We estimated the pooled risk of tobacco smoking for Parkinson's disease (PD). Inclusion criteria included systematic searches of MedLine, PsycLIT, Embase, Current Contents, previously published reviews, examination of cited reference sources, and personal contact and discussion with several investigators expert in the field. Published prospective studies on PD and cigarette smoking. When two or more studies were based on an identical study, the study that principally investigated the relationship or the study that was published last was used. Seven prospective studies were carried out between 1959 and 1997, of which six reported risk estimates. Four cohorts were based on standardised mortality rates, which were exclusively of male. Only one study included risk estimates for both males and females separately. The risk of ever smoker was 0.51 (95% confidence interval, 0.43 to 0.61). There was an obvious protective effect of current smoking in the pooled estimate (relative risk, 0.35; 95% CI, 0.26-0.47). Former smokers had lower risk compared with never smokers (relative risk, 0.66; 95% CI, 0.49-0.88). Although our pooled estimates show that smoking is inversely associated with the risk of PD, the four prospective studies that were based on follow-up of mortality of smokers had many limitations. Further studies evaluating the association between smoking and PD in women are strongly needed.

Although our pooled estimates show that coffee consumption is inversely associated with the risk of AD, the four studies had heterogeneous methodologies and results. Further prospective studies evaluating the association between coffee consumption and AD are strongly needed.

Perhaps one of the most important questions posed by the neurobiology of aging concerns the pathogenic mechanisms in Parkinson's disease (PD). Recently, it was suggested that exposure to pesticides could be the main cause of PD. Another study reported that the environmental endotoxin, lipopolysaccaride produced by Salmonella minnesota, might be a risk factor for PD. An alternative explanation is the genetic component, which has been suggested to be an important risk factor. Epidemiological studies have identified a positive family history of Parkinson as one of the most important risk factors for the disease. However, these studies neither examined nor reviewed the medical records of the family members. The twin study stated that the major factors in the etiology of PD are non-genetic. Meanwhile, epidemiological studies from China have shown that the prevalence of PD is much lower than in the Caucasian population, explained by the low frequency of cytochrome P-450 CYP2D6 debrisoquine hydroxylase gene polymorphism. The etiology of idiopathic PD is still a question for scientists, and calls for further research, especially with the growing proportion of elderly and the rising incidence of PD worldwide. Future research for PD risk factors should consider that multiple interactions occur in PD, resulting in a complex trait, which includes genetic, acquired, and environmental components.

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The Cox regression analysis with quantitative time-dependent variables is the most valid alternative for assessing the risk of nosocomial infection per day of exposure to an extrinsic risk factor in the ICU.

This study describes the behavior of eight statistical programs (BMDP, EGRET, JMP, SAS, SPSS, STATA, STATISTIX and SYSTAT)

Our aim was to estimate the pooled risk of current and former smoking for Parkinson’s disease (PD).We have reviewed all observational studies that evaluated the association between PD risk and smoking habit. Twenty six studies were identified: 21 case-control, 4 cohort and 1 cross-sectional. The cross-sectional study did not compare former with never smokers. These studies were carried out between 1968 and 2000.There was an obvious protective effect of current smoking in the pooled estimate [risk estimate 0.37 (95% confidence interval 0.33 to 0.41)]. Former versus never smokers had pooled risk estimate of 0.84 (95% confidence interval 0.76 to 0.92). Current and former smoking do not, therefore, exert the same protective effect against PD so that it is unnecessary to postulate a biological mechanism through which smoking protects against PD. The results show that the reverse direction of causation is a more probable explanation, i.e. movement disorders of PD protect against smoking. Another explanation is that failure to develop strong smoking habits in early adult life might be a prodromal symptom of the disease and could perhaps be its first clinical manifestation.

Tea consumption can protect against PD and this protective effect is clearer in Chinese populations. The low rate of tea consumption among persons with PD should provide us many valuable insights into the nature of the illness.