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Causality


Causality

Statistical Perspectives and Applications
Wiley Series in Probability and Statistics 1. Aufl.

von: Carlo Berzuini, Philip Dawid, Luisa Bernardinell

73,99 €

Verlag: Wiley
Format: EPUB
Veröffentl.: 04.06.2012
ISBN/EAN: 9781119941736
Sprache: englisch
Anzahl Seiten: 416

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Beschreibungen

<p><b>A state of the art volume on statistical causality</b></p> <p><i>Causality: Statistical Perspectives and Applications</i> presents a wide-ranging collection of seminal contributions by renowned experts in the field, providing a thorough treatment of all aspects of statistical causality. It covers the various formalisms in current use, methods for applying them to specific problems, and the special requirements of a range of examples from medicine, biology and economics to political science.</p> <p>This book:</p> <ul> <li>Provides a clear account and comparison of formal languages, concepts and models for statistical causality.</li> <li>Addresses examples from medicine, biology, economics and political science to aid the reader's understanding.</li> <li>Is authored by leading experts in their field.</li> <li>Is written in an accessible style.</li> </ul> <p>Postgraduates, professional statisticians and researchers in academia and industry will benefit from this book.</p>
<p>List of contributors xv</p> <p><b>An overview of statistical causality xvii<br /> </b><i>Carlo Berzuini, Philip Dawid and Luisa Bernardinelli</i></p> <p><b>1 Statistical causality: Some historical remarks 1<br /> </b><i>D.R. Cox</i></p> <p>1.1 Introduction 1</p> <p>1.2 Key issues 2</p> <p>1.3 Rothamsted view 2</p> <p>1.4 An earlier controversy and its implications 3</p> <p>1.5 Three versions of causality 4</p> <p>1.6 Conclusion 4</p> <p>References 4</p> <p><b>2 The language of potential outcomes 6<br /> </b><i>Arvid Sjölander</i></p> <p>2.1 Introduction 6</p> <p>2.2 Definition of causal effects through potential outcomes 7</p> <p>2.2.1 Subject-specific causal effects 7</p> <p>2.2.2 Population causal effects 8</p> <p>2.2.3 Association versus causation 9</p> <p>2.3 Identification of population causal effects 9</p> <p>2.3.1 Randomized experiments 9</p> <p>2.3.2 Observational studies 11</p> <p>2.4 Discussion 11</p> <p>References 13</p> <p><b>3 Structural equations, graphs and interventions 15<br /> </b><i>Ilya Shpitser</i></p> <p>3.1 Introduction 15</p> <p>3.2 Structural equations, graphs, and interventions 16</p> <p>3.2.1 Graph terminology 16</p> <p>3.2.2 Markovian models 17</p> <p>3.2.3 Latent projections and semi-Markovian models 19</p> <p>3.2.4 Interventions in semi-Markovian models 19</p> <p>3.2.5 Counterfactual distributions in NPSEMs 20</p> <p>3.2.6 Causal diagrams and counterfactual independence 22</p> <p>3.2.7 Relation to potential outcomes 22</p> <p>References 23</p> <p><b>4 The decision-theoretic approach to causal inference 25<br /> </b><i>Philip Dawid</i></p> <p>4.1 Introduction 25</p> <p>4.2 Decision theory and causality 26</p> <p>4.2.1 A simple decision problem 26</p> <p>4.2.2 Causal inference 27</p> <p>4.3 No confounding 28</p> <p>4.4 Confounding 29</p> <p>4.4.1 Unconfounding 29</p> <p>4.4.2 Nonconfounding 30</p> <p>4.4.3 Back-door formula 31</p> <p>4.5 Propensity analysis 33</p> <p>4.6 Instrumental variable 34</p> <p>4.6.1 Linear model 36</p> <p>4.6.2 Binary variables 36</p> <p>4.7 Effect of treatment of the treated 37</p> <p>4.8 Connections and contrasts 37</p> <p>4.8.1 Potential responses 37</p> <p>4.8.2 Causal graphs 39</p> <p>4.9 Postscript 40</p> <p>Acknowledgements 40</p> <p>References 40</p> <p><b>5 Causal inference as a prediction problem: Assumptions, identification and evidence synthesis 43<br /> </b><i>Sander Greenland</i></p> <p>5.1 Introduction 43</p> <p>5.2 A brief commentary on developments since 1970 44</p> <p>5.2.1 