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Cigarette smoking and depression: tests of causal linkages using a longitudinal birth cohort

  • Joseph M. Boden (a1), David M. Fergusson (a1) and L. John Horwood (a1)



Research on the comorbidity between cigarette smoking and major depression has not elucidated the pathways by which smoking is associated with depression.


To examine the causal relationships between smoking and depression via fixed-effects regression and structural equation modelling.


Data were gathered on nicotine-dependence symptoms and depressive symptoms in early adulthood using a birth cohort of over 1000 individuals.


Adjustment for confounding factors revealed persistent significant (P<0.05) associations between nicotine-dependence symptoms and depressive symptoms. Structural equation modelling suggested that the best-fitting causal model was one in which nicotine dependence led to increased risk of depression. The findings suggest that the comorbidity between smoking and depression arises from two routes; the first involving common or correlated risk factors and the second a direct path in which smoking increases the risk of depression.


This evidence is consistent with the conclusion that there is a cause and effect relationship between smoking and depression in which cigarette smoking increases the risk of symptoms of depression.

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Corresponding author

David M. Fergusson, Christchurch Health and Development Study, University of Otago, Christchurch School of Medicine and Health Sciences, PO Box 4345, Christchurch, New Zealand. Email:


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See editorial, pp. 425–426, this issue.

Declaration of interest




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Cigarette smoking and depression: tests of causal linkages using a longitudinal birth cohort

  • Joseph M. Boden (a1), David M. Fergusson (a1) and L. John Horwood (a1)


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Cigarette smoking and depression: tests of causal linkages using a longitudinal birth cohort

  • Joseph M. Boden (a1), David M. Fergusson (a1) and L. John Horwood (a1)
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Depression and Smoking - Reply to Sheikh

Joseph M. Boden, Senior Research Fellow
15 October 2010

Sheikh (1) has made a number of comments concerning our earlier published study (2), which we address below.

1. Sheikh noted that “It is possible that some teenagers experienced depression and smoked cigarettes before age 17”. In response we would point out that the purpose of the study was not to measure or compare the onset or first cause of either depression or cigarette smoking, but rather to examine the dynamic interplay between cigarette smoking and symptoms of depression during early adulthood, and the extent to which either cigarette smoking or depression played a causal role in the maintenance of this association across time.

2.Sheikh also asserted that “the data collected… were almost cross-sectional.” This is in fact not true. The data were discrete longitudinal data, in which both smoking and depression were assessed overseveral time periods. The separation of these assessments by unobserved periods was not sufficient to render the data cross-sectional.

3.Sheikh suggested that data observed at the same time periods couldnot be used to model causality. This is not strictly true. Given the availability of data observed at multiple points in time, it proves possible to fit structural equation models of the time-dynamic associations between two variables (such as cigarette smoking and depression) across time, comparing the relative fit of models that posit: a) a reciprocal causal effect between smoking and depression; b) a unidirectional causal effect from smoking to depression; and c) a unidirectional causal effect from depression to smoking. The present dataclearly show that the most parsimonious model is one in which there is a unidirectional causal effect from smoking to depression. This same approach has been used to examine the causal associations between numerousvariables using CHDS data (3, 4).

4.Sheikh argued that it might be possible that measures other than nicotine dependence might have led to differing results. We have in fact conducted several additional analyses using a range of measures of both cigarette smoking and depression, including: measures of smoking frequency; measures of the number of cigarettes smoked; and whether participants met criteria for DSM-IV nicotine dependence and major depression. In all cases the analyses were consistent with those reportedin the original study; measures of smoking and measures of depression demonstrated significant (p < .05) associations using fixed-effects regression models; and the results of structural equation modelling showedthat the best fitting model was one in which cigarette smoking (or nicotine dependence) predicted depression. In the original study, we reported on analyses of nicotine dependence symptoms and symptoms of depression in order to maintain a focus on measures germane to psychiatry,in view of the scope of the BJP.

5.Sheikh argued that depression must be caused by nicotine withdrawal rather than smoking. However, Benowitz (5) has shown that active smokers go through several withdrawal phases during each day, and that these withdrawal phases are one of the factors that causes self-administration of nicotine. Therefore, it could also be argued that depressive symptomatology may be increased amongst active smokers due to this continual cycle of withdrawal and satiety.

The authors declare no conflicts of interest.


