A Mendelian randomization study reveals a causal relationship between tea consumption and esophageal cancer

Research Article
Open access

A Mendelian randomization study reveals a causal relationship between tea consumption and esophageal cancer

Shuang Deng 1* , Hongling Zeng 2 , Pingping Zhou 3 , Zhongqiang Guo 4
  • 1 Tianhua College, Shanghai Normal University, Shanghai, China    
  • 2 Tianhua College, Shanghai Normal University, Shanghai, China    
  • 3 Tianhua College, Shanghai Normal University, Shanghai, China    
  • 4 School of Nursing and Health, Henan University, Kaifeng, China    
  • *corresponding author naidou1017@gmail.com
JCTT Vol.3 Issue 2
ISSN (Print): 3049-5466
ISSN (Online): 3049-5458

Abstract

This study aims to evaluate the causal relationship between tea consumption and esophageal cancer using a bidirectional Mendelian Randomization (MR) approach. Methodologically, genetic instruments for tea intake were derived from a Genome-Wide Association Study (GWAS) involving 447,485 participants in the UK Biobank. Thirty-nine tea-associated Single Nucleotide Polymorphisms (SNPs) were selected and analyzed using two-sample MR to examine causality. The esophageal cancer data were obtained from the NA consortium’s publicly available GWAS, which includes 998 cases and 475,308 controls. A reverse MR analysis was also conducted to explore potential reverse causality. The results demonstrate a causal link between tea consumption and esophageal cancer. Specifically, using the inverse-variance weighted (IVW) method, a one standard deviation increase in tea intake was associated with a 194.5% increase in esophageal cancer risk (OR = 2.945, 95% CI: 1.794–4.833). Similar results were observed using the weighted mode (OR = 5.590, 95% CI: 2.713–11.519) and weighted median (OR = 4.446, 95% CI: 2.260–8.748) methods. The IVW method again showed a consistent result (OR = 2.945, 95% CI: 1.551–5.592). However, there was no evidence supporting reverse causality (IVW: P > 0.05). Overall, genetic evidence from bidirectional MR analyses indicates that increased tea consumption raises the risk of esophageal cancer, although no reverse causal relationship was found.

Keywords:

tea consumption, esophageal cancer, mendelian randomization, causality, genetic epidemiology

Deng,S.;Zeng,H.;Zhou,P.;Guo,Z. (2025). A Mendelian randomization study reveals a causal relationship between tea consumption and esophageal cancer. Journal of Clinical Technology and Theory,3(2),23-29.
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References

[1]. Sheikh, M., Roshandel, G., McCormack, V., & Malekzadeh, R. (2023). Current status and future prospects for esophageal cancer. Cancers, 15(3), 765.

[2]. Li, J., Xu, J., Zheng, Y., Gao, Y., He, S., Li, H., ... & He, J. (2021). Esophageal cancer: Epidemiology, risk factors and screening. Chinese Journal of Cancer Research, 33(5), 535.

[3]. Napier, K. J., Scheerer, M., & Misra, S. (2014). Esophageal cancer: A review of epidemiology, pathogenesis, staging workup and treatment modalities. World journal of gastrointestinal oncology, 6(5), 112.

[4]. Testa, U., Castelli, G., & Pelosi, E. (2023). The molecular characterization of genetic abnormalities in esophageal squamous cell carcinoma may foster the development of targeted therapies. Current Oncology, 30(1), 610-640.

[5]. Zhang, W., Bailey-Wilson, J. E., Li, W., Wang, X., Zhang, C., Mao, X., ... & Wu, M. (2000). Segregation analysis of esophageal cancer in a moderately high–incidence area of northern China. The American Journal of Human Genetics, 67(1), 110-119.

[6]. Sohda, M., & Kuwano, H. (2017). Current status and future prospects for esophageal cancer treatment. Annals of Thoracic and Cardiovascular Surgery, 23(1), 1-11.

[7]. Tang, G. Y., Meng, X., Gan, R. Y., Zhao, C. N., Liu, Q., Feng, Y. B., ... & Li, H. B. (2019). Health functions and related molecular mechanisms of tea components: an update review. International journal of molecular sciences, 20(24), 6196.

[8]. Gao, Y. T., McLaughlin, J. K., Blot, W. J., Ji, B. T., Dai, Q., & Fraumeni, J. F. (1994). Reduced risk of esophageal cancer associated with green tea consumption. JNCI: Journal of the National Cancer Institute, 86(11), 855-858.

[9]. Trisha, A. T., Shakil, M. H., Talukdar, S., Rovina, K., Huda, N., & Zzaman, W. (2022). Tea polyphenols and their preventive measures against cancer: Current trends and directions. Foods, 11(21), 3349.

[10]. Sekula, P., Fabiola Del Greco, M., Pattaro, C., & Köttgen, A. (2016). Mendelian randomization as an approach to assess causality using observational data. Journal of the American Society of Nephrology, 27(11), 3253-3265.

[11]. Taschler, B., Smith, S. M., & Nichols, T. E. (2022). Causal inference on neuroimaging data with Mendelian randomisation. NeuroImage, 258, 119385.

[12]. Bowden, J., & Holmes, M. V. (2019). Meta‐analysis and Mendelian randomization: a review. Research synthesis methods, 10(4), 486-496.

[13]. Bucur, I. G., Claassen, T., & Heskes, T. (2020). Inferring the direction of a causal link and estimating its effect via a Bayesian Mendelian randomization approach. Statistical Methods in Medical Research, 29(4), 1081-1111.

[14]. Hemani, G., Zheng, J., Elsworth, B., Wade, K. H., Haberland, V., Baird, D., ... & Haycock, P. C. (2018). The MR-Base platform supports systematic causal inference across the human phenome. eLife, 7, e34408.

