Alcohol consumption and dementia risk: a dose–response meta-analysis of prospective studies

It is widely believed that light-to-moderate alcohol intake may protect against dementia while excessive drinking may instead increase the risk. Nonetheless, these findings need cautious interpretations due to varying methodologies and lack of standard definition, which hindered our transferring into preventative practice. The objective of this study is to investigate the potential dose–response association between alcohol consumption and risk of dementia. A systematic search was conducted in electronic databases to identify relevant studies. Risk estimates were combined using a random-effect model. Eleven studies with 73,330 participants and 4586 cases for all-cause dementia (ACD), five studies with 52,715 participants and 1267 cases for Alzheimer’s dementia (AD) and four studies with 49,535 participants and 542 cases for vascular dementia were included. We observed a nonlinear association between alcohol consumption and ACD risk (p _nonlinearity < 0.05). The alcohol dose associated with lower risk of dementia was confined to at most 12.5 g/day, with the risk hitting bottom (RR ≈ 0.9) at roughly 6 g/day. Of note, the ACD risk seemed to be elevated (≈10%) when the dose surpasses certain levels: 23 drinks/week or 38 g/day. For the alcohol type, recommendation for wine is prioritized. The subgroup analysis further indicated that the effect of alcohol may be greater in younger adults (<60 years old) with regard to fighting against dementia. Modest alcohol consumption (≤12.5 g/day) is associated with a reduced risk of dementia with 6 g/day of alcohol conferring a lower risk than other levels while excessive drinking (≥38 g/day) may instead elevate the risk.     

Dairy foods intake and risk of Parkinson’s disease: a dose–response meta-analysis of prospective cohort studies

Dairy foods have been linked to Parkinson’s disease (PD), and a meta-analysis of prospective cohort studies on dairy foods intake and PD risk was conducted. Eligible studies were identified in a literature search of EMBASE and PubMed up to April 2014. Seven results from prospective studies were included, including 1,083 PD cases among 304,193 subjects. The combined risk of PD for highest vs. lowest level of dairy foods intake was 1.40 (1.20–1.63) overall, 1.66 (1.29–2.14) for men and 1.15 (0.85–1.56) for women. For highest vs. lowest level, the PD risk was 1.45 (1.23–1.73) for milk, 1.26 (0.99–1.60) for cheese, 0.95 (0.76–1.20) for yogurt and 0.76 (0.51–1.13) for butter. The linear dose–response relationship showed that PD risk increased by 17 % [1.17 (1.06–1.30)] for every 200 g/day increment in milk intake (P_{for non-linearity} = 0.22), and 13 % [1.13 (0.91–1.40)] for every 10 g/day increment in cheese intake (P_{for non-linearity} = 0.39). The absolute risk differences were estimated to be 2–4 PD cases per 100,000 person-years for every 200 g/day increment in milk intake, and 1–3 PD cases per 100,000 person-years for every 10 g/day increment in cheese intake. Dairy foods (milk, cheese) might be positively associated with increased risk of PD, especially for men.     

Egg consumption and risk of GI neoplasms: dose–response meta-analysis and systematic review

Purpose

Previous epidemiological studies on egg consumption and the risk of gastrointestinal (GI) neoplasms suggest a positive association; however, data are limited and the evidence remains controversial. This study aims to investigate and quantify the potential dose–response relationship with an evaluation of cancer site-specific differences.

Methods

Relevant studies were identified after the literature search via electronic databases until January 2014. Subgroup analysis for serving portions was performed using two standardized classification methods: (1) less than 3, or 3 or more eggs per week; (2) less than 3, 3–5, or more than 5 eggs per week. Method two excludes studies that only reported consumption frequency. Pooled adjusted odds ratios (ORs) comparing highest and lowest categories of dietary pattern scores were calculated using a random-effects model.

