Association of coffee intake with bone mineral density: a Mendelian randomization study.

Background: In observational studies, the relationship between coffee intake and bone mineral density (BMD) is contradictory. However, residual confounding tends to bias the results of these studies. Therefore, we used a two-sample Mendelian randomization (MR) approach to further investigate the potential causal relationship between the two. Methods: Genetic instrumental variables (IVs) associated with coffee intake were derived from genome-wide association studies (GWAS) of the Food Frequency Questionnaire (FFQ) in 428,860 British individuals and matched using phenotypes in PhenoScanner. Summarized data on BMD were obtained from 537,750 participants, including total body BMD (TB-BMD), TB-BMD in five age brackets ≥60, 45-60, 30-45, 15-30, and 0-15 years, and BMD in four body sites: the lumbar spine, the femoral neck, the heel, and the ultradistal forearm. We used inverse variance weighting (IVW) methods as the primary analytical method for causal inference. In addition, several sensitivity analyses (MR-Egger, Weighted median, MR-PRESSO, Cochran's Q test, and Leave-one-out test) were used to test the robustness of the results. Results: After Bonferroni correction, Coffee intake has a potential positive correlation with total body BMD (effect estimate [Beta]: 0.198, 95% confidence interval [Cl]: 0.05-0.35, P=0.008). In subgroup analyses, coffee intake was potentially positively associated with TB-BMD (45-60, 30-45 years) (Beta: 0.408, 95% Cl: 0.12-0.69, P=0.005; Beta: 0.486, 95% Cl: 0.12-0.85, P=0.010). In addition, a significant positive correlation with heel BMD was also observed (Beta: 0.173, 95% Cl: 0.08-0.27, P=0.002). The results of the sensitivity analysis were generally consistent. Conclusion: The results of the present study provide genetic evidence for the idea that coffee intake is beneficial for bone density. Further studies are needed to reveal the biological mechanisms and offer solid support for clinical guidelines on osteoporosis prevention.

Coffee intake reduced gout risk by decreasing urate and urea while increasing SHBG levels in plasma: a mediation Mendelian randomization study.

OBJECTIVE: This study aims to investigate the causal relationships between specific dietary habits and the risk of gout, while identifying the mediators involved in these associations. METHODS: We initially assessed the causal effects of five dietary habits on gout by two-sample Mendelian randomization (MR). Subsequently, we identified mediators from five plasma metabolites by two-step MR, including urate, urea, sex hormone-binding globulin (SHBG), interleukin-18 (IL-18), and C-reactive protein (CRP). Next, we quantified the proportion of mediation effects by multivariable Mendelian randomization (MVMR). Last, we performed reverse MR analyses. Sensitivity analyses were conducted to enhance the robustness of our findings. RESULTS: Only coffee intake demonstrated a significant negative casual effect on gout (inverse variance weighted: OR = 0.444, p = 0.049). In two-step MR, coffee intake decreased urate and urea while increased SHBG levels, but did not affect IL-18 and CRP levels. Besides, urate and urea showed positive causal effects while SHBG exhibited a negative impact on gout. In mediation analysis, urate, urea, and SHBG respectively mediated 53.60%, 16.43%, and 4.81% of the total causal effect of coffee intake on gout. The three mediators collectively mediated 27.45% of the total effect. Reverse MR analyses suggested no significant reverse causal effects. Sensitivity analyses supported the reliability of our causal inferences. CONCLUSION: Coffee intake reduced gout risk by decreasing urate and urea while increasing SHBG levels in plasma. These findings accentuate the benefits of coffee intake for gout management. The mediators may provide a novel insight into potential therapeutic targets for gout prevention. Key Points • This study determines the causally protective effect of coffee intake on gout. • We reveal that coffee intake reduced the risk of gout by decreasing urate and urea while increasing SHBG levels in plasma. • Identifying specific mediators in the causal pathway from coffee intake to gout provides valuable information for clinical interventions of gout.

