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Personality Disorders and Time to Remission in Generalized Anxiety Disorder, Social Phobia, and Panic Disorder
Ann O. Massion, MD;
Ingrid R. Dyck, MPH;
M. Tracie Shea, PhD;
Katharine A. Phillips, MD;
Meredith G. Warshaw, MSS, MA;
Martin B. Keller, MD
Arch Gen Psychiatry. 2002;59:434-440.
ABSTRACT
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Background This investigation assessed the effect of personality disorders (PersDs)
on time to remission in patients with generalized anxiety disorder, social
phobia, or panic disorder.
Methods Selected Axis I and II predictors of time to remission during 5 years
of follow-up were assessed in 514 patients with 1 or more of these anxiety
disorders who participated in the Harvard/Brown Anxiety Research Program,
a multisite, prospective, longitudinal, naturalistic study.
Results The presence of a PersD predicted a 30% lower likelihood of generalized
anxiety disorder remission, a 39% lower likelihood of social phobia remission,
and no difference in likelihood of panic disorder remission. More specifically,
a lower likelihood of remission from generalized anxiety disorder was predicted
by the presence of avoidant PersD (34% lower) and dependent PersD (14% lower).
The presence of avoidant PersD predicted a 41% lower likelihood of social
phobia remission. The presence of major depressive disorder did not account
for these findings.
Conclusions Our findings provide new data on the pernicious effect of PersDs on
the course of generalized anxiety disorder and social phobia but not panic
disorder, suggesting that PersDs have a differential effect on the outcome
of anxiety disorders.
INTRODUCTION
STUDIES EXAMINING the effect of comorbid personality disorders (PersDs)
on the outcome of Axis I disorders generally have found that the presence
of a PersD is associated with worse outcome of Axis I disorders,1-2
particularly for depression.3 However, to our
knowledge, few prospective, naturalistic, longitudinal studies have assessed
the effect of Axis II disorders on the course of panic disorder, only 1 study4 has assessed the effect on generalized anxiety disorder
(GAD), and none have assessed the effect on social phobia (SP). The need for
such studies has been emphasized in the literature.5-6
Three prospective, longitudinal (1-3 years), naturalistic studies of
panic disorder7-10
found that the presence of a PersD was associated with worse outcome of panic
disorder symptoms and functioning; 1 study found an association with a lower
likelihood of remission.9-10 These
studies are limited by use of self-report PersD instruments,7, 9-10
only 1 follow-up assessment,8 follow-up of only
1 year,7, 9-10 and retrospective
recall.8 Only 1 study9-10
used DSM-III-R criteria for the PersDs, although
with a self-report instrument.
Regarding GAD, Yonkers et al4 reported
that the presence of cluster B or C PersDs predicted a lower likelihood of
remission. The only other longer-term, larger-sample studies on PersD and
GAD or SP were treatment studies,11-13
both of which showed that PersDs had a negative effect on outcome; specifically,
avoidant PersD predicted a worse outcome for SP.12-13
The present study used a prospective, naturalistic design to assess
the effect of PersDs on the outcome of anxiety disorders, which has not been
addressed in our previous studies.4, 14-18
Unlike other studies, this study has the advantages of longer follow-up (5
years), a larger sample (n = 514), assessment of several anxiety disorders,
and use of multiple assessments over time with standard structured or semistructured
instruments. Also, we accounted for the effect of major depression and analyzed
time to remission separately for GAD, SP, and panic disorder, enabling us
to determine differential course outcomes. Because panic disorder has a more
episodic course than does GAD or SP, we hypothesized that the effect of a
comorbid PersD would be less.
PARTICIPANTS AND METHODS
PARTICIPANTS
The Harvard/Brown Anxiety Research Program is a prospective, naturalistic,
longitudinal study of patients with DSM-III-R–defined
anxiety disorders.14 Participants had at least
1 past or current episode of 1 or more of the following disorders: (1) panic
disorder with agoraphobia (PDA) or without agoraphobia (PD), (2) agoraphobia
without a history of panic disorder, (3) GAD, or (4) SP. Individuals with
agoraphobia without a history of panic disorder were omitted owing to the
small number of patients (n = 8). No attempt was made to affect the treatment
received. Participants were recruited from and interviewed at 1 of 10 Boston
area, central Massachusetts, or Rhode Island hospitals or clinics from the
public and private sector (a complete list of these sites appears at the end
of this article). Exclusion criteria were age younger than 18 years, organic
mental disorder, schizophrenia, or psychosis within 6 months before study
enrollment.
