Yvonne H. C. Yau, MSc, Sarah W. Yip, MSc, PhD, and Marc N. Potenza, MD, PhD
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Addiction is often described as having four defining components: (1) continued engagement in behavior despite adverse consequences; (2) diminished self-control over engagement in the behavior; (3) compulsive engagement in the behavior; and (4) an appetitive urge or craving state prior to engagement in the behavior. In its original formulation, the term was not linked to substance use but gradually became primarily associated with substance use behaviors. More recently, the term addiction has been increasingly applied to describe excessive engagement in nondrug behaviors, such as gambling, sex, and eating. Aided by data from neurobiologic studies, this view is gaining momentum and has led to the renaming of the “Substance-Related Disorders” diagnostic category to “Substance-Related and Addictive Disorders” in the DSM-5. Currently, only gambling disorder (previously referred to in the DSM-IV as pathologic gambling [PG]) has been included in this category by the American Psychiatric Association, who concluded that there is presently insufficient research to warrant the consideration of other “behavioral addictions” in the main section.
IMPULSE CONTROL DISORDERS: “BEHAVIORAL ADDICTIONS”?
Several disorders that may be considered as behavioral addictions have been traditionally categorized in the DSM as “impulse control disorders (ICDs) not elsewhere classified.” Among issues being considered within research workgroups are whether ICDs might be best categorized separately, with substance use disorders (SUDs) as addictions, or with obsessive–compulsive disorders (OCDs) as obsessive–compulsive spectrum disorders.
PATHOLOGIC GAMBLING
PG and SUDs share clinical characteristics and diagnostic criteria. Individuals with PG often experience withdrawal, craving, tolerance, and failed attempts to reduce or abate gambling behaviors—all common features of SUDs. They also share phenomenologic features: both often begin in adolescence and young adulthood; prevalence estimates tend to decrease across adulthood; and the phenomenon of “telescoping” whereby the time between initiation and problematic engagement in the addictive behavior is shorter in females than males is observed in both conditions. These commonalities, in addition to high comorbidity rates for PG and SUDs, suggest common vulnerability factors for both disorders.
Neurocognitive research provides evidence for dysregulation of the ventromedial prefrontal cortex (vmPFC) and orbitofrontal cortex (OFC) in individuals with PG. Impaired performance on risk/reward decision-making tasks and on neurocognitive tasks involving inhibition, time estimation, cognitive estimating, and planning tasks has been observed among individuals with PG and individuals with SUDs.
Individuals with PG often make disadvantageous decisions, selecting small immediate rewards over larger delayed rewards. The rapid temporal discounting of rewards has been termed “delay discounting,” as rewards are more steeply discounted as a function of delay duration. Poorer performance on delay discounting measures has been observed in multiple populations, including those with SUDs and PG.
Among the most widely implicated brain regions in subjective reward valuation is the nucleus accumbens (NAcc), situated in the ventral striatum, and the vmPFC—both of which are also frequently implicated in SUDs. Research suggests that dysregulation of the mesocorticolimbic dopamine system—often referred to as the “reward pathway” and frequently implicated in SUDs—may contribute to PG. In particular, corticostriatal and forebrain neuromodulatory systems are frequently implicated.
In recent years, multiple studies have investigated the neurostructural correlates of psychiatric disorders using either diffusion tensor imaging (DTI) or voxel-based morphometry (VBM) to assess white and gray matter structures, respectively. Findings from DTI studies indicate similar alterations in white matter microstructure encompassing regions of callosal, association, and projection fiber tracts among individuals with PG and SUDs. Preliminary VBM data suggested no alteration in gray matter macrostructures in PG, although more recent data indicate smaller amygdalar and hippocampal volumes, as have been reported in SUDs.
Serotonin (5-HT) neurons project from the raphe nucleus of the brain stem to multiple brain regions including the hippocampus, amygdala, and prefrontal cortex (PFC). It has been hypothesized that dysregulated 5-HT functioning may underlie behavioral inhibition and impulsivity in PG. Selective serotonin reuptake inhibitors (SSRIs) have been found to improve social functioning and reduce gambling behaviors and thoughts about gambling in PG, although clinical trial findings involving SSRIs have generally been mixed.
Dopamine (DA) is involved in the encoding of rewarding and aversive stimuli and is implicated in the neurobiology of drug addictions. DA may influence the clinical presentation of PG, although the precise manner is not completely understood.
