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An important problem in causal inference is to break down the total effect of treatment into different causal pathways and quantify the causal effect in each pathway. Causal mediation analysis (CMA) is a formal statistical approach for identifying and estimating these causal effects. Central to CMA is the sequential ignorability assumption that implies all pre-treatment confounders are measured and they can capture different types of confounding, e.g., post-treatment confounders and hidden confounders. Typically unverifiable in observational studies, this assumption restrains both the coverage and practicality of conventional methods. This work, therefore, aims to circumvent the stringent assumption by following a causal graph with a unified confounder and its proxy variables. Our core contribution is an algorithm that combines deep latent-variable models and proxy strategy to jointly infer a unified surrogate confounder and estimate different causal effects in CMA from observed variables. Empirical evaluations using both synthetic and semi-synthetic datasets validate the effectiveness of the proposed method.
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Causal mediation analysis is used to evaluate direct and indirect causal effects of a treatment on an outcome of interest through an intermediate variable or a mediator.It is difficult to identify the direct and indirect causal effects because the mediator cannot be randomly assigned in many real applications. In this article, we consider a causal model including latent confounders between the mediator and the outcome. We present sufficient conditions for identifying the direct and indirect effects and propose an approach for estimating them. The performance of the proposed approach is evaluated by simulation studies. Finally, we apply the approach to a data set of the customer loyalty survey by a telecom company.
Interventional effects for mediation analysis were proposed as a solution to the lack of identifiability of natural (in)direct effects in the presence of a mediator-outcome confounder affected by exposure. We present a theoretical and computational study of the properties of the interventional (in)direct effect estimands based on the efficient influence fucntion (EIF) in the non-parametric statistical model. We use the EIF to develop two asymptotically optimal, non-parametric estimators that leverage data-adaptive regression for estimation of the nuisance parameters: a one-step estimator and a targeted minimum loss estimator. A free and open source texttt{R} package implementing our proposed estimators is made available on GitHub. We further present results establishing the conditions under which these estimators are consistent, multiply robust, $n^{1/2}$-consistent and efficient. We illustrate the finite-sample performance of the estimators and corroborate our theoretical results in a simulation study. We also demonstrate the use of the estimators in our motivating application to elucidate the mechanisms behind the unintended harmful effects that a housing intervention had on adolescent girls risk behavior.
Greater understanding of the pathways through which an environmental mixture operates is important to design effective interventions. We present new methodology to estimate the natural direct effect (NDE), natural indirect effect (NIE), and controlled direct effects (CDEs) of a complex mixture exposure on an outcome through a mediator variable. We implement Bayesian Kernel Machine Regression (BKMR) to allow for all possible interactions and nonlinear effects of 1) the co-exposures on the mediator, 2) the co-exposures and mediator on the outcome, and 3) selected covariates on the mediator and/or outcome. From the posterior predictive distributions of the mediator and outcome, we simulate counterfactuals to obtain posterior samples, estimates, and credible intervals of the mediation effects. Our simulation study demonstrates that when the exposure-mediator and exposure-mediator-outcome relationships are complex, BKMR-Causal Mediation Analysis performs better than current mediation methods. We applied our methodology to quantify the contribution of birth length as a mediator between in utero co-exposure to arsenic, manganese and lead, and childrens neurodevelopmental scores, in a prospective birth cohort in Bangladesh. Among younger children, we found a negative association between the metal mixture and neurodevelopment. We also found evidence that birth length mediates the effect of exposure to the metal mixture on neurodevelopment for younger children. If birth length were fixed to its $75^{th}$ percentile value, the effect of the metal mixture on neurodevelopment decreases, suggesting that nutritional interventions to help increase birth length could potentially block the harmful effects of the metal mixture on neurodevelopment.
Causal variance decompositions for a given disease-specific quality indicator can be used to quantify differences in performance between hospitals or health care providers. While variance decompositions can demonstrate variation in quality of care, causal mediation analysis can be used to study care pathways leading to the differences in performance between the institutions. This raises the question of whether the two approaches can be combined to decompose between-hospital variation in an outcome type indicator to that mediated through a given process (indirect effect) and remaining variation due to all other pathways (direct effect). For this purpose, we derive a causal mediation analysis decomposition of between-hospital variance, discuss its interpretation, and propose an estimation approach based on generalized linear mixed models for the outcome and the mediator. We study the performance of the estimators in a simulation study and demonstrate its use in administrative data on kidney cancer care in Ontario.
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.
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