A. R. Vieira
Imperial College London
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Annals of Oncology | 2014
D. S. M. Chan; A. R. Vieira; D. Aune; Elisa V. Bandera; Darren C. Greenwood; Anne McTiernan; D. A. Navarro Rosenblatt; Inger Thune; R. Vieira; Teresa Norat
The current systematic literature review and meta-analysis extends and confirms the associations of obesity with an unfavourable overall and breast cancer survival in pre and postmenopausal breast cancer, regardless of when BMI is ascertained. Increased risks of mortality in underweight and overweight women and J-shape associations with total mortality were also observed. The recommendation of maintaining a healthy body weight throughout life is important as obesity is a pandemic health concern.
Annals of Oncology | 2012
Dagfinn Aune; D. S. M. Chan; Darren C. Greenwood; A. R. Vieira; D. A. Navarro Rosenblatt; Rui Vieira; Teresa Norat
BACKGROUND Evidence from case-control studies suggest that dietary fiber may be inversely related to breast cancer risk, but it is unclear if this is supported by prospective data. We conducted a systematic review and meta-analysis of the evidence from prospective studies. METHODS PubMed was searched for prospective studies of fiber intake and breast cancer risk until 31st August 2011. Random effects models were used to estimate summary relative risks (RRs). RESULTS Sixteen prospective studies were included. The summary RR for the highest versus the lowest intake was 0.93 [95% confidence interval (CI) 0.89-0.98, I(2) = 0%] for dietary fiber, 0.95 (95% CI 0.86-1.06, I(2) = 4%) for fruit fiber, 0.99 (95% CI 0.92-1.07, I(2) = 1%) for vegetable fiber, 0.96 (95% CI 0.90-1.02, I(2) = 5%) for cereal fiber, 0.91 (95% CI 0.84-0.99, I(2) = 7%) for soluble fiber and 0.95 (95% CI 0.89-1.02, I(2) = 0%) for insoluble fiber. The summary RR per 10 g/day of dietary fiber was 0.95 (95% CI 0.91-0.98, I(2) = 0%, P(heterogeneity) = 0.82). In stratified analyses, the inverse association was only observed among studies with a large range (≥13 g/day) or high level of intake (≥25 g/day). CONCLUSION In this meta-analysis of prospective studies, there was an inverse association between dietary fiber intake and breast cancer risk.
British Journal of Nutrition | 2014
Itziar Abete; Dora Romaguera; A. R. Vieira; Adolfo López de Munain; Teresa Norat
An association between processed and red meat consumption and total mortality has been reported by epidemiological studies; however, there are many controversial reports regarding the association between meat consumption and CVD and IHD mortality. The present meta-analysis was carried out to summarise the evidence from prospective cohort studies on the association between consumption of meat (total, red, white and processed) and all-cause, CVD and IHD mortality. Cohort studies were identified by searching the PubMed and ISI Web of Knowledge databases. Risk estimates for the highest v. the lowest consumption category and dose-response meta-analysis were calculated using a random-effects model. Heterogeneity among the studies was also evaluated. A total of thirteen cohort studies were identified (1 674 272 individuals). Subjects in the highest category of processed meat consumption had 22 and 18 % higher risk of mortality from any cause and CVD, respectively. Red meat consumption was found to be associated with a 16 % higher risk of CVD mortality, while no association was found for total and white meat consumption. In the dose-response meta-analysis, an increase of 50 g/d in processed meat intake was found to be positively associated with all-cause and CVD mortality, while an increase of 100 g/d in red meat intake was found to be positively associated with CVD mortality. No significant associations were observed between consumption of any type of meat and IHD mortality. The results of the present meta-analysis indicate that processed meat consumption could increase the risk of mortality from any cause and CVD, while red meat consumption is positively but weakly associated with CVD mortality. These results should be interpreted with caution due to the high heterogeneity observed in most of the analyses as well as the possibility of residual confounding.