Beverage consumption and facial skin aging: Evidence from Mendelian randomization analysis.

BACKGROUND: Observational studies have linked coffee, alcohol, tea, and sugar-sweetened beverage (SSB) consumption to facial skin aging. However, confounding factors may influence these studies. The present two-sample Mendelian randomization (MR) investigated the potential causal association between beverage consumption and facial skin aging. METHODS: The single-nucleotide polymorphisms (SNPs) associated with coffee, alcohol, and tea intake were derived from the IEU project. The SSB-associated SNPs were selected from a genome-wide association study (GWAS). Data on facial skin aging were derived from the largest GWAS involving 16 677 European individuals. The inverse variance-weighted (IVW) was the main MR analysis method, supplemented by other methods (MR-Egger, weighted median, simple mode, and weighted mode). The MR-Egger intercept analysis was used for sensitivity analysis. Moreover, we conducted a replication analysis using data from another GWAS dataset on coffee consumption to validate our findings. RESULTS: Four instrumental variables (IVs) sets were used to examine the causal association between beverage consumption (coffee, alcohol, tea, SSB) and facial skin aging. Our results revealed that genetically predicted higher coffee consumption reduced the risk of facial skin aging (OR: 0.852; 95% CI: 0.753-0.964; p = 0.011, IVW method). The sensitivity analysis confirmed the robustness of the findings, with no evidence of pleiotropy or heterogeneity. The results of replicated MR analysis on coffee consumption were consistent with the initial analysis (OR = 0.997; 95% CI = 0.996-0.999; p = 0.003, IVW method). CONCLUSIONS: This study manifests that higher coffee consumption is significantly associated with a reduced risk of facial skin aging. These findings can offer novel strategies for identifying the underlying etiology of facial skin aging.

Causal relationships between coffee intake, apolipoprotein B and gastric, colorectal, and esophageal cancers: univariable and multivariable Mendelian randomization.

PURPOSE: Coffee intake and apolipoprotein B levels have been linked to gastric, colorectal, and esophageal cancers in numerous recent studies. However, whether these associations are all causal remains unestablished. This study aimed to assess the potential causal associations of apolipoprotein B and coffee intake with the risk of gastric, colorectal, and esophageal cancers using Mendelian randomization analysis. METHODS: In this study, we utilized a two-sample Mendelian randomization analysis to access the causal effects of coffee intake and apolipoprotein B on gastric, colorectal, and esophageal cancers. The summary statistics of coffee intake (n = 428,860) and apolipoprotein B (n = 439,214) were obtained from the UK Biobank. In addition, the summary statistics of gastric cancer, colorectal cancer, and esophageal cancer were obtained from the FinnGen biobank (n = 218,792). Inverse variance weighted, MR-Egger, weighted median, and weighted mode were applied to examine the causal relationship between coffee intake, apolipoprotein B and gastric, colorectal, and esophageal cancers. MR-Egger intercept test, Cochran's Q test, and leave-one-out analysis were performed to evaluate possible heterogeneity and pleiotropy. Steiger filtering and bidirectional mendelian randomization analysis were performed to evaluate the possible reverse causality. RESULTS: The result of the inverse variance weighted method indicated that apolipoprotein B levels were significantly associated with a higher risk of gastric cancer (OR = 1.392, 95% CI 1.027-1.889, P = 0.0333) and colorectal cancer (OR = 1.188, 95% CI 1.001-1.411, P = 0.0491). Furthermore, multivariable Mendelian randomization analysis also revealed a positive association between apolipoprotein B levels and colorectal cancer risk, but the effect of apolipoprotein B on gastric cancer risk disappeared after adjustment of coffee intake, body mass index or lipid-related traits. However, we did not discover any conclusive evidence linking coffee intake to gastric, colorectal, or esophageal cancers. CONCLUSIONS: This study suggested a causal association between genetically increased apolipoprotein B levels and higher risk of colorectal cancer. No causal relationship was observed between coffee intake and gastric, colorectal, or esophageal cancers.

