Background: Few studies have assessed the metabolic syndrome (MetS) as an entity in relation to breast cancer risk, and results have been inconsistent. We aimed to examine the association between MetS factors (individually and combined) and risk of breast cancer incidence and mortality.Methods: Two hundred ninety thousand women from Austria, Norway, and Sweden were enrolled during 1974-2005, with measurements of height, weight, blood pressure, and levels of glucose, cholesterol, and triglycerides. Relative risks (RR) of breast cancer were estimated using Cox proportional hazards regression for each MetS factor in quintiles and for standardized levels (z-scores) and for a composite z-score for the MetS.Results: There were 4,862 incident cases of breast cancer and 633 deaths from breast cancer identified. In women below age 50, there was a decreased risk of incident cancer for the MetS (per 1-unit increment of z-score; RR, 0.83; 95% confidence interval, 0.76-0.90) as well as for the individual factors (except for glucose). The lowest risks were seen among the heaviest women. In women above age 60, there was an increased risk of breast cancer mortality for the MetS (RR, 1.23; 95% confidence interval, 1.04-1.45) and for blood pressure and glucose. The strongest association with mortality was seen for increased glucose concentrations.Conclusions: The MetS was associated with a decreased risk of incident breast cancer in women below age 50 with high body mass index, and with an increased risk of breast cancer mortality in women above 60.Impact: Lifestyle interventions as recommended for cardiovascular disease prevention may be of value to prevent breast cancer mortality in postmenopausal women. Cancer Epidemiol Biomarkers Prev; 19(7); 1737-45.

Using data on cancer incidence for 2008 and our AF(p) estimates, about 270,000 new cancer diagnoses per year can be considered attributable to cigarette smoking in the eight European countries with available data for both men and women (Italy, Spain, United Kingdom, the Netherlands, Greece, Germany, Sweden, Denmark).

The authors examined the association between the metabolic syndrome and risk of incident endometrial and fatal uterine corpus cancer within a large prospective cohort study. Approximately 290,000 women from Austria, Norway, and Sweden were enrolled during 1974-2005, with measurements of height, weight, systolic and diastolic blood pressure, and circulating levels of glucose, total cholesterol, and triglycerides. Relative risks were estimated using Cox proportional hazards regression. The metabolic syndrome was assessed as a composite z score, as the standardized sum of z scores for body mass index, blood pressure, glucose, cholesterol, and triglycerides. A total of 917 endometrial carcinomas and 129 fatal cancers were identified. Increased risks of incident endometrial carcinoma and fatal uterine corpus cancer were seen for the metabolic syndrome factors combined, as well as for individual factors (except for cholesterol). The relative risk of endometrial carcinoma for the metabolic syndrome was 1.37 (95% confidence interval: 1.28, 1.46) per 1-unit increment of z score. The positive associations between metabolic syndrome factors (both individually and combined) and endometrial carcinoma were confined to the heaviest women. The association between the metabolic syndrome and endometrial carcinoma risk seems to go beyond the risk conferred by obesity alone, particularly in women with a high body mass index.

Results from case-control and prospective studies suggest a moderate positive association between obesity and height and differentiated thyroid carcinoma (TC). Little is known on the relationship between other measures of adiposity and differentiated TC risk. Here, we present the results of a study on body size and risk of differentiated TC based on a large European prospective study (EPIC). During follow-up, 508 incident cases of differentiated TC were identified in women, and 58 in men. 78% of cases were papillary TC. Cox proportional hazard models were used to estimate hazard ratios (HRs). In women, differentiated TC risk was significantly associated with body mass index (BMI, kg/m 2 ) (HR highest vs lowest quintile 5 1.41, 95% CI: 1.03-1.94); height (HR 5 1.61; 95% CI: 1.18-2.20); HR highest vs lowest tertile waist (HR 5 1.34, 95% CI: 1.00-1.79) and waist-to-hip ratio (HR 5 1.42, 95% CI: 1.05-1.91). The association with BMI was somewhat stronger in women below age 50. Corresponding associations for papillary TC were similar to those for all differentiated TC. In men the only body size factors significantly associated with differentiated TC were height (non linear), and leg length (HR highest vs. lowest tertile 5 3.03, 95% CI: 1.30-7.07). Our study lends further support to the presence of a moderate positive association between differentiated TC risk and overweight and obesity in women. The risk increase among taller individuals of both sexes suggests that some genetic characteristics or early environmental exposures may also be implicated in the etiology of differentiated TC.

