Association of serum 25-hydroxyvitamin D with the incidence of 16 cancers, cancer mortality, and all-cause mortality among individuals with metabolic syndrome: a prospective cohort study.

PURPOSE: The relationship between vitamin D levels and cancer incidence and mortality in individuals with metabolic syndrome (MetS) remains poorly explored. Herein, we aimed to determine the association between 25-hydroxyvitamin D [25(OH)D] concentrations and the risk of 16 cancer incidence types and cancer/all-cause mortality in patients with MetS. METHODS: We enrolled 97,621 participants with MetS at recruitment from the UK Biobank cohort. The exposure factor was baseline serum 25(OH)D concentrations. The associations were examined using Cox proportional hazards models, which were displayed as hazard ratios (HRs) with 95% confidence intervals (CIs). RESULTS: Over a median follow-up period of 10.92 years for cancer incidence outcomes, 12,137 new cancer cases were recorded. We observed that 25(OH)D concentrations were inversely related to the risk of colon, lung, and kidney cancer, and HRs (95% CI) for 25(OH)D ≥ 75.0 vs. < 25.0 nmol/L were 0.67 (0.45-0.98), 0.64 (0.45-0.91), and 0.54 (0.31-0.95), respectively. The fully adjusted model revealed a null correlation between 25(OH)D and the incidence of stomach, rectum, liver, pancreas, breast, ovary, bladder, brain, multiple myeloma, leukemia, non-Hodgkin lymphoma, esophagus, and corpus uteri cancer. Over a median follow-up period of 12.72 years for mortality outcomes, 8286 fatalities (including 3210 cancer mortalities) were documented. An "L-shaped" nonlinear dose-response correlation was detected between 25(OH)D and cancer/all-cause mortality; the respective HRs (95% CI) were 0.75 (0.64-0.89) and 0.65 (0.58-0.72). CONCLUSION: These findings emphasize the importance of 25(OH)D in cancer prevention and longevity promotion among patients with MetS.

Associations of genetic variation in CASP3 gene with noise-induced hearing loss in a Chinese population: a case-control study.

BACKGROUND: Noise-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. METHODS: A 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. RESULTS: Two 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). CONCLUSIONS: Genetic variations in the CASP3 gene and the joint effects of working time and CASP3 polymorphisms may modify the risk of developing NIHL.

Association of tea and coffee consumption with the risk of all-cause and cause-specific mortality among individuals with metabolic syndrome: a prospective cohort study.

BACKGROUND: The relationship between tea and coffee consumption and mortality among patients with metabolic syndrome (MetS) remains barely explored. Herein, this study aimed to examine the association between tea and coffee consumption and the likelihood of all-cause and cause-specific mortality in patients with MetS. METHODS: A total of 118,872 participants with MetS at baseline from the UK Biobank cohort were included. Information on tea and coffee consumption was obtained during recruitment using a touchscreen questionnaire. Hazard ratios (HRs) and 95% confidence intervals (CIs) for mortality were determined using Cox proportional hazards models. RESULTS: During a median follow-up of 13.87 years, 13,666 deaths were recorded, with 5913, 3362, and 994 deaths from cancer, cardiovascular diseases (CVD), and respiratory disease (RD), respectively. This research showed a significant inverse association between tea intake and the risk of all-cause and cancer mortality, the respective HRs (95% CI) for consuming tea 2 vs. 0 cup/day were 0.89 (0.84-0.95), and 0.91 (0.83-0.99), and tea intake ≥ 4 cups/day could reduce CVD mortality by 11% (HR 0.89; 95% CI 0.81-0.98). The U-shaped nonlinear association between coffee intake and all-cause/CVD mortality was examined (all p-nonlinear < 0.001). The HRs (95% CI) for coffee consumption 1 vs. 0 cup/day were 0.93 (0.89-0.98) and 0.89 (0.80-0.99), and for ≥ 4 vs. 0 cup/day were 1.05 (1.01-1.11) and 1.13 (1.03-1.25), respectively. Notably, the combined intake of tea and coffee presented a protective effect against all-cause mortality (HR < 1). CONCLUSIONS: The importance of daily tea and moderate coffee consumption in individuals with MetS to optimise health benefits are highlighted.

Noncausal effects of genetic predicted depression and colorectal cancer risk: A Mendelian randomization study.

Depression has been associated with colorectal cancer (CRC) in observational studies. However, the causality of depression on CRC risk remained unknown. This study aimed to evaluate the potential causal association between genetic variants related to depression and the risk of CRC using Mendelian randomization (MR). Two-sample MR analysis using summary data was performed to examine whether depression was causally associated with CRC risk. We used 2 sets of instrumental variables (IV) from the genome-wide association study results for analysis. A set of IV related to major depressive disorder contain 44 single-nucleotide polymorphisms. Another set of IV was related to major depression, including 53 single-nucleotide polymorphisms. Summary data of CRC was from the FinnGen consortium. Based on the results of MR using inverse-variance weighted method, we found that genetically determined major depressive disorder (odds ratio = 1.06, 95% confidence interval = 0.77-1.45) or major depression (odds ratio = 0.77, 95% confidence interval = 0.57-1.04) did not causally increase CRC risk. The results of MR-Egger and the weighted median method are consistent with the inverse-variance weighted method. The two-sample MR analysis showed that depression is not causally associated with CRC risk. Further research is needed to investigate the association between depression and CRC.