Coffee intake and risk of diabetic nephropathy: a Mendelian randomization study.

Rationale and objective: A causal relationship concerning coffee intake and diabetic nephropathy (DN) is controversial. We conducted a Mendelian randomization study to assess the causal nature of these associations. Methods: 40 independent single nucleotide polymorphisms (SNPs) associated with coffee intake were selected from the UK Biobank study. Summary-level data for diabetic nephropathy were obtained from publicly available genome-wide association studies (GWAS) and the FinnGen consortium. Inverse variance weighted (IVW), MR-Egger, and weighted median (WM) methods were used to examine a causal association. Sensitivity analyses included Cochran's Q test, the intercept of MR-Egger, MR-PRESSO, and the Outlier method. Leave-One-Out sensitivity analyses were also conducted to reduce the heterogeneity. Results: Our current study demonstrated positive associations of genetically predicted coffee intake with diabetic nephropathy (OR=1.939; P = 0.045 and type 2 diabetes with renal complications (OR = 2.787, P= 0.047). These findings were robust across several sensitivity analyses. Conclusions: This study found a positive correlation between coffee consumption and the risk of diabetic nephropathy using genetic data. For a more accurate and trustworthy conclusion, subgroup analysis on coffee intake, including preparing method, variety of coffee, and quantity, is required.

Coffee and tea intake with long-term risk of irritable bowel syndrome: a large-scale prospective cohort study.

BACKGROUND: To investigate prospective association of coffee and tea intake with incident irritable bowel syndrome (IBS) in a long-term cohort. METHODS: Participants free of IBS, coeliac disease, inflammatory bowel disease and any cancer at baseline from UK Biobank were included. Coffee and tea intake was measured separately via baseline touchscreen questionnaire, with four categories for each intake (0, 0.5-1, 2-3 and ≥4 cups/day). Primary outcome was incident IBS. Cox proportional hazard model was used to estimate associated risk. RESULTS: Among 425 387 participants, 83 955(19.7%) and 186 887(43.9%) consumed ≥4 cups/day of coffee and tea at baseline, respectively. During median 12.4-year follow-up, incident IBS was identified in 7736 participants. Compared with no coffee intake, consumption of 0.5-1, 2-3 and ≥4 cups/day was associated with lower IBS risk [hazard ratio (HR)=0.93, 95% CI: 0.87-0.99; 0.91, 0.85-0.97; 0.81, 0.76-0.88; Ptrend < 0.001]. Specifically, decreased risk was evident in individuals who consumed instant (HR = 0.83, 0.78-0.88) or ground coffee (HR = 0.82, 0.76-0.88) compared with no coffee drink. Regarding tea intake, protective association was only found in individuals who consumed 0.5-1 cup/day (HR = 0.87, 0.80-0.95), whereas no significant association was detected in those who consumed 2-3 (HR = 0.94, 0.88-1.01) or ≥4 cups/day (HR = 0.95, 0.89-1.02) compared with no-tea intake (Ptrend = 0.848). CONCLUSIONS: Higher intake of coffee, particularly instant and ground coffee, is associated with lower risk of incident IBS, with significant dose-response relationship. Moderate-tea intake (0.5-1 cup/day) is associated with lower IBS risk.

Understanding the Complex Interactions between Coffee, Tea Intake and Neurologically Relevant Tissues Proteins in the Development of Anxiety and Depression.

