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Associations between glycemic traits and colorectal cancer: a Mendelian randomization analysis

Abstract:

Background

Glycemic traits—such as hyperinsulinemia, hyperglycemia, and type 2 diabetes—have been associated with higher colorectal cancer risk in observational studies; however, causality of these associations is uncertain. We used Mendelian randomization (MR) to estimate the causal effects of fasting insulin, 2-hour glucose, fasting glucose, glycated hemoglobin (HbA1c), and type 2 diabetes with colorectal cancer.

Methods

Genome-wide association study summary data were used to identify genetic variants associated with circulating levels of fasting insulin (n = 34), 2-hour glucose (n = 13), fasting glucose (n = 70), HbA1c (n = 221), and type 2 diabetes (n = 268). Using 2-sample MR, we examined these variants in relation to colorectal cancer risk (48 214 case patient and 64 159 control patients).

Results

In inverse-variance models, higher fasting insulin levels increased colorectal cancer risk (odds ratio [OR] per 1-SD = 1.65, 95% confidence interval [CI] = 1.15 to 2.36). We found no evidence of any effect of 2-hour glucose (OR per 1-SD = 1.02, 95% CI = 0.86 to 1.21) or fasting glucose (OR per 1-SD = 1.04, 95% CI = 0.88 to 1.23) concentrations on colorectal cancer risk. Genetic liability to type 2 diabetes (OR per 1-unit increase in log odds = 1.04, 95% CI = 1.01 to 1.07) and higher HbA1c levels (OR per 1-SD = 1.09, 95% CI = 1.00 to 1.19) increased colorectal cancer risk, although these findings may have been biased by pleiotropy. Higher HbA1c concentrations increased rectal cancer risk in men (OR per 1-SD = 1.21, 95% CI = 1.05 to 1.40), but not in women.

Conclusions

Our results support a causal effect of higher fasting insulin, but not glucose traits or type 2 diabetes, on increased colorectal cancer risk. This suggests that pharmacological or lifestyle interventions that lower circulating insulin levels may be beneficial in preventing colorectal tumorigenesis.
Publication status:
Published
Peer review status:
Peer reviewed

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Publisher copy:
10.1093/jnci/djac011

Authors

More by this author
Institution:
University of Oxford
Division:
MSD
Department:
Nuffield Department of Population Health
Role:
Author
et al.


Publisher:
Oxford University Press
Journal:
Journal of the National Cancer Institute More from this journal
Volume:
114
Issue:
5
Pages:
740–752
Publication date:
2022-01-20
Acceptance date:
2022-01-12
DOI:
EISSN:
1460-2105
ISSN:
0027-8874


Language:
English
Keywords:
Pubs id:
1233127
Local pid:
pubs:1233127
Deposit date:
2022-01-20
ARK identifier:

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