A Bayesian nonparametric approach for causal inference with multiple mediators

TL;DR

This paper introduces a Bayesian nonparametric method for causal mediation analysis with multiple mediators, overcoming model misspecification and allowing flexible estimation of joint and individual effects.

Contribution

It proposes a novel BNP approach using an enriched Dirichlet process mixture to model complex mediator-outcome relationships in causal inference.

Findings

Demonstrates effectiveness through simulations.

Applied to VAP patient data revealing mediation effects.

Flexible modeling of multiple mediators and effects.

Abstract

Mediation analysis with contemporaneously observed multiple mediators is an important area of causal inference. Recent approaches for multiple mediators are often based on parametric models and thus may suffer from model misspecification. Also, much of the existing literature either only allow estimation of the joint mediation effect, or, estimate the joint mediation effect as the sum of individual mediator effects, which often is not a reasonable assumption. In this paper, we propose a methodology which overcomes the two aforementioned drawbacks. Our method is based on a novel Bayesian nonparametric (BNP) approach, wherein the joint distribution of the observed data (outcome, mediators, treatment, and confounders) is modeled flexibly using an enriched Dirichlet process mixture with three levels: the first level characterizing the conditional distribution of the outcome given the mediators, treatment and the confounders, the second level corresponding to the conditional distribution of each of the mediators given the treatment and the confounders, and the third level corresponding to the distribution of the treatment and the confounders. We use standardization (g-computation) to compute causal mediation effects under three uncheckable assumptions that allow identification of the individual and joint mediation effects. The efficacy of our proposed method is demonstrated with simulations. We apply our proposed method to analyze data from a study of Ventilator-associated Pneumonia (VAP) co-infected patients, where the effect of the abundance of Pseudomonas on VAP infection is suspected to be mediated through antibiotics.