OBJECTIVES: Coffee and tea intake might be associated with psychiatry diseases. However, it is unclear whether the effect of coffee/tea on anxiety and depression depending on the different types of proteins. DESIGN: This was a cross-sectional study. SETTING: Our datasets were downloaded from online. PARTICIPANTS: Phenotypic and genotypic data for coffee intake(N=376,196) and tea intake (N=376,078) were derived from UK Biobank. GWAS data of proteins (N=1,537) from neurologically relevant tissues (brain, cerebrospinal fluid (CSF) and plasma) were obtained from a recently published study. MEASUREMENTS: Multivariate linear analysis was then used to evaluate the potential interaction effect between coffee/tea intake and proteins polygenetic risk score (PRS) on the risks of anxiety and depression controlling for age, sex, Townsend deprivation index (TDI), smoke, drinking and education level. RESULTS: 34 coffee intake-proteins interactions and 15 tea intake-proteins interactions were observed in anxiety individuals, such as coffee intake-c-Jun interaction (ß=0.0169, P=4.131×10-3), coffee intake-Fas interaction (ß=-0.0190, P=8.132×10-4), tea intake-sL-Selectin interaction (ß=0.0112, P=5.412×10-3) and tea intake-IL-1F6 (ß=0.0083, P=4.471×10-2). 25 coffee intake-proteins and 14 tea intake-proteins interactions were observed in depression individuals, including coffee intake- IL-1 sRI (ß=0.0171, P=4.888×10-3) and coffee intake-NXPH1 interaction (ß=0.0156, P=9.819×10-3), tea intake-COLEC12 interaction (ß=0.0127, P=3.280×10-3), and tea intake-Layilin interaction (ß=0.0117, P=7.926×10-3). CONCLUSIONS: Our results suggested the important role of multiple proteins in neurologically relevant tissues in the associations between coffee/tea intake and psychiatry diseases, providing entry points to explore the mechanisms underlying anxiety and depression.

Functional single-nucleotide polymorphism (rs762551) in CYP1A2 gene affects white coffee intake in healthy 20- to 40-year-old adults.

Coffee is one of the most consumed beverages in the world, but the extent to which it is consumed is affected by both environmental and genetic factors. Genome-wide association studies and candidate date association studies have identified several gene variants associated with increased consumption of coffee. Functional single-nucleotide polymorphisms in rs762551 (cytochrome P450 1A2 [CYP1A2]) and rs5751876 (adenosine receptor A2A [ADORA2A]) has been linked to individual caffeine response. Coffee intake has been shown to affect lipid metabolism. We thus hypothesize that rs762551 (CYP1A2) A allele carriers consume more coffee than C allele carriers and that rs5751876 (ADORA2A) C allele carriers consume less coffee than T allele carriers. Additionally, we hypothesize that CYP1A2 genotype can modulate serum glucose concentrations and lipid profile. A total of 421 participants aged 20 to 40 years were recruited from 2016 to 2018 in Poznan, Poland. Genotyping of CYP1A2 and ADORA2A was performed using TaqMan probes. Individuals with AA CYP1A2 genotype consumed relatively more coffee with milk (72.81 ± 10.15 mL/1000 kcal vs 43.38 ± 6.42 mL/1000 kcal, P = .008) and with milk or cream than did C allele carriers, whereas the rs5751876 ADORA2A polymorphism was not associated with coffee or tea intake. Additionally, subjects with AA CYP1A2 genotype had 10% higher serum triacylglycerol (TG) concentrations than C allele carriers. This study suggests that CYP1A2 rs762551 polymorphism is associated with coffee intake and serum TG concentrations in healthy 20- to 40-year-old adults.

Coffee Types and Type 2 Diabetes Mellitus: Large-Scale Cross-Phenotype Association Study and Mendelian Randomization Analysis.

