humans (Clarke, Weiss, & Berrettini, 2011). Research on anorexia nervosa genetics in humans has identified abnormalities involving serotonin and dopamine receptor genes that are concentrated in the limbic system and, therefore, may play a role in altering emotion regulation in individuals with anorexia nervosa. The abnormal processing of emotions in people with anorexia nervosa may also be related to variations in another gene that relates to neuroticism, depressive mood, and selective processing of emotional stimuli. Such abnormalities may be at the core of altered nonconscious emotion-related disturbances that influence the individual’s thoughts, feelings, and self-regulation of eating behavior (Hatch et al., 2010).
               Although clinicians have used SSRIs to treat individuals with anorexia nervosa, they appear to have limited effectiveness until they administer them after clients have reached acceptable weight levels (Holtkamp et al., 2005). Similarly, SSRIs have limited effectiveness in treating bulimia nervosa (Herpertz et al., 2011). However, obese individuals with binge-eating disorder (i.e., nonpurging bulimia) may benefit from a 6-month treatment with SSRIs (Leombruni et al., 2008).
             Given the mixed evidence for pharmacological interventions for eating disorders, clinicians regard psychotherapeutic methods as the methods of choice. Psychological perspectives to eating disorders focus on the core eating disorders’ symptoms of disturbances in body image, a collection of several components (Figure 14.1). The cognitive-affective component involves attitudes and aff ects about one’s own body. The cognitiveaff ective component of body image includes evaluation of one’s own appearance (satisfaction or dissatisfaction) and the importance of weight and shape for an individual’s self-esteem. The perceptual component of body image includes the way individuals mentally represent their bodies. Individuals with eating disorders typically overestimate their own body size. The behavioral component includes body checking, such as frequent weighing or measuring body parts, and avoidance, which is the wearing of baggy clothing or avoiding social situations that expose the individual’s body to viewing by others (Ahrberg, Trojca, Nasrawi, & Vocks, 2011).
               Psychological treatments for eating disorders that follow this model take a multifaceted approach to targeting changes in body image. The primary aim of treatment involves identifying and changing the individual’s maladaptive assumptions that occur with his or her body shape and weight. In addition, clinicians attempt to reduce the frequency of such maladaptive behaviors as body checking and avoidance (Hrabosky, 2011). In cognitive-behavioral therapy, clinicians attempt to change what are selective biases in people with eating disorders that lead them to focus on the parts of their bodies they dislike. Second, by using exposure therapy in which clients view their own bodies (“mirror confrontation”), clinicians attempt to reduce the negative emotions that they would ordinarily experience. Behavioral interventions focus on reducing the frequency of body checking. Third, clinicians can address the component of body image involving size overestimation by helping clients view their bodies more holistically in front of a mirror, teaching them mindfulness techniques to reduce their negative cognitions and affect about their bodies, and giving them psychoeducation about the ways that their beliefs reinforce their negative body image (Delinsky, 2011).
          Within the sociocultural perspective, clinicians use interventions incorporating a family component for clients with eating disorders who are still in their teens and who have had symptoms for only a brief time. In the so-called “Maudsley model,” families enter treatment for 10 to 20 sessions over a 6- to 12-month period. In the first phase of treatment, parents completely take charge of their child’s eating and weight while they receive coaching in finding effective means of doing so. Gradually, the child can regain his or her autonomy. Although the Maudsley model has not withstood the test of controlled studies in terms of effectiveness compared to individual therapy, there are reasons for adopting this approach, particularly because it is so available on a widespread basis (Wilson, Grilo, & Vitousek, 2007).

Figure 14.1


People with impulse-control disorders repeatedly engage in behaviors, often ones that are harmful, that they feel they cannot control. Before they act on their impulses, these individuals experience tension and anxiety that they can relieve only by following through on their impulses. After acting on their impulses, they experience a sense of pleasure or gratification, although later they may regret that they engaged in the behavior.