From January 1, 1989, to November 1, 1991, 711 individuals were enrolled,
all of whom gave written informed consent. This article reports on the 514
individuals who had (1) a diagnosis of GAD, SP, PD, and/or PDA at study enrollment
and (2) a PersD assessment and course data available for at least 6 months
to 5 years (Table 1). Of the 514
participants, 232 had follow-up data for all 5 years and 282 had mean (SD)
follow-up of 83 (66) weeks (range, 1-251 weeks). These participants have less
than 5 years of follow-up data because of attrition or the fact that assessments
were not yet due at the time of data analysis. There was no significant difference
in PersD rates among participants with less than 5 years vs 5 years of follow-up
data ( 21 = 1.21; P = .27).
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Table 1. Subject Intake Demographic Data and Frequency of Comorbid
Personality Disorders*
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Analyses examining the predictive effect of PersDs on course were done
for the following current-at-enrollment diagnostic groups: 155 patients with
GAD, 141 with SP (70 with specific and 71 with generalized SP), 73 with PD,
and 313 with PDA. Except for PD and PDA, participants may have had 1, 2, or
all 3 of these anxiety disorders. Of participants with GAD, 51 (33%) had comorbid
SP, 16 (10%) had PD, and 65 (42%) had PDA. Of participants with SP, 50 (36%)
had comorbid GAD, 14 (10%) had PD, and 50 (36%) had PDA. Of participants with
PD, 16 (22%) had comorbid GAD and 12 (16%) had SP. Of participants with PDA,
65 (21%) had comorbid GAD and 52 (17%) had SP.
DIAGNOSTIC AND FOLLOW-UP ASSESSMENTS
Axis I disorders were diagnosed at study enrollment using the SCALUP,19 which consists of items from the Structured Clinical
Interview for the DSM-III-R, Patient Version (Nonaffective
Disorders Section and Psychosis Screen)20 and
the Research Diagnostic Criteria Schedule for Affective Disorders–Lifetime.21-22 The Global Assessment Scale also was
completed at enrollment.23 Follow-up interviews
were conducted at 6-month intervals for 3 years and then annually using the
Longitudinal Interval Follow-up Evaluation,24-25
which assesses information on course of illness, psychopharmacological treatment
received, and psychosocial functioning. The Longitudinal Interval Follow-up
Evaluation rates severity of psychopathologic symptoms over time using 6-point
Psychiatric Status Rating (PSR) scales for each disorder based on DSM-III-R criteria; these are scored on a week-by-week basis during
the interview period (6 or 12 months). A score of 5 or 6 indicates that full
criteria for the disorder are currently met (a score of 6 indicates more severe
symptoms than a score of 5); a score of 3 or 4 denotes subthreshold symptoms;
and a score of 1 or 2 denotes remission.
Remission was defined as occasional mild symptoms or no symptoms (PSR
of 2 or 1, respectively) for 8 consecutive weeks after the episode of illness
at enrollment, which is the definition used in the National Institute of Mental
Health Collaborative Depression Study.26 For
participants with PDA, remission was defined as a PSR of 2 or less for either
panic disorder or agoraphobia for at least 8 consecutive weeks. Probability
of first remission was analyzed for participants who met criteria for a current
episode of the index disorder at enrollment.
Receipt of psychosocial treatments was assessed every 6 months for 2
years and annually thereafter using the Psychosocial Treatments Interview,27 a reliable and valid instrument.
All assessments were conducted by experienced interviewers with 3 to
6 months of training in the study instruments. Most had a bachelor of science
or bachelor of arts degree, several had a master of arts degree, and 2 had
a doctor of medicine degree. To monitor interrater reliability, raters independently
rated 1 videotaped interview per month. Three substudies assessed interrater
reliability, participant recall, and validity of the Longitudinal Interval
Follow-up Evaluation PSR score.25 The PSR scores
had very good reliability,25 with test-retest
intraclass correlations ranging from 0.62 to 0.88 for PD, 0.49 to 0.98 for
agoraphobia, 0.78 to 1.00 for GAD, and 0.75 to 0.89 for SP.25
PersD ASSESSMENT
Personality disorders were assessed at the 1-year follow-up interview
using an earlier version of the International Personality Disorder Examination,
a reliable semistructured clinical interview based on DSM-III-R criteria,28-29 which differs
from the later expanded version only in its lack of International
Classification of Diseases, 10th Revision, diagnoses (referred to herein
as PDE). This instrument assesses characteristics typical throughout the participant's
life and uses scoring algorithms to determine the presence or absence of specific
PersDs.
