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Social Anxiety Disorder and the Risk of Depression
A Prospective Community Study of Adolescents and Young Adults
Murray B. Stein, MD;
Martina Fuetsch, MagRerNat;
Nina Müller, DiplPsych;
Michael Höfler, DiplStat;
Roselind Lieb, PhD;
Hans-Ulrich Wittchen, PhD
Arch Gen Psychiatry. 2001;58:251-256.
ABSTRACT
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Background Social anxiety disorder (SAD) (also known as "social phobia") is frequently
comorbid with major depression, and in such cases, almost always precedes
it. This has led to interest in SAD as a possible modifier of the risk and/or
course of mood disorders.
Methods Data come from a prospective, longitudinal epidemiologic study of adolescents
and young adults (aged 14-24 years) in Munich, Germany. Respondent diagnoses
(N = 2548) at baseline and follow-up (34-50 months later) are considered.
The influence of SAD at baseline on the risk, course, and characteristics
of depressive disorders (ie, major depression or dysthymia) at follow-up is
examined.
Results The baseline prevalence of SAD was 7.2% (95% confidence interval [CI],
6.1%-8.4%). Social anxiety disorder in nondepressed persons at baseline was
associated with an increased likelihood (odds ratio [OR] = 3.5; 95% CI, 2.0-6.0)
of depressive disorder onset during the follow-up period. Furthermore, comorbid
SAD and depressive disorder at baseline was associated with a worse prognosis
(compared with depressive disorder without comorbid SAD at baseline). This
is exemplified by the greater likelihood of depressive disorder persistence
or recurrence (OR = 2.3; 95% CI, 1.2-4.6) and attempted suicide (OR = 6.1;
95% CI, 1.2-32.2).
Conclusions Social anxiety disorder during adolescence or young adulthood is an
important predictor of subsequent depressive disorders. Moreover, the presence
of comorbid SAD in adolescents who are already depressed is associated with
a more malignant course and character of subsequent depressive illness. These
findings may inform targeted intervention efforts.
INTRODUCTION
SOCIAL ANXIETY disorder (SAD) (also known as "social phobia") is a prevalent
disorder with its onset almost universally in childhood or adolescence.1, 2, 3 Recent estimates indicate
that between 4% and 8% of adults in the general population suffer from SAD
in a given year, with even higher rates when lifetime prevalence is considered.4, 5 In a community study of adolescents
and young adults aged 14 to 24 years, from which the current report is derived,
we found a lifetime prevalence of DSM-IV SAD of 9.5%
in females and 4.9% in males.4, 6, 7
Another characteristic feature of the longitudinal course of SAD, in
addition to its early onset, is its frequent co-occurrence with depressive
illness.6, 7, 8, 9, 10, 11, 12
Social anxiety disorder is reported to be the most commonly occurring comorbid
anxiety disorder among patients with depressive disorders.13
Furthermore, when comorbidity does occur, SAD almost always starts first,
often many years prior to the onset of depression.14, 15
This consistent finding has spurred interest in the study of SAD as a possible
risk factor for major depression.
A possible link between social anxiety and earlier onset of major depression
has been reported in several studies.16, 17, 18, 19
In a longitudinal study, anxiety disorders in early adolescence predicted
clinically significant depressive and anxiety disorders (especially SAD) in
early adulthood.20 Furthermore, the association
between early-onset (eg, prepubertal) anxiety and depression in young adulthood
is evident when looking at family patterns of transmission in depressive high-risk
families.21, 22 These observations
have sparked interest in the possibility that early identification of and
intervention with socially anxious children or adolescents might reduce their
risk for depressive disorders in later life.6, 19
In this report, we examined data from the Early Developmental Stages
of Psychopathology (EDSP) Study,23 focusing
on the longitudinal relationship between SAD and depressive disorders. We
hypothesized that SAD at baseline would predict onset and severity of subsequent
depressive disorders.
SUBJECTS AND METHODS
SAMPLE
Data were collected as part of the EDSP study. The EDSP is a prospective
longitudinal study designed to collect data on the prevalence, risk factors,
comorbidity, and course of mental and substance use disorders in a representative
sample, which consisted of 3021 subjects aged 14 to 24 years at baseline.
