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Social Anxiety Disorder and Alcohol Use Disorder Comorbidity in the National Epidemiologic Survey on Alcohol and Related Conditions

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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 United States. 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. 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. 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.
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Social anxiety disorder and alcohol use disorder
co-morbidity in the National Epidemiologic Survey
on Alcohol and Related Conditions
F. R. Schneier
1
,
2
#, T. E. Foose
1
,
2
#, D. S. Hasin
1
,
2
,
3
, R. G. Heimberg
4
, S.-M. Liu
1
, B. F. Grant
5
* and
C. Blanco
1
,
2
1
New York State Psychiatric Institute, New York, New York, USA
2
Departments of Psychiatry, College of Physicians and Surgeons, Columbia University, New York, New York, USA
3
Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, New York, USA
4
Department of Psychology, Temple University, Philadelphia, Pennsylvania, USA
5
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
United States.
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.
Introduction
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 : bgrant@willco.niaaa.nih.gov)
#These authors contributed equally to this work.
Psychological Medicine, Page 1 of 12. fCambridge University Press 2009
doi:10.1017/S0033291709991231
ORIGINAL ARTICLE
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.
2006).
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.
Methods
Subjects
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.
Measures
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.
2007).
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.
2007).
Statistical analyses
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).
Results
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-
cant.
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
alone.
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
(n=88).
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
abuse.
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
Sociodemographic characteristics
Co-morbid SAD and
alcohol dependence (n=909)
Alcohol dependence,
ORs associated with co-morbid SAD
SAD, ORs associated with
co-morbid alcohol dependence
% 95% CI OR 95% CI OR 95 % CI
Sex
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)
Race
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)
Native
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)
Age (years)
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)
Education
<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)
Marital status
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
(n=30176)
Co-morbid SAD and alcohol
dependence (n=487)
Alcohol dependence, ORs
associated with co-morbid SAD
SAD, ORs associated with
co-morbid alcohol dependence
% 95% CI % 95 % CI aOR
a
95% CI aOR 95 % CI
Any psychiatric disorder
b
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
c
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.
a
These ORs are adjusted for sex, US born, income, marital status, education, race, age, urbanicity, and region.
b
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.
c
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
the other.
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.
Discussion
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
separately.
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
SAD without
AUD (n=1074)
Co–morbid SAD and alcohol
dependence (n=487)
Alcohol dependence
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)
SF-12 subscales
a
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.
a
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-
cohol dependence.
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.
2009).
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
more complex.
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
these individuals.
Acknowledgements
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
None.
Social anxiety and alcohol NESARC 9
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12 F. R. Schneier et al.
... El TAS es el segundo trastorno de ansiedad más frecuente (después de la fobia específica) y su prevalencia global a nivel mundial de 2,4% en los últimos 12 meses y de 4,0% a lo largo de la vida (Stein et al., 2017), lo sitúa en lo alto del ranking de problemas de salud mental, después de los trastornos depresivos y por consumo de sustancias, con los que suele presentarse de forma comórbida (p. ej., Beesdo et al., 2007;MacKenzie y Fowler, 2013;Pignon et al., 2018;Quevedo et al., 2020;Schneier et al., 2010;Smith y Randall, 2012;Stein et al., 2017). Una serie de estudios ha encontrado relación entre la ansiedad social y otros trastornos o problemas psicológicos, como la depresión, la baja autoestima, el exceso de preocupaciones, el consumo de alcohol, el déficit en habilidades sociales, etc. Así, por ejemplo, Ratnani et al. (2017) encontraron que las personas con ansiedad social eran más propensas a experimentar depresión y el nivel de gravedad de la depresión se correlacionaba con la gravedad de la ansiedad social (r de 0,36 a 0,45). ...
... En estudios con muestras clínicas (Tyrała et al., 2015) esta correlación es incluso mayor (r= 0,64), Adicionalmente, existe cierto apoyo empírico para considerar al TAS como un precursor de los trastornos depresivos (p. ej., Beesdo et al., 2007;MacKenzie y Fowler, 2013;Pignon et al., 2018;Quevedo et al., 2020;Schneier et al., 2010;Stein et al., 2017). ...