Rates of paranoid, sadistic, and antisocial PersDs were expected to
be low and therefore were excluded from the PDE to reduce participant fatigue.
Participants with a probable PersD diagnosis were combined with those with
a definite diagnosis because rates of PersDs were low.
Training for use of the PDE was conducted by its developer, Armand W.
Loranger, PhD, and included studying case examples, watching and rating tapes,
and conducting mock interviews. Raters were supervised by a trained rater
during the first 3 PDE assessments with study participants.
STATISTICAL ANALYSES
We examined the following as predictors of first remission for GAD,
SP, and PDA: any PersD and avoidant, passive-aggressive, obsessive-compulsive,
histrionic, dependent, narcissistic, and borderline PersDs. We do not report
on PersD clusters because cluster A and B disorders were excluded because
rates of schizoid and schizotypal PersDs (cluster A) were low. We tabulated
but did not analyze (as course predictors) schizoid, schizotypal, narcissistic,
borderline, and self-defeating PersDs because rates were low. Similarly, because
of the low rates, we did not analyze passive-aggressive or histrionic PersDs
for participants with SP, PDA, or both. To investigate the overlap between
generalized SP and avoidant PersD, we (1) separately analyzed generalized
and specific SP for predictors of remission and (2) further analyzed predictors
of remission for participants with generalized SP with and without avoidant
PersD. Also, we examined the effect of comorbid major depression at enrollment
on the relationship between PersDs and course of the anxiety disorders because
previous data30 suggested that the presence
of major depression is associated with a more chronic course of anxiety disorders.
Specifically, we examined the effect of major depression at enrollment on
overall remission and when occurring in the week before remission from the
anxiety disorder. Last, we separately analyzed the effect of past or current
substance abuse or dependence on remission.
Statistical analyses were conducted using a software program (SAS Version
6.07; SAS Institute Inc, Cary, NC) and PROC FREQ, PROC PHREG, PROC TTEST,
and PROC LIFETEST. We used an  cutoff level of .01, or 95% confidence
intervals (CIs), or both. To examine whether PersD variables or major depressive
disorder predicted the course of GAD, SP, or PD/PDA, we analyzed for individual
predictors of time to remission (which includes probability of remission)
over time using Kaplan-Meier survival curves. Kaplan-Meier life tables were
constructed for PersDs and substance abuse disorders to determine whether
the probability of remission over time was significantly different for presence
vs absence of the disorder. For comparison of demographics and comorbidity
between groups, 2 tests were used to examine categorical data,
and the Fisher exact test was used when expected cell counts were small. Noncomorbid
anxiety disorders were not compared because of the relatively large numbers
of participants who had comorbid disorders.
To determine whether participants with and without a PersD received
different treatment, we assessed the percentage of participants receiving
1 or more of the following: any psychotropic medication, selective serotonin
reuptake inhibitors, monoamine oxidase inhibitors, tricyclic antidepressants,
benzodiazepines, atypical antidepressants, any psychosocial treatment, relaxation
training, 1 or more cognitive techniques, 1 or more behavioral techniques,
or psychodynamic therapy.
RESULTS
Table 1 gives the frequency
of comorbid PersDs.31 There were no across-the-board
differences in the rates of treatment for participants with and without PersDs
(Table 2, including baseline Global
Assessment Scale scores).
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Table 2. Treatment Modality Received and Global Assessment Scale Scores
at Enrollment Related to Presence and Absence of Personality Disorder*
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The probability of remission/number of first remissions from the anxiety
disorders at 5 years was 0.38/53 for GAD, 0.29/38 for SP, 0.35/102 for PDA,
and 0.65/45 for PD. Regarding remission from GAD, participants with a PersD
had a lower probability of remission at 5 years (probability, 0.18; 95% CI,
0.07-0.29) than those with no PersD (probability, 0.50; 95% CI, 0.39-0.61;
log-rank test, 12.52; P<.001). The presence of
2 specific PersDs, avoidant or dependent, primarily explained this finding
(Figure 1 and Figure 2). No other PersD had a statistically significant effect
on remission of GAD.
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Figure 1. Cumulative probability of remission
from generalized anxiety disorder in patients with and without avoidant personality
disorder.
