Canynge Hall Whiteladies Road Bristol BS8 2PR, United Kingdom
Department of Primary Care and Population Science Royal Free and University College Medical School Rowland Hill Street London NW3 2PF, United Kingdom
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INTRODUCTION |
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Our paper was entitled, "Smoking as 'independent' risk factor for suicide: illustration of an artifact from observational epidemiology?" (3). However, it has been widely taken to illustrate that smoking does indeed cause suicide. Biologic mechanisms through which this could act (e.g., smoking suppressing brain serotonin levels) have been advanced, and a meta-analysis has been performed showing that most studies demonstrate the same thing. In our study (3
), however, smoking was strongly related to the risk of being murdered, with an "independent" relative risk of over 2 for smokers of two packs or more per day compared with nonsmokers. Unless health promoters have moved on to a direct action phase, during which they shoot smokers, this association is very unlikely to be causal.
We live in a world in which associations are more common than lack of associations, and the former are only worth drawing attention to if they increase our understanding of why the world is the way it is. The "independent" association between smoking and suicide is about as interesting as the equally strong "independent" association in which never wearing a seatbelt apparently increases the risk of dying of all-cause or respiratory disease mortality (5). These findings merely show for the thousandth time that smokers are different from nonsmokers and that the people who wear seatbelts differ from people who don't wear seatbelts. Indeed, lack of associations tell us at least as much as do associations. For example, the lack of association between socio-economic position and several causes of ill health demonstrates that strongly socially patterned exposures, which represent a large majority of the exposures that epidemiologists study, are unlikely to be importantly involved in the etiology of these particular conditions (6
).
Similar studies carried out in different social, cultural, geographic, and historical contexts tell us much more than mere replications within the same study population. For example, meta-analyses have demonstrated that smoking appears to be strongly related to cervical cancer risk, yet the few studies that fail to show this effect are the ones in which smoking among women is associated in a different way with the risk of acquisition of sexually transmitted viral infections than in the majority of studies carried out in North America or Western Europe (7). In these studies, smoking will not merely serve as a proxy for an unmeasured underlying causal (probably viral) factor (8
).
To prevent further ventures down unrewarding alleyways, perhaps an additional sectionwhich could be titled, "Why did we examine this association and consider it worth reporting?"should be added alongside the Introduction, Methods, Results, and Discussion in reports of observational epidemiologic studies.
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REFERENCES |
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Department of Health Policy and Management Harvard University School of Public Health Boston, MA 02115
Department of Social and Behavioral Sciences Boston University School of Public Health Boston, MA 02118
US Army Research Institute of Environmental Medicine Natick, MA 01760-5007
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INTRODUCTION |
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A recent study of several thousand teenagers suggests that the conclusion of Davey Smith and Phillips may have been premature. In this study, teenagers were followed longitudinally to assess the nature and direction of the relation between cigarette smoking and depression (3). Among nondepressed teens, cigarette smoking was the strongest predictor of developing depressive symptoms, but among teens who did not smoke at baseline, baseline depressive symptoms were not predictive of heavy smoking.
The arguments of Davey Smith and Phillips reiterate those they and their colleague, J. D. Neaton, made in their 1992 paper, where they expressed general disdain for observational epidemiology (4). They assert that associations are of value only if they increase our understanding of why the world is the way it is and imply that the purpose of science is only to determine causality. We disagree. The fact that the cock's crowing doesn't cause the sun to rise did not make the cock any less useful as an alarm clock throughout the ages. Similarly, smoking, regardless of whether or not there is a causal link with suicide, may prove an easily observable and useful marker of persons at risk.
We are not apologists for a causal relation between smoking and suicide nor do we claim that our paper supports this particular explanation for the relation we describe. It may well be that third variable explanations account for some of the relation we observe, that some soldiers who were depressed self-medicated with tobacco, and that others were depressed as a consequence of smoking. These explanations are not mutually exclusive. What troubles us is not that uncertainty remains about the likely explanation(s) for the relation we describe. Rather, we are troubled by the implication of Davey Smith and Phillips that they are properly the arbiters of what avenues investigators ought to pursue.
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