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Psychological Intervention and Antidepressant Treatment in Smoking Cessation
Sharon M. Hall, PhD;
Gary L. Humfleet, PhD;
Victor I. Reus, MD;
Ricardo F. Muñoz, PhD;
Diane T. Hartz, PhD;
Roland Maude-Griffin, BA
Arch Gen Psychiatry. 2002;59:930-936.
ABSTRACT
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Background Sustained-release bupropion hydrochloride and nortriptyline hydrochloride
have been shown to be efficacious in the treatment of cigarette smoking. It
is not known whether psychological intervention increases the efficacy of
these antidepressants. This study compared both drugs with placebo. It also
examined the efficacy of these 2 drugs and placebo with and without psychological
intervention.
Methods This was a 2 (medical management vs psychological intervention) x
3 (bupropion vs nortriptyline vs placebo) randomized trial. Participants were
220 cigarette smokers. Outcome measures were biologically verified abstinence
from cigarettes at weeks 12, 24, 36, and 52.
Results Psychological intervention produced higher 7-day point-prevalence rates
of biochemically verified abstinence than did medical management alone. With
the use of point-prevalence abstinence, both nortriptyline and bupropion were
more efficacious than placebo. On rates of 1-year continuous abstinence, the
2 drugs did not differ from each other or from placebo. Psychological intervention
did not differ from medical management alone on rates of 1-year continuous
abstinence.
Conclusions Both nortriptyline and bupropion are efficacious in producing abstinence
in cigarette smokers. Similarly, psychological intervention produces better
abstinence rates than simple medical management. Both drugs, and psychological
intervention, have limited efficacy in producing sustained abstinence. The
data also suggest that combined psychological intervention and antidepressant
drug treatment may not be more effective than antidepressant drug treatment
alone.
INTRODUCTION
THE ANTIDEPRESSANTS bupropion hydrochoride and nortriptyline hydrochloride
are useful adjuncts in the treatment of tobacco dependence. A multicenter
bupropion trial reported 1-year continuous abstinence rates of 24% for 300
mg/d, 18% for 150 mg/d, 14% for 100 mg/d, and 10% for placebo. The difference
from placebo was significant in the 150- and 300-mg/d groups.1
A trial comparing bupropion and nicotine patch reported 1-year continuous
abstinence rates of 36% for bupropion and nicotine patch, 33% for bupropion
alone, 16% for nicotine patch alone, and 15% for placebo. Bupropion alone
or with nicotine patch resulted in significantly higher abstinence rates than
did patch alone or placebo.2 Our group reported
1-year continuous abstinence rates of 24% for nortriptyline and 12% for placebo.3 A second study reported that 14% of patients receiving
nortriptyline and 3% of patients receiving placebo were abstinent 6 months
after treatment.4
Nicotine replacement treatment (NRT) is usually more effective when
provided with psychosocial treatment.5-6
The impact of psychosocial interventions in antidepressant treatment for cigarette
smoking is unknown. Antidepressants and NRT differ in ease of use, mode of
administration, adverse effects, and effects on mood and withdrawal symptoms,
all of which might contribute to differences in the role of psychosocial interventions.
Antidepressant studies have involved either psychotherapy or counseling
or extensive contact with project staff, including physician reinforcement
for quitting smoking,1-2 multiple
episodes of brief counseling by "research staff,"1-2
group meetings,3-4 and psychotherapy.3 According to the Agency for Health Care Policy and
Research guidelines7-8 available
at the time this study was conducted, a more typical practice-based medical
management (MM) protocol would entail physician advice to quit smoking and,
at most, 1 to 3 brief follow-up visits, and perhaps a referral to a smoking
cessation group. Antidepressant efficacy in such a context may differ from
that obtained from more extensive psychotherapy. One important question is
the effect of psychological intervention (PI) when added to antidepressant
therapy.
A second question is the relative efficacy of the 2 drugs. On the basis
of the extant literature, we deemed differences in efficacy between bupropion
and nortriptyline unlikely, and we did not predict differences between the
2. We did expect, however, that both would produce higher abstinence rates
than placebo.
