Social anxiety disorder and alcohol use disorder
co-morbidity in the National Epidemiologic Survey
on Alcohol and Related Conditions
F. R. Schneier
#, T. E. Foose
#, D. S. Hasin
, R. G. Heimberg
, S.-M. Liu
, B. F. Grant
New York State Psychiatric Institute, New York, New York, USA
Departments of Psychiatry, College of Physicians and Surgeons, Columbia University, New York, New York, USA
Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, New York, USA
Department of Psychology, Temple University, Philadelphia, Pennsylvania, USA
Laboratory of Epidemiology and Biometry, Division of Intramural Clinical and Biological Research, National Institute of Alcohol Abuse and
Alcoholism, National Institutes of Health, Bethesda, Maryland, USA
Background. To assess the prevalence and clinical impact of co-morbid 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
Method. Data came from a large representative sample of the US population. Face-to-face interviews of 43093 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.
Results. Lifetime prevalence of co-morbid AUD and SAD in the general population was 2.4 %. SAD was associated
with signiﬁcantly increased rates of alcohol dependence [odds ratio (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 co-morbid cases, but co-morbidity status did not inﬂuence age of onset for either
disorder. Co-morbid SAD was associated with increased severity of alcohol dependence and abuse. Respondents
with co-morbid SAD and alcohol dependence or abuse reported low rates of treatment-seeking.
Conclusions. Co-morbid lifetime AUD and SAD is a prevalent dual diagnosis, associated with substantial rates
of additional co-morbidity, but remaining largely untreated. Future research should clarify the etiology of this co-
morbid presentation to better identify eﬀective means of intervention.
Received 7 August 2008; Revised 28 July 2009; Accepted 1 August 2009
Key words : Alcohol dependence, alcohol abuse, anxiety disorders, epidemiology, social phobia.
Alcohol use disorders (AUD) and social anxiety dis-
order (SAD) are among the ﬁve most prevalent psy-
chiatric diagnoses (Kessler et al. 2005a). Estimates of
lifetime prevalence for AUD (including alcohol de-
pendence and alcohol abuse) range from 8.3 to 30.3 %,
and for SAD range from 5.0 to 12.1 % (Grant et al. 2005;
Kessler et al. 2005a; Hasin et al. 2007). AUD and SAD
frequently co-occur, are highly co-morbid with other
Axis I and II disorders (Burns and Teesson, 2002 ;
Bakken et al. 2005; Grant et al. 2005; Hasin et al. 2007)
and are associated with severe morbidity and func-
tional disability (Lecrubier and Weiller, 1997 ; Lepine
and Pelissolo, 1998; Kushner et al. 2000; Crum and
Pratt, 2001; Kessler, 2003; Bakken et al. 2005; Grant
et al. 2005; Kessler et al. 2005b; Hasin et al. 2007).
Despite the availability of eﬃcacious treatments, both
AUD and SAD frequently go untreated (Olfson et al.
2000; Grant et al. 2005; Cohen et al. 2007; Wang et al.
2005; Hasin et al. 2007), an important concern given
* Address for correspondence : Dr B. F. Grant, Laboratory of
Epidemiology and Biometry, Room 3077, Division of Intramural
Clinical and Biological Research, National Institute of Alcohol Abuse
and Alcoholism, National Institutes of Health, MS 9304, 5635 Fishers
Lane, Bethesda, MD 20892–9304, USA.
(Email : email@example.com)
#These authors contributed equally to this work.
Psychological Medicine, Page 1 of 12. fCambridge University Press 2009
evidence that recovery from either disorder is com-
promised by failure to treat the other (Lecrubier, 1998 ;
Moggi et al. 1999; Randall et al. 2001; Terra et al.
Studies investigating the co-morbidity of AUD with
anxiety disorders as a group have characterized a
pattern of co-morbidity 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 co-morbidity of AUD
and SAD, despite documentation of their strong as-
sociation, and the clear diﬀerences between the
phenomenology and course of SAD and other anxiety
disorders (Kushner et al. 2000, 2005; Schneider et al.
