Questions remain about the strength and shape of the dose-response relationship between fruit and vegetable intake and risk of cardiovascular disease, cancer and mortality, and the effects of ...specific types of fruit and vegetables. We conducted a systematic review and meta-analysis to clarify these associations.
PubMed and Embase were searched up to 29 September 2016. Prospective studies of fruit and vegetable intake and cardiovascular disease, total cancer and all-cause mortality were included. Summary relative risks (RRs) were calculated using a random effects model, and the mortality burden globally was estimated; 95 studies (142 publications) were included.
For fruits and vegetables combined, the summary RR per 200 g/day was 0.92 95% confidence interval (CI): 0.90-0.94, I 2 = 0%, n = 15 for coronary heart disease, 0.84 (95% CI: 0.76-0.92, I 2 = 73%, n = 10) for stroke, 0.92 (95% CI: 0.90-0.95, I 2 = 31%, n = 13) for cardiovascular disease, 0.97 (95% CI: 0.95-0.99, I 2 = 49%, n = 12) for total cancer and 0.90 (95% CI: 0.87-0.93, I 2 = 83%, n = 15) for all-cause mortality. Similar associations were observed for fruits and vegetables separately. Reductions in risk were observed up to 800 g/day for all outcomes except cancer (600 g/day). Inverse associations were observed between the intake of apples and pears, citrus fruits, green leafy vegetables, cruciferous vegetables, and salads and cardiovascular disease and all-cause mortality, and between the intake of green-yellow vegetables and cruciferous vegetables and total cancer risk. An estimated 5.6 and 7.8 million premature deaths worldwide in 2013 may be attributable to a fruit and vegetable intake below 500 and 800 g/day, respectively, if the observed associations are causal.
Fruit and vegetable intakes were associated with reduced risk of cardiovascular disease, cancer and all-cause mortality. These results support public health recommendations to increase fruit and vegetable intake for the prevention of cardiovascular disease, cancer, and premature mortality.
Objective To quantify the dose-response relation between consumption of whole grain and specific types of grains and the risk of cardiovascular disease, total cancer, and all cause and cause specific ...mortality.Data sources PubMed and Embase searched up to 3 April 2016.Study selection Prospective studies reporting adjusted relative risk estimates for the association between intake of whole grains or specific types of grains and cardiovascular disease, total cancer, all cause or cause specific mortality.Data synthesis Summary relative risks and 95% confidence intervals calculated with a random effects model.Results 45 studies (64 publications) were included. The summary relative risks per 90 g/day increase in whole grain intake (90 g is equivalent to three servings—for example, two slices of bread and one bowl of cereal or one and a half pieces of pita bread made from whole grains) was 0.81 (95% confidence interval 0.75 to 0.87; I2=9%, n=7 studies) for coronary heart disease, 0.88 (0.75 to 1.03; I2=56%, n=6) for stroke, and 0.78 (0.73 to 0.85; I2=40%, n=10) for cardiovascular disease, with similar results when studies were stratified by whether the outcome was incidence or mortality. The relative risks for morality were 0.85 (0.80 to 0.91; I2=37%, n=6) for total cancer, 0.83 (0.77 to 0.90; I2=83%, n=11) for all causes, 0.78 (0.70 to 0.87; I2=0%, n=4) for respiratory disease, 0.49 (0.23 to 1.05; I2=85%, n=4) for diabetes, 0.74 (0.56 to 0.96; I2=0%, n=3) for infectious diseases, 1.15 (0.66 to 2.02; I2=79%, n=2) for diseases of the nervous system disease, and 0.78 (0.75 to 0.82; I2=0%, n=5) for all non-cardiovascular, non-cancer causes. Reductions in risk were observed up to an intake of 210-225 g/day (seven to seven and a half servings per day) for most of the outcomes. Intakes of specific types of whole grains including whole grain bread, whole grain breakfast cereals, and added bran, as well as total bread and total breakfast cereals were also associated with reduced risks of cardiovascular disease and/or all cause mortality, but there was little evidence of an association with refined grains, white rice, total rice, or total grains.Conclusions This meta-analysis provides further evidence that whole grain intake is associated with a reduced risk of coronary heart disease, cardiovascular disease, and total cancer, and mortality from all causes, respiratory diseases, infectious diseases, diabetes, and all non-cardiovascular, non-cancer causes. These findings support dietary guidelines that recommend increased intake of whole grain to reduce the risk of chronic diseases and premature mortality.
