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Plasma lipid levels and colorectal adenoma risk

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Abstract

Purpose

Abnormalities in lipid levels have been associated with colorectal neoplasm risk; however, few studies have adjusted for use of cholesterol-lowering medications. The objective of this study was to determine the association of plasma lipid levels with adenoma risk while accounting for statin medication use.

Methods

We included 254 subjects with advanced adenoma, 246 with single small adenoma, 179 with multiple small adenoma cases, and 403 control participants in the Tennessee Colorectal Polyp Study who also had plasma lipid measurements performed. Data on the use of statin medications were available for 83.4 % of these participants. The association between plasma lipids and adenoma risk was evaluated using logistic regression models.

Results

Participants in the highest quartile of HDL cholesterol (range 52–106 mg/dl) had an adjusted odds ratio of 0.49 (95 % CI 0.23, 1.07), 0.35 (95 % CI 0.13, 0.91), and 0.22 (95 % CI 0.09, 0.54) for single small, multiple small, and advanced adenomas compared to the lowest quartile (range 12–34 mg/dl), respectively. Participants with the highest quartile of triglyceride levels (range 178–721 mg/dl) had an adjusted odds ratio of 2.40 (95 % CI 1.26, 4.55), 1.67 (95 % CI 0.66, 4.23), and 2.79 (95 % CI 1.25, 6.23) for single small, multiple small, and advanced adenoma, respectively, compared to the lowest quartile (range 40–84 mg/dl). When restricted to individuals with known statin medication use, adjusting for statin use did not appreciably affect these results.

Conclusion

We found a direct association between triglyceride plasma levels and an inverse association between plasma HDL cholesterol levels and adenoma risk. Both effects were not appreciably changed when accounting for the regular use of statin medication.

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Acknowledgments

We thank Regina Courtney and Jie Wu for their excellent laboratory assistant, and Kimberly Campbell for lipid assays. This study was supported through the National Institute of Health Grants P50CA 95103, R01CA97386, R01CA143288, and R01HL106845. Surveys and sample collection, processing, and preparation for this study were conducted by the Survey and Biospecimen Shared Resource, which is supported in part by P30CA068485. The content of this paper is solely the responsibility of the authors and does not necessarily represent the official views of the National Cancer Institute or the National Institutes of Health. A portion of this material is the result of work supported with resources and the use of facilities at the VA Tennessee Valley Healthcare System.

Conflict of interest

The authors declare that they have no conflict of interest.

Author information

Authors and Affiliations

  1. Florida State University College of Medicine, Tallahassee, FL, USA

    John-Anthony Coppola

  2. Division of General Internal Medicine and Public Health, Vanderbilt University School of Medicine, 6012 Medical Center East, 1215 21st Avenue South, Nashville, TN, 37232-8300, USA

    Harvey J. Murff

  3. Department of Veterans Affairs, GRECC, Tennessee Valley Healthcare System, Nashville, TN, USA

    Martha J. Shrubsole, Wei Zheng & Harvey J. Murff

  4. Division of Epidemiology, Vanderbilt University School of Medicine, Nashville, TN, USA

    Martha J. Shrubsole, Qiuyin Cai, Qi Dai & Wei Zheng

  5. Department of Preventive Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA

    Walter E. Smalley

  6. Division of Gastroenterology, Vanderbilt University School of Medicine, Nashville, TN, USA

    Walter E. Smalley & Reid M. Ness

  7. Center for Preventive Cardiology of the Knight Cardiovascular Institute, Oregon Health & Science University, Portland, Hillsboro, OR, USA

    Sergio Fazio

  8. Vanderbilt Ingram Cancer Center, Nashville, TN, USA

    Martha J. Shrubsole, Qiuyin Cai, Qi Dai, Wei Zheng & Harvey J. Murff

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  1. John-Anthony Coppola
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Correspondence to Harvey J. Murff.

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Coppola, JA., Shrubsole, M.J., Cai, Q. et al. Plasma lipid levels and colorectal adenoma risk. Cancer Causes Control 26, 635–643 (2015). https://doi.org/10.1007/s10552-015-0555-y

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  • DOI: https://doi.org/10.1007/s10552-015-0555-y

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