The study consists of a baseline (T0) survey, 2 follow-up surveys (T1 and
T2), and a family history component.
The baseline sample was drawn in 1994 from government registries in
metropolitan Munich, Germany, of registrants expected to be aged 14 to 24
years at the time of the baseline interview in 1995. Because the study was
designed as a longitudinal panel with special emphasis on early developmental
stages of psychopathology, 14- to 15-year-old individuals were sampled at
twice the probability of people aged 16 to 21 years, and 22- to 24-year-old
people were sampled at half the probability of the 16- to 21-year-old people.
Individuals were contacted first by letter, and then by telephone to
arrange a meeting. Most interviews took place in the respondents' homes or,
in some instances, at another location preferred by the respondent. Approximately
one third of the sample received a financial incentive (US $10-$20) to participate.
Participants provided informed consent; parental consent was provided for
respondents aged 18 years and younger.
The demographic distribution of the sampled population and the respondents
has been reported elsewhere.23, 24
Briefly, among the sampled subjects, a total of 3021 interviews were completed,
resulting in a response rate of 70.8%. At baseline, refusal to participate
in the survey (18.2%) was by far the most frequent reason for nonresponse,
followed by a reported lack of time (3.3%), failure to contact anyone in the
identified household (3.1%), and failure to contact the sampled individual
in the household (3.0%).
The first follow-up survey was conducted only for subjects aged 14 to
17 years at baseline, whereas the second follow-up survey was conducted for
all subjects. At the first follow-up survey 14 to 25 months after baseline
(mean interval, 20 months; SD, 3 months), a total of 1228 interviews were
completed, resulting in a response rate of 88%. From the 3021 subjects of
the baseline survey, a total of 2548 interviews were completed at the second
follow-up survey 34 to 50 months after baseline (mean duration, 42 months;
SD, 2 months), resulting in a response rate of 84%. A more detailed description
of the study is presented elsewhere.24
For those probands aged 14 to 17 years at baseline, the follow-up status
is assessed from the aggregation of information obtained from the first and
second follow-up interviews. For the probands older than 17 years at baseline,
the follow-up status is assessed from the the second set of follow-up questions,
which refer to the time between baseline and the second follow-up.
DIAGNOSTIC ASSESSMENT
The survey staff throughout the entire study period (including the family
history component of the study) consisted of 57 clinical interviewers, most
of whom were clinical psychologists with extensive experience in diagnostic
interviewing, including the Munich-Composite International Diagnostic Interview
(M-CIDI).25, 26 At baseline, 25
professional health research interviewers recruited from a survey company
were also involved. Formal training with the M-CIDI took place for 2 weeks,
followed by at least 10 closely monitored practice interviews and additional
1-day booster sessions throughout the study.
The M-CIDI allows for the assessment of symptoms, syndromes, and diagnoses
of 48 mental disorders, along with information about onset, duration, severity,
and psychosocial impairment. Diagnostic findings reported in this article
were obtained by using the M-CIDI/DSM-IV diagnostic
algorithms. Test-retest reliability and validity for the full M-CIDI have
been reported elsewhere,26, 27, 28
along with descriptions of the M-CIDI format and coding conventions.
Social anxiety disorder is defined here as
one meeting DSM-IV criteria per the M-CIDI diagnostic
algorithm.6 Depressive disorder is defined as one meeting DSM-IV criteria
for one or more episodes of major depression or dysthymia. One-week test-retest
reliability of these diagnostic categories was acceptable (all  values,
> 0. 64),26 as was their validity (
values range, 0.54 for dysthymia to 0.96 for single depressive episodes).
Descriptors of the course of depression (eg, number of depressive episodes),
which was also derived from the M-CIDI, refer to the time between baseline
and follow-up. Severity descriptors (eg, number of depressive symptoms) refer
to the self-identified worst episode of depression during this interval. The
variable "total duration of depression" was estimated in weeks by multiplying
the number of depressive episodes by the duration of the longest depressive
episode. The variable "suicidal ideas" refers to the number of endorsed items
from a total of 4 possibilities: (1) frequent thoughts of death, (2) desire
for death, (3) suicidal thoughts, and (4) concrete suicidal plans or attempts.