Dysregulation of norepinephrine (NE)—a neurotransmitter implicated in arousal, attention, and sensation-seeking behavior—has been reported in individuals with PG. Data suggest that there may be an elevation of NE activity among individuals with PG, and this elevation may be potentiated by gambling behaviors.
Pharmacologic challenge studies suggest a dysregulation of the opioid system in PG. Naltrexone and nalmefene, both opioid receptor antagonists, have been found to reduce gambling-related thoughts and behaviors in individuals with PG.
Family and twin-based studies of addiction indicate that genetic factors are important in the development of both SUDs and PG. Twin data suggest that roughly 50% of the probability of developing PG is attributable to inherited factors. This heritability rate is similar to that observed for SUDs. Molecular genetic research has identified specific genetic alleles involved in the encoding of DA- and 5-HT–related moieties that are associated with PG, although negative results have also been observed.
BINGE EATING DISORDER
Data suggest that both substance use and eating behaviors may be modulated by the same motivational neurocircuitry, leading to the conceptualization of “foods as drugs.” Binge eating disorder (BED)—distinct from bulimia nervosa as it does not include compensatory behaviors such as purging—is associated with obesity and other negative sequelae. The diagnostic features of BED are very similar to those for SUDs and ICDs: recurrent episodes, impaired control, and marked distress in relation to binge eating.
Leptin, an adipose-derived hormone, is a chemical modulator involved in the maintenance of energy homeostasis and feeding behaviors; it has been implicated in other reward-seeking behaviors including SUDs. Administration of leptin replacement treatment in individuals with leptin deficiency syndrome, a rare condition in humans, has decreased hyperphagia and reduced activation of reward centers such as the NAcc during feeding conditions, suggesting that leptin may help encode palatability.
The mesocorticolimbic reward pathways contribute importantly to eating behaviors. For example, increased activation of these brain regions have been observed subsequent to both presentation and consumption of palatable food. Preclinical research has demonstrated that knockdown of striatal DA D2 receptors rapidly accelerates the development of addiction-like reward deficits and the onset of compulsive-like food seeking. In addition to its metabolic function, leptin may help modulate mesolimbic DA reward circuits.
Partially modulated by adipose-derived hormones such as leptin and ghrelin, orexins are important modulators for eating behavior and help to maintain energy homeostasis. Orexin administration has been demonstrated to increase feeding behaviors and reinstate substance-using behavior while the opposite is observed with orexin receptor agonists. Preclinical research suggests orexin may directly influence DA pathways although further research investigating their relationship in clinical populations is needed. Unlike leptin and orexin, ghrelin is orexigenic and increases food intake and body weight. Ghrelin levels appear inversely correlated with BMI and have also been positively associated with synapse formation and DA turnover in the NAcc.
Stimulation of NAcc opioid receptors enhances palatability and food intake while opioid receptor antagonists extinguishes previously established preferences for hyperpalatable foods. The NAcc may also be important in general habit formation or basic motor control of feeding behaviors, independent of palatability.
Atrophy of frontal areas can increase food cravings/obsession, gluttony, and weight. Within the PFC, activation of dorsal regions has been associated with reductions in food craving and weight loss success, whereas activation of ventral regions, including the OFC, has been negatively correlated with greater dietary restraint. Individuals with BED, anorexia nervosa, or bulimia nervosa typically perform poorer on decision-making tasks—indirectly suggesting frontal lobe dysfunction.
Increases in both exogenous and endogenous 5-HT is associated with reductions in food intake and weight gain and increases in energy expenditure. Hypothalamic 5-HT may in part mediate the experience of satiety and has been implicated in management of eating behavior, in particular with meal termination. Some research suggests that SSRIs are effective in targeting binge eating, psychiatric, and weight symptoms, although the effectiveness and duration of these medications remain under debate.
COMPULSIVE SEXUAL BEHAVIOR
Characterized by excessive engagement in normative sexual behavior, compulsive sexual behavior (CSB) can be divided into paraphilic (i.e., disturbance in object selection) and nonparaphilic (i.e., engaging in sexual behavior in an excessive, obsessive, or compulsive manner) behaviors. While it is estimated that 5% to 6% of the adult population meet criteria for CSB, there lacks systematic examination, and most existing studies predominantly investigated male clinical populations. CSB frequently co-occurs with multiple psychiatric disorders where high impulsivity is implicated (e.g., SUDs, ICDs, attention-deficit/hyperactivity disorder [ADHD]), as well as with mood disorders. Nonparaphilic CSB is not specifically listed in the DSM; it can be classified as either as a ICD-NOS or a sexual disorder NOS.