The American Journal of Clinical Nutrition | 2015
Dagfinn Aune; Deborah A. Navarro Rosenblatt; D. S. M. Chan; A. R. Vieira; Rui Vieira; Darren C. Greenwood; Lars J. Vatten; Teresa Norat
BACKGROUND Dairy product and calcium intakes have been associated with increased prostate cancer risk, but whether specific dairy products or calcium sources are associated with risk is unclear. OBJECTIVE In the Continuous Update Project, we conducted a meta-analysis of prospective studies on intakes of dairy products and calcium and prostate cancer risk. DESIGN PubMed and several other databases were searched up to April 2013. Summary RRs were estimated by using a random-effects model. RESULTS Thirty-two studies were included. Intakes of total dairy products [summary RR: 1.07 (95% CI: 1.02, 1.12; n = 15) per 400 g/d], total milk [summary RR: 1.03 (95% CI: 1.00, 1.07; n = 14) per 200 g/d], low-fat milk [summary RR: 1.06 (95% CI: 1.01, 1.11; n = 6) per 200 g/d], cheese [summary RR: 1.09 (95% CI: 1.02, 1.18; n = 11) per 50 g/d], and dietary calcium [summary RR: 1.05 (95% CI: 1.02, 1.09; n = 15) per 400 mg/d] were associated with increased total prostate cancer risk. Total calcium and dairy calcium intakes, but not nondairy calcium or supplemental calcium intakes, were also positively associated with total prostate cancer risk. Supplemental calcium was associated with increased risk of fatal prostate cancer. CONCLUSIONS High intakes of dairy products, milk, low-fat milk, cheese, and total, dietary, and dairy calcium, but not supplemental or nondairy calcium, may increase total prostate cancer risk. The diverging results for types of dairy products and sources of calcium suggest that other components of dairy rather than fat and calcium may increase prostate cancer risk. Any additional studies should report detailed results for subtypes of prostate cancer.
The American Journal of Clinical Nutrition | 2012
Dagfinn Aune; D. S. M. Chan; A. R. Vieira; Deborah A. Navarro Rosenblatt; Rui Vieira; Darren C. Greenwood; Teresa Norat
BACKGROUND Measurement errors in the dietary assessment of fruit and vegetable intake may attenuate associations with breast cancer risk and might explain the weak associations observed in epidemiologic studies. Carotenoid concentrations in blood are biomarkers of fruit and vegetable intake; however, no systematic assessment has compared dietary intake with blood concentrations of carotenoids and breast cancer risk. OBJECTIVE We conducted a systematic review and meta-analysis of prospective studies of dietary intake and blood concentrations of carotenoids and breast cancer risk. DESIGN We searched PubMed and several other databases for relevant studies up to 31 August 2011. Random-effects models were used to estimate summary estimates. RESULTS Of the 6 dietary carotenoids assessed, only intake of β-carotene was significantly associated with a reduced breast cancer risk (summary RR: 0.95; 95% CI: 0.91, 0.99; I(2): 0%) per 5000 μg/d (n = 10). In contrast, the summary RR for blood concentrations of carotenoids was 0.78 (95% CI: 0.61, 0.99; I(2): 53%) per 100 μg total carotenoids/dL (n = 7), 0.74 (95% CI: 0.57, 0.97; I(2): 43%) per 50 μg β-carotene/dL (n = 13), 0.82 (95% CI: 0.73, 0.92, I(2): 3%) per 10 μg α-carotene/dL (n = 12), and 0.68 (95% CI: 0.52, 0.89; I(2): 0%) per 25 μg lutein/dL (n = 6). CONCLUSIONS Blood concentrations of carotenoids are more strongly associated with reduced breast cancer risk than are carotenoids assessed by dietary questionnaires. Our results suggest that the use of certain biomarkers may clarify inconsistent and weak results between dietary intake and breast cancer risk.
Annals of Oncology | 2015
Dagfinn Aune; D. A. Navarro Rosenblatt; D. S. M. Chan; Snieguole Vingeliene; Leila Abar; A. R. Vieira; Darren C. Greenwood; Elisa V. Bandera; Teresa Norat
BACKGROUND Greater body mass index (BMI) has been convincingly related to increased endometrial cancer risk, however, whether adiposity earlier in life or abdominal fatness is an independent risk factor and whether weight gain or greater height increases the risk is not clear. METHODS As part of the Continuous Update Project of the World Cancer Research Fund International, we conducted a systematic review and meta-analysis of prospective studies of the association between anthropometric measures and endometrial cancer risk and searched PubMed and several other databases up to February 2015. Summary relative risks (RRs) were calculated using a random-effects model. RESULTS Thirty prospective studies of BMI and endometrial cancer risk with 22 320 cases among 6 445 402 participants were included. The summary RR for a 5-unit increment was 1.54 [95% confidence interval (CI) 1.47-1.61, I(2) = 81%]. Although the test for non-linearity was significant, Pnon-linearity < 0.0001, and the curve was steeper within the overweight and obese BMI ranges, there was evidence of increased risk even within the high normal BMI range. The summary RR was 1.45 (95% CI 1.28-1.64, I(2) = 76%) per 5 BMI units for BMI in young adulthood, 1.18 (95% CI 1.14-1.23, I(2) = 67%) per 5 kg increase of weight, and 1.16 (95% CI 1.12-1.20, I(2) = 51%) per 5 kg of weight gained between young adulthood and study baseline, 1.27 (95% CI 1.17-1.39, I(2) = 71%) per 10 cm increase in waist circumference, 1.21 (95% CI 1.13-1.29, I(2) = 0%) per 0.1-unit increment in waist-to-hip ratio and 1.30 (95% CI 1.19-1.41, I(2) = 0%) per 10-cm increase in hips circumference. The summary RR was 1.15 (95% CI 1.09-1.22, I(2) = 61%) for a 10-cm increase in height. CONCLUSIONS All measures of adiposity were associated with increased risk of endometrial cancer, and in addition increasing height was associated with increased risk.