Thus, the following hypotheses were proposed: (1) Abstinence rates will
be higher in participants receiving active antidepressant treatment, whether
bupropion or nortriptyline, during a 52-week period, than for those receiving
placebo. (2) Independent of drug, abstinence rates will be higher for participants
receiving PI than for those receiving MM alone. (3) Active drug conditions
combined with PI will be more efficacious than the other experimental conditions
in producing abstinence.
SUBJECTS AND METHODS
SUBJECTS
Smokers of 10 or more cigarettes per day were recruited by advertising,
public service announcements, and flyers. After telephone screening, potential
participants were invited to an orientation meeting. Interested individuals
completed an informed consent and were invited to a baseline assessment including
a physical examination, electrocardiogram, and blood draws. The sections of
the Structured Clinical Interview for DSM-IV9 that diagnose depression, dysthymia, and bipolar disorder
were administered by master's-level clinicians. Participants were assessed
on demographic variables and mood by paper-and-pencil measures and interviews
administered by research staff.
Exclusionary criteria included cardiovascular disease, hyperthyroidism,
seizure or bulimia, use of a monoamine oxidase inhibitor within 2 weeks, severe
allergies including allergies to either experimental drug, life-threatening
disease, bipolar disease, current major depressive disorder (MDD), pregnancy
or lactation, use of levodopa, migraines, previous treatment for cigarette
smoking with nortriptyline or bupropion, treatment for alcohol or other drug
use within 6 months, psychiatric hospitalization within 1 year, use of any
psychiatric medication, suicidal or psychotic symptoms, and current NRT use.
PROCEDURES
Participants were stratified by number of cigarettes smoked, sex, and
history of depression vs no history, and randomly assigned to 1 of the 6 experimental
cells in a 3 (bupropion vs nortriptyline vs placebo) x 2 (MM alone vs
MM + PI).
Assessments were at baseline and at weeks 12 (end of treatment), 24,
36, and 52. Participants were coded as nonsmoking if they reported smoking
no cigarettes, not even a puff, during the previous 7 days, had expired carbon
monoxide levels of 10 ppm or less, and had urinary cotinine levels of 60 ng/mL
or less.10 Adverse effects were assessed by
checklist at baseline and weeks 1, 2, 3, and 6. At 52 weeks, participants
indicated which drug they believed they had received and its perceived helpfulness.
MEASURES
Negative affect was assessed with the Profile of Mood States (POMS).11 On the basis of the Structured Clinical Interview
for DSM-IV, participants were classified as positive
or negative for MDD. We also administered the Fagerstrom Test for Nicotine
Dependence12 and a adverse effects scale we
developed that includes the adverse effects reported for both bupropion and
nortriptyline.
COUNSELING INTERVENTIONS
Medical Management
Medical management was developed from the 1996 Agency for Health Care
Policy and Research guidelines7 and from the
MM condition in the Collaborative Depression Trials.13
Medical management included advice to stop smoking, antidepressant medication,
adverse effects monitoring, and educational materials. It did not introduce
complex or time-consuming interventions that would be impractical in primary
care.
Physicians were 5 licensed psychiatric and internal medicine residents.
Participants were provided written information about smoking cessation (Freedom
From Smoking).14 During week 1, the physician
reviewed the treatment rationale and prescription instructions, discussed
behavioral factors important to smoking cessation, and established a quit
date during week 5. This session lasted 10 to 20 minutes. Five-minute visits
were scheduled during weeks 2, 6, and 11, during which participants were queried
about cessation progress. The physician responded briefly to questions and
provided encouragement. Advice about specific quitting strategies was not
offered.
Psychological Intervention
All participants participated in the MM sessions previously described.
In addition, they participated in 5 group sessions.