A bidirectional Mendelian randomization study supports the causal effects of a high basal metabolic rate on colorectal cancer risk.

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 (ß = 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.

Association of sleep duration and noise exposure with hearing loss among Chinese and American adults: two cross-sectional studies.

OBJECTIVES: To examine the associations of sleep duration (SPD) and noise exposure with hearing loss (HL) among Chinese and American adults. DESIGN: Two cross-sectional studies. SETTING: The National Health and Nutrition Examination Survey (2011-2012), and Zhejiang Chinese participants between 1 January 2018 and 1 November 2021. PARTICIPANTS: 3322 adults from the USA and 4452 adults from Zhejiang, China. MAIN OUTCOME MEASURES: HL 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. RESULTS: SPD ≥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). CONCLUSIONS: Noise 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.

Association of a Healthy Lifestyle with All-Cause, Cause-Specific Mortality and Incident Cancer among Individuals with Metabolic Syndrome: A Prospective Cohort Study in UK Biobank.

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.

Consumption of fruits, vegetables, and legumes are associated with overweight/obesity in the middle- and old-aged Chongqing residents: A case-control study.

This study aimed to investigate the association of dietary habits with the risk of overweight/obesity among middle-and-old-aged Chongqing residents and also to examine the joint effects of behavioral lifestyles, dietary habits, and overweight/obesity. In this case-control study, age (±3 years), sex, and time of physical exercise matched 979 overweight/obesity residents, and 979 normal weight residents were recruited. A validated questionnaire was used to collect participants' information. Conditional logistic regression analysis was performed to determine the adjusted odds ratios (ORs) and 95% CIs of dietary habits and lifestyles associated with overweight/obesity risk. Overweight/obesity was defined as body mass index (BMI) ≥ 24 kg·m-2, and normal weight was defined as 18.5 ≤ BMI < 24 kg·m-2. The multivariate-adjusted models showed the weekly intake frequency of fruits 0-1 (day/week) (OR = 1.79, 95% CI = 1.04-3.10), and legumes 0-1 (day/week) (OR = 2.45, 95% CI = 1.28-4.67), as well as the weekly intake percentage of vegetables ≥ 15% (OR = 2.44, 95% CI = 1.04-5.71) were associated with a higher risk of overweight/obesity. Besides, there were joint effects of lifestyles (smoking or drinking) and dietary habits on overweight/obesity risk (P for interaction < 0.05). The consumption of vegetables, fruits, legumes, and the joint effects of behavioral habits (smoking or drinking) may modify the risk of being overweight/obese. It is essential to consume fruits and legumes at least 2 days/week, quit smoking, and stop consuming alcohol to avoid overweight/obesity among middle-aged and elderly people in Chongqing, China.

Genetic risk, incident colorectal cancer, and the benefits of adhering to a healthy lifestyle: A prospective study using data from UK Biobank and FinnGen.

Background: Genetic factors increase the individual risk of colorectal cancer (CRC); however, the extent to which a healthy lifestyle can offset increased genetic risk is unknown. This study investigated whether a healthy lifestyle is associated with lower CRC risk, regardless of genetic risk. Methods: We recruited 390,365 participants without cancer at baseline (2006-2010) from the UK Biobank. The primary outcome was CRC incidence. A healthy lifestyle score constructed using 16 factors of six dimensions (smoking, drinking, body mass index, diet, exercise, and sleep) was categorized into three risk categories: favorable, intermediate, and unfavorable. To calculate the polygenic risk scores (PRSs) of UK Biobank participants, we extracted 454,678 single nucleotide polymorphisms (SNPs) from the UK Biobank and FinnGen Biobank after quality control. Cox proportional hazards regression was performed to evaluate the associations and was expressed as hazard ratios (HRs) with 95% confidence intervals (CIs). Results: During a median follow-up of 10.90 years, 4,090 new CRC cases were reported in the UK Biobank. The "best-fit" PRSs were constructed using 59 SNPs based on the UK Biobank cohort and FinnGen genome-wide association study summary data (R2 = 0.23%) and were divided into low (lowest quintile), intermediate (including second-fourth quintile), and high (highest quintile) genetic risk categories. The multivariate-adjusted Cox model revealed that participants with favorable lifestyles had HRs of 0.66 (95% CI = 0.60-0.72) for developing CRC vs. those with unfavorable lifestyles; low genetic risk was associated with a decreased risk of CRC (HR = 0.67, 95% CI =0.61-0.74) compared with those with high genetic risk. The HRs for low genetic risk participants with favorable lifestyles were 0.44 (95% CI =0.36-0.55) vs. participants with high genetic risk and unfavorable lifestyles. Among the participants with low, intermediate, or high genetic risk, the HRs of favorable vs. unfavorable lifestyles were 0.74, 0.64, and 0.72 (all p< 0.05). Conclusions: Low genetic risk and a favorable lifestyle were significantly associated with a decreased risk of CRC. A favorable lifestyle was associated with a lower CRC risk, regardless of genetic risk.

Positive association between ALDH2 rs671 polymorphism and essential hypertension: A case-control study and meta-analysis.

BACKGROUND AND OBJECTIVE: Several 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. METHODS: One 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. RESULTS: Significant 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). CONCLUSION: The 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.