scholarly journals Meta-Analysis of Present-Bias Estimation Using Convex Time Budgets

2019 ◽  
Author(s):  
Taisuke Imai ◽  
Tom A. Rutter ◽  
Colin F. Camerer
2019 ◽  
Author(s):  
Taisuke Imai ◽  
Tom Rutter ◽  
Colin Camerer

We examine 220 estimates of the present-bias parameter from 28 articles using the Convex Time Budget protocol. The literature shows that people are on average present biased, but the estimates exhibit substantial heterogeneity across studies. There is evidence of modest selective reporting in the direction of overreporting present-bias. The primary source of the heterogeneity is the type of reward, either monetary or non-monetary reward, but the effect is weakened after correcting for potential selective reporting. In the studies using the monetary reward, the delay until the issue of the reward associated with the "current" time period is shown to influence the estimates of present bias parameter.


2020 ◽  
Author(s):  
Taisuke Imai ◽  
Tom A Rutter ◽  
Colin F Camerer

Abstract We examine 220 estimates of the present-bias parameter from 28 articles using the Convex Time Budget protocol. The literature shows that people are on average present-biased, but estimates exhibit substantial heterogeneity across studies. There is evidence of modest selective reporting in the direction of overreporting present-bias. The primary source of heterogeneity is the type of reward, either monetary or non-monetary, but this effect is weakened after correcting for selective reporting. In studies using monetary rewards, the delay until the issue of the reward associated with the “current” time period influences estimates of the present-bias parameter.


F1000Research ◽  
2018 ◽  
Vol 7 ◽  
pp. 146 ◽  
Author(s):  
Peter N. Lee ◽  
Barbara A. Forey ◽  
Katharine J. Coombs ◽  
Jan S. Hamling ◽  
Alison J. Thornton

Background: Some evidence suggests environmental tobacco smoke (ETS) might cause chronic obstructive pulmonary disease (COPD). We reviewed available epidemiological data in never smokers. Methods: We identified epidemiological studies providing estimates of relative risk (RR) with 95% confidence interval (CI) for various ETS exposure indices. Confounder-adjusted RRs for COPD were extracted, or derived using standard methods. Meta-analyses were conducted for each exposure index, with tests for heterogeneity and publication bias. For the main index (spouse ever smoked or nearest equivalent), analyses investigated variation in RR by location, publication period, study type, sex, diagnosis, study size, confounder adjustment, never smoker definition, and exposure index definition. Results: Twenty-eight relevant studies were identified; nine European or Middle Eastern, nine Asian, eight American and two from multiple countries. Five were prospective, seven case-control and 16 cross-sectional. The COPD definition involved death or hospitalisation in seven studies, GOLD stage 1+ criteria in twelve, and other definitions in nine. For the main index, random-effects meta-analysis of 33 heterogeneous (p<0.001) estimates gave a RR of 1.20 (95%CI 1.08-1.34). Higher estimates for females (1.59,1.16-2.19, n=11) than males (1.29,0.94-1.76, n=7) or sexes combined (1.10,0.99-1.22, n=15 where sex-specific not available), and lower estimates for studies of 150+ cases (1.08,0.97-1.20, n=13) partly explained the heterogeneity. Estimates were higher for Asian studies (1.34,1.08-1.67, n=10), case-control studies (1.55,1.04-2.32, n=8), and COPD mortality or hospitalisation (1.40,1.12-1.74, n=11). Some increase was seen for severer COPD (1.29,1.10-1.52, n=7). Dose-response evidence was heterogeneous. Evidence for childhood (0.88,0.72-1.07, n=2) and workplace (1.12,0.77-1.64, n=4) exposure was limited, but an increase was seen for overall adulthood exposure (1.20,1.03-1.39, n=17). We discuss study weaknesses that may bias estimation of the association of COPD with ETS. Conclusions: Although the evidence suggests ETS increases COPD, study weaknesses and absence of well-designed large studies precludes reliable inference of causality. More definitive evidence is required.


F1000Research ◽  
2020 ◽  
Vol 7 ◽  
pp. 146
Author(s):  
Peter N. Lee ◽  
Barbara A. Forey ◽  
Katharine J. Coombs ◽  
Jan S. Hamling ◽  
Alison J. Thornton