2001). Furthermore, prior studies of AUD and anxiety
disorders were often limited to treatment-seeking
samples (Randall et al. 2001; Gerlach et al. 2006; Terra
et al. 2006 ; Book et al. 2008) and utilized a unidirectional
approach, e.g. examining factors associated with co-
morbid 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 co-morbidity of
AUD with SAD, utilizing the 2001–2002 National In-
stitute on Alcohol Abuse and Alcoholism’s (NIAAA)
National Epidemiologic Survey on Alcohol and Re-
lated 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 examin-
ation of the association of co-morbid alcohol depen-
dence/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
co-morbid presentation and improve access to care.
Better characterization of persons with co-morbid
SAD and AUD will inform the development of eﬀec-
tive 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,
2005; Hasin et al. 2007). The NESARC targeted the
civilian, non-institutionalized population, aged 18
years and older, residing in households in the 50 states
and District of Columbia. The ﬁnal sample included
43093 respondents drawn from individual house-
holds and group living quarters. African Americans,
Latinos, and young adults (aged 18 to 24 years) were
over-sampled. Data were adjusted to account for over-
sampling 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 in-
come, 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 et al. 2001, Hasin et al. 2007), a
valid and reliable fully structured diagnostic interview
designed for use by lay interviewers. The test–test re-
liability and validity of AUDADIS-IV measures of
DSM-IV disorders is reported elsewhere (Grant et al.
2003, 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 as-
sessed. Consistent with DSM-IV, an AUDADIS-IV
diagnosis of alcohol abuse required one or more of
four abuse criteria in the last 12 months or any pre-
vious 12-month period. Alcohol dependence diag-
noses required three or more of seven DSM-IV
dependence criteria in the last 12 months or in any
previous 12-month period. For prior diagnoses of al-
cohol dependence, three 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 depen-
dence. The test–retest reliability of AUDADIS-IV al-
cohol diagnoses in clinical and general populations
ranges from good to excellent (k=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.
Consistent with DSM-IV, diagnosis of SAD required
a marked or persistent fear of social or performance
situations (here operationalized as at least one of 14
social or performance situations, such as speaking
in public, attending social gatherings, conversing with
an authority ﬁgure), in which embarrassment or
2F. R. Schneier et al.
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, oc-
cupational or other areas of functioning). The gen-
eralized subtype of SAD (GSAD), deﬁned by fear of
most social situations, was operationalized as fear of
more than seven of the 14 situations queried, with the
remainder of SAD respondents classiﬁed as having the
non-generalized subtype (NGSAD). Because scrutiny
fears in SAD have speciﬁcally been associated with
AUD (Buckner et al. 2008c), eight of the situations
were identiﬁed as instances of scrutiny fears for sep-
arate analysis. The test–retest reliability of the diag-
nosis of SAD was fair (k=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-12
v.2; Gandek et al. 1998), a reliable and valid measure in
population surveys. Controlling for sociodemographic
factors and other mental disorders, SAD and SF-12 v.2
scales (described below) showed highly signiﬁcant
relationships (p<0.0001) (Grant et al. 2005).
Mental health treatment
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. Respon-
dents 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 in-patient
ward of a hospital, an out-patient clinic, a detoxiﬁca-
tion 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 programme or through family/
social services or attended self-help groups. Treatment
utilization questions were disorder-speciﬁc.
Disability and impairment
Disability among respondents was determined with
the SF-12 v.2 scales assessing mental health, social
functioning (limitations due to emotional problems)
and role emotional functioning (role impairment due
to emotional problems). Each SF-12 v.2 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.
Weighted percentages, means and cross-tabulations
were computed to derive estimates of lifetime pre-
valence of alcohol dependence, alcohol abuse, SAD
and correlates. Odds ratios (ORs) indicated associa-
tions between each AUD and SAD and : (1) socio-
demographic variables ; (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 (CI) were estimated using
SUDAAN, statistical software that adjusts for charac-
teristics 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 GSAD and
NGSAD. To address possible concerns about pseudo-
co-morbidity 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 time-frame. We present
the results of secondary analyses of SAD subtypes and
12-month time-frame, which had more limited stat-
istical power, only where the pattern of results dif-
fered from that of the main analyses (results of all
secondary analyses available upon request).