... No obstante, los datos de la literatura sobre la relación entre la ansiedad social y el consumo de alcohol son confusos. Así, por ejemplo, Schneier et al. (2010) informaron que, en la población general estadounidense, la prevalencia conjunta y a lo largo de la vida del TAS y de un trastorno por consumo de alcohol era del 2,4% y que, entre los que padecían TAS, el 27,3% tenía dependencia del alcohol y el 20,9% abusaba de él. Pero, en otros estudios, se informa de la ausencia de dicha relación (p. ...
Article
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En un trabajo anterior (Caballo et al., 2021) comprobamos la eficacia del programa de Intervención multidimensional para la ansiedad social (IMAS) en la reducción de los síntomas de ansiedad social. En este estudio cuasiexperimental, con medidas pre/postratamiento y seguimiento, hallamos el impacto del programa IMAS en otros problemas relacionados con la ansiedad social. 57 personas diagnosticadas con un trastorno de ansiedad social (TAS), según el DSM-5, contestaron a cuestionarios que medían habilidades sociales, depresión, síntomas del trastorno de la personalidad por evitación, alcoholismo, autoestima, sensibilidad personal, preocupaciones y calidad de vida. Diferentes terapeutas llevaron a cabo el tratamiento en Ecuador, España y Paraguay. Los resultados mostraron importantes mejoras en el postratamiento en prácticamente todos los aspectos evaluados, mejoras que se mantenían a los seis meses. Los tamaños del efecto sobre la eficacia del tratamiento iban de medianos a grandes. Se comparó también el programa IMAS con terapia cognitivo conductual individual y tratamiento farmacológico, con resultados favorables para el programa IMAS. Este nuevo programa para el tratamiento de la ansiedad social tiene un impacto importante en otros problemas relacionados habitualmente con el TAS.
... Social anxiety disorder (SAD), also known as social phobia, is characterized, primarily, by an intense fear of being observed and negatively evaluated by others in social situations, whether performing in front of or interacting with others (American Psychiatric Association [APA], 2013). SAD is the second most common anxiety disorder (after specific phobia) and its overall worldwide prevalence of 2.4% in the past 12 months and 4.0% over a lifetime (Stein et al., 2017), places it at the top of the ranking of mental health problems, after depressive and substance use disorders, with which it often occurs comorbidly (e.g., Beesdo et al., 2007;MacKenzie & Fowler, 2013;Pignon et al., 2018;Quevedo et al., 2020;Schneier et al., 2010;Smith & Randall, 2012;Stein et al., 2017). There is a whole series of studies that have found relationships of social anxiety with other disorders or psychological problems, such as depression, low self-esteem, excessive worry, alcohol consumption, deficits in social skills, etc. ...
... In studies with clinical samples (Tyrała et al., 2015), this correlation is even higher (r= .64), Additionally, there is some empirical support for considering SAD as a precursor of depressive disorders (e.g., Beesdo et al., 2007;MacKenzie & Fowler, 2013;Pignon et al., 2018;Quevedo et al., 2020;Schneier et al., 2010;Stein et al., 2017). ...
... However, the data in the literature on the relationship between social anxiety and alcohol use are indeed confusing. Thus, for example, Schneier et al. (2010) reported that, in the general U.S. population, the joint lifetime prevalence of SAD and an alcohol use disorder was 2.4% and that among those with SAD, 27.3% had alcohol dependence and 20.9% abused alcohol. But other studies report a lack of such a relationship (e.g., Bartholomay et al., 2021;Villarosa et al., 2014) or even a negative correlation (e.g., Ham et al., 2007;Ham & Hope, 2005, 2006Papachristou et al., 2018;Schry & White, 2013). ...
Article
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In a previous work (Caballo et al., 2021) we tested the effectiveness of the Multidimensional Intervention for Social Anxiety (MISA) program in reducing social anxiety symptoms. In this quasi-experimental study, with pre/post-treatment and follow-up measures, we examined the impact of the MISA program on other problems related to social anxiety. 57 people diagnosed with social anxiety disorder (SAD), according to DSM-5, were assessed with a diagnostic interview and questionnaires measuring social skills, depression, avoidant personality disorder symptoms, alcoholism, self-esteem, personal sensitivity, worries, and quality of life. Different therapists carried out the treatment in Ecuador, Spain, and Paraguay. The results showed significant improvements at post-treatment in virtually all measures assessing the above variables, improvements that were maintained at six months. Effect sizes on treatment effectiveness ranged from medium to large. The MISA program was also compared with individual cognitive behavioral therapy and pharmacological treatment, with favorable results for the MISA program. In conclusion, this new program for the treatment of social anxiety has a significant impact on other problems usually related to SAD.
