Background: Breast cancer, especially postmenopausal, is one of the most common cancers in Western women. Although therapeutic options have improved, there still is a high mortality rate. Several of the known risk factors for breast cancer are lifestyle related and modifiable, providing an opportunity for primary prevention. Middle-aged women still have the chance to modify these factors to lower nearby breast cancer risk. We estimated the fraction of postmenopausal breast cancer cases that is attributable to lifestyle factors as currently present in middle-aged Dutch women. Methods: We estimated population attributable fractions (PAFs) of five potentially modifiable risk factors for Dutch women aged 45-54 years. Risk factors included overweight and obesity, alcohol use, physical inactivity, current use of hormone replacement therapy (HRT) and oral contraceptives. We based relative risks on literature search including meta-analyses and expert group consensus. Current prevalence rates of the risk factors were derived from several Dutch registration databases and national surveys (2009-2011). Results: Of all 45-54 year old contemporary Dutch women, 46% are estimated to be physically inactive, 43% to be overweight or obese, 42% to drink alcohol, 1% to use HRT and 17% to use contraceptives. These risk factors jointly account for an estimated 20.2% of all future breast cancer cases in these women. Physical inactivity and alcohol use are responsible for the highest population attributable fraction (PAF of 7.0% and 6.8% respectively), followed by overweight and obesity (4.3%), oral contraceptive use (3.4%) and hormone replacement therapy (0.6%). Conclusion: On a population level, lifestyle related factors play an important role in the development of postmenopausal breast cancer. Considering current prevalence rates in the Netherlands, our findings imply that modifiable risk factors present at middle-age are jointly responsible for 1 out of every 5 future breast cancer cases. This is in concordance with other studies in European countries. Our findings thus suggest that incidence rates can be lowered substantially by changing lifestyle habits, even in a woman's later life. Citation Format: WAM van Gemert, SG Elias, RA Bausch-Goldbohm, PA van den Brandt, HG Grooters, E Kampman, LALM Kiemeney, FE van Leeuwen, EM Monninkhof, E De Vries, PHM Peeters. The attribution of lifestyle related risk factors in middle age on breast cancer incidence in The Netherlands: Preliminary results. [abstract]. In: Proceedings of the Eleventh Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2012 Oct 16-19; Anaheim, CA. Philadelphia (PA): AACR; Cancer Prev Res 2012;5(11 Suppl):Abstract nr A90.

Skip to main content. Viewing from: Google Indexer. BMJ Journals. Subscribe; Log In More …

Background Chronic exposure to traffic-related air pollution (TRAP) may contribute to premature mortality, but few studies to date have addressed this topic. Objectives In this study we assessed the association between TRAP and mortality in Toronto, Ontario, Canada. Methods We collected nitrogen dioxide samples over two seasons using duplicate two-sided Ogawa passive diffusion samplers at 143 locations across Toronto. We calibrated land use regressions to predict NO2 exposure on a fine scale within Toronto. We used interpolations to predict levels of particulate matter with aerodynamic diameter ≤ 2.5 μm (PM2.5) and ozone levels. We assigned predicted pollution exposures to 2,360 subjects from a respiratory clinic, and abstracted health data on these subjects from medical billings, lung function tests, and diagnoses by pulmonologists. We tracked mortality between 1992 and 2002. We used standard and multilevel Cox proportional hazard models to test associations between air pollution and mortality. Results After controlling for age, sex, lung function, obesity, smoking, and neighborhood deprivation, we observed a 17% increase in all-cause mortality and a 40% increase in circulatory mortality from an exposure contrast across the interquartile range of 4 ppb NO2. We observed no significant associations with other pollutants. Conclusions Exposure to TRAP was significantly associated with increased all-cause and circulatory mortality in this cohort. A high prevalence of cardiopulmonary disease in the cohort probably limits inference of the findings to populations with a substantial proportion of susceptible individuals.