People with the impulse-control disorder kleptomania are driven by a persistent urge to steal. Unlike shoplift ers or thieves, they don’t actually wish to have the object, or the money that it’s worth. Instead, they seek excitement from the act of stealing. Despite the thrill that they get from stealing, people with kleptomania would rather not be driven to this behavior and feel that their urge is unpleasant, unwanted, intrusive, and senseless. Since they don’t really want or need the items that they steal, they don’t have specific uses for them and they may give or throw them away. In order to receive a diagnosis of kleptomania, clinicians cannot better account for the individual’s stealing by antisocial personality disorder, conduct disorder, or bipolar disorder (in a manic episode). Although shoplifting is relatively common, kleptomania appears to be far less so.
        Kleptomania has a number of significant effects on the individual’s life, not the least of which is the fear or actuality of arrest. In one study of 101 adults (73 percent female), 69 percent were arrested and 21 percent were incarcerated. Over half were arrested on two or more occasions. Their symptoms started when they were 19 years old, on average, and they shoplifted at least twice a week. The majority stole items of clothing, household goods, and grocery store items. To a lesser extent, they also stole from their friends, relatives, and places of employment. This study replicated those of smaller-scale investigations in reporting that people with kleptomania are likely to have high lifetime prevalence rates of co-occurring depressive disorders (43 percent), anxiety disorders (25 percent), other impulse control disorders (42 percent), and drug abuse or dependence (18 percent). Suicide attempts are common among people with kleptomania (Grant, Odlaug, Davis, & Kim, 2009).
         One reason kleptomania fits into the impulse-control disorders is that people with this disorder feel an urge or state of craving prior to stealing and a sense of gratification after they steal. Researchers believe that these features of kleptomania also bear similarities to substance dependence.
            Similar to tolerance, individuals with kleptomania report that they need to engage in increasingly riskier behavior in order to experience the same gratification. They also experience symptoms similar to withdrawal, in that in between episodes they experience insomnia, agitation, and irritability. Studies of the neurobiology of kleptomania suggest that, like substance abuse disorders, it occurs with altered dopamine, serotonin, and opioid receptor functions as well as changes in brain structures similar to those in people with cocaine dependence (Grant, Odlaug, & Kim, 2010).
         Naltrexone, a therapeutic medication that clinicians use in substance dependence treatment, appears to have value in treating people with kleptomania (Grant, Kim, & Odlaug, 2009). Cognitive behavioral treatments also are effective. These include covert sensitization, imaginal desensitization, systematic desensitization, aversion therapy, relaxation training, and helping clients find alternative sources of satisfaction (Hodgins & Peden, 2008).


People who have the impulse-control disorder known as pathological gambling are unable to resist recurrent urges to gamble despite knowing that the gambling will bring about negative consequences to themselves or others. The diagnosis of pathological gambling in DSM-IV-TR includes a set of criteria also seen in other impulse-control disorders and others that are unique to this disorder. The unique features of pathological gambling include behaviors seen when people engage in chasing a bad bet, lying about how much they have lost, seeking financial bailouts, and committing crimes to support their gambling.
          As venues for gambling continue to become available on a more widespread basis, including online gambling, the incidence of pathological gambling appears to be on the increase. Among countries with legalized gambling, lifetime prevalence estimates range from about 0.5 to as high as 3.5 percent of the adult population (Stucki & Rihs-Middel, 2007). In the United States, although the large majority of adults have gambled at some point in their lives, pathological gambling was estimated to be diagnosable in 0.6 percent. Moreover, the greater the number of occasions on which people gambled, the higher their chances of developing pathological gambling—with the highest prevalence occurring after people had gambled 1,000 times in their lives.
            Like other impulse control disorders, pathological gambling often co-occurs with other psychological disorders. The highest risk of developing pathological gambling occurs among people who engage in gambling on games involving mental skill (such as cards), followed by sports betting, gambling machines, and horse races or cock/dog fights (Kessler et al., 2008). Pathological gamblers who bet on sports tend to be young men who have substance disorders. Those who bet on slot machines are more likely to be older women who have higher rates of other psychological disorders and begin gambling at a later age (Petry, 2003). In general, women are less likely than men to engage in the type of gambling that depends on strategy, such as poker (Odlaug, Marsh, Kim, & Grant, 2011).