Providers were 3 master's-level counselors, the most common smoking
treatment provider in the health care organizations we consulted. The group
intervention was an adaptation of an intervention described in detail elsewhere3, 15-17 and
is available from the first author (S.M.H.). The first 90-minute session was
during week 4. Sessions 2 and 3 were during week 5; sessions 4 and 5 were
during weeks 7 and 11, respectively. Group size ranged from 3 to 11. The intervention
provided health-related information for mood management and smoking cessation,
and discussion of cessation. A core element was the development of a quit-smoking
plan and weekly modification of it. Methods used included monitoring of cigarette
use and affective states; paper-and-pencil exercises focusing on health-related
information, motivation to quit, and decreasing relapse-related thoughts;
informational handouts; and brief didactic presentations.
PHARMACOLOGIC INTERVENTIONS
Medication was placebo controlled and double blind. The sustained-release
properties of bupropion rest on the formulation of the tablet's coating; placebo
bupropion was not available. We encapsulated both drugs to maintain the patency
of the bupropion formulation and to provide a blinded drug. All participants
received capsules that were identical in number and appearance.
The University of California, San Francisco Drug Product Services prepared
medication capsules. For nortriptyline, lactose placebo and active drug were
encapsulated in powdered form. For bupropion, Wellbutrin SR tablets (Glaxo
Wellcome Inc, Research Triangle Park, NC) or similar-sized placebo tablets
were inserted into lactose-filled capsules. All capsules were secured with
a gelatin mixture to prevent opening.
Nortriptyline drug dose was titrated for each participant until a therapeutic
serum level (50-150 ng/mL) was obtained. All participants assigned to active
nortriptyline hydrochloride received 25 mg/d for 3 days, followed by 50 mg/d
for 4 days. At the end of the week, serum levels of nortriptyline were assessed.
Dosage was increased to 75 mg/d if a therapeutic serum level had not been
reached. At week 4, serum levels were assessed again and, if necessary, drug
dosage was increased to 100 mg/d. At week 6, serum levels were assessed to
determine final dose. At the end of week 12, drug dose was decreased by 25
mg every 2 days, with the final drug administration being 25 mg over 3 days.
Whenever a dose was titrated for a participant receiving active drug, the
dose was titrated for a participant receiving placebo. Titration was performed
by a physician who had no contact with participants or clinical staff. The
mean nortriptyline blood level for participants abstinent at week 6 was 59.9
ng/mL (SD, 25.2 ng/mL). We report only blood levels for abstinent participants,
since nicotine is known to result in lowered nortriptyline levels.18 Daily nortriptyline hydrochloride dosages at week
7 were as follows: 50 mg/d, n = 2; 75 mg/d, n = 26; 100 mg/d, n = 25, and
125 mg/d, n = 5.
Bupropion hydrochloride dosage began at 150 mg/d for the first 3 days.
The dosage was increased to 300 mg/d, where it remained until week 12, when
the dose was decreased to 150 mg for 3 days, then discontinued. Dose reductions
occurred if participants reported unpleasant adverse effects. Mean bupropion
blood level for abstinent subjects was 36.0 ng/mL. At week 7, all participants
receiving bupropion were receiving 300 mg/d.
Participants returned pill bottles at each clinic visit. Pills were
counted and number of pills taken was recorded. If a patient failed to return
a bottle, he or she was asked to call clinic staff with the pill count.
STATISTICAL METHODS
The principal data analysis method was a generalized linear model (GLM),
a generalization of the classic linear model that computes estimates by means
of likelihood functions instead of least squares. A GLM allows use of repeated
measurements when there are missing data, without dropping participants with
data missing or assuming that missing data equate to smoking.19-21
We used SAS PROC MIXED version 6.12 software (SAS Institute Inc, Cary, NC).
When abstinence was the dependent variable, we also used the GLIMMIX Macro
for SAS (SAS Institute Inc), which interacts with PROC MIXED to modify it
so that it is appropriate for dichotomous data.22
A single GLM was used to evaluate the 3 hypotheses. Abstinence status at weeks
12, 24, 38, and 52 were the dependent variables. The design was a 2 (active
drug vs placebo) x 2 (MM vs MM/PI) x 2 (MDD history vs no history)
model with assessment entered as a repeated variable. Since no interactions
of assessment with independent variables were predicted, these interactions
were dropped from the final model when no significant effects emerged. Since
we performed a single test for each hypothesis, the hypothesis-wise error
rate was held at P = .05.
