|Home | About | Journals | Submit | Contact Us | Français|
To assess the prevalence and clinical impact of comorbid Social Anxiety Disorder (SAD) and Alcohol Use Disorders (AUD, i.e., alcohol abuse and alcohol dependence) in a nationally representative sample of adults in the United States.
Data came from a large representative sample of the United States population. Face-to-face interviews of 43,093 adults residing in households were conducted during 2001–2002. Diagnoses of mood, anxiety, alcohol and drug use disorders, and personality disorders were based on the Alcohol Use Disorder and Associated Disabilities Interview Schedule—DSM-IV Version.
Lifetime prevalence of comorbid AUD and SAD in the general population was 2.4%. SAD was associated with significantly increased rates of alcohol dependence (OR=2.8) and alcohol abuse (OR=1.2). Among respondents with alcohol dependence, SAD was associated with significantly more mood, anxiety, psychotic, and personality disorders. Among respondents with SAD, alcohol dependence and abuse were most strongly associated with more substance use disorders, pathological gambling, and antisocial personality disorders. SAD occurred before alcohol dependence in 79.7% of comorbid cases, but comorbidity status did not influence age of onset for either disorder. Comorbid SAD was associated with increased severity of alcohol dependence and abuse. Respondents with comorbid SAD and alcohol dependence or abuse reported low rates of treatment-seeking.
Comorbid lifetime AUD and SAD is a prevalent dual diagnosis, associated with substantial rates of additional comorbidity, but remaining largely untreated. Future research should clarify the etiology of this comorbid presentation to better identify effective means of intervention.
Alcohol use disorders (AUD) and social anxiety disorder (SAD) are among the five most prevalent psychiatric diagnoses (Kessler et al., 2005a). Estimates of lifetime prevalence for AUD (including alcohol dependence and alcohol abuse) range from 8.3% to 30.3%, and for SAD range from 5.0% to 12.1% (Grant et al., 2005, Hasin et al., 2007, Kessler et al., 2005a). AUD and SAD frequently co-occur, are highly comorbid with other Axis I and II disorders (Bakken et al., 2005, Burns and Teesson, 2002, Grant et al., 2005, Hasin et al., 2007), and are associated with severe morbidity and functional disability (Bakken et al., 2005, Book et al., 2007, Crum and Pratt, 2001, Grant et al., 2005, Hasin et al., 2007, Kessler, 2003, Kessler et al., 2005b, Kushner et al., 2000, Lecrubier and Weiller, 1997, Lepine and Pelissolo, 1998). Despite the availability of efficacious treatments, both AUD and SAD frequently go untreated (Cohen et al., 2007, Grant et al., 2005, Olfson et al., 2000, Wang et al., 2005; Hasin et al., 2007), an important concern given evidence that recovery from either disorder is compromised by failure to treat the other (Lecrubier, 1998, Moggi et al., 1999, Randall et al., 2001, Terra et al., 2006).
Studies investigating the comorbidity of AUD with anxiety disorders as a group have characterized a pattern of comorbidity in which anxiety and alcohol use are each a cause and a consequence of the other (Kushner et al., 2000). However, no epidemiologic study has specifically characterized comorbidity of AUD and SAD, despite documentation of their strong association, and the clear differences between the phenomenology and course of SAD and other anxiety disorders (Kushner et al., 2000, Kushner et al., 2005, Schneider et al., 2001). Furthermore, prior studies of AUD and anxiety disorders were often limited to treatment-seeking samples (Book et al., 2008, Gerlach et al., 2006, Randall et al., 2001, Terra et al., 2006) and utilized a unidirectional approach, e.g., examining factors associated with comorbid AUD among patients with anxiety disorders, but not the reverse. This approach provides only a partial view of the relationship between disorders.
We seek to build on previous work by employing a bidirectional approach to explore comorbidity of AUD with SAD, utilizing the 2001–2002 National Institute on Alcohol Abuse and Alcoholism’s (NIAAA) National Epidemiologic Survey on Alcohol and Related Conditions (NESARC). This approach provides a unique opportunity to investigate the incremental effect of having both disorders relative to either alone in regard to strength of association with particular sociodemographic features and with other DSM-IV disorders. Furthermore, it enables detailed examination of the association of comorbid alcohol dependence/SAD and alcohol abuse/SAD with age of onset of each disorder, treatment-seeking behavior, family history, and illness severity. Such information could be used to identify population characteristics that may help generate hypotheses about the etiology of this comorbid presentation and improve access to care. Better characterization of persons with comorbid SAD and AUD will inform the development of effective integrated treatment models, which is an active interest of members of our research group.
