It has been suggested that dietary phytoestrogen intake during adolescence may reduce the risk of developing breast cancer. This population-based case-control study evaluated the association between adolescent dietary phytoestrogen intake and adult breast cancer risk among women in Ontario, Canada.
Pathology-confirmed, population-based breast cancer cases, aged 25-74 years, diagnosed between June 2002 and April 2003, were identified using the Ontario Cancer Registry. Population-based controls were recruited, and matched to cases within 5-year age groups. Adolescent phytoestrogen intake was obtained using a brief food frequency questionnaire (n = 3,024 cases, n = 3,420 controls). Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs).
Higher phytoestrogen intake (both isoflavones and lignans) during adolescence was associated with a reduced breast cancer risk, and a monotonic trend was observed from the lowest to the highest quartile (OR [Q2] = 0.91, 95% CI 0.79-1.04, OR[Q3] = 0.86, 95% CI 0.75-0.98, and OR[Q4] = 0.71, 95% CI 0.62-0.82, p-trend
A secondary analysis of data from a study of nutritional vulnerability among 153 women in families seeking charitable food assistance was undertaken to estimate the extent and nutritional significance of at-home food preparation activity for these women. At-home food preparation was estimated from women's reported food intakes from three 24-hour recalls. The relationships between food preparation and energy and nutrient intake, food intake, and 30-day household food security status were characterized. Almost all participants (97%) consumed foods prepared from scratch at least once during the three days of observation; 57% did so each day. Both the frequency and complexity of at-home food preparation were positively related to women's energy and nutrient intakes and their consumption of fruits and vegetables, grain products, and meat and alternates. The intakes by women in households with food insecurity with hunger reflected less complex food preparation but no less preparation from scratch than women in households where hunger was not evident, raising questions about the extent to which food skills can protect very poor families from food insecurity and hunger. Our findings indicate the need for nutrition professionals to become effective advocates for policy reforms to lessen economic constraints on poor households.
Animal and human studies have reported an association between antidepressant (AD) medication use and breast cancer risk. A population-based case-control study was designed specifically to examine this association among women in Ontario, Canada.
The Ontario Cancer Registry (OCR) identified women diagnosed with primary breast cancer. Controls, randomly sampled from the female population of Ontario, were frequency matched by 5-year age groups. A mailed self-administered questionnaire included questions about lifetime use of AD and potential confounders. Multivariate logistic regression yielded odds ratio estimates.
'Ever' use of AD was reported by 14% (441/3077) cases versus 12% (372/2994) controls. The age-adjusted odds ratio (AOR) for 'ever' use was 1.17, (95% CI: 1.01, 1.36). An increased risk was also observed for selective serotonin reuptake inhibitors = 1.33 (95% CI: 1.07, 1.66), Sertraline = 1.58 (95% CI: 1.03, 2.41), and Paroxetine = 1.55 (95% CI: 1.00, 2.40). None of the 30 variables assessed for confounding altered the risk estimate by more than 10%. Multivariate adjustment including all possible breast cancer risk factors yielded an unchanged, but not significant, point estimate (MVOR = 1.2, 95% CI: 0.96, 1.51). No relationship was observed for duration or timing of AD use.
A modest association between 'ever' use of AD and breast cancer was found using the most parsimonious multivariate model. OR estimates did not change, but CI were widened and statistical significance lost, after adjustment for factors associated with breast cancer risk.
Comment In: Int J Epidemiol. 2003 Dec;32(6):966-714681257
Animal and human studies have suggested that antidepressant medications may be associated with several cancers. The authors evaluated the association between antidepressant medication use and the risk of non-Hodgkin's lymphoma using a Canadian population-based case-control study, the National Enhanced Cancer Surveillance Study. Non-Hodgkin's lymphoma cases (n=638) diagnosed in 1995-1996 were identified using the Ontario Cancer Registry, and controls (n=1,930) were identified from the Ontario Ministry of Finance Property Assessment Database. Antidepressant medication use was ascertained using a self-administered questionnaire. Multivariate logistic regression was used to estimate odds ratios. "Ever" use of antidepressant medications was not associated with non-Hodgkin's lymphoma risk. The odds ratio for non-Hodgkin's lymphoma with 25 or more months of tricyclic antidepressant medication use was 1.6; however, this was nonsignificant. Duration or history of use or individual types of antidepressant medications were not associated with non-Hodgkin's lymphoma risk. These findings do not support an increased risk of non-Hodgkin's lymphoma with antidepressant medication use.
Antihistamines are structurally similar to DPPE, a tamoxifen derivative known to promote tumor growth, and to antidepressants. Animal experiments have linked certain antihistamines and antidepressants with enhanced tumor growth in mice. The few epidemiologic studies examining antihistamine use have not indicated an increased risk. In light of suggestive animal data, structural similarities between antihistamines and DPPE, the widespread use of antihistamines, and the lack of epidemiologic investigation into their use and breast cancer risk, it is important to examine this issue. Female cases aged 25-74 years, diagnosed 1996 to 1998, were identified through the Ontario Cancer Registry. Controls were a random, age-matched sample of women. Cases (n=3,133) and controls (n=3,062) completed a mailed questionnaire that included questions about antihistamines used regularly (undefined), type and duration. Age-adjusted odds ratio (OR) estimates and 95% confidence intervals (CIs) were obtained using logistic regression. Antihistamine users were at no increased risk for breast cancer (OR=0.93, 95% CI: 0.81, 1.06), and no trend in risk was observed for age starting or duration of use. Antihistamine users were at no increased risk. No confounding or effect modification was identified in multivariate modeling. Our findings do not support the hypothesis that women who use antihistamines are at a greater breast cancer risk than those who do not.
