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Book ; Online ; E-Book: Systematic reviews in health research

Egger, Matthias / Davey Smith, George / Altman, Douglas G.

meta-analysis in context

2022

Abstract: This book has become the standard text on the use of systematic reviews in health research. It is recommended reading for anyone undertaking systematic reviews or needing to understand the principles and methodology used in research papers. It goes ... ...

Author's details	edited by Matthias Egger, Julian P. T. Higgins, George Davey Smith
Abstract	"This book has become the standard text on the use of systematic reviews in health research. It is recommended reading for anyone undertaking systematic reviews or needing to understand the principles and methodology used in research papers. It goes beyond explanation, to provide debate on key issues in systematic reviewing. Written by leading, internationally respected researchers, this is a reference for the informed reviewer but also a valuable resource for those coming to the field for the first time. It is both comprehensive and stimulating -- a classic text in its own right"-- "In this Third Edition of the classic Systematic Reviews textbook, now titled Systematic Reviews in Health Research, a team of distinguished researchers deliver a comprehensive and authoritative guide to the rapidly evolving area of systematic reviews and meta-analysis. The book demonstrates why systematic reviews—when conducted properly—provide the highest quality evidence on clinical and public health interventions and shows how they contribute to inference in many other contexts. The new edition reflects the broad role of systematic reviews, including: Twelve new chapters, covering additional study designs, methods and software, for example, on genetic association studies, prediction models, prevalence studies, network and dose-response meta-analysis; Thorough update of 15 chapters focusing on systematic reviews of interventions; Access to a companion website offering supplementary materials and practical exercises (www.systematic-reviews3.org). A key text for health researchers, Systematic Reviews in Health Research is also an indispensable resource for practitioners, students, and instructors in the health sciences needing to understand research synthesis."--Provided by publisher.
MeSH term(s)	Systematic Reviews as Topic ; Meta-Analysis as Topic ; Research Design ; Evidence-Based Medicine ; Controlled Clinical Trials as Topic
Keywords	Evidence-based medicine ; Systematic reviews (Medical research)
Subject code	610/.7/2
Language	English
Dates of publication	2022-2022
Size	1 online resource (xxxiii, 568 pages) :, illustrations (some colour)
Edition	Third edition.
Publisher	John Wiley & Sons, Inc
Publishing place	Hoboken, NJ
Document type	Book ; Online ; E-Book
Note	Previous edition: Systematic reviews in health care / edited by Matthias Egger, George Davey Smith and Douglas G. Altman. 2nd edition, 2001.
Remark	Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
ISBN	1-119-09937-4 ; 1-119-09936-6 ; 9781405160506 ; 978-1-119-09937-6 ; 978-1-119-09936-9 ; 1405160500
DOI	10.1002/9781119099369
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Article ; Online: Time-varying and tissue-dependent effects of adiposity on leptin levels: A Mendelian randomization study.

Richardson, Tom G / Leyden, Genevieve M / Davey Smith, George

eLife

2023 Volume 12

Abstract: Background: Findings from Mendelian randomization (MR) studies are conventionally interpreted as lifelong effects, which typically do not provide insight into the molecular mechanisms underlying the effect of an exposure on an outcome. In this study, we ...

