The article provides a comprehensive review of the epidemiology and etiology of Parkinson's disease (PD). It highlights the complex nature of PD, which involves both genetic and environmental factors. The incidence and prevalence of PD vary significantly, with higher rates in men than in women. Several genes associated with PD have been identified, supporting a genetic component. However, consistent findings on lifestyle and environmental risk factors are limited. Smoking and coffee are reported to have protective effects, but the biological mechanisms are not well understood. Uric acid is also associated with lower PD risk. Evidence suggests that pesticides may increase PD risk, but further research is needed to identify specific compounds. Metals, other chemicals, and magnetic fields have limited evidence of their role in PD. Methodological limitations, such as crude exposure classification and inadequate sample sizes, are common in PD studies. Future research should focus on large, detailed studies that include detailed exposure assessments and genetic polymorphisms. The article also discusses the diagnostic criteria for PD, the impact of different diagnostic criteria on incidence and prevalence estimates, and the influence of age and gender on these measures. It reviews the mortality rates and causes of death in PD patients, noting a two-fold increase in mortality compared to the general population. The article concludes by emphasizing the need for more robust and consistent research to better understand the etiology of PD.The article provides a comprehensive review of the epidemiology and etiology of Parkinson's disease (PD). It highlights the complex nature of PD, which involves both genetic and environmental factors. The incidence and prevalence of PD vary significantly, with higher rates in men than in women. Several genes associated with PD have been identified, supporting a genetic component. However, consistent findings on lifestyle and environmental risk factors are limited. Smoking and coffee are reported to have protective effects, but the biological mechanisms are not well understood. Uric acid is also associated with lower PD risk. Evidence suggests that pesticides may increase PD risk, but further research is needed to identify specific compounds. Metals, other chemicals, and magnetic fields have limited evidence of their role in PD. Methodological limitations, such as crude exposure classification and inadequate sample sizes, are common in PD studies. Future research should focus on large, detailed studies that include detailed exposure assessments and genetic polymorphisms. The article also discusses the diagnostic criteria for PD, the impact of different diagnostic criteria on incidence and prevalence estimates, and the influence of age and gender on these measures. It reviews the mortality rates and causes of death in PD patients, noting a two-fold increase in mortality compared to the general population. The article concludes by emphasizing the need for more robust and consistent research to better understand the etiology of PD.