Prevalence and sociodemographic characteristics
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 co-morbid AUD (either de-
pendence 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, preva-
lence of SAD was 10.9% (95% CI 9.7–12.2%) and
among respondents with alcohol abuse, it was 5.8 %
Social anxiety and alcohol NESARC 3
(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 NGSAD and 4.8 %
(95% CI 4.1–5.7%) for GSAD. Among respondents
with alcohol abuse, lifetime prevalences of SAD sub-
types were 3.6% (95% CI 3.07–4.2) for NGSAD and
2.2% (95% CI 1.8–2.7%) for GSAD. Because only
alcohol dependence was strongly associated with
SAD, subsequent analyses focus on dependence
and mention speciﬁc ﬁndings for abuse where signiﬁ-
Prevalence data for alcohol dependence and SAD is
shown stratiﬁed by sociodemographic characteristics
in Table 1. Co-morbid prevalence ranged from 0.6 %
among blacks to 2.6% among Native Americans.
Among respondents with alcohol dependence, the
odds of co-morbid SAD were signiﬁcantly greater for
women and lower for blacks and Hispanics relative to
non-Hispanic whites. Individuals aged 45–64 years
had higher odds of co-morbid SAD than those aged
18–29 years. Respondents with less than high school
education had signiﬁcantly greater odds of SAD than
those with a college education. Respondents with in-
dividual income less than $35000/year had signiﬁ-
cantly greater odds of SAD relative to those with
income of $35000 or greater. Among respondents with
SAD, odds of co-morbid alcohol dependence were
signiﬁcantly greater for men, lower for blacks and
lower for those aged o65 years.
For alcohol abuse, sociodemographic patterns were
similarly associated in respect of gender, but diﬀered
in that, among respondents with SAD, co-morbid al-
cohol abuse was associated with being native-born,
aged 30–64 years and having income of $20000/year
or greater, and was negatively associated with having
never married. Among respondents with alcohol
abuse, co-morbid SAD was associated with being
Native American and aged 30–64 years, and was
negatively associated with income of $70000/year or
greater. For SAD subtypes, co-morbid 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 psychi-
atric disorders among respondents with co-morbid
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 co-morbid alcohol de-
pendence and SAD had a mean of 4.6 (95 % CI 4.3–4.9)
additional DSM-IV disorders, compared with 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
Among respondents with alcohol dependence, co-
morbid SAD was signiﬁcantly associated with all Axis
I disorders except for conduct disorder and patho-
logical 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, respect-
ively) and the weakest with antisocial personality
disorder (OR 2.3). Among respondents with SAD, co-
morbid alcohol dependence was most strongly asso-
ciated with drug and nicotine dependence, pathologi-
cal gambling and histrionic and antisocial personality
disorders (OR 3.2–7.9) and was more modestly asso-
ciated with bipolar disorder, panic disorder, speciﬁc
phobia and psychotic disorders, as well as avoidant,
obsessive-compulsive, paranoid and schizoid person-
ality disorders (OR 1.5–2.4).
For alcohol abuse, co-morbidity patterns were
similar, but co-morbid alcohol abuse was signiﬁcantly
associated only with drug abuse and nicotine depen-
dence, 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 co-
morbidity, the overall pattern of direction and mag-
nitude of associations remained the same and the only
changes observed were in the level of signiﬁcance of
some of the associations due to smaller sample size
Table 3 shows that age of onset of SAD was signiﬁ-
cantly earlier than age of onset of alcohol dependence.