STATISTICAL ANALYSES
Data were weighted to consider different sampling probabilities as well
as systematic nonresponse at baseline. The Stata Software29
package was used to compute robust confidence intervals (eg, by applying the
Huber-White sandwich matrix in the case of regression models)30
required when basing analyses on weighted sample sizes. Logistic regressions
with odds ratios (OR) were used to describe associations with onset and stability
of depressive disorders, recognizing confounding variables such as subjects'
age, sex, or substance abuse or dependence.31
We also conducted most analyses omitting the subjects (n = 600) who suffered
from alcohol abuse or illicit drug abuse or dependence at any time point.
The results of these analyses did not differ meaningfully from those in which
the full sample was included; we have therefore elected to report only results
for the full sample. The quantitative outcomes of severity of depressive disorder
considered here (eg, number of depressive episodes) constitute count variables
with a strongly positively skewed distribution. For this, negative binomial
regressions were used with multiplicative effects described by so-called incidence
rate ratios (IRR) (ie, the factor by which the mean differs from the one in
the comparison group). Negative binomial regressions allow for extra-Poisson
variation or overdispersion that is likely to be owing to unobserved heterogeneity
in the outcome between subjects as well as correlated events that are counted
(eg, symptoms),32 and 95% confidence intervals
(CI) are used throughout this article.
RESULTS
CHARACTERISTICS OF THE SAMPLE AT BASELINE AND THE SECOND FOLLOW-UP
PERIOD
Sociodemographic characteristics of the sample at baseline are summarized
in Table 1. A total of 3021 cases
were available at baseline, with data from the second follow-up available
for 2548 cases.
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Table 1. Sociodemographic Characteristics of the Sample*
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PREVALENCE RATES AT BASELINE
Baseline prevalence rates (lifetime and past 12 months) of SAD and depressive
disorder are presented in Table 2;
27.3% of cases with lifetime social phobia were of the generalized subtype.
These disorders are categorized into 3 mutually exclusive combinations (ie,
SAD without depressive disorder, depressive disorder without SAD, depressive
disorder with SAD) to permit comparison of their longitudinal outcomes at
follow-up. Depressive disorders (OR = 1.9; 95% CI, 1.5-2.5) and SAD (OR =
2.0; 95% CI, 1.4-2.9) were more common in women than men; associations were
therefore adjusted for sex.
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Table 2. Baseline Lifetime and 12-Month Prevalence of Social Anxiety
Disorder and Depressive Disorder in the EDSP*
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LIKELIHOOD OF DEPRESSION AT FOLLOW-UP
Rates of depression during the period between baseline and the second
follow-up are presented in Table 3.
Persons with SAD but no depression (current or previous) at baseline were
significantly more likely (OR = 3.5; 95% CI, 2.0-6.0) than persons with no
mental disorder to have experienced a depressive disorder during the follow-up
period. This effect, however, could be detected only for the older (ie, aged
18-24 years at baseline) (OR = 5.3; 95% CI, 1.6-3.8), but not the younger
(ie, aged 14-17 years at baseline) subsample (OR = 0.6; 95% CI, 0.1-2.7).
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Table 3. Depressive Disorder Status at Follow-up by Baseline Diagnostic
Status*
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A similar significant increase in odds (OR = 3.8; 95% CI, 2.6-5.5) was
seen for persons with depression but no SAD at baseline. Persons with depression
and SAD (current or previous) at baseline were also at significantly amplified
odds for subsequent depression (OR = 8.7; 95% CI, 4.5-16.8) compared with
persons with no mental disorder at baseline. In persons with depressive disorder
at baseline, SAD (current or previous) at baseline approximately doubled the
odds for subsequent (or persistent, as this might reflect a continuous episode
from baseline to follow-up) depressive disorder (OR = 2.3; 95% CI, 1.2-4.6).
Among persons with SAD, age at onset of social anxiety symptoms (not
disorder, which was unavailable)33 was found
to predict neither depressive disorder onset (OR = 1.1; 95% CI, 0.9-1.2) nor
persistence or recurrence (OR = 1.0; 95% CI, 0.9-1.1).
