Causal Inference with Unobserved Confounding

We introduce DeDiCa, a practical framework for efficient causal inference with discrete variables and hidden confounding that revisits classical probabilistic modeling through a tensorized parameterization of causal Bayesian networks, enabling tractable inference. Given a causal graph, DeDiCa is trained once on observational data by maximum likelihood, exactly marginalizing over hidden confounders, and can then estimate any (proxy-)identifiable interventional query. Despite this deliberately simple parameterization, DeDiCa matches state-of-the-art neural causal generative models in ATE estimation, while supporting memory-efficient CPU training and exact interventional inference in milliseconds. Compared with causal foundation models, DeDiCa scales more effectively with additional observational samples and achieves competitive accuracy at substantially lower inference time and memory. DeDiCa provides a tractable, accurate, and scalable approach to causal inference in discrete settings with hidden confounding.

Standard causal identification methods often assume no unmeasured confounding and can fail when relevant confounders are unobserved. Proximal causal inference instead uses proxy variables to identify effects under hidden confounding. However, nonparametric proximal estimation can be challenging in practice: recovering causal estimands such as the conditional average treatment effect (CATE) requires solving an ill-posed integral equation that is data-hungry, hyperparameter-sensitive, and optimization-unstable. Bayesian inference for such models provides a desirable alternative, mitigating these difficulties by regularizing through the prior. However, computing a posterior is itself challenging, as a typical likelihood function will include latent variables. Following the recent success of tabular foundation models in backdoor, instrumental variable, and frontdoor settings, we propose that prior-data fitted networks (PFNs) are uniquely suited to resolve this bottleneck. Indeed, by training on synthetic data sampled from compliant structural causal models with access to oracle counterfactuals, we simplify the task substantially, amortizing the implied Bayesian operator inversion into a single transformer forward pass. Compared to prior literature that focuses primarily on point estimation, our model, ProximalFM, explicitly targets the Bayesian posterior distribution of the CATE. One unique aspect of this problem is that we need to provide Monte Carlo estimates of the oracle CATEs, leading to a novel variation of PFNs that accounts for the added stochastic error. Across a diverse suite of proximal regimes, ProximalFM achieves consistently strong CATE-estimation performance without dataset-specific tuning, with its largest advantage when latent confounding is substantial and the proxies are weakly informative; it also provides fast inference through a single amortized forward pass.

Estimating treatment effects from observational data typically relies on the No Unmeasured Confounding Assumption (NUCA), which rarely holds in practice. Proximal causal learning (PCL) addresses unmeasured confounding via proxy variables, yet existing methods require the proxy variables to be pre-specified. Thus, we propose PCL-U, a framework that learns proxy variables directly from observed covariates. PCL-U uses neural encoders to decompose covariates into treatment-inducing, outcome-inducing, and shared proxies, guided by minimax mutual information objectives, and obtains causal estimates through a practical moment-based risk function. Experiments on benchmarks show that PCL-U matches or outperforms existing baselines. Besides, there are two types of synthetic datasets with varying dimensions and confounding strengths that illustrate that our method maintains stable estimation accuracy.

Estimating causal effects from observational data is central to science and policy, but the effects are not identified when confounders are unmeasured. Proximal causal inference addresses this problem with proxies of the unmeasured confounders. However, existing proxy-based approaches either designate proxy roles and solve an inverse problem, which is ill-posed and hard to estimate with high-dimensional proxies, or use a latent-variable model, which assumes that the learned latent variable matches the hidden confounder and leaves bias when it does not. To address these challenges, we introduce proximal balancing. It carries the classical idea of covariate balancing to confounders that are observed only through proxies: it learns a low-dimensional summary of the covariates and proxies that makes the treatment groups comparable, and then adjusts for this summary. It needs no designated proxy roles, inverse problem, or latent model. We give identification theory, finite-sample guarantees, and a practical algorithm, PROBE. We demonstrate the method on low-dimensional, high-dimensional, and image proxies and on real-world data.