The NESARC is a nationally representative sample of the adult population of the United States, conducted by the US Census Bureau under direction of the NIAAA, as previously described (Grant et al., 2003, Grant, 2003, Grant et al., 2005, Hasin et al., 2007). The NESARC targeted the civilian, non-institutionalized population, 18 years and older, residing in households in the 50 states and District of Columbia. The final sample included 43,093 respondents drawn from individual households and group living quarters. African Americans, Latinos, and young adults (aged 18 to 24 years) were oversampled. Data were adjusted to account for oversampling and respondent and household response. The overall survey response rate was 81%. Weighted data were adjusted using the 2000 Decennial Census, to be representative of the US civilian population for a variety of sociodemographic variables.
Sociodemographic measures included age, sex, race, nativity, marital status, education, and personal income, assessed as categorical variables.
All psychiatric diagnoses except psychotic disorder were made according to DSM-IV criteria using the NIAAA Alcohol Use Disorder and Associated Disabilities Interview Schedule-DSM IV Version (AUDADIS-IV) (Grant, 2001, Hasin et al., 2007), a valid and reliable fully structured diagnostic interview designed for use by lay interviewers. The test-test reliability and validity of AUDADIS-IV measures of DSM-IV disorders is reported elsewhere (Grant et al., 2003, Grant et al., 2005, Hasin et al., 2007). We also included data on family history of AUD (not specified as alcohol dependence or abuse), but the AUDADIS-IV does not collect data on family history of SAD.
Both 12-month and lifetime diagnoses were assessed. Consistent with DSM-IV, an AUDADIS-IV diagnosis of alcohol abuse required 1 or more of 4 abuse criteria in the last 12 months or any previous 12-month period. Alcohol dependence diagnoses required 3 or more of 7 DSM-IV dependence criteria in the last 12 months or in any previous 12-month period. For prior diagnoses of alcohol dependence, 3 or more criteria must have occurred at the same time within a 12-month period. Persons who met criteria for both alcohol abuse and dependence were classified as having alcohol dependence. The test-retest reliability of AUDADIS-IV alcohol diagnoses in clinical and general populations ranges from good to excellent (κ = 0.70–0.84) (Hasin et al., 2007). Convergent, discriminant, and construct validity of AUDADIS-IV alcohol use disorder criteria and diagnoses are also good to excellent (Hasin et al., 2007).
Consistent with DSM-IV, diagnosis of SAD required a marked or persistent fear of social or performance situations (here operationalized as at least 1 of 14 social or performance situations such as speaking in public, attending social gatherings, conversing with an authority figure) in which embarrassment or humiliation may occur. In addition, the fear had to be recognized as excessive or unreasonable, and the feared social situation must have been avoided or endured with intense anxiety. All SAD diagnoses required that the clinical significance criterion of DSM-IV be met (i.e. symptoms of the disorder must have caused clinically significant distress and/or impairment in social, occupational, or other areas of functioning). The generalized subtype of SAD (GSAD), defined by fear of most social situations, was operationalized as fear of more than 7 of the 14 situations queried, with the remainder of SAD respondents classified as having the nongeneralized subtype (NGSAD). Because scrutiny fears in SAD have specifically been associated with AUD (Buckner et al., 2008a), eight of the situations were identified as instances of scrutiny fears for separate analysis. The test-retest reliability of the diagnosis of SAD was fair (κ = 0.42–0.46) (Grant et al., 2005), similar to other instruments used in epidemiological studies (Ruscio et al., 2008). Validity of AUDADIS-IV SAD diagnoses has been supported by assessment of impairment using the Short Form 12, version 2 (SF-12v2; Gandek et al., 1998), a reliable and valid measure in population surveys. Controlling for sociodemographic factors and other mental disorders, SAD and SF-12v2 scales (described below) showed highly significant relationships (p<.0001) (Grant et al., 2005).
To estimate rates of mental health service utilization, respondents were classified as receiving treatment for SAD if they: (1) visited a physician, psychologist, or any other health professional; (2) were a patient in a hospital for at least one night; (3) visited an emergency room; or (4) were prescribed medications. Respondents were classified as receiving treatment for AUD (not specified as alcohol dependence or abuse). if they: (1) visited a physician, psychologist, or any other health professional; (2) were a patient in an inpatient ward of a hospital, an outpatient clinic, a detoxification or rehabilitation unit; (3) visited an emergency department or crisis center; or (4) received treatment by a paraprofessional (e.g., a member of the clergy), an employee assistance program or through family/social services, or attended self-help groups. Treatment utilization questions were disorder-specific.
