beta-carotene and Atrial-Fibrillation

Chocolate consumption has been shown to protect against various cardiovascular end points; however, little is known about the association between chocolate consumption and incident atrial fibrillation (AF). Therefore, we prospectively examined the association between chocolate consumption and incident AF in a cohort of 18,819 US male physicians. Chocolate consumption was ascertained from 1999 to 2002 through a self-administered food frequency questionnaire. Incident AF was ascertained through yearly follow-up questionnaires. Cox regression was used to estimate relative risks of AF. The average age at baseline was 66 years (±9.1). During a mean follow-up of 9.0 years (±3.0), 2,092 cases of AF occurred. Using <1 per month of chocolate consumption as the reference group, multivariable adjusted hazard ratios (95% confidence interval) for AF were 1.04 (0.93 to 1.18), 1.10 (0.96 to 1.25), 1.14 (0.99 to 1.31), and 1.05 (0.89 to 1.25) for chocolate intake of 1 to 3 per month and 1, 2 to 4, and ≥5 per week (p for trend 0.25), respectively. In a secondary analysis, there was no evidence of effect modification by adiposity (p interaction = 0.71) or age (p interaction = 0.26). In conclusion, our data did not support an association between chocolate consumption and risk of AF in US male physicians.

Topics: Aged; Aspirin; Atrial Fibrillation; beta Carotene; Cacao; Cohort Studies; Diet; Humans; Incidence; Male; Middle Aged; Neoplasms; Physicians; Platelet Aggregation Inhibitors; Proportional Hazards Models; Risk Factors; Sex Factors; Surveys and Questionnaires; Vitamins

Although sleep quality and duration have been related to cardiovascular end points, little is known about the association between sleep duration and incident atrial fibrillation (AF). Hence, we prospectively examined the association between sleep duration and incident AF in a cohort of 18,755 United States male physicians. Self-reported sleep duration was ascertained during a 2002 annual follow-up questionnaire. Incident AF was ascertained through annual follow-up questionnaires. Cox regression analysis was used to estimate the relative risks of AF. The average age at baseline was 67.7 ± 8.6 years. During a mean follow-up of 6.9 ± 2.1 years, 1,468 cases of AF occurred. Using 7 hours of sleep as the reference group, the multivariate adjusted hazard ratio for AF was 1.06 (95% confidence interval 0.92 to 1.22), 1.0 (reference), and 1.13 (95% confidence interval 1.00 to 1.27) from the lowest to greatest category of sleep duration (p for trend = 0.26), respectively. In a secondary analysis, no evidence was seen of effect modification by adiposity (p for interaction = 0.69); however, prevalent sleep apnea modified the relation of sleep duration with AF (p for interaction = 0.01). From the greatest to the lowest category of sleep duration, the multivariate-adjusted hazard ratio for AF was 2.26 (95% confidence interval 1.26 to 4.05), 1.0 (reference), and 1.34 (95% confidence interval 0.73 to 2.46) for those with prevalent sleep apnea and 1.01 (95% confidence interval 0.87 to 1.16), 1.0 (reference), and 1.12 (95% confidence interval 0.99 to 1.27) for those without sleep apnea, respectively. Our data showed a modestly elevated risk of AF with long sleep duration among United States male physicians. Furthermore, a shorter sleep duration was associated with a greater risk of AF in those with prevalent sleep apnea.

Topics: Aged; Aspirin; Atrial Fibrillation; beta Carotene; Confidence Intervals; Cyclooxygenase Inhibitors; Dose-Response Relationship, Drug; Double-Blind Method; Drug Therapy, Combination; Follow-Up Studies; Humans; Incidence; Male; Physicians; Prevalence; Retrospective Studies; Risk Factors; Sleep; Sleep Wake Disorders; Surveys and Questionnaires; United States; Vitamins

The causal association between circulating β-carotene concentrations and cardiovascular disease (CVD) remains controversial. We conducted a Mendelian randomization study to explore the effects of β-carotene on various cardiovascular diseases, including myocardial infarction, atrial fibrillation, heart failure, and stroke. Three single nucleotide polymorphisms (SNPs) associated with the β-carotene levels were obtained by searching published data and used as instrumental variables. Genetic association estimates for 4 CVDs (including myocardial infarction, atrial fibrillation, heart failure, and stroke) in the primary analysis, blood pressure and serum lipids (high-density lipoprotein [HDL] cholesterol, LDL cholesterol, and triglycerides) in the secondary analysis were obtained from large-scale genome-wide association studies (GWASs). We applied inverse variance-weighted as the primary analysis method, and 3 others were used to verify as sensitivity analysis. Genetically predicted circulating β-carotene levels (natural log-transformed, µg/L) were positively associated with myocardial infarction (odds ratio [OR] 1.10, 95% confidence interval [CI] 1.02-1.18, P = .011) after Bonferroni correction. No evidence supported the causal effect of β-carotene on atrial fibrillation (OR 1.02, 95% CI 0.96-1.09, P = .464), heart failure (OR 1.07, 95% CI 0.97-1.19, P = .187), stroke (OR 1.03, 95% CI 0.93-1.15, P = .540), blood pressure (P > .372) and serum lipids (P > .239). Sensitivity analysis produced consistent results. This study provides evidence for a causal relationship between circulating β-carotene and myocardial infarction. These findings have important implications for understanding the role of β-carotene in CVD and may inform dietary recommendations and intervention strategies for preventing myocardial infarction.

Topics: Atrial Fibrillation; beta Carotene; Cardiovascular Diseases; Cholesterol, HDL; Genome-Wide Association Study; Heart Failure; Humans; Mendelian Randomization Analysis; Myocardial Infarction; Polymorphism, Single Nucleotide; Stroke; Triglycerides

Observational studies reported conflicting results regarding the association between circulating concentrations of nutrition-related factors and atrial fibrillation (AF). The aim of this study was to evaluate the potential causal effect of 8 circulating nutrition-related factors (vitamin B12, vitamin E, folate, retinol, β-carotene, iron, zinc, and copper) on AF risk using mendelian randomization (MR). Summary-level data for the nutrition-related factors and AF were obtained from genome-wide association studies conducted among individuals of European ancestry. The genome-wide association study on AF included 60,620 cases and 970,216 controls. A 2-sample MR design was applied for evaluating the causal association. In the primary MR analyses, the inverse variance-weighted method did not identify any causal effect of circulating concentrations of vitamin B12 [β = 0.000, standard error (SE) = 0.021, P = 0.994], vitamin E (β = 0.080, SE = 0.152, P = 0.600), retinol (β = 0.098, SE = 0.397, P = 0.806), folate (β = -0.006, SE = 0.052, P = 0.901), β-carotene (β = 0.014, SE = 0.025, P = 0.560), iron (β = -0.009, SE = 0.072, P = 0.905), zinc (β = 0.038, SE = 0.032, P = 0.239), and copper (β = -0.012, SE = 0.023, P = 0.589) on AF. The MR-Egger and MR pleiotropy residual sum and outlier (MR-PRESSO) analyses did not suggest the presence of pleiotropy. In addition, the lack of association remained in the leave-one-out analysis. This MR study indicates no causal association of circulating concentrations of vitamin B12, vitamin E, folate, retinol, β-carotene, iron, zinc, and copper with AF.

Topics: Atrial Fibrillation; beta Carotene; Copper; Folic Acid; Genome-Wide Association Study; Humans; Iron; Mendelian Randomization Analysis; Polymorphism, Single Nucleotide; Vitamin A; Vitamin B 12; Vitamins; Zinc