Background and objectiveSeveral studies have been conducted to examine the association between aldehyde dehydrogenase 2 family (ALDH2) rs671 polymorphism and essential hypertension (EH). However, the results remain inconsistent. This study aimed to clarify the association between ALDH2 rs671 polymorphism and EH susceptibility.MethodsOne thousand and ninety-four cases and 1236 controls who were ethnic Han Chinese were collected for this population-based case-control study. A meta-analysis was performed to calculate the pooled odds ratio and 95% confidence interval, using allele contrast, dominant, recessive, and co-dominant models using fixed or random-effect models.ResultsSignificant differences were observed between EH cases and controls at the level of both genotype (χ2 = 6.656, P<0.05) and alleles (χ2 = 6.314, P<0.05). An additional meta-analysis using 4204 cases and 5435 controls established that rs671 was significantly associated with EH (P<0.00001).ConclusionThe results of our case-control study and meta-analysis showed that there is a significant association between ALDH2 rs671 polymorphism and EH susceptibility. In addition, the results of the breakdown analysis by gender suggest a male-specific association between the ALDH2 rs671 polymorphism and EH.
BackgroundNoise-induced hearing loss (NIHL) is a complex disease caused by environmental and genetic risk factors. This study explored the relationship between the genetic variations in the CASP gene and the risk of developing NIHL among Chinese workers exposed to occupational noise.MethodsA case–control study of 272 NIHL workers and 272 normal-hearing workers matched for age, sex and years of noise exposure was conducted. Fifteen single-nucleotide polymorphisms (SNP) in the CASP1, CASP3, CASP4, CASP5, CASP6, CASP8, CASP9, CASP10 and CASP14 genes were genotyped using the polymerase chain reaction–ligase detection reaction method. Using conditional logistic regression models, the adjusted odds ratios (ORs) and 95% confidence intervals (CIs) of genetic variations associated with NIHL risk were calculated.ResultsTwo SNPs in the CASP3 gene were associated with NIHL risk. For rs1049216, TT genotype was associated with a decreased risk of NIHL (OR = 0.246, 95% CI = 0.069–0.886) when compared with the CC genotype. For rs6948, the AC and CC genotype were associated with a decreased NIHL risk (OR = 0.568, 95% CI = 0.352–0.916) compared with AA genotype. There were joint effects of working time and CASP3 polymorphisms on NIHL risk (P < 0.05).ConclusionsGenetic variations in the CASP3 gene and the joint effects of working time and CASP3 polymorphisms may modify the risk of developing NIHL.Electronic supplementary materialThe online version of this article (doi:10.1186/s12940-017-0280-y) contains supplementary material, which is available to authorized users.
Purpose We conducted a bidirectional two-sample Mendelian randomization (MR) study to determine whether genetically predicted basal metabolic rate (BMR) was a causal risk factor for colorectal cancer (CRC) or whether a genetically predicted CRC risk can influence the BMR level (i.e., reverse causation). Methods We employed 1,040 genetic variants as proxies for BMR to obtain effect estimates on CRC risk. Another 58 CRC-associated variants were used to estimate effects on BMR levels. Stratified analysis by tumor site was used to examine the causal associations between BMR and colon/rectal cancer risk. Results The inverse variance weighted (IVW) method indicated a significant causal effect of genetically determined BMR on CRC risk (ORSD = 1.27, 95% CI = 1.07–1.51). No significant reverse causal association was identified between genetically increased CRC risk and BMR levels [IVW (β = 0, 95% CI = -0.01 to 0)]. The results of MR-Egger and the weighted median method were consistent with the IVW method. Stratified analysis by CRC sites identified significant causal associations between BMR and colon cancer [IVW (ORSD = 1.45, 95% CI = 1.16-1-80)], and null evidence of a causal association between BMR and rectal cancer risk was found (p > 0.05). Conclusion Our findings add to the current literature by validating a positive relationship between high BMR levels and CRC risk instead of reverse causality. The genetically predicted BMR level was causally associated with colon cancer risk but not rectal cancer risk.
ObjectivesTo examine the associations of sleep duration (SPD) and noise exposure with hearing loss (HL) among Chinese and American adults.DesignTwo cross-sectional studies.SettingThe National Health and Nutrition Examination Survey (2011–2012), and Zhejiang Chinese participants between 1 January 2018 and 1 November 2021.Participants3322 adults from the USA and 4452 adults from Zhejiang, China.Main outcome measuresHL was defined as a pure-tone average >20 dB in the better ear at low frequency (500, 1000 and 2000 Hz), speech frequency (500, 1000, 2000 and 4000 Hz) or high frequency (3000, 4000, 6000 and 8000 Hz). Binary logistic regression analysis quantified the associations between SPD, noise exposure (at work or off-work) and HL.ResultsSPD ≥8 hours/night had an OR of 0.71 (95% CI 0.59 to 0.84) for high-frequency HL vs. an SPD of 6–8 hours/night among the Chinese participants but had an OR of 1.28 (95% CI 1.03 to 1.58) among American participants. Noise exposure (both at work and off-work) was associated with poorer low-frequency (OR 1.58, 1.43; p<0.05), speech-frequency (OR 1.63, 1.29; p<0.05) and high-frequency (OR 1.37, 1.23; p<0.05) hearing among the Chinese participants; and it was associated with worse high-frequency hearing (OR 1.43, 1.66; p<0.05) among the American participants. The negative relationship between SPD ≥8 hours/night and HL was mainly observed in the Chinese participants with noise exposure (OR <1, p<0.05), and SPD ≥8 hours/night associated with poorer HF hearing was only identified in the American participants without noise exposure (OR >1, p<0.05).ConclusionsNoise exposure was associated with poorer hearing. SPD ≥8 hours/night was negatively associated with HL in the Chinese participants especially when exposed to noise. SPD ≥8 hours/night was related to poorer high-frequency hearing in the American participants when they had no noise exposure.
This study investigated the association between a healthy lifestyle with all-cause, cause-specific mortality, and cancer incidence among individuals with metabolic syndrome (MetS). Healthy lifestyle scores were created based on MetS management guidelines, including never/quitting smoking, moderate drinking, good sleep, healthy diet, sufficient exercise, social support, and less sedentary behaviour. Weighted healthy lifestyle scores were further constructed and classified into three groups: unfavourable (lowest quintile), intermediate (quintiles 2–4), and favourable (highest quintile) lifestyles. We included 87,342 MetS participants from the UK Biobank. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated using multivariate-adjusted Cox proportional hazards regression. During a median follow-up of 12.54 years, 6739 deaths were reported; during a median follow-up of 10.69 years, 10,802 new cancer cases were documented. We found a favourable lifestyle was inversely associated with all-cause mortality (HR: 0.57; 95%CI: 0.53–0.62), cause-specific mortality from respiratory disease, cancer, digestive disease, cardiovascular disease (HR < 1; p-trend < 0.001), and overall cancer incidence (HR: 0.84; 95% CI: 0.79–0.90). Our results indicate that adherence to healthy lifestyles is associated with lower overall cancer incidence and all-cause mortality risk among MetS individuals. However, causality cannot be made due to the nature of observational studies.
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