Disability among respondents was determined with the SF-12v2 scales assessing mental health, social functioning (limitations due to emotional problems), and role emotional functioning (role impairment due to emotional problems). Each SF-12v2 norm-based disability score is a continuous variable with a mean of 50 in the general population, standard deviation of 10, and range of 0 to 100. Lower scores indicate greater disability and have been associated with psychopathology in prior studies (e.g. Compton et al., 2007).
Weighted percentages, means, and cross-tabulations were computed to derive estimates of lifetime prevalence of alcohol dependence, alcohol abuse, SAD and correlates. Odds ratios (ORs) indicated associations between each AUD and SAD and: (1) sociodemographic variables and (2) other psychiatric disorders. Multiple linear or logistic regression (as appropriate) were used to estimate means and ORs after adjusting for sociodemographic covariates. Standard errors and 95% confidence intervals were estimated using SUDAAN, statistical software that adjusts for characteristics of the NESARC.
Because previous analyses of the NESARC have documented that SAD is significantly associated with alcohol dependence but not abuse (Hasin et al., 2007), we focused our main analyses on alcohol dependence, but also summarize results on alcohol abuse (detailed results of analyses for abuse available upon request). We also conducted secondary analyses for generalized and nongeneralized subtypes of SAD. To address possible concerns about pseudocomorbidity that could arise from analyses of lifetime diagnoses, we repeated our analyses using a 12-month timeframe. For data on disability, however, primary analyses used the 12-month timeframe. We present the results of secondary analyses of SAD subtypes and 12-month timeframe, which had more limited statistical power, only where the pattern of results differed from that of the main analyses (results of all secondary analyses available upon request).
As has been previously reported, lifetime prevalences in the general population were 5.0% for SAD, 12.5% for alcohol dependence, and 17.8% for alcohol abuse. The lifetime prevalence of comorbid AUD (either dependence or abuse) and SAD in the general population was 2.4% (95% CI: 2.2–2.7%). Among respondents with SAD, prevalence was significantly elevated for alcohol dependence (27.3%, adjusted OR = 2.8, 95% CI: 2.5–3.3), and abuse (20.9%, OR = 1.2, 95% CI: 1.1–1.4). Among respondents with alcohol dependence, prevalence of SAD was 10.9% (95% CI: 9.7–12.2%) and among respondents with alcohol abuse, it was 5.8% (95% CI: 5.2–6.6%). Among respondents with alcohol dependence, lifetime prevalences of SAD subtypes were 6.0% (95% CI: 5.1–7.0%) for nongeneralized SAD and 4.8% (95%CI: 4.1–5.7%) for generalized. Among respondents with alcohol abuse, lifetime prevalences of SAD subtypes were 3.6% (95% CI: 3.07–4.2) for nongeneralized SAD and 2.2% (95% CI: 1.8–2.7%) for generalized. Because only alcohol dependence was strongly associated with SAD, subsequent analyses focus on dependence and mention specific findings for abuse where significant.
Prevalence data for alcohol dependence and SAD is shown stratified by sociodemographic characteristics in Table I. Comorbid prevalence ranged from 0.6% among Blacks to 2.6% among Native Americans. Among respondents with alcohol dependence, the odds of comorbid SAD were significantly greater for women and lower for Blacks and Hispanics relative to non-Hispanic Whites. Individuals 45–64 had higher odds of comorbid SAD than those aged 18–29. Respondents with less than high school education had significantly greater odds of SAD than those with a college education. Respondents with individual income less that $35,000/year had significantly greater odds of SAD relative to those with income of $35,000 or greater. Among respondents with SAD, odds of comorbid alcohol dependence were significantly greater for men, lower for Blacks, and lower for those 65 and older.
For alcohol abuse, sociodemographic patterns were similarly associated in respect to gender, but differed in that among respondents with SAD, comorbid alcohol abuse was associated with being native-born, age 30–64, and having income of $20,000/year or greater, and was negatively associated with having never married. Among respondents with alcohol abuse, comorbid SAD was associated with being Native American and age 30–64, and was negatively associated with income of $70,000/year or greater..For SAD subtypes, comorbid GSAD but not NGSAD was significantly associated with less than high school education. Other minor differences related to the level of significance of the findings.