Results

Thirty-seven case–control and seven cohort studies were included for meta-analysis, which contained a total of 424,867 participants and 18,852 GI neoplasm cases. The combined odds ratio (OR) was calculated to 1.15 (95 % CI 1.09–1.22; p value heterogeneity <0.001), showing only a slight increase in risk. The correlation was stronger for colon cancers 1.29 (95 % CI 1.14–1.46; p value heterogeneity <0.22). Dose–response analysis revealed similar results with stratification methods, and the ORs for an intake of <3 and ≥3 eggs per week were 1.14 (95 % CI 1.07–1.22; p value heterogeneity = 0.38) and 1.25 (95 % CI 1.14–1.38; p value heterogeneity = 0.25), respectively. With method 2, the ORs for an intake of <3, 3–5, and >5 eggs per week were 1.13 (95 % CI 1.06–1.21; p value heterogeneity = 0.25), 1.14 (95 % CI 1.01–1.29; p value heterogeneity = 0.06), and 1.19 (95 % CI 1.01–1.39; p value heterogeneity <0.001), respectively.

Conclusion

This study provides evidence that egg consumption is associated with a positive dose–response association with the development of GI neoplasms.     

Whole grain and refined grain consumption and the risk of type 2 diabetes: a systematic review and dose–response meta-analysis of cohort studies

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, p _nonlinearity < 0.0001, but not for refined grains, p _nonlinearity = 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.     

Physical activity and the risk of heart failure: a systematic review and dose–response meta-analysis of prospective studies

European Journal of Epidemiology - Although physical activity is an established protective factor for cardiovascular diseases such as ischemic heart disease and stroke, less is known with regard to...     

Tea consumption and lung cancer risk: A meta-analysis of case–control and cohort studies

ObjectiveRecent epidemiologic studies, especially cohort and case–control studies, have yielded inconsistent findings regarding the association between tea consumption and risk for lung cancer. The aim of this study was to assess a potential relationship between tea consumption and the incidence of lung cancer worldwide.MethodsA systematic literature search of PubMed, Web of Science, the Cochrane Library, Google Scholar, the Chinese Biomedical Database, and Wanfang Database was conducted from 1966 to January 2014 by two investigators. All cohort studies and case–control studies that evaluated the association of tea and lung cancer were included. Summary relative risks (RR) and the corresponding 95% confidence intervals (CIs) were calculated using a random-effects model. Quality assessments were performed using the Newcastle–Ottawa Scale. Heterogeneity was assessed using the Q and I² tests, and the source of heterogeneity was detected by meta-regression analysis. Publication bias was evaluated with Egger's regression symmetry test. Subgroup analyses and sensitivity analysis were performed.ResultsThirty-eight lung cancer studies (26 case–control studies and 12 cohort studies) with 59,041 cases and 396,664 controls were included. Overall tea consumption was significantly associated with decreased risk for lung cancer (RR, 0.78; 95% CI, 0.70–0.87). Subgroup analyses showed that tea consumption was associated with reduced risk for lung cancer in women (RR, 0.76; 95% CI, 0.62–0.93), case–control studies (RR 0.72; 95% CI 0.63–0.83), Western studies (RR, 0.85; 95% CI, 0.75–0.97), and studies in China and Japan (RR, 0.74; 95% CI, 0.62–0.88). Both green tea (RR, 0.75; 95% CI, 0.62–0.91) and black tea (RR, 0.82; 95% CI, 0.71–0.94) were significantly associated with reduced lung cancer risk. No significant association was found in men or in cohort studies.ConclusionTea consumption may offer some protection against lung cancer.     