BACKGROUND:The evidence for red meat as a determinant of colorectal cancer remains equivocal, which might be explained by differences in heme content. Heme is the pro-oxidant, iron-containing porphyrin pigment of meat and its content depends on the type of meat. Chlorophyll from green vegetables might modify this association.METHODS:The Netherlands Cohort Study was initiated in 1986 when a self-administered questionnaire on risk factors for cancer was completed by 120,852 subjects ages 55 to 69 years. After 9.3 years of follow-up through the Cancer Registry, 1,535 incident colorectal cancer cases (869 men and 666 women) were available. Nineteen of the 150 items in the validated dietary questionnaire related to consumption of specific types of fresh and processed meat. Heme iron content was calculated as a type-specific percentage of the total iron content and chlorophyll content of vegetables was derived from the literature.RESULTS:Multivariate rate ratios for quintiles of heme iron intake and colon cancer were 1.00, 0.98, 1.04, 1.13, and 1.29 (P(trend) = 0.10) among men and 1.00, 1.31, 1.44, 1.18, and 1.20 (P(trend) = 0.56) among women, respectively. No consistent associations were observed for rectal cancer. Rate ratios for colon cancer increased across successive quintiles of the ratio of heme/chlorophyll among men only (1.00, 1.08, 1.01, 1.32, and 1.43; P(trend) = 0.01). No associations were observed between fresh meat and colorectal cancer.CONCLUSION:Our data suggest an elevated risk of colon cancer in men with increasing intake of heme iron and decreasing intake of chlorophyll. Further research is needed to confirm these results.

Background Atopic parents may adopt lifestyle characteristics that allegedly protect against atopic disease. If this is true, infants from atopic parents will be characterized by low-risk behaviour. Consequently, aetiologic studies on lifestyle factors and allergic disease in childhood may be biased by confounding by indication.Objective We explored whether the prevalence of 'prudent' lifestyle characteristics differs between atopic and non-atopic families.Methods Information about a family history of atopic manifestations and lifestyle characteristics was collected by repeated questionnaires in the Dutch KOALA Birth Cohort Study in 2469 infants from families with divergent lifestyle practices (conventional vs. alternative).Results In conventional lifestyle families, infants were less often exposed to environmental tobacco smoke when parents were atopic than when they were non-atopic (10.0% vs. 14.7%, P=0.001). In alternative lifestyle families, exposure to smoking was very rare in both groups (1.7% vs. 2.6%). Pets were less often present in families with than without parental atopy (38.8% vs. 51.1%, P=0.008 for conventional lifestyle families; 43.0% vs. 48.4%, P=0.014 for alternative lifestyle families). Infants with atopic siblings had less often been vaccinated according to the standard scheme than infants with non-atopic siblings in conventional lifestyle families (76.6% vs. 85.5%, P < 0.001). In alternative lifestyle families, the difference was in the same direction but not statistically significant (30.1% vs. 40.5%, P=0.143). Antibiotic use, breastfeeding and consumption of organic foods were unrelated to a family history of atopic manifestations.Conclusion Some 'prudent' lifestyle characteristics differed between atopic and non-atopic families, depending on whether atopic manifestations were present in parents or older siblings. This has important consequences for the validity in epidemiological studies on the aetiology of allergy in children. Confounding by indication because of a family history of atopic manifestations can best be controlled for by considering atopy in parents and siblings as separate confounders.

BACKGROUND. To the authors' knowledge, only a few prospective studies to date have investigated the correlation between vegetable and fruit consumption and the risk of ovarian carcinoma and their results have been inconclusive.METHODS. Vegetable and fruit intake was assessed in relation to ovarian carcinoma, among 62,573 postmenopausal women participating in The Netherlands Cohort Study on Diet and Cancer. Women reported on dietary habits and on other risk factors for cancer in a self-administered questionnaire in 1986. Follow-up of cancer was implemented by annual record linkage with The Netherlands Cancer Registry and a pathology register. After 11.3 years of follow-up, data regarding 252 incident invasive epithelial ovarian carcinoma cases and of 2216 subcohort members were available for case-cohort analyses.RESULTS. Multivariable-adjusted rate ratios (RR) of ovarian carcinoma for women in the highest compared with the lowest quintile of intake (RRQ5 (vs.) (Q1)) were 0.98 (95% confidence interval [95% CI], 0.61-1.58) for total vegetables and 1.11 (95% CI, 0.70-1.78) for total fruit. The RRQ5 (vs.) (Q1) values of ovarian carcinoma with intake of cooked vegetables, raw vegetables, brassicas, legumes, cooked leafy vegetables, and raw leafy vegetables were 1.35 (95% CI, 0.83-2.21), 0.75 (95% CI, 0.48-1.18), 1.42 (95% CI, 0.88-2.29), 0.93 (95% CI, 0.60-1.44), 1.05 (95% CI, 0.66-1.67), and 1.23 (95% CI, 0.75-2.02), respectively. With the exception of raw endive (multivariable-adjusted RR, 0.24; 95% CI, 0.07-0.78), none of the individual vegetable or fruit items showed a statistically significant association with ovarian carcinoma.CONCLUSIONS. The results of the current study did not support a significant association between vegetable or fruit consumption and ovarian carcinoma risk in a cohort of postmenopausal women.

