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Low physical activity and high sedentary behaviour have been clearly linked with colorectal cancer development, yet data on their potential role in colorectal cancer survival is limited. Better characterisation of these relationships is needed for the development of post‐diagnosis physical activity and sedentary behaviour guidance for colorectal cancer survivors. We searched PubMed and Embase through 28 February 2022 for studies assessing post‐diagnosis physical activity, and/or sedentary behaviour in relation to all‐cause and cause‐specific mortality and recurrence after colorectal cancer diagnosis. Total and recreational physical activity were assessed overall and by frequency, duration, intensity, and volume using categorical, linear, and non‐linear dose–response random‐effects meta‐analyses. The Global Cancer Update Programme (CUP Global) independent Expert Committee on Cancer Survivorship and Expert Panel interpreted and graded the likelihood of causality. We identified 16 observational studies on 82,220 non‐overlapping patients from six countries. Physical activity was consistently inversely associated with colorectal cancer morbidity and mortality outcomes, with 13%–60% estimated reductions in risk. Sedentary behaviour was positively associated with all‐cause mortality. The evidence had methodological limitations including potential confounding, selection bias and reverse causation, coupled with a limited number of studies for most associations. The CUP Global Expert panel concluded limited‐suggestive evidence for recreational physical activity with all‐cause mortality and cancer recurrence. Total physical activity and its specific domains and dimensions, and sedentary behaviour were all graded as limited‐no conclusion for all outcomes. Future research should focus on randomised trials, while observational studies should obtain objective and repeated physical activity measures and better adjustment for confounders. [ABSTRACT FROM AUTHOR]

Background and objective: Physical activity has benefits for the cardiovascular system, however, what levels and types of activity provide optimal cardiovascular health is unclear. We aimed to determine the level of physical activity that has the most benefits against cardiovascular diseases (CVD). Methods: PubMed, Scopus, and Web of Science were searched for prospective cohort studies on leisure-time (LTPA) or occupational physical activity (OPA) as the exposure and major types of CVD (total CVD, coronary heart disease [CHD], stroke, and atrial fibrillation [AF]) incidence as the outcome. Risk of bias of studies was evaluated using the ROBINS-I tool. Summary hazard ratios (HR) were calculated using random-effects pairwise model. Results: A total of 103 studies were included in the analysis. The highest versus the lowest LTPA was associated with a lower risk of overall CVD (HR = 0.81; 95% CI: 0.77–0.86), CHD (HR = 0.83; 0.79–0.88), and stroke (HR = 0.83; 0.79–0.88), but not AF (HR = 0.98; 0.92–1.05). Linear dose-response analyses showed a 10%, 12%, 9%, and 8% risk reduction in CVD, CHD, stroke, and AF incidence, respectively, for every 20 MET-hours/week increase in LTPA. In nonlinear dose-response analyses, there were inverse associations up to 20 MET-hours/week with 19% and 20% reduction in CVD and CHD risk, and up to 25 MET-hours/week with 22% reduction in stroke, with no further risk reduction at higher LTPA levels. For AF, there was a U-shaped nonlinear association with the maximum 8% risk reduction at 10 MET-hours/week of LTPA. Higher levels of OPA were not associated with risk of CVD, CHD, stroke, or AF. Conclusions: Overall, results showed an inverse dose-response relationship between LTPA and risk of CVD, CHD, stroke, and AF. Running was the most beneficial LTPA but the risk was similar among various LTPA intensities. OPA showed no benefits in total or any type of CVD. [ABSTRACT FROM AUTHOR]