Potential outcomes and missing data 45</p> <p>5.2.2 The prognostic view 45</p> <p>5.3 Ambiguities of observational extensions 46</p> <p>5.4 Causal diagrams and structural equations 47</p> <p>5.5 Compelling versus plausible assumptions, models and inferences 47</p> <p>5.6 Nonidentification and the curse of dimensionality 50</p> <p>5.7 Identification in practice 51</p> <p>5.8 Identification and bounded rationality 53</p> <p>5.9 Conclusion 54</p> <p>Acknowledgments 55</p> <p>References 55</p> <p><b>6 Graph-based criteria of identifiability of causal questions 59<br /> </b><i>Ilya Shpitser</i></p> <p>6.1 Introduction 59</p> <p>6.2 Interventions from observations 59</p> <p>6.3 The back-door criterion, conditional ignorability, and covariate adjustment 61</p> <p>6.4 The front-door criterion 63</p> <p>6.5 Do-calculus 64</p> <p>6.6 General identification 65</p> <p>6.7 Dormant independences and post-truncation constraints 68</p> <p>References 69</p> <p><b>7 Causal inference from observational data: A Bayesian predictive approach 71<br /> </b><i>Elja Arjas</i></p> <p>7.1 Background 71</p> <p>7.2 A model prototype 72</p> <p>7.3 Extension to sequential regimes 76</p> <p>7.4 Providing a causal interpretation: Predictive inference from data 80</p> <p>7.5 Discussion 82</p> <p>Acknowledgement 83</p> <p>References 83</p> <p><b>8 Assessing dynamic treatment strategies 85<br /> </b><i>Carlo Berzuini, Philip Dawid, and Vanessa Didelez</i></p> <p>8.1 Introduction 85</p> <p>8.2 Motivating example 86</p> <p>8.3 Descriptive versus causal inference 87</p> <p>8.4 Notation and problem definition 88</p> <p>8.5 HIV example continued 89</p> <p>8.6 Latent variables 89</p> <p>8.7 Conditions for sequential plan identifiability 90</p> <p>8.7.1 Stability 90</p> <p>8.7.2 Positivity 91</p> <p>8.8 Graphical representations of dynamic plans 92</p> <p>8.9 Abdominal aortic aneurysm surveillance 94</p> <p>8.10 Statistical inference and computation 95</p> <p>8.11 Transparent actions 97</p> <p>8.12 Refinements 98</p> <p>8.13 Discussion 99</p> <p>Acknowledgements 99</p> <p>References 99</p> <p><b>9 Causal effects and natural laws: Towards a conceptualization of causal counterfactuals for nonmanipulable exposures, with application to the effects of race and sex 101<br /> </b><i>Tyler J. VanderWeele and Miguel A. Hernán</i></p> <p>9.1 Introduction 101</p> <p>9.2 Laws of nature and contrary to fact statements 102</p> <p>9.3 Association and causation in the social and biomedical sciences 103</p> <p>9.4 Manipulation and counterfactuals 103</p> <p>9.5 Natural laws and causal effects 104</p> <p>9.6 Consequences of randomization 107</p> <p>9.7 On the causal effects of sex and race 108</p> <p>9.8 Discussion 111</p> <p>Acknowledgements 112</p> <p>References 112</p> <p><b>10 Cross-classifications by joint potential outcomes 114<br /> </b><i>Arvid Sjölander</i></p> <p>10.1 Introduction 114</p> <p>10.2 Bounds for the causal treatment effect in randomized trials with imperfect compliance 115</p> <p>10.3 Identifying the complier causal effect in randomized trials with imperfect compliance 119</p> <p>10.4 Defining the appropriate causal effect in studies suffering from truncation by death 121</p> <p>10.5 Discussion 123</p> <p>References 124</p> <p><b>11 Estimation of direct and indirect effects 126<br /> </b><i>Stijn Vansteelandt</i></p> <p>11.1 Introduction 126</p> <p>11.2 Identification of the direct and indirect effect 127</p> <p>11.2.1 Definitions 127</p> <p>11.2.2 Identification 129</p> <p>11.3 Estimation of controlled direct effects 132</p> <p>11.3.1 G-computation 132</p> <p>11.3.2 Inverse probability of treatment weighting 133</p> <p>11.3.3 G-estimation for additive and multiplicative models 137</p> <p>11.3.4 G-estimation for logistic models 141</p> <p>11.3.5 Case-control studies 142</p> <p>11.3.6 G-estimation for additive hazard models 143</p> <p>11.4 Estimation of natural direct and