Abstract	Background: Findings from Mendelian randomization (MR) studies are conventionally interpreted as lifelong effects, which typically do not provide insight into the molecular mechanisms underlying the effect of an exposure on an outcome. In this study, we apply two recently developed MR approaches (known as 'lifecourse' and 'tissue-partitioned' MR) to investigate lifestage-specific effects and tissues of action in the relationship between adiposity and circulating leptin levels. Methods: Genetic instruments for childhood and adult adiposity were incorporated into a multivariable MR (MVMR) framework to estimate lifestage-specific effects on leptin levels measured during early life (mean age: 10 y) in the Avon Longitudinal Study of Parents and Children and in adulthood (mean age: 55 y) using summary-level data from the deCODE Health study. This was followed by partitioning body mass index (BMI) instruments into those whose effects are putatively mediated by gene expression in either subcutaneous adipose or brain tissues, followed by using MVMR to simultaneously estimate their separate effects on childhood and adult leptin levels. Results: There was strong evidence that childhood adiposity has a direct effect on leptin levels at age 10 y in the lifecourse (β = 1.10 SD change in leptin levels, 95% CI = 0.90-1.30, p=6 × 10 Conclusions: Our findings demonstrate the use of lifecourse MR to disentangle direct and indirect effects of early-life exposures on time-varying complex outcomes. Furthermore, by integrating tissue-specific data, we highlight the etiological importance of appetite regulation in the effect of adiposity on leptin levels. Funding: This work was supported by the Integrative Epidemiology Unit, which receives funding from the UK Medical Research Council and the University of Bristol (MC_UU_00011/1).
MeSH term(s)	Adult ; Child ; Humans ; Middle Aged ; Leptin/genetics ; Adiposity/genetics ; Longitudinal Studies ; Mendelian Randomization Analysis ; Obesity
Chemical Substances	Leptin
Language	English
Publishing date	2023-10-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.84646
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Genetic variation and elevated liver enzymes during childhood, adolescence and early adulthood.

Stender, Stefan / Davey Smith, George / Richardson, Tom G

International journal of epidemiology

2023 Volume 52, Issue 5, Page(s) 1341–1349

Abstract: Background: Genetic factors influence the risk of fatty liver disease (FLD) in adults. The aim of this study was to test if, and when, genetic risk factors known to affect FLD in adults begin to exert their deleterious effects during childhood, ... ...

Abstract	Background: Genetic factors influence the risk of fatty liver disease (FLD) in adults. The aim of this study was to test if, and when, genetic risk factors known to affect FLD in adults begin to exert their deleterious effects during childhood, adolescence and early adulthood. Methods: We included up to 4018 British children and adolescents from the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort. Three genetic variants known to associate robustly with FLD in adults (PNPLA3 rs738409, TM6SF2 rs58542926 and HSD17B13 rs72613567) were tested for association with plasma levels of alanine transaminase (ALT) and aspartate transaminase (AST) during childhood (mean age: 9.9 years), early adolescence (15.5 years), late adolescence (17.8 years), and early adulthood (24.5 years). We also tested the associations of a 17-variant score and whole-genome polygenic risk scores (PRS) derived from associations in adults with plasma ALT and AST at the same four time points. Associations with elastography-derived liver steatosis and fibrosis were tested in early adulthood. Results: Genetic risk factors for FLD (individually, combined into a 3-variant score, a 17-variant score and as a genome-wide PRS), were associated with higher liver enzymes, beginning in childhood and throughout adolescence and early adulthood. The ALT-increasing effects of the genetic risk variants became larger with increasing age. The ALT-PRS was associated with liver steatosis in early adulthood. No genetic associations with fibrosis were observed. Conclusions: Genetic factors that promote FLD in adults associate with elevated liver enzymes already during childhood, and their effects get amplified with increasing age.
MeSH term(s)	Adolescent ; Adult ; Child ; Humans ; Alanine Transaminase/blood ; Alanine Transaminase/genetics ; Aspartate Aminotransferases/blood ; Aspartate Aminotransferases/genetics ; Fibrosis ; Genetic Predisposition to Disease ; Longitudinal Studies ; Non-alcoholic Fatty Liver Disease/genetics ; Polymorphism, Single Nucleotide
Chemical Substances	Alanine Transaminase (EC 2.6.1.2) ; Aspartate Aminotransferases (EC 2.6.1.1)
Language	English
Publishing date	2023-04-27
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	187909-1
ISSN	1464-3685 ; 0300-5771
ISSN (online)	1464-3685
ISSN	0300-5771
DOI	10.1093/ije/dyad048
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Article ; Online: Characterizing the Causal Pathway From Childhood Adiposity to Right Heart Physiology and Pulmonary Circulation Using Lifecourse Mendelian Randomization.