... People with social anxiety disorder (SAD) are two to three times more likely to develop an alcohol use disorder (AUD) than the general population (Kushner et al., 2000). Among those diagnosed with comorbid SAD and AUD, SAD precedes the onset of AUD approximately 79% of the time (Schneier et al., 2010), suggesting SAD prospectively increases risk for alcohol-related problems. Given this temporal ordering, links between social anxiety and alcohol use are often explained with classic theories that suggest alcohol, an anxiolytic, is consumed to reduce distress, which in turn negatively reinforces alcohol use (e.g., tension-reduction; Conger, 1956). ...
... Fifth, AUD was not an inclusion or exclusion criterion. Given that comorbid SAD and AUD is associated with greater impairment than either alone (Schneier et al., 2010), research on this subgroup is important. Sixth, levels of coping motives were relatively low (especially depression), which might have limited ability to detect effects. ...
Article
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People with social anxiety disorder (SAD) are at increased risk for alcohol-related problems. Most research exploring social anxiety and alcohol use has examined negative drinking consequences, with less consideration of positive consequences—namely positive social experiences—that may reinforce alcohol use. In this daily diary study, we examined how adults diagnosed with SAD (N = 26) and a psychologically healthy control group (N = 28) experienced positive drinking consequences in naturally occurring drinking episodes during the study period. For 14 consecutive days, participants answered questions about alcohol use, motives for drinking, and positive consequences of drinking. On days when participants drank, those with SAD were more likely than healthy controls to perceive a reduction in anxiety, but the two groups did not differ in their likelihood of experiencing positive social drinking consequences. For both groups, on days when they were more motivated to drink to enhance social experiences (affiliation motives) or cope with distress (coping motives), they were more likely to obtain positive consequences from drinking. Compared to controls, participants with SAD endorsed stronger trait and daily coping motives (anxiety-coping, social anxiety-coping, and depression-coping). Results are discussed in the context of reinforcement mechanisms that may maintain social anxiety and alcohol use.
... Alcohol use disorder (AUD) is a major public health concern and the third leading preventable disease in the United States (Bouchery et al., 2011;GBD 2016Alcohol Collaborators, 2018. AUD is a complex and chronic disease that is often accompanied by affective disorders such as anxiety and depression (Koob and Volkow, 2010;Fink et al., 2016), and studies show that patients with depression and anxiety have increased alcohol use compared to their counterparts (Schneier et al., 2010;Wiener et al., 2018). Because of the complex pathogenesis, treatments for the comorbidity of AUD with mood disorders have not been very successful and improved pharmacotherapy is needed in this direction. ...
Article
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Background Alcohol use disorder (AUD) is a complex and chronic relapsing brain disease, which is often co-morbid with psychiatric disorders such as anxiety and depression. AUD phenotypes differ in men and women. Although genetic factors play an important role in its pathophysiology, epidemiologic evidence suggests that during prenatal development, individuals are more vulnerable to the negative effects of environmental factors that may predispose them to AUD later in life. We explored the effects of prenatal stress on the development of AUD phenotypes as well as anxiety- and depression-like behaviors using rat model. Methods In this study, timed-pregnant Sprague Dawley dams were used. Dams in the control group were left undisturbed throughout gestation, whereas dams in stress groups were either subjected to protracted or acute restraint stress under bright light. At adulthood, the anxiety-like, ethanol drinking, and sucrose drinking behaviors were measured using the Light/Dark Box test and two-bottle free-choice procedure. Results Compared to the control group, both the male and female offspring in the stress groups exhibited anxiety-like behavior and consumed significantly higher amounts of ethanol in which the acute stress group demonstrated the higher ethanol preference. Moreover, male but not female offspring from the stress groups had decreased sucrose preferences. Conclusion These findings suggest that protracted and acute prenatal stress in late pregnancy can induce in anxiety-, depressive-like behaviors, and excessive ethanol intake in adult offspring.
