scholarly journals BMI and all cause mortality: systematic review and non-linear dose-response meta-analysis of 230 cohort studies with 3.74 million deaths among 30.3 million participants

BMJ ◽  
2016 ◽  
pp. i2156 ◽  
Author(s):  
Dagfinn Aune ◽  
Abhijit Sen ◽  
Manya Prasad ◽  
Teresa Norat ◽  
Imre Janszky ◽  
...  
2018 ◽  
Vol 22 (2) ◽  
pp. 295-306 ◽  
Author(s):  
Alireza Milajerdi ◽  
Kurosh Djafarian ◽  
Sakineh Shab-Bidar

AbstractObjectiveHigh Na intake has been associated with different health problems. However, serious controversies exist over studies investigating associations of Na intake with mortality from all-causes and CVD. The present systematic review and meta-analysis was done to investigate, for the first time, the dose–response association of dietary Na intake with all-cause and CVD mortality among prospective studies.DesignRelevant papers published up to August 2017 were searched in MEDLINE, EMBASE and Google Scholar databases. Prospective cohort studies on the association of dietary Na intake with all-cause or/and CVD mortality were included. Linear and non-linear dose–response associations between Na intake and CVD and all-cause mortality were examined.ResultsOverall, twenty publications met inclusion criteria. A significant non-linear association (P<0·001) was found between Na intake and CVD mortality risk among studies assessing urinary Na excretion, with a relatively steep slope at Na intakes above 2400mg/d. However, the association was not significant in studies using dietary Na intake (P=0·61). Additionally, the non-linear association of Na intake with all-cause mortality was also non-significant. No linear association (effect size; 95 % CI; I2) was seen between 100mg/d increment in Na intake and CVD mortality (1·01; 0·97, 1·05; 98·4 %) or all-cause mortality (1·01; 1·00, 1·02; 89·2 %). Following subgroup analyses, the association between Na intake and CVD mortality was observed only among studies conducted in the USA (0·99; 0·99, 1·00; 20·0 %).ConclusionsThe study showed a direct association between urinary Na excretion and CVD mortality which was more considerable at intakes above 2400mg/d. In contrast, no significant association was found between Na intake and all-cause mortality. Further long-term prospective studies on different populations are required to confirm these findings.


Heart ◽  
2019 ◽  
Vol 105 (9) ◽  
pp. 686-692 ◽  
Author(s):  
Ahmad Jayedi ◽  
Kazem Rahimi ◽  
Leonelo E Bautista ◽  
Milad Nazarzadeh ◽  
Mahdieh Sadat Zargar ◽  
...  

ObjectiveTo systematically assess the association of circulating inflammation markers with the future risk of hypertension.MethodsWe did a systematic literature search of PubMed and Scopus, from database inception to July 10, 2018. Prospective and retrospective cohort studies evaluating the association of circulating C reactive protein (CRP), high-sensitive CRP (hs-CRP), interleukin 6 (IL-6) and IL-1β to the risk of developing hypertension in the general population were included. The relative risks (RRs) for the top versus bottom tertiles of circulating biomarkers were calculated using a fixed-effects/random-effects model. A potential non-linear dose-response association was tested.ResultsFourteen prospective cohort studies, two retrospective cohort studies and five nested case-control studies involving 142 640 participants and 20 676 cases were identified. The RR for the third versus first tertiles of circulating CRP was 1.23 (95% CI 1.11 to 1.35; I2=59%, n=12). The association remained unchanged after adjustment for body mass index. The RRs for other biomarkers were as follows: hs-CRP (RR 1.20, 95% CI 1.02 to 1.37; I2=74%, n=7), IL-6 (RR 1.51, 95% CI 1.30 to 1.71; I2=0%, n=5), and IL-1β (RR 1.22, 95% CI 0.92 to 1.51; I2=0%, n=3). A non-linear dose-response meta-analysis demonstrated that the risk of hypertension increased linearly with increasing circulating inflammation markers, even within the low-risk and intermediate-risk categories.ConclusionsHigher levels of circulating CRP, hs-CRP and IL-6, but not IL-1β, were associated with the risk of developing hypertension. The association persisted in subgroups of studies defined by major sources of heterogeneity.


Author(s):  
Quanman Li ◽  
Yu Liu ◽  
Xizhuo Sun ◽  
Honghui Li ◽  
Cheng Cheng ◽  
...  

