Amber coloured plasma-Case for illustration.

INTRODUCTION: Abnormal colour of plasma is infrequently identified during processing of blood and blood components. Common reasons include haemolysis, medications or diet related. Sometimes, the aetiology is unknown. It is a dilemma for every transfusion specialist encountering this situation. Effort should be made to find the aetiology of discolouration of plasma, so that the blood donor can be suitably advised, and a decision can be made regarding the use of blood products. MATERIALS AND METHODS: We encountered two cases of orange coloured (amber coloured) plasma in our regular blood donors. All the common reasons for abnormal plasma discolouration were evaluated, including the donor's medication and diet. Spectrophotometry along with Liquid Chromatography-Mass Spectrometry (LC-MS) in both the positive and negative ion modes with literature search helped in arriving at a conclusion. RESULTS: Haemolysis was ruled out by estimation of plasma haemoglobin. Spectrophotometric analysis of the coloured plasma samples showed a peak, which was absent in normal coloured plasma. This was further investigated using Liquid Chromatography-Mass Spectrometry (LC-MS) in both the positive and negative ion modes. There was no significant difference between the coloured and normal samples in the positive ion mode. But in the negative ion mode, there was a peak observed at 110.5 and 191 m/z value in the profile of the coloured samples in comparison with the normal sample. Literature review shows the peak was corresponding to the presence of quinic acid residues-a substance found in coffee, and potentially excreted into the plasma of an individual with high coffee consumption. CONCLUSION: Reporting unusual causes associated with plasma discolouration is important. Present guidelines forbid issue of abnormal coloured blood and blood components for transfusion. Further such reports are necessary to confirm the safety of recipients receiving such units. This is the first case report to our knowledge of quinic acid discolouring blood products.

Caffeine intake enhances bowel recovery after colorectal surgery: a meta-analysis of randomized and non-randomized studies.

Postoperative ileus (POI) after colorectal surgery is a major problem that affects both patient recovery and hospital costs highlighting the importance of preventive strategies. Therefore, we aimed to perform a systematic analysis of the effects of postoperative caffeine consumption on bowel recovery and surgical morbidity after colorectal surgery. A comprehensive literature search was conducted through September 2023 for randomized and non-randomized trials comparing the effect of caffeinated versus non-caffeinated drinks on POI by evaluating bowel movement resumption, time to first flatus and solid food intake, and length of hospital stay (LOS). Secondary outcome analysis included postoperative morbidity in both groups. After data extraction and inclusion in a meta-analysis, odds ratios (ORs) for dichotomous variables and standardized mean differences (SMDs) for continuous outcomes with 95% confidence intervals (CIs) were calculated. Subgroup analyses were performed in cases of substantial heterogeneity. Six randomized and two non-randomized trials with a total of 610 patients were included in the meta-analysis. Caffeine intake significantly reduced time to first bowel movement [SMD -0.39, (95% CI -0.66 to -0.12), p = 0.005] and time to first solid food intake [SMD -0.41, (95% CI -0.79 to -0.04), p = 0.03] in elective laparoscopic colorectal surgery, while time to first flatus, LOS, and the secondary outcomes did not differ significantly. Postoperative caffeine consumption may be a reasonable strategy to prevent POI after elective colorectal surgery. However, larger randomized controlled trials (RCTs) with homogeneous study protocols, especially regarding the dosage form of caffeine and coffee, are needed.

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.

Effects of common lifestyle factors on obstructive sleep apnea: precautions in daily life based on causal inferences.

Background: This study aimed to evaluate the causal impact of common modifiable lifestyles on obstructive sleep apnea (OSA), which is beneficial for recommendations to prevent and manage OSA. Method: Published genome-wide association study (GWAS) summary statistics were used to perform two-sample Mendelian randomization (MR). Variants associated with each exposure of smoking, drinking, and leisure sedentary behaviors at the genetic level were used as instrumental variables (IVs). Then, inverse-variance weighting (IVW) was considered the primary result for causality. Moreover, several complimented approaches were also included to verify the observed associations. MR-PRESSO and MR-Egger intercept were applied to test the horizontal pleiotropy. To assess heterogeneity, Cochran's Q test by IVW and MR-Egger were applied. Results: Regular smoking history increased OSA risk in all applied approaches [OR (95% CI)IVW = 1.28 (1.12, 1.45), p = 1.853 × 10-4], while the causality of lifetime smoking index [OR (95% CI)IVW = 1.39 (1.00, 1.91), p = 0.048], alcohol intake frequency [outliers removed OR (95% CI)IVW = 1.26 (1.08, 1.45), p = 0.002], and coffee intake behavior [OR (95% CI)IVW = 1.66 (1.03, 2.68), p = 0.039] on OSA risk were not always consistent in other approaches. In addition, no robust causal associations were observed for the effect of sedentary leisure behaviors on OSA risk. In sensitivity analysis, we observed no sign of horizontal pleiotropy or heterogeneity. Conclusion: Ever regularly smoking has a robust causal role in increasing OSA risk, which should be discouraged as precautions from developing OSA.