... Alcohol use disorder (AUD) is a leading cause of worldwide disease burden, affecting over 280 million people worldwide, and harmful alcohol consumption is responsible for over 3 million deaths per year (WHO, 2018). AUD is comorbid with a variety of neuropsychiatric disorders, and nearly all cases present with negative mood symptoms, including depression (Brière, Rohde, Seeley, Klein, & Lewinsohn, 2014), bipolar disorder (Farren, Hill, & Weiss, 2012), and anxiety disorders (Grant et al., 2004;Lai, Cleary, Sitharthan, & Hunt, 2015;Schneier et al., 2010). Some studies have reported that up to 40% of AUD patients have a mood disorder, and a third suffer from an anxiety disorder. ...
Article
Alcohol use disorder (AUD) is frequently comorbid with mood disorders, and these co-occurring neuropsychiatric disorders contribute to the development and maintenance of alcohol dependence and relapse. In preclinical models, mice chronically exposed to alcohol display anxiety-like and depressive-like behaviors during acute withdrawal and protracted abstinence. However, in total, results from studies using voluntary alcohol drinking paradigms show variable behavioral outcomes in assays measuring negative affective behaviors. Thus, the main objective of this review is to summarize the literature on the variability of negative affective behaviors in mice after chronic alcohol exposure. We compare the behavioral phenotypes that emerge during abstinence across different exposure models, including models of alcohol and stress interactions. The complicated outcomes from these studies highlight the difficulties of assessing negative affective behaviors in mouse models designed for the study of AUD. We discuss new behavioral assays, comprehensive platforms, and unbiased machine-learning algorithms as promising approaches to better understand the interaction between alcohol and negative affect in mice. New data-driven approaches in the understanding of mouse behavior hold promise for improving the identification of mechanisms, cell subtypes, and neurocircuits that mediate negative affect. In turn, improving our understanding of the neurobehavioral basis of alcohol-associated negative affect will provide a platform to test hypotheses in mouse models that aim to improve the development of more effective strategies for treating individuals with AUD and co-occurring mood disorders.
... Not only are these comorbidities extremely common, but also they can often result in significantly worse outcomes for the individual. Individuals with comorbid affective disorders and AUD are less likely to seek treatment and even in treatment centers, report increased rates of relapse (Driessen et al. 2001;Schellekens et al. 2015;Schneier et al. 2010;Haver and Gjestad, 2005). ...
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Full-text available
Alcohol use disorders (AUDs) are a major problem across the USA. While AUD remains a complex human condition, it is difficult to isolate the directionality of anxiety and ethanol (EtOH) drinking from outside influences. The present study sought to investigate the relationship between affective states and EtOH intake using male and female Sprague–Dawley rats. Using complementary tests of anxiety- and depressive-like behavior, we found sex- and test-specific differences in basal affective behavior such that females displayed enhanced anxiety-like behavior in the splash test and males displayed enhanced anxiety-like behavior in the novelty-suppressed feeding test. Although, there were no sex differences in EtOH intake and no correlation between baseline anxiety-like behavior and subsequent EtOH intake, we did find that depressive-like behavior predicted future EtOH intake in female rats only. In addition, we observed an increase in depressive-like behavior is male rats in both the water and EtOH drinking groups (compared to baseline levels). Furthermore, post-drinking anxiety-like behavior, but not depressive-like behavior predicted subsequent EtOH intake in female rats. Lastly, we found a history of EtOH intake decreased pain thresholds in male and female rats, but increased anxiety-like and depressive-like behavior was associated with decreased thermal sensitivity only in EtOH-drinking males. Together, these experiments provide important information on the complex interaction between negative affect and EtOH intake and how these two contexts reciprocally do, or do not, influence each other in a sex-specific manner.
... At the diagnostic level, epidemiological studies have shown relationships between specific anxiety disorders and Cannabis Use Disorder (CUD) or Alcohol Use Disorder (AUD; Grant et al., 2015;Hasin et al., 2016). Of studies examining co-occurring anxiety disorders, evidence suggests co-morbidity between AUD or CUD and select disorders, such as Generalized Anxiety Disorder (GAD) and Social Anxiety Disorder (Social Phobia; Grant et al., 2015;Hasin et al., 2016;Schneier et al., 2010). Metaanalytic work has shown that social anxiety is negatively associated with alcohol use, but positively associated with alcohol-related problems (Schry & White, 2013), prompting work to examine possible moderators (Adams et al., 2019). ...