Purpose: To explore whether coffee intake is associated with the risk of type 2 diabetes mellitus (T2DM) from a genetic perspective, and whether this association remains the same among different types of coffee consumers. Methods: We utilized the summary-level results of 12 genome-wide association studies. First, we used linkage disequilibrium score regression and cross-phenotype association analysis to estimate the genetic correlation and identify shared genes between coffee intake and T2DM in addition to some other T2DM-related phenotypes. Second, we used Mendelian randomization (MR) analysis to test whether there is a significant genetically predicted causal association between coffee intake and the risk of T2DM or other T2DM-related phenotypes. For all the analyses above, we also conducted a separate analysis for different types of coffee consumers, in addition to total coffee intake. Results: Genetically, choice for ground coffee was significantly negatively associated with the risk of T2DM and some other related risks. While coffee intake and choice for decaffeinated/instant coffee had significant positive correlation with these risks. Between these genetically related phenotypes, there were 1571 genomic shared regions, of which 134 loci were novel. Enrichment analysis showed that these shared genes were significantly enriched in antigen processing related biological processes. MR analysis indicated that higher genetically proxied choice for ground coffee can reduce the risk of T2DM (T2DM: b: -0.2, p-value: 4.70×10-10; T2DM adjusted for body mass index (BMI): b: -0.11, p-value: 4.60×10-5), and BMI (b: -0.08, p-value: 6.50×10-5). Conclusions: Compared with other types of coffee, ground coffee has a significant negative genetic and genetically predicated causal relationship with the risk of T2DM. And this association is likely to be mediated by immunity. The effect of different coffee types on T2DM is not equal, researchers on coffee should pay more attention to distinguishing between coffee types.

Cardiovascular symptoms affect the patterns of habitual coffee consumption.

BACKGROUND: Excessive coffee consumption can lead to unpleasant sensations such as tachycardia and heart palpitations. OBJECTIVES: Our aim was to investigate if cardiovascular symptoms can lead to alterations in habitual patterns of coffee consumption. METHODS: We used information from up to 390,435 European ancestry participants in the UK Biobank, aged 39-73 y. Habitual coffee consumption was self-reported, and systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate were measured at baseline. Cardiovascular symptoms at baseline were based on hospital diagnoses, primary care records, and/or self-report. Mendelian randomization (MR) was used to examine genetic evidence for a causal association between SBP, DBP, and heart rate with habitual coffee consumption. RESULTS: Participants with essential hypertension, angina, or heart arrhythmia were all more likely to drink less caffeinated coffee and to be non-habitual or decaffeinated coffee drinkers compared with those who did not report related symptoms (P ≤ 3.5 × 10-8 for all comparisons). Higher SBP and DBP were associated with lower caffeinated coffee consumption at baseline, with consistent genetic evidence to support a causal explanation across all methods [MR-Egger regression (MREggr) ß: -0.21 cups/d (95% CI: -0.34, -0.07) per 10 mm Hg higher SBP and -0.33 (-0.61, -0.07) per 10 mm Hg higher DBP)]. In genetic analyses, higher resting heart rate was associated with a greater odds of being a decaffeinated coffee drinker (MREggr OR: 1.71; 95% CI: 1.31, 2.21) per 10 beats/min). CONCLUSIONS: We provide causal genetic evidence for cardiovascular system-driven influences on habitual coffee intakes, suggesting that people tend to naturally regulate their coffee consumption based on blood pressure levels and heart rate. These findings suggest that observational studies of habitual coffee intakes are prone to influences by reverse causation, and caution is required when inferred health benefits result from comparisons with coffee abstainers or decaffeinated coffee drinkers.

Habitual coffee intake and plasma lipid profile: Evidence from UK Biobank.

BACKGROUND & AIMS: There is evidence that long-term heavy coffee consumption may adversely affect individuals' cardiovascular disease (CVD) risk. As hyperlipidemia is a well-established contributor to CVD risk, we investigated the association between habitual coffee intake and plasma lipid profile. METHODS: We used data from up to 362,571 UK Biobank participants to examine phenotypic associations between self-reported coffee intake and plasma lipid profiles, including low-density-lipoproteins cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), total cholesterol (total-C), triglycerides, and apolipoproteins A1 and B (ApoA1 and ApoB). Mendelian randomization (MR) analysis using genetically instrumented coffee intake was used to interrogate the causal nature of coffee-lipid associations. RESULTS: We observed a positive dose-dependent association between self-reported coffee intake and plasma concentration of LDL-C, ApoB and total-C, with the highest lipid levels seen among participants reported drinking >6 cups/day (Plinear trend≤ 3.24E-55 for all). Consistently, in MR analyses using genetically instrumented coffee intake one cup higher coffee intake was associated with a 0.07 mmol/L (95% CI 0.03 to 0.12), 0.02 g/L (95% CI 0.01 to 0.03), and 0.09 mmol/L (95% CI 0.04 to 0.14) increase in plasma concentration of LDL-C, ApoB, and total-C, respectively. CONCLUSIONS: Our phenotypic and genetic analyses suggest that long-term heavy coffee consumption may lead to unfavourable lipid profile, which could potentially increase individuals' risk for CVD. These findings may have clinical relevance for people with elevated LDL cholesterol.