Vegetable and fruit consumption is generally inversely associated with various cancer types, including renal cell carcinoma (RCC). The Netherlands cohort study on diet and cancer (NLCS) consists of 120,852 men and women, aged 55-69 years, who filled out a self-administered questionnaire that includes 150-item food-frequency questions and additional questions on lifestyle factors, at baseline in 1986. A case-cohort approach was used. After 9.3 years of follow-up, 275 microscopically confirmed incident cases were identified. Subjects with incomplete or inconsistent dietary data were excluded, leaving 260 RCC cases for analyses on fruit consumption and 249 RCC cases for analyses on vegetable consumption. Incidence rate ratios (RR) and corresponding 95% confidence intervals (CI) were estimated using Cox proportional hazard models. RRs for exposure variables are expressed per increment of 25 g/day and are adjusted for age, sex, smoking, body mass index and history of hypertension at baseline. The RRs for vegetable consumption were further adjusted for fruit consumption and vice versa. Total vegetable and fruit consumption (RR: 1.00; 95% CI 0.97-1.02), vegetable (RR: 1.00, 95% CI 0.96-1.06) and fruit consumption (RR: 1.00; 95% CI 0.97-1.03) were not associated with RCC risk. Also, no association existed for botanical subgroups of vegetables and fruit. For 30 individual vegetables and fruits, we observed one that significantly increased RR (mandarin consumption, RR: 1.76; 95% CI 1.28-2.42), which must be regarded cautiously because of multiple testing. These results suggest the absence of an association between vegetable and/or fruit consumption and RCC risk. (c) 2005 Wiley-Liss, Inc.

Background: The aim of the current study was to evaluate the relation between physical activity and prostate cancer risk with specific emphasis on interaction with body mass index (BMI) and baseline energy intake. Methods: The association between prostate cancer and physical activity was evaluated in the Netherlands Cohort Study, conducted among 58,279 men ages 55 to 69 years at entry. Information regarding baseline nonoccupational physical activity, history of sports participation, and occupational physical activity was collected with a questionnaire in 1986. After 9.3 years, 1,386 incident prostate cancer cases were available for case-cohort analyses. Multivariate incidence rate ratios (RR) and corresponding 95% confidence intervals (95% CI) were calculated using Cox regression analyses. Results: Neither baseline nonoccupational physical activity (RR, 1.01; 95% CI, 0.81-1.25 for >90 versus <30 minutes per day), history of sports participation (RR, 1.04; 95% CI, 0.90-1.22 for ever versus never participated), nor occupational physical activity (RR, 0.91; 95% CI, 0.70-1.18 for >12 versus <8 KJ/min energy expenditure in the longest held job) showed an inverse relation with prostate cancer risk. We found an increased risk of prostate cancer for men who were physically active for >1 hour per day in obese men (BMI > 30) and men with a high baseline energy intake. Discussion: The results of this current study do not support the hypothesis that physical activity protects against prostate cancer in men.

