Lifestyle habits, diet, drugs, comorbidities may lower risk for PD

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Lifestyle habits, diet, drugs, comorbidities may lower risk for PD

Eleven lifestyle factors including physical activity, drinking coffee and tea, and fat intake were associated with a lower risk for Parkinson’s disease development, according to a systematic review in Journal of Parkinson’s Disease.

“Although the exact cause of PD remains unknown, it is well recognized that both genetic and non-genetic factors contribute to its development,” Yancong Chen, of Central South University’s Xiangya School of Public Health in China, and colleagues wrote. “As the majority of PD cases are sporadic, and genetic factors can only explain to a small degree the risk of sporadic PD, research on non-genetic factors involved in PD development is vital.”

Chen and colleagues aimed to investigate which non-genetic factors correlated with the development of PD from published systematic reviews and analyze the reasons behind the conflicting results. They included 46 systematic reviews published between January 2011 and June 2020 in their investigation and reviewed various habits, environmental agents, dietary factors, medical history and comorbidities, drugs and biomarkers that may affect PD development.

The analysis showed the following habits were linked to a decreased risk for PD: physical activity (pooled RR = 0.79; 95% CI, 0.68-0.91; I² = 0.0%), smoking (pooled RR = 0.64; 95% CI, 0.60-0.69; I² = 49.6%; 67 case-control and cohort studies), coffee drinking (pooled RR = 0.67; 95% CI, 0.58-0.76; I² = 42.9%; 19 case-control and cohort studies), tea drinking (pooled RR = 0.64; 95% CI, 0.5-0.82; I² = 16.2%; four cohort and nested case-control studies) and caffeine intake (pooled RR = 0.55; 95% CI, 0.43-0.71; I² = 53%; seven case-control, cohort and nested case-control studies).

Additionally, fat intake (pooled RR = 0.8; 95% CI, 0.68-0.95; I² = 3%; six cohort studies); use of calcium channel blockers (pooled RR = 0.74; 95% CI, 0.64-0.85; I² = 42.6%; three cohort studies), statins (pooled RR = 0.82; 95% CI, 0.68-0.99; I² = 55.5%; six cohort studies) and thiazolidinediones (pooled OR = 0.7; 95% CI, 0.51-0.96; I² = 86%; five cohort studies); and high urate levels in blood (pooled RR = 0.68; 95% CI, 0.5-0.91; I² = 42.1%; six cohort and nested case-control studies) also correlated with a decreased the risk for PD.

Chen and colleagues also reported data showing factors that increased the risk for PD. These included dairy consumption (pooled RR for milk intake = 1.45; 95% CI, 1.23-1.73; I² = 16.1%; five cohort studies), having diabetes (pooled RR = 1.31; 95% CI, 1.1-1.57; I² = 34.7%; four cohort studies), depression (pooled OR = 1.92; 95% CI, 1.66-2.22; I² = 0%; six cohort studies), mood disorder (pooled RR = 1.79; 95% CI, 1.72-1.87; I² = 0%; two cohort studies), bipolar disorder (pooled OR = 3.12; 95% CI, 1.66-5.88; I² = 95%), hormone replacement therapy (pooled RR = 1.24; 95% CI, 1.1-1.41; I² = 0%; four cohort studies) and taking aspirin (pooled RR = 1.12; 95% CI, 1.01-1.23; I² not reported; six cohort and nested case-control studies).

The investigators wrote that due to opposing conclusions of studies, 31 factors could not be definitively linked to PD development. They said other limitations included variety of study designs, long prodromal period of PD, poor methodology of most studies and analysis of systematic reviews from only the past 10 years.

Chen and colleagues provided clinical and research suggestions to lower public risk for PD and refine research results.

“Promotion of the health benefits of physical activity and coffee and tea consumption should be considered for the general population,” they wrote. “The methodological quality of future [systematic reviews] strongly requires improvement, and international standards such as Conducting Systematic Reviews and Meta-Analyses of Observational Studies of Etiology (COSMOS-E) should be adhered to when conducting [systematic reviews].”