Plasma metabolite biomarkers of boiled and filtered coffee intake and their association with type 2 diabetes risk.

BACKGROUND: Habitual coffee intake has been associated with a lower risk of developing type 2 diabetes (T2D), but few studies used biomarkers to reflect intake and investigated different coffee brews, that is boiled and filtered, separately. OBJECTIVES: To identify plasma metabolites associated with boiled or filtered coffee intake and to examine their association with T2D risk in Swedish adults. METHODS: In a case-control study nested within the Västerbotten Intervention Programme, baseline plasma samples from 421 case-control pairs and samples from a subset of 149 pairs at a 10-year follow-up were analysed using untargeted LC-MS metabolomics. We identified metabolites associated with food frequency questionnaires (FFQ)-estimated coffee intake and assessed odds ratios of T2D. RESULTS: In total, 24 and 32 metabolites were associated with boiled or filtered coffee intake. We determined robust metabolite panels for highly specific prediction of boiled or filtered coffee. We observed an inverse association between the metabolite panel of filtered coffee and T2D risk. No association with T2D was observed for the panel of boiled coffee intake. Similar results were observed for FFQ-estimated coffee intake. CONCLUSIONS: We identified plasma metabolites specifically associated with boiled or filtered coffee intake, which might be used as selective biomarkers. Our study supports a protective role of habitual intake of filtered coffee on T2D development. The lack of association for boiled coffee intake might be due to the lack of a protective effect of boiled coffee or due to the limited number of boiled coffee consumers in this population, but it warrants further investigation.

The relationship between coffee intake, obstructive sleep apnea risk, and type 2 diabetes glycemic control, in Tabuk City, The Kingdom of Saudi Arabia: a case-control study.

OBJECTIVES: The study aimed to assess the relationship between coffee intake, obstructive sleep apnea risk (OSA), and glycemic control among patients with diabetes mellitus. RESULTS: There were 110 patients with diabetes and 96 healthy control subjects (matched for age and sex) attending a diabetes center زinTabuk, Saudi Arabia during the period from June 2018-October 2019. Stop-Bang questionnaire was used to assess OSA risk, and Epworth Sleepiness Scale to investigate daytime sleepiness. OSA risk and daytime sleepiness were higher among patients with diabetes compared to controls (4.34 ± 1.61 vs. 2.86 ± 1.24, and 8.31 ± 4.40 vs. 6.39 ± 3.70 respectively, P < 0.5), while coffee consumption was not (4.64 ± 3.95 vs. 3.45 ± 3.06, P > 0.05). Women with diabetes were younger with short duration since the diagnosis of diabetes and consumed less coffee compared to men, P < 0.5. A negative correlation was found between coffee consumption and the duration of diabetes, while no correlation was found between coffee intake, the glycated hemoglobin, OSA risk, sex, and daytime sleepiness. Daytime sleepiness and OSA risk were commoners among patients with diabetes, they were not correlated with coffee consumption which was negatively correlated with the duration since diabetes diagnosis. Further larger multi-center studies investigating coffee intake among patients newly diagnosed with diabetes are recommended.

Coffee Intake and Obesity: A Meta-Analysis.

