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Associations between six dietary habits and risk of hepatocellular carcinoma: A Mendelian randomization study.

ABSTRACT: Diet is reported to be associated with hepatocellular carcinoma (HCC), but whether there is a causal relationship remains unclear. This study aimed to explore the potential causal associations between dietary habits and HCC risk using Mendelian randomization in an East Asian population. From the BioBank Japan, we obtained summary-level genome-wide association studies data for the following six dietary habits: ever/never drinker (n = 165,084), alcohol consumption (n = 58,610), coffee consumption (n = 152,634), tea consumption (n = 152,653), milk consumption (n = 152,965), and yoghurt consumption (n = 152,097). We also obtained data on HCC (1866 cases and 195,745 controls). Single-nucleotide polymorphisms (SNPs) that were associated with exposures (p < 5 × 10^-8 ) were selected as instrumental variables (IVs). Five, two, and six SNPs were identified for ever/never drinkers, alcohol consumption, and coffee consumption. One SNP was used for consumption of tea, milk, and yoghurt. The odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by inverse variance weighted (for an IV with more than one SNP) or Wald ratio (for an IV with one SNP). Ever/never drinkers (OR, 1.11; 95% CI, 1.05-1.18; p < 0.001) and alcohol consumption (OR, 1.57; 95% CI, 1.32-1.86; p < 0.001) were positively associated with HCC risk. Conversely, coffee consumption was inversely related to HCC risk (OR, 0.69; 95% CI, 0.53-0.90; p = 0.007). Similar inverse associations were observed for consumption of tea, milk, and yoghurt, with ORs (95% CIs) of 0.11 (0.05-0.26), 0.18 (0.09-0.34), and 0.18 (0.09-0.34), respectively (all p < 0.001). Conclusion: There are potential causal associations between six dietary habits and HCC risk. Our findings inform clinical practice by providing evidence on the impact of dietary habits on HCC.

SUBMITTER: Deng Y

PROVIDER: S-EPMC9315115 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundOxidative stress is currently considered to be closely related to the occurrence of respiratory tumors, especially lung cancer. Many observational studies have shown that increased antioxidant intake can reduce the risk of lung cancer, but the results are still controversial. Therefore, we performed a two-sample Mendelian randomized (MR) analysis to clarify the causal relationship between antioxidant vitamins and lung cancer.MethodsTo assess the causal effect of dietary antioxidant vitamin intake on lung cancer, we conducted a two-sample MR analysis and we extracted single-nucleotide polymorphisms (SNPs) that are associated with antioxidants from genome-wide association studies (GWASs) of the UK biobank. We gathered summary data for lung cancer from the International Lung Cancer Consortium (ILCCO), including 11,348 cases and 15,861 controls, and applied the inverse-variance weighted (IVW) method as the primary MR analysis, and performed a sensitivity analysis to verify the results.ResultsThe results showed that higher dietary retinol intake was causally associated with lung cancer overall [odds ratio (OR) = 1.844, 95% CI, 1.359-2.502, p = 0.00009], squamous cell lung cancer (OR = 2.162, 95% CI, 1.117-4.183, p = 0.022), and lung adenocarcinoma (OR = 1.706, 95% CI, 1.084-2.685, p = 0.021). Additionally, carotene was positively correlated with lung adenocarcinoma (OR = 1.510, 95% CI, 1.002-2.276, p = 0.049). However, there was a non-significant relationship between the intake of other dietary antioxidants (vitamin C and vitamin E) and lung cancer.ConclusionOur research showed that dietary retinol intake has an adverse impact on lung cancer, and carotene might increase the risk of adenocarcinoma. This highlights the importance of revealing the underlying mechanisms of dietary antioxidant vitamins in lung cancer and delivers an important health message that dietary antioxidant vitamin intake may not be necessary for the prevention of lung cancer. It also provides a basis for future research.

Project description:ObjectiveObservational research has indicated a potential link between dietary salt intake and susceptibility to dementia. However, it is important to note that these types of studies are prone to the issues of reverse causation and residual confounding. Therefore, we conducted a two-sample Mendelian randomization (MR) study to explore the causality.MethodTo explore the causal relationship between them, this Mendelian randomization (MR) study incorporated summary statistics of dietary salt intake and dementia. We estimated the causality between salt intake and the risk of overall dementia and various subtypes of dementia, including Alzheimer's disease (AD), Vascular dementia (VaD), and Lewy body dementia (LBD). The inverse variance-weighted (IVW) method was the major MR analysis. To conduct sensitivity analyses, we employed various MR methods, the pleiotropy residual sum and outlier (MR-PRESSO) method, and the leave-one-out approach. The MR-Egger intercept and Cochran's Q test were conducted to test pleiotropy and heterogeneity respectively.ResultsA suggestive association was observed for genetically predicted higher dietary salt intake and increased risk of overall dementia in the European ancestry [odds ratio (OR): 1.542; 95% confidence interval (95% CI): 1.095-2.169; P = 0.013]. The causal relationship between dietary salt intake and overall dementia is robust with respect to the choice of statistical methods and is validated through extensive sensitivity analyses that guard against various model assumption violations. Meanwhile, no clear heterogeneity or pleiotropy was identified. However, we failed to detect a causal effect of dietary salt intake on the risk of various dementia subtypes.ConclusionThe results of this research present strong evidence that established a significant association between dietary salt intake and the likelihood of developing dementia. These findings reinforce the notion that the amount of dietary salt intake plays a crucial role in determining the risk of acquiring this cognitive condition. By establishing a definitive correlation, this study highlights the importance of reducing salt consumption as a preventive measure against dementia.

Project description:Observational studies have shown an association between liver dysfunction and hepatocellular carcinoma (HCC), but the causality relationship between them is unclear. We aimed to determine whether there is a bidirectional causal relationship between liver function indicators (alanine aminotransferase, ALT; aspartate aminotransferase, AST; alkaline phosphatase, ALP; γ-glutamyltransferase, GGT) and HCC. Our two-sample Mendelian randomization (MR) study acquired single nucleotide polymorphisms (SNPs) associated with liver function indicators (ALT, n = 134,182; AST, n = 134,154; GGT, n = 118,309; ALP, n = 105,030) and with HCC (n = 197,611) from publicly available genome-wide association studies (GWAS) of East Asian ancestry in Japan (BioBank Japan, BBJ). Univariable MR analyses were performed to identify whether the genetic evidence of exposure was significantly associated with outcome. Multivariable MR analysis was conducted to estimate the independent effects of exposures on outcome. Univariable MR analysis indicated that the level of ALT, AST, and GGT was the risk factor for HCC incidence. Meanwhile, multivariable MR analysis revealed that AST was an independent risk factor for HCC. The hazard ratio (HR) of the probability of HCC was 3.045 [95% confidence interval (95%CI), 1.697-5.463, p = 0.003] for AST. The results of reverse MR analyses showed that gene-predictive HCC incidence could increase the levels of AST (HR = 1.031, 95%CI: 1.009-1.054, p = 2.52 × 10-4) and ALT (HR = 1.040, 95%CI: 1.019-1.063, p = 0.005). Meanwhile, HCC may be negatively correlated with ALP levels (HR = 0.971, 95%CI: 0.947-0.995, p = 0.018). This study provides evidence to support that genetically predicted higher levels of AST are related to increased risk of HCC, with no strong evidence of a causal effect of genetically predicted ALP, ALP, and GGT on HCC. In addition, genetic predisposition to HCC could influence blood concentration of ALT, AST, and ALP. Thus, this may create a vicious cycle.

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Associations between six dietary habits and risk of hepatocellular carcinoma: A Mendelian randomization study.

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