We evaluated effects of sex and its interaction with the 3 design variables
on abstinence rates at weeks 12 to 52 by means of 3 GLM models computed with
the GLIMMIX Macro. We used a parallel procedure to compare the 3 drug conditions
(bupropion, nortriptyline, and placebo). Effect sizes are expressed as odds
ratios and confidence intervals.
Analysis of variance and  2 tests were used to evaluate
baseline differences among treatment conditions, continuous abstinence rates,
and the rate of occurrence of adverse effects. Tests were 2-tailed, with P<.05, all comparisons.
RESULTS
PARTICIPANT CHARACTERISTICS
Demographic, smoking, and psychiatric characteristics of participants
in each experimental condition are given in Table 1. There were no significant differences between conditions
at baseline.
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Table 1. Baseline Variables by Psychological Intervention and Drug
Condition*
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ATTRITION
Figure 1 shows participant
flow from first telephone contact to week 52. Smokers (N = 220) were randomly
assigned to 1 of 3 pharmacologic treatments (nortriptyline, bupropion, or
placebo) and 1 of 2 counseling treatments (MM or PI). A history of MDD was
present in 33% of the participants. Because of a medical emergency, it was
necessary to break the blind for 1 participant, who was receiving placebo
drug. Thus, the usable sample (N = 219) consisted of 122 men and 97 women.
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Figure 1. Attrition flow chart. ECG indicates
electrocardiogram; MM, medical management; and PI, psychological intervention.
Asterisk indicates n = 219, because the blind was broken for 1 female subject
in the group receiving placebo and PI.
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Thirty-seven participants (17%) failed to complete treatment: 15 for
personal reasons, 12 because of perceived medication adverse effects (bupropion,
6; nortriptyline, 3; placebo, 3), 1 because of an unrelated medical condition,
and 9 for undisclosed reasons. There were no significant differences between
psychological treatment conditions (21 [N = 219]
= 1.37, P = .24) or diagnostic categories (21 [N = 219] = 3.19, P = .07) in
treatment dropout. There were significant differences between the drug conditions
(22 [N = 219] = 7.29, P
= .03; bupropion, 15.1% [n = 11]; nortriptyline, 10.0% [n = 7]; placebo, 26.0%
[n = 19]). The rate for placebo was significantly greater than the rate for
nortriptyline (21 [N = 219] = 6.74, P = .009), but not for bupropion (21 [N
= 219] = 2.69, P = .10). The 2 active drugs did not
differ from one another (21 [N = 219] = 1.01, P = .31). The mean number of counseling sessions attended
was 3.58 (SD, 1.61).
The percentages and numbers of participants for whom we were unable
to collect smoking data were as follows: week 12, 15% (n = 33); week 26, 16%
(n = 35); week 36, 17% (n = 38); and week 52, 19% (n = 42), with no significant
differences between drug, psychological treatment, or diagnostic categories.
ABSTINENCE
Main effects for drug, psychological treatment condition, and assessment
time were each significant at P<.05 (Table 2). There were no other significant
effects. Neither main effects for MDD diagnosis nor the interaction of this
variable with other variables was significant. Thus, both the first and second
hypotheses—that active drug would be more effective than placebo (Figure 2) and that the PI would be more effective
than MM alone (Figure 3)—were supported. The lack of a significant interaction between drug and PI condition
indicated lack of support for the hypothesis that active medication plus PI
would be the most efficacious condition.
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Table 2. Percent Abstinent, Number Assessed, and Number Abstinent by
Assessment Time, Treatment Condition, and Drug*
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Figure 2. Seven-day point-prevalence abstinence
rates by pharmacologic intervention.
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Figure 3. Seven-day point-prevalence abstinence
rates by psychological intervention (PI) and drug. MM indicates medical management.
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We did not hypothesize a difference in efficacy between the 2 active
drugs. None was found (21 [N = 126] = 1.88, P = .17).
