Objective: Previous studies have suggested that diabetes mellitus (DM) increases the risk of Parkinson disease (PD); however, this has not been conclusively established. We analyzed the risk of PD based on baseline glucose tolerance status in a large-scale cohort representative of the general Korean population.

Research Design and Methods: This analysis was performed in a cohort of 15,168,021 adults aged ≥40 years who underwent health checkups under the National Health Insurance Service between January 2009 and December 2010. The clinical course of subjects was followed until December 2016. Subjects were classified into the following groups: non-diabetes (non-DM), impaired fasting glucose (IFG), DM duration <5 years, and DM duration ≥5 years. We analyzed the adjusted hazard ratio of PD for each group.

Results: During the observation period of 49,076,148.74 person-years, PD occurred in 31,577 patients. Compared with the non-DM subjects, the adjusted hazard ratio was 1.038 (95% confidence interval [CI], 1.009–1.067) in the IFG group, 1.185 (95% CI, 1.143–1.229) in the DM duration <5 years group, and 1.618 (95% CI, 1.566–1.672) in the DM duration ≥5 years group. These results were consistent with those of the subgroup analysis, and the presence of DM further increased the risk of PD regardless of comorbidities such as cardiovascular, cerebrovascular, and chronic kidney diseases.

Conclusion: This population-based cohort study suggests that DM is an independent risk factor for PD.

Objective: Previous studies have suggested that diabetes mellitus (DM) increases the risk of Parkinson disease (PD); however, this has not been conclusively established. We analyzed the risk of PD based on baseline glucose tolerance status in a large-scale cohort representative of the general Korean population.

Research Design and Methods: This analysis was performed in a cohort of 15,168,021 adults aged ≥40 years who underwent health checkups under the National Health Insurance Service between January 2009 and December 2010. The clinical course of subjects was followed until December 2016. Subjects were classified into the following groups: non-diabetes (non-DM), impaired fasting glucose (IFG), DM duration <5 years, and DM duration ≥5 years. We analyzed the adjusted hazard ratio of PD for each group.

Results: During the observation period of 49,076,148.74 person-years, PD occurred in 31,577 patients. Compared with the non-DM subjects, the adjusted hazard ratio was 1.038 (95% confidence interval [CI], 1.009–1.067) in the IFG group, 1.185 (95% CI, 1.143–1.229) in the DM duration <5 years group, and 1.618 (95% CI, 1.566–1.672) in the DM duration ≥5 years group. These results were consistent with those of the subgroup analysis, and the presence of DM further increased the risk of PD regardless of comorbidities such as cardiovascular, cerebrovascular, and chronic kidney diseases.

Conclusion: This population-based cohort study suggests that DM is an independent risk factor for PD.

It remains unknown how different glucose tolerance status affects the relationships between dietary intake of different tocopherol isoforms (α-, β-, γ-, and δ-tocopherol) and cellular aging, oxidative stress, and inflammatory markers. The authors conducted a cross-sectional study among 582 Chinese adults with different glucose tolerance status to explore the association between dietary intake of different tocopherol isoforms and cellular aging, oxidative stress, and inflammatory markers. The inverse correlations between non-α-tocopherols and tumor necrosis factor-alpha (TNF-α) varied substantially across different glucose tolerance status, with the strongest observed in prediabetes (r=−0.33 for β-/γ-tocopherol, r=−0.37 for δ-tocopherol, p<0.01), followed by normal glucose tolerance (NGT). While such correlations were abolished in established diabetes. Furthermore, within prediabetes, the strongest inverse correlations between non-α-tocopherols and TNF-α were observed in impaired fasting glucose (IFG) (r=−0.42 for β-/γ-tocopherol, r=−0.55 for δ-tocopherol, p<0.01), while such correlations were significantly attenuated in individuals with impaired glucose tolerance (IGT) and IFG+IGT. And mediation model analysis displayed that TNF-α mediated the protective effect of non-α-tocopherols on leukocyte telomere length and mitochondrial DNA copy number, which was uniquely observed in prediabetes, while such mediation effect was statistically nonsignificant in NGT and established diabetes. In conclusion, our findings indicate that dietary intake of non-α-tocopherols might protect against cellular aging markers mediated by TNF-α in prediabetes. Individuals with prediabetes, especially for IFG, might benefit from increasing dietary intake of non-α-tocopherol in alleviating inflammation and cellular aging, which might provide a new dietary avenue for delaying diabetes onset.

Abstract Background: Few studies have examined how maternal body mass index (BMI), mode of delivery and ethnicity affect the microbial composition of human milk and none have examined associations with maternal metabolic status. Given the high prevalence of maternal adiposity and impaired glucose metabolism, and the importance of human milk in the colonization of the infant gut, we systematically investigated the associations between these maternal factors and milk microbial composition and functionality. Methods: Women ≥20 years were recruited during pregnancy and milk samples were collected at 3 months post-partum (NCT01405547). Demographic data, weight, height, and a 3-hour oral glucose tolerance test were conducted at 30 (95% CI: 25-33) weeks gestation. Metagenomic DNA extraction and 16S ribosomal RNA gene sequencing of the V4 hypervariable region (Illumina MiSeq) was carried out on 113 milk samples. Results: Multivariable linear regression analyses demonstrated no significant associations between maternal characteristics (maternal BMI [pre-pregnancy, 3 months post-partum], glucose tolerance, mode of delivery and ethnicity) and microbiota alpha-diversity; however, pre-pregnancy BMI was associated with human milk beta-diversity (Bray-Curtis p=0.040). Women with a pre-pregnancy BMI >30 kg/m2 (obese) had a greater incidence of Bacteroidetes (incidence rate ratio [IRR]: 3.70 [95% CI: 1.61-8.48]) and a reduced incidence of Proteobacteria (0.62 [0.43-0.90]), compared to overweight women (BMI 25.0-29.9 kg/m2) as assessed by multivariable Poisson regression. Increased incidence of Gemella was observed among overweight (versus healthy) mothers with gestational diabetes (5.96 [1.85-19.21]) and obese (versus healthy) mothers with impaired glucose tolerance (4.04 [1.63-10.01]). An increased incidence of Brevundimonas (16.70 [5.99-46.57]) was found in the milk of women who underwent an unscheduled C-section versus vaginal delivery. Lastly, functional gene inference demonstrated that obesity was associated with increased abundance of genes encoding for the biosynthesis of secondary metabolites in milk (coefficient=0.00028, p=0.0070). Conclusions: Mother’s milk has a diverse microbiota of which its diversity and differential abundance appear associated with maternal body size, glucose tolerance status, mode of delivery, and ethnicity. Further research is warranted to determine whether this variability in the milk microbiota impacts colonization of the infant gut.