To date, there have been no published functional imaging studies of CSB. Bilateral temporal lobe and amygdala lesions have been associated with the Kluver-Bucy syndrome, of which a symptom is hypersexuality. However, Kluver-Bucy syndrome is extremely rare in humans. There has been one small-scale DTI study of white matter microstructures in CSB suggesting higher mean diffusivity in the superior frontal region among individuals with CSB compared to healthy controls.
Open-label prescriptions of various antidepressants and antipsychotics have been used to treat CSB, but their efficacy remains to be systematically examined. While serotonin has been implicated in sexual functioning and desire and sexual dysfunction, there is mixed evidence to support the efficacy of SSRIs in treating CSB symptoms. Moreover, it is presently unclear whether the reduction in CSB symptoms is a result of actual reduction of sexual thoughts, or to the sexual side effects of the medication. Evidence from pharmacologic studies also implicates the opioid and dopaminergic system in CSB although the precise relationship remains unclear.
PROBLEMATIC INTERNET USE
Problematic Internet use (PIU) or “Internet addiction” is characterized by excessive or poorly controlled urges and a maladaptive obsession with the Internet. As with other ICDs, PIU involves excessive engagement in socially normative activities. Although considered for inclusion in the DSM-5, it was concluded there is currently insufficient evidence to warrant PIU’s addition. The lack of a universal assessment tool may contribute to the wide range of prevalence estimates among adolescents (4.0% to 19.1%) and adults (0.7% to 18.3%). PIU frequently co-occurs with SUDs as well as other psychiatric conditions.
While evidence remains scarce, emerging research suggests increased resting state regional homogeneity in frontal areas among individuals with PIU. Other evidence suggests differences in brain function, such as in the anterior and posterior cingulate cortices, during cognitive tasks that may reflect a sensitization to reward and desensitization to loss. Decreased gray matter density in brain areas implicated in decision making has been observed among individuals with PIU. Alterations in white matter microstructures have also been reported among individuals with PIU, although further research is needed.
Two small-scale ligand-based studies of dopaminergic functioning among individuals with PIU indicate that PIU individuals have reduced dopamine transporter expression and dopamine D2 receptor availability in striatal regions.
Specific genetic alleles related to encoding for 5-HT– and nicotinic acetylcholine–related moieties have been implicated in PIU. However, replication of these findings is needed.
Data suggest that ADHD, depression, and aggression may be vulnerability factors for PIU. However, certain factors (such as aggression) were associated with increased severity in PIU only among males. Moreover, some data suggest that men are more likely to have PIU, although this gender gap may be diminishing.
PROBLEMATIC VIDEO GAME PLAYING
Problematic video game playing (PVG) or “video game addiction” is both similar to and distinct from other behavioral addictions in its availability and use of visual and auditory rewards. Previous research on PVG has often included online games; thus, video game findings cannot be clearly separated from Internet findings based on existing data.
While no DSM-based diagnostic criteria exist in the main DSM text, assessment tools for PVG are often based on the DSM-IV definitions for SUDs and PG. Prevalence estimates have ranged from 4.2% to 20.0% for adolescents and roughly 11.9% for adults. Psychiatric comorbidities remain poorly researched, although preliminary findings suggest links with ADHD, mood disorders, and SUDs.
A recent large-scale MRI study observed both structural and functional differences in the ventral striatum when comparing frequent versus infrequent gamers. Other brain regions have also been implicated in other studies. In particular, the OFC, striatum, and anterior cingulate—all of which are involved with subjective reward valuation—have been frequently shown to be hyperactivated among PVG individuals.
Playing video games has been shown to increase release of DA, particularly in the ventral striatum, at levels comparable to that induced by psychostimulant drugs. Moreover, bupropion (a drug with dopaminergic/noradrenergic reuptake–blocking properties) administration decreased craving, time spent playing, and cue-induced brain activity in PVG individuals.
While adolescent boys were more likely to endorse PVG symptoms, no associations between PVG and negative health measures were observed, suggesting that video gaming may be a normative behavior among boys. Research pertaining to gender-related differences in adults has yielded mixed results.
COMPULSIVE BUYING DISORDER
While compulsive buying disorder (CBD) has long been recognized, little is known regarding its pathophysiology. To date, only one imaging-based study has been conducted. Findings from this study suggest CBD individuals find shopping cues more rewarding (increased NAcc activation) and have poorer cognitive control (attenuated insula and anterior cingulate activation) while making purchasing decisions.
