Parity and All-cause Mortality in Women and Men: A Dose-Response Meta-Analysis of Cohort Studies.
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ABSTRACT:
SUBMITTER: Zeng Y
PROVIDER: S-EPMC4725925 | biostudies-other | 2016 Jan
REPOSITORIES: biostudies-other
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Project description:Parity has been shown to inversely associate with cardiovascular disease (CVD) mortality, but the evidence of epidemiological studies is still controversial. Therefore, we quantitatively assessed the relationship between parity and CVD mortality by summarizing the evidence from prospective studies. We searched MEDLINE (PubMed), EMBASE and ISI Web of Science databases for relevant prospective studies of parity and CVD mortality through the end of March 2015. Fixed- or random-effects models were used to estimate summary relative risks (RRs) and 95% confidence intervals (CIs). Heterogeneity among studies was assessed using the I(2) statistics. All statistical tests were two-sided. Ten prospective studies were included with a total of 994,810 participants and 16,601 CVD events. A borderline significant inverse association was observed while comparing parity with nulliparous, with summarized RR?=?0.79 (95% CI: 0.60-1.06; I(2)?=?90.9%, P?<?0.001). In dose-response analysis, we observed a significant nonlinear association between parity number and CVD mortality. The greatest risk reduction appeared when the parity number reached four. The findings of this meta-analysis suggests that ever parity is inversely related to CVD mortality. Furthermore, there is a statistically significant nonlinear inverse association between parity number and CVD mortality.
| S-EPMC4547137 | biostudies-literature
Project description:We performed this meta-analysis of epidemiological studies to comprehensively assess the association between parity and gastric cancer risk, because previous studies have shown conflicting results regarding this topic. Relevant prospective studies were identified by searching the following databases: PubMed, EMBASE, and Web of Science, and random-effects models were used to estimate summary relative risks (SRRs) and 95% confidence intervals (CIs). Our search yielded 10 prospective cohort studies involving a total of 6624 gastric cancer cases and 5,559,695 non-cases. The SRRs for ever parity vs. nulliparous and highest vs. lowest parity number were 0.96 (95%CI = 0.87-1.05, I(2)?= 0%) and 1.03 (95%CI = 0.94-1.13, I(2)?= 0%), respectively. Additionally, the SRR for an increment of one live birth was 1.00 (95%CI = 0.97-1.03, I(2) = 18.6%). These non-significant associations were observed in all subgroups as stratified by the number of gastric cases, follow-up years, geographic location, menopausal status, anatomic subsite of gastric cancer, and adjustment for potential confounders, as well as in sensitivity analyses. Our meta-analysis found no significant association between parity and gastric cancer risk. However, further studies should be conducted to validate our findings and could provide more detailed results by stratifying their findings by Lauren's subtype, histology, and anatomic site, as well as fully adjusting for potential confounding factors.
| S-EPMC4698715 | biostudies-literature
Project description:ObjectiveTo quantify the association of indices of central obesity, including waist circumference, hip circumference, thigh circumference, waist-to-hip ratio, waist-to-height ratio, waist-to-thigh ratio, body adiposity index, and A body shape index, with the risk of all cause mortality in the general population, and to clarify the shape of the dose-response relations.DesignSystematic review and meta-analysis.Data sourcesPubMed and Scopus from inception to July 2019, and the reference lists of all related articles and reviews.Eligibility criteria for selecting studiesProspective cohort studies reporting the risk estimates of all cause mortality across at least three categories of indices of central fatness. Studies that reported continuous estimation of the associations were also included.Data synthesisA random effects dose-response meta-analysis was conducted to assess linear trend estimations. A one stage linear mixed effects meta-analysis was used for estimating dose-response curves.ResultsOf 98 745 studies screened, 1950 full texts were fully reviewed for eligibility. The final analyses consisted of 72 prospective cohort studies with 2 528 297 participants. The summary hazard ratios were as follows: waist circumference (10 cm, 3.94 inch increase): 1.11 (95% confidence interval 1.08 to 1.13, I2=88%, n=50); hip circumference (10 cm, 3.94 inch increase): 0.90 (0.81 to 0.99, I2=95%, n=9); thigh circumference (5 cm, 1.97 inch increase): 0.82 (0.75 to 0.89, I2=54%, n=3); waist-to-hip ratio (0.1 