Unobserved common causes are pervasive in real-world time series and can induce spurious associations that causal discovery methods mistake for direct edges. We propose LUCID (Learning Under Confounding for Inference and Discovery, a regime-adaptive deconfounding layer that first estimates the confounding regime from data using a Marčenko--Pastur spectral router, then applies a deconfounding strategy matched to that regime. When the spectrum indicates pervasive factor confounding, LUCID attenuates factor-dominated variation and recovers contemporaneous (lag-$0$) structure from the resulting innovations, with edge selection calibrated against a data-driven edge-free null. Rather than being tied to a particular discovery algorithm, it can wrap existing discovery engines; we demonstrate consistent improvements across three such methods. On a diverse synthetic out-of-distribution benchmark spanning changes in confounder strength and sparsity, loading density, lag structure, volatility dynamics, edge heterogeneity, persistence, intermittency, and tail behavior, LUCID achieves the best family-weighted directed, lag-resolved graph $F_1$ ($0.60$), improving over the strongest baseline by $0.19$ absolute ($\approx\!46\%$ relative). Its advantage widens relative to looser lag-collapsed scoring, and remains robust under intermittent and heavy-tailed confounding. Code reproducing the method, the benchmark generators, and every reported experiment is available at https://github.com/bloomberg/causal-ts.

We consider the problem of learning risk scores to prioritize individuals for scarce resources or interventions, from historical observational data affected by unobserved confounding. Decisions about who receives scarce resources are often guided by risk scores based on recorded characteristics, such as responses to a survey. These risk scores are increasingly being learned directly from observational data: historical records of individuals' characteristics, allocation decisions, and outcomes. Standard methods such as inverse propensity weighting (IPW), which corrects for the bias introduced by the historical allocation policy, can be used to learn accurate risk scores if the historical decision process is fully explained by the recorded characteristics. In practice, however, historical decisions often depend on unrecorded information, causing learned risk scores to systematically under-prioritize exactly the individuals whose unrecorded circumstances drove past prioritization. We propose a method for learning risk scores that are robust to this kind of unobserved confounding, building on IPW. Since propensity weights cannot be reliably estimated under unobserved confounding, we instead treat them as belonging to an uncertainty set determined by the observable data and domain-informed estimates of the degree of confounding, combining sensitivity analysis from causal inference with Wasserstein distributionally robust optimization. The resulting robust risk score learning problem admits a sample-based approximation that we reformulate as an exponential cone program compatible with off-the-shelf solvers. We demonstrate the effectiveness of our approach on semi-synthetic data derived from datasets in the UCI Machine Learning Repository. Our method improves calibration by up to 29.2% over traditional benchmarks and up to 11.1% over the state of the art, without compromising other metrics.

Unobserved confounding is a fundamental challenge in causal inference from observational data. This article develops a mixture-learning perspective, viewing latent confounders as sources of heterogeneity that induce mixture structure in observed data. Under suitable structural and identifiability assumptions, recovering the mixing distribution and component mechanisms enables estimation of interventional distributions and causal estimands. Using variants of Bernoulli mixtures as a running example, we contextualize mixture-learning techniques and their structural assumptions, and connect them to causal inference in panel-data settings, including latent factor models and synthetic interventions.We then consider high-dimensional exponential-family mixtures with dependent outcome trajectories, moving beyond counterfactual means to model counterfactual distributions. We situate this perspective relative to complementary approaches for unobserved confounding. Together, these ideas provide a bridge between mixture learning and causal inference, connecting recent advances in high-dimensional mixture learning to scalable identification and estimation of causal effects while raising new challenges for mixture learning.

Causal discovery aims to recover causal relationships from observed data. In various fields, exploring causal relationships among variables remains an important topic, but this task becomes challenging due to the existence of latent confounders. Ignoring such confounders can lead to false associations and incorrect edge directions. In this paper, we study the linear structural equation model with latent confounders. We propose an algorithm that iteratively identifies terminal (observed) nodes and reconstructs the directed acyclic graph of the observed variables. To do this, we recover the precision matrix of the observed variables as a sparse plus low-rank matrix: a sparse matrix captures the conditional dependencies among observed variables, while a low-rank matrix captures the combined influence of a few latent confounders. We establish that for $p$ observed variables, $r$ latent confounders and $s$ edges, our procedure correctly identifies the directed causal relationship among observed variables, for $n \gtrsim \max\{s\log p,\ r p\}$ samples. Experimental results validate our theoretical contributions.