Delirium is a neuropsychiatric syndrome represented by an acute disturbance in attention, awareness and cognition, highly prevalent in older, and critically ill patients, and associated with poor outcomes. This review synthesized existing evidence on the effectiveness of music interventions on delirium in adults, and music interventions (MIs), psychometric assessments and outcome measures used. We searched MEDLINE, PsychINFO, SCOPUS, Clinical Trials and CENTRAL for quantitative designs comparing any MIs to standard care or another intervention. From 1150 studies 12 met the inclusion criteria, and 6 were included in the meta-analysis. Narrative synthesis showed that most studies focused on prevention, few assessed delirium severity, with the majority of studies reporting beneficial effects. The summary relative risk for incident delirium comparing music vs. no music in postsurgical and critically ill older patients was 0.52 (95% confidential interval (CI): 0.20–1.35, I2 = 79.1%, heterogeneity <0.0001) for the random effects model and 0.47 (95% CI: 0.34–0.66) using the fixed effects model. Music listening interventions were more commonly applied than music therapy delivered by credentialed music therapists, and delirium assessments methods were heterogeneous, including both standardized tools and systematic observations. Better designed studies are needed addressing effectiveness of MIs in specific patient subgroups, exploring the correlations between intervention-types/dosages and delirium symptoms. [ABSTRACT FROM AUTHOR]

Background: Earlier evidence on the association between dietary polyunsaturated fatty acids and risk of diabetes has been conflicting.Purpose: To quantitatively summarize previous studies on the association between dietary LA intake, its biomarkers, and the risk of type 2 diabetes mellitus (T2DM) in the general population.Data Sources: Our data sources included PubMed/MEDLINE, Scopus, and ISI Web of Science until 24 October 2020; reference lists of all related articles; and key journals.Study Selection: We included prospective cohort studies that examined the associations of linoleic acid (LA) with the risk of T2DM in adults.Data Synthesis: The inverse variance method was applied to calculate summary relative risk (RR) of LA intake and its biomarkers, and dose-response associations were modeled using restricted cubic splines. Twenty-three publications, covering a total of 31 prospective cohorts, were included; these studies included 297,685 participants (22,639 incident diabetes cases) with dietary intake assessment and 84,171 participants (18,458 incident diabetes cases) with biomarker measurements. High intake of LA was associated with a 6% lower risk of T2DM (summary relative risk [RR] 0.94, 95% CI 0.90, 0.99; I2 = 48.5%). In the dose-response analysis, each 5% increment in energy from LA intake was associated with a 10% lower risk of T2DM. There was also evidence of a linear association between LA intake and diabetes, with the lowest risk at highest intakes. The summary RR for diabetes per SD increment in LA concentrations in adipose tissue/blood compartments was 0.85 (95% CI 0.80, 0.90; I2 = 66.2%). The certainty of the evidence was assessed as moderate.Limitations: A limitation of our work was the observational design of studies included in the analyses.Conclusions: We found that a high intake of dietary LA and elevated concentrations of LA in the body were both significantly associated with a lower risk of T2DM. These findings support dietary recommendations to consume dietary LA. [ABSTRACT FROM AUTHOR]

Diabetes mellitus has been associated with increased risk of pancreatitis in several studies, however, not all studies have found an association. We conducted a systematic review and meta-analysis of prospective studies on diabetes mellitus and pancreatitis to clarify the association. PubMed and Embase databases were searched for studies on diabetes mellitus and pancreatitis up to 8th of January 2020. Cohort studies that reported adjusted relative risk (RR) estimates and 95% confidence intervals (CIs) for the association between diabetes diagnosis and pancreatitis were included and summary RRs (95% CIs) were calculated using a random effects model. Eight cohort studies were included in the meta-analysis, and seven of these were included in the analysis of diabetes mellitus and acute pancreatitis (14124 cases, 5.7 million participants). Comparing diabetes patients with persons without diabetes the summary RRs (95% CIs) were 1.74 (95% CI: 1.33–2.29, I2 = 95%) for acute pancreatitis, 1.40 (95% CI: 0.88–2.22, I2 = 0%, n = 2) for chronic pancreatitis, and 1.39 (95% CI: 1.07–1.80, I2 = 54%, n = 3) for pancreatitis overall. Although there was some indication of publication bias in the analysis of acute pancreatitis this appeared to be explained by one outlying study which when excluded did not substantially alter the association. The results persisted in several subgroup and sensitivity analyses. These results suggest that diabetes patients are at an increased risk of acute pancreatitis. Further studies are needed on diabetes and risk of chronic pancreatitis, pancreatitis overall and on gallstone-related and non-gallstone-related pancreatitis. [ABSTRACT FROM AUTHOR]

