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Objectives: This systematic review of the literature was carried out to see whether coffee consumption could affect Parkinson’s disease (PD) symptoms. Methods: Randomized controlled trials (RCTs), crossover studies, and quasi-experimental studies were assessed to evaluate the effect of caffeine on PD. The databases including Medline/PubMed, ProQuest, Embase, Cochrane Library, and ClinicalTrials.gov were systematically searched. The Cochrane Collaboration’s tool for assessing the risk of bias in randomized clinical trials and the Cochrane risk of bias assessment tool for non-randomized studies of interventions (ROBINS-I) were used to assess the quality of RCTs and non-randomized clinical trials, respectively. A meta-analysis of the results was not possible because of reporting different outcomes. Results: Four papers were included in this study. Only one study reported the significant effect of caffeine on ESS and UPDRS. Another study observed no significant effect of caffeine on ESS during three- and six-week interventions. However, a significant reduction in ESS scores in the sixth week was reported after excluding four protocol violations. This study reported that the UPDRS score reduced in the third week, but significant changes were observed after six weeks. The other two studies did not show a significant effect of caffeine on ESS and UPDRS. Conclusions: Since a meta-analysis was not conducted, there was insufficient evidence to evaluate the effect of caffeine on PD. Thus, it is recommended to conduct more well-designed RCTs with a larger sample size to assess the effect of caffeine on PD.

Background: There is generally a strong link between smoking, more particularly, passive smoking, and the occurrence of various illnesses and health-related disorders. Also, there is a globally recognized epidemiological link between smoking and Parkinson’s disease (PD). However, the current data on passive smoking are contradictory. Thus, this paper extracted the inconsistent existing studies to systematically shed light on the slightly ambiguous protective properties of dietary nicotine and passive smoking as an influential factor against PD. Method: This systematic review was registered in PROSPERO (CRD042020160707). Two independent researchers searched through the following databases: PubMed, Cochrane Library, Scopus, Ovid, Embase, Google Scholar, and ProQuest to find relevant dissertations and theses. This paper involved the data of papers published until 30 September 2020. The paper used the Newcastle-Ottawa scale (NOS) for case-control and cohort studies for quality assessment. The study extracted cases without a history of smoking and the number of patients with PD in the workspace, home, and lifetime and organized them based on each research. The study implemented Q-statistic to investigate the selected papers based on statistical heterogeneity. Result: In total, four cohorts and five case-control papers were included. Our findings indicated that life time exposure to smoking had protective effect against PD risks (OR: 0.84; 95% CI: 0.70-0.99; p=0.04). However, the settings, workspace, home exposure, and PD risk did not display to have any considerable relationship. It should be noted that the papers on the relationship between dietary nicotine and PD risks have revealed the protective effect of nicotine-rich foods like potatoes, tomatoes, and peppers on PD risks. Conclusion: In light of the observational studies covered in this paper, its findings should receive an organized interpretation while identifying the relevant mechanisms of this association.