The interaction of bupropion vs nortriptyline with diagnosis fell short
of traditional levels of significance (21 [N =
126] = 3.39, P = .07). There were few differences
between the 2 drugs for participants without a history of depression, but
there were higher abstinence rates for bupropion than nortriptyline for participants
with a history of depressive disorder. For example, with missing data omitted,
the 52-week abstinence rate for participants without a history of MDD was
27% for nortriptyline and 24% for bupropion (20% with missing data coded as
smoking for both drugs), whereas for participants with a history of MDD, the
52-week abstinence rate was 16% for nortriptyline (13% with missing data coded
as relapsed) and 38% for bupropion (33% with missing data coded as relapsed).
Continuous abstinence rates for the 1-year period were 20.7% for bupropion,
13.2% for nortriptyline, and 11.8% for placebo (22
[N = 162] = 1.96, P = .38). For the 2 psychosocial
conditions, they were 13% for MM and 18% for PI (22
[N = 162]<1).
Main effects for sex approached significance (21 [N = 189] = 2.68, P = .10), favoring better
abstinence rates for men when compared with women. Abstinence rates for men
were as follows: week 12, 44%; week 24, 29%; week 36, 26%; and week 52, 24%.
For women, these rates were as follows: week 12, 41%; week 24, 20%; week 36,
28%; and week 52, 23%.
For all analyses, there were no differences in significance when the
data were reanalyzed with missing data coded as smoking. With missing data
coded as smoking, continuous abstinence rates were as follows: bupropion,
16.4%; nortriptyline, 9.6%; and placebo, 8.2% (22
[N = 219] = 2.80, P = .25); and MM, 10%, and PI,
13% (22 [N = 219]<1).
Fifty-four participants, or 25% of the sample, reported using out-of-study
NRT (n = 34) or bupropion during follow-up (15 in the bupropion group, 14
in the nortriptyline group, and 25 in the placebo group). Placebo recipients
were more likely than active-drug recipients to use nonstudy pharmacological
therapies (21 [N = 219] = 5.42, P = .20).
Of the 54 subjects who reported use of extrastudy medications, however,
only 14 were abstinent at the time of the report, and they were distributed
fairly equally across the treatment conditions. At week 24, 1 participant
who reported out-of-study medication was abstinent (nortriptyline condition);
at week 36, 1 abstinent participant in each of the antidepressant conditions
and 2 in the placebo condition were using out-of-study medications. At week
52, the out-of-study medication count was 4 in the bupropion group, 2 in the
nortriptyline group, and 3 in the placebo group.
MAINTENANCE OF THE BLIND
As part of the informed consent procedures, participants were informed
about the adverse effects of each drug. It is not surprising that participants
receiving active drug were more likely to guess that they had received active
drug (87%) than placebo participants were to believe they were receiving active
drug (67%; 21 [N = 160] = 9.06, P = .003; odds ratio, 3.29; 95% confidence interval, 1.48-7.30). Of
the active drug participants who were able to correctly guess their assignment
to active or placebo drug, 49% of the nortriptyline recipients and 58% of
the bupropion recipients correctly guessed drug assignment (21 [N = 96]<1, P = .35). Thus, bupropion
recipients were no more likely than nortriptyline participants to correctly
identify which drug they had received.
ADVERSE EFFECTS
Of the potential adverse effects (dry mouth, rash, weight gain, light-headedness,
shaky hands, constipation, blurry vision, sexual problems, difficulty in urinating,
racing heart, swollen legs, chest pain or pressure, shortness of breath, weight
loss, headaches, agitation, nausea or vomiting, dizziness, difficulty sleeping,
and sweating), postbaseline endorsement rates differed between nortriptyline
and placebo on the following: (1) dry mouth: nortriptyline, 72%; placebo,
33% (21 [N = 131] = 19.71, P<.001; odds ratio, 5.16; 95% confidence interval, 2.45-10.86); and
(2) constipation: nortriptyline, 32%; placebo, 14% (21 [N = 131]=5.91, P
= .02; odds ratio, 2.87; 95% confidence interval, 1.20-6.85). Bupropion did
not differ from placebo on any item.