unit increase): 1.20 (1.15 to 1.25, I2=90%, n=31); waist-to-height ratio (0.1 unit increase): 1.24 (1.12 to 1.36, I2=94%, n=11); waist-to-thigh ratio (0.1 unit increase): 1.21 (1.03 to 1.39, I2=97%, n=2); body adiposity index (10% increase): 1.17 (1.00 to 1.33, I2=75%, n=4); and A body shape index (0.005 unit increase): 1.15 (1.10 to 1.20, I2=87%, n=9). Positive associations persisted after accounting for body mass index. A nearly J shaped association was found between waist circumference and waist-to-height ratio and the risk of all cause mortality in men and women. A positive monotonic association was observed for waist-to-hip ratio and A body shape index. The association was U shaped for body adiposity index.ConclusionsIndices of central fatness including waist circumference, waist-to-hip ratio, waist-to-height ratio, waist-to-thigh ratio, body adiposity index, and A body shape index, independent of overall adiposity, were positively and significantly associated with a higher all cause mortality risk. Larger hip circumference and thigh circumference were associated with a lower risk. The results suggest that measures of central adiposity could be used with body mass index as a supplementary approach to determine the risk of premature death.
| S-EPMC7509947 | biostudies-literature
Project description:BackgroundPrevious epidemiologic studies have reported inconsistent results between parity and pancreatic cancer (PC) risk. To our knowledge, a comprehensive and quantitative assessment of this association has not been conducted.MethodsRelevant published studies of parity and PC were identified using MEDLINE (PubMed) and Web of Science databases until November 2013. Two authors (H-BG and LW) independently assessed eligibility and extracted data. Eleven prospective and 11 case-control studies reported relative risk (RR) estimates and 95% confidence intervals (CIs) of PC associated with parity. Fixed- and random-effects models were used to estimate the summary RR depending on the heterogeneity of effects.ResultsThe summary RR for PC comparing the highest versus lowest parity was 0.86 (95% CI: 0.73-1.02; Q = 50.49, P<0.001, I2 = 58.4%). Significant inverse associations were also observed in the studies that adjusted for cigarette smoking (RR = 0.81; 95% CI: 0.68-0.98), Type 2 diabetes mellitus (RR = 0.83; 95% CI: 0.75-0.93), and those that included all confounders or important risk factors (RR = 0.85; 95% CI: 0.76-0.96). Additionally, in the dose-response analysis, the summary RR for per one live birth was 0.97 (95% CI: 0.94-1.01; Q = 62.83, P<0.001, I2 = 69.8%), which also indicated a borderline statistically significant inverse effect of parity on PC risk. No evidence of publication bias and significant heterogeneity between subgroups were detected by meta-regression analyses.ConclusionIn summary, these findings suggest that higher parity is associated with a decreased risk of PC. Future large consortia or pooled studies are warranted to fully adjust for potential confounders to confirm this association.
| S-EPMC3962437 | biostudies-literature
Project description:With a growing number of prospective cohort studies, an updated dose-response meta-analysis of milk and dairy products with all-cause mortality, coronary heart disease (CHD) or cardiovascular disease (CVD) have been conducted. PubMed, Embase and Scopus were searched for articles published up to September 2016. Random-effect meta-analyses with summarised dose-response data were performed for total (high-fat/low-fat) dairy, milk, fermented dairy, cheese and yogurt. Non-linear associations were investigated using the spine models and heterogeneity by subgroup analyses. A total of 29 cohort studies were available for meta-analysis, with 938,465 participants and 93,158 mortality, 28,419 CHD and 25,416 CVD cases. No associations were found for total (high-fat/low-fat) dairy, and milk with the health outcomes of mortality, CHD or CVD. Inverse associations were found between total fermented dairy (included sour milk products, cheese or yogurt; per 20 g/day) with mortality (RR 0.98, 95% CI 0.97-0.99; I2 = 94.4%) and CVD risk (RR 0.98, 95% CI 0.97-0.99; I2 = 87.5%). Further analyses of individual fermented dairy of cheese and yogurt showed cheese to have a 2% lower risk of CVD (RR 0.98, 95% CI 0.95-1.00; I2 = 82.6%) per 10 g/day, but not yogurt. All of these marginally inverse associations of totally fermented dairy and cheese were attenuated in sensitivity analyses by removing one large Swedish study. This meta-analysis combining data from 29 prospective cohort studies demonstrated neutral associations between dairy products and cardiovascular and all-cause mortality. For future studies it is important to investigate in more detail how dairy products can be replaced by other foods.