There were no signiﬁcant diﬀerences in age of onset of
either disorder between those with co-morbid alcohol
dependence and SAD and those with only one of the
disorders. Among co-morbid cases, SAD occurred ﬁrst
in 79.7% (95% CI 76.5–85.9), Alcohol dependence oc-
curred 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 depen-
dence 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
Among respondents with SAD, co-morbid alcohol
dependence was not associated with severity of SAD,
as measured by number of situations feared or sever-
ity of scrutiny fears. Among respondents with alcohol
dependence, co-morbid SAD was associated with
greater severity of dependence, as indicated by more
dependence criteria (Hasin et al. 2006), but not alcohol
4F. R. Schneier et al.
Table 1. Prevalence and sociodemographic characteristics
Co-morbid SAD and
alcohol dependence (n=909)
ORs associated with co-morbid SAD
SAD, ORs associated with
co-morbid alcohol dependence
% 95% CI OR 95% CI OR 95 % CI
Male n=18518 1.5 (1.3–1.8) 0.6 (0.4–0.7) 2.2 (1.7–2.8)
Female n=24575 1.2 (1.0–1.4) 1.0 (1.0–1.0) 1.0 (1.0–1.0)
White n=24507 1.6 (1.4–1.8) 1.0 (1.0–1.0) 1.0 (1.0–1.0)
Black n=8245 0.6 (0.4–1.0) 0.6 (0.4–1.0) 0.5 (0.3–0.9)
Native American n=701 2.6 (1.4–4.7) 1.1 (0.6–2.2) 1.1 (0.5–2.1)
Asian n=1332 0.7 (0.3–1.4) 0.9 (0.4–2.2) 0.6 (0.3–1.3)
Hispanic n=8308 0.7 (0.5–1.1) 0.6 (0.4–1.0) 0.7 (0.4–1.1)
Yes n=35622 1.5 (1.3–1.7) 1.0 (1.0–1.0) 1.0 (1.0–1.0)
No n=7320 0.4 (0.2–0.9) 0.7 (0.3–1.4) 0.5 (0.2–1.1)
18–29 n=8666 1.7 (1.3–2.1) 1.0 (1.0–1.0) 1.0 (1.0–1.0)
30–44 n=13382 1.5 (1.2–1.8) 1.0 (0.8–1.4) 0.8 (0.6–1.1)
45–64 n=12840 1.6 (1.3–1.9) 1.6 (1.2–2.1) 0.8 (0.6–1.1)
o65 n=8205 0.3 (0.2–0.5) 1.0 (0.6–1.7) 0.2 (0.1–0.4)
<High school n=7849 1.4 (1.0–1.9 ) 1.4 (1.0–2.0) 1.1 (0.7–1.6 )
High school n=12547 1.4 (1.1–1.7 ) 1.2 (0.9–1.5) 0.9 (0.7–1.2)
College n=22697 1.3 (1.1–1.6) 1.0 (1.0–1.0) 1.0 (1.0–1.0)
Individual income ($)
0–19000 n=21075 1.5 (1.2–1.8) 1.0 (1.0–1.0) 1.0 (1.0–1.0)
20–34000 n=9999 1.5 (1.2–1.9) 0.8 (0.6–1.1) 1.1 (0.8–1.6)
35–64000 n=9031 1.1 (0.8–1.5) 0.6 (0.4–0.8) 1.0 (0.7–1.4)
>70000 n=2988 1.0 (0.6–1.5) 0.6 (0.4–1.0) 1.2 (0.7–1.9)
Married n=22081 1.3 (1.1–1.5) 1.0 (1.0–1.0) 1.0 (1.0–1.0)
Widowed n=11117 1.5 (1.2–1.9) 1.1 (0.8–1.4) 1.2 (0.9–1.6)
Never married n=9895 1.5 (1.2–2.0) 0.8 (0.5–1.0) 1.2 (0.9–1.6)
CI, Conﬁdence interval.
The sample sizes in the second column provide denominators for the prevalence of co-morbid social anxiety disorder (SAD)/alcohol dependence by sociodemographic group, but not
for the two odds ratio (OR) columns.