Because fruits and vegetables are rich in bioactive compounds with potential cancer-preventive actions, increased consumption may reduce the risk of ovarian cancer. Evidence on the association between fruit and vegetable intake and ovarian cancer risk has not been consistent. We analyzed and pooled the primary data from 12 prospective studies in North America and Europe. Fruit and vegetable intake was measured at baseline in each study using a validated food-frequency questionnaire. To summarize the association between fruit and vegetable intake and ovarian cancer, study-specific relative risks (RR) were estimated using the Cox proportional hazards model, and then combined using a random-effects model. Among 560,441 women, 2,130 cases of invasive epithelial ovarian cancer occurred during a maximum follow-up of 7 to 22 years across studies. Total fruit intake was not associated with ovarian cancer risk—the pooled multivariate RR for the highest versus the lowest quartile of intake was 1.06 [95% confidence interval (95% CI), 0.92-1.21; P value, test for trend = 0.73; P value, test for between-studies heterogeneity = 0.74]. Similarly, results for total vegetable intake indicated no significant association (pooled multivariate RR, 0.90; 95% CI, 0.78-1.04, for the highest versus the lowest quartile; P value, test for trend = 0.06; P value, test for between-studies heterogeneity = 0.31). Intakes of botanically defined fruit and vegetable groups and individual fruits and vegetables were also not associated with ovarian cancer risk. Associations for total fruits and vegetables were similar for different histologic types. These results suggest that fruit and vegetable consumption in adulthood has no important association with the risk of ovarian cancer.

The contribution of cigarette smoking to sporadic colorectal cancer may differ according to molecular aspects of the tumor or according to glutathione S-transferase M1 (GSTM1) or glutathione S-transferase T1 (GSTT1) genotype. In the prospective Netherlands Cohort Study on Diet and Cancer, adjusted incidence rate ratios for 1986-1993 were computed for overall colorectal cancer, tumors with and without adenomatous polyposis coli (APC) mutations, and tumors with and without human mut-L homologue 1 (hMLH1) expression, according to cigarette smoking characteristics (661 cases, 2,948 subcohort members). Case-only analyses were performed to estimate odds ratios for interaction between cigarette smoking and GSTM1 and GSTT1 genotypes. In comparison with never smokers, a high smoking frequency increased the risk of colorectal cancer (for a five-cigarette/day increment, incidence rate ratio (IRR) = 1.07, 95% confidence interval (CI): 1.03, 1.12), and this association was stronger in 371 tumors without a truncating APC mutation (IRR = 1.11, 95% CI: 1.05, 1.17). Long-term smoking was associated with lack of hMLH1 expression in 56 tumors (for a 10-year increment, IRR = 1.17, 95% CI: 1.00, 1.37). No statistically significant interactions between smoking and GSTM1 or GSTT1 genotype were observed. These results indicate that cigarette smoking is associated with risk of colorectal cancer, and this association may depend on molecular characteristics of the tumor as defined by APC mutation and hMLH1 expression status.

Background: Clinical and pathologic differences exist between colon carcinomas deficient and proficient in the mismatch repair protein hMLH1. Animal and in vitro studies suggest that fruits, vegetables, folate, and antioxidants are associated with colonic expression of mismatch repair genes. Methods: Associations between consumption of fruits and vegetables and hMLH1 protein–deficient and –proficient colon cancer were evaluated in the Netherlands Cohort Study on diet and cancer using a case-cohort approach. A self-administered food frequency questionnaire was completed, in 1986, by 120,852 individuals ages 55 to 69 years. Using immunohistochemistry, hMLH1 protein expression was assessed in colon cancer tissue obtained from 441 patients who were identified over 7.3 years of follow-up excluding the initial 2.3 years. Incidence rate ratios (RR) were estimated for hMLH1 protein–deficient and –proficient colon cancer. Results: hMLH1 protein expression was absent in 54 tumors (12.2%) and present in 387 tumors. Fruit consumption was associated with hMLH1 protein–deficient colon cancer [highest versus lowest tertile, RR, 0.46; 95% confidence interval (95% CI), 0.23-0.90; Ptrend = 0.029] but not with hMLH1 protein–proficient tumors (highest versus lowest tertile, RR, 1.03; 95% CI, 0.78-1.35; Ptrend = 0.81). Total consumption of vegetables was not associated with either type of tumor (hMLH1 protein deficient: RR, 0.86; 95% CI, 0.45-1.65; Ptrend = 0.67; hMLH1 protein proficient: RR, 0.94; 95% CI, 0.72-1.23; Ptrend = 0.72). No associations were observed for folate, fiber, antioxidants, or subgroups of vegetables. Conclusion: These analyses indicate that an inverse association between consumption of fruits and colon cancer may be confined to the subgroup of tumors with a deficient mismatch repair system.

