Background: Metabolic syndrome may predict endometrial cancer risk better than diabetes, hypertension, dyslipidemia, dysglycemia, or weight alone, but few studies have examined this issue.Methods: We conducted a population-based case-control study in Alberta, Canada (2002) that included 515 incident endometrial cancer cases and 962 frequency age-matched controls. Data were collected through in-person interviews, anthropometric measurements, and 8-hour fasting bloods drawn either pre-or postsurgery. Bloods were analyzed using quantitative colorimetric or absorbance-based assays (ELISA), specific to metabolic syndrome markers. Metabolic syndrome was defined using harmonized guidelines requiring presence of !3 of the following risk factors: waist circumference !88 cm, triglycerides !150 mg/dL, high-density lipoprotein cholesterol <50 mg/dL, treatment of previously diagnosed hypertension, and fasting blood glucose !100 mg/dL. OR and 95% CIs for endometrial cancer risk with presence of metabolic syndrome and individual metabolic syndrome components were estimated using logistic regression analysis.Results: Metabolic syndrome was significantly more prevalent among cases (62%) than controls (38%). A statistically significant increased risk for endometrial cancer was observed for metabolic syndrome (OR ¼ 1.53; 95% CI: 1.17-2.00), as well as for some of the individual components of metabolic syndrome including waist circumference !88 cm (OR ¼ 1.57; 95% CI: 1.18-2.08), hypertension (OR ¼ 1.57; 95% CI: 1.18-2.09), and fasting blood glucose !100 mg/dL (OR ¼ 1.31; 95% CI: 1.03-1.67). Some evidence for effect modification by menopausal status and body mass index was also found.Conclusion: Metabolic syndrome is clearly associated with increased endometrial cancer risk. Impact: Targeting the entire metabolic syndrome may optimize endometrial cancer risk reduction. Cancer Epidemiol Biomarkers Prev; 20(11); 2384-95. Ó2011 AACR.

Objective: Intake of nutrients may influence the risk of endometrial cancer (EC). We aimed to estimate the association of intake of individual nutrients from food and from food plus supplements with EC occurrence. Design: A population-based case-control study conducted in Canada (2002Canada ( -2006. Setting: Nutrient intakes from food and supplements were assessed using an FFQ. Logistic regression was used to estimate EC risk within quartile levels of nutrient intakes. Subjects: Incident EC cases (n 506) were identified from the Alberta Cancer Registry, and population controls were frequency-and age-matched to cases (n 981). Results: There existed little evidence of an association with EC for the majority of macronutrients and micronutrients examined. We observed a statistically significant increased risk associated with the highest, compared with the lowest, quartile of intake of dietary cholesterol (multivariable-adjusted OR 5 1?51, 95 % CI 1?08, 2?11; P for trend 5 0?02). Age-adjusted risk at the highest level of intake was significantly reduced for Ca from food sources (OR 5 0?73, 95 % CI 0?54, 0?99) but was attenuated in the multivariable model (OR 5 0?82, 95 % CI 0?59, 1?13). When intake from supplements was included in Ca intake, risk was significantly reduced by 28 % with higher Ca (multivariable-adjusted OR 5 0?72, 95 % CI 0?51, 0?99, P for trend 5 0?04). We also observed unexpected increased risks at limited levels of intakes of dietary soluble fibre, vitamin C, thiamin, vitamin B 6 and lutein/zeaxanthin, with no evidence for linear trend. Conclusions: The results of our study suggest a positive association between dietary cholesterol and EC risk and an inverse association with Ca intake from food sources and from food plus supplements.