Article
Using ecological momentary assessment (EMA), we assessed momentary patterns of alcohol and cannabis co-use in college students and whether state-level and baseline reports of anxiety varied based on type of substance(s) consumed. Students (N=109) reporting regular cannabis use completed a baseline assessment and two-week signal-contingent EMA, with three random prompts/day. At each EMA instance, we categorized instances of substance "usage" as: 1) no use, 2) cannabis-only, 3) alcohol-only, or 4) co-use of alcohol and cannabis (i.e., reports of alcohol and cannabis use within the same prompt). Using temporal sequenced data, we explored how state-level anxiety varied before and after usage type using multiple multilevel structural equation models (MSEMs) and whether baseline factors (general anxiety, social anxiety, and sex) influenced the relation between usage type and state-level anxiety. Participants were 63.3% White, 58.7% female, used cannabis near-daily, and commonly reported co-use. Models examining whether usage type predicted subsequent state-level anxiety were predominantly significant, with the majority of relationships being more pronounced for participants with higher baseline general anxiety. In examining whether momentary state-level anxiety predicted usage type, in instances when participants reported higher levels of momentary anxiety, they were more likely to report no use compared to co-use and cannabis-only, with sex moderating some of the relationships. Social anxiety did not moderate any of the within-person associations between state-level anxiety and usage type. This study provides preliminary evidence that report of momentary anxiety varies based on substance type. Future research is needed to establish co-use related synergistic effects and correlates.
... Not only are these comorbidities extremely common, they can often result in significantly worse outcomes for the individual. Indeed, individuals with comorbid affective disorders and AUD are less likely to seek treatment and even in treatment centers, report increased rates of relapse (Driessen et al., 2001, Schellekens et al., 2015, Schneier et al., 2010, Haver and Gjestad, 2005. ...
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Alcohol use disorders (AUDs) are a major problem across the United States. While AUD remains a complex human condition, it is difficult to isolate the directionality of anxiety and ethanol (EtOH) drinking from outside influences. The present study sought to investigate the relationship between affective states and EtOH intake using male and female Sprague Dawley rats. Using complementary tests of anxiety- and depressive-like behavior, we found sex- and test-specific differences in basal affective behavior such that females displayed enhanced anxiety-like behavior in the Splash Test and males displayed enhanced anxiety-like behavior in the Novelty Suppressed Feeding Test. Although there were no sex differences in EtOH intake and no correlation between anxiety-like behavior and subsequent EtOH intake, we did find that depressive-like behavior predicted future EtOH intake in females rats only. In addition, we observed an increase in depressive-like behavior is male rats in both the water and EtOH drinking groups. Furthermore, anxiety-like behavior, but not depressive-like behavior predicted subsequent EtOH intake in female rats. Lastly, we found a history of EtOH intake decreased pain thresholds in male and female rats. Together, these experiments provide important information on the complex interaction between negative affect and alcohol intake and how these two contexts reciprocally do, or do not, influence each other in a sex-specific manner.
Article
Understanding factors that contribute to the escalation of alcohol consumption is key to understanding how an individual transitions from non/social drinking to AUD and to providing better treatment. In this review, we discuss how the way ethanol is consumed as well as individual and environmental factors contribute to the escalation of ethanol consumption from intermittent low levels to consistently high levels. Moreover, we discuss how these factors are modelled in animals. It is clear a vast array of complex, interacting factors influence changes in alcohol consumption. Some of these factors act early in the acquisition of ethanol consumption and initial escalation, while others contribute to escalation of ethanol consumption at a later stage and are involved in the development of alcohol dependence. There is considerable need for more studies examining escalation associated with the formation of dependence and other hallmark features of AUD, especially studies examining mechanisms, as it is of considerable relevance to understanding and treating AUD.