OTHER ANXIETY DISORDERS
Specificity of the effects attributable to SAD (vis-á-vis other
anxiety disorders) in predicting onset and recurrence or persistence of depressive
disorder was not high. Other anxiety disorders (specific phobias and generalized
anxiety disorder in particular) at baseline were also associated with similarly
increased odds (data not shown). We therefore examined the possibility that
the associations we had linked to SAD might be due to comorbidity with other
anxiety disorders. Analyses were repeated where SAD groups were stratified
for the presence or absence of at least one other comorbid anxiety disorder
at baseline. The association with the onset of depressive disorder was somewhat
higher in cases with SAD plus another comorbid anxiety disorder (OR = 6.0;
95% CI, 2.6-13.3) than in cases with SAD alone (OR = 2.4; 95% CI, 1.2-4.9),
though not significantly so. No appreciable difference in association was
found for the persistence or recurrence of depressive disorder in cases with
SAD alone (OR = 7.7; 95% CI, 2.5-23.7) compared with SAD plus another comorbid
anxiety disorder (OR = 9.2; 95% CI, 4.2-19.9).
CLINICAL CHARACTERISTICS AND COURSE OF DEPRESSIVE DISORDER AT FOLLOW-UP
Several clinical characteristics and descriptors of the course of depressive
illness during the follow-up period were compared between groups (Table 4). Compared with persons with no
mental disorder at baseline, there were few significant differences in these
parameters for persons with either a depressive disorder alone or SAD alone
at baseline. The sole exception was a small but statistically significant
increase in the severity of depression (as indicated by the number of depressive
symptoms experienced during an episode) for persons with depression alone
at baseline compared with persons not mentally ill at baseline (IRR, 1.2;
95% CI, 1.1-1.4).
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Table 4. Selected Description of Course of Depression During Follow-up
Period by Baseline Diagnostic Status*
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A very different portrait of risk emerged, however, for persons who
had both depressive disorder and SAD at baseline (Table 4). During the follow-up period, these persons were significantly
more likely to experience (compared with persons with no mental disorder)
more intense suicidal ideation (IRR, 2.2; 95% CI, 1.4-3.4), more depressive
symptoms (IRR, 1.4; 95% CI, 1.2-1.7), and a longer duration of major depressive
episode(s) (IRR, 3.2; 95% CI, 1.5-6.8). They also had much greater odds (OR
= 7.0; 95% CI, 1.5-32.2) of having attempted suicide during the follow-up
period. Similarly increased magnitudes of effects were seen for this comorbid
group (ie, positive for both depressive disorder and SAD at baseline) in comparison
with persons with depressive disorder alone at baseline (Table 4, bottom row).
COMMENT
In this prospective study, we found that the presence of SAD in adolescence
or early adulthood is a strong risk factor for the subsequent occurrence of
depressive illness during young adulthood. Moreover, the combination of depression
and SAD in adolescence markedly augments the risk for subsequent depressive
disorder, over and above the risk conferred by either disorder alone. Thus,
in addition to confirming the findings from retrospective reports that preexisting
SAD increases the risk for "early-onset" depression,16, 17, 19
our observations suggest that those persons with the combination of SAD and
depression in adolescence or early adulthood are at the greatest risk for
subsequent depression.
Individuals with this early form of comorbidity (ie, SAD plus depressive
disorder) are not only at highest risk for subsequent depression, they also
experience a more malignant course of depressive illness. This is manifested
in more suicidal ideation and suicide attempts, and more depressive symptoms
during episodes, as well as more frequent and/or more protracted depressive
episodes. These findings are consistent with observations from other settings
(eg, primary care) where the presence of SAD comorbidity predicts poorer depressive
outcomes.34 Remaining to be shown is whether
or not these associations are unique to SAD or whether they are seen with
other forms of anxiety disorder comorbidity. Our preliminary look at these
data suggests that the association with SAD is not specific, but that it must
be scrutinized more closely in future analyses. Regardless, the fact that
SAD may be the most common form of anxiety disorder comorbidity seen in depressed
patients13 makes this a particularly salient
observation.
It is important to emphasize that causal inferences cannot be drawn
from these observational data. We may speculate, however, about the mechanism(s)
by which preexisting SAD might increase the risk of subsequent depression.
