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Cancer Causes & Control
Published in: Cancer Causes & Control 3/2015

01-03-2015 | Original paper

Blood lipids and colorectal polyps: testing an etiologic hypothesis using phenotypic measurements and Mendelian randomization

Authors: Michael N. Passarelli, Polly A. Newcomb, Karen W. Makar, Andrea N. Burnett-Hartman, John D. Potter, Melissa P. Upton, Lee-Ching Zhu, Michael E. Rosenfeld, Stephen M. Schwartz, Carolyn M. Rutter

Published in: Cancer Causes & Control | Issue 3/2015

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Abstract

Purpose

Studies linking cholesterol levels to the development of colorectal neoplasia are inconsistent, and Mendelian randomization has been suggested as a way to help avoid problems with confounding and reverse causation.

Methods

We genotyped individuals who received a colonoscopy at Group Health (1998–2007) for 96 of 102 single-nucleotide polymorphisms identified by the Global Lipids Genetics Consortium. Participants included 139 advanced adenoma cases, 518 non-advanced adenoma cases, 380 non-adenomatous polyp cases, and 754 polyp-free controls. All had at least one available pre-colonoscopy lipid measurement from electronic records maintained by Group Health.

Results

Advanced adenoma cases were more likely than controls to have higher pre-colonoscopy zenith low-density lipoprotein (LDL), triglycerides (TG), and total cholesterol (TC) (odds ratio, OR per 20 mg/dL LDL increase: 1.16, 95 % confidence interval, CI 1.03–1.30; per 40 mg/dL TG increase: 1.09, 1.03–1.16; and per 20 mg/dL TC increase: 1.09, 1.02–1.18). For these traits, genotype–polyp ORs using weighted allele scores were not statistically significant (OR per increase in score scaled to a 20 mg/dL LDL increase: 1.17, 0.78–1.75; a 40 mg/dL TG increase: 1.12, 0.91–1.38; a 20 mg/dL TC increase: 0.99, 0.71–1.38).

Conclusions

Cholesterol levels may be associated with advanced adenomas, but larger studies are warranted to determine whether this association can be attributed to genetics.
Appendix
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Metadata
Title
Blood lipids and colorectal polyps: testing an etiologic hypothesis using phenotypic measurements and Mendelian randomization
Authors
Michael N. Passarelli
Polly A. Newcomb
Karen W. Makar
Andrea N. Burnett-Hartman
John D. Potter
Melissa P. Upton
Lee-Ching Zhu
Michael E. Rosenfeld
Stephen M. Schwartz
Carolyn M. Rutter
Publication date
01-03-2015
Publisher
Springer International Publishing
Published in
Cancer Causes & Control / Issue 3/2015
Print ISSN: 0957-5243
Electronic ISSN: 1573-7225
DOI
https://doi.org/10.1007/s10552-015-0526-3

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