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Figure 2. Cumulative probability of remission
from generalized anxiety disorder in patients with and without dependent personality
disorder.
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Participants with a PersD also were significantly less likely to remit
from SP than were those with no PersD (probability, 0.39; CI, 0.15-0.91; P = .03). In particular, participants with avoidant PersD
were significantly less likely to remit from SP (Figure 3). Furthermore, the presence of avoidant PersD predicted
remission of generalized (log-rank 21, 4.05; P = .04) but not specific (log-rank 21, 1.88; P = .17) SP. None of the other PersDs
had a significant effect.
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Figure 3. Cumulative probability of remission
from social phobia in patients with and without avoidant personality disorder.
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The presence of a PersD did not have a differential effect on probability
of remission from PD or PDA.
The presence of major depression at enrollment was not a significant
predictor of partial (PSR of 3 or 4) or full (PSR of 1 or 2) remission of
PD, SP, or GAD. However, the presence of major depression during the week
before remission resulted in a lower probability of remission from PDA (risk
ratio, 0.88; 95% CI, 0.79-0.99; 2 = 4.42; P = .04) but not from SP (risk ratio, 1.11; 95% CI, 0.93-1.33; 2 = 1.42; P = .23). There was only a trend
for lower probability of GAD remission (risk ratio, 0.80; 95% CI, 0.64-1.01; 2 = 3.49; P = .06). Panic disorder without
agoraphobia was not analyzed because there were too few patients in that group.
The presence of past or current alcohol abuse or dependence was associated
with a lower probability of SP remission (present: probability, 0.84; 95%
CI, 0.74-0.94, 8/54 remitted vs absent: probability, 0.6; 95% CI, 0.53-0.74,
30/87 remitted; log-rank 2, 6.09; P
= .01) but not GAD or PD/PDA remission.
COMMENT
This is the first study, to our knowledge, of a large sample of patients
with multiple assessments and prospective longitudinal data for up to 5 years
of follow-up that examines the effect of PersDs on probability of remission
from 3 anxiety disorders. The presence of 1 or more PersDs was a significant
predictor of lower probability of remission of GAD and SP but not PD/PDA,
taking into account the effect of major depression. Regarding specific PersDs,
avoidant PersD predicted a lower likelihood of remitting from GAD and SP but
not from PD/PDA, and dependent PersD predicted a lower likelihood of remitting
from GAD.
The finding that avoidant PersD predicts a lower likelihood of remitting
from SP is consistent with the overlap in the diagnostic criteria for these
disorders and with previous reports that individuals with comorbid SP and
avoidant PersD tend to have more symptoms and avoidance than those with SP
without avoidant PersD.32 In addition, because
avoidant PersD and generalized SP tend to be chronic, the 2 would not be easily
distinguished by their course.33 The finding
that avoidant PersD also predicted a lower probability of GAD remission was
unexpected, as this has not been previously investigated. Because 12 of the
31 individuals with GAD and avoidant PersD did not have comorbid SP, and only
1 of these had a later onset of SP (between the enrollment and PDE assessments),
this finding cannot be completely explained by the presence of comorbid SP.
This supports a distinction between SP and avoidant PersD, supported by the DSM-IV criteria that most people with generalized SP also
will have avoidant PersD, but not necessarily the
reverse.
Our findings are inconsistent with those of previously cited naturalistic
studies7-10
of PD/PDA, which showed that the presence of a PersD predicted a worse outcome
for PD/PDA. A possible explanation may be that 2 of the studies7, 9-10
used self-report PersD instruments, which overdiagnose PersDs compared with
semistructured interview instruments.34 The
other study8 had only a single follow-up interview
after 3 years, which involved retrospective recall. Also, because these patients
originally had participated in a treatment study, they might not be broadly
representative of patients with PD/PDA.
Because the rate of lifetime alcohol abuse or dependence was low for
participants with SP (12 of 141 individuals), we could not assess whether
alcohol abuse or dependence accounted for the predictive effect of avoidant
PersD on remission of SP. The rates of all substance abuse or dependence disorders
in this sample were low, thus limiting our ability to assess the predictive
effect.
