Depression and Smoking Cessation: Evidence from a Smoking Cessation Clinic with 1-Year Follow-Up

The present data were routinely collected as part of smoking cessation treatment at the Center for Tobacco Dependence at the General University Hospital in Prague, Czech Republic. Patients could be referred by their physician or self-refer to the treatment centre. Treatment followed evidence-based guidelines [21, 22] and was tailored to the individual patient’s needs. Treatment consisted of face-to-face counselling and a choice of pharmacotherapy for all patients and was provided by a nurse and a physician; all physicians had completed training courses developed by the Czech Medical chamber or the Tobacco Treatment Specialist Certification Program at the Mayo Clinic, Rochester, Minnesota.

All patients were treated as outpatients, and over the course of a year, each patient visited the clinic several times. The first visit took about 1 h and was used to complete a basic physical examination and to collect data on demographics, smoking characteristics and dependence, quit attempt history and medical history including self-reported mental health problems and completion of the Beck Depression Inventory (BDI-II) [23]. Patients also provided informed consent for their data to be used in research. The second visit took up to 2 h; it included discussion of physical and psychosocial dependence on smoking and nicotine, strategies to reduce exposure to smoking cues and to cope with cravings. Pharmacotherapy options for smoking cessation were discussed and selected cooperatively and a target date to quit smoking was set. Follow-up visits took about 30 min each. The first one was arranged to occur 1 week after the quit date, followed by fortnightly visits during the first 3 months and monthly visits during months 3 to 6. The final follow-up took place 1 year after the actual quit date; the basic physical examination and BDI-II were repeated and total duration of pharmacotherapy for cessation recorded. At all visits, carbon monoxide (CO) was measured, and information on smoking cessation pharmacotherapy and any changes in medical history were recorded.

The treatment did not include any specific treatment for depression or other mental health problems. The counselling/behavioural support was covered by health insurance, but the cost of pharmacotherapy had to be covered by the patient. A full description of the intervention is available at www.​slzt.​cz/​intervention-structure. Previous analysis showed that at 1-year follow-up, 38% of patients were biochemically verified abstinent from smoking [24]. These are very high success rates compared for example with around 8% achieved in UK stop smoking services [25] (which also deliver a combination of behavioural support and pharmacotherapy, albeit usually restricted to a shorter period of time ) and compared with the Mayo clinic which uses a similar treatment model and reported 28% self-reported abstinence at 6 months [26].

Between January 2008 and December 2014, 4415 smokers began treatment at the Centre for Tobacco Dependence. Patients without information on baseline depression were excluded from all analyses (n = 998). Patients younger than 16 (n = 16) or older than 80 years (n = 5) were also excluded.

To address aim 1 (association between baseline level of depression and outcome), patients missing information on age or dependence (n = 16) were excluded, leaving n = 3380 patients for analyses. An additional analysis included length of pharmacotherapy so that only patients taking any pharmacotherapy could be included (n = 2545).

To address aim 2 (change in depression), only patients with information on depression level at baseline and 1-year follow-up were included (n = 864). Among patients who were not abstinent at 1 year, depression at follow-up was generally not recorded; so, analysis had to be restricted to abstinent patients (n = 835).

Baseline characteristics of the sample, treatment characteristics and 1-year outcomes were described. The association between baseline level of depression and outcome was assessed in logistic regressions of 1-year abstinence onto baseline level of depression (none, mild, moderate/severe); a first bivariate model was followed by the primary model, a multiple logistic regression that included baseline patient characteristics (age, gender, education, marital status, cigarette dependence and other mental health problems) and treatment characteristics (number of visits, type of pharmacotherapy). A further model added an interaction for level of depression and gender. Separate models replaced depression level with antidepressant use at baseline. Finally, a separate analysis added length of pharmacotherapy to the primary model; this was repeated with an interaction term for length of pharmacotherapy and type of pharmacotherapy.