          People with pathological gambling also have high rates of other disorders, particularly nicotine dependence (60 percent), dependence on other substances (58 percent), mood disorder (38 percent), and anxiety disorder (37 percent). Mood and anxiety disorders are more likely to precede, rather than follow, the onset of pathological gambling (Lorains, Cowlishaw, & Th omas, 2011). Unfortunately, the likelihood of an individual always having symptoms of pathological gambling continues to predict gambling behavior. A follow-up of Vietnam War veterans showed that even after controlling for family genetics, education, substance dependence, and other disorders, the men most likely to have symptoms were the ones who showed symptoms 10 years earlier (Scherrer et al., 2007).
        As is true for kleptomania, pathological gambling seems to involve abnormalities in multiple neurotransmitters including dopamine, serotonin, noradrenaline, and opioid. The repetitive behaviors characteristic of this disorder may be viewed as resulting from an imbalance between two competing and relatively separate neurobiological mechanisms—those that are involved in urges and those that are involved in cognitive control (Grant, Chamberlain, Odlaug, Potenza, & Kim, 2010). There may also be genetic contributions, perhaps involving abnormalities in dopamine receptor genes (Lobo et al., 2010).
         Pathological gambling may develop in part because gambling follows a variable ratio reinforcement schedule when rewards occur, on average, every “X” number of times. This pattern of reinforcement produces behaviors that are highly resistant to extinction. Slot machines, in particular, produce payoffs on this type of schedule, maintaining high rates of responding by gamblers. Classical conditioning is also involved in maintaining this behavior, because gamblers learn to associate certain cues to gambling including their internal states or moods and external stimuli such as advertisements for gambling.
           Cognitive factors also play an important role in pathological gambling. People with this disorder seem to engage in a phenomenon known as “discounting of probabilistic rewards,” in which they discount or devalue rewards they could obtain in the future compared to rewards they could obtain right away (Petry, 2011). They also engage in other cognitive distortions many of which involve poor judgment of the probabilities that their gambling will lead to successful outcomes, as shown in Table 14.1.
          The biopsychosocial perspective seems particularly relevant for understanding pathological gambling. According to the pathways model, the genetic vulnerability interacts with the poor coping and problem-solving skills of the pathological gambler to make the individual particularly susceptible to early gambling experiences, such as having early gambling luck (“the big win”). These, combined with sociocultural factors can propel the individual into more serious symptoms. The pathways model predicts that there are three main paths leading to three subtypes of pathological gamblers. The behaviorally conditioned subtype had few symptoms prior to developing the disorder but through frequent exposure to gambling, develops positive associations, distorted cognitions, and poor decision making about gambling. The emotionally vulnerable pathological gambler had pre-existing depression, anxiety, and perhaps a history of trauma; gambling helps this individual feel better. The third type of pathological gambler has pre-existing impulsivity, attentional difficulties, and antisocial characteristics. For this individual, the risk of gambling provides thrills and excitement (Hodgins & Peden, 2008).
           Researchers are beginning to investigate the possibility of treating pathological gambling with medications that target particular neurotransmitters. One set of medications are the opioid-acting medications to reduce the urge to drink in people with alcohol dependence, such as naltrexone and its long-acting form, nalmefene (Grant, Odlaug, Potenza, Hollander, & Kim, 2010). Another medication that shows promise is memantine, used as a treatment for Alzheimer’s disease. People with pathological gambling showed improved cognitive control presumably due to the medication’s effect on glutamate receptors (Grant, Chamberlain, et al., 2010).
