Abstract
Background
The role of the metabolic syndrome in the etiology of esophageal and gastric cancer is unclear.
Methods
This was a large nationwide cohort study based on data from 11 prospective population-based cohorts in Norway with long-term follow-up, the Cohort of Norway (CONOR) and the third Nord-Trøndelag Health Study (HUNT3). The metabolic syndrome was assessed by objective anthropometric and metabolic biochemical measures and was defined by the presence of at least three of the following five factors: increased waist circumference, elevated triglycerides, low high-density lipoprotein cholesterol, hypertension and high glucose. Newly diagnosed cases of esophageal adenocarcinoma, esophageal squamous-cell carcinoma and gastric adenocarcinoma were identified from the Norwegian Cancer Registry. Hazard ratios (HRs) and 95 % confidence intervals (CIs) were estimated using Cox proportional hazard models with adjustment for potential confounders.
Result
Among 192,903 participants followed up for an average of 10.6 years, 62 developed esophageal adenocarcinoma, 64 had esophageal squamous-cell carcinoma and 373 had gastric adenocarcinoma. The metabolic syndrome was significantly associated with an increased risk of gastric adenocarcinoma (HR 1.44, 95 % CI 1.14–1.82), but not associated with esophageal adenocarcinoma (HR 1.32, 95 % CI 0.77–2.26) or esophageal squamous-cell carcinoma (HR 1.08, 95 % CI 0.64–1.83). Increased waist circumference was associated with an increased HR of esophageal adenocarcinoma (HR 2.48, 95 % CI 1.27–4.85). No significant association was found between any single component of the metabolic syndrome and risk of esophageal squamous-cell carcinoma. High waist circumference (HR 1.71, 95 % CI 1.05–2.80), hypertension (HR 2.41, 95 % CI 1.44–4.03) and non-fasting glucose (HR 1.74, 95 % CI 1.18–2.56) were also related to an increased risk of gastric adenocarcinoma in women, but not in men.
Conclusion
Metabolic syndrome was associated with an increased risk of gastric adenocarcinoma in women. Of the individual components of the metabolic syndrome, high waist circumference was positively associated with risk of esophageal adenocarcinoma. Positive associations were also observed for women between high waist circumference, hypertension, high non-fasting glucose and risk of gastric adenocarcinoma. However, further evidence is warranted due to the limited number of cases and the inability to effectively identify gastric cardia adenocarcinoma.
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Acknowledgments
The authors wish to acknowledge the services of CONOR, the contributing research centers delivering data to CONOR and all the study participants. The following cohorts from CONOR were used in the analysis: Tromsø IV and V, TROFINN, HUNT2, Oslo I, HUBRO, The Immigrant Study, MoRo, Oslo II, OPPHED, and HUSK. The Nord-Trøndelag Health Study (The HUNT Study) is performed through collaboration between HUNT Research Centre (Faculty of Medicine, Norwegian University of Science and Technology NTNU), Nord-Trøndelag County Council, Central Norway Health Authority, and the Norwegian Institute of Public Health. The study has used data from the Cancer Registry of Norway. The interpretation and reporting of these data are the sole responsibility of the authors, and no endorsement by the Cancer Registry of Norway is intended nor should be inferred.
Author contributions
All authors designed and conceptualized the article. Eivind Ness-Jensen and Kristian Hveem provided provision of study materials. Eivind Ness-Jensen, Kristian Hveem and Yunxia Lu collected and assembled data. Yulan Lin, Eivind Ness-Jensen, Jesper Lagergren and Yunxia Lu analyzed and interpreted the data. All authors wrote the manuscript.
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This work was supported by the Faculty Funds for Partial Financing of New Doctoral Students from Karolinska Institutet (12059012/KID-medel 2010); the Swedish Research Council (SIMSAM); and the Swedish Society of Medicine.
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The authors declare that they have no conflict of interests.
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Lin, Y., Ness-Jensen, E., Hveem, K. et al. Metabolic syndrome and esophageal and gastric cancer. Cancer Causes Control 26, 1825–1834 (2015). https://doi.org/10.1007/s10552-015-0675-4
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DOI: https://doi.org/10.1007/s10552-015-0675-4