Metabolic syndrome risk in adult coffee drinkers with the rs301 variant of the LPL gene.

BACKGROUND: Metabolic syndrome (MetS), a cluster of metabolic and cardiovascular risk factors is influenced by environmental, lifestyle, and genetic factors. We explored whether coffee consumption and the rs301 variant of the lipoprotein lipase (LPL) gene are related to MetS. METHODS: We conducted multiple logistic regression analyses using data gathered from 9523 subjects in Taiwan Biobank (TWB). RESULTS: Our findings indicated that individuals who consumed coffee had a reduced odds ratio (OR) for MetS (0.750 (95% confidence interval [CI] 0.653-0.861) compared to non-coffee drinkers. Additionally, the risk of MetS was lower for individuals with the 'TC' and 'CC' genotypes of rs301 compared to those with the 'TT' genotype. Specifically, the OR for MetS was 0.827 (95% CI 0.721-0.949) for the 'TC' genotype and 0.848 (95% CI 0.610-1.177) for the 'CC' genotype. We observed an interaction between coffee consumption and the rs301 variant, with a p-value for the interaction of 0.0437. Compared to the reference group ('no coffee drinking/TT'), the ORs for MetS were 0.836 (95% CI 0.706-0.992) for 'coffee drinking/TT', 0.557 (95% CI 0.438-0.707) for 'coffee drinking/TC', and 0.544 (95% CI 0.319-0.927) for 'coffee drinking/CC'. Notably, MetS was not observed in non-coffee drinkers regardless of their rs301 genotype. CONCLUSION: Our findings suggest that rs301 genotypes may protect against MetS in Taiwanese adults who consume coffee compared to non-coffee drinkers.

Susceptibility to hypertension based on MTHFR rs1801133 single nucleotide polymorphism and MTHFR promoter methylation.

Background: The aetio-pathologenesis of hypertension is multifactorial, encompassing genetic, epigenetic, and environmental factors. The combined effect of genetic and epigenetic changes on hypertension is not known. We evaluated the independent and interactive association of MTHFR rs1801133 single nucleotide polymorphism (SNP) and MTHFR promoter methylation with hypertension among Taiwanese adults. Methods: We retrieved data including, MTHFR promoter methylation, MTHFR rs1801133 genotypes (CC, CT, and TT), basic demography, personal lifestyle habits, and disease history of 1,238 individuals from the Taiwan Biobank (TWB). Results: The distributions of hypertension and MTHFR promoter methylation quartiles (ß < 0.1338, 0.1338 ≤ ß < 0.1385, 0.1385 ≤ ß < 0.1423, and ß ≥ 0.1423 corresponding to

Risk of gout in Taiwan Biobank participants pertaining to their sex and family history of gout among first-degree relatives.

BACKGROUND: Family history of gout and sex are independently associated with gout. However, there is a paucity of research regarding the joint role of both factors in gout pathogenesis. Therefore, we assessed the independent and combined association of family history of gout and sex with gout. METHODS: Our analysis included 132,311 Taiwan Biobank (TWB)-enrolled individuals comprising 21,159 gout cases and 111,152 controls. We subcategorized the family history of gout as (1) both siblings and parents had gout), (2) only parents had gout, and (3) only siblings had gout. RESULTS: Generally, sex (men compared to women) and family history of gout were independently associated with a higher risk of gout. The odds ratio (OR); 95% confidence interval (CI) was 9.175; 8.801-9.566 for sex, and 2.306; 2.206-2.410 for family history. For the subcategories 'both siblings and had gout,' 'only parents had gout,' and 'only siblings had gout,' the odds ratios (ORs); 95% confidence intervals (CIs) were 4.944; 4.414-5.538, 2.041; 1.927-2.161, and 2.162; 2.012-2.323, respectively. The interaction between sex and family history was significant (p value = 0.0001). After stratification by sex, family history of gout remained significantly associated with a higher risk of gout in both sexes, even though the odds ratios were higher in men. For the subcategories 'both siblings and parents had gout,' 'only parent had gout,' and 'only siblings had gout,' the corresponding ORs; 95% CIs were 6.279; 5.243-7.520, 2.211; 2.062-2.371, and 2.148; 1.955-2.361 in men and 4.199; 3.566-4.945, 1.827; 1.640-2.035, and 2.093; 1.876-2.336 in women. After integrating sex and family history (reference: women with no family history), the highest risk of gout was observed in men who had at least one parent and sibling with a history of gout (OR; 95% CI 55.774; 46.360-67.101). CONCLUSION: Sex and family history of gout were independently and interactively associated with gout. Sex-wise, men had a higher risk of gout than women. Family history was associated with a higher risk of gout in both sexes, but men had a higher risk. Notably, men having both siblings and parents with gout had the highest risk of gout.

Epigenetic regulation of Parkinson's disease risk variant GPNMB cg17274742 methylation by sex and exercise from Taiwan Biobank.