COMMENT
As predicted, bupropion and nortriptyline were more efficacious than
placebo in producing abstinence when measured by point-prevalence abstinence
during the course of a year. Similarly, PI was more efficacious than MM alone.
The hypothesis that PI would add to antidepressant treatment was not supported.
As has been the case in other recent studies (eg, Hall et al3),
MDD did not predict failure to quit smoking.
The equivalent effectiveness of bupropion and nortriptyline, a generic
drug, and nortriptyline's much lower cost, suggest that it might be a useful
alternative to bupropion for some smokers. The drugs have different adverse
effect and risk profiles, however. Nortriptyline has been shown to be related
to an increased rate of serious cardiac events in patients with ischemic heart
disease.23
The present study does not indicate whether it is the content of the
PI or increased contact that increases abstinence. Visual inspection of data
values in Figure 3 suggests potential
differences between MM-placebo, and the remaining 3 conditions (MM–active
drug, MM/PI–placebo, and MM/PI–active drug) at weeks 12, 24, and
52. The PI did not increase abstinence rates when added to the active drug;
it may bring abstinence rates in the placebo condition to about the same level
as active drug. Additional research in the role of psychological treatment
with antidepressants is warranted. The interaction of drug with history of
MDD did not reach statistically significant levels (P
= .07). Inspection of the data suggests potential superiority of bupropion
for smokers with a history of MDD, but virtually no difference in patients
without a history of MDD. The effect may warrant further examination in a
study designed to address this question.
Abstinence rates in the present study were lower than those reported
in earlier work with nortriptyline3 and bupropion.1-2 This difference may reflect the changing
nature of participants entering smoking treatment trials. Smokers in the present
study smoked fewer cigarettes, were less likely to have a partner or spouse,
were more likely to be blue collar or service workers, and were less likely
to be white. A recent study24 has shown decreasing
abstinence rates in smoking cessation studies during the past 25 years. The
authors of that study attribute this to increasing difficulty in quitting
cigarettes among individuals who continue to smoke despite current pressures.
Although nortriptyline and bupropion were significantly more efficacious
than placebo when point-prevalence rates were compared, this was not the case
when 1-year continuous abstinence rates were evaluated. Also, as the modest
week 24 and 52 abstinence rates indicate, the field must continue to seek
more efficacious treatments. Two recent clinical trials, both with acceptable
rigor, one published in 199625 and the second
in 1999,2 failed to find differences between
placebo and active NRT. Recent reviews of NRT effectiveness have suggested
decreasing efficacy of nicotine patch, but not nicotine gum, since they were
introduced in the 1980s.26 As the population
of smokers changes, interventions may experience a declining efficacy.
Given the information provided to participants as part of the informed
consent procedures, it is not surprising that they were able to correctly
guess which drug they had received. Indeed, in studies of drugs with detectable
effects that report the maintenance of the blind, participants are often able
to correctly guess which drug they received.27-29
Nevertheless, given the complex blinding procedures we used because a placebo
bupropion sustained-release capsule was unavailable, it was reassuring that
the bupropion recipients were no more likely than the nortriptyline recipients
to guess their drug.
To our knowledge, this is the first clinical trial to report the use
of out-of-study medication during the follow-up period. We found a high rate
of such use (54 patients [25% of the sample]), but only 14 of these 54 participants
were abstinent. Recoding these abstinent participants as smoking does not
change the overall findings. They represent less than 6% of the sample and
were fairly equally distributed across conditions. Nevertheless, given the
increasing availability of smoking cessation medications, we recommend that
studies routinely report these data to better understand outcomes and the
processes of abstinence and relapse.
The results of the present study are limited by the select nature of
the sample resulting from the need to meet both criteria necessary to complete
the research, such as availability during the course of the year, and medical
exclusionary criteria.
AUTHOR INFORMATION
Submitted for publication July 20, 2001; final revision received November
12, 2001; accepted December 11, 2001.
