Association of 25-hydroxyvitamin D with Parkinson’s disease based on the results from the NHANES 2007 to 2018 and Mendelian randomization analysis

An abundance of observational researches had suggested that vitamin D insufficient was related to Parkinson's disease (PD) risk. However, their relationships were debatable and the causality remains uncertain. We intended to evaluate the association between 25-hydroxyvitamin D [25(OH)D] and Parkinson's disease (PD) risk using NHANES data (2007–2018) and Mendelian randomization (MR) analyses with the genome-wide association study (GWAS) summary data. Demographic characteristics and multivariable-adjusted logistic regression were conducted to assess the relationship between the serum 25(OH)D levels and risk of PD prevalence by utilizing NHANES database. Besides, a two-sample MR analysis was applied to evaluate the causal association between serum 25(OH)D levels and PD risk. The main analysis was conducted by citing the inverse-variance-weighted (IVW) approach, while additional MR approaches and multiple sensitivity analysis were cited to evaluate the robustness and pleiotropy for the discoveries. In total, 30,796 adults from NHANES 2007–2018 were selected for the present research. As a result, 1.1% participants with PD (mean age: 61.9 ± 15.5 years), while 68.5% reported vitamin D insufficient. Compared with participants without PD, those with PD had a greater level of 25(OH)D (P < 0.01). However, after adjusted for demographic characteristics and comorbid factors, this association was not observed. Furthermore, no potential causal relationships between the serum level of 25(OH)D and PD risk were found via MR analysis (IVW-MR: OR = 1.082; 95% CI, 0.902 to 1.297; P = 0.395). After eliminating variants with horizontal pleiotropy risk, pleiotropy-robust MR analysis presented similar results. In conclusion, this research suggested that serum 25(OH)D levels was not correlated with PD risk. Additionally, the MR analyses revealed no significant causal association between serum 25(OH)D levels and PD risk at the genetic level. Awareness of these findings may improve personalized prevention and treatment of PD.