Baseline characteristics of the sample and treatment characteristics are described in Table 1. Overall, CO-verified 1-year abstinence was 37.1%. Overall, 29.7% of the sample reported at least some level of depression, and 444 patients (13.1%) were taking antidepressants at baseline. Bivariate analysis results indicate that in comparison with patients without depression, patients with mild depression (OR = 0.71; 95% CI: 0.58 to 0.87, p = 0.01) were less likely to be abstinent and patients who reported moderate to severe depression were considerably less likely to be abstinent (OR = 0.51; 95% CI: 0.41 to 0.63, p < 0.001). These associations remained very similar in adjusted analysis (Table 1). Higher education, being married and lower dependence were also associated with increased abstinence; gender, age and other mental health problems were not significantly associated with abstinence (Table 1). Compared with those not taking any pharmacotherapy, patients taking any type of pharmacotherapy were more likely to be abstinent, with the exception of the small groups of those using a combination of NRT and varenicline or ‘other’ combinations where differences were not significant (Table 1). More visits during the year increased odds of abstinence, particularly having had 5 or more visits was associated with vastly increased odds of abstinence at the 1-year follow-up (Table 1). In the additional model including interaction terms, there was no evidence of an interaction between gender and baseline level of depression (gender * mild depression: OR = 1.23, 95% CI: 0.77 to 1.98, p = 0.40; gender * moderate/severe depression: OR = 1.24, 95% CI: 0.76 to 2.04, p = 0.39).

In the models replacing level of depression with antidepressant use, patients using antidepressants at baseline were marginally less likely to be abstinent at 1 year than those not using antidepressants (32.9% versus 37.7%, OR = 0.81, 95% CI: 0.65 to 0.999, p = 0.049). This association was similar in adjusted analysis, albeit with a wider confidence interval crossing 1 (OR = 0.79, 95% CI: 0.62 to 1.01, p = 0.061). The associations of other predictors were very similar to those in the primary model.

When adding length of pharmacotherapy to the primary model (Table 2), the results for mild and moderate/severe depression were very similar to each other. Longer use of pharmacotherapy use was associated with increased abstinence. For pharmacotherapy, the reference category in this model was NRT; patients on a combination of NRT and varenicline or using any of the options in the mixed other category were less likely to be abstinent than those using NRT; other differences were not significant. The ORs associated with a higher number of visits were not as large as in the main model, but the number of visits remained a strong predictor of abstinence (Table 2). No significant interaction was found for length of pharmacotherapy * type of pharmacotherapy (all p ≥ 0.05).

The majority of patients with depression at baseline who remained abstinent from smoking reported improvements in their level of depression, while only a very small minority reported a higher level of depression at follow-up (Fig. 1, χ² = 100.1, p < 0.001). Across all successful patients, mean (SD) BDI-II scores improved significantly from 9.2 (8.6) to 5.3 (6.1); t(834) = 14.6, p < 0.001. The median decreased significantly from 7 to 3 (Wilcoxon signed-rank Z = −14.1, p < 0.001; sign test Z = −12.9, p < 0.001).

The mixed model ANOVA assessing the change in depression by baseline level of depression indicated large significant main effects of time (F(1, 832) = 880.8, p < 0.001, partial η² = 0.51) and baseline level of depression (F(2, 832) = 666.4, p < 0.001, partial η² = 0.62) and a significant depression * time interaction (F(2832) = 296.5, p < 0.001, partial η² = 0.42; Fig. 2). Median scores decreased significantly from baseline to follow-up for those with no/minimal depression (from 5 to 3, Wilcoxon Z = −8.4, sign Z = −8.4, both p < 0.001), mild depression (from 16 to 7, Wilcoxon Z = −7.8, sign Z = −7.5, both p < 0.001) and moderate/severe depression (from 25 to 10, Wilcoxon Z = −8.1, sign Z = −8.2, both p < 0.001).

The mixed model ANOVA assessing the change in depression by pharmacotherapy indicated a small significant main effect of pharmacotherapy (F(5, 829) = 12.34, p < 0.001, partial η² = 0.07) and a significant interaction of pharmacotherapy with time (F(5, 829) = 3.47, p = 0.004, partial η² = 0.02), illustrated by a steep gradient for those on bupropion (Fig. 3).