Dynamic Structural Causal Modeling for Sleep

Objective sleep assessment relies on polysomnography (PSG), yet clinical impact is often better reflected in patient-reported outcomes (PROs) such as sleepiness and fatigue. Existing summary indices, including the Apnea-Hypopnea Index (AHI), provide limited insight into the multidomain physiology underlying functional recovery. We propose an interpretable, causal-discovery-guided framework for deriving a hierarchical Sleep Recovery Score (SRS) from multimodal PSG. Using two large population cohorts (MESA: $n=1{,}540$; MrOS: $n=825$), we apply directed acyclic graph (DAG) learning to identify candidate physiological drivers spanning respiratory burden, hypoxic burden, sleep fragmentation, sleep architecture, and autonomic regulation. Although derived from clinical PSG, these domains map naturally to sensing streams increasingly available in connected health technologies, including wearable ECG, oximetry, and sleep-stage estimation devices. To preserve mechanistic plausibility, we introduce a two-stage screening process that combines physiology-based constraints with constrained LLM-assisted auditing to identify and remove structural confounders and construct-overlapping variables. Across cohorts, these five domains emerge as recurrent physiological domains associated with recovery, and the resulting SRS shows up to $3.4\times$ stronger alignment with perceived recovery than AHI. By linking multimodal sleep physiology to patient-centered outcomes through an interpretable, bias-aware, and domain-structured framework, this work provides a practical foundation for recovery modeling across both clinical sleep studies and emerging smart and connected health settings.

Personalized healthcare decisions require reasoning about how physiological and behavioral variables influence an individual patient over time. Existing temporal causal discovery methods are poorly matched to this setting: cohort-level models provide stable but non-personalized structures, while per-patient discovery is unreliable because individual trajectories are short, noisy, irregular, and non-stationary. This creates a fundamental gap between population-level causal modeling and the patient-specific, time-varying mechanisms needed for intervention reasoning. We introduce PerCaM-Health, a framework for learning personalized dynamic causal graphs from longitudinal health data. The framework learns a knowledge-guided population temporal graph, then conservatively adapts and evolves it using patient-specific temporal evidence and rolling-window updates, producing interpretable and auditable graph sequences. By coupling these graphs with temporal structural equations, the framework enables patient-level counterfactual queries, such as estimating short-horizon outcome changes under hypothetical behavioral interventions. Experiments on a semi-synthetic dynamic health benchmark show that PerCaM-Health improves graph recovery, dynamic edge tracking, and intervention direction accuracy compared to cohort-level, per-patient, and non-personalized temporal baselines. These results demonstrate that jointly modeling personalization and temporal evolution yields more reliable causal structure and intervention reasoning.

Sleep occupies roughly one-third of human life, yet many aspects of its physiology remain poorly understood. Large polysomnography (PSG) datasets offer new opportunities to study sleep and its links to disease, but extracting insight from these recordings requires substantial expert effort and remains difficult for general-purpose AI systems. We developed AI Sleep Co-Scientist, an expert-guided environment in which human scientists direct specialist agents for hypothesis development, signal preprocessing, and statistical analysis, reviewing intermediate outputs. Each reported result is linked to the executable code that produced it. Across four cohorts of approximately 124,000 PSG recordings and more than 50 TB of raw signals, we conducted five case studies spanning how sleep physiology relates to future disease, how it distinguishes clinical phenotypes, and how sleep is organized and regulated. Diminished network-level physiological coupling during sleep was associated with incident Parkinson's disease (HR 1.48) and Alzheimer's disease (HR 1.38). A physiologically structured late-fusion sleep-age model outperformed an unconstrained early-fusion approach, and its age residual was associated with incident disease across multiple organ systems. Arousal dynamics characterized comorbid insomnia and sleep apnoea as an intermediate phenotype skewed towards obstructive sleep apnoea, distinguished by prolonged post-arousal wakefulness. Rapid eye movement (REM) bout duration tracked preceding non-REM sleep more closely than intervening wakefulness. Transient-oscillation analysis identified a fast-sigma deficit and excess centrofrontal theta activity in narcolepsy type 1. Together, these findings connect sleep to disease risk, clinical classification, and its own regulation, and show how agentic AI can support large-scale, multimodal discovery.