Results have been mixed with regard to the efficacy of pharmacologic treatment using SSRIs for CBD. Moreover, substantial placebo effects have been observed, raising questions regarding the clinical utility of SSRIs in treating CBD. There have been several case reports of successful naltrexone treatment (typically of high dosage) in CBD.
KLEPTOMANIA
“Kleptomania” differs from “shoplifting” in that individuals steal not for personal gains but for symptomatic relief. DSM diagnostic criteria reflect aspects of diminished ability to inhibit impulses to steal, consequential distress, and subjective pleasure/relief associated with theft. Kleptomania generally begins in adolescence or early adulthood and appears to be more common in women than men. However, the illegal nature of kleptomania may significantly contribute to a reluctance to seek treatment; therefore, its true prevalence remains unclear.
Currently, only one multisubject imaging study exists, although lesion and imaging data from case reports exist. Together, existing data suggest frontal lobe involvement. Findings regarding serotonergic dysfunction in kleptomania have been inconsistent. Opioid antagonists have shown some efficacy in decreasing urge intensity and frequency of kleptomania symptoms.
TRICHOTILLOMANIA
Trichotillomania is a heterogeneous disorder involving the pulling of hair, most frequently from the scalp, and can co-occur with trichophagia (eating hair). The duration of trichotillomania varies widely and may present as chronic and persistent across the life span or may abate without treatment. Onset generally occurs during adolescence, and prevalence rates appear approximately equal for both genders. Trichotillomania is classified in the DSM-5 as an “obsessive–compulsive and related disorder.”
A SPECT analysis of female identical twins found positive associations between temporal pole abnormalities and trichotillomania symptomatology. In contrast, an fMRI study reported no between-group differences in corticostriatal function. Preliminary structural MRI studies have shown mixed results. Recent DTI data suggest decreased white matter integrity in regions of anterior cingulate, presupplementary motor area, and temporal cortex.
Pharmacologic research with SSRIs has yielded conflicting results. A meta-analysis suggests that certain SSRIs have greater efficacy than placebo in reducing trichotillomania severity, while other SSRIs show no significant effects on symptoms. Naltrexone, not effective in treating OCD symptoms, has been shown to effectively treat features of trichotillomania.
PATHOLOGIC SKIN PICKING
Pathologic skin picking (PSP) is characterized by pathologic attention to, and extended duration of, skin picking behavior that is impulsive, ritualistic, and repetitive. Excoriation (skin picking) disorder is included in the DSM-5 as an OC-related disorder. Reluctance to seek treatment has occluded prevalence estimates. Among community samples, prevalence estimates have ranged from 1.4% to 5.4%. PSP appears to be a chronic, often lifelong, condition. PSP has been associated with different disorders including OCD, body dysmorphic disorder, and delusions.
However, the neurobiology of this disorder remains incompletely understood. Preliminary data suggest the endogenous opioid system contributes to the pathophysiology of PSP. Some—but not all—individuals with PSP may be successfully treated with SSRIs, suggesting possible serotonergic involvement in the disorder. Glutamatergic agents have also shown early promise as treatments. Twin studies suggest significant genetic influence on skin picking with genetic factors accounting for slightly over 40% of the variance in skin picking.
INTERMITTENT EXPLOSIVE DISORDER
Under the DSM-5 criteria, intermittent explosive disorder (IED) has been defined as a failure to control aggressive impulses. Data from the National Comorbidity Survey Replication indicate that as many as 7.3% of adults (approximately 11.5 to 16 million Americans) may meet lifetime criteria for IED and 3.9% may meet criteria for 12-month IED.
fMRI data suggest a dysregulation of inhibitory “top-down” OFC processes in individuals with IED. Moreover, differences in the function of areas implicated in emotion regulation and impulse control have been observed among individuals with IED. Levels of 5-HT have been inversely related to the frequency and severity of impulsive aggression. Specifically, alterations in 5-HT transporter and receptors have been reported in areas such as the anterior cingulate and OFC. Psychopharmacotherapy targeting the serotonergic system has been found to reduce aggressive and impulsive behaviors. Norepinephrine and corticotrophin-releasing factor have also been implicated in IED.
KEY POINTS
1. Research suggests similarities between substance addiction and excessive engagement in nondrug behaviors.
2. This has led to growing support for the conceptualization of “behavioral addictions.”
3. Disordered gambling has been recategorized under “Substance-Related and Addictive Disorders” in DSM-5.
4. Behavioral addiction remains a debated topic and merits further research.
REVIEW QUESTIONS
1. Which behavioral addiction has been added to the DSM-5’s new category, “Substance-Related and Addictive Disorders”?
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