Social anxiety and alcohol NESARC 5
Table 2. Prevalence and odds ratios (ORs)of lifetime DSM-IV disorders among respondents with co-morbid social anxiety disorder (SAD)and alcohol dependence
Associated psychiatric disorders
Neither SAD nor AUD
Co-morbid SAD and alcohol
Alcohol dependence, ORs
associated with co-morbid SAD
SAD, ORs associated with
co-morbid alcohol dependence
% 95% CI % 95 % CI aOR
95% CI aOR 95 % CI
Any psychiatric disorder
30.7 (29.5–31.9) 97.0 (94.6–98.3) 8.0 (4.3–15.1) 7.1 (3.8–13.3)
Any Axis I disorder
27.2 (26.0–28.4) 93.9 (90.7–96.0) 4.4 (2.8–7.0) 5.1 (3.2–8.2)
Any drug use disorder 2.8 (2.5–3.1) 45.7 (39.9–51.6) 1.3 (1.0–1.7) 4.4 (3.2–6.1)
Drug abuse disorder 2.4 (2.1–2.6) 19.5 (15.6–24.1) 0.7 (0.5–0.9) 1.7 (1.2–2.5)
Drug dependence disorder 0.4 (0.3–0.5) 26.2 (21.1–32.1) 2.4 (1.7–3.3) 7.9 (4.9–13.0)
Nicotine dependence disorder 9.6 (8.9–10.3) 59.2 (53.6–64.6) 1.5 (1.1–1.9) 4.7 (3.5–6.3)
Any mood disorder 13.2 (12.6–13.9) 64.1 (58.1–69.7) 3.5 (2.6–4.6) 2.0 (1.5–2.7)
Major depressive disorder 10.5 (9.9–11.1) 35.4 (30.5–40.7) 1.9 (1.4–2.4) 1.2 (0.9–1.5)
Dysthymia 2.3 (2.1–2.5) 12.9 (9.7–16.8) 2.0 (1.4–3.0) 1.3 (0.9–1.9)
Bipolar I disorder 1.5 (1.3–1.6) 21.9 (17.4–27.3) 3.1 (2.3–4.3) 2.2 (1.5–3.2)
Bipolar II disorder 0.7 (0.6–0.8) 5.8 (3.6–9.2) 2.1 (1.2–3.6) 2.2 (1.2–4.0)
Any anxiety disorder 10.7 (10.0–11.4) 63.1 (57.7–68.1) 4.9 (3.9–6.2) 1.7 (1.4–2.2)
Panic disorder 3.4 (3.1–3.6) 30.0 (25.5–34.8) 3.5 (2.6–4.6) 1.6 (1.2–2.1)
Speciﬁc phobia 6.7 (6.2–7.2) 46.0 (40.5–51.6) 4.7 (3.7–6.0) 1.7 (1.3–2.2)
Generalized anxiety disorder 2.5 (2.2–2.8) 27.3 (22.6–32.6) 4.7 (3.5–6.4) 1.3 (0.9–1.8)
Conduct disorder 0.8 (0.7–1.0) 0.8 (0.3–2.1) 0.5 (0.2–1.3) 0.2 (0.1–0.7)
Pathological gambling 0.1 (0.1–0.2) 1.4 (0.8–2.5) 0.9 (0.4–1.7) 3.2 (1.3–7.6)
Psychotic disorder 0.2 (0.2–0.3) 2.9 (1.4–6.3) 3.5 (1.3–9.2) 2.5 (1.0–6.8)
Any personality disorder 9.0 (8.5–9.6) 71.7 (66.6–76.3) 6.3 (4.8–8.2) 2.6 (2.0–3.4)
Avoidant 1.1 (0.9–1.2) 29.4 (24.5–34.8) 13.4 (9.5–18.8) 1.5 (1.1–2.1)
Dependant 0.3 (0.2–0.3) 5.6 (3.5–9.1) 7.7 (3.9–15.0) 1.1 (0.6–2.1)
Obsessive–compulsive 5.1 (4.7–5.5) 38.9 (33.9–44.2) 4.1 (3.2–5.3) 1.5 (1.1–1.9)
Paranoid 2.6 (2.3–2.8) 33.8 (28.5–39.5) 5.6 (4.3–7.4) 2.4 (1.8–3.3)
Schizoid 1.8 (1.6–2.0) 21.2 (17.3–25.7) 4.7 (3.5–6.3) 1.4 (1.0–1.9)
Histrionic 0.9 (0.8–1.0) 15.4 (11.9–19.6) 3.5 (2.5–5.0) 3.2 (2.0–5.0)
Antisocial 1.2 (1.0–1.3) 23.8 (19.5–28.7) 2.3 (1.7–3.2) 3.7 (2.5–5.6)
AUD, Alcohol use disorders ; CI, conﬁdence intervals ; aOR, adjusted odds ratio.
