Tailoring messages to individual differences in monitoring-blunting styles to increase fruit and vegetable intake.

OBJECTIVE: To examine whether messages matched to individuals' monitoring-blunting coping styles (MBCS) are more effective in increasing fruit and vegetable intake than mismatched messages. MBCS refers to the tendency to either attend to and amplify, or distract oneself from and minimize threatening information. DESIGN/SETTING: Randomly assigned messages were tailored to resonate with either monitors or blunters and delivered at baseline, 1 week, 2 months, and 3 months later. Surveys were conducted at baseline and 2 and 4 months later. PARTICIPANTS: 531 callers to a cancer information hotline who did not meet the 5 A Day guideline. INTERVENTION: A brief telephone-delivered message and 3 mailings of booklets and promotional items encouraging fruit and vegetable intake, tailored for either monitors or blunters. MAIN OUTCOME MEASURE: Fruit and vegetable intake 2 and 4 months post-baseline. ANALYSIS: Hierarchical regression modeling. RESULTS: Messages matched to MBCS were more effective than mismatched messages, particularly for the monitor message, in increasing intake at 2 months but not at 4 months. CONCLUSIONS AND IMPLICATIONS: These minimal interventions influenced fruit and vegetable intake. MBCS may be a promising target for developing tailored messages aimed at increasing intake, although additional research is needed to verify the robustness of these findings.

Intake of coffee and tea and risk of ovarian cancer: a prospective cohort study.

There is some evidence from case-control studies that coffee consumption might be positively associated with ovarian cancer risk, whereas the epidemiologic evidence regarding tea consumption and ovarian cancer is inconsistent. To date, there have been few prospective studies of these associations. Therefore, we examined ovarian cancer risk in association with both coffee and tea intake in a prospective cohort study of 49,613 Canadian women enrolled in the National Breast Screening Study (NBSS) who completed a self-administered food frequency questionnaire between 1980 and 1985. Linkages to national mortality and cancer databases yielded data on deaths and cancer incidence, with follow-up ending between 1998 and 2000. Data from the food frequency questionnaire were used to estimate daily intake of coffee and tea. Cox proportional hazards models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) for the association between categories of coffee and tea intake and ovarian cancer risk. During a mean 16.4 years of follow-up, we observed 264 incident ovarian cancer cases. Tea intake was not associated with ovarian cancer risk in our study population. In contrast, a borderline positive association was observed among women who drank > 4 cups coffee/day compared to women who did not drink coffee (HR = 1.62, 95% CI = 0.95-2.75, P(trend) = 0.06). Given the pervasive use of these beverages, the associations between coffee and tea consumption and ovarian cancer risk warrant investigation in further prospective studies.

Glycaemic index, glycaemic load and ovarian cancer risk: a prospective cohort study.

BACKGROUND: There is some evidence that plasma insulin levels might influence ovarian cancer risk. Glycaemic index (GI) and glycaemic load (GL) are measures that allow the carbohydrate content of individual foods to be classified according to their postprandial glycaemic effects and hence their effects on circulating insulin levels. Therefore, we examined ovarian cancer risk in association with GI and GL, and intake of dietary carbohydrate and sugar. METHODS: The study was conducted in a prospective cohort of 49 613 Canadian women enrolled in the National Breast Screening Study (NBSS) who completed a self-administered food-frequency questionnaire (FFQ) between 1980 and 1985. Linkages to national mortality and cancer databases yielded data on deaths and cancer incidence, with follow-up ending between 1998 and 2000. Data from the FFQ were used to estimate overall GI and GL, and Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between energy-adjusted quartile levels of GL, overall GI, total carbohydrates, total sugar and ovarian cancer risk. RESULTS: During a mean 16.4 years of follow-up, we observed 264 incident ovarian cancer cases. GI and total carbohydrate and sugar intakes were not associated with ovarian cancer risk in the total cohort. GL was positively associated with a 72% increase in risk of ovarian cancer (HR=1.72, 95% CI=1.13-2.62, Ptrend=0.01) and the magnitude of the association was slightly greater among postmenopausal (HR=1.89, 95% CI=0.98-3.65, Ptrend=0.03) than among premenopausal women (HR=1.64, 95% CI=0.95-2.88, Ptrend=0.07). CONCLUSIONS: Our data suggest that consumption of diets with high GL values may be associated with increased risk of ovarian cancer.

Dietary fiber intake and ovarian cancer risk: a prospective cohort study.

There is some evidence from case-control studies that dietary fiber intake might be inversely associated with ovarian cancer risk, but there are limited prospective data. Therefore, we examined ovarian cancer risk in association with intake of dietary fiber in a prospective cohort of 49,613 Canadian women enrolled in the National Breast Screening Study (NBSS), who completed a self-administered food frequency questionnaire between 1980 and 1985. Linkages to national mortality and cancer databases yielded data on deaths and cancer incidence, with follow-up ending between 1998 and 2000. Data from the food frequency questionnaire were used to estimate intake of total dietary fiber, of fiber fractions, and of fiber from various sources. Cox proportional hazards models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) for the association between energy-adjusted quartile levels of fiber intake and ovarian cancer risk. During a mean 16.4 years of follow-up, we observed 264 incident ovarian cancer cases. Total dietary fiber and fiber fractions were not associated with ovarian cancer risk in this study population.