        Based on the pathways model, even if a medication is found that can reduce pathological gambling, individuals with this disorder would nevertheless require psychosocial interventions. Although many gamblers turn to help from Gamblers Anonymous, there are few studies of its efficacy. The most thoroughly studied intervention is cognitivebehavioral therapy. A typical cognitive-behavioral treatment would involve these steps. First, the clinician teaches clients to understand the triggers for their gambling by having them describe their pattern of gambling behaviors. For example, common triggers include unstructured or free time, negative emotional states, reminders such as watching sports or advertisements, and having some available money. The clinician would also ascertain the times when clients do not gamble. Clinicians use this information to help their clients analyze the times they gamble and the times they do not. Following this assessment, clinicians continue in subsequent sessions to work on helping their clients increase pleasant activities, think of ways to handle cravings or urges, become more assertive, and correct their irrational cognitions. At the end of treatment, clinicians would help prepare their clients for setbacks using relapse-prevention methods (Morasco, Ledgerwood, Weinstock, & Petry, 2009).

Table 14.1


People with pyromania deliberately set fires, feel tension and arousal before they commit the act, are fascinated with and curious about fire and its situational contexts, derive pleasure, gratification, or relief when setting or witnessing fires or while participating in their aftermath. To be diagnosed with pyromania, the individual must not set fires for monetary reasons or have other medical or psychiatric conditions. Arson is deliberate firesetting for an improper purpose (e.g., monetary gain), and an arsonist does not experience the relief shown by people with pyromania. Among hospitalized psychiatric patients, 3.4 percent had current symptoms and 5.9 percent had lifetime symptoms consistent with a diagnosis of pyromania (Grant, Levine, Kim, & Potenza, 2005). The majority of people with pyromania are male. Pyromania appears to be rare, however, even among arsonists. Among a sample of 90 repeated offenders, Finnish researchers found that only 3 met the DSM-IV-TR criteria for pyromania (Lindberg, Holi, Tani, & Virkkunen, 2005).
          Pyromania appears to be a chronic condition if the individual does not receive treatment. Some individuals with pyromania, however, may switch to another addictive or impulsive behavior such as kleptomania or pathological gambling. An intensive study of 21 participants with a lifetime history of pyromania described the most likely triggers for their behavior as stress, boredom, feelings of inadequacy, and interpersonal conflict (Grant & Kim, 2007).
        As is true for the other impulse control disorders, pyromania may reflect abnormalities in dopamine functioning in areas of the brain involving behavioral addictions. Treatment for pyromania that follows the cognitive-behavioral model seems to show the most promise, however. The techniques used in cognitive-behavioral therapy for pyromania include imaginal exposure and response prevention, cognitive restructuring of responding to urges, and relaxation training (Grant, 2006).


A diagnosis of trichotillomania is given to individuals who pull out their hair in response to an increasing sense of tension or urge. After they pull their hair, they feel relief, pleasure, or gratification. People with trichotillomania are upset by their uncontrollable behavior and may find that their social, occupational, or other areas of functioning are impaired because of this disorder. They feel unable to stop this behavior, even when the pulling results in bald patches and lost eyebrows, eyelashes, armpit hair, and pubic hair. As individuals get older, they increase the number of bodily sites from which they pull hair (Flessner, Woods, Franklin, Keuthen, & Piacentini, 2009).
           People with this disorder experience significant impairment in areas of life ranging from sexual intimacy to social activities, medical examinations, and haircuts. They may also develop a range of physical symptoms including the development of hairballs (trichobezoars), which settle in their gastrointestinal tract, causing abdominal pain, nausea and vomiting, weakness, and weight loss. They can also develop skin infections, scalp pain or bleeding, and carpal tunnel syndrome. Psychologically, they may suffer low selfesteem, shame and embarrassment, depressed mood, irritability, and argumentativeness. Their impairments appear early in life and continue through to middle and late adulthood (Duke, Keeley, Geffken, & Storch, 2010).