The literature on the effect of depression on anxiety disorder outcome
is mixed,8-9,35 with
1 review36 reporting that 3 of 5 studies showed
that comorbid major depression did not affect panic disorder outcome. Our
findings on the effect of comorbid major depression are similar to those of
2 previously cited studies9, 35 (ie,
that comorbid depression was not associated with outcome of panic disorder
at 1-year follow-up). However, we did find that the presence of major depression
in the week before remission predicted a lower probability of remission of
PDA but not GAD or SP. Possibly we were not able to detect an effect for GAD
or SP because there was such a low rate of remissions for these two; after
10 years of follow-up and more remissions, we may be able to determine the
presence or absence of such an effect.
We found that other comorbid individual PersDs, such as borderline PersD,
did not predict a worse outcome for any anxiety disorder. This finding, which
previously has not been investigated, is contrary to what clinical wisdom
might suggest. However, because few participants had certain individual PersDs,
this finding may reflect type II error.
The strengths of this study include a large sample size; a prospective,
naturalistic, longitudinal design with multiple assessments over time; the
use of structured clinical interviews to diagnose both DSM-III-R Axis I and II disorders; detailed course information over
5 years of follow-up; and assessment of the predictive effect of individual
PersDs on the course of anxiety disorders. Because this was not a treatment
study that excluded comorbid conditions, our sample may be more representative
of patients treated in clinical settings. Therefore, we cannot draw conclusions
about the course of these disorders in a nonclinical setting. Another limitation
is that our participants had a high rate of comorbid anxiety disorders, making
statistical comparisons of remission rates for noncomorbid anxiety disorders
unfeasible. Last, the PDE was given 1 year after enrollment, and a state effect
(eg, remission at 1 year from an Axis I disorder) could have affected the
results.
Despite these limitations, the strength of the association between the
presence of a PersD and longer time to remission from GAD and SP but not PD/PDA,
and the findings on specific PersDs, suggest that there is a differential
effect of PersDs on the outcomes of anxiety disorders. Future studies are
needed to confirm these findings and to address the limitations of this study.
Because anxiety disorders and PersDs are relatively common conditions that
are associated with considerable morbidity, this clinically important issue
deserves further investigation.
AUTHOR INFORMATION
Submitted for publication March 3, 1999; final revision received August
8, 2001; accepted September 4, 2001.
Dr Shea has received honorarium from Organon, West Orange, NJ. Dr Phillips
has a significant interest that derives from her service to the following
entities: Eli Lilly and Co, Indianapolis, Ind; Solvay Pharmaceuticals, Marietta,
Ga; Forest Laboratories, Inc, St Louis, Mo; Gate Pharmaceuticals, North Wales,
Pa; Wyeth-Ayerst Pharmaceuticals, Philadelphia, Pa; Bristol-Myers Squibb,
Co, Wallingford, Conn; Glaxo-Wellcome Inc, Research Triangle Park, NC; and
SmithKline Beecham Pharmaceuticals, Philadelphia. Dr Keller has a significant
interest that derives from his service to the following entities: Pfizer,
Inc, New York, NY; Bristol-Myers Squibb, Co; Forest Laboratories, Inc; Wyeth-Ayerst
Pharmaceuticals; Merck & Co, Inc, Whitehouse Station, NJ; Janssen Pharmaceutica,
Titusville, NJ; Eli Lilly and Co; Organon; Pharmacia/Upjohn Inc, Kalamazoo,
Mich; SmithKline Beecham Pharmaceuticals; Zeneca Pharmaceuticals, Wilmington,
Del; Mitsubishi Pharmaceuticals, Tokyo, Japan; Scirex, Philadelphia; Vela
Pharmaceuticals Inc, Princeton, NJ; Sepracor Pharmaceuticals, Marlborough,
Mass; Somerset Pharmaceuticals, Inc, Tampa, Fla; and Sanofi-Synthelabo, New
York.
This study was supported in part by Wyeth-Ayerst Pharmaceuticals through
its Global Research Program on Anxiety Disorders; grant MH 51415 from the
National Institute of Mental Health, Bethesda, Md; and the Department of Psychiatry
and Human Behavior, Brown University.