Tobacco smoking has been associated with increased risk of pancreatitis in several studies, however, not all studies have found an association and it is unclear whether there is a dose-response relationship between increasing amount of tobacco smoked and pancreatitis risk. We conducted a systematic review and meta-analysis of prospective studies on tobacco smoking and pancreatitis to clarify the association. PubMed and Embase databases were searched for relevant studies up to April 13th, 2019. Prospective studies that reported adjusted relative risk (RR) estimates and 95% confidence intervals (CIs) for the association between tobacco smoking and pancreatitis were included and summary RRs were calculated using a random effects model. Ten prospective studies were included. The summary RR for acute pancreatitis was 1.49 (95% CI: 1.29–1.72, I2 = 68%, n = 7) for current smokers, 1.24 (95% CI: 1.15–1.34, I2 = 0%, n = 7) for former smokers, and 1.39 (95% CI: 1.25–1.54, I2 = 69%, n = 7) for ever smokers compared to never smokers. Similar results were observed for chronic pancreatitis and acute/chronic pancreatitis combined. The summary RR per 10 cigarettes per day was 1.30 (95% CI: 1.18–1.42, I2 = 42%, n = 3) and per 10 pack-years in current smokers was 1.13 (95% CI: 1.08–1.17, I2 = 14%, n = 4) for acute pancreatitis and results were similar for chronic pancreatitis and acute/chronic pancreatitis combined. These results suggest that tobacco smoking increases the risk of acute and chronic pancreatitis and acute and chronic pancreatitis combined and that there is a dose-response relationship between increasing number of cigarettes and pack-years and pancreatitis risk. [ABSTRACT FROM AUTHOR]

Background: Adiposity has been associated with elevated risk of urinary incontinence in epidemiological studies; however, the strength of the association has differed between studies.Objectives: To conduct a systematic literature review and dose-response meta-analysis of prospective studies on adiposity and risk of urinary incontinence.Search Strategy: We searched PubMed and Embase databases up to 19 July 2017.Selection Criteria: Prospective cohort studies were included.Data Collection and Analysis: Data were extracted by one reviewer and checked for accuracy by a second reviewer. Summary relative risks (RRs) and 95% confidence intervals (CIs) were calculated using random effects models.Main Results: Twenty-four prospective studies were included. The summary RR per 5 kg/m2 increment in body mass index (BMI) was 1.20 (95% CI 1.16-1.25, I2  = 62%, n = 11) for population-based studies and 1.19 (95% CI 1.08-1.30, I2  = 87.1%, n = 8) for pregnancy-based studies, 1.18 (95% CI 1.14-1.22, I2  = 0%, n = 2) per 10 cm increase in waist circumference and 1.34 (95% CI 1.11-1.62, I2  = 90%, n = 2) per 10 kg of weight gain. Although the test for nonlinearity was significant for BMI, P = 0.04, the association was approximately linear. For subtypes of urinary incontinence the summary RR per 5 BMI units was 1.45 (95% CI 1.25-1.68, I2  = 85%, n = 3) for frequent incontinence, 1.52 (95% CI 1.37-1.68, I2  = 34%, n = 4) for severe incontinence, 1.33 (95% CI 1.26-1.41, I2  = 0%, n = 8) for stress incontinence, 1.26 (95% CI 1.14-1.40, I2  = 70%, n = 7) for urge incontinence, and 1.52 (95% CI 1.36-1.69, I2  = 0%, n = 3) for mixed incontinence.Conclusion: These results suggest excess weight may increase risk of urinary incontinence.Tweetable Abstract: Overweight and obesity increase the risk of urinary incontinence. [ABSTRACT FROM AUTHOR]