Leyden, Genevieve M / Urquijo, Helena / Hughes, Alun D / Davey Smith, George / Richardson, Tom G

Journal of the American Heart Association

2024 Volume 13, Issue 6, Page(s) e030453

Abstract: Background: Observational epidemiological studies have reported an association between childhood adiposity and altered cardiac morphology and function in later life. However, whether this is due to a direct consequence of being overweight during ... ...

Abstract	Background: Observational epidemiological studies have reported an association between childhood adiposity and altered cardiac morphology and function in later life. However, whether this is due to a direct consequence of being overweight during childhood has been difficult to establish, particularly as accounting for other measures of body composition throughout the lifecourse can be exceptionally challenging. Methods and results: In this study, we used human genetics to investigate this using a causal inference technique known as lifecourse Mendelian randomization. This approach allowed us to evaluate the effect of childhood body size on 11 measures of right heart and pulmonary circulation independent of other anthropometric traits at various stages in the lifecourse. We found strong evidence that childhood body size has a direct effect on an enlarged right heart structure in later life (eg, right ventricular end-diastolic volume: β=0.24 [95% CI, 0.15-0.33]; Conclusions: Our findings suggest that, although childhood body size has a long-term influence on an enlarged heart structure in adulthood, associations with the other structural components of the cardiovascular system and their function may be largely attributed to body composition at other stages in the lifecourse.
MeSH term(s)	Humans ; Adiposity/genetics ; Overweight/complications ; Mendelian Randomization Analysis/methods ; Pulmonary Circulation ; Body Mass Index ; Pediatric Obesity/diagnosis ; Pediatric Obesity/epidemiology ; Pediatric Obesity/genetics ; Genome-Wide Association Study ; Polymorphism, Single Nucleotide
Language	English
Publishing date	2024-03-08
Publishing country	England
Document type	Journal Article
ZDB-ID	2653953-6
ISSN	2047-9980 ; 2047-9980
ISSN (online)	2047-9980
ISSN	2047-9980
DOI	10.1161/JAHA.123.030453
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Article ; Online: Leveraging family history data to disentangle time-varying effects on disease risk using lifecourse mendelian randomization.

Richardson, Tom G / Urquijo, Helena / Holmes, Michael V / Davey Smith, George

European journal of epidemiology

2023 Volume 38, Issue 7, Page(s) 765–769

Abstract: Lifecourse Mendelian randomization is a causal inference technique which harnesses genetic variants with time-varying effects to develop insight into the influence of age-dependent lifestyle factors on disease risk. Here, we apply this approach to ... ...

Abstract	Lifecourse Mendelian randomization is a causal inference technique which harnesses genetic variants with time-varying effects to develop insight into the influence of age-dependent lifestyle factors on disease risk. Here, we apply this approach to evaluate whether childhood body size has a direct consequence on 8 major disease endpoints by analysing parental history data from the UK Biobank study.Our findings suggest that, whilst childhood body size increases later risk of outcomes such as heart disease (odds ratio (OR) = 1.15, 95% CI = 1.07 to 1.23, P = 7.8 × 10
MeSH term(s)	Humans ; Female ; Risk Factors ; Overweight/epidemiology ; Overweight/genetics ; Mendelian Randomization Analysis/methods ; Smoking ; Breast Neoplasms ; Genome-Wide Association Study ; Polymorphism, Single Nucleotide
Language	English
Publishing date	2023-05-08
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	632614-6
ISSN	1573-7284 ; 0393-2990
ISSN (online)	1573-7284
ISSN	0393-2990
DOI	10.1007/s10654-023-01001-8
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: A lifecourse Mendelian randomization study uncovers age-dependent effects of adiposity on asthma risk.

Urquijo, Helena / Leyden, Genevieve M / Davey Smith, George / Richardson, Tom G

iScience

2023 Volume 26, Issue 12, Page(s) 108356

Abstract: Evaluating the long-term consequences of childhood lifestyle factors on asthma risk can be exceptionally challenging in epidemiology given that cases are typically diagnosed at various timepoints throughout the lifecourse. In this study, we used human ... ...