These ORs are adjusted for sex, US born, income, marital status, education, race, age, urbanicity, and region.
Any psychiatric disorder includes any drug use disorder, nicotine dependence disorder, any mood disorder, panic disorder, speciﬁc phobia, generalized anxiety disorder, conduct
disorder, pathological gambling and psychotic disorder.
Any Axis I disorder includes any drug use disorder, nicotine dependence disorder, any mood disorder, panic disorder, speciﬁc phobia, generalized anxiety disorder, conduct disorder,
pathological gambling, psychotic disorder and any personality disorder.
6F. R. Schneier et al.
abuse. Family history of AUD was more prevalent
among individuals with co-morbid SAD and alcohol
dependence compared with those with either disorder
alone. SF-12 scores for social functioning, role
emotional and mental health scales were worse among
individuals with co-morbid alcohol dependence and
SAD, or with SAD alone, compared with individuals
with alcohol dependence alone, but there were no
signiﬁcant diﬀerences between those with SAD alone
and those with co-morbid alcohol dependence and
SAD. Rates of treatment-seeking for either disorder
were not signiﬁcantly aﬀected by co-morbidity with
When alcohol abuse was examined separately,
and SAD subtypes were examined separately, patterns
of association with SAD severity remained non-
signiﬁcant. Individuals with either subtype of SAD co-
morbid 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, co-morbidity, disability
and treatment-seeking patterns of individuals with
co-morbid SAD and AUD. We found that: (1) co-
morbid AUD (dependence or abuse) and SAD is a
prevalent dual diagnosis that is associated with in-
creased co-morbidity with other psychiatric disorders ;
(2) SAD is associated with increased alcohol depen-
dence (and weakly, with alcohol abuse) ; (3) in persons
with alcohol dependence, SAD is associated with in-
creased family history of AUD and severity of AUD,
impairment and co-morbidity ; (4) treatment rates are
low for SAD and AUD, whether occurring together or
Consistent with prior studies documenting high
rates of SAD among AUD patients and high rates of
AUD among SAD patients, we found that co-morbid
SAD and AUD had a lifetime prevalence of 2.4 %. The
ﬁnding that co-morbid SAD is associated with alcohol
dependence, in particular, increased severity of de-
pendence, and increased impairment relative to al-
cohol dependence or abuse alone is consistent with
ﬁndings from clinical samples (Thomas et al. 1999).
Unlike some other reports from community and clini-
cal samples (e.g. Schneier et al. 1989 ; Buckner et al.