We thank the Quintiles Corporation, Research Triangle Park, NC, for
providing valuable consultation services to this project.
| Harvard/Brown Anxiety Research Program
Investigators
Martin B. Keller, MD (Chairperson), Providence,
RI; M. Tracie Shea, PhD, Providence (Veterans Administration Hospital, Brown
University School of Medicine); Jane Eisen, MD, Providence; Katharine A. Phillips,
MD, Providence; Robert Stout, PhD, Providence (Butler Hospital, Brown University
School of Medicine); Steven E. Bruce, PhD, Providence; Risa B. Weisberg, PhD,
Providence (Brown University School of Medicine); Meredith G. Warshaw, MSS,
MA, Boston, Mass (Massachusetts Veterans Epidemiology Research and Information
Center, Boston VA Healthcare System, and Department of Epidemiology and Biostatistics,
Boston University School of Public Health); Robert M. Goisman, MD, Boston
(Massachusetts Mental Health Center, Harvard University School of Medicine);
Ann O. Massion, MD, Worcester, Mass (University of Massachusetts Medical School,
Worcester); Malcom P. Rogers, MD, Boston (Brigham and Women's Hospital, Harvard
University School of Medicine); Carl Salzman, MD, Boston (Massachusetts Mental
Health Center); Gail Steketee, PhD, Boston (Boston University School of Social
Work); Kimberly Yonkers, MD, New Haven, Conn (Yale University School of Medicine);
Idell Goldenberg, PsyD, Medway, Mass; Gopi Mallya, MD, Belmont, Mass (McLean
Hospital, Harvard University School of Medicine); Timothy Mueller, MD, Providence
(Butler Hospital, Brown University School of Medicine); Fernando Rodriguez-Villa,
MD, Belmont (McLean Hospital, Harvard University School of Medicine); Russell
Vasile, MD, Boston (New England Deaconess Hospital, Harvard University School
of Medicine); Caron Zlotnick, PhD, Providence (Butler Hospital, Brown University
School of Medicine); Eugene Fierman, MD, Brookline, Mass.
Additional Contributors
Paul Alexander, MD, Providence (Butler Hospital, Brown University School
of Medicine); James Curran, MD, Providence; Jonathan Cole, MD, Belmont (McLean
Hospital, Harvard University School of Medicine); James Ellison, MD, MPH,
Somerville, Mass (Harvard Pilgrim Health Care, Harvard University School of
Medicine); Alan Gordon, MD, Providence (Butler Hospital, Brown University
School of Medicine); Steven Rasmussen, MD, Providence (Butler Hospital, Brown
University School of Medicine); Robert Hirschfeld, PhD, Galveston, Tex (University
of Texas, Galveston); Jill Hooley, DPhil, Cambridge, Mass (Harvard University);
Philip Lavori, PhD, Stanford, Calif (Stanford University); John C. Perry,
MD, Montreal, Quebec (Jewish General Hospital, McGill University School of
Medicine, Montreal); Linda G. Peterson, Rockport, Me (Midcoast Medicine, Rockport);
James Reich, MD, MPH, Brockton, Mass (Renard Hospital–Washington University
School of Medicine); John Rice, PhD, St Louis, Mo (Renard Hospital–Washington
University School of Medicine); Harriet Samuelson, MA, Boston (Brigham and
Women's Hospital); David Shera, MS, Somerville (Harvard School of Public Health);
Naomi Weinshenker, MD, Newark, NJ (New Jersey Medical School); Myrna Weissman,
PhD, New York, NY (Columbia University); Kerrin White, MD, Seattle, Wash.
Recruitment Sites
McLean Hospital, Belmont; Brown Medical School (Rhode Island and Butler
Hospitals), Providence; University of Massachusetts Medical School, Worcester;
Cambridge City Hospital, Cambridge; Massachusetts Mental Health Center, Boston;
Brighton/Allston Mental Health Center, Brighton, Mass; Brigham and Women's
Hospital, Boston; Worcester VA Medical Clinic, Worcester; Beth Israel Hospital,
Boston; Deaconess Hospital, Boston.
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Corresponding author and reprints: Ann O. Massion, MD, Department
of Psychiatry, University of Massachusetts Medical School, 55 Lake Ave N,
Worcester, MA 01655 (e-mail: ann.massion{at}umassmed.edu).
From the Department of Psychiatry, University of Massachusetts Medical
School, Worcester (Dr Massion); the Department of Psychiatry and Human Behavior,
Brown University School of Medicine, Providence, RI (Drs Shea, Phillips, and
Keller and Ms Dyck); and the Massachusetts Veterans Epidemiology Research
and Information Center, Boston VA Healthcare System, and Department of Epidemiology
and Biostatistics, Boston University School of Public Health (Ms Warshaw).
Drs Shea, Phillips, and Keller are or have been consultants for, received
honoraria or grant support from, or serve on the advisory board of several
pharmaceutical companies.
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