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BFBNIB, CMK, NMLJ, NUK, PNG, SAZU, UL, UM, UPUK
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.
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.
We searched PubMed and Embase up to 14 February 2018. Summary RRs and 95% CIs were calculated with the use of random-effects models.
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.
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.
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CMK, GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Background: The association between intake of dairy products and the risk of type 2 diabetes has been investigated in several studies, but the evidence is not conclusive.Objective: We conducted an ...updated systematic review and dose-response meta-analysis of dairy product intake and the risk of type 2 diabetes.Design: We searched the PubMed database for prospective cohort and nested case-control studies of dairy product intake and risk of type 2 diabetes up to 5 June 2013. Summary RRs were estimated by use of a random-effects model.Results: Seventeen cohort studies were included in the meta-analysis. In the dose-response analysis, the summary RRs (95% CIs) were 0.93 (0.87, 0.99; I2 = 33%) per 400 g total dairy products/d (n = 12), 0.98 (0.94, 1.03; I2 = 8%) per 200 g high-fat dairy products/d (n = 9), 0.91 (0.86, 0.96; I2 = 40%) per 200 g low-fat dairy products/d (n = 9), 0.87 (0.72, 1.04; I2 = 94%) per 200 g milk/d (n = 7), 0.92 (0.86, 0.99; I2 = 0%) per 50 g cheese/d (n = 8), and 0.78 (0.60, 1.02; I2 = 70%) per 200 g yogurt/d (n = 7). Nonlinear inverse associations were observed for total dairy products (P-nonlinearity < 0.0001), low-fat dairy products (P-nonlinearity = 0.06), cheese (P-nonlinearity = 0.05), and yogurt (P-nonlinearity = 0.004), and there was a flattening of the curve at higher intakes.Conclusions: This meta-analysis suggests that there is a significant inverse association between intakes of dairy products, low-fat dairy products, and cheese and risk of type 2 diabetes. Any additional studies should assess the association between other specific types of dairy products and the risk of type 2 diabetes and adjust for more confounding factors.
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CMK, GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Several studies have suggested a protective effect of intake of whole grains, but not refined grains on type 2 diabetes risk, but the dose-response relationship between different types of grains and ...type 2 diabetes has not been established. We conducted a systematic review and meta-analysis of prospective studies of grain intake and type 2 diabetes. We searched the PubMed database for studies of grain intake and risk of type 2 diabetes, up to June 5th, 2013. Summary relative risks were calculated using a random effects model. Sixteen cohort studies were included in the analyses. The summary relative risk per 3 servings per day was 0.68 (95 % CI 0.58-0.81, I² = 82 %, n = 10) for whole grains and 0.95 (95 % CI 0.88-1.04, I² = 53 %, n = 6) for refined grains. A nonlinear association was observed for whole grains, Pnoniinearity < 0.0001, but not for refined grains, Pnoniinearity = 0.10. Inverse associations were observed for subtypes of whole grains including whole grain bread, whole grain cereals, wheat bran and brown rice, but these results were based on few studies, while white rice was associated with increased risk. Our meta-analysis suggests that a high whole grain intake, but not refined grains, is associated with reduced type 2 diabetes risk. However, a positive association with intake of white rice and inverse associations between several specific types of whole grains and type 2 diabetes warrant further investigations. Our results support public health recommendations to replace refined grains with whole grains and suggest that at least two servings of whole grains per day should be consumed to reduce type 2 diabetes risk.
