The relationships between body mass index (BMI) during early and middle-late adulthood and incidence of prostate cancer (PCa) by subtype of the disease (localised, advanced) and fatal PCa is unclear.
A population-based cohort of 36,959 Swedish men aged 45-79 years was followed up from January 1998 through December 2008 for incidence of PCa (1530 localised and 554 advanced cases were diagnosed) and through December 2007 for PCa mortality (225 fatal cases).
From a competing-risks analysis, incidence of localised PCa was observed to be inversely associated with BMI at baseline (middle-late adulthood; rate ratio (RR) for 35 kg m(-2) when compared with 22 kg m(-2) was 0.69 (95% CI 0.52-0.92)), but not at age 30. For fatal PCa, BMI at baseline was associated with a nonstatistically significant increased risk (RR for every five-unit increase: 1.12 (0.88-1.43)) and BMI at age 30 with a decreased risk (RR for every five-unit increase: 0.72 (0.51-1.01)).
Our results indicate an inverse association between obesity during middle-late, but not early adulthood, and localised PCa. They also suggest a dual association between BMI and fatal PCa--a decreased risk among men who were obese during early adulthood and an increased risk among those who were obese during middle-late adulthood.
Dietary antioxidant vitamins and retinol have been proposed to be protective against breast cancer on the basis of their ability to reduce oxidative DNA damage and their role in cell differentiation. Epidemiologic studies have not been convincing in supporting this hypothesis, but women with high exposure to free radicals and oxidative processes have not been specifically considered. We explored these issues in the Swedish Mammography Screening Cohort, a large population-based prospective cohort study in Sweden that comprised 59,036 women, 40-76 years of age, who were free of cancer at baseline and who had answered a validated 67-item food frequency questionnaire. During 508,267 person-years of follow-up, 1,271 cases of invasive breast cancer were diagnosed. Cox proportional hazards models were used to obtain hazard ratios (HRs) and 95% confidence intervals (CIs). There was no overall association between intake of ascorbic acid, beta-carotene, retinol or vitamin E and breast cancer incidence. High intake of ascorbic acid was inversely related to breast cancer incidence among overweight women (HR=0.61; 95% CI 0.45-0.82, for highest quintile of intake among women with body mass index>25 kg/m(2)) and women with high consumption of linoleic acid (HR=0.72; 95% CI 0.52-1.02, for highest quintile of ascorbic acid intake and average consumption of more than 6 grams of linoleic acid per day). Among women with a body mass index of 25 or below, the hazard ratio for breast cancer incidence was 1.27 (95% CI 0.99-1.63), comparing the highest to the lowest quintile of ascorbic acid intake. Consumption of foods high in ascorbic acid may convey protection from breast cancer among women who are overweight and/or have a high intake of linoleic acid.
A number of prospective cohort studies have examined the relations of individual dietary variables to risk of colorectal cancer. Few studies have addressed the broader eating patterns that reflect many dietary exposures working together. Using data from a prospective study of 61,463 women, with an average follow-up period of 9.6 years (between 1987 and 1998) and 460 incident cases of colorectal cancer, the authors conducted a factor analysis to identify and examine major dietary patterns in relation to colorectal cancer risk. Using proportional hazards regression to estimate relative risks, the authors found no clear association between a "Western," "healthy," or "drinker" dietary pattern and colorectal cancer risk. However, the data suggested that consuming low amounts of foods that constitute a "healthy" dietary pattern may be associated with increased risks of colon and rectal cancers. An inverse association with the "healthy" dietary pattern was found among women under age 50 years, although the number of cancers in this age group was limited and interpretation of this finding should be cautious. In this age group, relative risks for women in increasing quintiles of the "healthy" dietary pattern, compared with the lowest quintile, were 0.74 (95% confidence interval (CI): 0.41, 1.31), 0.69 (95% CI: 0.39, 1.24), 0.59 (95% CI: 0.32, 1.07), and 0.45 (95% CI: 0.23, 0.88) (p for trend = 0.03). The role of overall eating patterns in predicting colorectal cancer risk requires further investigation.
OJECTIVE: We evaluated the relation between obesity and the risks for various forms of cancer. METHODS: In a population-based cohort of 28,129 hospital patients (8165 men, 19,964 women) with any discharge diagnosis of obesity (9557 only diagnosis, 5266 primary, 13,306 secondary) during 1965-1993, cancer incidence was ascertained through 1993 by record linkage to the nationwide Swedish Cancer Registry. Cancer risk was estimated using the standardized incidence ratio (SIR, with 95% confidence interval), which is the ratio of the observed number of cancers to that expected. RESULTS: Overall, a 33% excess incidence of cancer was seen in obese persons, 25% in men and 37% in women. Significant risk elevations were observed for cancers of the small intestine (SIR = 2.8; 95% CI 1.6-4.5), colon (1.3; 1.1-1.5), gallbladder (1.6; 1.1-2.3), pancreas (1.5; 1.1-1.9), larynx (2.1; 1.1-3.5), renal parenchyma (2.3; 1.8-2.8), bladder (1.2; 1.0-1.6), cervix uteri (1.4; 1.1-1.9), endometrium (2.9; 2.5-3.4), ovary (1.2; 1.1-1.5), brain (1.5; 1.2-1.9), and connective tissue (1.9; 1.1-3.0), and for lymphomas (1.4; 1.0-1.7), with higher risk observed for Hodgkin's disease only in men (3.3; 1.4-6.5) and for non-Hodgkin's lymphoma only in women (1.6; 1.2-2.1). The association of obesity with risk of breast, prostate and pancreas cancers was modified by age. CONCLUSIONS: Obesity is associated with more forms of cancer than previously reported.
Notwithstanding its biologic plausibility, the association between physical activity and endometrial cancer has been analyzed in only a few epidemiological studies. Retrospective assessment of exposure and small sample size often hampers interpretation of published data. We studied risk for endometrial cancer in relation to physical activity at work in a large cohort of Swedish women identified in the nationwide censuses in 1960 and 1970, with jobs that could be consistently classified into one of 4 levels of physical demands. Follow-up from 1971 through 1989 was accomplished through record linkages. Multivariate Poisson regression models were used to estimate relative risk. The risk for endometrial cancer increased regularly with decreasing level of occupational physical activity (p for trend