This study was supported by grants R01 DA02538 and 2 P50 DA09253 from
the National Institute on Drug Abuse, Bethesda, Md, and grant R01 CA71378
from the National Cancer Institute, Bethesda.
We thank Kevin Delucchi, PhD, for his statistical consultation and Heather
Kenna for manuscript preparation.
Corresponding author and reprints: Sharon M. Hall, PhD, University
of California, San Francisco, 401 Parnassus Ave, Box 0984, San Francisco,
CA 94143-0984 (e-mail: smh{at}itsa.ucsf.edu).
From the Department of Psychiatry, University of California, San Francisco
(Drs Hall, Humfleet, Reus, Muñoz, and Hartz); and Edina, Minn (Mr Maude-Griffin).
REFERENCES
| |
1. Hurt RD, Sachs DPL, Glover ED, Offord KP, Johnston JA, Dale LC, Khayralla MA, Schroeder DR, Glover PN, Sullivan R, Croghan IT, Sullivan PM. A comparison of sustained-release bupropion and placebo for smoking
cessation. N Engl J Med. 1997;337:1195-1202.
FREE FULL TEXT
2. Jorenby DE, Leischow SJ, Nides MA, Rennard SI, Johnston JA, Hughes AR, Smith SS, Muramoto ML, Daughton DM, Doan K, Fiore MC, Baker TB. A controlled trial of sustained-release bupropion, a nicotine patch,
or both for smoking cessation. N Engl J Med. 1999;340:685-691.
FREE FULL TEXT
3. Hall SM, Reus VI, Muñoz RF, Sees KL, Humfleet G, Hartz DT, Frederick S, Triffleman E. Nortriptyline and cognitive-behavioral therapy in the treatment of
cigarette smoking. Arch Gen Psychiatry. 1998;55:683-690.
FREE FULL TEXT
4. Prochazka AV, Weaver MJ, Keller RT, Fryer GE, Licari PA, Lofaso D. A randomized trial of nortriptyline for smoking cessation. Arch Intern Med. 1998;158:2035-2039.
FREE FULL TEXT
5. Hughes J, Gust S, Skoog K, Keenan R, Fenwick J. Symptoms of tobacco withdrawal: a replication and extension. Arch Gen Psychiatry. 1991;48:52-59.
FREE FULL TEXT
6. Fiore MC, Jorenby DE, Baker TB, Kenford SL. Tobacco dependence and the nicotine patch: clinical guidelines for
effective use. JAMA. 1992;268:2687-2694.
FREE FULL TEXT
7. Fiore MC, Bailey WC, Cohen SJ. Smoking Cessation Clinical Practice Guidelines No. 18. Rockville, Md: Public Health Service, Agency for Health Care
Policy and Research, US Dept of Health and Human Services; 1996. Publication
96-0692.
8. Fiore MC. A clinical practice guideline for treating tobacco use and dependence:
a US Public Health Service report. JAMA. 2000;283:3244-3254.
FREE FULL TEXT
9. First M, Gibbons M, Spitzer R, Williams J. Structured Clinical Interview for DSM-IV: Users Guide. New York: Biometrics Research Dept, New York State Psychiatric Institute;
1996.
10. Jarvis MJ, Tunstall-Pedeo H, Feyerabend C, Vesy C, Saloojee Y. Comparison of tests used to distinguish smokers from non-smokers. Am J Public Health. 1987;77:1435-1483.
FREE FULL TEXT
11. McNair DM, Lorr M, Droppleman LF. Manual for the Profile of Mood States. San Diego, Calif: Educational & Instructional Testing Service;
1981.
12. Payne T, Smith P, McCracken L, McSherry WC, Antony M. Assessing nicotine dependence: a comparison of the Fagerstrom Tolerance
Questionnaire (FTQ) with the Fagerstrom Test for Nicotine Dependence (FTND)
in a clinical sample. Addict Behav. 1994;19:307-317.