Coffee and the risk of osteoarthritis: a two-sample, two-step multivariable Mendelian randomization study.

Purpose: To investigate the potential causal relationship between coffee consumption and osteoarthritis (OA), and to disentangle whether body mass index (BMI) and Bone mineral density (BMD) mediate this relationship. Methods: We performed two-sample and two-step Mendelian randomization (MR) analyses utilizing publicly available genome-wide association studies (GWAS) summary statistics to estimate the association between coffee intake and OA risk (including knee OA, hip OA, knee or hip OA, and total OA), as well as the possible mediating effects of BMI and BMD. In addition, data of different coffee types (decaffeinated coffee, instant coffee, ground coffee-including espresso, filter, etc., and other coffee types) were used to explore the effect of coffee type on the risk of OA. Results: In two-sample MR, coffee intake increased the risk of OA in various sites, with the most significant impact observed in knee osteoarthritis (KOA) (odds ratio [OR] 2.03, 95% confidence interval [CI] 1.57-2.61, p < 0.001). The effect on self-reported OA was minimal (OR 1.03, 95% CI 1.01-1.05, p = 0.006). Further analysis of different types of coffee revealed that only decaffeinated coffee was causally associated with both KOA (OR 4.40, 95% CI 1.71-11.33, p = 0.002) and self-reported OA (OR 1.13, 95% CI 1.02-1.26, p = 0.022). In two-step MR, BMI explained over half of the coffee intake-all OA risk association, while BMD accounted for less than 5% of the mediation effect. Conclusion: Our study suggests that coffee intake increase the risk of OA, with BMI playing a significant mediating role. Decaffeinated coffee appears to have the greatest impact on OA risk compared to other types of coffee. Therefore, managing BMI and selecting appropriate types of coffee should be included in the health management of individuals who frequently consume coffee.

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.

Moderate or greater daily coffee consumption is associated with lower incidence of metabolic syndrome in Taiwanese militaries: results from the CHIEF cohort study.

Background: Daily moderate coffee intake was found with a lower risk of specific metabolic abnormalities, e.g., hypertension and hyperglycemia, while the association of coffee intake and incident metabolic syndrome (MetS) has not been clarified in prior studies, particularly in young adults. Methods: A total of 2,890 military personnel, aged 18-39 years, free of MetS were followed for incident MetS from baseline (2014) until the end of 2020 in Taiwan. Daily coffee amount consumed was grouped to those ≥3 cups or 600 mL (moderate or more amount) and those without. Incidence of MetS was identified in annual health examinations. MetS was diagnosed on the basis of the guideline of the International Diabetes Federation. Multivariable Cox regression model with adjustments for sex, age, body mass index, physical activity and substance use status at baseline was performed to determine the association. Results: At baseline, there were 145 subjects with daily coffee intake ≥3 cups or 600 mL (5.0%) in the overall cohort. During a mean follow-up of 6.0 years, 673 incident MetS (23.3%) were found. As compared to those consuming less coffee or none, those consuming daily coffee ≥3 cups had a lower risk of MetS [hazard ratio (HR): 0.69 (95% confidence interval: 0.48, 0.99)]. Conclusion: This study suggests that adhering to the guideline recommended moderate or greater daily coffee consumption for promoting health, may confer advantages in preventing the development of MetS among young adults.

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

[This corrects the article DOI: 10.3389/fendo.2023.1169933.].

Lifestyle habits and gastric cancer in an East Asian population: a Mendelian randomization study.

Background: Epidemiological evidence suggests an association between lifestyle habits (smoking, alcohol consumption, tea, coffee intake, etc.) and gastric cancer (GC). However, the causal relationship remains uncertain. Therefore, the purpose of this study was to ascertain whether there is a causal connection between them. Methods: Two-sample Mendelian randomization (MR) analysis was performed using the publicly available Genome Wide Association Study summary datasets using six methods: inverse variance weighting (IVW), weighted median, MR using a Robust Adjusted Profile Score (MR.Raps), MR using a Robust Adjusted Profile Score (MR-PRESSO), Radial regression of MR, and Causal Analysis Using Summary Effect Estimates (CAUSE). A sensitivity analysis was conducted to assess the robustness of the results. Results: In an East Asian population, we found that increased tea intake reduced the risk of GC [odds ratio (OR)= 0.90, 95% confidence interval (CI)= 0.82-0.99, P = 0.037] while there was a positive association between smoking and GC (OR = 1.58, 95% CI = 1.04-2.39, P = 0.032). No causal relationship between alcohol and coffee intake and GC. Sensitivity analyses demonstrated the robustness of these causal associations. Conclusions: Our study suggests that tea intake may reduce the risk of GC, for which smoking is a potential risk factor. Nevertheless, a larger and more diverse sample size is needed for further validation.