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BFBNIB, EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
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.
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.
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, I
= 47%, n = 11), stroke, 0.93 (95% CI: 0.83-1.05, I
= 14%, n = 11), cardiovascular disease, 0.79 (95% CI: 0.70-0.88, I
= 60%, n = 12), total cancer, 0.85 (95% CI: 0.76-0.94, I
= 42%, n = 8), all-cause mortality, 0.78 (95% CI: 0.72-0.84, I
= 66%, n = 15), and for mortality from respiratory disease, 0.48 (95% CI: 0.26-0.89, I
= 61%, n = 3), diabetes, 0.61 (95% CI: 0.43-0.88, I
= 0%, n = 4), neurodegenerative disease, 0.65 (95% CI: 0.40-1.08, I
= 5.9%, n = 3), infectious disease, 0.25 (95% CI: 0.07-0.85, I
= 54%, n = 2), and kidney disease, 0.27 (95% CI: 0.04-1.91, I
= 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.
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.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Objective To conduct a systematic review and meta-analysis of cohort studies of body mass index (BMI) and the risk of all cause mortality, and to clarify the shape and the nadir of the dose-response ...curve, and the influence on the results of confounding from smoking, weight loss associated with disease, and preclinical disease.Data sources PubMed and Embase databases searched up to 23 September 2015.Study selection Cohort studies that reported adjusted risk estimates for at least three categories of BMI in relation to all cause mortality.Data synthesis Summary relative risks were calculated with random effects models. Non-linear associations were explored with fractional polynomial models.Results 230 cohort studies (207 publications) were included. The analysis of never smokers included 53 cohort studies (44 risk estimates) with >738 144 deaths and >9 976 077 participants. The analysis of all participants included 228 cohort studies (198 risk estimates) with >3 744 722 deaths among 30 233 329 participants. The summary relative risk for a 5 unit increment in BMI was 1.18 (95% confidence interval 1.15 to 1.21; I2=95%, n=44) among never smokers, 1.21 (1.18 to 1.25; I2=93%, n=25) among healthy never smokers, 1.27 (1.21 to 1.33; I2=89%, n=11) among healthy never smokers with exclusion of early follow-up, and 1.05 (1.04 to 1.07; I2=97%, n=198) among all participants. There was a J shaped dose-response relation in never smokers (Pnon-linearity <0.001), and the lowest risk was observed at BMI 23-24 in never smokers, 22-23 in healthy never smokers, and 20-22 in studies of never smokers with ≥20 years’ follow-up. In contrast there was a U shaped association between BMI and mortality in analyses with a greater potential for bias including all participants, current, former, or ever smokers, and in studies with a short duration of follow-up (<5 years or <10 years), or with moderate study quality scores.Conclusion Overweight and obesity is associated with increased risk of all cause mortality and the nadir of the curve was observed at BMI 23-24 among never smokers, 22-23 among healthy never smokers, and 20-22 with longer durations of follow-up. The increased risk of mortality observed in underweight people could at least partly be caused by residual confounding from prediagnostic disease. Lack of exclusion of ever smokers, people with prevalent and preclinical disease, and early follow-up could bias the results towards a more U shaped association.
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BFBNIB, CMK, NMLJ, NUK, PNG, SAZU, UL, UM, UPUK
A history of hypertension has been associated with increased risk of endometrial cancer in several studies, but the results have not been consistent. We conducted a systematic review and ...meta-analysis of case-control and cohort studies to clarify the association between hypertension and endometrial cancer risk. PubMed and Embase databases were searched up to 27
of February 2016. Prospective and case-control studies which reported adjusted relative risk estimates and 95% confidence intervals of endometrial cancer associated with a hypertension diagnosis were included. Summary relative risks were estimated using a random effects model. Nineteen case-control studies and 6 cohort studies were included. The summary RR was 1.61 (95% CI: 1.41-1.85, I
= 86%) for all studies, 1.73 (95% CI: 1.45-2.06, I
= 89%) for case-control studies and 1.32 (95% CI: 1.12-1.56, I
= 47%) for cohort studies. The association between hypertension and endometrial cancer was weaker, but still significant, among studies with adjustment for smoking, BMI, oral contraceptive use, and parity, compared to studies without such adjustment. This meta-analysis suggest an increased risk of endometrial cancer among patients with hypertension, however, further studies with more comprehensive adjustments for confounders are warranted to clarify the association.