Background: Diabetes mellitus has been associated with reduced risk of abdominal aortic aneurysm in a number of epidemiological studies, however, until recently little data from prospective studies have been available. We therefore conducted a systematic review and meta-analysis of prospective studies to quantify the association.Material and Methods: Two investigators searched the PubMed and Embase databases for studies of diabetes and abdominal aortic aneurysm up to May 8th 2018. Prospective studies were included if they reported adjusted relative risk (RR) estimates and 95% confidence intervals (95% CIs) of abdominal aortic aneurysm associated with a diabetes diagnosis. Summary relative risks were estimated by use of a random effects model.Results: We identified 16 prospective studies with 16,572 cases among 4,563,415 participants that could be included in the meta-analysis. The summary RR for individuals with diabetes compared to individuals without diabetes was 0.58 (95% CI: 0.51-0.66, I2 = 40.4%, pheterogeneity = 0.06). The results persisted when stratified by sex, duration of follow-up, and in most of the other subgroup analyses. There was no evidence of publication bias with Egger's test, p = 0.64 or by inspection of the funnel plots.Conclusions: These results suggest that individuals with diabetes mellitus are at a reduced risk of abdominal aortic aneurysm, however, whether pharmacological agents for diabetes mellitus explain this observation needs to be clarified in future studies. [ABSTRACT FROM AUTHOR]

Background: High dietary intake or blood concentrations (as biomarkers of dietary intake) of vitamin C, carotenoids, and vitamin E have been associated with reduced risk of cardiovascular disease, cancer, and mortality, but these associations have not been systematically assessed. Objective: We conducted a systematic review and meta-analysis of prospective studies of dietary intake and blood concentrations of vitamin C, carotenoids, and vitamin E in relation to these outcomes. Design: We searched PubMed and Embase up to 14 February 2018. Summary RRs and 95% CIs were calculated with the use of randomeffects models. Results: Sixty-nine prospective studies (99 publications) were included. The summary RR per 100-mg/d increment of dietary vitamin C intake was 0.88 (95% CI: 0.79, 0.98, I2 = 65%, n = 11) for coronary heart disease, 0.92 (95% CI: 0.87, 0.98, I2 = 68%, n = 12) for stroke, 0.89 (95% CI: 0.85, 0.94, I2 = 27%, n = 10) for cardiovascular disease, 0.93 (95% CI: 0.87, 0.99, I2 = 46%, n = 8) for total cancer, and 0.89 (95% CI: 0.85, 0.94, I2 = 80%, n = 14) for all-cause mortality. Corresponding RRs per 50-µmol/L increase in blood concentrations of vitamin C were 0.74 (95% CI: 0.65, 0.83, I2 = 0%, n = 4), 0.70 (95% CI: 0.61, 0.81, I2 = 0%, n = 4), 0.76 (95% CI: 0.65, 0.87, I2 = 56%, n = 6), 0.74 (95% CI: 0.66, 0.82, I2 = 0%, n = 5), and 0.72 (95% CI: 0.66, 0.79, I2 = 0%, n = 8). Dietary intake and/or blood concentrations of carotenoids (total, β-carotene, α-carotene, β-cryptoxanthin, lycopene) and α-tocopherol, but not dietary vitamin E, were similarly inversely associated with coronary heart disease, stroke, cardiovascular disease, cancer, and/or all-cause mortality. Conclusions: Higher dietary intake and/or blood concentrations of vitamin C, carotenoids, and α-tocopherol (as markers of fruit and vegetable intake) were associated with reduced risk of cardiovascular disease, total cancer, and all-cause mortality. These results support recommendations to increase fruit and vegetable intake, but not antioxidant supplement use, for chronic disease prevention. [ABSTRACT FROM AUTHOR]

