Membership Testing in Markov Equivalence Classes via Independence Query Oracles
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Understanding causal relationships between variables is a fundamental problem with broad impact in numerous scientific fields. While extensive research has been dedicated to learning causal graphs from data, its complementary concept of testing causal relationships has remained largely unexplored. While learning involves the task of recovering the Markov equivalence class (MEC) of the underlying causal graph from observational data, the testing counterpart addresses the following critical question: Given a specific MEC and observational data from some causal graph, can we determine if the data-generating causal graph belongs to the given MEC? We explore constraint-based testing methods by establishing bounds on the required number of conditional independence tests. Our bounds are in terms of the size of the maximum undirected clique ($s$) of the given MEC. In the worst case, we show a lower bound of $\exp(Ω(s))$ independence tests. We then give an algorithm that resolves the task with $\exp(O(s))$ tests, matching our lower bound. Compared to the learning problem, where algorithms often use a number of independence tests that is exponential in the maximum in-degree, this shows that testing is relatively easier. In particular, it requires exponentially less independence tests in graphs featuring high in-degrees and small clique sizes. Additionally, using the DAG associahedron, we provide a geometric interpretation of testing versus learning and discuss how our testing result can aid learning.
Background: Generalized Odds (Gen Odds) provide summaries for ordinal outcomes without requiring the proportional odds assumption. However, conventional Gen Odds compares independently drawn treatment and control outcomes and targets a population-level contrast rather than an individual-level contrast. We developed an individual-level causal formulation of Gen Odds and examined its identification. Methods: We defined the Causal Gen Odds using the joint distribution of…
We develop a semiparametric continuous time inferential framework for testing cumulative treatment effects, including both immediate and carryover effects. The latent state process is modeled by an ordinary differential equation (ODE) whose drift depends on state and treatment, while the observed data are noisy measurements of this latent state at irregular, multi resolution time points. We define the average treatment effect (ATE) as the difference of expected cumulative…
We study inference for continuous linear functionals of solutions to ill-posed inverse problems, including Euclidean parameters arising in nonparametric instrumental variables, proximal causal inference, and shadow-variable models. Although pointwise root-$n$ inference is possible under standard conditions, we show that this need not translate into locally reliable inference. Under a model imposing only minimal regularity conditions, the target is Hellinger discontinuous…
Motivation: Mediation analysis is an important tool for elucidating causal mechanisms in biomedical research and has recently gained increasing attention in microbiome studies. Motivated by a microbiome study of acute myeloid leukemia (AML) patients, we investigate whether the effect of induction chemotherapy intensity on infection status is mediated through gut microbial taxa. This problem poses substantial methodological challenges due to the high dimensionality, zero…
观测因果推断中不完全识别下的相对偏差
To conduct causal inference in observational settings, researchers must rely on certain identifying assumptions. In practice, these assumptions are unlikely to hold exactly. This paper considers the bias of selection-on-observables, instrumental variables, and proximal inference estimates under violations of their identifying assumptions. We develop bias expressions for IV and proximal inference that show how violations of their respective assumptions are amplified by any…
组间不平衡下的风险异质性稳健推断
Population-level heterogeneity is ubiquitous in biomedical data, where differences across demographic or clinical subgroups can substantially alter risk patterns. For example, in intensive care unit (ICU) studies, the mortality risk associated with specific admission diagnoses can vary across ethnic groups. Existing approaches for detecting risk heterogeneity are often sensitive to baseline model misspecification and regularization bias, both of which commonly arise in…