Coffee consumption and the risk of incident gastric cancer—A meta-analysis of prospective cohort studies

As several epidemiological studies on the association of coffee consumption with gastric cancer risk have produced inconsistent results, this meta-analysis was designed to synthesize current evidence of this potential relationship. We searched PubMed, EMBASE, and the Cochrane Library up to September 2014 to retrieve relevant articles. Prospective cohort studies were included if the relative risks (RRs) or hazard ratios and 95% confidence intervals (CIs) for gastric cancer according to coffee consumption were reported. Fixed- or random-effects models were used based on heterogeneity. The search yielded 13 eligible cohort studies of 3484 incident gastric cancer patients from among 1,324,559 participants. A significantly increased risk was found between gastric cardia cancer and coffee consumption (RR = 1.50, 95% CI: 1.09–2.07). Compared with Europeans (RR = 1.12, 95% CI: 0.86–1.46) and Asians (RR = 0.96, 95% CI: 0.72–1.27), Americans (RR = 1.36, 95% CI: 1.06–1.74) demonstrated a significantly positive association. However, the significant differences of the pooled results vanished after adjusting for smoking or body mass index. Our meta-analysis results suggest that a high level of coffee consumption is a risk factor for gastric cancer. However, these results should not be overinterpreted because residual confounding effects of other factors could exist.     

Coffee consumption and risk of pancreatic cancer: a systematic review and dose–response meta-analysis

The association between coffee consumption and pancreatic cancer risk has been extensively studied; however, there is no consistent conclusion. Therefore, this meta-analysis study sought to evaluate dose–response relationship between them. A search was conducted using the PubMed and Web of Science databases. Thirteen high-quality cohort studies were identified, involving in 959,992 study participants and 3831 pancreatic cancer cases. Comparing the highest with lowest categories of coffee intake, the pooled relative risk (RR) was 1.08 (95% CI 0.94–1.25). For dose–response analysis, no evidence of a nonlinear dose–response association between coffee consumption and pancreatic cancer (p for nonlinearity =0.171) was found. The risk of pancreatic cancer was increased by 5.87% (RR =1.06, 95% CI 1.05–1.07) with the increment of one cup/day. Coffee consumption was identified to be related with the increasing risk of pancreatic cancer in a dose–response manner. Nevertheless, further mechanistic studies are needed to clarify the concerned issues.     

Dietary fiber intake and risk of type 2 diabetes: a dose–response analysis of prospective studies

Observational studies suggest an association between dietary fiber intake and risk of type 2 diabetes, but the results are inconclusive. We conducted a meta-analysis of prospective studies evaluating the associations of dietary fiber intake and risk of type 2 diabetes. Relevant studies were identified by searching EMBASE (from 1974 to April 2013) and PubMed (from 1966 to April 2013). The fixed or random-effect model was selected based on the homogeneity test among studies. In addition, a 2-stage random-effects dose–response meta-analysis was performed. We identified 17 prospective cohort studies of dietary fiber intake and risk of type 2 diabetes involving 19,033 cases and 488,293 participants. The combined RR (95 % CI) of type 2 diabetes for intake of total dietary fiber, cereal fiber, fruit fiber and insoluble fiber was 0.81 (0.73–0.90), 0.77 (0.69–0.85), 0.94 (0.88–0.99) and 0.75 (0.63–0.89), respectively. A nonlinear relationship was found of total dietary fiber intake with risk of type 2 diabetes (P _{for nonlinearity} < 0.01), and the RRs (95 % CI) of type 2 diabetes were 0.98 (0.90–1.06), 0.97 (0.87–1.07), 0.89 (0.80–0.99), 0.76 (0.65–0.88), and 0.66 (0.53–0.82) for 15, 20, 25, 30, and 35 g/day. The departure from nonlinear relationship was not significant (P _{for nonlinearity} = 0.72), and the risk of type 2 diabetes decreased by 6 % (RR 0.94, 95 % CI 0.93–0.96) for 2 g/day increment in cereal fiber intake. Findings from this meta-analysis indicate that the intakes of dietary fiber may be inversely associated with risk of type 2 diabetes.     