Smoking is an established risk factor for cardiovascular disease including coronary heart disease and stroke, however, data regarding smoking and sudden cardiac death have not been summarized in a meta-analysis previously. We therefore conducted a systematic review and meta-analysis to clarify this association. We searched the PubMed and Embase databases for studies of smoking and sudden cardiac death up to July 20th 2017. Prospective studies were included if they reported adjusted relative risk (RR) estimates and 95% confidence intervals (CIs) for smoking and sudden cardiac death. Summary RRs were estimated by use of a random effects model. Twelve prospective studies were included. The summary RR was 3.06 (95% CI 2.46-3.82, I2 = 41%, pheterogeneity = 0.12, n = 7) for current smokers and 1.38 (95% CI 1.20-1.60, I2 = 0%, pheterogeneity = 0.55, n = 7) for former smokers compared to never smokers. For four studies using non-current (never + former) smokers as the reference category the summary RR among current smokers was 2.08 (95% CI 1.70-2.53, I2 = 18%, pheterogeneity = 0.30). The results persisted in most of the subgroup analyses. There was no evidence of publication bias. These results confirm that smoking increases the risk of sudden cardiac death. Any further studies should investigate in more detail the effects of duration of smoking, number of cigarettes per day, pack-years, and time since quitting smoking and sudden cardiac death. [ABSTRACT FROM AUTHOR]

Background: Diabetes and elevated blood glucose have been associated with increased risk of atrial fibrillation in a number of epidemiological studies, however, the findings have not been entirely consistent. We conducted a systematic review and meta-analysis to clarify the association.Material and Methods: We searched the PubMed and Embase databases for studies of diabetes and blood glucose and atrial fibrillation up to July 18th 2017. Cohort studies were included if they reported relative risk (RR) estimates and 95% confidence intervals (CIs) of atrial fibrillation associated with a diabetes diagnosis, prediabetes or blood glucose. Summary RRs were estimated using a random effects model.Results: Thirty four studies were included in the meta-analysis of diabetes, pre-diabetes or blood glucose and atrial fibrillation. Thirty two cohort studies (464,229 cases, >10,244,043 participants) were included in the analysis of diabetes mellitus and atrial fibrillation. The summary RR for patients with diabetes mellitus versus patients without diabetes was 1.30 (95% CIs: 1.03-1.66), however, there was extreme heterogeneity, I2 = 99.9%) and evidence of publication bias with Begg's test, p < 0.0001. After excluding a very large and outlying study the summary RR was 1.28 (95% CI: 1.22-1.35, I2 = 90%, n = 31, 249,772 cases, 10,244,043 participants). The heterogeneity was mainly due to differences in the size of the association between studies and the results persisted in a number of subgroup and sensitivity analyses. The summary RR was 1.20 (95% CI: 1.03-1.39, I2 = 30%, n = 4, 2392 cases, 58,547 participants) for the association between prediabetes and atrial fibrillation. The summary RR was 1.11 (95% CI: 1.04-1.18, I2 = 61%, n = 4) per 20 mg/dl increase of blood glucose in relation to atrial fibrillation (3385 cases, 247,447 participants) and there was no evidence of nonlinearity, pnonlinearity = 0.34.Conclusions: This meta-analysis suggest that prediabetes and diabetes increase the risk of atrial fibrillation by 20% and 28%, respectively, and there is a dose-response relationship between increasing blood glucose and atrial fibrillation. Any further studies should clarify whether the association between diabetes and blood glucose and atrial fibrillation is independent of adiposity. [ABSTRACT FROM AUTHOR]