Certainly, common genetic risk factors may exist.35, 36
Investigators have theorized a role of social anxiety and avoidance in contributing
to demoralization and social isolation,8 all
of which are known depressive risk factors. Socially anxious children are
more likely than their less socially anxious peers to develop problems with
self-esteem and lack friendships.37 It is therefore
reasonable to posit that a cause-and-effect relationship between social anxiety
and depression exists at least in some cases, but this remains to be empirically
proven.
Limitations of our study should be considered. Although we did not find
selective attrition for persons with social phobia from baseline to second
follow-up investigation in our sample, it is possible that persons most impaired
by SAD did not participate in our study. It is also possible that our findings
from this urban German sample, consisting of persons who are well educated
with relatively high economic status, may not generalize to other populations.
Diagnoses at baseline are retrospective and therefore subject to possible
recall problems or biases, though these should be attenuated in this relatively
young sample. Some of our findings (eg, increased suicide attempts in comorbid
cases) rest on relatively few cases, and though statistically significant,
should be interpreted with caution. Also, as mentioned earlier, it seems that
the association with subsequent depressive disorder is not specific for SAD.
It is also possible that depressive disorders are not the most common (or
important) kinds of mental disorders predicted by SAD. We intend to conduct
additional analyses to further explore these latter issues.
Our findings are consistent with other longitudinal studies showing
anxiety disorders in youth to be a predictor of more serious depression in
adulthood, particularly in those at risk for depression on the basis of family
history.22 Though we caution once again about
imparting causality to our findings, they do support the proposal made by
numerous investigators that early intervention with socially phobic youth
be tested as a primary prevention of depressive illness.6, 12, 15, 19
Furthermore, our results suggest that the union of depression with SAD (and
probably other anxiety disorders as well) in adolescence or early adulthood
is a particularly sinister combination that heralds an increased risk for
subsequent depressive episode(s) of increased severity, with amplified suicide
risk. Given the substantial morbidity and mortality risks associated with
adolescent-onset major depressive disorder,38, 39
serious efforts should be initiated to identify and test treatments for youth
who fit this clinical profile (ie, early-onset anxiety and depressive disorders).
AUTHOR INFORMATION
Accepted for publication September 25, 2000.
This work is part of the Early Developmental Stages of Psychopathology
(EDSP) Study and is funded by the German Ministry of Research and Technology,
project 01 EB 9405/6.
The principal investigators are Hans-Ulrich Wittchen, PhD, and Roselind
Lieb, PhD. Current or former staff members of the EDSP group are Kirsten vonSydow,
PhD; Gabriele Lachner, PhD; Axel Perkonigg, PhD; Peter Schuster, PhD; Franz
Gander, PhD; Michael Höfler, DiplStat; and Holger Sonntag, DiplPsych,
as well as Esther Beloch, Mag Phil; Martina Fuetsch, MagRerNat; Elzbieta Garczynski,
DiplPsych; Alexandra Holly, DiplPsych; Barbara Isensee, DiplPsych; Marianne
Mastaler, DiplPsych; Nina Müller, DiplPsych; Chris Nelson, PhD; Hildegard
Pfister, DiplInf; Victoria Reed, DiplPsych; Dilek Türk, DiplPsych; Antonia
Vossen, DiplPsych; Ursula Wunderlich, PhD; and Petra Zimmermann, DiplPsych.
Scientific advisors are Jules Angst, PhD (Zurich, Switzerland); Jürgen
Margraf, PhD (Basel, Switzerland); Günther Esser, PhD (Mannheim, Germany);
Kathleen Merikangas, PhD (New Haven, Conn); and Ron Kessler, PhD (Boston,
Mass).
From the Department of Psychiatry, University of California San Diego,
and the Veterans Administration San Diego Healthcare System, La Jolla, Calif
(Dr Stein); and the Department of Clinical Psychology and Epidemiology, Max
Planck Institute of Psychiatry, Munich, Germany (Mss Fuetsch and Müller,
Mr Höfler, and Drs Lieb and Wittchen).
Corresponding author and reprints: Murray B. Stein, MD, Department
of Psychiatry, University of California San Diego, 8950 Villa La Jolla Dr,
Suite 2243, La Jolla, CA 92037 (e-mail: mstein{at}ucsd.edu).
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