Article
Objectives Social anxiety disorder (SAD) and alcohol use disorder (AUD) are highly comorbid and this comorbidity is associated with poorer clinical outcomes. Integrating exposure-based treatment for SAD into the context of typical AUD treatment programs should improve engagement and treatment outcomes for this population. Methods After initial development of a fully integrated, intensive outpatient program (IOP) for individuals with comorbid SAD and AUD, patients with SAD and AUD were recruited from a community-based SUD specialty clinic (N = 56) and randomized to either (a) usual care (UC), consisting of the evidence-based Matrix Model of Addiction IOP; or (b) the Fully Integrated Treatment (FIT) for comorbid SAD and AUD IOP. Participants were assessed on indices of social anxiety and alcohol use. Results By the 6-month follow-up, those in FIT showed superior improvement to UC on number of drinking days in the past 30 days and social anxiety severity at follow-up, but there were no differences between groups on quantity of alcohol consumed on drinking days. Alcohol-related problems improved in both groups, with no statistically significant differences. Within-group improvement was observed in FIT (but not in UC) on drinking to cope with social anxiety and avoidance of social situations without alcohol, but between-group effects were non-significant. In sum, the integrated treatment of SAD and AUD led to greater reductions in both the frequency of drinking and in social anxiety symptoms than usual care. Conclusions Targeting social anxiety in the context of AUD treatment is a promising approach to improving the treatment of this common comorbidity.
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Ninety-eight outpatients meeting DSM-III-R criteria for social phobia were evaluated for past history of RDC alcoholism using the SADS-LA structured interview. The resulting 16 subjects with a history of alcoholism were then compared to the 82 nonalcoholic social phobics. The alcoholic social phobics had more severe social phobia and tended to be less likely to be married. Both groups were similar in other measures of demographics. The mean age of onset of social phobia was significantly earlier than the mean age of onset of alcoholism, and social phobia preceded alcoholism in 15 of the 16 dual diagnosis subjects. Most of the dual diagnosis subjects reported using alcohol to self-medicate social phobic symptoms. These findings are consistent with the hypothesis that social phobia can be an important factor in the development of alcoholism.
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Methods: Data were obtained from the first and sec- ond measurement of the Netherlands Mental Health Sur- vey and Incidence Study (NEMESIS) (response rate at baseline: 69.7%, n=7076; 1 year later, 79.4%, n=5618). Nine common DSM-III-R diagnoses were assessed twice with the Composite International Diagnostic Interview with a time lapse of 1 year. Using structural equation mod- eling, the number of latent dimensions underlying these diagnoses was determined, and the structural and dif- ferential stability were assessed. Results: A 3-dimensional model was established as hav- ing the best fit: a first dimension underlying substance use disorders (alcohol dependence, drug dependence); a second dimension for mood disorders (major depres- sion, dysthymia), including generalized anxiety disor- der; and a third dimension underlying anxiety disorders (simple phobia, social phobia, agoraphobia, and panic disorder). The structural stability of this model during a 1-year period was substantial, and the differential stabil- ity of the 3 latent dimensions was considerable. Conclusions: Our results confirm the 3-dimensional model for 12-month prevalence of mental disorders. Re- sults underline the argument for focusing on core psy- chopathological processes rather than on their manifes- tation as distinguished disorders in future population studies on common mental disorders. Arch Gen Psychiatry. 2001;58:597-603
Article
Errors in Byline, Author Affiliations, and Acknowledgment. In the Original Article titled “Prevalence, Severity, and Comorbidity of 12-Month DSM-IV Disorders in the National Comorbidity Survey Replication,” published in the June issue of the ARCHIVES (2005;62:617-627), an author’s name was inadvertently omitted from the byline on page 617. The byline should have appeared as follows: “Ronald C. Kessler, PhD; Wai Tat Chiu, AM; Olga Demler, MA, MS; Kathleen R. Merikangas, PhD; Ellen E. Walters, MS.” Also on that page, the affiliations paragraph should have appeared as follows: Department of Health Care Policy, Harvard Medical School, Boston, Mass (Drs Kessler, Chiu, Demler, and Walters); Section on Developmental Genetic Epidemiology, National Institute of Mental Health, Bethesda, Md (Dr Merikangas). On page 626, the acknowledgment paragraph should have appeared as follows: We thank Jerry Garcia, BA, Sara Belopavlovich, BA, Eric Bourke, BA, and Todd Strauss, MAT, for assistance with manuscript preparation and the staff of the WMH Data Collection and Data Analysis Coordination Centres for assistance with instrumentation, fieldwork, and consultation on the data analysis. We appreciate the helpful comments of William Eaton, PhD, Michael Von Korff, ScD, and Hans-Ulrich Wittchen, PhD, on earlier manuscripts. Online versions of this article on the Archives of General Psychiatry Web site were corrected on June 10, 2005.