Context: The investigation of dose-response associations between carbohydrate intake, glycemic index, glycemic load, and risk of breast cancer stratified by menopausal status, hormone receptor status, and body mass index (BMI) remains inconclusive. Objective: A systematic review and dose-response meta-analyses was conducted to investigate these associations. Data Sources: As part of the World Cancer Research Fund/American Institute for Cancer Research Continuous Update Project, PubMed was searched up to May 2015 for relevant studies on these associations. Study Selection: Prospective studies reporting associations between carbohydrate intake, glycemic index, or glycemic load and breast cancer risk were included. Data Extraction: Two investigators independently extracted data from included studies. Results: Random-effects models were used to summarize relative risks (RRs) and 95%CIs. Heterogeneity between subgroups, including menopausal status, hormone receptor status, and BMI was explored using meta-regression. Nineteen publications were included. The summary RRs (95%CIs) for breast cancer were 1.04 (1.00-1.07) per 10 units/d for glycemic index, 1.01 (0.98-1.04) per 50 units/d for glycemic load, and 1.00 (0.96-1.05) per 50g/d for carbohydrate intake. For glycemic index, the association appeared slightly stronger among postmenopausal women (summary RR per 10 units/d, 1.06; 95%CI, 1.02-1.10) than among premenopausal women, though the difference was not statistically significant (Pheterogeneity = 0.15). Glycemic load and carbohydrate intake were positively associated with breast cancer among postmenopausal women with estrogen-negative tumors (summary RR for glycemic load, 1.28; 95%CI, 1.08-1.52; and summary RR for carbohydrates, 1.13; 95%CI, 1.02-1.25). No differences in BMI were detected. Conclusions: Menopausal and hormone receptor status, but not BMI, might be potential influencing factors for the associations between carbohydrate intake, glycemic index, glycemic load, and breast cancer. [ABSTRACT FROM AUTHOR]

Background: Although nut consumption has been associated with a reduced risk of cardiovascular disease and all-cause mortality, data on less common causes of death has not been systematically assessed. Previous reviews missed several studies and additional studies have since been published. We therefore conducted a systematic review and meta-analysis of nut consumption and risk of cardiovascular disease, total cancer, and all-cause and cause-specific mortality. Methods: PubMed and Embase were searched for prospective studies of nut consumption and risk of cardiovascular disease, total cancer, and all-cause and cause-specific mortality in adult populations published up to July 19, 2016. Summary relative risks (RRs) and 95% confidence intervals (CIs) were calculated using random-effects models. The burden of mortality attributable to low nut consumption was calculated for selected regions. Results: Twenty studies (29 publications) were included in the meta-analysis. The summary RRs per 28 grams/day increase in nut intake was for coronary heart disease, 0.71 (95% CI: 0.63-0.80, I2 = 47%, n = 11), stroke, 0.93 (95% CI: 0.83-1.05, I2 = 14%, n = 11), cardiovascular disease, 0.79 (95% CI: 0.70-0.88, I2 = 60%, n = 12), total cancer, 0.85 (95% CI: 0.76-0.94, I2 = 42%, n = 8), all-cause mortality, 0.78 (95% CI: 0.72-0.84, I2 = 66%, n = 15), and for mortality from respiratory disease, 0.48 (95% CI: 0.26-0.89, I2 = 61%, n = 3), diabetes, 0.61 (95% CI: 0.43-0.88, I2 = 0%, n = 4), neurodegenerative disease, 0.65 (95% CI: 0.40-1.08, I2 = 5.9%, n = 3), infectious disease, 0.25 (95% CI: 0.07-0.85, I2 = 54%, n = 2), and kidney disease, 0.27 (95% CI: 0.04-1.91, I2 = 61%, n = 2). The results were similar for tree nuts and peanuts. If the associations are causal, an estimated 4.4 million premature deaths in the America, Europe, Southeast Asia, and Western Pacific would be attributable to a nut intake below 20 grams per day in 2013. Conclusions: Higher nut intake is associated with reduced risk of cardiovascular disease, total cancer and all-cause mortality, and mortality from respiratory disease, diabetes, and infections. [ABSTRACT FROM AUTHOR]

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, β-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 β-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 β-carotene and retinol were observed only in men and not in women. Nonlinear associations were observed for β-carotene, β-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. [ABSTRACT FROM AUTHOR]

