This epidemiological study examined demographic and clinical correlates, comorbidity, disability, and treatment-seeking patterns of individuals with comorbid SAD and AUD. We found that: 1) comorbid AUD (dependence or abuse) and SAD is a prevalent dual diagnosis that is associated with increased comorbidity with other psychiatric disorders; 2) SAD is associated with increased alcohol dependence (and weakly, with alcohol abuse); 3) in persons with alcohol dependence, SAD is associated with increased family history of AUD, and severity of AUD, impairment, and comorbidity; 4) treatment rates are low for SAD and AUD, whether occurring together or separately.
Consistent with prior studies documenting high rates of SAD among AUD patients and high rates of AUD among SAD patients, we found that comorbid SAD and AUD had a lifetime prevalence of 2.4%. The finding that comorbid SAD is associated with alcohol dependence in particular, increased severity of dependence, and increased impairment relative to alcohol dependence or abuse alone is consistent with findings from clinical samples (Thomas et al., 1999
). Unlike some other reports from community and clinical samples (e.g. Buckner et al., 2008a
; Schneier et al., 1989
), the comorbid condition was not associated with greater severity of SAD, scrutiny fears or impairment relative to SAD alone. This may be due to different approaches to the assessment of severity and impairment. Separate analyses of alcohol abuse showed some sociodemographic differences from findings for dependence, but generally, analyses of alcohol abuse and subtypes of SAD did not yield consistent qualitative differences from the findings for alcohol dependence and SAD overall.
Sociodemographic correlates of comorbid alcohol dependence and SAD were intermediate to those of each disorder; but patterns of additional comorbidity associated with the combined condition appear to be the sum of comorbidity separately associated with alcohol dependence and SAD. Among persons with SAD, comorbid alcohol dependence was particularly associated with increased comorbidity of drug and nicotine dependence, pathological gambling, and histrionic and antisocial personality disorders. Among persons with alcohol dependence, comorbid SAD was most strongly associated with mood disorders, other anxiety disorders, and dependent and avoidant personality disorders. The high comorbidity with avoidant personality disorder is likely due in part to the substantial overlap in its diagnostic criteria with those of SAD (Chambless et al., 2008
). While comorbid SAD conferred a broad increase in psychiatric comorbidity, it was associated with decreased rates of externalizing disorders such as conduct disorder, pathological gambling, and drug abuse, suggesting that SAD may be an indicator of protective factors in respect to externalizing disorders among persons with alcohol dependence. Alcohol abuse was generally associated with lower rates of comorbidity, compared to alcohol dependence.
In current models of the structure of common mental disorders, SAD is generally conceptualized as an internalizing disorder, shown to have greatest comorbidity with other internalizing disorders (i.e., mood and anxiety disorders and avoidant personality disorder). AUD are considered externalizing disorders, having the strongest association with other externalizing disorders, such as other substance use disorders and antisocial personality disorder (Kendler et al., 2003
, Krueger, 1999
, Vollebergh et al., 2001
). Yet the clinical presentation of comorbid AUD and SAD includes features of internalizing and externalizing disorders and does not resemble the clinical fingerprint of either AUD or SAD alone. Our findings suggest that externalizing and internalizing features can exist in tandem and thus should not be conceptualized as opposites on a spectrum.. This is consistent with recent findings that a subset of persons with SAD paradoxically evidence risk-prone behavior (Kashdan et al., 2009
Our study replicates previous findings that SAD precedes and increases risk for AUD (Buckner et al., 2008b
, Crum and Pratt, 2001
, Merikangas et al., 1998
, Zimmermann et al., 2003
, Schneier et al., 1989
), supporting the hypothesis of a directional etiological link from SAD to alcohol dependence and abuse. On the other hand, comorbid SAD did not appear to accelerate the onset of either alcohol dependence or abuse, which has also been noted previously (Buckner et al., 2008b
), and the comorbid condition was not associated with a greater number of social fears. The true relationship between these disorders is undoubtedly more complex.
Animal studies have shown that stress and substance use disorders share common circuitry and the potentiating effect of corticotropin-releasing factor (CRF) on mesolimbic dopaminergic reward pathways (Piazza and Le Moal, 1998
), suggesting that stress may reinforce the addictive properties of substances of abuse. Human studies have documented that alcohol can play an anxiolytic role by interfering with appraisal of stressful information (Sayette et al., 2001
), attenuating anxiety reactions during the stressor (Dai et al., 2007
, Kushner et al., 2000
, Thomas et al., 2003
), and interfering with the consolidation of memories related to stressful events (Gerlach et al., 2006
). Our finding that individuals with AUD (dependence or abuse) and SAD have greater prevalence of familial AUD than individuals with either AUD alone is consistent with previous findings suggesting the offspring of alcoholics differ from controls with regard to HPA-axis hormonal response to subjective psychological stress (Dai et al., 2007
, Uhart et al., 2006
). However, though alcohol is a short-term anxiolytic, it is also disinhibiting, which may both release the excess inhibition present in SAD and increase the risk of traumatic or anxiety-inducing social interactions (Brady et al., 2007
). The amnesic effects of alcohol may contribute to the persistence of social anxiety by impairing extinction of fear response and possibly interfering with desensitization (Cameron et al., 1987
). Furthermore, alcohol withdrawal is anxiogenic in the setting of autonomic hyperactivation (Duka et al., 2002
, Johnston et al., 1991
). The etiology of joint AUD and SAD may therefore be heterogeneous, multifactorial, and bidirectional.