This paper investigates the development of causal foundation models for bounding the effect of interventions and counterfactuals from observational data. We show that a canonical prior can be defined with full support over the space of structural causal models with discrete observables. With this canonical prior, we translate the problem of bounding counterfactuals into that of learning distributions over functions that map data (and possibly structural assumptions) to a causal query of interest. This extends the promising causal foundational modelling paradigm to the estimation of partially-identifiable causal effects, i.e., under unobserved confounding, where multiple values are equally compatible with the observed data and prior structural assumptions.

Estimating causal effects from real-world spatiotemporal data is challenging due to hidden confounders and interference. Standard causal identification methods assume conditional exchangeability given observed covariates, which fails whenever hidden confounders affect both treatment and outcomes - a common setting in domains such as climate, environmental policy, epidemiology, and regional economics. In this paper, we propose a novel spatiotemporal proximal causal inference framework that extends proximal identification theory to spatiotemporal settings. The proposed method jointly captures local and neighborhood-level confounding information by introducing treatment- and outcome-inducing proxies, and we derive a spatiotemporal outcome confounding bridge function that identifies the potential outcome without requiring direct recovery of the hidden confounder. We establish the identifiability of this bridge function under proxy exclusion restrictions and a spatiotemporal completeness condition, and show that the resulting estimator recovers the outcome through a proximal generalization of the g-computation formula. To operationalize this identification result, we propose a neural architecture that learns proxies via transformer-based spatiotemporal encoders - coupled with a conditional mutual information critic to enforce exclusion restrictions and a moment-matching network to guarantee that the learned bridge function satisfies the underlying identifying equation. We further introduce a stabilized weighting scheme to address treatment support imbalance. Experiments on synthetic datasets demonstrate that our approach achieves comparable performance to baseline causal inference methods, while providing, to our knowledge, the first theoretically grounded outcomes for the hidden confounding in the presence of spatiotemporal interference through a proximal causal inference framework.

We study causal inference under outcome interference for sequential, observational settings. Specifically, we consider settings where the binary outcomes over N units are Markovian across T time steps. At each time step, the outcomes of N units have dependencies captured through an Ising model; each outcome is also impacted through an external field capturing the effects of its treatment as well as latent confounders. Similar to panel data literature, these latent confounders are modeled to have a low-rank factor structure. Our data is a single sample from this high-dimensional distribution. To estimate causal quantities of interest, we provide a computationally efficient method based on Maximum Pseudo-Likelihood Estimation (MPLE) for learning the model parameters. Under mild assumptions, we establish non-asymptotic consistency for parameter estimation and show this translates to faithful estimation of causal quantities of interest after sampling from the learned model. We demonstrate the efficacy of the method through synthetic experiments as well as a real-world case-study investigating causal effects of vaccine rates on COVID-19 death rates within US counties nationwide.

Uplift modeling, crucial for estimating individual treatment effects (ITE), faces dual challenges: flexibly leveraging inter-group similarity to enhance discriminative power and debiasing under unobserved confounding scenarios. In this paper, we propose the Cross-Head Attention Uplift Network (CHAUN) and Robust Adversarial Inverse Propensity Score (RA-IPS) method to address these limitations. CHAUN employs shared feature embeddings and cross-head attention mechanisms to dynamically integrate treatment-specific and control-specific representations, enhancing inter-group correlation modeling. Theoretically, we prove that access to the true propensity scores ensures ITE identifiability even with unobserved confounders. For practical scenarios lacking true propensity scores, RA-IPS adversarially optimizes propensity weights within constrained uncertainty sets to mitigate bias from unobserved variables. Experiments on public datasets (CRITEO-UPLIFT, LAZADA) and a production e-commerce dataset demonstrate CHAUN's superiority over state-of-the-art uplift models, achieving relative improvements of up to 25.6% in QINI scores. RA-IPS further enhances robustness, outperforming standard IPS by 5.4% under unobserved confounding. The results validate the effectiveness of our proposed methods in real-world causal inference tasks.

