On combining dose—response data from epidemiological studies by meta-analysis

1995 ◽  
Vol 14 (5-7) ◽  
pp. 531-544 ◽  
Author(s):  
S. Jay Smith ◽  
Samue L. P. Caudill ◽  
Karen K. Steinberg ◽  
Stephen B. Thacker
Epidemiology ◽  
1993 ◽  
Vol 4 (3) ◽  
pp. 218-228 ◽  
Author(s):  
Jesse A. Berlin ◽  
Matthew P. Longnecker ◽  
Sander Greenland

2016 ◽  
Vol 115 (4) ◽  
pp. 737-750 ◽  
Author(s):  
Dominik D. Alexander ◽  
Lauren C. Bylsma ◽  
Ashley J. Vargas ◽  
Sarah S. Cohen ◽  
Abigail Doucette ◽  
...  

AbstractInverse associations between dairy consumption and CVD have been reported in several epidemiological studies. Our objective was to conduct a meta-analysis of prospective cohort studies of dairy intake and CVD. A comprehensive literature search was conducted to identify studies that reported risk estimates for total dairy intake, individual dairy products, low/full-fat dairy intake, Ca from dairy sources and CVD, CHD and stroke. Random-effects meta-analyses were used to generate summary relative risk estimates (SRRE) for high v. low intake and stratified intake dose–response analyses. Additional dose–response analyses were performed. Heterogeneity was examined in sub-group and sensitivity analyses. In total, thirty-one unique cohort studies were identified and included in the meta-analysis. Several statistically significant SRRE below 1.0 were observed, namely for total dairy intake and stroke (SRRE=0·91; 95 % CI 0·83, 0·99), cheese intake and CHD (SRRE=0·82; 95 % CI 0·72, 0·93) and stroke (SRRE=0·87; 95 % CI 0·77, 0·99), and Ca from dairy sources and stroke (SRRE=0·69; 95 % CI 0·60, 0·81). However, there was little evidence for inverse dose–response relationships between the dairy variables and CHD and stroke after adjusting for within-study covariance. The results of this meta-analysis of prospective cohort studies have shown that dairy consumption may be associated with reduced risks of CVD, although additional data are needed to more comprehensively examine potential dose–response patterns.


2020 ◽  
Author(s):  
Xiao Wang ◽  
Yang Zhou ◽  
Xiaofei Ye ◽  
Fangchen Liu ◽  
Xi Zhu ◽  
...  

Abstract Background: Bilirubin, a marker of hepatic and hematological diseases in clinical practice, is not only a waste end-product but also an antioxidant that may protect against diseases associated with oxidative stress. Numerous epidemiological studies have shown an inverse relationship between the serum total bilirubin (TBIL) level and the risk of ischemic stroke (IS). However, markedly elevated TBIL levels may exert neurotoxic effects. Based on this, we conducted a dose-response meta-analysis to quantify the relationship between blood TBIL and IS as well as between TBIL and all types of stroke (AS) in the physiological range of bilirubin.Methods: PubMed, Embase, Web of Science, and Cochrane Central databases were searched up to March 2019. Additional studies were identified by reviewing references and contacting authors. Categorical and dose-response meta-analyses were performed to quantify the relationship between TBIL and IS. The primary outcome was ischemic stroke, and the secondary outcome was all types of stroke.Results: Nine observational studies (seven publications) involving 110,032 participants and 3710 stroke cases were included for analysis. The average OR of IS for every 1 µmol/L increment in TBIL level was 0.978 (95% CI: 0.957–0.999). The summary OR of AS for every 1 µmol/L increment in TBIL level was 0.974 (95% CI: 0.956–0.992). Subgroup analysis based on gender showed a negative dose-response relationship between the circulating TBIL level and IS or AS in males, but not in females.Conclusions: The present study found a negative dose-response relationship between the circulating TBIL level and the risk of IS or AS within physiologic range of serum TBIL in males. Moderately elevated blood TBIL levels might be associated with a diminished prevalence of IS. Every 1 µmol/L increment in serum TBIL level was associated with a 2.2% decrease in the risk of IS and a 2.6% decrease in the risk of AS. However, due to the limitations in the number of included studies and their quality, large-scaled prospective cohort studies are needed to confirm the conclusion of the current analysis.Trial registration: This study was registered at PROSPERO (https://www.crd. york.ac.uk/PROSPERO/[CRD42017075988]).


2011 ◽  
Vol 4 (1) ◽  
pp. 70-77
Author(s):  
Dale Hattis

Perceived needs for extensive chemical-specific toxicological information have impeded efforts to assess risks and evaluate likely public health protection benefits of possible standards for hazardous air pollutants (HAPs). This paper discusses opportunities to use effects of HAPs on early effect biomarkers, such as birth weights, to predict likely changes in rare quantal effects of concern that would be relevant for the quantification of likely regulatory benefits from exposure reductions. In the birth weight example, even modest exposures to common air pollutants can be seen as producing a kind of tax on the limited resources available to the fetus to grow and develop. In contrast to teratogenic effects, dose response relationships for fetal growth restriction in animals are often nearly linear, suggesting that the developing fetus may not generally have untapped ”functional reserve capacity“ that is expected to buffer the effects of modest exposures to toxicants in the traditional toxicological paradigm. Given this mechanistic perspective, supported in part by parallel dose response relationships between reported cigarette smoking and both birth weight and infant mortality, restriction on fetal growth can be associated with changes in quantal end effects of concern that are more difficult to assess directly in epidemiological studies.


2016 ◽  
Vol 35 (5) ◽  
pp. 1039-1046 ◽  
Author(s):  
Xingyang Yi ◽  
Jingjing Zhu ◽  
Xiao Zhu ◽  
Guang Jian Liu ◽  
Lang Wu

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