| S-EPMC5437143 | biostudies-literature
Project description:BackgroundThe consumption of dairy products may influence the risk of cardiovascular disease (CVD) and total mortality, but conflicting findings have been reported.ObjectiveThe objective was to examine the associations of milk, total dairy products, and high- and low-fat dairy intakes with the risk of CVD [including coronary heart disease (CHD) and stroke] and total mortality.DesignPubMed, EMBASE, and SCOPUS were searched for articles published up to February 2010. Of > 5000 titles evaluated, 17 met the inclusion criteria, all of which were original prospective cohort studies. Random-effects meta-analyses were performed with summarized dose-response data. Milk as the main dairy product was pooled in these analyses.ResultsIn 17 prospective studies, there were 2283 CVD, 4391 CHD, 15,554 stroke, and 23,949 mortality cases. A modest inverse association was found between milk intake and risk of overall CVD [4 studies; relative risk (RR): 0.94 per 200 mL/d; 95% CI: 0.89, 0.99]. Milk intake was not associated with risk of CHD (6 studies; RR: 1.00; 95% CI: 0.96, 1.04), stroke (6 studies; RR: 0.87; 95% CI: 0.72, 1.05), or total mortality (8 studies; RR per 200 mL/d: 0.99; 95% CI: 0.95, 1.03). Limited studies of the association of total dairy products and of total high-fat and total low-fat dairy products (per 200 g/d) with CHD showed no significant associations.ConclusionThis dose-response meta-analysis of prospective studies indicates that milk intake is not associated with total mortality but may be inversely associated with overall CVD risk; however, these findings are based on limited numbers.
| S-EPMC3361013 | biostudies-literature
Project description:Effects of extreme sleep duration on risk of mortality and cardiovascular outcomes remain controversial. We aimed to quantify the dose-response relationships of sleep duration with risk of all-cause mortality, total cardiovascular disease, coronary heart disease, and stroke.PubMed and Embase were systematically searched for prospective cohort studies published before December 1, 2016, that examined the associations between sleep duration and at least 1 of the 4 outcomes in generally healthy populations. U-shaped associations were indicated between sleep duration and risk of all outcomes, with the lowest risk observed for ?7-hour sleep duration per day, which was varied little by sex. For all-cause mortality, when sleep duration was <7 hours per day, the pooled relative risk (RR) was 1.06 (95% CI, 1.04-1.07) per 1-hour reduction; when sleep duration was >7 hours per day, the pooled RR was 1.13 (95% CI, 1.11-1.15) per 1-hour increment. For total cardiovascular disease, the pooled RR was 1.06 (95% CI, 1.03-1.08) per 1-hour reduction and 1.12 (95% CI, 1.08-1.16) per 1-hour increment of sleep duration. For coronary heart disease, the pooled RR was 1.07 (95% CI, 1.03-1.12) per 1-hour reduction and 1.05 (95% CI, 1.00-1.10) per 1-hour increment of sleep duration. For stroke, the pooled RR was 1.05 (95% CI, 1.01-1.09) per 1-hour reduction and 1.18 (95% CI, 1.14-1.21) per 1-hour increment of sleep duration.Our findings indicate that both short and long sleep duration is associated with an increased risk of all-cause mortality and cardiovascular events.