The presence of confounding bias poses a key challenge in policy evaluation, as the target causal effects of actions are not identifiable (i.e., underdetermined) from observational data. On the other hand, existing confounding-robust evaluation strategies require detailed prior knowledge about the environment or apply only to discrete treatments and outcomes. This paper investigates causal effect evaluation over the continuous domain from confounded observations, while requiring only basic temporal ordering between the treatment and the outcome. We introduce a universal discretization of the exogenous domains that approximates the observational and interventional distributions of any causal model with arbitrary accuracy using a finite number of latent states. Building on this newfound universal approximation property, we develop a novel family of Causal Gaussian process (CGP) models that effectively approximate the observational and interventional distributions of any causal model with confounded observations.

Finding the source of failures, known as Root Cause Analysis (RCA), is essential for identifying the root causes of anomalies and maintaining the reliability of complex systems. While causal theory has advanced data-driven RCA, existing frameworks assume causal sufficiency, failing to account for the unobserved latent variables prevalent in real-world environments. To address this gap, we propose PAG-RCA. This framework models system failures as parametric interventions over Partial Ancestral Graphs (PAGs) to perform RCA in the presence of latent variables. We use standard causal identification algorithms to find the source of failures by quantifying causal effects over the PAG. When an effect is identifiable, candidate root causes are ranked based on their exact intervention effects. When effects are structurally unidentifiable, our framework (for the first time in the RCA literature) integrates partial identification to evaluate and score candidates using analytical causal bounds. By integrating latent variables and partial identification at once our framework ensures robust RCA even under data scarcity and latent-variable scenarios where traditional methods degrade. Evaluations on synthetic data, microservice anomaly benchmarks and power-grid cascading failures demonstrate that PAG-RCA consistently outperforms state-of-the-art data-driven baselines. By improving data-driven RCA performance under data scarcity, this methodology advances reliable automated diagnostics in partially observable complex networks.

Causal discovery from observational data remains challenging due to the need to recover directed structure and latent confounding without interventions. We propose FoundCause, an amortized causal discovery model trained entirely on synthetic data that maps datasets directly to causal graphs in a single forward pass. By learning from large collections of simulated structural causal models, FoundCause captures transferable statistical patterns that generalize beyond individual datasets. The architecture incorporates several key inductive biases for causal discovery. It uses a permutation-invariant transformer encoder with alternating attention over samples and variables to jointly model cross-variable dependence and per-variable distributions. Pairwise statistical features derived from classical asymmetry measures are injected through statistics-conditioned attention, guiding the model toward known causal signals. A factorized decoder separates edge existence from direction, while a triangular refinement module enables reasoning over higher-order causal motifs such as chains and colliders. In addition, a dedicated confounder module based on learnable latent tokens explicitly models hidden common causes, and the model explicitly handles missing data via its masked input representation. To our knowledge, FoundCause is the first amortized causal discovery approach to explicitly model latent confounding. FoundCause outperforms 11 classical non-amortized methods (e.g., PC, GES, NOTEARS-style optimization) and 4 amortized causal discovery methods on 15 real-world datasets, achieving +9.6% improvement in $F_1$, +1.2% in AUROC, and an 18.9% reduction in structural Hamming distance relative to the strongest non-amortized methods, while performing inference in a single forward pass.

Understanding the effects of interventions is central to scientific progress, with randomized controlled trials (RCTs) regarded as the gold standard for causal inference in many applied fields. However, RCTs are costly, time-consuming, and often constrained by ethical or practical limitations, motivating the need for causal methods able to draw conclusions from observational data. While such data is collected at ever larger scale, making its use for causal inference is often hindered by the fact that not all variables affecting treatment allocation and the outcome are observed: an issue known as unobserved confounding. In this paper, we introduce a new study design called confounder detection via treatment intent. The idea is to query a human expert who makes treatment decisions, and ask them to compare pairs of units proposed by a principled matching strategy, with the goal of eliciting unobserved variables that explain why treatment decisions differ. We provide a theoretical basis for such a procedure, ascertaining conditions under which such a study design may elicit unobserved confounders. Building on this newly established foundations, we study treatment effects of interventions in the intensive care unit (ICU). First, we show empirical evidence strongly indicating that electronic health records (EHRs) collected in ICUs are subject to unobserved confounding. By using clinical text notes as a proxy for physicians' knowledge and leveraging natural language processing, we provide a proof of concept for our methodology in a semi-synthetic environment with a known ground truth.

