Abstract
The aim of this study was to investigate the possible reduced risk of Parkinson Disease (PD) due to coffee, alcohol, and/or cigarette consumption. In addition, we explored the potential effect modification by intensity, duration and time-since-cessation of smoking on the association between cumulative pack-years of cigarette smoking (total smoking) and PD risk. Data of a hospital based case-control study was used including 444 PD patients, diagnosed between 2006 and 2011, and 876 matched controls from 5 hospitals in the Netherlands. A novel modeling method was applied to derive unbiased estimates of the potential modifying effects of smoking intensity, duration, and time-since-cessation by conditioning on total exposure. We observed no reduced risk of PD by alcohol consumption and only a weak inverse association between coffee consumption and PD risk. However, a strong inverse association of total smoking with PD risk was observed (OR = 0.27 (95%CI: 0.18–0.42) for never smokers versus highest quartile of tobacco use). The observed protective effect of total smoking was significantly modified by time-since-cessation with a diminishing protective effect after cessation of smoking. No effect modification by intensity or duration of smoking was observed indicating that both intensity and duration have an equal contribution to the reduced PD risk. Understanding the dynamics of the protective effect of smoking on PD risk aids in understanding PD etiology and may contribute to strategies for prevention and treatment.
Highlights
Coffee, alcohol and cigarette consumption are potential protective factors for the development of Parkinson disease (PD) [1]
The evidence for an association between cigarette smoking and PD risk is strong with studies consistently showing an exposure dependent reduction in risk with total lifetime exposure to cigarette smoke, the product of smoking intensity and duration of smoking [2,3,4]
In our hospital based case-control study, we found a strong inverse association between cigarette smoking and Parkinson disease, which is in correspondence with earlier studies
Summary
Alcohol and cigarette consumption are potential protective factors for the development of Parkinson disease (PD) [1]. Insight into the relative importance of duration, intensity, and time-since-cessation of cigarette smoking on PD risk may offer important clues to PD etiology and to strategies for prevention and treatment [5]. To circumvent this problem Lubin et al described a model in which the modifying effects of intensity or duration can be investigated by conditioning the model on total exposure, allowing a comparison of the risk of low intensity exposures at long duration with risk of high intensity exposures at short duration [7] This method was extended by including a term for time-since-cessation of smoking [8]
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