indirect effects 146</p> <p>11.5 Discussion 147</p> <p>Acknowledgements 147</p> <p>References 148</p> <p><b>12 The mediation formula: A guide to the assessment of causal pathways in nonlinear models 151<br /> </b><i>Judea Pearl</i></p> <p>12.1 Mediation: Direct and indirect effects 151</p> <p>12.1.1 Direct versus total effects 151</p> <p>12.1.2 Controlled direct effects 152</p> <p>12.1.3 Natural direct effects 154</p> <p>12.1.4 Indirect effects 156</p> <p>12.1.5 Effect decomposition 157</p> <p>12.2 The mediation formula: A simple solution to a thorny problem 157</p> <p>12.2.1 Mediation in nonparametric models 157</p> <p>12.2.2 Mediation effects in linear, logistic, and probit models 159</p> <p>12.2.3 Special cases of mediation models 164</p> <p>12.2.4 Numerical example 169</p> <p>12.3 Relation to other methods 170</p> <p>12.3.1 Methods based on differences and products 170</p> <p>12.3.2 Relation to the principal-strata direct effect 171</p> <p>12.4 Conclusions 173</p> <p>Acknowledgments 174</p> <p>References 175</p> <p><b>13 The sufficient cause framework in statistics, philosophy and the biomedical and social sciences 180<br /> </b><i>Tyler J. VanderWeele</i></p> <p>13.1 Introduction 180</p> <p>13.2 The sufficient cause framework in philosophy 181</p> <p>13.3 The sufficient cause framework in epidemiology and biomedicine 181</p> <p>13.4 The sufficient cause framework in statistics 185</p> <p>13.5 The sufficient cause framework in the social sciences 185</p> <p>13.6 Other notions of sufficiency and necessity in causal inference 187</p> <p>13.7 Conclusion 188</p> <p>Acknowledgements 189</p> <p>References 189</p> <p><b>14 Analysis of interaction for identifying causal mechanisms 192<br /> </b><i>Carlo Berzuini, Philip Dawid, Hu Zhang and Miles Parkes</i></p> <p>14.1 Introduction 192</p> <p>14.2 What is a mechanism? 193</p> <p>14.3 Statistical versus mechanistic interaction 193</p> <p>14.4 Illustrative example 194</p> <p>14.5 Mechanistic interaction defined 196</p> <p>14.6 Epistasis 197</p> <p>14.7 Excess risk and superadditivity 197</p> <p>14.8 Conditions under which excess risk and superadditivity indicate the presence of mechanistic interaction 200</p> <p>14.9 Collapsibility 201</p> <p>14.10 Back to the illustrative study 202</p> <p>14.11 Alternative approaches 204</p> <p>14.12 Discussion 204</p> <p>Ethics statement 205</p> <p>Financial disclosure 205</p> <p>References 206</p> <p><b>15 Ion channels as a possible mechanism of neurodegeneration in multiple sclerosis 208<br /> </b><i>Luisa Bernardinelli, Carlo Berzuini, Luisa Foco, and Roberta Pastorino</i></p> <p>15.1 Introduction 208</p> <p>15.2 Background 209</p> <p>15.3 The scientific hypothesis 209</p> <p>15.4 Data 210</p> <p>15.5 A simple preliminary analysis 211</p> <p>15.6 Testing for qualitative interaction 213</p> <p>15.7 Discussion 214</p> <p>Acknowledgments 216</p> <p>References 216</p> <p><b>16 Supplementary variables for causal estimation 218<br /> </b><i>Roland R. Ramsahai</i></p> <p>16.1 Introduction 218</p> <p>16.2 Multiple expressions for causal effect 220</p> <p>16.3 Asymptotic variance of causal estimators 222</p> <p>16.4 Comparison of causal estimators 222</p> <p>16.4.1 Supplement C with L or not 223</p> <p>16.4.2 Supplement L with C or not 224</p> <p>16.4.3 Replace C with L or not 225</p> <p>16.5 Discussion 226</p> <p>Acknowledgements 226</p> <p>Appendices 227</p> <p>16.A Estimator given all X’s recorded 227</p> <p>16.B Derivations of asymptotic variances 227</p> <p>16.C Expressions with correlation coefficients 229</p> <p>16.D Derivation of I’s 230</p> <p>16.E Relation between ρ2 rl|t and ρ2 rl|c 231</p> <p>References 232</p> <p><b>17 Time-varying confounding: Some practical considerations in a likelihood framework 234<br /> </b><i>Rhian Daniel, Bianca De Stavola and Simon Cousens</i></p> <p>17.1 Introduction 234</p> <p>17.2 General setting 235</p> <p>17.2.1 