Annals of Oncology | 2016
A. R. Vieira; Leila Abar; Snieguole Vingeliene; D. S. M. Chan; Dagfinn Aune; D. Navarro-Rosenblatt; Christophe Stevens; Darren C. Greenwood; Teresa Norat
BACKGROUND Lung cancer is the most common cause of cancer death. Fruits and vegetables containing carotenoids and other antioxidants have been hypothesized to decrease lung cancer risk. As part of the World Cancer Research Fund International Continuous Update Project, we conducted a systematic review and meta-analysis of prospective studies. METHODS We searched PubMed and several databases up to December 2014 for prospective studies. We conducted meta-analyses comparing the highest and lowest intakes and dose-response meta-analyses to estimate summary relative risks (RRs) and 95% confidence intervals (CIs), and examine possible non-linear associations. We combined results from the Pooling Project with the studies we identified to increase the statistical power of our analysis. RESULTS When comparing the highest with the lowest intakes, the summary RR estimates were 0.86 [95% CI 0.78-0.94; n (studies) = 18] for fruits and vegetables, 0.92 (95% CI 0.87-0.97; n = 25) for vegetables and 0.82 (95% CI 0.76-0.89; n = 29) for fruits. The association with fruit and vegetable intake was marginally significant in current smokers and inverse but not significant in former or never smokers. Significant inverse dose-response associations were observed for each 100 g/day increase: for fruits and vegetables [RR: 0.96; 95% CI 0.94-0.98, I(2) = 64%, n = 14, N (cases) = 9609], vegetables (RR: 0.94; 95% CI 0.89-0.98, I(2) = 48%, n = 20, N = 12 563) and fruits (RR: 0.92; 95% CI 0.89-0.95, I(2) = 57%, n = 23, N = 14 506). Our results were consistent among the different types of fruits and vegetables. The strength of the association differed across locations. There was evidence of a non-linear relationship (P < 0.01) between fruit and vegetable intake and lung cancer risk showing that no further benefit is obtained when increasing consumption above ∼400 g per day. CONCLUSIONS Eliminating tobacco smoking is the best strategy to prevent lung cancer. Although residual confounding by smoking cannot be ruled out, the current evidence from prospective studies is consistent with a protective role of fruit and vegetables in lung cancer aetiology.
Annals of Oncology | 2017
A. R. Vieira; Leila Abar; Doris S. M. Chan; Snieguole Vingeliene; Elli Polemiti; Christophe Stevens; Darren C. Greenwood; Teresa Norat
Objective As part of the World Cancer Research Fund International Continuous Update Project, we updated the systematic review and meta-analysis of prospective studies to quantify the dose-response between foods and beverages intake and colorectal cancer risk. Data sources PubMed and several databases up to 31 May 2015. Study selection Prospective studies reporting adjusted relative risk estimates for the association of specific food groups and beverages and risk of colorectal, colon and rectal cancer. Data synthesis Dose-response meta-analyses using random effect models to estimate summary relative risks (RRs). Results About 400 individual study estimates from 111 unique cohort studies were included. Overall, the risk increase of colorectal cancer is 12% for each 100 g/day increase of red and processed meat intake (95% CI = 4-21%, I2=70%, pheterogeneity (ph)<0.01) and 7% for 10 g/day increase of ethanol intake in alcoholic drinks (95% CI = 5-9%, I2=25%, ph = 0.21). Colorectal cancer risk decrease in 17% for each 90g/day increase of whole grains (95% CI = 11-21%, I2 = 0%, ph = 0.30, 6 studies) and 13% for each 400 g/day increase of dairy products intake (95% CI = 10-17%, I2 = 18%, ph = 0.27, 10 studies). Inverse associations were also observed for vegetables intake (RR per 100 g/day =0.98 (95% CI = 0.96-0.99, I2=0%, ph = 0.48, 11 studies) and for fish intake (RR for 100 g/day = 0.89 (95% CI = 0.80-0.99, I2=0%, ph = 0.52, 11 studies), that were weak for vegetables and driven by one study for fish. Intakes of fruits, coffee, tea, cheese, poultry and legumes were not associated with colorectal cancer risk. Conclusions Our results reinforce the evidence that high intake of red and processed meat and alcohol increase the risk of colorectal cancer. Milk and whole grains may have a protective role against colorectal cancer. The evidence for vegetables and fish was less convincing.