Abstract Background We conducted a systematic review and meta-analysis from published cohort studies to examine the association of adult height and all-cause mortality and to further explore the dose–response association. Methods PubMed, The Cochrane Library, The Ovid, CNKI, CQVIP and Wanfang databases were searched for articles published from database inception to 6 February 2018. We used the DerSimonian–Laird random-effects model to estimate the quantitative association between adult height and all-cause mortality and the restricted cubic splines to model the dose–response association. Results We included 15 articles, with 1 533 438 death events and 2 854 543 study participants. For each 5-cm height increase below the average, the risk of all-cause mortality was reduced by 7% [relative risk (RR) = 0.93, 95% confidence interval (CI), 0.89–0.97] for men and 5% (RR = 0.95, 95% CI, 0.90–0.99) for women. All-cause mortality had a U-shaped association with adult height, the lowest risk occurring at 174 cm for men and 158 cm for women (both Pnonlinearity &lt; 0.001). Relative to the shortest adult height (147 cm for men and 137 cm for women), men at 174 cm had a 47% lower likelihood of all-cause mortality and women at 158 cm a 33% lower risk of all-cause mortality. Conclusions Our study suggests that the relation between adult height and all-cause mortality is approximately U-shaped in both men and women.


BMJ ◽  
2019 ◽  
pp. l4570 ◽  
Author(s):  
Ulf Ekelund ◽  
Jakob Tarp ◽  
Jostein Steene-Johannessen ◽  
Bjørge H Hansen ◽  
Barbara Jefferis ◽  
...  

AbstractObjectiveTo examine the dose-response associations between accelerometer assessed total physical activity, different intensities of physical activity, and sedentary time and all cause mortality.DesignSystematic review and harmonised meta-analysis.Data sourcesPubMed, PsycINFO, Embase, Web of Science, Sport Discus from inception to 31 July 2018.Eligibility criteriaProspective cohort studies assessing physical activity and sedentary time by accelerometry and associations with all cause mortality and reported effect estimates as hazard ratios, odds ratios, or relative risks with 95% confidence intervals.Data extraction and analysisGuidelines for meta-analyses and systematic reviews for observational studies and PRISMA guidelines were followed. Two authors independently screened the titles and abstracts. One author performed a full text review and another extracted the data. Two authors independently assessed the risk of bias. Individual level participant data were harmonised and analysed at study level. Data on physical activity were categorised by quarters at study level, and study specific associations with all cause mortality were analysed using Cox proportional hazards regression analyses. Study specific results were summarised using random effects meta-analysis.Main outcome measureAll cause mortality.Results39 studies were retrieved for full text review; 10 were eligible for inclusion, three were excluded owing to harmonisation challenges (eg, wrist placement of the accelerometer), and one study did not participate. Two additional studies with unpublished mortality data were also included. Thus, individual level data from eight studies (n=36 383; mean age 62.6 years; 72.8% women), with median follow-up of 5.8 years (range 3.0-14.5 years) and 2149 (5.9%) deaths were analysed. Any physical activity, regardless of intensity, was associated with lower risk of mortality, with a non-linear dose-response. Hazards ratios for mortality were 1.00 (referent) in the first quarter (least active), 0.48 (95% confidence interval 0.43 to 0.54) in the second quarter, 0.34 (0.26 to 0.45) in the third quarter, and 0.27 (0.23 to 0.32) in the fourth quarter (most active). Corresponding hazards ratios for light physical activity were 1.00, 0.60 (0.54 to 0.68), 0.44 (0.38 to 0.51), and 0.38 (0.28 to 0.51), and for moderate-to-vigorous physical activity were 1.00, 0.64 (0.55 to 0.74), 0.55 (0.40 to 0.74), and 0.52 (0.43 to 0.61). For sedentary time, hazards ratios were 1.00 (referent; least sedentary), 1.28 (1.09 to 1.51), 1.71 (1.36 to 2.15), and 2.63 (1.94 to 3.56).ConclusionHigher levels of total physical activity, at any intensity, and less time spent sedentary, are associated with substantially reduced risk for premature mortality, with evidence of a non-linear dose-response pattern in middle aged and older adults.Systematic review registrationPROSPERO CRD42018091808.


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