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 intake one hour prior to phlebotomy produces no clinically significant changes in routine biochemical test results.

Introduction: Although current guidelines recommend not drinking coffee prior to phlebotomy, our hypothesis is that drinking coffee does not affect the clinical interpretation of biochemical and haematological test results. Materials and methods: Twenty-seven volunteers were studied in basal state (T0) and 1h after (T1) drinking coffee. Routine haematological (Sysmex-XN1000 analyser) and biochemistry parameters (Vitros 4600 analyser) were studied. Results were compared using the Wilcoxon test (P < 0.05). A clinical change was considered when mean percent difference (MD%) was higher than the reference change value (RCV). Results: Coffee intake produced statistically, but not clinically, significant: i) increases in haemoglobin (P = 0.009), mean cell haemoglobin concentration (P = 0.044), neutrophils (P = 0.001), albumin (P = 0.001), total protein (P = 0.000), cholesterol (P = 0.025), high density lipoprotein cholesterol (P = 0.007), uric acid (P = 0.011), calcium (P = 0.001), potassium (P = 0.010), aspartate aminotransferase (P = 0.001), amylase (P = 0.026), and lactate dehydrogenase (P = 0.001), and ii) decreases in mean cell volume (P = 0.002), red cell distribution width (P = 0.001), eosinophils (P = 0.002), and lymphocytes (P = 0.001), creatinine (P = 0.001), total bilirubin (P = 0.012), phosphorus (P = 0.001), magnesium (P = 0.007), and chloride (P = 0.001). Conclusion: Drinking a cup of coffee 1 hour prior to phlebotomy produces no clinically significant changes in routine biochemical and haematological test results.

The association between coffee consumption and risk of incident depression and anxiety: Exploring the benefits of moderate intake.

Accumulating evidence has reported the associations of coffee consumption with physical conditions and mortality, but the associations with mental disorders were limited. The objective of this study was to examine the associations of coffee consumption with incident depression and anxiety, and to assess whether the associations differed by coffee subtypes (instant, ground, and decaffeinated coffee) or additives (milk, sugar-sweetened, and artificial-sweetened). In this prospective cohort study, we utilized data from the UK Biobank and included a total of 146,566 participants who completed the touchscreen questionnaire at baseline between 2006 and 2010. During the follow-up, incident depression and anxiety were measured in 2016 using the Patient Health Questionnaire (PHQ)-9 and the Generalised Anxiety Disorder Assessment (GAD)-7, respectively. Multivariable-adjusted logistic regression models and restricted cubic splines were used to assess the associations. Approximately 80.7% of participants reported consuming coffee, and most drank 2 to 3 cups per day (41.2%). We found J-shaped associations between coffee consumption and both incident depression and anxiety, with the lowest risk of the mental disorders occurring at around 2-3 cups per day. Results were similar for participants who drank 2-3 cups of ground coffee, milk-coffee, or unsweetened coffee. Our findings highlight that 2-3 cups of coffee consumption could be recommended as part of a healthy lifestyle to improve mental health.

Smoking, Coffee Consumption, Alcohol Intake, and Obstructive Sleep Apnea: A Mendelian Randomization Study.

BACKGROUND: Previous studies revealed that obstructive sleep apnea (OSA) and smoking, alcohol consumption, and coffee intake are closely related. This study aimed to evaluate the causal effect between these factors and OSA. METHODS: The published genome-wide association study data (GWAS) provided genetic tools. We conducted a univariable two-sample Mendelian Randomization (MR) to estimate the causal effect between smoking initiation, never smoking, alcohol consumption, coffee intake, and coffee consumption with the risk of incidence OSA. Inverse variance weighting (IVW) was used as the main method for effect evaluation, and other MR methods were used for sensitivity analysis. After adjusting for body mass index (BMI), hypertension, and diabetes respectively by multivariable MR (MVMR), we further evaluate the causal effect of these factors on OSA. RESULTS: Under univariable MR analysis, we observed that smoking initiation was associated with an increased risk of incidence OSA (OR 1.326, 95% CI 1.001-1.757, p =0.049). Never smoking was associated with decreased risk of OSA (OR 0.872, 95% CI 0.807-0.942, p <0.001). Coffee intake and coffee consumption was associated with an increased incidence of OSA (OR 1.405, 95% CI 1.065-1.854, p =0.016) and (OR 1.330, 95% CI 1.013-1.746, p =0.040). Further multivariate MR showed that the causal relationship between never smoking and OSA existed but not coffee consumption, after adjusting for diabetes and hypertension. However, the all results did not support causality after adjusting for BMI. CONCLUSION: This two-sample MR study showed that genetically predicted smoking and higher coffee intake are causally associated with an increased risk of OSA.