Background: Randomized controlled trials (RCTs) are costly, time-consuming, and often infeasible, while treatment-effect estimation from observational data is limited by unobserved confounding. Methods: We developed a three-step framework to address unobserved confounding in observational survival data. First, we infer a latent prognostic factor (U) from restricted mean survival time (RMST) discrepancies between patients with similar observed factors, the same treatment, and divergent outcomes, leveraging the idea that the aggregate effect of unmeasured factors can be inferred even if individual factors cannot. Second, we balance U with observed baseline covariates using prognostic matching, entropy balancing, or inverse probability of treatment weighting. Third, we apply multivariable survival analysis to estimate hazard ratios (HRs). We evaluated the framework in three observational cohorts with RCT benchmarks, two RCT cohorts, and six multicenter observational cohorts. Results: In three observational cohorts (nine comparisons), balancing U improved agreement with trial HRs in all cases; in the strongest settings, it reduced absolute log-HR error by approximately ten-fold versus using observed covariates alone (mean reduction 0.344; p=0.001). In two RCT cohorts, U was balanced across arms (most SMDs <0.1) and adjustment had minimal impact on log-HRs (mean absolute change 0.08). Across six multicenter cohorts, balancing U within centers reduced cross-center dispersion in chemotherapy log-HR estimates (mean reduction 0.147; p=0.016); when populations were directly balanced across centers to account for case-mix differences, cross-center survival differences were narrowed in 75%-100% of comparisons. Conclusions: Inferring and balancing a latent prognostic signal may reduce unobserved confounding and improve treatment-effect estimation from real-world data.

Unobserved confounding is a key challenge when estimating causal effects from a treatment on an outcome. In this work, we assume that we observe a single, potentially multi-dimensional proxy variable of the unobserved confounder and that we know the mechanism that generates the proxy from the confounder. Under an assumption called Single Proxy Identifiability of Causal Effects or simply SPICE, we prove that this error mechanism is complete and causal effects are identifiable. We extend the proxy-based causal identifiability results by Kuroki and Pearl (2014); Pearl (2010) to multi-dimensional continuous settings, more flexible functional relationships and a broader class of distributions. Further, we develop a neural network based estimation framework, SPICE-Net, to estimate causal effects, which is applicable to both discrete and continuous treatments.

A key challenge in travel demand analysis is the presence of unobserved factors that may generate non-causal dependencies, obscuring the true causal effects. To address the issue, the study introduces a novel deep learning based fully interpretable joint modelling framework, Copula-ResLogit, which integrates the flexibility of Residual Neural Network (ResNet) architectures with the dependence capturing capabilities of copula models. This hybrid structure enables us to first detect unobserved confounding through traditional copula function based joint modelling and then mitigate these hidden associations by incorporating deep learning components. The study applies this framework to two case studies, including the relationship between stress levels and wait time of pedestrians when crossing mid block in VR and the dependencies between travel mode choice and travel distance in London travel behaviour data. Results show that Copula-ResLogit substantially reduces or eliminates the dependencies, demonstrating the ability of residual layers to account for hidden confounding effects.

Instrumental variable (IV) and proximal causal learning (Proxy) methods are central frameworks for causal inference in the presence of unobserved confounding. Despite substantial methodological advances, existing approaches rarely provide reliable epistemic uncertainty (EU) quantification. We address this gap through a Deconditional Gaussian Process (DGP) framework for uncertainty-aware causal learning. Our formulation recovers popular kernel estimators as the posterior mean, ensuring predictive precision, while the posterior variance yields principled and well-calibrated EU. Moreover, the probabilistic structure enables systematic model selection via marginal log-likelihood optimization. Empirical results demonstrate strong predictive performance alongside informative EU quantification, evaluated via empirical coverage frequencies and decision-aware accuracy rejection curves. Together, our approach provides a unified, practical solution for causal inference under unobserved confounding with reliable uncertainty.

