Multiply Robust Causal Mediation Analysis with Continuous Treatments

There is a precise sense in which drawing causal inferences from observational data is hard, even when identifiability is assumed. In particular, Robins and Ritov (1997) and Robins et al. (2003) showed that causal effects can be discontinuous as a function of the data distribution: two arbitrarily close data distributions might correspond to different causal effects. This is a fact independent of the choice of estimator; however, not all estimators are equally unstable. Our contribution is to surface a second layer of instability that depends on the choice of estimator. We show that many standard point estimates can be read as point summaries of multimodal distributions over the space of structural causal models. As such, estimators can jump discontinuously in the data distribution. This defines a taxonomy of estimators that admits a decision-theoretic reading: stability depends on whether the implicit loss function an estimator optimizes is aligned with the causal effect itself. Specifically, inverse propensity weighted estimators and regression estimators are examples of discontinuous summaries, while explicit posterior means and medians are shown to be continuous.

Causal mediation analysis decomposes a treatment effect into indirect pathways through mediators and direct pathways not operating through them. Modern biomedical studies often involve high-dimensional covariates and mediators that are noisy proxies for lower-dimensional latent biological processes. Existing methods typically rely on sparsity, linear factor models, or ignore the connection among variables in the learned representations, which can be restrictive when measurements are nonlinear and covariate and mediator factors are structurally dependent. We propose MediEncoder, a representation-learning framework for nonlinear high-dimensional mediation analysis. MediEncoder jointly learns low-dimensional covariate and mediator representations using a coupled encoder-decoder architecture with a cross-factor network that links treatment and covariate representations to mediator representations. The learned features are then used in a cross-fitted efficient influence function-based estimator of natural direct and indirect effects. The resulting estimator is multiply robust and asymptotically normal under suitable regularity conditions. Simulations show that MediEncoder improves estimation accuracy over competing dimension-reduction approaches, and an application to Alzheimer's Disease Neuroimaging Initiative data illustrates its utility in high-dimensional biomedical causal mediation analysis.

We propose a two-stage estimator for structural mediation parameters that combines deep representation learning with G-estimation under the "no essential heterogeneity" (NEH) assumption. We call the method UNIT. In the first stage,TARNet estimates the heterogeneous effect of a randomized treatment on a mediator by learning a shared covariate representation across treatment arms.The resulting conditional average treatment effect (CATE) estimate provides a plug-in approximation to the heterogeneity-dependent component of the weight function entering the G-estimating equation of Zheng and Zhou (2015), which identifies the structural parameters even in the presence of unmeasured mediator-outcome confounding. We show that more accurate first-stage representation learning can yield a more informative plug-in weight and thereby improve the precision of the structural parameter estimator. In simulations with non-Gaussian covariates and nonlinear mediator effects, TARNet weights reduce the Stage-2 standard error of the mediation coefficient by a factor of $1.45$ to $1.51$ (median across replications, $n \ge 2000$) relative to the classical approach, at no cost to bias or coverage.