The study aim is to evaluate benzodiazepine use and risk for breast cancer in Ontario, Canada, by using a population-based case-control study design.
Cases were a random sample of women aged 25 to 74 years identified through the Ontario Cancer Registry and diagnosed with breast cancer between 1996 and 1998 (n = 3133). Controls were an age-matched random sample of women (n = 3062). Cases and controls completed a self-administered questionnaire that included questions about their past use of benzodiazepines (defined as daily use for at least 2 months) and potential confounders. Individual classes of benzodiazepines also were evaluated. Multivariate logistic regression analysis was conducted, and odds ratios (ORs) and 95% confidence intervals (CIs) were estimated.
Compared with nonusers, ever use of benzodiazepines was not significantly associated with risk for breast cancer (OR, 1.06; 95% CI, 0.88-1.27). No apparent trends were observed for duration of use, time since first use, or time since last use. Estimates according to individual classes of benzodiazepines, including diazepam, lorazepam, and chlordiazepoxide, also were not statistically significant.
Our data show no association between benzodiazepine use and breast cancer risk. Results confirm findings from previous studies that diazepam use does not increase the risk for breast cancer and also suggest no association with the use of other benzodiazepine compounds.
Calcium and vitamin D are recommended for bone health, but there are concerns about adverse risks. Some clinical studies suggest that calcium intake may be cardioprotective, whereas others report increased risk associated with calcium supplements. Both low and high serum levels of 25-hydroxyvitamin D have been associated with increased mortality.
The purpose of this study was to determine the association between total calcium and vitamin D intake and mortality and heterogeneity by source of intake.
The Canadian Multicentre Osteoporosis Study cohort is a population-based longitudinal cohort with a 10-year follow-up (1995-2007).
This study included randomly selected community-dwelling men and women.
A total of 9033 participants with nonmissing calcium and vitamin D intake data and follow-up were studied.
Total calcium intake (dairy, nondairy food, and supplements) and total vitamin D intake (milk, yogurt, and supplements) were recorded.
The outcome variable was all-cause mortality.
There were 1160 deaths during the 10-year period. For women only, we found a possible benefit of higher total calcium intake, with a hazard ratio of 0.95 (95% confidence interval, 0.89-1.01) per 500-mg increase in daily calcium intake and no evidence of heterogeneity by source; use of calcium supplements was also associated with reduced mortality, with hazard ratio of 0.78 (95% confidence interval, 0.66-0.92) for users vs nonusers with statistically significant reductions remaining among those with doses up to 1000 mg/d. These associations were not modified by levels of concurrent vitamin D intake. No definitive associations were found among men.
Calcium supplements, up to 1000 mg/d, and increased dietary intake of calcium may be associated with reduced risk of mortality in women. We found no evidence of mortality benefit or harm associated with vitamin D intake.
For proper interpretation of results from epidemiological studies that use food-frequency questionnaires (FFQs), it is necessary to know the relationship between reported intakes from the FFQ and true usual intake. In this paper, we report a calibration study conducted to investigate the performance of the FFQ used in a cohort study, the Canadian Study of Diet, Lifestyle and Health.
Over a 1-year period, 151 men and 159 women completed a full set of questionnaires including a self-administered baseline FFQ, three 24-hour diet recalls administered by telephone, and a second FFQ self-administered subsequently. The association between the nutrient estimates derived from the FFQs and the diet recalls was evaluated by calculating deattenuated Pearson's correlation coefficients.
FFQs estimated mean daily nutrient intakes higher than the diet recalls. When the log-transformed and energy-adjusted nutrient intakes from the average of three 24-hour recalls were compared against the baseline FFQ, the following deattenuated correlations were obtained in men and women, respectively: total energy 0.44 and 0.32, total fat 0.64 and 0.68, saturated fat 0.68 and 0.70, dietary fibre 0.65 and 0.44, vitamin E 0.32 and 0.37, vitamin C 0.40 and 0.37, beta-carotene 0.34 and 0.29, alcohol 0.74 and 0.67, caffeine 0.81 and 0.76, with a median correlation of 0.49 and 0.53. Correlations between the second FFQ and diet recalls were similar. The correlations between the two FFQs as a test of reliability had a median value 0.64 for men and 0.63 for women for selected nutrients.
The study suggests that the FFQ method gives acceptable levels of nutrients or food component estimates, as assessed by this calibration study against diet recalls, when limited to energy-adjusted and deattenuated values.
We have established a new cohort study, the Canadian Study of Diet, Lifestyle, and Health, to investigate the relationship between diet, lifestyle factors, molecular markers, and cancer incidence in Canada.
The cohort was established predominantly by recruiting alumni from the Universities of Alberta, Toronto, and Western Ontario between 1995 and 1998, but also includes a small contingent recruited mostly in 1992 through the Canadian Cancer Society. Participants completed baseline lifestyle and food frequency questionnaires, measured waist and hip circumferences, and provided hair and toenail specimens.
Seventy-three thousand nine hundred and nine individuals (34,291 males and 39,618 females) were recruited, with representation from all Canadian provinces and territories; 97% provided biological specimens. The mean (S.D.) ages of the male and female participants at recruitment were 51.6 (15.6) and 46.1 (15.2) years, respectively. Data from a random sample of the study subjects at baseline show that approximately one-half of the males and one-third of the females were overweight (BMI>or=25kg/m(2)), and approximately one-quarter of all participants reported that they walked at least 4h/week. Mean (S.D.) daily caloric intake was 2341 (697)kcal for males and 2091 (612)kcal for females.
Given the rich repository of questionnaire and biological data, and an average follow-up time for cohort members of 10.4 years, the study is poised to make a major Canadian contribution towards understanding the roles of diet, lifestyle factors, and molecular markers in influencing cancer risk.