Glycaemic index, glycaemic load and risk of endometrial cancer: a prospective cohort study.

OBJECTIVE: High-glycaemic-load diets may increase endometrial cancer risk by increasing circulating insulin levels and, as a consequence, circulating oestrogen levels. Given the paucity of epidemiological data regarding the relationship between dietary glycaemic index and glycaemic load and endometrial cancer risk, we sought to examine these associations using data from a prospective cohort study. DESIGN, SETTING AND SUBJECTS: We examined the association between dietary glycaemic load and endometrial cancer risk in a cohort of 49,613 Canadian women aged between 40 and 59 years at baseline who completed self-administered food-frequency questionnaires between 1982 and 1985. Linkages to national mortality and cancer databases yielded data on deaths and cancer incidence, with follow-up ending between 1998 and 2000. RESULTS: During a mean of 16.4 years of follow-up, we observed 426 incident cases of endometrial cancer. Hazard ratios for the highest versus the lowest quartile level of overall glycaemic index and glycaemic load were 1.47 (95% confidence interval (CI) = 0.90-2.41; P for trend = 0.14) and 1.36 (95% CI = 1.01-1.84; P for trend = 0.21), respectively. No association was observed between total carbohydrate or total sugar consumption and endometrial cancer risk. Among obese women (body mass index >30 kg m(-2)) the hazard ratio for the highest versus the lowest quartile level of glycaemic load was 1.88 (95% CI = 1.08-3.29; P for trend = 0.54) and there was a 55% increased risk for the highest versus the lowest quartile level of glycaemic load among premenopausal women. There was also evidence to support a positive association between glycaemic load and endometrial cancer risk among postmenopausal women who had used hormone replacement therapy. CONCLUSIONS: Our data suggest that diets with high glycaemic index or high glycaemic load may be associated with endometrial cancer risk overall, and particularly among obese women, premenopausal women and postmenopausal women who use hormone replacement therapy.

Oral contraceptive use and risk of breast cancer among women with a family history of breast cancer: a prospective cohort study.

Family history of breast cancer is an established risk factor for breast cancer. In addition, there is evidence that oral contraceptive use may be associated with a moderate increase in breast cancer risk. The three cohort studies that have investigated the relationship between oral contraceptive use and breast cancer risk among women with a family history of breast cancer have yielded mixed results, possibly due to the relatively small sample sizes employed and/or differences in the selection of covariates for inclusion in multivariate models. Therefore, we examined the association between oral contraceptive use and breast cancer risk in a large cohort study in Canada. The cohort consisted of the 27,318 women in the Canadian National Breast Screening Study who reported a family history of breast cancer on enrollment into the study. Linkages to national mortality and cancer databases yielded data on deaths and cancer incidence, with follow-up ending between 1998 and 2000, depending upon the province. During a mean of 16.0 years of follow-up, we observed 1707 incident cases of breast cancer among women with any history of breast cancer of which 795 cases occurred among women with a mother, sister, and/or daughter with breast cancer. Among women with any family history of breast cancer, ever use of oral contraceptives was associated with a 12% reduction in risk of breast cancer (95% confidence interval [CI]=0.73-1.07), and there was an inverse trend with increasing duration of use of borderline statistical significance (p(trend)=0.03). Although we also observed a 25% lower risk of breast cancer associated with oral contraceptive use of greater than 84 months versus never use among women with a first degree relative with breast cancer, this finding was not statistically significant (95% CI=0.47-1.19, p(trend)=0.48). Our data raise the possibility that relatively long duration of oral contraceptive use may be inversely associated with risk among women with a family history of breast cancer.

Glycemic index, glycemic load, and pancreatic cancer risk (Canada).

There is some evidence that plasma insulin and postload plasma glucose may be associated with risk of pancreatic cancer. Glycemic index and glycemic load are measures, which allow the carbohydrate content of individual foods to be classified according to their postprandial glycemic effects and hence their effects on circulating insulin levels. Therefore, we examined pancreatic cancer risk in association with glycemic index (GI), glycemic load (GL), and intake of dietary carbohydrate and sugar in a prospective cohort of 49,613 Canadian women enrolled in the National Breast Screening Study (NBSS) who completed a self-administered food frequency questionnaire between 1980 and 1985. Linkages to national cancer and mortality databases yielded data on cancer incidence and deaths, with follow-up ending between 1998 and 2000. During a mean 16.5 years of follow-up, we observed 112 incident pancreatic cancer cases. There was no association between overall glycemic index, glycemic load, total carbohydrate and total sugar intake and pancreatic cancer risk. In multivariate adjusted models, the hazard ratio (HR) for the highest versus lowest quartile levels of overall GI and GL were 1.43 (95% confidence interval [CI]=0.56-3.65, P(trend)=0.58) and 0.80 (95% CI=0.45-1.41, P(trend)=0.41), respectively. Our data suggest that overall glycemic index and glycemic load, as well as total sugar and total carbohydrate intake, are not associated with pancreatic cancer risk. However, given the limited literature regarding the role of diet in the etiology of pancreatic cancer, particularly with respect to glycemic index/load, further investigation is warranted.