Associations of Serum Lipids with Risk of Incident, Sporadic Colorectal Adenoma 公开

Yu, Randy Rueyn (2011)

Permanent URL: https://etd.library.emory.edu/concern/etds/ww72bc31p?locale=zh
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Abstract

Background: Colorectal cancer is the third most common cancer in the United States. There has been substantial evidence that environmental factors affect the risk of developing colorectal adenoma, precursors of colorectal cancer.

Objective: This study was conducted to investigate whether serum lipids are associated with risk of incident, sporadic colorectal adenomatous polyps.

Methods: Data were analyzed from a case-control study of incident, sporadic colorectal adenoma (n = 534) and colonoscopy negative controls (n = 644) conducted in Minnesota between 1990 and 1994. Self-administered questionnaires were used to collect demographic, dietary, and lifestyle information from all participants. Blood samples were drawn from participants to measure information on serum levels of total cholesterol, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), very-low-density lipoprotein cholesterol (VLDL-C), and triglycerides. Multivariate logistic regression analyses were conducted to investigate the associations between serum lipid levels and risk of incident, sporadic colorectal adenoma.

Results: In the crude analyses, higher levels of HDL-C were associated with lower risk of colorectal adenoma (odds ratio (OR) = 0.57; 95% confidence interval (CI): 0.41, 0.80, highest quartile vs. lowest quartile), and higher levels of LDL-C were associated with higher risk (OR = 1.46; CI: 1.04-2.04, highest quartile vs. lowest quartile). Total cholesterol, VLDL-C, and triglycerides were not associated with risk of colorectal adenoma. In the multivariable analysis, higher levels of HDL-C were not associated with risk of colorectal adenoma (OR = 0.77; CI: 0.47-1.27, highest quartile vs. lowest quartile) and higher levels of LDL-C were not associated with risk of colorectal adenoma (OR = 1.05; CI: 0.68-1.61).

Discussions: Overall, serum lipid levels were not associated with risk for incident, sporadic colorectal adenoma. After adjustment for risk factors that tend to play a role in determining blood lipid levels, the associations of HDL-C and LDL-C were attenuated to close to the null value. These findings suggest that blood lipid levels may not affect risk for colorectal neoplasms; however, it is possible that exposures that influence HDL and LDL cholesterol levels may be more relevant to risk for the disease.

Table of Contents

INTRODUCTION..................................................................................................................................... 1 CHAPTER 1: BACKGROUND ...................................................................................................................... 3 Definition .................................................................................................................................... 3 Descriptive Epidemiology ................................................................................................................ 3 International Differences ................................................................................................................ 5 Colorectal Cancer Pathogenesis ....................................................................................................... 6 Obesity and Body Size ................................................................................................................... 9 Dietary Factors ........................................................................................................................... 10 Lifestyle Factors ......................................................................................................................... 16 Medication Use ........................................................................................................................... 18 Hyperlipidemia/Dyslipidemia ........................................................................................................... 20 Conclusion ................................................................................................................................. 25 CHAPTER 2: MANUSCRIPT CHAPTER ........................................................................................................ 26 Abstract .................................................................................................................................... 26 Introduction ............................................................................................................................... 27 Materials and Methods ................................................................................................................. 28 Results ..................................................................................................................................... 31 Discussion ................................................................................................................................. 33 CHAPTER 3: CONCLUSIONS ................................................................................................................... 37 Summary ................................................................................................................................... 37 Possible Future Directions ............................................................................................................. 38 REFERENCES ....................................................................................................................................... 40 TABLES .............................................................................................................................................. 50 APPENDIX ........................................................................................................................................... 64

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