2008b,c), the co-morbid condition was not associated
with greater severity of SAD, scrutiny fears or im-
pairment 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
Table 3. Age of onset, severity, family history, treatment-seeking and disability among respondents with alcohol dependence, social
anxiety disorder (SAD)and co-morbid disorders
Co–morbid SAD and alcohol
without SAD (n=4294)
Mean 95% CI Mean 95% CI Mean 95% CI
Age of onset (SAD) 15.7 (14.8–16.6) 14.3 (13.2–15.4)
Age of onset (AUD) 21.7 (20.9–22.5) 21.1 (20.8–21.4)
No. of social fears 7.2 (6.9–7.4) 7.1 (6.7–7.5)
No. of scrutiny fears 4.7 (4.5–4.8) 4.5 (4.3–4.8)
No. of AUD abuse criteria 2.0 (1.9–2.1) 1.8 (1.8–1.9)
No. of AUD dependence criteria 4.7 (4.5–4.8) 4.3 (4.2–4.4)
Social functioning scale 45.2 (44.1–46.3) 41.4 (37.2–45.6) 49.8 (49.2–50.5)
Role emotional scale 44.9 (43.8–46.0) 41.5 (38.1–44.8) 48.7 (47.9–49.4)
Mental health scale 44.0 (43.1–44.9) 41.2 (37.0–45.5) 47.9 (47.2–48.6)
Family history of AUD ( %) 43.6 (40.3–47.1) 64.6 (59.3–69.5) 52.4 (50.5–54.3)
Treatment sought for SAD ( %) 17.5 (14.8–20.6) 23.8 (19.5–28.8)
Treatment sought for AUD ( %) 25.7 (21.5–30.5) 24.0 (22.5–25.5)
CI, Conﬁdence intervals.
SF-12 Subscale data are reported for 12-month samples : SAD without alcohol use disorders (AUD) ( n=999) ; co-morbid SAD
and alcohol dependence (n=88) ; alcohol dependence (n=1484).
Social anxiety and alcohol NESARC 7
consistent qualitative diﬀerences from the ﬁndings for
alcohol dependence and SAD overall.
Sociodemographic correlates of co-morbid alcohol
dependence and SAD were intermediate to those of
each disorder; but patterns of additional co-morbidity
associated with the combined condition appear to be
the sum of co-morbidity separately associated with
alcohol dependence and SAD. Among persons with
SAD, co-morbid alcohol dependence was particularly
associated with increased co-morbidity of drug and
nicotine dependence, pathological gambling and his-
trionic and antisocial personality disorders. Among
persons with alcohol dependence, co-morbid SAD was
most strongly associated with mood disorders, other
anxiety disorders and dependent and avoidant per-
sonality disorders. The high co-morbidity with avoi-
dant personality disorder is likely due in part to the
substantial overlap in its diagnostic criteria with those
of SAD (Chambless et al. 2008). While co-morbid SAD
conferred a broad increase in psychiatric co-morbidity,
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 of ex-
ternalizing disorders among persons with alcohol de-
pendence. Alcohol abuse was generally associated
with lower rates of co-morbidity, compared with al-
In current models of the structure of common men-
tal disorders, SAD is generally conceptualized as an
internalizing disorder, shown to have greatest co-
morbidity with other internalizing disorders (i.e. mood
and anxiety disorders and avoidant personality dis-
order). AUD are considered externalizing disorders,
having the strongest association with other externaliz-
ing disorders, such as other substance use disorders
and antisocial personality disorder (Krueger, 1999 ;
Vollebergh et al. 2001; Kendler et al. 2003). However,
the clinical presentation of co-morbid AUD and SAD
includes features of internalizing and externalizing
disorders and does not resemble the clinical ﬁnger-
print of either AUD or SAD alone. Our ﬁndings sug-
gest that externalizing and internalizing features can
exist in tandem and thus should not be conceptualized
as opposites on a spectrum. This is consistent with re-
cent ﬁndings that a subset of persons with SAD para-
doxically evidence risk-prone behavior (Kashdan et al.
The present study replicates previous ﬁndings that
SAD precedes and increases risk for AUD (Schneier
et al. 1989; Merikangas et al. 1998; Crum & Pratt, 2001;
Zimmermann et al. 2003; Buckner et al. 2008b), sup-
porting the hypothesis of a directional etiological
link from SAD to alcohol dependence and abuse.
On the other hand, co-morbid 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 co-morbid condition was not as-
sociated with a greater number of social fears. The true
relationship between these disorders is undoubtedly
Animal studies have shown that stress and sub-
stance use disorders share common circuitry and the
potentiating eﬀect of corticotropin-releasing factor on
mesolimbic dopaminergic reward pathways (Piazza
and Le Moal, 1998), suggesting that stress may re-
inforce 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 (Kushner et al.