Background Diabetes has been hypothesized to increase the risk of gallbladder disease based on the observation that obesity and insulin resistance are associated with gallbladder disease. Although several studies have investigated the association between a diabetes diagnosis and risk of gallbladder disease, the results have not been entirely consistent. For this reason we conducted a systematic review and meta-analysis of the available cohort studies. Materials and methods We searched the PubMed and Embase databases for studies of diabetes and gallbladder disease (defined as gallstones, cholecystectomy, or cholecystitis) up to January 9th 2015. Prospective studies were included if they reported relative risk estimates and 95% confidence intervals of gallbladder disease associated with a diabetes diagnosis. Summary relative risks were estimated by use of a random effects model. Results We identified 10 prospective studies that could be included in the meta-analysis which included 223,651 cases among 7,365,198 participants. The summary RR for diabetes patients was 1.56 (95% CI: 1.26–1.93, I 2 = 99.4%, p heterogeneity < 0.0001). The results persisted when stratified by gender, and in most subgroup analyses and there was no heterogeneity among studies with more than 10 years duration of follow-up. There was no evidence of publication bias. Conclusions Our analysis provides further support for an increased risk of gallbladder disease among diabetes patients. [ABSTRACT FROM AUTHOR]

Background: Obesity has been associated with increased risk of heart failure, but whether overweight also increases risk is unclear. It is also unclear whether abdominal adiposity is more strongly associated with heart failure risk than general adiposity. We conducted a systematic review and meta-analysis of prospective studies to clarify the strength and shape of the dose-response relationship between general and abdominal adiposity and the risk of heart failure.Methods and Results: PubMed and Embase databases were searched up to October 10, 2014. Summary relative risks were calculated using random-effects models. A total of 28 studies (27 publications) were included. Twenty-three prospective studies with >15 905 incident cases among 647 388 participants were included in the analysis of body mass index and heart failure incidence, and 4 studies were included for heart failure mortality. The summary relative risk for a 5-unit increment in body mass index was 1.41 (95% confidence interval, 1.34-1.47; I(2)=83%) for heart failure incidence and 1.26 (95% confidence interval, 0.85-1.87; I(2)=95%) heart failure mortality. Although the test for nonlinearity was significant (P<0.0001), this appeared to be attributable to a threshold at a body mass index of ≈23 to 24 kg/m(2); however, there was evidence of increased risk even in the overweight body mass index range. The summary relative risk for a 10-cm increase in waist circumference was 1.29 (95% confidence interval, 1.21-1.37; I(2)=89%) and per 0.1-unit increase in waist-to-hip ratio was 1.29 (95% confidence interval, 1.13-1.47; I(2)=82%).Conclusion: Overweight and obesity and abdominal adiposity are associated with increased risk of heart failure. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Mechanistic and epidemiologic studies provide considerable evidence for a protective association between calcium intake and incident colorectal cancer (CRC). While the relationship has not been substantiated by short-duration randomized controlled trials (RCTs) of CRC, trials do show a benefit on adenomas, a precursor to CRC. To address some of this inconsistency, we conducted dose-response meta-analyses by sources of calcium intake, based on prospective observational studies published up to December 2013 identified from PubMed, Embase, and BIOSIS. Summary relative risks (RRs) and 95% confidence intervals (CIs) were calculated using a random-effects model. For total calcium intake, each 300 mg/day increase was associated with an approximately 8% reduced risk of CRC (summary RR = 0.92, 95% CI = 0.89-0.95, I2 = 47%, 15 studies with 12,305 cases, intake = 250-1,900 mg/day, follow-up = 3.3-16 years). While the risk decreased less steeply in higher range of total calcium intake ( Pnon-linearity = 0.04), the degree of curvature was mild and statistical significance of non-linearity was sensitive to one study. For supplementary calcium, each 300 mg/day increase was associated with an approximately 9% reduced risk of CRC (summary RR = 0.91, 95% CI = 0.86-0.98, I2 = 67%, six studies with 8,839 cases, intake = 0-1,150 mg/day, follow-up = 5-10 years). The test for non-linearity was not statistically significant ( Pnon-linearity = 0.11). In conclusion, both dietary and supplementary calcium intake may continue to decrease CRC risk beyond 1,000 mg/day. Calcium supplements and non-dairy products fortified with calcium may serve as additional targets in the prevention of CRC. RCTs of calcium supplements with at least 10 years of follow-up are warranted to confirm a benefit of calcium supplements on CRC risk. [ABSTRACT FROM AUTHOR]