Causal inference from observational data can provide strong evidence for finding the best action in a decision-making scenario without having to perform expensive randomized trials. The causal effect of an action is often not pointwise identifiable even with infinite data due to unobserved confounding factors. Furthermore, having only finitely many samples adds another layer of uncertainty to causal effect estimation. Several existing methods can be used to obtain upper and lower bounds to the causal effect, ranging from symbolic methods to the more recent neural network-based approaches, which implicitly incorporate both sources of uncertainty. However, these methods do not inform whether collecting more samples may or may not help identify the best action from observational data, leaving experts in the dark about their data collection strategies. We address this problem with a novel framework that can distinguish the range of causal effect values that might be eliminated by collecting more samples from the range of values that, with high probability, cannot be eliminated with more observational samples. We show that this partitioning can be obtained by solving max-min and min-max optimization problems. We leverage neural causal models to approximately recover this decomposition in practice. We demonstrate via experiments on synthetic and real-world datasets that our algorithm can determine when collecting more samples will not help determine the best action. Our framework can help practitioners decide when to resort to non-observational studies or seek to measure some of the unmeasured confounders for optimal decision-making.

Granger causality characterizes directed predictive dependencies in multivariate time series, but recovering such dependencies becomes challenging in the presence of latent confounding. Cross-environment invariance provides a natural source of information in heterogeneous settings, yet invariance alone can be insufficient: when latent-to-observed mechanisms remain stable, hidden confounders can induce predictive dependencies that are just as invariant as genuine Granger-causal relations. We show that interventions provide an additional source of identifying information by inducing structured variation in observed mechanisms, while stable latent pathways need not exhibit the same cross-environment changes. In practice, however, neither the intervened environments nor the affected mechanisms are known. We propose GRACE, a framework for learning Granger causality under latent confounding from intervention-induced heterogeneity. GRACE decomposes multivariate dynamics into a shared Granger mechanism, sparse environment-specific deviations that capture edge-level interventions, and a latent component that accounts for confounding. Under a linear generative model, we show that GRACE can recover which environments intervene on a given edge when the edge is perturbed in at least one but fewer than half of the environments and the intervention effect is sufficiently large to survive sparsity shrinkage; the recovered intervention pattern then provides a certificate for the corresponding Granger causal edge. Experiments on synthetic and real-world time series demonstrate improved Granger causal structure recovery under latent confounding and unknown interventions.

Causal inference in spatial domains faces two intertwined challenges: (1) unmeasured spatial factors, such as weather, air pollution, or mobility, that confound treatment and outcome, and (2) interference from nearby treatments that violate standard no-interference assumptions. While existing methods typically address one by assuming away the other, we show they are deeply connected: interference reveals structure in the latent confounder. Leveraging this insight, we propose the Spatial Deconfounder, a two-stage method that reconstructs a substitute confounder from local treatment vectors using a conditional variational autoencoder (C-VAE) with a spatial prior, then estimates causal effects with a flexible outcome model. We show that this enables nonparametric identification of direct and spillover effects under weak assumptions--without multiple treatment types or a known latent-field model. Empirically, we extend SpaCE, a benchmark suite for spatial confounding, to include treatment interference, and show that the Spatial Deconfounder consistently improves effect estimation across real-world environmental health and social science datasets. By turning local interference into a multi-cause proxy for latent spatial confounding, our framework advances robust causal inference for spatial data.

Causal discovery aims to learn causal structures up to certain symmetries. Diverse populations or changing environments give rise to heterogeneous data in the following sense: each population/environment is a ``source'' which idiosyncratically determines the forms of causal effects. From this perspective, the source is a latent common cause for every observed variable. While some methods for causal discovery can work around latent confounding in special cases, a global confounder poses a significant challenge. The only known ways to deal with latent global confounding involve making assumptions that limit structural equations and/or noise functions. We demonstrate that globally confounded causal structures can still be identified with arbitrary structural equations and noise functions, so long as the number of latent classes remains small relative to the size and sparsity of the underlying DAG. The approach relies on agglomerating variables into large-enough matrices of moments, whose ranks directly reveal graphical properties of the causal structure. We also provide a statistical test to test the rank of these matrices.