Background: Parkinson's disease (PD) is a complex neurodegenerative disease with an elusive etiology that involves the interaction between genetic, behavioral, and environmental factors. Recently, epigenetic modifications, particularly DNA methylation, have been recognized to play an important role in the onset of PD. Glycoprotein non-metastatic melanoma protein B (GPNMB), a type I transmembrane protein crucial for immune cell activation and maturation, has emerged as a potential biomarker for the risk of PD. This research aims to investigate the influence of exercise and gender on the regulation of methylation levels of GPNMB cg17274742 in individuals. Methods: We analyze data from 2,474 participants in the Taiwan Biobank, collected from 2008 and 2016. Methylation levels at the GPNMB cg17274742 CpG site were measured using Illumina Infinium MethylationEPIC beads. After excluding individuals with incomplete data or missing information on possible risk factors, our final analysis included 1,442 participants. We used multiple linear regression models to assess the association between sex and exercise with adjusted levels of GPNMB cg17274742 for age, BMI, smoking, drinking, coffee consumption, serum uric acid levels, and hypertension. Results: Our results demonstrated that exercise significantly influenced the methylation levels of GPNMB cg17274742 in males (ß = -0.00242; p = 0.0026), but not in females (ß = -0.00002362; p = 0.9785). Furthermore, male participants who exercised showed significantly lower levels of methylation compared to the reference groups of the female and non-exercising reference groups (ß = -0.00357; p = 0.0079). The effect of the interaction between gender and exercise on the methylation of GPNMB cg17274742 was statistically significant (p = 0.0078). Conclusion: This study suggests that gender and exercise can modulate GPNMB cg17274742, with hypomethylation observed in exercise men. More research is needed to understand the underlying mechanisms and implications of these epigenetic changes in the context of risk and prevention strategies.

Risk of gout among Taiwanese adults with ALDH-2 rs671 polymorphism according to BMI and alcohol intake.

BACKGROUND: Gout stems from both modifiable and genetic sources. We evaluated the risk of gout among Taiwanese adults with aldehyde dehydrogenase-2 (ALDH2) rs671 single nucleotide polymorphism (SNP) according to body mass index (BMI) and alcohol drinking. METHODS: We obtained information of 9253 individuals having no personal history of cancer from the Taiwan Biobank (2008-2016) and estimated the association between gout and independent variables (e.g., rs671, BMI, and alcohol drinking) using multiple logistic regression. RESULTS: Alcohol drinking and abnormal BMI were associated with a higher risk of gout whereas the rs671 GA+AA genotype was associated with a lower risk. The odds ratios (ORs) and 95% confidence intervals (CIs) were 1.297 and 1.098-1.532 for alcohol drinking, 1.550 and 1.368-1.755 for abnormal BMI, and 0.887 and 0.800-0.984 for GA+AA. The interaction between BMI and alcohol on gout was significant for GG (p-value = 0.0102) and GA+AA (p-value = 0.0175). When we stratified genotypes by BMI, alcohol drinking was significantly associated with gout only among individuals with a normal BMI (OR; 95% CI = 1.533; 1.036-2.269 for GG and 2.109; 1.202-3.699 for GA+AA). Concerning the combination of BMI and alcohol drinking among participants stratified by genotypes (reference, GG genotype, normal BMI, and no alcohol drinking), the risk of gout was significantly higher in the following categories: GG, normal BMI, and alcohol drinking (OR, 95% CI = 1.929, 1.385-2.688); GG, abnormal BMI, and no alcohol drinking (OR, 95% CI, = 1.721, 1.442-2.052); GG, abnormal BMI, and alcohol drinking (OR, 95% CI = 1.941, 1.501-2.511); GA+AA, normal BMI, and alcohol drinking (OR, 95% CI = 1.971, 1.167-3.327); GA+AA, abnormal BMI, and no alcohol drinking (OR, 95% CI = 1.498, 1.256-1.586); and GA+AA, abnormal BMI, and alcohol drinking (OR, 95% CI = 1.545, 1.088-2.194). CONCLUSIONS: Alcohol and abnormal BMI were associated with a higher risk of gout, whereas the rs671 GA+AA genotype was associated with a lower risk. Noteworthy, BMI and alcohol had a significant interaction on gout risk. Stratified analyses revealed that alcohol drinking especially among normal-weight individuals might elevate the risk of gout irrespective of the genotype.

Interactive Effect of IGF2BP2 rs4402960 Variant, Smoking and Type 2 Diabetes.

PURPOSE: Genetic and environmental factors are related to type 2 diabetes (T2D). Genetic modifiers of T2D have not been widely determined among smoking individuals. In this population-based study, we investigated the interactive association between rs4402960 polymorphism of the insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) gene and smoking with T2D among Taiwanese adults. MATERIALS AND METHODS: We obtained genetic data collected between 2008 and 2018 for 22,039 participants (aged 30-70 years) from the Taiwan Biobank (TWB) database. These data were analyzed using the t-test, Chi-square (χ 2) test, and multiple logistic regression. RESULTS: The mean ages for participants with and without diabetes were 58.11±8.75 and 48.58±11, respectively. Compared with the rs4402960 GG genotype, the odds ratio (OR) for T2D was 1.261 among GT and 1.545 among TT genotype individuals (p<0.05). Current smokers compared to nonsmokers were associated with a higher risk of T2D (OR=1.266, p=0.0404). There was a significant interaction between the IGF2BP2 rs4402960 variant and smoking on T2D (p = 0.0497). After stratification by rs4402960 genotypes and smoking status, the OR was substantial only in current smokers with GG genotype (OR, 1.663, p = 0.0008). CONCLUSION: This population-based study indicated that the risk for T2D was stronger among current smoking rs4402960 GG individuals recruited between 2008 and 2019 in Taiwan.