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The metabolic syndrome and risk of incident colorectal cancer.
Cancer 2006; 107(1):28-36C

Abstract

BACKGROUND

The authors tested the hypothesis that the metabolic syndrome (> or =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 (> or =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.

Authors+Show Affiliations

Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, Minnesota 55454-1015, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Multicenter Study
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16721800

Citation

Ahmed, Rehana L., et al. "The Metabolic Syndrome and Risk of Incident Colorectal Cancer." Cancer, vol. 107, no. 1, 2006, pp. 28-36.
Ahmed RL, Schmitz KH, Anderson KE, et al. The metabolic syndrome and risk of incident colorectal cancer. Cancer. 2006;107(1):28-36.
Ahmed, R. L., Schmitz, K. H., Anderson, K. E., Rosamond, W. D., & Folsom, A. R. (2006). The metabolic syndrome and risk of incident colorectal cancer. Cancer, 107(1), pp. 28-36.
Ahmed RL, et al. The Metabolic Syndrome and Risk of Incident Colorectal Cancer. Cancer. 2006 Jul 1;107(1):28-36. PubMed PMID: 16721800.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The metabolic syndrome and risk of incident colorectal cancer. AU - Ahmed,Rehana L, AU - Schmitz,Kathryn H, AU - Anderson,Kristin E, AU - Rosamond,Wayne D, AU - Folsom,Aaron R, PY - 2006/5/25/pubmed PY - 2006/8/17/medline PY - 2006/5/25/entrez SP - 28 EP - 36 JF - Cancer JO - Cancer VL - 107 IS - 1 N2 - BACKGROUND: The authors tested the hypothesis that the metabolic syndrome (> or =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 (> or =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. SN - 0008-543X UR - https://www.unboundmedicine.com/medline/citation/16721800/The_metabolic_syndrome_and_risk_of_incident_colorectal_cancer_ L2 - https://doi.org/10.1002/cncr.21950 DB - PRIME DP - Unbound Medicine ER -