RESUMO
Background: Several studies have explored the potential relationship between fruit consumption and non-small cell lung cancer (NSCLC). However, the impact of dried fruit on NSCLC risk remains unclear. Additionally, the presence of confounding variables in these observational investigations could not be avoided. Therefore, the aim of this article was to explore the potential relationship between fruits intake and NSCLC. Methods: We extracted fruit intake data from the UK Biobank and utilized a genome-wide association study (GWAS) encompassing 218,792 individuals for NSCLC data. We employed a two-sample Mendelian randomization (MR) analysis to investigate the potential causal associations between fruit intake and the risk of NSCLC. The major method of analysis was the inverse variance weighted (IVW). Furthermore, we conducted sensitivity analyses to corroborate the robustness of our findings. Results: The result of our study showed convincing evidence suggesting that dried fruit intake is effective in reducing the risk of NSCLC. Specifically, the odds ratios (ORs) for NSCLC exhibited a noteworthy reduction at 0.32 [95% confidence interval (CI): 0.15, 0.67; P=0.003] with respect to dried fruit intake. Conclusions: Our study underscores a significant correlation between dried fruit consumption and reduced NSCLC risk. In contrast, the association with fresh fruit intake did not reach statistical significance. To substantiate and validate these findings, further prospective randomized controlled trials (RCTs) are warranted in the future.
RESUMO
Background: Studying the relationship between strenuous sports or other exercises (SSOE) and lung cancer risk remains underexplored. Traditional observational studies face challenges like confounders and inverse causation. However, Mendelian randomization (MR) provides a promising approach in epidemiology and genetics, using genetic variants as instrumental variables to investigate causal relationships. By leveraging MR, we have scrutinized the causal link between SSOE and lung cancer development. Methods: Twelve single-nucleotide polymorphisms (SNPs) associated with SSOE, as identified in previously published genome-wide association studies, were utilized as instrumental variables in our investigation. Summary genetic data at the individual level were obtained from relevant studies and cancer consortia. The study encompassed a total of 11,348 cases and 15,861 controls. The statistical technique of inverse variance-weighting (IVW), commonly employed in meta-analyses and MR studies, was employed to assess the causal relationship between SSOE and lung cancer risk. Results: The MR risk analysis indicated a causal relationship between SSOE and the incidence of lung cancer, with evidence of a reduced risk for overall lung cancer [odds ratio (OR) =0.129; 95% confidence interval (CI): 0.021-0.779; P=0.03], lung adenocarcinoma (OR =0.161; 95% CI: 0.012-2.102; P=0.16) and squamous cell lung cancer (OR =0.045; 95% CI: 0.003-0.677; P=0.03). The combined OR for lung cancer from SSOE (controlling for waist circumference and smoking status) was 0.054 (95% CI: 0.010-0.302, P<0.001). Conclusions: Our MR analysis findings indicate a potential correlation between SSOE and a protective effect against lung cancer development. Further investigation is imperative to uncover the precise mechanistic link between them.
