Realizing Common Random Numbers: Event-Keyed Hashing for Causally Valid Stochastic Models
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实现共同随机数:用于因果有效随机模型的事件键控哈希AI 解读 ↓
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Agent-based models (ABMs) are widely used to estimate causal treatment effects via paired counterfactual simulation. A standard variance reduction technique is common random numbers (CRNs), which couples replicates across intervention scenarios by sharing the same random inputs. In practice, CRNs are implemented by reusing the same base seed, but this relies on a critical assumption: that the same draw index corresponds to the same modeled event across scenarios. Stateful pseudorandom number generators (PRNGs) violate this assumption whenever interventions alter the simulation's execution path, because any change in control flow shifts the draw index used for all downstream events. We argue that this execution-path-dependent draw indexing is not only a variance-reduction nuisance, but represents a fundamental mismatch between the scientific causal structure ABMs are intended to encode and the program-level causal structure induced by stateful PRNG implementations. Formalizing this through the lens of structural causal models (SCMs), we show that standard PRNG practices yield causally incoherent paired counterfactual comparisons even when the mechanistic specification is otherwise sound. We show that a remedy is to combine counter-based random number generators (e.g., Philox/Threefry) with event identifiers. This decouples random number generation from simulation execution order by making random draws explicit functions of the particular modeled event that called them, restoring the stable event-indexed exogenous structure assumed by SCMs.
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…
While causal discovery methods have matured for complete data, such algorithms for handling missing values remain limited. We establish general sufficient conditions under which causal graphs remain identifiable (i.e., uniquely determined from the available data distribution) under various missingness categories, including Missing Not At Random, and provide a framework to extend correctness guarantees from causal discovery algorithms for complete data to missing data…