Notation 235</p> <p>17.2.2 Observed data structure 235</p> <p>17.2.3 Intervention strategies 236</p> <p>17.2.4 Potential outcomes 237</p> <p>17.2.5 Time-to-event outcomes 237</p> <p>17.2.6 Causal estimands 238</p> <p>17.3 Identifying assumptions 238</p> <p>17.4 G-computation formula 239</p> <p>17.4.1 The formula 239</p> <p>17.4.2 Plug-in regression estimation 240</p> <p>17.5 Implementation by Monte Carlo simulation 242</p> <p>17.5.1 Simulating an end-of-study outcome 242</p> <p>17.5.2 Simulating a time-to-event outcome 242</p> <p>17.5.3 Inference 242</p> <p>17.5.4 Losses to follow-up 243</p> <p>17.5.5 Software 243</p> <p>17.6 Analyses of simulated data 243</p> <p>17.6.1 The data 243</p> <p>17.6.2 Regimes to be compared 244</p> <p>17.6.3 Parametric modelling choices 245</p> <p>17.6.4 Results 246</p> <p>17.7 Further considerations 249</p> <p>17.7.1 Parametric model misspecification 249</p> <p>17.7.2 Competing events 249</p> <p>17.7.3 Unbalanced measurement times 250</p> <p>17.8 Summary 251</p> <p>References 251</p> <p><b>18 ‘Natural experiments’ as a means of testing causal inferences 253<br /> </b><i>Michael Rutter</i></p> <p>18.1 Introduction 253</p> <p>18.2 Noncausal interpretations of an association 253</p> <p>18.3 Dealing with confounders 255</p> <p>18.4 ‘Natural experiments’ 256</p> <p>18.4.1 Genetically sensitive designs 257</p> <p>18.4.2 Children of twins (CoT) design 259</p> <p>18.4.3 Strategies to identify the key environmental risk feature 261</p> <p>18.4.4 Designs for dealing with selection bias 263</p> <p>18.4.5 Instrumental variables to rule out reverse causation 264</p> <p>18.4.6 Regression discontinuity (RD) designs to deal with unmeasured confounders 265</p> <p>18.5 Overall conclusion on ‘natural experiments’ 266</p> <p>18.5.1 Supported causes 266</p> <p>18.5.2 Disconfirmed causes 267</p> <p>Acknowledgement 267</p> <p>References 268</p> <p><b>19 Nonreactive and purely reactive doses in observational studies 273<br /> </b><i>Paul R. Rosenbaum</i></p> <p>19.1 Introduction: Background, example 273</p> <p>19.1.1 Does a dose–response relationship provide information that distinguishes treatment effects from biases due to unmeasured covariates? 273</p> <p>19.1.2 Is more chemotherapy for ovarian cancer more effective or more toxic? 274</p> <p>19.2 Various concepts of dose 277</p> <p>19.2.1 Some notation: Covariates, outcomes, and treatment assignment in matched pairs 277</p> <p>19.2.2 Reactive and nonreactive doses of treatment 278</p> <p>19.2.3 Three test statistics that use doses in different ways 279</p> <p>19.2.4 Randomization inference in randomized experiments 280</p> <p>19.2.5 Sensitivity analysis 281</p> <p>19.2.6 Sensitivity analysis in the example 283</p> <p>19.3 Design sensitivity 284</p> <p>19.3.1 What is design sensitivity? 284</p> <p>19.3.2 Comparison of design sensitivity with purely reactive doses 286</p> <p>19.4 Summary 287</p> <p>References 287</p> <p><b>20 Evaluation of potential mediators in randomised trials of complex interventions (psychotherapies) 290<br /> </b><i>Richard Emsley and Graham Dunn</i></p> <p>20.1 Introduction 290</p> <p>20.2 Potential mediators in psychological treatment trials 291</p> <p>20.3 Methods for mediation in psychological treatment trials 293</p> <p>20.4 Causal mediation analysis using instrumental variables estimation 297</p> <p>20.5 Causal mediation analysis using principal stratification 301</p> <p>20.6 Our motivating example: The SoCRATES trial 302</p> <p>20.6.1 What are the joint effects of sessions attended and therapeutic alliance on the PANSS score at 18 months? 303</p> <p>20.6.2 What is the direct effect of random allocation on the PANSS score at 18 months and how is this influenced by the therapeutic alliance? 304</p> <p>20.6.3 Is the direct effect of the number of sessions attended on the PANSS score at 18 months influenced by therapeutic alliance? 