FULL TEXT
|
ISI
| PUBMED
13. Fawcett J, Epstein P, Fiester SJ, Elkin I, Autry JH. Clinical management—imipramine/placebo administration manual:
NIMH Treatment of Depression Collaborative Research Program. Psychopharmacol Bull. 1987;23:309-324.
ISI
| PUBMED
14. American Lung Association. Freedom From Smoking. New York, NY: American Lung Association; 1993.
15. Hall SM, Munoz RF, Reus VI. Cognitive-behavioral intervention increases abstinence rates for depressive-history
smokers. J Consult Clin Psychol. 1994;62:141-146.
FULL TEXT
|
ISI
| PUBMED
16. Hall SM, Tunstall C, Rugg D, Jones RT, Benowitz H. Nicotine gum and behavioral treatment in smoking cessation. J Consult Clin Psychol. 1985;53:256-258.
FULL TEXT
|
ISI
| PUBMED
17. Hall SM, Tunstall CD, Ginsberg D, Benowitz NL, Jones RT. Nicotine gum and behavioral treatment: a placebo controlled trial. J Consult Clin Psychol. 1987;55:603-605.
FULL TEXT
|
ISI
| PUBMED
18. Linnoila M, George L, Guthrie S, Leventhal B. Effects of alcohol consumption and cigarette smoking in antidepressant
levels of depressed patients. Am J Psychiatry. 1981;138:841-842.
FREE FULL TEXT
19. McCullagh P, Nelder JA. Generalized Linear Models. 2nd ed. London, England: Chapman Hall; 1989.
20. Gibbons RD, Hedeker D, Waternaux C, Davis JM. Random regression models: a comprehensive approach to the analysis
of longitudinal psychiatric data. Psychopharmacol Bull. 1988;24:438-443.
ISI
| PUBMED
21. Gibbons RD, Hedeker D, Elkin I, Waternaux C, Kraemer H, Greenhouse JB, Shea TM, Imber SD, Sotsky SM, Watkins JT. Some conceptual and statistical issues in analysis of longitudinal
psychiatric data. Arch Gen Psychiatry. 1993;50:739-750.
FREE FULL TEXT
22. Little RC, Milliken GA, Stroup WW. SAS System for Mixed Models. Cary, NC: SAS Institute Inc; 1996.
23. Roose SP, Laghrissi-Thode F, Kennedy JS, Nelson JC, Bigger JT, Pollock BG, Gaffney A, Narayan M, Finkel MS, McCafferty J, Gergel I. Comparison of paroxetine and nortriptyline in depressed patients with
ischemic heart disease. JAMA. 1998;279:287-291.
FREE FULL TEXT
24. Irvin JE, Brandon TH. The increasing recalcitrance of smokers in clinical trials. Nicotine Tob Res. 2000;2:79-84.
25. Hall SM, Munoz RF, Reus VI, Sees KL, Duncan C, Humfleet GL, Hartz D. Mood management and nicotine gum in smoking treatment: a therapeutic
content and placebo-controlled study. J Consult Clin Psychol. 1996;64:1003-1009.
FULL TEXT
|
ISI
| PUBMED
26. Fox BJ, Welsh SK, Fiore MC, Baker TB. Have nicotine patch and nicotine gum lost their efficacy over time? Paper presented at: 7th Annual Meeting of the Society for Research
on Nicotine and Tobacco; March 2001; Seattle, Wash.
27. Moscucci M, Byrne L, Weintraub M, Cox C. Blinding, unblinding, and the placebo effect: an analysis of patients'
guesses of treatment assignment in a double-blind clinical trial. Clin Pharmacol Ther. 1987;41:259-265.
ISI
| PUBMED
28. Ney P, Collins C, Spensor C. Double blind: double talk or are there ways to do better research? Med Hypotheses. 1986;21:119-126.
FULL TEXT
|
ISI
| PUBMED
29. Rabkin J, Markowitz J, Stewart J, McGrath P, Harrison W, Quitkin F, Klein D. How blind is blind? assessment of patient and doctor medication guesses
in a placebo-controlled trial of imipramine and phenelzine. Psychiatry Res. 1986;19:75-86.
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