Association Between Antioxidant Nutrients, Oxidative Stress-Related Gene Polymorphism and Skeletal Fluorosis in Guizhou, China.

Background: Oxidative stress plays an important role in the pathogenesis of endemic fluorosis. We analyzed associations between oxidative stress-related gene polymorphisms (PON1 rs662, CAT rs769217, rs2300182, and SOD2 rs11968525) and skeletal fluorosis, and examined potential gene-environment interactions with dietary vitamin C, vitamin E, zinc, and selenium intake. Methods: A cross-sectional study was conducted in the Zhijin County, Guizhou Province of China. Skeletal fluorosis was identified according to the Chinese Diagnostic Criteria of Endemic Skeletal Fluorosis. Dietary information was assessed through face-to-face interviews by trained interviewers using a 75-item food frequency questionnaire. The genotype was detected by high throughput TaqMan-MGB RT-PCR technology. Odds ratios (ORs) and 95% CIs were calculated using an unconditional logistic regression model. Results: Intake of vitamin E, zinc, and selenium was found to be inversely associated with the risk of skeletal fluorosis. The multivariable-adjusted ORs were 0.438 (95% CI: 0.268 to 0.715, P-trend < 0.001) for vitamin E, 0.490 (95% CI: 0.298 to 0.805, P-trend = 0.001) for zinc, and 0.532 (95% CI: 0.324 to 0.873, P-trend = 0.010) for selenium when comparing the highest with the lowest quartile. The relationship for vitamin C was not observed after adjustment for risk factors. Furthermore, participants with PON1 rs662 AA genotype had a significantly decreased risk of skeletal fluorosis compared with those with the GG genotype (OR = 0.438, 95% CI: 0.231 to 0.830). GG + AG genotype carriers were 2.212 times more likely to have skeletal fluorosis than AA carriers (OR = 2.212, 95% CI: 1.197 to 4.090). Compared with AA carriers, AG carriers had a 2.182 times higher risk of skeletal fluorosis (OR = 2.182, 95% CI: 1.143 to 4.163). Although we observed the risk of skeletal fluorosis was higher with a lower intake of antioxidant nutrients, the potential interactions between nutrient intake and genetic polymorphisms were not observed. Conclusion: Participants with a higher intake of vitamin E, zinc, and selenium have a lower likelihood of skeletal fluorosis. In addition, the PON1 rs662 polymorphism is related to skeletal fluorosis.

Association Between Dietary Intake of One-Carbon Metabolism-Related Nutrients and Fluorosis in Guizhou, China.

Objective: This study aimed to investigate the associations between dietary one-carbon metabolism-related nutrients (betaine, choline, methionine, folate, vitamin B6, and vitamin B12) and fluorosis among the Chinese population in an area known for coal-burning fluorosis. Methods: A cross-sectional study was conducted, with 653 fluorosis patients and 241 non-fluorosis participants. Dietary intake was acquired using a validated semi-quantitative 75-item food frequency questionnaire. The risk associations were assessed by unconditional logistical regression. Results: We observed a significant inverse association between dietary betaine, total choline, methionine, folate, vitamin B6, and choline species and fluorosis. The adjusted OR (95% CI) in the highest quartile of consumption compared with the lowest were 0.59 (0.37-0.94) (P-trend = 0.010) for betaine intake, 0.45 (0.28-0.73) (P-trend = 0.001) for total choline intake, 0.45 (0.28-0.72) (P-trend < 0.001) for methionine intake, 0.39 (0.24-0.63) (P-trend < 0.001) for folate intake, 0.38 (0.24-0.62) (P-trend < 0.001) for vitamin B6 intake, and 0.46 (0.28-0.75) (P-trend = 0.001) for total choline plus betaine intake. Dietary intakes of choline-containing compounds, phosphatidylcholine, free choline, glycerophosphocholine, and phosphocholine were also inversely associated with lower fluorosis (all P-trend < 0.05). No significant associations were observed between dietary vitamin B12 or sphingomyelin and fluorosis. Conclusion: The present study suggested that the higher dietary intakes of specific one-carbon metabolism-related nutrients, such as betaine, choline, methionine, folate, and vitamin B6, are associated with lower fluorosis prevalence.

The Association between Interleukin-6 Gene Polymorphisms and Risk of Systemic Lupus Erythematosus: A Meta-analysis with Trial Sequential Analysis.

BACKGROUND: Molecular epidemiological studies have sought associations between interleukin-6 (IL-6) polymorphisms and the risk of systemic lupus erythematosus (SLE); however, the results are controversial. Therefore, we conducted a meta-analysis with trial sequential analysis to evaluate a more accurate estimation of the associations. METHODS: Published literatures reporting the relationships of two IL-6 polymorphisms (G-174C and G-572C) and SLE risk were retrieved from electronic databases such as PubMed and EMBASE. The most appropriate genetic model was chosen for each polymorphism. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated. Trial sequential analysis (TSA) was introduced to assess the information size and the positive results. RESULTS: With 17 studies (2780 cases and 3100 controls) included, a dominant association (CC+GC vs. GG) was suggested for G-174C polymorphism, and compared with the GG genotype, the CC+GC genotype of G-174C was associated with a decreased SLE risk (OR = 0.71; 95% CI = 0.56-0.88, P =.02). No association was found for G-572C under all genetic models (e.g. OR and 95%CI for CC+GC vs. GG: 0.89, 0.73-1.08, P =.22). Subgroup analyses indicated that SLE risk decreased in G-174C polymorphism by subgroups of Caucasian population, publications after 2010, studies with high quality, and studies complied with Hardy-Weinberg equilibrium (HWE). TSA suggested that the sample sizes used for G-572C were insufficient. CONCLUSION: We found that the minor allele C of IL6G-174C polymorphism is a protective factor in SLE. Further studies with a larger sample size are needed to confirm the null association for G-572C.