         Diagnosable trichotillomania is relatively rare, with an estimated current prevalence rate of 0.6 percent of the community population. However, trichotillomania may be underreported because people with this disorder are secretive about what they are doing and tend to engage in hair-pulling only when alone (Duke, Bodzin, Tavares, Geffken, & Storch, 2009).
          In DSM-IV-TR, trichotillomania is included in the category of impulse-control disorders, but in DSM-5, it will move to the category that includes obsessive-compulsive and related disorders. In addition, the name will change to hair-pulling, which the DSM-5 authors concur will be a better description of the disorder than calling it a “mania,” which they regard as inappropriate for this disorder.
           There may be two types of hair-pulling. In the “focused” type, which may account for one-quarter of cases, the individual is aware of having the urge to pull, and may develop compulsive behaviors or rituals to avoid doing so. In “automatic” hair-pulling, the individual is involved in another task or is absorbed in thought while engaging in the behavior. Individuals who fall into the automatic category of hair-pulling experience pronounced stress and anxiety. For people in the focused type, depression and disability are also likely to occur along with stress and anxiety (Duke et al., 2010).
          Heritability seems to play an important role in trichotillomania, with an estimated 80 percent heritability (Novak, Keuthen, Stewart, & Pauls, 2009). Abnormalities in a gene on chromosome 1 known as SLTRK1 may play a role in the disorder; this gene is also linked to Tourette’s syndrome (Abelson et al., 2005). Researchers have also identified abnormalities in SAPAP3, a gene related to glutamate which, in turn, is involved in obsessive-compulsive disorder (Zuchner et al., 2009). The neurotransmitters serotonin, dopamine, and glutamate are, in turn, thought to play a role in the development of trichotillomania (Duke, et al., 2009). Brain imaging studies of individuals with trichotillomania suggest that they may also have abnormalities in neural pathways in the brain involved in generating and suppressing motor habits; these pathways also seem to be involved in regulating affect (Chamberlain et al., 2010).
           Corresponding to these abnormalities in neurotransmitter and brain functioning, the regulation model of trichotillomania suggests that individuals with this disorder seek an optimal state of emotional arousal providing them with greater stimulation when they are understimulated, and calming them when they are overstimulated. At the same time, hair-pulling may bring them from a negative to a positive affective state. Using the Trichotillomania Symptoms Questionnaire (Table 14.2), researchers conducting an online survey found that individuals who engaged in hair-pulling experienced more difficulty controlling their emotions than those who did not. There were subgroups within those who engaged in hair-pulling. These subgroups varied in whether they were more likely to experience boredom vs. anxiety or tension and in the overall intensity of emotions they felt that seemed to drive them toward hair-pulling. The researchers suggested that these subgroups on the questionnaire seemed to correspond to the automatic vs. focused subtypes of the disorder (Shusterman, Feld, Baer, & Keuthen, 2009).
          Various pharmacological treatments for trichotillomania include antidepressants, atypical antipsychotics, lithium, and naltrexone. Of these, naltrexone seems to have shown the most promising results. However, the results of controlled studies are not compelling and do not seem to justify the use of medications when weighed against the side effects that can include obesity, diabetes, neurotoxicity, delirium, encephalopathy, tremors, and hyperthyroidism, among others (Duke et al., 2010).
          The behavioral treatment of habit reversal training (HRT) is regarded as the most effective approach to treating trichotillomania. Not only does this method prevent the side effects of medication, but it is more successful in reducing the symptoms of hair-pulling (Duke et al., 2010). However, for treatment-resistant individuals, a combination of medication and HRT may be required (Franklin, Zagrabbe, & Benavides, 2011).
            In HRT, the individual learns a new response to compete with the habit of hairpulling, such as fist-clenching. The key feature is that the new response is incompatible with the undesirable habit. When it was first developed several decades ago, HRT was given for only one session. Since that time, clinicians have extended the length of treatment and added several cognitive components, including self-monitoring and cognitive restructuring. For example, clients may learn to challenge their cognitive distortions such as their perfectionistic beliefs. Combining Acceptance and Commitment Therapy (ACT) with HRT is also shown to produce relief from hair-pulling symptoms. Cognitivebehavioral therapy can help in treating children and adolescents with trichotillomania, with very little alteration from the basic protocol used for adults. In one study, 77 percent of those who received treatment remained symptom-free after 6 months (Tolin, Franklin, Diefenbach, Anderson, & Meunier, 2007).