Many studies have explored the relationship between coffee-one of the most commonly consumed beverages today-and obesity. Despite inconsistent results, the relationship has not been systematically summarized. Thus, we conducted a meta-analysis by compiling data from 12 epidemiologic studies identified from PubMed and Embase through February 2019. The included studies assessed obesity by body mass index (BMI, a measure of overall adiposity) or waist circumference (WC, a measure of central adiposity); analyzed the measure as a continuous outcome or binary outcome. Using random effects model, weighted mean difference (WMD) and 95% confidence interval (CI) were obtained for continuous outcomes; summary relative risk (RR) and 95% CI for the highest vs. lowest categories of coffee intake were estimated for binary outcome. For BMI, WMD was -0.08 (95% CI -0.14, -0.02); RR was 1.49 (95% CI 0.97, 2.29). For WC, WMD was -0.27 (95% CI -0.51, -0.02) and RR was 1.07 (95% CI 0.84, 1.36). In subgroup analysis by sex, evidence for an inverse association was more evident in men, specifically for continuous outcome, with WMD -0.05 (95% CI -0.09, -0.02) for BMI and -0.21 (95% CI -0.35, -0.08) for WC. Our meta-analysis suggests that higher coffee intake might be modestly associated with reduced adiposity, particularly in men.

Habitual coffee intake reduces all-cause mortality by decreasing heart rate.

It is well known that subjects with metabolic syndrome show an elevated resting heart rate. We previously reported that elevated heart rate was significantly related to all-cause mortality, and that coffee consumption was inversely associated with metabolic syndrome. We hypothesized that higher coffee consumption may decrease all-cause mortality by reducing resting heart rate. We performed a longitudinal epidemiological study in Tanushimaru (a cohort of the Seven Countries Study). A total of 1920 residents aged over 40 years received health checkups in 1999. We measured components of metabolic syndrome, and eating and drinking patterns were evaluated by a food frequency questionnaire. We followed up the participants annually for 15 years. During the follow-up period, 343 of the participants died. Of these, 102 subjects died of cancer, 48 of cerebro-cardiovascular diseases, and 44 of infectious diseases. Multivariate analyses revealed that higher coffee consumption was inversely associated with resting heart rate. Kaplan-Meier curves found lower mortality rates in the higher coffee consumption groups. In the lower coffee consumption groups, elevated hazard ratios of all-cause death were observed in the increased heart rate quintiles, whereas heart rate was not associated with all-cause death in the higher coffee consumption groups. These significant associations remained after further adjustment for confounders. This prospective study suggests that higher coffee consumption may have a protective effect against all-cause death due to reducing resting heart rate.

Coffee intake, health-related quality of life, and associated factors of overactive bladder in older Korean women living in rural South Korea.

Overactive bladder (OAB) is a common health problem in older women. The aim of the study was to investigate coffee consumption, health-related quality of life (HRQOL), and associated factors of OAB in older Korean women living in rural South Korea. A total of 248 women aged 65 years and older participated in this study. Chi-square tests, t-tests, and multivariable logistic regressions were performed. The means of coffee consumption between OAB and non-OAB groups were not significantly different. Women with OAB showed significantly lower HRQOL than women with stress urinary incontinence only. OAB was associated with high body mass index and poor health status.

High genetic risk scores of SLIT3, PLEKHA5 and PPP2R2C variants increased insulin resistance and interacted with coffee and caffeine consumption in middle-aged adults.