Background: Although smoking is the primary cause of lung cancer, much is unknown about lung cancer etiology, including risk determinants for nonsmokers and modifying factors for smokers.

The objective of this article was to study the association between dietary patterns and lung cancer incidence in the Netherlands Cohort Study on Diet and Cancer. The baseline measurement of this prospective case cohort study that was completed by 58,279 men in 1986 included a self-administered questionnaire on dietary intake, smoking habits, and other covariates. Follow-up was established by computerized record linkage to cancer registries and a pathology register. After 9.3 years of follow-up, 1,426 confirmed cases of incident male lung cancer were detected. Five dietary patterns were identified by exploratory factor analysis in a randomly sampled subcohort (n = 2,190). The dietary pattern labeled "salad vegetables" was associated with decreased risk of lung cancer [rate ratios (RR)(Q5), 0.75; 95% confidence interval (CI), 0.55-1.01], after multivariate adjustment. This inverse association was most evident among current and former smokers. A dietary pattern labeled "sweet foods" was also inversely associated with lung cancer risk (RRQ5, 0.62; 95% CI, 0.43-0.89). However, the higher intake of monosaccharides and disaccharides, fruits, and lower consumption of alcohol associated with this pattern could not account for its full protective effect. The "pork, processed meat, and potatoes" pattern was nonsignificantly associated with increased risk (RRQ5, 1.44; 95% CI, 0.99-2.09), and this positive association was most evident among current smokers. The other dietary patterns characterized by brown/white bread substitution and by consumption of cooked vegetables were not associated with lung cancer risk. These results show how studying both single factors and dietary patterns gives more insight into the complex, and often seemingly inconsistent, associations between diet and cancer.

The proportions of X and Y chromosome bearing sperms in human semen are equal, but more boys than girls are born. Male embryos and fetuses have a greater risk of attrition in utero than their female counterparts, and therefore male excess is likely to be still larger at the time of conception. It remains unexplained, however, what is responsible, presumably at some point between insemination and conception, for the greater probability of Y bearing sperms fusing with the ovum. One hypothesis relates to experiments showing that Y bearing sperms swim faster than X bearing sperms in viscous fluids.1 For natural conception, human sperms have to penetrate cervical mucus, the viscosity of which varies among and within women.2 Since mucal viscosity also influences the probability of conception,2 we expected that natural conceptions that take longer to achieve are more likely to be male than quick conceptions. We tested our prediction by assessing the relation between time to pregnancy and sex of the offspring.We …

Background. Studies in animals have suggested that calcium may reduce the risk of colorectal cancer. However, results from epidemiologic studies of intake of calcium or dairy foods and colorectal cancer risk have been inconclusive. Methods: We pooled the primary data from 10 cohort studies in five countries that assessed usual dietary intake by using a validated food frequency questionnaire at baseline. For most studies, follow-up was extended beyond that in the original publication. The studies included 534 536 individuals, among whom 4992 incident cases of colorectal cancer were diagnosed between 6 and 16 years of follow-up. Pooled multivariable relative risks for categories of milk intake and quintiles of calcium intake and 95% confidence intervals (CIs) were calculated. All statistical tests were two-sided. Results: Milk intake was related to a reduced risk of colorectal cancer. Compared with the lowest category of intake (<70 g/day), relative risks of colorectal cancer for increasing categories (70-174, 175-249, and greater than or equal to250 g/day) of milk intake were 0.94 (95% CI = 0.86 to 1.02), 0.88 (95% CI = 0.81 to 0.96), and 0.85 (95% CI = 0.78 to 0.94), respectively (P-trend<.001). Calcium intake was also inversely related to the risk of colorectal cancer. The relative risk for the highest versus the lowest quintile of intake was 0.86 (95% CI = 0.78 to 0.95; P-trend = .02) for dietary calcium and 0.78 (95% CI = 0.69 to 0.88; P-trend<.001) for total calcium (combining dietary and supplemental sources). These results were consistent across studies and sex. The inverse association for milk was limited to cancers of the distal colon (P-trend<.001) and rectum (P-trend = .02). Conclusion: Higher consumption of milk and calcium is associated with a lower risk of colorectal cancer.