Body mass index,abdominal fatness,and the risk of sudden cardiac death: a systematic review and dose–response meta-analysis of prospective studies

Although overweight and obesity are established risk factors for some types of heart disease including ischemic heart disease, heart failure and atrial fibrillation, less is known about the association between adiposity and sudden cardiac death. We conducted a systematic review and meta-analysis of prospective studies to clarify the association between adiposity and risk of sudden cardiac death. PubMed and Embase databases were searched up to July 20th 2017. Summary relative risks (RRs) and 95% confidence intervals (CIs) were calculated using random effects models. The summary RR was 1.16 (95% CI 1.05–1.28, I² = 68%, n = 14) per 5 unit increment in BMI, and 1.82 (95% CI 1.61–2.07, I² = 0%, n = 3) per 0.1 unit increase in waist-to-hip ratio, and 1.03 (95% CI 0.93–1.15, I² = 0%, n = 2) per 10 cm increase in waist circumference. The heterogeneity in the analysis of BMI and sudden cardiac death persisted across most subgroup analyses. The association was stronger among studies with longer follow-up compared to short follow-up and was observed in the European and American studies, but not in the Asian studies. There was a J-shaped association between BMI and sudden cardiac death and the lowest risk was observed in the normal weight range, however, the increased risk with a low BMI was attenuated among studies with a longer duration of follow-up. This meta-analysis suggest an increased risk of sudden cardiac death with increasing BMI and waist-to-hip ratio, however, further studies with stratification for smoking status are needed of waist circumference, weight changes and adiposity at younger ages.     

Body mass index,abdominal fatness,weight gain and the risk of psoriasis: a systematic review and dose–response meta-analysis of prospective studies

Greater body mass index (BMI) has been associated with increased risk of psoriasis in case–control and cross-sectional studies, however, the evidence from prospective studies has been limited. We conducted a systematic review and dose–response meta-analysis of different adiposity measures and the risk of psoriasis to provide a more robust summary of the evidence based on data from prospective studies. PubMed and Embase databases were searched for relevant studies up to August 8th 2017. Summary relative risks (RRs) and 95% confidence intervals (CIs) were calculated using a random effects model. The summary relative risk (RR) for a 5 unit increment in BMI was 1.19 (95% CI 1.10–1.28, I² = 83%, n = 7). The association appeared to be stronger at higher compared to lower levels of BMI, p_nonlinearity < 0.0001, and the lowest risk was observed at a BMI around 20. The summary RR was 1.24 (95% CI 1.17–1.31, I² = 0%, p_{heterogeneity} = 0.72, n = 3) per 10 cm increase in waist circumference, 1.37 (95% CI 1.23–1.53, I² = 0%, p_{heterogeneity} = 0.93, n = 3) per 0.1 unit increase in waist-to-hip ratio, and 1.11 (95% CI 1.07–1.16, I² = 47%, p_{heterogeneity} = 0.15, n = 3) per 5 kg of weight gain. Adiposity as measured by BMI, waist circumference, waist-to-hip ratio, and weight gain is associated with increased risk of psoriasis.     

Physical activity and the risk of gestational diabetes mellitus: a systematic review and dose–response meta-analysis of epidemiological studies

Physical activity has been inconsistently associated with risk of gestational diabetes mellitus in epidemiological studies, and questions remain about the strength and shape of the dose–response relationship between the two. We therefore conducted a systematic review and meta-analysis of cohort studies and randomized trials on physical activity and gestational diabetes mellitus. PubMed, Embase and Ovid databases were searched for cohort studies, and randomized controlled trials of physical activity and risk of gestational diabetes mellitus, up to August 5th 2015. Summary relative risks (RRs) were estimated using a random effects model. Twenty-five studies (26 publications) were included. For total physical activity the summary RR for high versus low activity was 0.62 (95 % CI 0.41–0.94, I² = 0 %, n = 4) before pregnancy, and 0.66 (95 % CI 0.36–1.21, I² = 0 %, n = 3) during pregnancy. For leisure-time physical activity the respective summary RRs for high versus low activity was 0.78 (95 % CI 0.61–1.00, I² = 47 %, n = 8) before pregnancy, and it was 0.80 (95 % CI 0.64–1.00, I² = 17 %, n = 17) during pregnancy. The summary RR for pre-pregnancy activity was 0.70 (95 % CI 0.49–1.01, I² = 72.6 %, n = 3) per increment of 5 h/week and for activity during pregnancy was 0.98 (95 % CI 0.87–1.09, I² = 0 %, n = 3) per 5 h/week. There was evidence of a nonlinear association between physical activity before pregnancy and the risk of gestational diabetes mellitus, p_nonlinearity = 0.005, with a slightly steeper association at lower levels of activity although further reductions in risk were observed up to 10 h/week. There was also evidence of nonlinearity for physical activity in early pregnancy, p_nonlinearity = 0.008, with no further reduction in risk above 8 h/week. There was some indication of inverse associations between walking (before and during pregnancy) and vigorous activity (before pregnancy) and the risk of gestational diabetes mellitus. This meta-analysis suggests that there is a significant inverse association between physical activity before pregnancy and in early pregnancy and the risk of gestational diabetes mellitus. Further studies are needed to clarify the association between specific types and intensities of activity and gestational diabetes mellitus.     