| S-EPMC5634263 | biostudies-other
Project description:BACKGROUND: Association between parity and colorectal cancer (CRC) risk has been investigated by several epidemiological studies but results are controversial, yet a comprehensive and quantitative assessment of this association has not been reported so far. METHODS: Relevant published studies of parity and CRC were identified using MEDLINE, EMBASE and Web of Science databases through end of April 2013. Two authors independently assessed eligibility and extracted data. Eleven prospective studies reported relative risk (RR) estimates and 95% confidence intervals (CIs) of CRC risk associated with parity. We pooled the RR from individual studies using fixed- or random-effects models and carried out heterogeneity and publication bias analyses. RESULTS: The summary RR for the ever parity vs. nulliparous was 0.95 (95% CI: 0.88-1.02), with no heterogeneity (Q?=?9.04, P?=?0.443, I (2)?=?0.5%). Likewise, no significant association was yielded for the highest vs. lowest parity number (RR?=?1.02, 95% CI: 0.89-1.17), with moderate heterogeneity (Q?=?17.48, P?=?0.094, I (2)?=?37.1%). Dose-response analysis still indicated no effect of parity on CRC risk and the summary RR of per one livebirth was 0.99 (95% CI: 0.96-1.02), with moderate of heterogeneity (Q?=?16.50, P<0.021, I (2)?=?57.6%). Similar results were observed among all the subgroup analyses. No evidence of publication bias and significant heterogeneity between subgroups were detected by meta-regression analyses. CONCLUSION: Results of this dose-response meta-analysis of prospective studies found that there was little evidence of an association between parity and CRC risk.
| S-EPMC3787107 | biostudies-literature
Project description:A previous meta-analysis provided convincing evidence for an inverse association between adherence to a Mediterranean diet (MedDiet) and the risk of all-cause mortality. Since then, 19 prospective studies have been published. We updated the evidence from these prospective studies and conducted a dose-response meta-analysis to test the linear and potential nonlinear dose-response associations between adherence to a MedDiet and the risk of all-cause mortality. The PubMed, Scopus, ISI Web of Knowledge, and Embase bibliographic databases were systematically searched up to August 24, 2018. Summary HRs were estimated with the use of a random-effects meta-analysis to assess the association between a 2-point increment in MedDiet adherence and the risk of all-cause mortality. Sensitivity and subgroup analyses were performed and potential publication bias was tested. Twenty-nine prospective studies with 1,676,901 participants and 221,603 cases of all-cause mortality were included in the final analysis. The pooled HR of all-cause mortality was 0.90 (95% CI: 0.89, 0.91; I2 = 81.1%) for a 2-point increment in adherence to a MedDiet. Subgroup analyses showed that a significant inverse association was stronger in participants who lived in the Mediterranean region compared with non-Mediterranean areas (HRs: 0.82 compared with 0.92, respectively), and in studies that used the Panagiotakos MedDiet score. A nonlinear dose-response meta-analysis indicated that the risk of all-cause mortality linearly decreased with the increase in adherence to a MedDiet. The robustness of findings was confirmed in the sensitivity analyses. In conclusion, low-quality evidence from prospective cohort studies suggests an inverse association between adherence to a MedDiet and the risk of all-cause mortality, especially in Mediterranean regions. An inverse linear dose-response relation was also observed between adherence to a MedDiet and the risk of all-cause mortality.
| S-EPMC6855973 | biostudies-literature
Project description:BackgroundSerum gamma-glutamyltransferase (GGT) elevation likely contributes to cardiovascular (CV) mortality, however it has remained unknown whether a dose-response relationship exists between serum GGT and CV mortality.MethodsWe searched the PubMed, EMBASE, and Cochrane library databases for prospective cohort studies published up to October 2, 2016. Summary hazard ratios (HRs) with their corresponding 95% confidence intervals (CIs) were calculated using a fixed effects model.FindingsNine prospective studies, including 527,589 participants and more than 7,011 cases, were included in this meta-analysis. For the moderate, high, and highest levels of GGT, the pooled HRs of CV mortality were 1.11 (95% CI = 1.04-1.19), 1.29 (95% CI = 1.21-1.38) and 1.59 (95% CI = 1.47-1.72), respectively (all p < 0.05 as compared to the lowest levels of GGT). Additionally, the HR per incremental increase of GGT by 10 U/L was 1.10 (95% CI = 1.08-1.11). Evidence of a positive relationship with nonlinear trend for GGT elevation with CV mortality in females was found (P = 0.04 for nonlinearity). However, a linear model was better fit to illustrate the GGT-CV mortality among males (P = 0.304 for nonlinearity).ConclusionsThese findings indicate that serum GGT activity within the reference interval is positively associated with increased risk of CV mortality in a dose-response manner.
| S-EPMC5322906 | biostudies-literature