2000; Thomas et al. 2003; Dai et al. 2007) and inter-
fering with the consolidation of memories related to
stressful events (Gerlach et al. 2006). The current ﬁnd-
ing 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 al-
coholics diﬀer from controls with regard to HPA-axis
hormonal response to subjective psychological stress
(Uhart et al. 2006; Dai et al. 2007). However, though
alcohol is a short-term anxiolytic, it is also disinhibit-
ing, which may 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 per-
sistence of social anxiety by impairing extinction of
fear response and possibly interfering with desensiti-
zation (Cameron et al. 1987). Furthermore, alcohol
withdrawal is anxiogenic in the setting of autonomic
hyperactivation (Johnston et al. 1991; Duka et al. 2002).
The etiology of joint AUD and SAD may therefore be
heterogeneous, multi-factorial and bidirectional.
Despite the ﬁnding that co-morbid AUD (depend-
ence or abuse) and SAD was more impairing than
either AUD alone, and the known tendency for co-
morbid cases in general to be more likely to receive
treatment, the majority of respondents with co-morbid
AUD and SAD did not receive treatment for either
disorder. The current ﬁndings are consistent with data
from previous epidemiological studies (Olfson et al.
2000; Wang et al. 2005; Cohen et al. 2007) and suggest
that eﬀorts to increase treatment rates for AUD
and SAD represent an important opportunity for im-
proving quality of care in this population with joint
co-morbidity. Earlier onset of SAD than of AUD and
expectations of individuals with SAD that alcohol will
alleviate anxiety symptoms (Ham et al. 2007) suggests
that psychoeducation and treatment for SAD, es-
pecially in the presence of family history of AUD, may
8F. R. Schneier et al.
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 co-morbid AUD (dependence
or abuse) and SAD, including the low rates of treat-
ment-seeking associated with each disorder. SAD
patients may be reluctant to seek treatment due to
avoidance of interaction with authority ﬁgures or em-
barrassment 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 dis-
order 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 co-
morbid SAD and AUD constitutes another major ob-
stacle to eﬀective care of this population. Use of ben-
zodiazepines, 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 addic-
tion (Blanco et al. 2002), increased risk of relapse to
alcohol (Chick et al. 2004) and dietary restrictions, re-
spectively (Balon et al. 1999). Popular group treatment
approaches to AUD, such as Alcoholic Anonymous,
present speciﬁc social obstacles for persons with co-
morbid 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 co-morbid AUD and SAD, poss-
ibly due to the focus of most research and treatment
programmes on pure rather than co-morbid disorders
or to the assumption that treatments eﬃcacious for a
pure disorder work in the presence of co-morbidity
(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 cogni-
tive behavioral therapy (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 im-
portant elements in the treatment of co-morbidity,
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 co-morbidity, based on an
integration of cognitive behavioral and motivational
enhancement strategies, and preliminary data are en-
couraging (Buckner et al. 2008a).
This study shares limitations common to most
large epidemiological studies. Because the NESARC
sample only included civilian households and group-
living populations aged >18 years, information was
unavailable on adolescents or individuals in prison.
The cross-sectional design does not permit us to es-
tablish directionality between symptoms of social an-
xiety and use of alcohol, or between lifetime disorders
and current impairment in functioning. Some covari-
ates in our analyses may be causes, correlates or con-
sequences 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 aﬀec-
ted individuals who received mental health care for
disorders other than SAD or AUD.
Our study details the impact of co-morbid AUD
and SAD. Co-morbid AUD (dependence or abuse) and
SAD are 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
The National Epidemiologic Survey on Alcohol and
Related Conditions was sponsored by the National
Institute on Alcohol Abuse and Alcoholism and fun-
ded, 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). The views and opinions expressed in this re-
port are those of the authors and should not be con-
strued to represent the views of any of the sponsoring
organizations, agencies or the US government.
Declaration of Interest
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