Background: Some evidence suggests environmental tobacco smoke (ETS) might cause chronic obstructive pulmonary disease (COPD). We reviewed available epidemiological data in never smokers. Methods: We identified epidemiological studies providing estimates of relative risk (RR) with 95% confidence interval (CI) for various ETS exposure indices. Confounder-adjusted RRs for COPD were extracted, or derived using standard methods. Meta-analyses were conducted for each exposure index, with tests for heterogeneity and publication bias. For the main index (spouse ever smoked or nearest equivalent), analyses investigated variation in RR by location, publication period, study type, sex, diagnosis, study size, confounder adjustment, never smoker definition, and exposure index definition. Results: Twenty-eight relevant studies were identified; nine European or Middle Eastern, nine Asian, eight American and two from multiple countries. Five were prospective, seven case-control and 16 cross-sectional. The COPD definition involved death or hospitalisation in seven studies, GOLD stage 1+ criteria in twelve, and other definitions in nine. For the main index, random-effects meta-analysis of 33 heterogeneous (p<0.001) estimates gave a RR of 1.20 (95%CI 1.08-1.34). Higher estimates for females (1.59,1.16-2.19, n=11) than males (1.29,0.94-1.76, n=7) or sexes combined (1.10,0.99-1.22, n=15 where sex-specific not available), and lower estimates for studies of 150+ cases (1.08,0.97-1.20, n=13) partly explained the heterogeneity. Estimates were higher for Asian studies (1.34,1.08-1.67, n=10), case-control studies (1.55,1.04-2.32, n=8), and COPD mortality or hospitalisation (1.40,1.12-1.74, n=11). Some increase was seen for severer COPD (1.29,1.10-1.52, n=7). Dose-response evidence was heterogeneous. Evidence for childhood (0.88,0.72-1.07, n=2) and workplace (1.12,0.77-1.64, n=4) exposure was limited, but an increase was seen for overall adulthood exposure (1.20,1.03-1.39, n=17). We discuss study weaknesses that may bias estimation of the association of COPD with ETS. Conclusions: Although the evidence strongly suggests that ETS increases COPD, study weaknesses and absence of well-designed large studies preclude reliable effect estimation. More definitive evidence is required.


F1000Research ◽  
2019 ◽  
Vol 7 ◽  
pp. 146
Author(s):  
Peter N. Lee ◽  
Barbara A. Forey ◽  
Katharine J. Coombs ◽  
Jan S. Hamling ◽  
Alison J. Thornton

Background: Some evidence suggests environmental tobacco smoke (ETS) might cause chronic obstructive pulmonary disease (COPD). We reviewed available epidemiological data in never smokers. Methods: We identified epidemiological studies providing estimates of relative risk (RR) with 95% confidence interval (CI) for various ETS exposure indices. Confounder-adjusted RRs for COPD were extracted, or derived using standard methods. Meta-analyses were conducted for each exposure index, with tests for heterogeneity and publication bias. For the main index (spouse ever smoked or nearest equivalent), analyses investigated variation in RR by location, publication period, study type, sex, diagnosis, study size, confounder adjustment, never smoker definition, and exposure index definition. Results: Twenty-eight relevant studies were identified; nine European or Middle Eastern, nine Asian, eight American and two from multiple countries. Five were prospective, seven case-control and 16 cross-sectional. The COPD definition involved death or hospitalisation in seven studies, GOLD stage 1+ criteria in twelve, and other definitions in nine. For the main index, random-effects meta-analysis of 33 heterogeneous (p<0.001) estimates gave a RR of 1.20 (95%CI 1.08-1.34). Higher estimates for females (1.59,1.16-2.19, n=11) than males (1.29,0.94-1.76, n=7) or sexes combined (1.10,0.99-1.22, n=15 where sex-specific not available), and lower estimates for studies of 150+ cases (1.08,0.97-1.20, n=13) partly explained the heterogeneity. Estimates were higher for Asian studies (1.34,1.08-1.67, n=10), case-control studies (1.55,1.04-2.32, n=8), and COPD mortality or hospitalisation (1.40,1.12-1.74, n=11). Some increase was seen for severer COPD (1.29,1.10-1.52, n=7). Dose-response evidence was heterogeneous. Evidence for childhood (0.88,0.72-1.07, n=2) and workplace (1.12,0.77-1.64, n=4) exposure was limited, but an increase was seen for overall adulthood exposure (1.20,1.03-1.39, n=17). We discuss study weaknesses that may bias estimation of the association of COPD with ETS. Conclusions: Although the evidence suggests ETS increases COPD, study weaknesses and absence of well-designed large studies preclude reliable estimation of the effect. More definitive evidence is required.


2021 ◽  
Author(s):  
Stephen L. Cheung ◽  
Agnieszka Tymula ◽  
Xueting Wang
Keyword(s):  

2021 ◽  
Author(s):  
Stephen L. Cheung ◽  
Agnieszka Tymula ◽  
Xueting Wang
Keyword(s):  

2021 ◽  
Author(s):  
Yali Wei ◽  
Yan Meng ◽  
Na Li ◽  
Qian Wang ◽  
Liyong Chen

The purpose of the systematic review and meta-analysis was to determine if low-ratio n-6/n-3 long-chain polyunsaturated fatty acid (PUFA) supplementation affects serum inflammation markers based on current studies.


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