Objective To observe the changes in vitamin D receptor (VDR) gene polymorphisms and serum 25-hydroxyvitamin D (25 (OH)D) levels in patients with Parkinson’s disease (PD), and to analyze their correlations with the onset of PD and their predictive efficiency on the onset of PD in order to clarify the significance of VDR gene polymorphisms and changes in serum 25 (OH)D levels. Methods Totally 178 PD patients (PD group) and 185 healthy subjects (control group) during the same period were included. PCR and DNA sequencing methods were used to detect the genotyping of VDR gene FokI (rs2228570) and BsmI (rs1544410) sites, and enzyme-linked immunosorbent assay was used to detect peripheral serum 25 (OH)D. The above indicators between the two groups were compared. Multivariate Logistic regression was used to analyze the independent risk factors for the onset of PD; ROC was used to analyze the predictive efficacy of vitamin D receptor gene polymorphisms and serum 25-hydroxyvitamin D levels for the onset of PD. Results The frequencies of T allele and TT genotype of FokI site in the PD group were 48.6% and 25.3% respectively, and 37.7% and 15.1% in the control group, respectively. Comparing the two groups, χ2 were 8.516 and 10.383, respectively, and P were 0.004 and 0.001, respectively. There were no statistically significant differences in the alleles or genotypes of the BsmI locus between the PD group and the control group (all P＞0.05). The serum 25 (OH)D level in the PD group was (16.06±6.04) ng/mL, and that in the control group was (19.22±6.32) ng/mL (t=–4.873, P=0.000). The serum 25 (OH)D levels of patients with TC type and CC type in the PD group were lower than those in the control group (t=–3.093, 3.329, respectively; P=0.002, 0.001, respectively). When the serum 25 (OH)D levels were consistent, patients with genotypes TT and TC were 2. 527 and 1. 888 times more likely to develop PD than patients with genotype CC, respectively (all P＜0.05). When the genotypes were consistent, patients with deficient serum 25 (OH)D level were 1.918 times more likely to develop PD than those with sufficient level (P＜0.05). As for genotype TT patients with 25 (OH)D deficiency, and genotype TC patients with 25 (OH)D deficiency, their risks of developing PD were 4.818 and 3.822 times that of genotype CC patients with sufficient 25 (OH)D, respectively (all P＜0.05). The AUC under ROC of FokI locus genotype TT in predicting the onset of PD was 0. 610, 95%CI was 0. 532–0.687, the diagnostic cut-off value was 0.502, the sensitivity was 74.5%, and the specificity was 47.4%; The AUC under the ROC of lack of serum 25 (OH)D level in predicting the onset of PD was 0.576, the 95%CI was 0.517–0.635, the diagnostic cut-off value was 0.466, the sensitivity was 72. 5%, and the specificity was 42.7%, respectively; the AUC under ROC of genotype TT combined with serum 25 (OH)D deficiency in predicting the onset of PD was 0. 693, 95%CI was 0.588–0.798, the sensitivity was 64.2%, and the specificity was 74. 5%, respectively. Conclusions The frequencies of the T allele and TT genotype at the FokI site of the VDR gene are high, and the serum 25 (OH)D level is low; the T allele at the FokI site and vitamin D deficiency can promote the occurrence of PD individually or together, and both of them have poor predictive efficiency for the risk of PD onset. [ABSTRACT FROM AUTHOR]