Table 14.2


The primary features of intermittent explosive disorder are aggressive outbursts in which individuals become assaultive or destructive in ways that are out of proportion to any stress or provocation. Their actions can cause serious physical harm to themselves, other people, and property. Like other impulse-control disorders, people with this disorder may feel a sense of arousal or tension just before having an outburst. Although they feel justified for their anger during the outburst, aft erwards they feel genuinely upset, regretful, bewildered, or embarrassed by their loss of control.
        An estimated 4 to 7 percent of people in the U.S. population have intermittent explosive disorder; of these, 70 percent have at least three outbursts per year with an average of 27 on a yearly basis (Kessler et al., 2006). People with this disorder are more vulnerable to a number of threats to their physical health, including coronary heart disease, hypertension, stroke, diabetes, arthritis, back/neck pain, ulcer, headaches, and other chronic pain (McCloskey, Kleabir, Berman, Chen, & Coccaro, 2010). People with this disorder often have co-occurring bipolar disorder, personality disorder such as antisocial or borderline, substance use disorder (particularly alcohol), and cognitive disorders.
           Intermittent explosive disorder appears to have a strong familial component not accounted for by any comorbid conditions associated with the disorder (Coccaro, 2010).
         Researchers believe that the disorder may result from abnormalities in the serotonin system causing a loss of the ability to inhibit movement (Coccaro, Lee, & Kavoussi, 2010). Other studies show altered EEG patterns that predispose individuals to these explosive outbursts (Bars, Heyrend, Simpson, & Munger, 2001).
        Faulty cognitions further contribute to the individual’s development of intermittent explosive disorder. People with this disorder have a set of negative beliefs that other people wish to harm them, beliefs that they may have acquired through harsh punishments they received as children from their parents or caregivers. They feel that, therefore, their violence is justified. In addition, they may have learned through modeling that aggression is the way to cope with conflict or frustration. Adding to these psychological processes is the sanctioning of violence associated with the masculine gender role, a view that would explain in part the greater prevalence of this disorder in men.
       Given the possible role of serotonergic abnormalities in this disorder, researchers have investigated the utility of SSRIs in treatment. Though effective in reducing aggressive behaviors, however, SSRIs only result in full or partial remission in less than 50 percent of cases (Coccaro, Lee, & Kavoussi, 2009). Mood stabilizers used in the treatment of bipolar disorder (lithium, oxcarbazepine, carbamazepine) also have some effects in reducing aggressive behavior but there are few well-controlled studies (Jones et al., 2011).
         Cognitive behavioral therapy can also be beneficial for individuals with this disorder. In one approach, a variant of anger management therapy uses relaxation training, cognitive restructuring, hierarchical imaginal exposure, and relapse prevention for a 12-week period in individual or group modalities. A controlled investigation of this model of therapy showed improvements in levels of anger, aggression, and depression that persisted for at least 3 months following treatment (McCloskey, Noblett, Deffenbacher, Gollan, & Coccaro, 2008).


The impulses that underlie the destructive or detrimental behaviors of people with eating and impulse control disorders seem to be ones that reflect an interaction of genetic, neurophysiological, cognitive, and social factors. Past psychological approaches to these disorders gave greater weight than is true now to psychodynamic theories; evidence-based treatment now seems virtually to mandate that clinicians use cognitive-behavioral treatment either alone or in combination with pharmacological interventions. Although the behaviors involved in these disorders maintain themselves, in some ways, through strongly reinforcing consequences, they do seem to respond to interventions that help people gain insight into thoughts that, ultimately, individuals can learn to control given appropriate treatment.