Dataset Information

Identification and Estimation Of Causal Effects from Dependent Data.

ABSTRACT: The assumption that data samples are independent and identically distributed (iid) is standard in many areas of statistics and machine learning. Nevertheless, in some settings, such as social networks, infectious disease modeling, and reasoning with spatial and temporal data, this assumption is false. An extensive literature exists on making causal inferences under the iid assumption [17, 11, 26, 21], even when unobserved confounding bias may be present. But, as pointed out in [19], causal inference in non-iid contexts is challenging due to the presence of both unobserved confounding and data dependence. In this paper we develop a general theory describing when causal inferences are possible in such scenarios. We use segregated graphs [20], a generalization of latent projection mixed graphs [28], to represent causal models of this type and provide a complete algorithm for nonparametric identification in these models. We then demonstrate how statistical inference may be performed on causal parameters identified by this algorithm. In particular, we consider cases where only a single sample is available for parts of the model due to full interference, i.e., all units are pathwise dependent and neighbors' treatments affect each others' outcomes [24]. We apply these techniques to a synthetic data set which considers users sharing fake news articles given the structure of their social network, user activity levels, and baseline demographics and socioeconomic covariates.

SUBMITTER: Sherman E

PROVIDER: S-EPMC6330046 | biostudies-literature | 2018 Dec

REPOSITORIES: biostudies-literature

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Publications

Identification and Estimation Of Causal Effects from Dependent Data.

Sherman Eli E Shpitser Ilya I

Advances in neural information processing systems 20181201

The assumption that data samples are independent and identically distributed (iid) is standard in many areas of statistics and machine learning. Nevertheless, in some settings, such as social networks, infectious disease modeling, and reasoning with spatial and temporal data, this assumption is false. An extensive literature exists on making causal inferences under the iid assumption [17, 11, 26, 21], even when unobserved confounding bias may be present. But, as pointed out in [19], causal infer ...[more]

PMID: 30643365

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Project description:BACKGROUND: In recent years, there has been great interest in using transcriptomic data to infer gene regulatory networks. For the time being, methodological development in this area has primarily made use of graphical Gaussian models for observational wild-type data, resulting in undirected graphs that are not able to accurately highlight causal relationships among genes. In the present work, we seek to improve the estimation of causal effects among genes by jointly modeling observational transcriptomic data with arbitrarily complex intervention data obtained by performing partial, single, or multiple gene knock-outs or knock-downs. RESULTS: Using the framework of causal Gaussian Bayesian networks, we propose a Markov chain Monte Carlo algorithm with a Mallows proposal model and analytical likelihood maximization to sample from the posterior distribution of causal node orderings, and in turn, to estimate causal effects. The main advantage of the proposed algorithm over previously proposed methods is its flexibility to accommodate any kind of intervention design, including partial or multiple knock-out experiments. Using simulated data as well as data from the Dialogue for Reverse Engineering Assessments and Methods (DREAM) 2007 challenge, the proposed method was compared to two alternative approaches: one requiring a complete, single knock-out design, and one able to model only observational data. CONCLUSIONS: The proposed algorithm was found to perform as well as, and in most cases better, than the alternative methods in terms of accuracy for the estimation of causal effects. In addition, multiple knock-outs proved to contribute valuable additional information compared to single knock-outs. Finally, the simulation study confirmed that it is not possible to estimate the causal ordering of genes from observational data alone. In all cases, we found that the inclusion of intervention experiments enabled more accurate estimation of causal regulatory relationships than the use of wild-type data alone.

Dataset Information

Identification and Estimation Of Causal Effects from Dependent Data.

Publications

Identification and Estimation Of Causal Effects from Dependent Data.

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