Article
Errors in Byline, Author Affiliations, and Acknowledgment. In the Original Article titled “Lifetime Prevalence and Age-of-Onset Distributions of DSM-IV Disorders in the National Comorbidity Survey Replication,” published in the June issue of the ARCHIVES (2005;62:593-602), an author’s name was inadvertently omitted from the byline and author affiliations footnote on page 592, and another author’s affiliation was listed incorrectly. The byline should have appeared as follows: “Ronald C. Kessler, PhD; Patricia Berglund, MBA; Olga Demler, MA, MS; Robert Jin, MA; Kathleen R. Merikangas, PhD; Ellen E. Walters, MS.” The author affiliations footnote should have appeared as follows: “Author Affiliations: Department of Health Care Policy, Harvard Medical School, Boston, Mass (Dr Kessler; Mss Demler and Walters; and Mr Jin); Institute for Social Research, University of Michigan, Ann Arbor (Ms Berglund); and Section on Developmental Genetic Epidemiology, National Institute of Mental Health, Rockville, Md (Dr Merikangas).” On page 601, the first sentence of the acknowledgment should have appeared as follows: “The authors appreciate the helpful comments of William Eaton, PhD, and Michael Von Korff, ScD.” Online versions of this article on the Archives of General Psychiatry Web site were corrected on June 10, 2005.
Article
The goals of this study were to describe demographic variables, drinking history, and the 6-month prevalence of Axis I comorbidity among alcohol-dependent subjects in Germany. The variables: amount of alcohol consumption, age at onset of the firs t alcohol consumed, age at onset of daily alcohol consumption, age at onset of withdrawal symptoms and number of detoxifications were related to the different comorbid disorders and gender. In this study, 556 patients from 25 alcohol treatment centres were enro lled between 1 January 1999 and 30 April 1999. After a minimum of 10 days of sobriety patients who fulfilled ICD-10 and DSM-IV crite ria of alcohol dependence were interviewed for data collection using the Mini-DIPS (German version of the Anxiety Disorders Intervi ew Schedule) and a standardized psychosocial interview. The 6-month prevalence of comorbid Axis I disorders was 53.1%. Among the patients with comorbidity, affective and anxiety disorders were most frequent. Comorbid stress disorder was associated with an early start of drinking, an early beginning of withdrawal symptoms, highest number of detoxifications, and the highest amount of alco hol consumed. Female patients with anxiety disorder consumed more alcohol and started earlier than females without this comorbid di s- order. The data do not answer the question of the pathogenesis of comorbid disorders and alcoholism, but indicate that stress d isorders in alcoholic patients and anxiety disorders in female alcoholics influence the course and severity of alcoholism.
Article
The aim of this paper is to report the prevalence of 12-month comorbidity between DSM-IV alcohol use disorders (abuse or dependence) and anxiety, affective and drug use disorders in the adult Australian general population and to examine the disability and health service utilisation associated with this comorbidity. The study uses data from the National Survey of Mental Health and Well Being (NSMH&WB). The NSMH&WB is a cross-sectional survey of 10,641 Australian adults conducted in 1997 that measured the prevalence of DSM-IV mental disorders in the previous 12 months and associated disability and health service utilisation. Results show approximately one-third of respondents with an alcohol use disorder (abuse or dependence) met criteria for at least one comorbid mental disorder in the previous 12 months. They were 10 times more likely to have a drug use disorder, four times more likely to have an affective disorder and three times more likely to have an anxiety disorder. Respondents with an alcohol use disorder and a comorbid mental disorder were significantly more disabled and higher users of health services than respondents with an alcohol disorder and no comorbid mental disorders. These results reinforce the need for both mental health and drug and alcohol professionals to be provided with education to assist with appropriate identification, management and referral of clients presenting with this complex range of disorders.