1.Sheikh K. Depression and Smoking [Letter]. Br J Psychiatry. 2010.

2.Boden JM, Fergusson DM, Horwood LJ. Cigarette smoking and depression: Tests of causal linkages using a longitudinal birth cohort. BrJ Psychiatry. 2010:440-446.

3.Fergusson DM, Horwood LJ, Ridder EM. Tests of causal linkages between cannabis use and psychotic symptoms. Addiction. 2005;100:354-366.

4.Fergusson DM, Boden JM, Horwood LJ. Structural models of the comorbidity of internalising disorders and substance use disorders in a longitudinal birth cohort. Soc Psych Psych Epid. In Press.

5.Benowitz NL. Nicotine addiction. New Engl J Med. 2010;362:2295-2303.
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Conflict of interest: None Declared

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Depression and Smoking

Kazim Sheikh, Physician
06 October 2010

In their study of a birth cohort (n=1265) in Christchurch, New Zealand, Boden et al (1) found that cigarette smoking increased the risk of depression. The cohort was “studied” at birth, 4 months, 1 year, and annually to age 16 years, and at age 18, 21 and 25 years. At the last three assessments, the study subjects were interviewed and data on depression and smoking were collected. The Composite International Diagnostic Interview (CIDI) was used to ascertain the symptoms of major depression and data on the number of cigarettes smoked and the symptoms ofnicotine dependence were recorded. The authors utilized a variety of regression analyses to determine the causal relationship between depression and smoking adjusted for covariates.

No matter how sophisticated the analyses are, the results of the study reflect the quality of data. The data for this study (1) were incomplete and flawed. The data on depression and smoking were for three 12-month periods and three 1-month periods, respectively, prior to the interviews. Consequently, the data on the prevalence of depression before age 17 and during periods from age 18 to 20 and from age 21 to 24 were missing. Except for three 1-month periods between age 18 and 25, all data on smoking and nicotine dependence were also missing. It is possible that some teenagers experienced depression and smoked cigarettes before age 17.It is also possible that the study subjects started and quit smoking or recovered from depression between age 18 and 20, and between age 21 and 24, periods for which data were not collected. In effect, the data collected at age 18, 21 and 25 were almost cross-sectional, which cannot provide evidence for the direction of the association. If a study subject reported smoking at age 18 interview and gave history of depression prevalent in the year prior to age 21, the authors would conclude that smoking caused depression because according to their data, smoking preceded depression. But, the authors did not know that this subject had quit smoking before the onset of depression at age 19 because they did notobtain the data for the two years prior to age 20. In this situation, depression was caused by smoking cessation, not by smoking.

As Munafo and Araya’s editorial (2) remarked, CIDI uses symptoms to determine the diagnosis of depression, not its severity. The number of cigarettes smoked is an appropriate measure of exposure to tobacco smoke, not the number of symptoms of nicotine dependence. Consequently, an association between the number of symptoms of depression and those of nicotine dependence is meaningless.

The fact that tobacco smoke has anti-anxiety and anti-depressant properties (2,3) and that attempted or successful smoking cessation results in depression regardless of prophylactic nicotine replacement or antidepressant therapy (4,5), smoking cannot cause depression. If smoking causes depression, smoking cessation would relieve depression. The authorsneglected to describe data on smokers developing depression when they quitsmoking and data on anti-depressant therapy during the observation period.Any study that does not use data on depression following reduction in or cessation, even transient, of tobacco smoking and data on pharmacotherapy cannot reliably determine the direction of the cause-and-effect relationship between smoking and depression.


1. Boden JM, Fergusson DM, Horwood LJ. Cigarette smoking and depression: tests of causal linkage using a longitudinal birth cohort. Br J Psychiatry 2010; 196: 440-46.

2. Munafo MR, Araya R. Cigarette smoking and depression: a question of causation. Br J Psychiatry 2010; 196: 425-26.

3. Balfour DJ, Ridley DL. The effects of nicotine on neural pathways implicated in depression: a factor in nicotine addiction? Pharmacol Biochem Behav 2000;66:79-85.

4. Wilhhelm K, Wedgwood L, Niven H, et al. Smoking cessation and depression: current knowledge and future. Drug Alcohol Rev 2006;25:97-107.

5. Glassman AH, Covey LS, Stetner F, et al. Smoking cessation and thecourse of major depression: a follow-up study. Lancet 2001;357:1929-32.
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