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Nutrition in acute and chronic diseases

High-density lipoprotein, low-density lipoprotein and triglyceride levels and upper gastrointestinal cancers risk: a trans-ancestry Mendelian randomization study

European Journal of Clinical Nutrition volume 76, pages 995–1002 (2022)Cite this article

Subjects

Abstract

Objective

This study was conducted to explore the causal associations of high-density lipoprotein (HDL), low-density lipoprotein (LDL) and triglyceride (TG) with the risk of upper gastrointestinal cancers (esophageal cancer [EC] and gastric cancer [GC]).

Methods

A total of 5623 Chinese and 4133 Europeans afforded the individual-level genotyping data, and 203,608 Japanese from Biobank Japan project and 393,926 Europeans from UK Biobank supported summary statistics of cancer genetic associations. Mendelian randomization (MR) analyses, including weighted genetic risk scores (wGRSs), inverse-variance weighted (IVW), weighted median and Egger-regression, were utilized to evaluate the causal effects of three blood lipids on upper gastrointestinal cancers risk.

Results

There was no significantly causal relationships between three blood lipids and EC or GC risk among Chinese or Europeans but a potential causal association between TG and GC risk among Japanese (IVW: odds ratio [OR] = 1.11, P = 0.034; Phet = 0.679). In stratified subgroups, higher genetically predicted TG levels were causally associated with an increased risk of GC among Chinese males (wGRS: OR = 1.61, P = 0.021; IVW: OR = 1.57, P = 0.009; Phet = 0.653) and Japanese females (IVW: OR = 1.33, P = 0.024; Phet = 0.378).

Conclusion

This trans-ancestry MR study suggested null significant causality between serum HDL, LDL or TG and the risk of upper gastrointestinal cancers among Chinese and Europeans, but provided evidence for a causal role of TG involved in GC etiology in Japanese (especially females), which would support a prevention guide for high-risk groups of GC. Further research with more comprehensive information is needed to explore the underlying mechanism.

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Fig. 1: Flow chart for process of our study.

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Data availability

Individual genotyping data of Chinese and European ancestry were obtained from dbGaP datasets (phs000361.v1.p1 and phs000869.v1.p1, respectively). Summary statistics of genetic associations with gastric cancer risk were extracted from UK Biobank single variant association analysis results at Lee Lab (https://www.leelabsg.org/resources). 1Shanxi and Linxian NIT: dbGaP, phs000361.v1.p1. 2BEAGESS: dbGaP, phs000869.v1.p1. 3BBJ GWAS summary statistics: http://jenger.riken.jp/en/result. 4UK Biobank GWAS summary statistics at Lee Lab: https://www.leelabsg.org/resources.

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Acknowledgements

The authors gratefully acknowledge the participants and staff involved in the development of dbGaP, Biobank Japan project and UK Biobank database for their dedication and effort. This study was supported by the National Key R&D Program of China (grants 2018YFC1313100, 2018YFC1313102), and partially by the National Key R&D Program of China (2017YFC1309201), and the Priority Academic Program Development of Jiangsu Higher Education Institutions (Public Health and Preventive Medicine).

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Author notes

  1. These authors contributed equally: Yanling Wu, Junyi Xin.

Authors and Affiliations

  1. Department of Environmental Genomics, Jiangsu Key Laboratory of Cancer Biomarkers, Prevention and Treatment, Collaborative Innovation Center for Cancer Personalized Medicine, School of Public Health, Nanjing Medical University, Nanjing, China

    Yanling Wu, Junyi Xin, Shuwei Li, Meilin Wang, Haiyan Chu & Zhengdong Zhang

  2. Department of Genetic Toxicology, The Key Laboratory of Modern Toxicology of Ministry of Education, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, China

    Yanling Wu, Junyi Xin, Shuwei Li, Meilin Wang, Haiyan Chu & Zhengdong Zhang

  3. Center for Disease Control and Prevention of Wuzhong District in Suzhou, Suzhou, China

    Yanling Wu

  4. Department of Clinical Genetics, Erasmus MC University Medical Center, Rotterdam, the Netherlands

    Elizabeth A. Loehrer

  5. Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institute, Nobels vagen 13, Stockholm, Sweden

    Xia Jiang

  6. Departments of Environmental Health, Harvard T.H. Chan School of Public Health, 677 Huntington Avenue, Boston, MA, 02115, USA

    Qianyu Yuan & David C. Christiani

  7. Department of Medicine, Massachusetts General Hospital, 55 Fruit Street, Boston, MA, 02114, USA

    David C. Christiani

  8. Departments of Gastrointestinal Surgery and Department of Clinical Nutrition, Beijing Shijitan Hospital, Capital Medical University, Beijing, China

    Hanping Shi

  9. Department of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China

    Lingxiang Liu

  10. Department of Biostatistics, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, China

    Mulong Du

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  1. Yanling Wu
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Contributions

ZZ, MD and HC are coresponders for this study. YW and JX contributed equally. ZZ, MD, JX and YW developed the study concept and design. YW and JX performed data analysis and interpretation. EL, XJ, QY, DC, HS, LL, MW, SL and HC assisted interpretation of results. YW and JX drafted the article. All authors revised the text and approved the final manuscript.

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Correspondence to Haiyan Chu, Mulong Du or Zhengdong Zhang.

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Wu, Y., Xin, J., Loehrer, E.A. et al. High-density lipoprotein, low-density lipoprotein and triglyceride levels and upper gastrointestinal cancers risk: a trans-ancestry Mendelian randomization study. Eur J Clin Nutr 76, 995–1002 (2022). https://doi.org/10.1038/s41430-022-01078-6

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