Article
Objective: To present nationally representative data on 12-month and lifetime prevalence, correlates and comorbidity of social anxiety disorder (SAD) among adults in the United States as determined by the 2001-2002 National Epidemiologic Survey on Alcohol and Related Conditions. Design: Face-to-face survey. Setting: The United States. Participants: Adults (aged 18 and over) residing in households and group quarters (N = 43,093). Main outcome measures: Prevalence and associations of SAD with sociodemographic and psychiatric correlates and Axis I and II disorders. Results: The prevalence of 12-month and lifetime DSM-IV SAD was 2.8% (95% CI = 2.5 to 3.1) and 5.0% (95% CI = 4.6 to 5.4), respectively. Being Native American, being young, or having low income increased risk, while being male, being of Asian, Hispanic, or black race/ethnicity, or living in urban or more populated regions reduced risk. Mean age at onset of SAD was 15.1 years, with a mean duration of 16.3 years. Over 80% of individuals with SAD received no treatment, and the mean age at first treatment was 27.2 years. Current and lifetime SAD were significantly related to other specific psychiatric disorders, most notably generalized anxiety, bipolar I, and avoidant and dependent personality disorders. The mean number of feared social situations among individuals with SAD was 7.0, with the majority reporting anxiety in performance situations. Conclusions: Social anxiety disorder was associated with substantial unremitting course and extremely early age at onset. Social anxiety disorder often goes untreated, underscoring the need for health care initiatives geared toward increasing recognition and treatment. Comprehensive evaluation of patients with SAD should include a systematic assessment of comorbid disorders, and novel approaches to the treatment of comorbid SAD are needed.
Article
Background: Social anxiety disorder (also called social phobia) is an anxiety disorder in which affected individuals fear the scrutiny of others. Clinical reports suggest that individuals with social anxiety disorder often use alcohol to alleviate anxiety symptoms, a practice that leads to alcohol abuse and/or dependence in approximately 20% of affected individuals. The present study investigated whether simultaneous treatment of social phobia and alcoholism, compared with treatment of alcoholism alone, improved alcohol use and social anxiety for clients with dual diagnoses of social anxiety disorder and alcohol dependence. Methods: The design was a two-group, randomized clinical trial that used 12 weeks of individual cognitive behavioral therapy for alcoholism only (n = 44) or concurrent treatment for both alcohol and social anxiety problems (n = 49). Outcome data were collected at the end of 12 weeks of treatment and at 3 months after the end of treatment. Results: Results with intent-to-treat analyses showed that both groups improved on alcohol-related outcomes and social anxiety after treatment. With baseline scores covaried, there was a significant effect of treatment group on several drinking measures. Counter to the hypothesis, the group treated for both alcohol and social anxiety problems had worse outcomes on three of the four alcohol use indices. No treatment group effects were observed on social anxiety indices. Conclusions: Implications for the staging of treatments for coexisting social phobia and alcoholism are discussed, as well as ways that modality of treatments might impact outcomes.
Article
Individuals with social anxiety have difficulty participating in group settings. Although it makes intuitive sense that social anxiety could present a challenge in addiction treatment settings, which often involve small groups and encouragement to participate in self-help groups like Alcoholics Anonymous (AA) and Narcotics Anonymous (NA), to our knowledge no study has yet assessed the impact of shyness on the treatment experience. Assessment surveys were given to 110 individuals seeking intensive outpatient substance abuse treatment at three community treatment programs. Established cut-offs for presence of clinically-significant social anxiety indicated a prevalence of 37%. Controlling for depression and worry, social anxiety was a unique predictor of endorsement that shyness interfered with willingness to talk to a therapist, speak up in group therapy, attend AA/NA, and ask somebody to be a sponsor. Socially anxious substance abusers were 4–8 times more likely to endorse that shyness interfered with addiction treatment activities. These findings have clinical and research implications.
Article
It is generally agreed that problems related to alcohol use and anxiety tend to occur within the same individual (“comorbidity”); however, the cause of this association remains controversial. Three prominent perspectives are that anxiety disorder promotes pathological alcohol use, that pathological alcohol use promotes anxiety disorder and that a third factor promotes both conditions. We review laboratory, clinical, family, and prospective studies bearing on the validity of these explanatory models. Findings converge on the conclusion that anxiety disorder and alcohol disorder can both serve to initiate the other, especially in cases of alcohol dependence versus alcohol abuse alone. Further, evidence from clinical studies suggests that anxiety disorder can contribute to the maintenance of and relapse to pathological alcohol use. Relying heavily on pharmacological and behavioral laboratory findings, we tentatively propose that short-term anxiety reduction from alcohol use, in concert with longer-term anxiety induction from chronic drinking and withdrawal, can initiate a vicious feed-forward cycle of increasing anxiety symptoms and alcohol use that results in comorbidity.