Aim The optimal initial fraction of oxygen ( iFiO2) for resuscitating/stabilising premature infants is not known. We aimed to study currently available information and provide guidelines regarding the iFiO2 levels needed to resuscitate/stabilise premature infants of ≤32 weeks' gestation. Methods Our systematic review and meta-analysis studied the effects of low and high iFiO2 during the resuscitation/stabilisation of 677 newborn babies ≤32 weeks' gestation. Results Ten randomised studies were identified covering 321 infants receiving low (0.21-0.30) iFiO2 levels and 356 receiving high (0.60-1.0) levels. Relative risk for mortality was 0.62 (95% CI: 0.37-1.04, I2 = 0%, pheterogeneity = 0.88) for low versus high iFiO2 ; for bronchopulmonary dysplasia, it was 1.11 (95% CI: 0.73-1.68, I2 = 46%, pheterogeneity = 0.06); and for intraventricular haemorrhage, it was 0.90 (95% CI: 0.53-1.53, I2 = 9%, pheterogeneity = 0.36). Conclusion These data show that reduced mortality approached significance when a low iFiO2 (0.21-0.30) was used for initial stabilisation, compared to a high iFiO2 (0.60-1.0). There was no significant association for bronchopulmonary dysplasia or intraventricular haemorrhage when comparing low and high iFiO2. Based on present data, premature babies ≤32 weeks' gestation in need of stabilisation in the delivery room should be given an iFiO2 of 0.21-0.30. [ABSTRACT FROM AUTHOR]

Background: The role of chorioamnionitis (CA) in the development of retinopathy of prematurity (ROP) has not been well established. Objective: To conduct a systematic review and meta-analysis of the association between CA and ROP in preterm infants. Data Sources: The authors searched MEDLINE, Embase, CINAHL, Cochrane Central Register of Controlled Trials and PubMed, reviewed reference lists of relevant articles, abstracts and conference proceedings (Society for Pediatric Research, European Society for Paediatric Research 1990-2012), sought results of unpublished trials, and contacted the primary authors of relevant studies. Study Selection: Studies were included if they had a comparison group, examined preterm infants, and reported primary data that could be used to measure the association between exposure to CA and the development of ROP. Data Extraction: Two reviewers independently screened the search results, applied inclusion criteria and assessed methodological quality using the Newcastle-Ottawa Scale. One reviewer extracted data and a second reviewer checked data extraction. Summary relative risks (RRs) were calculated using a random effects model. Data Synthesis: We identified 1,249 potentially relevant studies from the electronic databases. Twenty-seven studies involving 10,590 preterm neonates with 2,562 cases of ROP were included. Taking into account all included studies without adjusting for gestational age (GA), CA was significantly associated with ROP (any stage) [summary RR 1.33 (95% CI 1.14-1.55, I2 = 77%, pheterogeneity < 0.0001)], and a borderline significant association was observed for severe ROP (stage ≥3) [summary RR 1.27 (95% CI 0.99-1.63, I2 = 74%, pheterogeneity < 0.0001)]. There was no publication bias with Begg's test. However, subgroup analysis of studies adjusting for GA showed no significant association on CA with ROP [summary RR 0.98 (95% CI 0.77-1.26, I2 = 0%, pheterogeneity = 0.89)]. Conclusion: Unadjusted analyses showed that CA was significantly associated with ROP (any stage) as well as with severe ROP (stage ≥ 3). However, the association disappeared on analysis of studies adjusting for GA. Hence, CA cannot be definitively considered as a risk factor for ROP, and further studies should adjust for potential confounding factors and report results by stage to clarify the association with severe ROP. © 2014 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]