Social anxiety disorder and drug addiction commonly co-occur in the same individual, complicating the presentation, course and treatment of both disorders. Using drugs or alcohol may be a coping mechanism for social anxiety; however, many treatments for addiction are group-based approaches, which would be especially challenging for people with social anxiety disorder. This article provides a brief overview of what is known about the co-occurrence of these disorders, as well as possible treatment interventions for this population.
Social anxiety is a very common disorder and is especially common amongindividuals with substance abuse or dependence (substance use disorders [SUDs]). Several epidemiologic surveys have estimated theprevalence of social anxiety disorder (also called social phobia) in thegeneral population to be between 3% and 13% (Kessler et al., 1994; Schneier et al., 1992). However, in SUD clinics, the rateis significantly greater. Zimmermann and colleagues (2004) surveyed 150individuals seeking treatment for an SUD in Switzerland, using theclinician-administered Leibowitz Social Anxiety Scale(LSAS), and found that 20% of the participants screened positive forgeneralized social phobia and 42.6% screened positive for nongeneralizedsocial phobia. Myrick and Brady (1997) evaluated 158 individuals entering anoutpatient clinical treatment trial for cocaine dependence and found that 13%met criteria for social anxiety disorder. Finally, of 159 individuals seekingtreatment for heroin dependence, 18% to 25% screened positive for socialanxiety disorder (Grenyer et al., 1992).
In addition to social anxiety being prevalent in the drug treatment setting,addiction is also commonly found in anxiety treatment clinics and may beresponsible for resistance to traditional anxiety disorder treatments (Coplan et al., 1993). In Australia, 146 individuals seekingtreatment for either social phobia or panic disorder at an anxiety treatmentprogram were evaluated (Page and Andrews, 1996). The researchers hypothesizedthat they would see higher rates of sedative-hypnotic abuse and dependenceamong the participants with panic disorder and higher rates of alcohol misuseamong the individuals with social phobia. They found, however, that both theparticipants with social phobia and those with panic disorder had a rate ofsedative-hypnotic misuse that was eight times that of the general population.Also, only the participants with social phobia had elevated rates of an alcoholuse disorder (Page and Andrews, 1996).
When two disorders co-occur, like social anxiety disorderand addiction, causality (if it exists) is often difficult to unravel.For example, chronic alcohol or illicit drug use can be anxiogenic.Some treatment providers would argue that if an individual with an anxietydisorder and co-occurring substance dependence has successful treatment for the substance dependence, recovering into asober lifestyle, their anxiety disorder will also be ameliorated. This line ofreasoning would be based on the assumption that the substance dependencepreceded the anxiety disorder and the direction of causality would be fromaddiction to anxiety. As a disorder co-occurring with substance dependence,social anxiety disorder most likely does not fit into these assumptions. Theaverage age of onset of social anxiety disorder is in the mid-teens (Schneier et al., 1992), at a time when social interpersonalattitudes and relationships are being formed--also a time when experimentationwith illicit drugs and alcohol generally would begin. The average age ofalcohol dependence, for example, is roughly a decade later, in the mid-20s (Schuckit et al., 1998), making the direction of causality,if it exists, more likely to be from social anxiety to substance dependence.
One possible neurobiological link between social anxiety disorder andsubstance dependence may be the neurotransmitter dopamine. Individuals withsocial anxiety disorder have been shown to have a decreased binding of dopaminein the basal ganglia (Tiihonen et al., 1997) andsocial anxiety disorder has been shown to have a high incidence in individualswith parkinsonism (Stein et al., 1990), a diseaseknown to be associated with decreased dopamine binding. Some have theorizedthat dopamine, especially striatal dopamine, is a keycomponent in the manifestation of social anxiety disorder and that it acts as agatekeeper for the involvement of other neurochemicals,such as serotonin or γ-aminobutyric acid (GABA)(Li et al., 2001).
Interestingly, all drugs of abuse ultimately increase dopamine in the basalganglia (Kalivas, 2001). Although it does not explainthe ultimate development of substance dependence, if the hypoactive dopaminergic tone associated with social anxiety can betemporarily ameliorated with drugs of abuse, this may explain why a person withsocial anxiety disorder may find using drugs to be effective self-medication.
Another possible neurochemical link between socialanxiety disorder and substance dependence may involve the neurotransmitterGABA. Although an animal model of social anxiety disorder has been somewhatelusive, there is considerable preclinical evidence to support a role for GABAin anxiety disorders in general. Several studies have shown that, in a mousemodel, an inhibited ability to synthesize GABA results in increased anxiety (Kash et al., 1999; Stork et al., 2003, 2002). In additionto preclinical data that support the role of GABA in anxiety in general,pharmaceutical agents that enhance GABA-for example, benzodiazepines andnon-benzodiazepine anticonvulsants-have been shown to be effective in thetreatment of social anxiety disorder (Davidson et al., 1991; Pande et al., 2004, 1999; Van Ameringenet al., 2004). Although not quite as central as dopamine, GABA also plays animportant role in addiction (Malcolm, 2003).
If a patient presents with both disorders to either an addiction or ananxiety treatment setting, what is the optimal treatment approach?Unfortunately, there has been little work done in this area. As most treatmentfacilities rely heavily on traditional group therapy and 12-step treatmentapproaches (such as Narcotics Anonymous or Alcoholics Anonymous) for thetreatment of SUDs, individuals with social anxietymay have considerable difficulty engaging and participating in suchgroup-oriented activities. As such, a tailored approach to treatment includingmore individualized treatment and strategy development for participation ingroups is needed.
Some of the medications used for social anxiety, for example thebenzodiazepines, may not be safe to use if the patient has a co-occurringaddiction (Book and Randall, 2002). The selective serotonin reuptake inhibitorsare the first line treatment of social anxiety disorder (Ballenger et al.,1998) and, although there is some evidence that they can worsen addiction insome populations (Kranzler et al., 1996; Pettinati et al., 2000), in the right patient with socialanxiety disorder and co-occurring addiction, they may be the best choice. Theefficacy of paroxetine (Paxil)for individuals with social anxiety disorder and a co-occurring alcohol usedisorder has been evaluated (Randall et al., 2001). They found that the paroxetine-treated participants had significantly moreimprovement of social anxiety than did the placebo-treated participants overthe eight-week study. However, although the alcohol use variables also weremore improved in the paroxetine group than they werein the placebo group, the difference was not significant. This pilot study iscurrently being followed up on a larger scale. Although the work of Zimmermannet al. (2004) and of Myrick and Brady (1997) would indicate that treatmentsolutions are needed for individuals with social anxiety disorder and drugaddiction, no such studies have been done. Clearly, research trials involvingtherapeutic approaches to treat comorbid socialanxiety and substance use disorders are needed.
Supported by National Institute ofAlcohol Abuse and Alcoholism grants 2 P50 AA10761-03, K23 AA014430 (SWB) andK23 AA00314-01 (HM), and a U.S. Department of Veterans Affairs Merit Grant(HM).
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