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IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
Objectives This study sought to investigate whether obesity in the absence of metabolic abnormalities might be a relatively benign condition in relation to acute myocardial infarction (AMI) and heart ...failure (HF). Background The results of previous studies are conflicting for AMI and largely unknown for HF, and the role of the duration of obesity has not been investigated. Methods In a population-based prospective cohort study, a total of 61,299 men and women free of cardiovascular disease were classified according to body mass index (BMI) and metabolic status at baseline. BMI also was measured 10 and 30 years before baseline for 27,196 participants. Results During 12 years of follow-up, 2,547 participants had a first AMI, and 1,201 participants had a first HF. Compared with being normal weight (BMI <25 kg/m2 ) and metabolically healthy, the multivariable-adjusted hazard ratio (HR) for AMI was 1.1 (95% confidence interval CI: 0.9 to 1.4) among obese (BMI ≥30 kg/m2 ) and metabolically healthy participants and 2.0 (95% CI: 1.7 to 2.3) among obese and metabolically unhealthy participants. We found similar results for severe (BMI ≥35 kg/m2 ), long-lasting (>30 years), and abdominal obesity stratified for metabolic status. For HF, the HRs associated with obesity were 1.7 (95% CI: 1.3 to 2.3) and 1.7 (95% CI: 1.4 to 2.2) for metabolically healthy and unhealthy participants, respectively. Severe and long-lasting obesity were particularly harmful in relation to HF, regardless of metabolic status. Conclusions In relation to AMI, obesity without metabolic abnormalities did not confer substantial excess risk, not even for severe or long-lasting obesity. For HF, even metabolically healthy obesity was associated with increased risk, particularly for long-lasting or severe obesity.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Epidemiological studies have indicated a positive association between adiposity and gallbladder disease risk, however, the shape of the dose-response relationship and differences between overall and ...abdominal adiposity remains to be clarified. We conducted a systematic review and dose-response meta-analysis of cohort studies of body mass index (BMI), waist circumference and waist-to-hip ratio and risk of gallbladder disease. PubMed and Embase databases were searched up to January 9th 2015. Summary relative risks were calculated using a random effects model. Seventeen prospective studies of BMI and gallbladder disease risk with 55,670 cases among 1,921,103 participants were included. The summary relative risk (RR) for a 5 unit increment in BMI was 1.63 (95 % CI 1.49-1.78, I² = 98 %). There was evidence of a nonlinear association overall and among women, Pnoniinearity < 0.0001, but not among men, pnonlinearity = 0.99, with a slight flattening of the curve at very high BMI levels (BMI 40-45), however, the risk of gallbladder disease increased almost twofold even within the "normal" BMI range. The summary RR for a 10 cm increase in waist circumference was 1.46 (95 % CI 1.24-1.72, I² = 98 %, n = 5) and for a 0.1 unit increment in waist-to-hip ratio was 1.44 (95 % CI 1.26-1.64, I² = 92 %, n = 4). Associations were attenuated, but still significant, when BMI and abdominal adiposity measures were mutually adjusted. Our results confirm a positive association between both general and abdominal fatness and the risk of gallbladder disease. There is an almost twofold increase in the risk even within the "normal" BMI range, suggesting that even moderate increases in BMI may increase risk.
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BFBNIB, EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