Search

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. [ABSTRACT FROM AUTHOR]

Purpose: The perceived benefits and risks associated with seed oil intake remain controversial, with a limited number of studies investigating the impact of intake on a range of compounds used as cardiometabolic markers. This study aimed to explore the proteomic and cardiometabolic effects of commonly consumed seed oils in the UK, with different fatty acid profiles. Methods: In a parallel randomised control design, healthy adults (n = 84), aged 25–72 with overweight or obesity were randomised to one of three groups: control (habitual diet, CON); 20 mL rapeseed oil per day (RO), or 20 mL sunflower oil per day (SO). Blood, spot urine and anthropometric measures were obtained at 0, 6 and 12 weeks. Proteomic biomarkers analysis was conducted for coronary arterial disease (CAD) and chronic kidney disease (CKD) using capillary electrophoresis coupled to mass spectrometry (CE-MS). Blood lipids, fasting blood glucose, glycative/oxidative stress and inflammatory markers were also analysed. Results: No differences in change between time points were observed between groups for CAD or CKD peptide fingerprint scores. No change was detected within groups for CAD or CKD scores. No detectable differences were observed between groups at week 6 or 12 for the secondary outcomes, except median 8-isoprostane, ~ 50% higher in the SO group after 12-weeks compared to RO and CON groups (p = 0.03). Conclusion: The replacement of habitual fat with either RO or SO for 12 weeks does not lead to an improvement or worsening in cardiovascular health markers in people with overweight or obesity. Trial registration: Trial registration clinicaltrials.gov NCT04867629, retrospectively registered 30/04/2021. [ABSTRACT FROM AUTHOR]

Fat mass and fat-free mass are found to be associated with different health outcomes in observational studies, but the underlying causality remains unclear. We aimed to investigate the causal relationships between body composition and cardiometabolic traits using a two-sample Mendelian randomization (MR) approach. Independent genetic variants associated with body fat mass, fat-free mass, and fat percentage in UK Biobank population were used as genetic instrumental variables, and their causal effects on circulatory diseases, type 2 diabetes, glycemic traits, and lipid fractions were estimated from large-scale genome-wide association studies (GWAS) in European populations. Univariable, multivariable, and bidirectional MR analyses were performed. Genetically predicted high fat mass and fat percentage significantly increased risks of most cardiometabolic diseases, and high fat-free mass had protective effects on most cardiometabolic diseases after accounting for fat mass. Fat mass, fat-free mass, and fat percentage were all positively associated with higher risks of atrial fibrillation and flutter, varicose veins, and deep vein thrombosis and pulmonary embolism. High fat mass increased fasting glucose, homeostasis model assessment-insulin resistance (HOMA-IR), triglycerides, decreased high-density lipoprotein cholesterol, and high fat-free mass reduced HOMA-IR, triglycerides, and low-density lipoprotein cholesterol. Genetically predicted fat-free mass was bidirectionally negatively associated with 2-h glucose and total cholesterol. The findings may be helpful in risk stratification and tailoring management of body composition in patients with different cardiometabolic statuses. [ABSTRACT FROM AUTHOR]