International Journal of Cancer | 2015
Dagfinn Aune; Deborah A. Navarro Rosenblatt; Doris S. M. Chan; Leila Abar; Snieguole Vingeliene; A. R. Vieira; Darren C. Greenwood; Teresa Norat
In the World Cancer Research Fund/American Institute for Cancer Research report from 2007 the evidence relating body fatness to ovarian cancer risk was considered inconclusive, while the evidence supported a probably causal relationship between adult attained height and increased risk. Several additional cohort studies have since been published, and therefore we conducted an updated meta‐analysis of the evidence as part of the Continuous Update Project. We searched PubMed and several other databases up to 20th of August 2014. Summary relative risks (RRs) were calculated using a random effects model. The summary relative risk for a 5‐U increment in BMI was 1.07 (95% CI: 1.03–1.11, I2 = 54%, n = 28 studies). There was evidence of a nonlinear association, pnonlinearity < 0.0001, with risk increasing significantly from BMI∼28 and above. The summary RR per 5 U increase in BMI in early adulthood was 1.12 (95% CI: 1.05–1.20, I2 = 0%, pheterogeneity= 0.54, n = 6), per 5 kg increase in body weight was 1.03 (95% CI: 1.02–1.05, I2 = 0%, n = 4) and per 10 cm increase in waist circumference was 1.06 (95% CI: 1.00–1.12, I2 = 0%, n = 6). No association was found for weight gain, hip circumference or waist‐to‐hip ratio. The summary RR per 10 cm increase in height was 1.16 (95% CI: 1.11–1.21, I2 = 32%, n = 16). In conclusion, greater body fatness as measured by body mass index and weight are positively associated risk of ovarian cancer, and in addition, greater height is associated with increased risk. Further studies are needed to clarify whether abdominal fatness and weight gain is associated with risk.
Cancer Medicine | 2015
A. R. Vieira; Snieguole Vingeliene; Doris S. M. Chan; Dagfinn Aune; Leila Abar; Deborah A. Navarro Rosenblatt; Darren C. Greenwood; Teresa Norat
Smoking is estimated to cause about half of all bladder cancer cases. Case–control studies have provided evidence of an inverse association between fruit and vegetable intake and bladder cancer risk. As part of the World Cancer Research/American Institute for Cancer Research Continuous Update Project, we conducted a systematic review and meta‐analysis of prospective studies to assess the dose–response relationship between fruit and vegetables and incidence and mortality of bladder cancer. We searched PubMed up to December 2013 for relevant prospective studies. We conducted highest compared with lowest meta‐analyses and dose–response meta‐analyses using random effects models to estimate summary relative risks (RRs) and 95% confidence intervals (CIs), and used restricted cubic splines to examine possible nonlinear associations. Fifteen prospective studies were included in the review. The summary RR for an increase of 1 serving/day (80 g) were 0.97 (95% CI: 0.95–0.99) I2 = 0%, eight studies for fruits and vegetables, 0.97 (95% CI: 0.94–1.00, I2 = 10%, 10 studies) for vegetables and 0.98 (95% CI: 0.96–1.00, I2 = 0%, 12 studies) for fruits. Results were similar in men and women and in current, former and nonsmokers. Amongst fruits and vegetables subgroups, for citrus fruits the summary RR for the highest compared with the lowest intake was 0.87 (95% CI: 0.76–0.99, I2 = 0%, eight studies) and for cruciferous vegetables there was evidence of a nonlinear relationship (P = 0.001). The current evidence from cohort studies is not consistent with a role for fruits and vegetables in preventing bladder cancer.