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A treatment policy defines when and what treatments are applied to affect some outcome of interest. Data-driven decision-making requires the ability to predict what happens if a policy is changed. Existing methods that predict how the outcome evolves under different scenarios assume that the tentative sequences of future treatments are fixed in advance, while in practice the treatments are determined stochastically by a policy and may depend, for example, on the efficiency of previous treatments. Therefore, the current methods are not applicable if the treatment policy is unknown or a counterfactual analysis is needed. To handle these limitations, we model the treatments and outcomes jointly in continuous time, by combining Gaussian processes and point processes. Our model enables the estimation of a treatment policy from observational sequences of treatments and outcomes, and it can predict the interventional and counterfactual progression of the outcome after an intervention on the treatment policy (in contrast with the causal effect of a single treatment). We show with real-world and semi-synthetic data on blood glucose progression that our method can answer causal queries more accurately than existing alternatives.

Causal discovery methods have demonstrated the ability to identify the time series graphs representing the causal temporal dependency structure of dynamical systems. However, they do not include a measure of the confidence of the estimated links. Here, we introduce a novel bootstrap aggregation (bagging) and confidence measure method that is combined with time series causal discovery. This new method allows measuring confidence for the links of the time series graphs calculated by causal discovery methods. This is done by bootstrapping the original times series data set while preserving temporal dependencies. Next to confidence measures, aggregating the bootstrapped graphs by majority voting yields a final aggregated output graph. In this work, we combine our approach with the state-of-the-art conditional-independence-based algorithm PCMCI+. With extensive numerical experiments we empirically demonstrate that, in addition to providing confidence measures for links, Bagged-PCMCI+ improves the precision and recall of its base algorithm PCMCI+. Specifically, Bagged-PCMCI+ has a higher detection power regarding adjacencies and a higher precision in orienting contemporaneous edges while at the same time showing a lower rate of false positives. These performance improvements are especially pronounced in the more challenging settings (short time sample size, large number of variables, high autocorrelation). Our bootstrap approach can also be combined with other time series causal discovery algorithms and can be of considerable use in many real-world applications, especially when confidence measures for the links are desired.

There are well-established methods for identifying the causal effect of a time-varying treatment applied at discrete time points. However, in the real world, many treatments are continuous or have a finer time scale than the one used for measurement or analysis. While researchers have investigated the discrepancies between estimates under varying discretization scales using simulations and empirical data, it is still unclear how the choice of discretization scale affects causal inference. To address this gap, we present a framework to understand how discretization scales impact the properties of causal inferences about the effect of a time-varying treatment. We introduce the concept of "identification bias", which is the difference between the causal estimand for a continuous-time treatment and the purported estimand of a discretized version of the treatment. We show that this bias can persist even with an infinite number of longitudinal treatment-outcome trajectories. We specifically examine the identification problem in a class of linear stochastic continuous-time data-generating processes and demonstrate the identification bias of the g-formula in this context. Our findings indicate that discretization bias can significantly impact empirical analysis, especially when there are limited repeated measurements. Therefore, we recommend that researchers carefully consider the choice of discretization scale and perform sensitivity analysis to address this bias. We also propose a simple and heuristic quantitative measure for sensitivity concerning discretization and suggest that researchers report this measure along with point and interval estimates in their work. By doing so, researchers can better understand and address the potential impact of discretization bias on causal inference.

Learning individualized treatment rules (ITRs) is an important topic in precision medicine. Current literature mainly focuses on deriving ITRs from a single source population. We consider the observational data setting when the source population differs from a target population of interest. Compared with causal generalization for the average treatment effect which is a scalar quantity, ITR generalization poses new challenges due to the need to model and generalize the rules based on a prespecified class of functions which may not contain the unrestricted true optimal ITR. The aim of this paper is to develop a weighting framework to mitigate the impact of such misspecification and thus facilitate the generalizability of optimal ITRs from a source population to a target population. Our method seeks covariate balance over a non-parametric function class characterized by a reproducing kernel Hilbert space and can improve many ITR learning methods that rely on weights. We show that the proposed method encompasses importance weights and overlap weights as two extreme cases, allowing for a better bias-variance trade-off in between. Numerical examples demonstrate that the use of our weighting method can greatly improve ITR estimation for the target population compared with other weighting methods.

In this work we connect two notions: That of the nonparametric mode of a probability measure, defined by asymptotic small ball probabilities, and that of the Onsager-Machlup functional, a generalized density also defined via asymptotic small ball probabilities. We show that in a separable Hilbert space setting and under mild conditions on the likelihood, modes of a Bayesian posterior distribution based upon a Gaussian prior exist and agree with the minimizers of its Onsager-Machlup functional and thus also with weak posterior modes. We apply this result to inverse problems and derive conditions on the forward mapping under which this variational characterization of posterior modes holds. Our results show rigorously that in the limit case of infinite-dimensional data corrupted by additive Gaussian or Laplacian noise, nonparametric maximum a posteriori estimation is equivalent to Tikhonov-Phillips regularization. In comparison with the work of Dashti, Law, Stuart, and Voss (2013), the assumptions on the likelihood are relaxed so that they cover in particular the important case of white Gaussian process noise. We illustrate our results by applying them to a severely ill-posed linear problem with Laplacian noise, where we express the maximum a posteriori estimator analytically and study its rate of convergence in the small noise limit.

