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      Coffee Consumption and Mortality From All Causes, Cardiovascular Disease, and Cancer: A Dose-Response Meta-Analysis

      , , , ,
      American Journal of Epidemiology
      Oxford University Press (OUP)

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          Abstract

          Several studies have analyzed the relationship between coffee consumption and mortality, but the shape of the association remains unclear. We conducted a dose-response meta-analysis of prospective studies to examine the dose-response associations between coffee consumption and mortality from all causes, cardiovascular disease (CVD), and all cancers. Pertinent studies, published between 1966 and 2013, were identified by searching PubMed and by reviewing the reference lists of the selected articles. Prospective studies in which investigators reported relative risks of mortality from all causes, CVD, and all cancers for 3 or more categories of coffee consumption were eligible. Results from individual studies were pooled using a random-effects model. Twenty-one prospective studies, with 121,915 deaths and 997,464 participants, met the inclusion criteria. There was strong evidence of nonlinear associations between coffee consumption and mortality for all causes and CVD (P for nonlinearity < 0.001). The largest risk reductions were observed for 4 cups/day for all-cause mortality (16%, 95% confidence interval: 13, 18) and 3 cups/day for CVD mortality (21%, 95% confidence interval: 16, 26). Coffee consumption was not associated with cancer mortality. Findings from this meta-analysis indicate that coffee consumption is inversely associated with all-cause and CVD mortality.

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          Facilitating meta-analyses by deriving relative effect and precision estimates for alternative comparisons from a set of estimates presented by exposure level or disease category.

          Epidemiological studies relating a particular exposure to a specified disease may present their results in a variety of ways. Often, results are presented as estimated odds ratios (or relative risks) and confidence intervals (CIs) for a number of categories of exposure, for example, by duration or level of exposure, compared with a single reference category, often the unexposed. For systematic literature review, and particularly meta-analysis, estimates for an alternative comparison of the categories, such as any exposure versus none, may be required. Obtaining these alternative comparisons is not straightforward, as the initial set of estimates is correlated. This paper describes a method for estimating these alternative comparisons based on the ideas originally put forward by Greenland and Longnecker, and provides implementations of the method, developed using Microsoft Excel and SAS. Examples of the method based on studies of smoking and cancer are given. The method also deals with results given by categories of disease (such as histological types of a cancer). The method allows the use of a more consistent comparison when summarizing published evidence, thus potentially improving the reliability of a meta-analysis. Copyright (c) 2007 John Wiley & Sons, Ltd.
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            A meta-analysis of coffee drinking, cigarette smoking, and the risk of Parkinson's disease.

            We conducted a systematic review to summarize the epidemiological evidence on the association between cigarette smoking, coffee drinking, and the risk of Parkinson's disease. Case-control and cohort studies that reported the relative risk of physician-confirmed Parkinson's disease by cigarette smoking or coffee drinking status were included. Study-specific log relative risks were weighted by the inverse of their variances to obtain a pooled relative risk and its 95% confidence interval (CI). Results for smoking were based on 44 case-control and 4 cohort studies, and for coffee 8 case-control and 5 cohort studies. Compared with never smokers, the relative risk of Parkinson's disease was 0.59 (95% CI, 0.54-0.63) for ever smokers, 0.80 (95% CI, 0.69-0.93) for past smokers, and 0.39 (95% CI, 0.32-0.47) for current smokers. The relative risk per 10 additional pack-years was 0.84 (95% CI, 0.81-0.88) in case-control studies and 0.78 (95% CI, 0.73-0.84) in cohort studies. Compared with non-coffee drinkers, relative risk of Parkinson's disease was 0.69 (95% CI, 0.59-0.80) for coffee drinkers. The relative risk per three additional cups of coffee per day was 0.75 (95% CI, 0.64-0.86) in case-control studies and 0.68 (95% CI, 0.46-1.00) in cohort studies. This meta-analysis shows that there is strong epidemiological evidence that smokers and coffee drinkers have a lower risk of Parkinson's disease. Further research is required on the biological mechanisms underlying this potentially protective effect.
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              Is Open Access

              Caffeinated and Decaffeinated Coffee Consumption and Risk of Type 2 Diabetes: A Systematic Review and a Dose-Response Meta-analysis

              OBJECTIVE Previous meta-analyses identified an inverse association of coffee consumption with the risk of type 2 diabetes. However, an updated meta-analysis is needed because new studies comparing the trends of association for caffeinated and decaffeinated coffee have since been published. RESEARCH DESIGN AND METHODS PubMed and Embase were searched for cohort or nested case-control studies that assessed the relationship of coffee consumption and risk of type 2 diabetes from 1966 to February 2013. A restricted cubic spline random-effects model was used. RESULTS Twenty-eight prospective studies were included in the analysis, with 1,109,272 study participants and 45,335 cases of type 2 diabetes. The follow-up duration ranged from 10 months to 20 years. Compared with no or rare coffee consumption, the relative risk (RR; 95% CI) for diabetes was 0.92 (0.90–0.94), 0.85 (0.82–0.88), 0.79 (0.75–0.83), 0.75 (0.71–0.80), 0.71 (0.65–0.76), and 0.67 (0.61–0.74) for 1–6 cups/day, respectively. The RR of diabetes for a 1 cup/day increase was 0.91 (0.89–0.94) for caffeinated coffee consumption and 0.94 (0.91–0.98) for decaffeinated coffee consumption (P for difference = 0.17). CONCLUSIONS Coffee consumption was inversely associated with the risk of type 2 diabetes in a dose-response manner. Both caffeinated and decaffeinated coffee was associated with reduced diabetes risk.
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                Author and article information

                Journal
                American Journal of Epidemiology
                Oxford University Press (OUP)
                0002-9262
                1476-6256
                October 15 2014
                August 24 2014
                October 15 2014
                August 24 2014
                : 180
                : 8
                : 763-775
                Article
                10.1093/aje/kwu194
                25156996
                027b680b-53ca-41ec-bac7-db9e3eb39e1f
                © 2014
                History

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