Dr Sheikh notes 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.
He also asserts that ‘the data collected… were almost cross-sectional’. This is not true. The data were discrete longitudinal data, in which both smoking and depression were assessed over several time periods. The separation of these assessments by unobserved periods was not sufficient to render the data cross-sectional.
It is also not strictly true to suggest that data observed at the same time periods could not be used to model causality. 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. Our data clearly 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 numerous variables using the Christchurch Health and Development Study (CHDS) data. 1,2
Dr Sheikh argues 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 reported in the original study; measures of smoking and measures of depression demonstrated significant (P<0.05) associations using fixed-effects regression models; and the results of structural equation modelling showed that 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 this Journal.
Finally, Dr Sheikh argues that depression must be caused by nicotine withdrawal rather than smoking. However, Benowitz 3 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 among active smokers because of this continual cycle of withdrawal and satiety.
Edited by Kiriakos Xenitidis and Colin Campbell