Causal mediation analysis (CMA) is a powerful method to dissect the total effect of a treatment into direct and mediated effects within the potential outcome framework. This is important in many scientific applications to identify the underlying mechanisms of a treatment effect. However, in many scientific applications the mediator is unobserved, but there may exist related measurements. For example, we may want to identify how changes in brain activity or structure mediate an antidepressant's effect on behavior, but we may only have access to electrophysiological or imaging brain measurements. To date, most CMA methods assume that the mediator is one-dimensional and observable, which oversimplifies such real-world scenarios. To overcome this limitation, we introduce a CMA framework that can handle complex and indirectly observed mediators based on the identifiable variational autoencoder (iVAE) architecture. We prove that the true joint distribution over observed and latent variables is identifiable with the proposed method. Additionally, our framework captures a disentangled representation of the indirectly observed mediator and yields accurate estimation of the direct and mediated effects in synthetic and semi-synthetic experiments, providing evidence of its potential utility in real-world applications.

We propose strategies to estimate and make inference on key features of heterogeneous effects in randomized experiments. These key features include best linear predictors of the effects using machine learning proxies, average effects sorted by impact groups, and average characteristics of most and least impacted units. The approach is valid in high dimensional settings, where the effects are proxied (but not necessarily consistently estimated) by predictive and causal machine learning methods. We post-process these proxies into estimates of the key features. Our approach is generic, it can be used in conjunction with penalized methods, neural networks, random forests, boosted trees, and ensemble methods, both predictive and causal. Estimation and inference are based on repeated data splitting to avoid overfitting and achieve validity. We use quantile aggregation of the results across many potential splits, in particular taking medians of p-values and medians and other quantiles of confidence intervals. We show that quantile aggregation lowers estimation risks over a single split procedure, and establish its principal inferential properties. Finally, our analysis reveals ways to build provably better machine learning proxies through causal learning: we can use the objective functions that we develop to construct the best linear predictors of the effects, to obtain better machine learning proxies in the initial step. We illustrate the use of both inferential tools and causal learners with a randomized field experiment that evaluates a combination of nudges to stimulate demand for immunization in India.

Causal discovery and causal reasoning are classically treated as separate and consecutive tasks: one first infers the causal graph, and then uses it to estimate causal effects of interventions. However, such a two-stage approach is uneconomical, especially in terms of actively collected interventional data, since the causal query of interest may not require a fully-specified causal model. From a Bayesian perspective, it is also unnatural, since a causal query (e.g., the causal graph or some causal effect) can be viewed as a latent quantity subject to posterior inference -- other unobserved quantities that are not of direct interest (e.g., the full causal model) ought to be marginalized out in this process and contribute to our epistemic uncertainty. In this work, we propose Active Bayesian Causal Inference (ABCI), a fully-Bayesian active learning framework for integrated causal discovery and reasoning, which jointly infers a posterior over causal models and queries of interest. In our approach to ABCI, we focus on the class of causally-sufficient, nonlinear additive noise models, which we model using Gaussian processes. We sequentially design experiments that are maximally informative about our target causal query, collect the corresponding interventional data, and update our beliefs to choose the next experiment. Through simulations, we demonstrate that our approach is more data-efficient than several baselines that only focus on learning the full causal graph. This allows us to accurately learn downstream causal queries from fewer samples while providing well-calibrated uncertainty estimates for the quantities of interest.

This PhD thesis contains several contributions to the field of statistical causal modeling. Statistical causal models are statistical models embedded with causal assumptions that allow for the inference and reasoning about the behavior of stochastic systems affected by external manipulation (interventions). This thesis contributes to the research areas concerning the estimation of causal effects, causal structure learning, and distributionally robust (out-of-distribution generalizing) prediction methods. We present novel and consistent linear and non-linear causal effects estimators in instrumental variable settings that employ data-dependent mean squared prediction error regularization. Our proposed estimators show, in certain settings, mean squared error improvements compared to both canonical and state-of-the-art estimators. We show that recent research on distributionally robust prediction methods has connections to well-studied estimators from econometrics. This connection leads us to prove that general K-class estimators possess distributional robustness properties. We, furthermore, propose a general framework for distributional robustness with respect to intervention-induced distributions. In this framework, we derive sufficient conditions for the identifiability of distributionally robust prediction methods and present impossibility results that show the necessity of several of these conditions. We present a new structure learning method applicable in additive noise models with directed trees as causal graphs. We prove consistency in a vanishing identifiability setup and provide a method for testing substructure hypotheses with asymptotic family-wise error control that remains valid post-selection. Finally, we present heuristic ideas for learning summary graphs of nonlinear time-series models.

This paper focuses on the expected difference in borrower's repayment when there is a change in the lender's credit decisions. Classical estimators overlook the confounding effects and hence the estimation error can be magnificent. As such, we propose another approach to construct the estimators such that the error can be greatly reduced. The proposed estimators are shown to be unbiased, consistent, and robust through a combination of theoretical analysis and numerical testing. Moreover, we compare the power of estimating the causal quantities between the classical estimators and the proposed estimators. The comparison is tested across a wide range of models, including linear regression models, tree-based models, and neural network-based models, under different simulated datasets that exhibit different levels of causality, different degrees of nonlinearity, and different distributional properties. Most importantly, we apply our approaches to a large observational dataset provided by a global technology firm that operates in both the e-commerce and the lending business. We find that the relative reduction of estimation error is strikingly substantial if the causal effects are accounted for correctly.