305</p> <p>20.7 Conclusions 305</p> <p>Acknowledgements 306</p> <p>References 307</p> <p><b>21 Causal inference in clinical trials 310<br /> </b><i>Krista Fischer and Ian R. White</i></p> <p>21.1 Introduction 310</p> <p>21.2 Causal effect of treatment in randomized trials 312</p> <p>21.2.1 Observed data and notation 312</p> <p>21.2.2 Defining the effects of interest via potential outcomes 312</p> <p>21.2.3 Adherence-adjusted ITT analysis 314</p> <p>21.3 Estimation for a linear structural mean model 316</p> <p>21.3.1 A general estimation procedure 316</p> <p>21.3.2 Identifiability and closed-form estimation of the parameters in a linear SMM 317</p> <p>21.3.3 Analysis of the EPHT trial 319</p> <p>21.4 Alternative approaches for causal inference in randomized trials comparing experimental treatment with a control 321</p> <p>21.4.1 Principal stratification 321</p> <p>21.4.2 SMM for the average treatment effect on the treated (ATT) 322</p> <p>21.5 Discussion 324</p> <p>References 325</p> <p><b>22 Causal inference in time series analysis 327<br /> </b><i>Michael Eichler</i></p> <p>22.1 Introduction 327</p> <p>22.2 Causality for time series 328</p> <p>22.2.1 Intervention causality 328</p> <p>22.2.2 Structural causality 331</p> <p>22.2.3 Granger causality 332</p> <p>22.2.4 Sims causality 334</p> <p>22.3 Graphical representations for time series 335</p> <p>22.3.1 Conditional distributions and chain graphs 336</p> <p>22.3.2 Path diagrams and Granger causality graphs 337</p> <p>22.3.3 Markov properties for Granger causality graphs 338</p> <p>22.4 Representation of systems with latent variables 339</p> <p>22.4.1 Marginalization 341</p> <p>22.4.2 Ancestral graphs 342</p> <p>22.5 Identification of causal effects 343</p> <p>22.6 Learning causal structures 346</p> <p>22.7 A new parametric model 349</p> <p>22.8 Concluding remarks 351</p> <p>References 352</p> <p><b>23 Dynamic molecular networks and mechanisms in the biosciences: A statistical framework 355<br /> </b><i>Clive G. Bowsher</i></p> <p>23.1 Introduction 355</p> <p>23.2 SKMs and biochemical reaction networks 356</p> <p>23.3 Local independence properties of SKMs 358</p> <p>23.3.1 Local independence and kinetic independence graphs 358</p> <p>23.3.2 Local independence and causal influence 361</p> <p>23.4 Modularisation of SKMs 362</p> <p>23.4.1 Modularisations and dynamic independence 362</p> <p>23.4.2 MIDIA Algorithm 363</p> <p>23.5 Illustrative example – MAPK cell signalling 365</p> <p>23.6 Conclusion 369</p> <p>23.7 Appendix: SKM regularity conditions 369</p> <p>Acknowledgements 370</p> <p>References 370</p> <p>Index 371</p>
<p><strong>Carlo Berzuini</strong> and <strong>Philip Dawid</strong>, Statistical Labority, centre for Mathematical Sciences, University of Cambridge, UK. <p.<strong>Luisa Bernardinelli</strong>, MRC Biostatistics Unit, Institute of Public Health, Cambridge, UK.
<b>A state of the art volume on statistical causality</b> <p><i>Causality: Statistical Perspectives and Applications</i> presents a wide-ranging collection of seminal contributions by renowned experts in the field, providing a thorough treatment of all aspects of statistical causality. It covers the various formalisms in current use, methods for applying them to specific problems, and the special requirements of a range of examples from medicine, biology and economics to political science.</p> <p>This book:</p> <ul> <li>Provides a clear account and comparison of formal languages, concepts and models for statistical causality.</li> <li>Addresses examples from medicine, biology, economics and political science to aid the reader's understanding.</li> <li>Is authored by leading experts in their field.</li> <li>Is written in an accessible style.</li> </ul> <p>Postgraduates, professional statisticians and researchers in academia and industry will benefit from this book</p>

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