The metabolic syndrome and risk of incident colorectal cancer

Authors

  • Rehana L. Ahmed Ph.D.,

    1. Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, Minnesota
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  • Kathryn H. Schmitz Ph.D.,

    1. Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, Minnesota
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  • Kristin E. Anderson Ph.D.,

    1. Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, Minnesota
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  • Wayne D. Rosamond Ph.D.,

    1. Collaborative Studies Coordinating Center, School of Public Health, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina
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  • Aaron R. Folsom M.D.

    Corresponding author
    1. Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, Minnesota
    • Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, 1300 South Second Street, Suite 300, Minneapolis, MN 55454-1015
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    • Fax: (612) 624-0315


Abstract

BACKGROUND

The authors tested the hypothesis that the metabolic syndrome (≥3 of the following components: high blood pressure, increased waist circumference, hypertriglyceridemia, low levels of high-density lipoprotein cholesterol, or diabetes/hyperglycemia) is a risk factor for colorectal cancer.

METHODS

Data from the Atherosclerosis Risk in Communities (ARIC) multicenter prospective cohort study were used. Metabolic syndrome components and other risk factors were collected during 1987 to 1989 from the 14,109 men and women in these analyses. One hundred ninety-four incident colorectal cancers were identified through the Year 2000. Multivariate Cox proportional hazards regression analyses were used to examine associations.

RESULTS

Baseline metabolic syndrome (≥3 components vs. 0 components) had a positive association with age-adjusted and gender-adjusted colorectal cancer incidence (relative risk [RR], 1.49; 95% confidence interval [95%CI], 1.0-2.4); this association was attenuated after multivariate adjustment (RR, 1.39; 95%CI, 0.9-2.2). There was a dose-response association between colorectal cancer incidence and the number of metabolic syndrome components present at baseline (P for trend = .006) after multivariate adjustment. Analysis of gender revealed that the multivariate-adjusted association of metabolic syndrome with colorectal cancer was stronger in men (RR, 1.78; 95%CI, 1.0-3.6) and weaker in women (RR, 1.16; 95%CI, 0.6-2.2).

CONCLUSIONS

In this population-based cohort, metabolic syndrome was a risk factor for incident colorectal cancer in men but not women. Evidence is growing that the metabolic syndrome may be a marker for a physiologic milieu of growth that encourages tumor initiation, promotion, and/or progression. Cancer 2006. © 2006 American Cancer Society.

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