Table 2 shows lifetime prevalence of other psychiatric disorders among respondents with comorbid alcohol dependence and SAD. Among them, 97.0% had at least one additional psychiatric disorder, 93.9% another Axis I disorder, 64.1% a mood disorder, 63.1% a second anxiety disorder, and 71.7% a personality disorder. Respondents with comorbid alcohol dependence and SAD had a mean of 4.6 (95% CI: 4.3–4.9) additional DSM-IV disorders, compared to 2.7 (95% CI: 2.5–2.9) among those with SAD alone and 2.1 (95% CI: 2.0–2.2) among those with alcohol dependence alone.
Among respondents with alcohol dependence, comorbid SAD was significantly associated with all Axis I disorders except for conduct disorder and pathological gambling, and was negatively associated with drug dependence. Within personality disorders, the greatest strength of association was observed with avoidant and dependent (ORs 13.4 and 7.7 respectively) and the weakest with antisocial personality disorder (OR 2.3). Among respondents with SAD, comorbid alcohol dependence was most strongly associated with drug and nicotine dependence, pathological gambling, and histrionic and antisocial personality disorders (ORs 3.2–7.9) and was more modestly associated with bipolar disorder, panic disorder, specific phobia, and psychotic disorders, as well as avoidant, obsessive-compulsive, paranoid and schizoid personality disorders (ORs 1.5–2.4).
For alcohol abuse, comorbidity patterns were similar, but comorbid alcohol abuse was significantly associated only with drug abuse and nicotine dependence, and negatively associated with specific phobia, avoidant and schizoid personality disorders. When analyses were examined by SAD subtypes, patterns of associations remained the same. When restricting the sample to respondents with 12-month SAD/AUD comorbidity, the overall pattern of direction and magnitude of associations remain the same, and the only changes observed were in the level of significance of some of the associations due to smaller sample size (N = 88).
Table 3 shows that age of onset of SAD was significantly earlier than age of onset of alcohol dependence. There were no significant differences in age of onset of either disorder between those with comorbid alcohol dependence and SAD and those with only one of the disorders. Among comorbid cases, SAD occurred first in 79.7% (95% CI: 76.5 – 85.9%), Alcohol dependence occurred first in 14.7%, (95% CI: 10.9 – 19.6%) and the disorders co-occurred in 3.6% (95% CI: 2.0 – 6.5%). Secondary analyses for alcohol abuse, and for SAD subtypes, yielded similar findings. For cases in which SAD occurred first, mean lag time to alcohol dependence was 13.3 years (95% CI: 12.1 – 14.4 years), and to alcohol abuse was 10.6 years (95% CI: 9.6 – 11.7 years). For cases in which an AUD occurred first, mean lag time to SAD was 6.6 years (95% CI: 4.0 – 9.3 years) for dependence and 13.0 years (95% CI: 9.6 – 16.4 years) for abuse.
Among respondents with SAD, comorbid alcohol dependence was not associated with severity of SAD, as measured by number of situations feared, or severity of scrutiny fears. Among respondents with alcohol dependence, comorbid SAD was associated with greater severity of dependence, as indicated by more dependence criteria (Hasin et al., 2006), but not alcohol abuse. Family history of AUD was more prevalent among individuals with comorbid SAD and alcohol dependence compared to those with either disorder alone. SF-12 scores for social functioning, role emotional, and mental health scales were worse among individuals with comorbid alcohol dependence and SAD, or with SAD alone, compared to individuals with alcohol dependence alone, but there were no significant differences between those with SAD alone and those with comorbid alcohol dependence and SAD. Rates of treatment-seeking for either disorder were not significantly affected by comorbidity with the other.
When alcohol abuse was examined separately, and SAD subtypes were examined separately, patterns of association with SAD severity remained nonsignificant. Individuals with either subtype of SAD comorbid with alcohol abuse had higher rates of family history of AUD than those with the respective SAD subtype alone, or alcohol abuse alone. Measures of disability and treatment rates for alcohol abuse and SAD subtypes followed the same pattern as for alcohol dependence and SAD, and 12 month cases followed the same pattern as lifetime.
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, 2008b; 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.
The National Epidemiologic Survey on Alcohol and Related Conditions was sponsored by the National Institute on Alcohol Abuse and Alcoholism and funded, in part, by the Intramural Program, NIAAA, National Institutes of Health. This study is supported by NIH grants DA019606, DA020783, DA023200 and MH076051 (Dr. Blanco), AA08159 and AA00161 (Dr. Hasin), the American Foundation for Suicide Prevention (Dr. Blanco) and the New York State Psychiatric Institute (Drs. Foose, Hasin, Schneier and Blanco).
Publisher's Disclaimer: Disclaimer: The views and opinions expressed in this report are those of the authors and should not be construed to represent the views of any of the sponsoring organizations, agencies, or the U.S. government.
Declaration of Interest