BACKGROUND:The metabolic syndrome (MetS) has been related to an increased risk of colorectal cancer, but the modest size of previous studies precluded detailed characterization of the role of individual MetS factors and their interaction on risk. METHODS: In the Metabolic Syndrome and Cancer Project (Me-Can), data on body mass index (BMI), blood pressure, and blood levels of glucose, cholesterol, and triglycerides were available for 578,700 men and women. The mean age of participants at baseline was 44 years, and the mean follow-up was 12 years. Relative risks (RR) of colorectal cancer per 1 standard deviation increment in Z score of factors and for a combined MetS score, were calculated from Cox regression models, including adjustment for potential confounders. RESULTS: During follow-up, 2834 men and 1861 women were diagnosed with colorectal cancer. The RR of colorectal cancer for the MetS score was 1.25 (95% confidence interval [CI], 1.18-1.32) in men, and 1.14 (95% CI, 1.06-1.22) in women. Significant associations also were observed in men for BMI (RR, 1.07; 95% CI, 1.02-1.13), blood pressure (RR, 1.10; 95% CI, 1.02-1.18), and triglycerides (RR, 1.17; 95% CI, 1.06-1.28) and, in women, for BMI (RR, 1.08; 95% CI, 1.01-1.15). There was no significant positive interaction between the metabolic factors on risk. CONCLUSIONS: The combination of metabolic factors and some separate factors was related to an increased risk of colorectal cancer, but there was no interaction between metabolic factors.

ObjectiveTo investigate the association between total serum cholesterol (TSC) and cancer incidence in the Metabolic syndrome and Cancer project (Me-Can).MethodsMe-Can consists of seven cohorts from Norway, Austria, and Sweden including 289,273 male and 288,057 female participants prospectively followed up for cancer incidence (n = 38,978) with a mean follow-up of 11.7 years. Cox regression models with age as the underlying time metric were used to estimate hazard ratios (HR) and their 95% confidence intervals (CI) for quintiles of cholesterol levels and per 1 mmol/l, adjusting for age at first measurement, body mass index (BMI), and smoking status. Estimates were corrected for regression dilution bias. Furthermore, we performed lag time analyses, excluding different times of follow-up, in order to check for reverse causation.ResultsIn men, compared with the 1st quintile, TSC concentrations in the 5th quintile were borderline significantly associated with decreasing risk of total cancer (HR = 0.94; 95%CI: 0.88, 1.00). Significant inverse associations were observed for cancers of the liver/intrahepatic bile duct (HR = 0.14; 95%CI: 0.07, 0.29), pancreas cancer (HR = 0.52, 95% CI: 0.33, 0.81), non-melanoma of skin (HR = 0.67; 95%CI: 0.46, 0.95), and cancers of the lymph−/hematopoietic tissue (HR = 0.68, 95%CI: 0.54, 0.87). In women, hazard ratios for the 5th quintile were associated with decreasing risk of total cancer (HR = 0.86, 95%CI: 0.79, 0.93) and for cancers of the gallbladder (HR = 0.23, 95%CI: 0.08, 0.62), breast (HR = 0.70, 95%CI: 0.61, 0.81), melanoma of skin (HR = 0.61, 95%CI: 0.42, 0.88), and cancers of the lymph−/hematopoietic tissue (HR = 0.61, 95%CI: 0.44, 0.83).ConclusionTSC was negatively associated with risk of cancer overall in females and risk of cancer at several sites in both males and females. In lag time analyses some associations persisted, suggesting that for these cancer sites reverse causation did not apply.

Previous studies indicate that calcium and its regulating hormones, i.e., parathyroid hormone (PTH) and vitamin D, might affect breast cancer risk. Evidence also suggests that this relationship could be influenced by menopausal status and BMI. We examined breast cancer risk related to prediagnostic serum levels of vitamin D (25OHD(2) and 25OHD(3)), PTH and calcium using a nested case-control design within the Malmö Diet and Cancer Study. There were 764 incident breast cancer cases, and 764 controls were selected by incidence density matching, using age as the underlying time scale, matching on calendar time at inclusion, menopausal status and age at inclusion. Using logistic regression analysis, odds ratios (OR) with 95% confidence intervals were calculated for breast cancer risk in different quartiles of the analyzed factors. All analyses were adjusted for risk factors for breast cancer, and for levels of albumin, creatinine and phosphate. Analyses were repeated stratified for BMI and menopausal status, and for low vs. high levels of 25OHD(3), PTH and calcium. There was a weak, nonsignificant inverse association between breast cancer risk and 25OHD(3), and the OR for the 2nd, 3rd and 4th quartiles, as compared to the first, were 0.84 (0.60-1.15), 0.84 (0.60-1.17) and 0.93 (0.66-1.33). Serum calcium was positively associated with breast cancer in premenopausal women (OR for the 4th quartile = 3.10:1.33-7.22 and p for quartile trend = 0.04), and in women with BMI > 25 (OR for the 4th quartile = 1.94:1.12-3.37 and p for trend < 0.01). There was no association between baseline serum PTH and breast cancer risk.

2b Laryngoscope, 126:1260-1266, 2016.