Associations between vitamin D levels and dietary patterns in patients with Hashimoto's thyroiditis.

Introduction: Vitamin D insufficiency is a global health problem affecting healthy and diseased individuals, including patients with Hashimoto's thyroiditis (HT). Identifying dietary factors that may affect vitamin D levels and providing dietary guidelines accordingly can alleviate this problem. We therefore aimed to identify still unknown associations of dietary patterns, assessed through the Food Frequency Questionnaire (FFQ) with vitamin D blood levels. Materials and methods: FFQ was collected from 459 patients from Croatian Biobank of Patients with Hashimoto's thyroiditis (CROHT), while total 25(OH)D was measured from their stored serum samples. We performed linear regression analysis between vitamin D levels and weekly intake of 24 food groups in 459 patients with HT (ALL), and in two disease-severity groups (MILD and OVERT). Results: The main results of our study are observations of: (1) an inverse association between vitamin D levels and coffee consumption (ALL: ß = -0.433, p = 0.005; OVERT: ß = -0.62, p = 0.008); (2) an inverse association between vitamin D levels and sweets consumption (ALL: ß = -0.195, p = 0.034; OVERT: ß = -0.431, p = 0.006); (3) positive association between vitamin D levels and vegetable consumption (ALL: ß = 0.182, p = 0.019; OVERT, ß = 0.311, p = 0.009). Importantly, effect sizes of all three associations were more prominent in HT patients with prolonged and more severe disease (OVERT). Conclusion: Further research into the functional and causal relationships of the observed associations is important to provide guidance regarding coffee/sugar intake on vitamin D status. A well-balanced diet can help prevent vitamin D deficiency and improve the quality of life of patients with HT, especially those in later stages of disease characterized by greater metabolic imbalance.

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.

Assessing the effect of interaction between lifestyle and longitudinal changes in brain structure on sleep phenotypes.

Longitudinal changes in brain structure and lifestyle can affect sleep phenotypes. However, the influence of the interaction between longitudinal changes in brain structure and lifestyle on sleep phenotypes remains unclear. Genome-wide association study dataset of longitudinal changes in brain structure was obtained from published study. Phenotypic data of lifestyles and sleep phenotypes were obtained from UK Biobank cohort. Using genotype data from UK Biobank, we calculated polygenetic risk scores of longitudinal changes in brain structure phenotypes. Linear/logistic regression analysis was conducted to evaluate interactions between longitudinal changes in brain structure and lifestyles on sleep duration, chronotype, insomnia, snoring and daytime dozing. Multiple lifestyle × longitudinal changes in brain structure interactions were detected for 5 sleep phenotypes, such as physical activity×caudate_age2 for daytime dozing (OR = 1.0389, P = 8.84 × 10-3) in total samples, coffee intake×cerebellar white matter volume_age2 for daytime dozing (OR = 0.9652, P = 1.13 × 10-4) in females. Besides, we found 4 overlapping interactions in different sleep phenotypes. We conducted sex stratification analysis and identified one overlapping interaction between female and male. Our results support the moderate effects of interaction between lifestyle and longitudinal changes in brain structure on sleep phenotypes, and deepen our understanding of the pathogenesis of sleep disorders.

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.

Self-reported and genetically predicted effects of coffee intake on rheumatoid arthritis: Epidemiological studies and Mendelian randomization analysis.

Background and aims: Causal research concerning coffee intake and rheumatoid arthritis (RA) risk is controversial. The objective of this study was to further explore the causal relationship between coffee intake and RA risk. Methods: The 4,310 participants from NHANES 2003-2006 were included in an epidemiological study to assess the association between coffee intake and RA by weighted multivariate logistic regression. The inverse variance weighted (IVW) method of two-sample Mendelian randomization (MR), employing genetic data from UK Biobank (428,860 cases) of coffee intake and MR-Base platform (14,361 cases and 43,923 controls) of RA, was performed to estimate the causal relationship between coffee intake and RA. Results: Weighted multivariate logistic regression suggested no significant correlation between coffee intake and RA. Compared to the no-coffee group, the odds ratio for RA in the <1, 1-3, ≥4 cups/day group were 1.297, 1.378, and 1.125 (P = 0.204, 0.098, and 0.698, respectively). In the IVW of MR analysis, there was no causal relationship between coffee intake and RA (OR = 1.47, P = 0.218). Conclusion: Our study did not support a causal association between coffee intake and RA risk. However, it is necessary to consider valid information on coffee intake, including brewing method, type of coffee, and quantity, in further analysis of coffee intake and RA.