Abstract	Evaluating the long-term consequences of childhood lifestyle factors on asthma risk can be exceptionally challenging in epidemiology given that cases are typically diagnosed at various timepoints throughout the lifecourse. In this study, we used human genetic data to evaluate the effects of childhood and adulthood adiposity on risk of pediatric (n = 13,962 cases) and adult-onset asthma (n = 26,582 cases) with a common set of controls (n = 300,671) using a technique known as lifecourse Mendelian randomization. We found that childhood adiposity directly increases risk of pediatric asthma (OR = 1.20, 95% CI = 1.03-1.37, p = 0.03), but limited evidence that it has an effect on adult-onset asthma after accounting for adiposity during adulthood (OR = 1.05, 95% CI = 0.93-1.17, p = 0.39). Conversely, there was strong evidence that adulthood adiposity increases asthma risk in midlife (OR = 1.37, 95% CI = 1.28-1.46, P = 7 × 10
Language	English
Publishing date	2023-10-29
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2023.108356
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Article ; Online: Reappraising the role of instrumental inequalities for mendelian randomization studies in the mega Biobank era.

Sanderson, Eleanor / Davey Smith, George

European journal of epidemiology

2023 Volume 38, Issue 9, Page(s) 917–919

MeSH term(s)	Humans ; Biological Specimen Banks ; Mendelian Randomization Analysis ; Research
Language	English
Publishing date	2023-08-27
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	632614-6
ISSN	1573-7284 ; 0393-2990
ISSN (online)	1573-7284
ISSN	0393-2990
DOI	10.1007/s10654-023-01035-y
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Adiposity may confound the association between vitamin D and disease risk - a lifecourse Mendelian randomization study.

Richardson, Tom G / Power, Grace M / Davey Smith, George

eLife

2022 Volume 11

Abstract: Background: Vitamin D supplements are widely prescribed to help reduce disease risk. However, this strategy is based on findings using conventional epidemiological methods which are prone to confounding and reverse causation.: Methods: In this short ... ...

Abstract	Background: Vitamin D supplements are widely prescribed to help reduce disease risk. However, this strategy is based on findings using conventional epidemiological methods which are prone to confounding and reverse causation. Methods: In this short report, we leveraged genetic variants which differentially influence body size during childhood and adulthood within a multivariable Mendelian randomization (MR) framework, allowing us to separate the genetically predicted effects of adiposity at these two timepoints in the lifecourse. Results: Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC), there was strong evidence that higher childhood body size has a direct effect on lower vitamin D levels in early life (mean age: 9.9 years, range = 8.9-11.5 years) after accounting for the effect of the adult body size genetic score (beta = -0.32, 95% CI = -0.54 to -0.10, p=0.004). Conversely, we found evidence that the effect of childhood body size on vitamin D levels in midlife (mean age: 56.5 years, range = 40-69 years) is putatively mediated along the causal pathway involving adulthood adiposity (beta = -0.17, 95% CI = -0.21 to -0.13, p=4.6 × 10 Conclusions: Our findings have important implications in terms of the causal influence of vitamin D deficiency on disease risk. Furthermore, they serve as a compelling proof of concept that the timepoints across the lifecourse at which exposures and outcomes are measured can meaningfully impact overall conclusions drawn by MR studies. Funding: This work was supported by the Integrative Epidemiology Unit which receives funding from the UK Medical Research Council and the University of Bristol (MC_UU_00011/1).
MeSH term(s)	Adiposity/genetics ; Adult ; Aged ; Body Mass Index ; Child ; Genome-Wide Association Study ; Humans ; Longitudinal Studies ; Mendelian Randomization Analysis ; Middle Aged ; Obesity ; Polymorphism, Single Nucleotide ; Vitamin D ; Vitamins
Chemical Substances	Vitamins ; Vitamin D (1406-16-2)
Language	English
Publishing date	2022-08-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.79798
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Using the global randomization test as a Mendelian randomization falsification test for the exclusion restriction assumption.