[15]. Deng, Y., Ge, W., Xu, H., & Zhang, J. (2022). A Mendelian randomization study of the effect of tea intake on breast cancer. Frontiers in Nutrition, 9, 956969.

[16]. Chen, S., Chen, T., Chen, Y., Huang, D., Pan, Y., & Chen, S. (2022). Causal association between tea consumption and bone health: a mendelian randomization study. Frontiers in Nutrition, 9, 872451.

[17]. Sun, Q., Gao, N., Song, J., Jia, J., Dong, A., & Xia, W. (2024). The association between tea consumption and non-malignant digestive system diseases: a Mendelian randomized study. Clinical Nutrition ESPEN, 60, 327-332.

[18]. Kim, Y., & Je, Y. (2024). Tea consumption and risk of all-cause, cardiovascular disease, and cancer mortality: a meta-analysis of thirty-eight prospective cohort data sets. Epidemiology and Health, 46, e2024056.

Cite this article

Deng,S.;Zeng,H.;Zhou,P.;Guo,Z. (2025). A Mendelian randomization study reveals a causal relationship between tea consumption and esophageal cancer. Journal of Clinical Technology and Theory,3(2),23-29.

Data availability

The datasets used and/or analyzed during the current study will be available from the authors upon reasonable request.

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Journal：Journal of Clinical Technology and Theory

Volume number: Vol.3
Issue number: Issue 2
ISSN：3049-5458(Print) / 3049-5466(Online)

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References

[1]. Sheikh, M., Roshandel, G., McCormack, V., & Malekzadeh, R. (2023). Current status and future prospects for esophageal cancer. Cancers, 15(3), 765.

[2]. Li, J., Xu, J., Zheng, Y., Gao, Y., He, S., Li, H., ... & He, J. (2021). Esophageal cancer: Epidemiology, risk factors and screening. Chinese Journal of Cancer Research, 33(5), 535.

[3]. Napier, K. J., Scheerer, M., & Misra, S. (2014). Esophageal cancer: A review of epidemiology, pathogenesis, staging workup and treatment modalities. World journal of gastrointestinal oncology, 6(5), 112.

[4]. Testa, U., Castelli, G., & Pelosi, E. (2023). The molecular characterization of genetic abnormalities in esophageal squamous cell carcinoma may foster the development of targeted therapies. Current Oncology, 30(1), 610-640.

[5]. Zhang, W., Bailey-Wilson, J. E., Li, W., Wang, X., Zhang, C., Mao, X., ... & Wu, M. (2000). Segregation analysis of esophageal cancer in a moderately high–incidence area of northern China. The American Journal of Human Genetics, 67(1), 110-119.

[6]. Sohda, M., & Kuwano, H. (2017). Current status and future prospects for esophageal cancer treatment. Annals of Thoracic and Cardiovascular Surgery, 23(1), 1-11.

[7]. Tang, G. Y., Meng, X., Gan, R. Y., Zhao, C. N., Liu, Q., Feng, Y. B., ... & Li, H. B. (2019). Health functions and related molecular mechanisms of tea components: an update review. International journal of molecular sciences, 20(24), 6196.

[8]. Gao, Y. T., McLaughlin, J. K., Blot, W. J., Ji, B. T., Dai, Q., & Fraumeni, J. F. (1994). Reduced risk of esophageal cancer associated with green tea consumption. JNCI: Journal of the National Cancer Institute, 86(11), 855-858.

[9]. Trisha, A. T., Shakil, M. H., Talukdar, S., Rovina, K., Huda, N., & Zzaman, W. (2022). Tea polyphenols and their preventive measures against cancer: Current trends and directions. Foods, 11(21), 3349.

[10]. Sekula, P., Fabiola Del Greco, M., Pattaro, C., & Köttgen, A. (2016). Mendelian randomization as an approach to assess causality using observational data. Journal of the American Society of Nephrology, 27(11), 3253-3265.

[11]. Taschler, B., Smith, S. M., & Nichols, T. E. (2022). Causal inference on neuroimaging data with Mendelian randomisation. NeuroImage, 258, 119385.

[12]. Bowden, J., & Holmes, M. V. (2019). Meta‐analysis and Mendelian randomization: a review. Research synthesis methods, 10(4), 486-496.

[13]. Bucur, I. G., Claassen, T., & Heskes, T. (2020). Inferring the direction of a causal link and estimating its effect via a Bayesian Mendelian randomization approach. Statistical Methods in Medical Research, 29(4), 1081-1111.

[14]. Hemani, G., Zheng, J., Elsworth, B., Wade, K. H., Haberland, V., Baird, D., ... & Haycock, P. C. (2018). The MR-Base platform supports systematic causal inference across the human phenome. eLife, 7, e34408.

[15]. Deng, Y., Ge, W., Xu, H., & Zhang, J. (2022). A Mendelian randomization study of the effect of tea intake on breast cancer. Frontiers in Nutrition, 9, 956969.

[16]. Chen, S., Chen, T., Chen, Y., Huang, D., Pan, Y., & Chen, S. (2022). Causal association between tea consumption and bone health: a mendelian randomization study. Frontiers in Nutrition, 9, 872451.

[17]. Sun, Q., Gao, N., Song, J., Jia, J., Dong, A., & Xia, W. (2024). The association between tea consumption and non-malignant digestive system diseases: a Mendelian randomized study. Clinical Nutrition ESPEN, 60, 327-332.

[18]. Kim, Y., & Je, Y. (2024). Tea consumption and risk of all-cause, cardiovascular disease, and cancer mortality: a meta-analysis of thirty-eight prospective cohort data sets. Epidemiology and Health, 46, e2024056.

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