BACKGROUNDS AND AIMS: Insulin resistance is a common feature of metabolic syndrome that may be influenced by genetic risk factors. We hypothesized that genetic risk scores (GRS) of SNPs that influence insulin resistance and signaling interact with lifestyles to modulate insulin resistance in Korean adults. METHODS AND RESULTS: Genome-wide association studies (GWAS) of subjects aged 40-65 years who participated in the Ansung/Ansan cohorts (8842 adults) in Korea revealed 52 genetic variants that influence insulin resistance. The best gene-gene interaction model was explored using the generalized multifactor dimensionality reduction (GMDR) method. GRS from the best model were calculated and the GRS were divided into low, medium and high groups. The best model for representing insulin resistance included SLIT3_rs2974430, PLEKHA5_rs1077044, and PPP2R2C_rs16838853. The odds ratios for insulin resistance were increased by 150% in the High-GRS group compared to the Low-GRS group. However, ORs for insulin secretion capacity, measured by HOMA-B, were not associated with GRS. Coffee and caffeine intake and GRS had an interaction with insulin resistance: In subjects with high coffee (≥10 cups/week) or caffeine intake (≥220 mg caffeine/day), insulin resistance was significantly elevated in the High-GRS group, but not in the Low-GRS. However, alcohol intake, smoking and physical activity did not have an interaction with GRS. Insulin secretion capacity was not significantly influenced by GRS when evaluating the adjusted odds ratios. CONCLUSIONS: Subjects with High-GRS may be susceptible to increased insulin resistance by 50% and its risk may be exacerbated by consuming more than 10 cups coffee/week or 220 mg caffeine/day.

Does Caffeine Consumption Increase the Risk of New-Onset Atrial Fibrillation?

OBJECTIVE: Caffeine has been considered a trigger for atrial fibrillation (AF). We conducted a meta-analysis including a dose-response analysis to assess the relationship between caffeine consumed and incidence of AF. METHODS: Data from selected studies represented 176,675 subjects (AF in 9,987 [5.7%]). Caffeine content varied widely, ranging from 40 to 180 mg per cup of coffee. For purposes of the calculations in this study, we assumed 140 mg of caffeine in a standard 12-oz cup of coffee. RESULTS: No significant difference was found in AF incidence when the subjects consuming less than 2 cups of coffee per day were compared to subjects with higher consumption, 1.068 (0.937-1.216). The risk of AF was higher among subjects consuming less than 2 cups of coffee daily when compared to higher daily consumption subjects. A lower incidence of AF was found among people consuming more than 436 mg daily. CONCLUSION: The incidence of AF is not increased by coffee consumption. In fact, we found a lower incidence of AF when caffeine consumption exceeded 436 mg/day. Therefore, based on available evidence there is no association between caffeine intake and AF risk.

Effects of Coffee Intake on Incident Chronic Kidney Disease: A Community-Based Prospective Cohort Study.

BACKGROUND: Drinking coffee can raise public health problems, but the association between coffee and kidney disease is unknown. We studied whether coffee intake can affect the development of chronic kidney disease in the general population. METHODS: We analyzed 8717 subjects with normal renal function recruited from the Korean Genome and Epidemiology Study (KoGES) cohort. Based on a food frequency questionnaire, coffee consumption was categorized into 5 groups: 0 per week, <1 cup per week, 1-6 cups per week, 1 cup per day, and ≥2 cups per day. The primary outcome was incident chronic kidney disease, defined as an estimated glomerular filtration rate <60 mL/min/1.73 m2. RESULTS: The mean age (standard deviation) of study subjects was 52.0 (8.8) years, and 47.8% were male. Among the subjects, 52.8% were daily coffee consumers. During a mean follow-up of 11.3 (range, 5.9-11.5) years, 9.5% of participants developed chronic kidney disease. The incident chronic kidney disease occurred less in daily coffee consumers. Unadjusted hazard ratios (HRs) was significantly lower in daily coffee consumers. In multivariable Cox model even after adjustment of blood pressure, hypertension, cardiovascular disease, diabetes, and amount of daily intake for caffeine-containing foods such as tea and chocolate, coffee consumers with 1 cup per day (HR, 0.76; 95% confidence interval, 0.63-0.92) and ≥2 cups per day (HR, 0.80; 95% confidence interval, 0.65-0.98) were associated with a lower risk of chronic kidney disease development than nondrinkers. Time-averaged and time-varying Cox models yielded similar results. The rates of decline in glomerular filtration were lower in daily coffee consumers. CONCLUSIONS: Our findings suggest that daily coffee intake is associated with decreased risk of the development of chronic kidney disease.