The last decade witnessed the development of algorithms that completely solve the identifiability problem for causal effects in hidden variable causal models associated with directed acyclic graphs. However, much of this machinery remains underutilized in practice owing to the complexity of estimating identifying functionals yielded by these algorithms. In this paper, we provide simple graphical criteria and semiparametric estimators that bridge the gap between identification and estimation for causal effects involving a single treatment and a single outcome. First, we provide influence function based doubly robust estimators that cover a significant subset of hidden variable causal models where the effect is identifiable. We further characterize an important subset of this class for which we demonstrate how to derive the estimator with the lowest asymptotic variance, i.e., one that achieves the semiparametric efficiency bound. Finally, we provide semiparametric estimators for any single treatment causal effect parameter identified via the aforementioned algorithms. The resulting estimators resemble influence function based estimators that are sequentially reweighted, and exhibit a partial double robustness property, provided the parts of the likelihood corresponding to a set of weight models are correctly specified. Our methods are easy to implement and we demonstrate their utility through simulations.
This brief note is meant to complement our previous comment on "The Blessings of Multiple Causes" by Wang and Blei (2019). We provide a more succinct and transparent explanation of the fact that the deconfounder does not control for multi-cause confounding. The argument given in Wang and Blei (2019) makes two mistakes: (1) attempting to infer independence conditional on one variable from independence conditional on a different, unrelated variable, and (2) attempting to infer joint independence from pairwise independence. We give two simple counterexamples to the deconfounder claim.
(This comment has been updated to respond to Wang and Blei's rejoinder [arXiv:1910.07320].) The premise of the deconfounder method proposed in "Blessings of Multiple Causes" by Wang and Blei [arXiv:1805.06826], namely that a variable that renders multiple causes conditionally independent also controls for unmeasured multi-cause confounding, is incorrect. This can be seen by noting that no fact about the observed data alone can be informative about ignorability, since ignorability is compatible with any observed data distribution. Methods to control for unmeasured confounding may be valid with additional assumptions in specific settings, but they cannot, in general, provide a checkable approach to causal inference, and they do not, in general, require weaker assumptions than the assumptions that are commonly used for causal inference. While this is outside the scope of this comment, we note that much recent work on applying ideas from latent variable modeling to causal inference problems suffers from similar issues.
Recently there has been sustained interest in modifying prediction algorithms to satisfy fairness constraints. These constraints are typically complex nonlinear functionals of the observed data distribution. Focusing on the causal constraints proposed by Nabi and Shpitser (2018), we introduce new theoretical results and optimization techniques to make model training easier and more accurate. Specifically, we show how to reparameterize the observed data likelihood such that fairness constraints correspond directly to parameters that appear in the likelihood, transforming a complex constrained optimization objective into a simple optimization problem with box constraints. We also exploit methods from empirical likelihood theory in statistics to improve predictive performance, without requiring parametric models for high-dimensional feature vectors.
Missing data is a pervasive problem in data analyses, resulting in datasets that contain censored realizations of a target distribution. Many approaches to inference on the target distribution using censored observed data, rely on missing data models represented as a factorization with respect to a directed acyclic graph. In this paper we consider the identifiability of the target distribution within this class of models, and show that the most general identification strategies proposed so far retain a significant gap in that they fail to identify a wide class of identifiable distributions. To address this gap, we propose a new algorithm that significantly generalizes the types of manipulations used in the ID algorithm, developed in the context of causal inference, in order to obtain identification.
Classical causal and statistical inference methods typically assume the observed data consists of independent realizations. However, in many applications this assumption is inappropriate due to a network of dependences between units in the data. Methods for estimating causal effects have been developed in the setting where the structure of dependence between units is known exactly, but in practice there is often substantial uncertainty about the precise network structure. This is true, for example, in trial data drawn from vulnerable communities where social ties are difficult to query directly. In this paper we combine techniques from the structure learning and interference literatures in causal inference, proposing a general method for estimating causal effects under data dependence when the structure of this dependence is not known a priori. We demonstrate the utility of our method on synthetic datasets which exhibit network dependence.
Constraint-based structure learning algorithms infer the causal structure of multivariate systems from observational data by determining an equivalent class of causal structures compatible with the conditional independencies in the data. Methods based on additive-noise (AN) models have been proposed to further discriminate between causal structures that are equivalent in terms of conditional independencies. These methods rely on a particular form of the generative functional equations, with an additive noise structure, which allows inferring the directionality of causation by testing the independence between the residuals of a nonlinear regression and the predictors (nrr-independencies). Full causal structure identifiability has been proven for systems that contain only additive-noise equations and have no hidden variables. We extend the AN framework in several ways. We introduce alternative regression-free tests of independence based on conditional variances (cv-independencies). We consider conditionally-additive-noise (CAN) models, in which the equations may have the AN form only after conditioning. We exploit asymmetries in nrr-independencies or cv-independencies resulting from the CAN form to derive a criterion that infers the causal relation between a pair of variables in a multivariate system without any assumption about the form of the equations or the presence of hidden variables.
Causal understanding is essential for many kinds of decision-making, but causal inference from observational data has typically only been applied to structured, low-dimensional datasets. While text classifiers produce low-dimensional outputs, their use in causal inference has not previously been studied. To facilitate causal analyses based on language data, we consider the role that text classifiers can play in causal inference through established modeling mechanisms from the causality literature on missing data and measurement error. We demonstrate how to conduct causal analyses using text classifiers on simulated and Yelp data, and discuss the opportunities and challenges of future work that uses text data in causal inference.
The goal of personalized decision making is to map a unit's characteristics to an action tailored to maximize the expected outcome for that unit. Obtaining high-quality mappings of this type is the goal of the dynamic regime literature. In healthcare settings, optimizing policies with respect to a particular causal pathway may be of interest as well. For example, we may wish to maximize the chemical effect of a drug given data from an observational study where the chemical effect of the drug on the outcome is entangled with the indirect effect mediated by differential adherence. In such cases, we may wish to optimize the direct effect of a drug, while keeping the indirect effect to that of some reference treatment. [16] shows how to combine mediation analysis and dynamic treatment regime ideas to defines policies associated with causal pathways and counterfactual responses to these policies. In this paper, we derive a variety of methods for learning high quality policies of this type from data, in a causal model corresponding to a longitudinal setting of practical importance. We illustrate our methods via a dataset of HIV patients undergoing therapy, gathered in the Nigerian PEPFAR program.
We consider the problem of learning optimal policies from observational data in a way that satisfies certain fairness criteria. The issue of fairness arises where some covariates used in decision making are sensitive features, or are correlated with sensitive features. (Nabi and Shpitser 2018) formalized fairness in the context of regression problems as constraining the causal effects of sensitive features along certain disallowed causal pathways. The existence of these causal effects may be called retrospective unfairness in the sense of already being present in the data before analysis begins, and may be due to discriminatory practices or the biased way in which variables are defined or recorded. In the context of learning policies, what we call prospective bias, i.e., the inappropriate dependence of learned policies on sensitive features, is also possible. In this paper, we use methods from causal and semiparametric inference to learn optimal policies in a way that addresses both retrospective bias in the data, and prospective bias due to the policy. In addition, our methods appropriately address statistical bias due to model misspecification and confounding bias, which are important in the estimation of path-specific causal effects from observational data. We apply our methods to both synthetic data and real criminal justice data.