Millard, Louise A C / Davey Smith, George / Tilling, Kate

European journal of epidemiology

2024

Abstract: Mendelian randomization may give biased causal estimates if the instrument affects the outcome not solely via the exposure of interest (violating the exclusion restriction assumption). We demonstrate use of a global randomization test as a falsification ... ...

Abstract	Mendelian randomization may give biased causal estimates if the instrument affects the outcome not solely via the exposure of interest (violating the exclusion restriction assumption). We demonstrate use of a global randomization test as a falsification test for the exclusion restriction assumption. Using simulations, we explored the statistical power of the randomization test to detect an association between a genetic instrument and a covariate set due to (a) selection bias or (b) horizontal pleiotropy, compared to three approaches examining associations with individual covariates: (i) Bonferroni correction for the number of covariates, (ii) correction for the effective number of independent covariates, and (iii) an r
Language	English
Publishing date	2024-02-29
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	632614-6
ISSN	1573-7284 ; 0393-2990
ISSN (online)	1573-7284
ISSN	0393-2990
DOI	10.1007/s10654-024-01097-6
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Article ; Online: Life course effects of genetic susceptibility to higher body size on body fat and lean mass: prospective cohort study.

Waterfield, Scott / Richardson, Tom G / Davey Smith, George / O'Keeffe, Linda M / Bell, Joshua A

International journal of epidemiology

2023 Volume 52, Issue 5, Page(s) 1377–1387

Abstract: Background/objectives: Different genetic variants are associated with larger body size in childhood vs adulthood. Whether and when these variants predominantly influence adiposity are unknown. We examined how genetic variants influence total body fat ... ...

Abstract	Background/objectives: Different genetic variants are associated with larger body size in childhood vs adulthood. Whether and when these variants predominantly influence adiposity are unknown. We examined how genetic variants influence total body fat and total lean mass trajectories. Methods: Data were from the Avon Longitudinal Study of Parents and Children birth cohort (N = 6926). Sex-specific genetic risk scores (GRS) for childhood and adulthood body size were generated, and dual-energy X-ray absorptiometry scans measured body fat and lean mass six times between the ages of 9 and 25 years. Multilevel linear spline models examined associations of GRS with fat and lean mass trajectories. Results: In males, the sex-specific childhood and adulthood GRS were associated with similar differences in fat mass from 9 to 18 years; 8.3% [95% confidence interval (CI) 5.1, 11.6] and 7.5% (95% CI 4.3, 10.8) higher fat mass at 18 years per standard deviation (SD) higher childhood and adulthood GRS, respectively. In males, the sex-combined childhood GRS had stronger effects at ages 9 to 15 than the sex-combined adulthood GRS. In females, associations for the sex-specific childhood GRS were almost 2-fold stronger than the adulthood GRS from 9 to 18 years: 10.5% (95% CI 8.5, 12.4) higher fat mass at 9 years per SD higher childhood GRS compared with 5.1% (95% CI 3.2, 6.9) per-SD higher adulthood GRS. In females, the sex-combined GRS had similar effects, with slightly larger effect estimates. Lean mass effect sizes were much smaller. Conclusions: Genetic variants for body size are more strongly associated with adiposity than with lean mass. Sex-combined childhood variants are more strongly associated with increased adiposity until early adulthood. This may inform future studies that use genetics to investigate the causes and impact of adiposity at different life stages.
MeSH term(s)	Male ; Child ; Female ; Humans ; Adolescent ; Young Adult ; Adult ; Longitudinal Studies ; Prospective Studies ; Genetic Predisposition to Disease ; Life Change Events ; Body Mass Index ; Obesity/genetics ; Adipose Tissue ; Adiposity/genetics ; Body Size/genetics
Language	English
Publishing date	2023-03-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	187909-1
ISSN	1464-3685 ; 0300-5771
ISSN (online)	1464-3685
ISSN	0300-5771
DOI	10.1093/ije/dyad029
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