Blood concentrations of carotenoids and retinol and lung cancer risk: an update of the WCRF-AICR systematic review of published prospective studies.

Carotenoids and retinol are considered biomarkers of fruits and vegetables intake, and are of much interest because of their anti-inflammatory and antioxidant properties; however, there is inconsistent evidence regarding their protective effects against lung cancer. We conducted a meta-analysis of prospective studies of blood concentrations of carotenoids and retinol, and lung cancer risk. We identified relevant prospective studies published up to December 2014 by searching the PubMed and several other databases. We calculated summary estimates of lung cancer risk for the highest compared with lowest carotenoid and retinol concentrations and dose-response meta-analyses using random effects models. We used fractional polynomial models to assess potential nonlinear relationships. Seventeen prospective studies (18 publications) including 3603 cases and 458,434 participants were included in the meta-analysis. Blood concentrations of α-carotene, ß-carotene, total carotenoids, and retinol were significantly inversely associated with lung cancer risk or mortality. The summary relative risk were 0.66 (95% confidence interval [CI]: 0.55-0.80) per 5 µg/100 mL of α-carotene (studies [n] = 5), 0.84 (95% CI: 0.76-0.94) per 20 µg/100 mL of ß-carotene (n = 9), 0.66 (95% CI: 0.54-0.81) per 100 µg/100 mL of total carotenoids (n = 4), and 0.81 (95% CI: 0.73-0.90) per 70 µg/100 mL of retinol (n = 8). In stratified analysis by sex, the significant inverse associations for ß-carotene and retinol were observed only in men and not in women. Nonlinear associations were observed for ß-carotene, ß-cryptoxanthin, and lycopene, with stronger associations observed at lower concentrations. There were not enough data to conduct stratified analyses by smoking. In conclusion, higher blood concentrations of several carotenoids and retinol are associated with reduced lung cancer risk. Further studies in never and former smokers are needed to rule out confounding by smoking.

Anthropometric factors and ovarian cancer risk: a systematic review and nonlinear dose-response meta-analysis of prospective studies.

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, I(2) = 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, I(2) = 0%, pheterogeneity = 0.54, n = 6), per 5 kg increase in body weight was 1.03 (95% CI: 1.02-1.05, I(2) = 0%, n = 4) and per 10 cm increase in waist circumference was 1.06 (95% CI: 1.00-1.12, I(2) = 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, I(2) = 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.

Dairy products, calcium, and prostate cancer risk: a systematic review and meta-analysis of cohort studies.

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.

Red and processed meat intake and risk of colorectal adenomas: a systematic review and meta-analysis of epidemiological studies.

BACKGROUND: Current evidence indicates that red and processed meat intake increases the risk of colorectal cancer; however, the association with colorectal adenomas is unclear. OBJECTIVE: To conduct a systematic review and meta-analysis of epidemiological studies of red and processed meat intake and risk of colorectal adenomas as part of the Continuous Update Project of the World Cancer Research Fund. DESIGN: PubMed and several other databases were searched for relevant studies from their inception up to 31 December 2011. Summary relative risks (RRs) were estimated using a random effects model. RESULTS: Nineteen case-control studies and seven prospective studies were included in the analyses. The summary RR per 100 g/day of red meat was 1.27 (95 % CI 1.16-1.40, I (2) = 5 %, n = 16) for all studies combined, 1.20 (95 % CI 1.06-1.36, I (2) = 0 %, n = 6) for prospective studies, and 1.34 (95 % CI 1.12-1.59, I (2) = 31 %, n = 10) for case-control studies. The summary RR per 50 g/day of processed meat intake was 1.29 (95 % CI 1.10-1.53, I (2) = 27 %, n = 10) for all studies combined, 1.45 (95 % CI 1.10-1.90, I (2) = 0 %, n = 2) for prospective studies, and 1.23 (95 % CI 0.99-1.52, I (2) = 37 %, n = 8) for case-control studies. There was evidence of a nonlinear association between red meat (p nonlinearity < 0.001) and processed meat (p nonlinearity = 0.01) intake and colorectal adenoma risk. CONCLUSION: These results indicate an elevated risk of colorectal adenomas with intake of red and processed meat, but further prospective studies are warranted.

Dietary compared with blood concentrations of carotenoids and breast cancer risk: a systematic review and meta-analysis of prospective studies.

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 ß-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 ß-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.

Height and pancreatic cancer risk: a systematic review and meta-analysis of cohort studies.

BACKGROUND: Greater height has been associated with increased risk of several cancers, but epidemiological data on height and pancreatic cancer are inconclusive. We conducted a systematic review and meta-analysis of prospective studies to clarify these results. METHODS: PubMed and several other databases were searched up to September 2011. Prospective studies of height and pancreatic cancer were included. Summary relative risks were estimated by the use of a random effects model. RESULTS: We identified twelve cohort studies that were included in the meta-analysis. The summary RR per 5-cm increase in height was 1.07 (95 % CI: 1.03-1.12, I (2) = 57 %). The results were similar among men and women. The summary estimate was attenuated when we included results from two pooled analyses together with these studies, summary RR = 1.03 (95 % CI: 1.00-1.07, I (2) = 44 %). CONCLUSIONS: This meta-analysis of cohort studies provides further evidence that greater adult attained height is associated with increased pancreatic cancer risk. However, given the unexplained heterogeneity, further studies are needed before a conclusion can be drawn.