Body mass index,abdominal fatness,fat mass and the risk of atrial fibrillation: a systematic review and dose–response meta-analysis of prospective studies

Different adiposity measures have been associated with increased risk of atrial fibrillation, however, results have previously only been summarized for BMI. We therefore conducted a systematic review and meta-analysis of prospective studies to clarify the association between different adiposity measures and risk of atrial fibrillation. PubMed and Embase databases were searched up to October 24th 2016. Summary relative risks (RRs) were calculated using random effects models. Twenty-nine unique prospective studies (32 publications) were included. Twenty-five studies (83,006 cases, 2,405,381 participants) were included in the analysis of BMI and atrial fibrillation. The summary RR was 1.28 (95% confidence interval: 1.20–1.38, I² = 97%) per 5 unit increment in BMI, 1.18 (95% CI: 1.12–1.25, I² = 73%, n = 5) and 1.32 (95% CI: 1.16–1.51, I² = 91%, n = 3) per 10 cm increase in waist and hip circumference, respectively, 1.09 (95% CI: 1.02–1.16, I² = 44%, n = 4) per 0.1 unit increase in waist-to-hip ratio, 1.09 (95% CI: 1.02–1.16, I² = 94%, n = 4) per 5 kg increase in fat mass, 1.10 (95% CI: 0.92–1.33, I² = 90%, n = 3) per 10% increase in fat percentage, 1.10 (95% CI: 1.08–1.13, I² = 74%, n = 10) per 5 kg increase in weight, and 1.08 (95% CI: 0.97–1.19, I² = 86%, n = 2) per 5% increase in weight gain. The association between BMI and atrial fibrillation was nonlinear, p _nonlinearity < 0.0001, with a stronger association at higher BMI levels, however, increased risk was observed even at a BMI of 22–24 compared to 20. In conclusion, general and abdominal adiposity and higher body fat mass increase the risk of atrial fibrillation.     

Folate intake and pancreatic cancer risk: an overall and dose–response meta-analysis

Objective

Inconsistent findings of association between supplemental folate consumption and pancreatic cancer risk have been observed in the literature. This study aims to summarize the relationship between folate intake and risk of pancreatic cancer.

Study design

Pertinent studies published before November 2011 were identified by searching PubMed and Embase and by reviewing the reference lists of retrieved articles. The summary relative risks were estimated by the random effects model. A linear regression analysis of the natural logarithm of the relative risk (RR) was carried out to assess a possible dose–response relationship between folate intake and pancreatic cancer risk.

Results

Ten studies on dietary and supplemental folate intake and pancreatic cancer (4 case–control and 6 cohort studies) were included in the meta-analysis. The pooled RRs of pancreatic cancer for the highest vs lowest categories of dietary folate intake and supplemental folate intake were 0.66 (95% CI: 0.49–0.88) and 1.08 (95% CI, 0.82–1.41), respectively. The dose–response meta-analysis indicated that a 100 μg/day increment in dietary folate intake conferred a RR of 0.93 (95% CI: 0.90–0.97). These findings support the hypothesis that dietary folate may play a protective role in carcinogenesis of pancreatic cancer.