Behavioral Addictions _ _______________________________________________________________________
suggest both interventions are equally effective compared with control groups [122]. Gambling Disorder and Comorbid Problem Drinking Changes in alcohol use patterns during gambling treatment were examined in a study of 163 patients with gambling disorder followed 36 weeks pre-, during, and post-treatment. Overall, alcohol use was decreased during and after treatment, but 31% showed risky drinking during and after treatment. Latent risky drinking was predicted by recent at-risk drinking, male sex, younger age, lower gambling severity, treatment con- dition, and gambling during treatment. This greater-drinking profile suggested ambivalence about gambling changes during treatment, and those less motivated to change their gambling may be less motivated to reduce their alcohol use [123]. One study found that problem gamblers with co-occurring lifetime alcohol dependence demonstrate addictive behavior across multiple domains and resistance to externally motivated treat- ment approaches [124]. Treatment for patients with gambling disorder and comorbid risky alcohol use may differ from non-risky drinkers. Disor- dered gamblers with low-risk alcohol use tend to have posi- tive outcomes with group CBT, while high-risk drinkers tend to respond better to motivational interviewing. Screens for alcohol problems, such as the Alcohol Use Disorders Identi- fication Test (AUDIT), may be used to help guide treatment selection [125]. Pharmacologic Interventions The most studied medication class in gambling disorder is SSRIs, but results have been mixed at best [85]. Based on pos- sible efficacy in impulsivity treatment, several mood stabilizers have been evaluated in gambling disorder treatment. In one study, lithium was superior to placebo in reducing gambling symptoms during 10 weeks of treatment in patients with gambling disorder and bipolar spectrum disorders. However, olanzapine was found no more effective than placebo [85]. Opioid Receptor Antagonists Multiple studies have demonstrated the efficacy of opioid receptor antagonists in the treatment of gambling disorder. Opioid antagonists dampen gambling-related excitement and cravings by decreasing dopamine neurotransmission in the nucleus accumbens and interconnected reward and motiva- tional neurocircuitry [85]. In the initial study, naltrexone (mean dose: 188 mg/day) dem- onstrated superiority to placebo in reducing gambling-related behaviors, thoughts, and urges, and was particularly effective in gamblers with more severe gambling urges [126]. A second naltrexone study confirmed the findings of the initial study over a longer (18-week) period [127]. The efficacy of as-needed placebo or naltrexone (50 mg) and psychosocial support on reduction of gambling severity, gambling-related thoughts and urges, and gambling frequency and expenditures was assessed among 101 problem gamblers over 20 weeks [128]. Overall,
the as-needed naltrexone provided no substantial benefit over psychosocial support. Nalmefene is a long-acting analog of naltrexone administered by injection. Nalmefene efficacy was demonstrated in 207 subjects treated for 16 weeks, with significant reductions in gambling urges, thoughts, and behavior observed in 59% with nalmefene, compared with 34% with placebo [129]. A second nalmefene trial failed to show statistically significant differences from placebo [130]. Subsequent research found low- dose nalmefene significantly more effective than higher doses. Over 16 weeks, nalmefene (25 mg and 50 mg per day) led to significantly greater reductions in pathologic gambling severity than placebo. With nalmefene (25 mg/day), 59.2% of patients were rated as “much improved” or “very much improved,” compared with 34.0% with placebo. Nalmefene at a dosage of 25 mg/day was effective and showed few adverse events, but 50-mg and 100-mg doses had intolerable side effects [131]. Catechol-O-Methyl-Transferase Inhibitors Catechol-O-methyl-transferase (COMT) is an enzyme that degrades dopamine to regulate cognitive functioning in the PFC. As discussed, PFC-mediated cognitive dysfunction is implicated in the pathophysiology of gambling disorder, and a small uncontrolled study evaluated the COMT inhibitor tolca- pone in 24 patients with gambling disorder who also received fMRI before and after treatment. Compared with controls, the subjects with gambling disorder showed underactivation during executive planning tasks pretreatment. Tolcapone was associated with statistically significant reductions on measures of pathologic gambling, the extent of which significantly correlated with increased activity in brain areas previously underactive during executive planning challenge [132]. Dopaminergic Modulators Dopamine binding is positively correlated with gambling severity and impulsivity, and dopamine release in disordered gamblers is related to excitement and worsened behavioral per- formance. The dopamine-1 (D1) receptor antagonist ecopipam was evaluated in patients with gambling disorder when taken as needed for nine weeks. Compared with placebo, ecopipam led to statistically significant reductions in Yale-Brown Obses- sive Compulsive Scale Modified for Pathological Gambling (PG-YBOCS) total score (25.6 baseline vs. 14.0 at study end) and subscales of thought-urge and behavior. Ecopipam may reduce pathologic gambling behavior [133]. Glutamate-Modulating Agents Another promising area of pharmacotherapy in gambling dis- order is glutamate-modulating agents. N-acetylcysteine (NAC), one such agent, was studied in subjects with gambling disorder over eight weeks; responders during open-label were then ran- domized to NAC or placebo for six weeks. In the open-label phase, 59% experienced significant symptom reductions and were classified as responders. At the end of the double-blind phase, 83% of those assigned to NAC remained responders (vs. 28.6% assigned to placebo) [134].
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