Despite the finding that comorbid AUD (dependence or abuse) and SAD was more impairing than either AUD alone, and the known tendency for comorbid cases in general to be more likely to receive treatment, the majority of respondents with comorbid AUD and SAD did not receive treatment for either disorder. Our findings are consistent with data from previous epidemiological studies (Cohen et al., 2007
, Olfson et al., 2000
, Wang et al., 2005
) and suggest that efforts to increase treatment rates for AUD and SAD represent an important opportunity for improving quality of care in this population with joint comorbidity. Earlier onset of SAD than of either AUD, and expectations of individuals with SAD that alcohol will alleviate anxiety symptoms (Ham et al.,
2002), suggest that psychoeducation and treatment for SAD, especially in the presence of family history of AUD, may prevent a subset of cases of AUD. Efforts to identify and target at-risk populations may have greater impact during adolescence, around the time of SAD onset (Grant et al., 2005
), especially given evidence that alcohol exposure during adolescence may result in structural brain changes and dysregulation of drinking later in life (Chambers et al., 2003
, Dawson et al., 2007
Several factors may contribute to the cumulatively poor treatment rates of comorbid AUD (dependence or abuse) and SAD, including the low rates of treatment-seeking associated with each disorder. SAD patients may be reluctant to seek treatment due to avoidance of interaction with authority figures or embarrassment about their symptoms (Olfson et al., 2000
). AUD patients may avoid treatment due to stigma or low perceived need (Brady et al., 2007
). The unique clinical presentation of SAD and AUD in combination may also present a diagnostic challenge contributing to low treatment rates. Clinicians whose primary focus lies in anxiety or AUD may identify and treat the disorder most familiar to them, but fail to identify or be less familiar with treatments for the other disorder.
Lack of an evidence-based treatment model for comorbid SAD and AUD constitutes another major obstacle to effective care of this population. Use of benzodiazepines, SSRIs or monoamine oxidase inhibitors, the medications with strongest empirical support for the treatment of SAD (Blanco et al., 2003
) require caution due to concerns about potential risk of addiction (Blanco et al., 2002
), increased risk of relapse to alcohol (Chick et al., 2004
), and dietary restrictions, respectively (Balon et al., 1999
). Popular group treatment approaches to AUD, such as Alcoholic Anonymous, present specific social obstacles for persons with comorbid SAD (Book et al., 2009
To date, there has been a dearth of research and treatment-development efforts to meet specific needs of individuals with comorbid AUD and SAD, possibly due to the focus of most research and treatment programs on pure rather than comorbid disorders, or to the assumption that treatments efficacious for a pure disorder work in the presence of comorbidity (Randall et al., 2001
). Data from this study suggest the need to accelerate our understanding of this large population to improve their outcome. At present, there are no empirically-supported integrated CBT models for the joint treatment of SAD and alcohol dependence or abuse. A study comparing CBT for the combined treatment of AUD and SAD versus CBT for AUD alone resulted in worse outcomes for the combined CBT, indicating the difficulty of developing such approaches (Randall et al., 2001
). Although there is some agreement about important elements in the treatment of comorbidity, empirical support for the superiority of an integrated treatment versus separate or sequential treatments of the two disorders is lacking (Watkins et al., 2004
). Our group is currently developing alternative CBT models to treat joint AUD and SAD comorbidity, based on an integration of cognitive behavioral and motivational enhancement strategies, and preliminary data are encouraging (Buckner, et al., 2008c
This study shares limitations common to most large epidemiological studies. Because the NESARC sample only included civilian households and group living populations 18 years and older, information was unavailable on adolescents or individuals in prison. The cross-sectional design does not permit us to establish directionality between symptoms of social anxiety and use of alcohol, or between lifetime disorders and current impairment in functioning. Some covariates in our analyses may be causes, correlates or consequences of other variables in this model, including the outcome variable. Mental health treatment results, because they rely on respondent linkage to specific disorders, may underestimate the proportion of affected individuals who received mental health care for disorders other than SAD or AUD.
Our study details the impact of comorbid AUD and SAD. Comorbid AUD (dependence or abuse) and SAD is highly prevalent for a dual diagnosis, more disabling than AUD alone, and largely untreated. Treatment and preventive interventions are needed to decrease the public health burden and the suffering of these individuals.