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Register a new userEstimating Causal Effects with the Neural Autoregressive Density Estimator
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Estimation of causal effects is fundamental in situations were the underlying system will be subject to active interventions. Part of building a causal inference engine is defining how variables relate to each other, that is, defining the functional relationship between variables given conditional dependencies. In this paper, we deviate from the common assumption of linear relationships in causal models by making use of neural autoregressive density estimators and use them to estimate causal effects within the Pearls do-calculus framework. Using synthetic data, we show that the approach can retrieve causal effects from non-linear systems without explicitly modeling the interactions between the variables.
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We introduce RNADE, a new model for joint density estimation of real-valued vectors. Our model calculates the density of a datapoint as the product of one-dimensional conditionals modeled using mixture density networks with shared parameters. RNADE learns a distributed representation of the data, while having a tractable expression for the calculation of densities. A tractable likelihood allows direct comparison with other methods and training by standard gradient-based optimizers. We compare the performance of RNADE on several datasets of heterogeneous and perceptual data, finding it outperforms mixture models in all but one case.
Forest-based methods have recently gained in popularity for non-parametric treatment effect estimation. Building on this line of work, we introduce causal survival forests, which can be used to estimate heterogeneous treatment effects in a survival and observational setting where outcomes may be right-censored. Our approach relies on orthogonal estimating equations to robustly adjust for both censoring and selection effects. In our experiments, we find our approach to perform well relative to a number of baselines.
When interested in a time-to-event outcome, competing events that prevent the occurrence of the event of interest may be present. In the presence of competing events, various statistical estimands have been suggested for defining the causal effect of treatment on the event of interest. Depending on the estimand, the competing events are either accommodated or eliminated, resulting in causal effects with different interpretation. The former approach captures the total effect of treatment on the event of interest while the latter approach captures the direct effect of treatment on the event of interest that is not mediated by the competing event. Separable effects have also been defined for settings where the treatment effect can be partitioned into its effect on the event of interest and its effect on the competing event through different causal pathways. We outline various causal effects that may be of interest in the presence of competing events, including total, direct and separable effects, and describe how to obtain estimates using regression standardisation with the Stata command standsurv. Regression standardisation is applied by obtaining the average of individual estimates across all individuals in a study population after fitting a survival model. With standsurv several contrasts of interest can be calculated including differences, ratios and other user-defined functions. Confidence intervals can also be obtained using the delta method. Throughout we use an example analysing a publicly available dataset on prostate cancer to allow the reader to replicate the analysis and further explore the different effects of interest.
Evaluating causal effects in the presence of interference is challenging in network-based studies of hard to reach populations. Like many such populations, people who inject drugs (PWID) are embedded in social networks and often exert influence on others in their network. In our setting, the study design is observational with a non-randomized network-based HIV prevention intervention. The information is available on each participant and their connections that confer possible shared HIV risk behaviors through injection and sexual risk behaviors. We consider two inverse probability weighted (IPW) estimators to quantify the population-level effects of non-randomized interventions on subsequent health outcomes. We demonstrated that these two IPW estimators are consistent, asymptotically normal, and derived a closed form estimator for the asymptotic variance, while allowing for overlapping interference sets (groups of individuals in which the interference is assumed possible). A simulation study was conducted to evaluate the finite-sample performance of the estimators. We analyzed data from the Transmission Reduction Intervention Project, which ascertained a network of PWID and their contacts in Athens, Greece, from 2013 to 2015. We evaluated the effects of community alerts on HIV risk behavior in this observed network, where the links between participants were defined by using substances or having unprotected sex together. In the study, community alerts were distributed to inform people of recent HIV infections among individuals in close proximity in the observed network. The estimates of the risk differences for both IPW estimators demonstrated a protective effect. The results suggest that HIV risk behavior can be mitigated by exposure to a community alert when an increased risk of HIV is detected in the network.
Support vector machine (SVM) is one of the most popular classification algorithms in the machine learning literature. We demonstrate that SVM can be used to balance covariates and estimate average causal effects under the unconfoundedness assumption. Specifically, we adapt the SVM classifier as a kernel-based weighting procedure that minimizes the maximum mean discrepancy between the treatment and control groups while simultaneously maximizing effective sample size. We also show that SVM is a continuous relaxation of the quadratic integer program for computing the largest balanced subset, establishing its direct relation to the cardinality matching method. Another important feature of SVM is that the regularization parameter controls the trade-off between covariate balance and effective sample size. As a result, the existing SVM path algorithm can be used to compute the balance-sample size frontier. We characterize the bias of causal effect estimation arising from this trade-off, connecting the proposed SVM procedure to the existing kernel balancing methods. Finally, we conduct simulation and empirical studies to evaluate the performance of the proposed methodology and find that SVM is competitive with the state-of-the-art covariate balancing methods.
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