This study quantifies the association between non-adherence to antipsychotic medications and adverse outcomes in individuals with schizophrenia. We frame the problem using survival analysis, focusing on the time to the earliest of several adverse events (early death, involuntary hospitalization, jail booking). We extend standard causal inference methods (T-learner, S-learner, nearest neighbor matching) to utilize various survival models to estimate individual and average treatment effects, where treatment corresponds to medication non-adherence. Analyses are repeated using different amounts of longitudinal information (3, 6, 9, and 12 months). Using data from Allegheny County in western Pennsylvania, we find strong evidence that non-adherence advances adverse outcomes by approximately 1 to 4 months. Ablation studies confirm that county-provided risk scores adjust for key confounders, as their removal amplifies the estimated effects. Subgroup analyses by medication formulation (injectable vs. oral) and medication type consistently show that non-adherence is associated with earlier adverse events. These findings highlight the clinical importance of adherence in delaying psychiatric crises and show that integrating survival analysis with causal inference tools can yield policy-relevant insights. We caution that although we apply causal inference, we only make associative claims and discuss assumptions needed for causal interpretation.

Causal inference across multiple data sources has the potential to improve the generalizability, transportability, and replicability of scientific findings. However, data integration methods for time-to-event outcomes -- common in medical contexts such as clinical trials -- remain underdeveloped. Existing data fusion methods focus on binary or continuous outcomes, neglecting the distinct challenges of survival analysis, including right-censoring and the unification of discrete and continuous time frameworks. To address these gaps, we propose two novel approaches for multi-source causal survival analysis. First, considering a target site-specific causal effect, we introduce a semiparametric efficient estimator for scenarios where data-sharing is feasible. Second, we develop a federated learning framework tailored to privacy-constrained environments. This framework dynamically adjusts source site-specific contributions, downweighting biased sources and upweighting less biased ones relative to the target population. Both approaches incorporate nonparametric machine learning models to enhance robustness and efficiency, with theoretical guarantees applicable to both continuous and discrete time-to-event outcomes. We demonstrate the practical utility of our methods through extensive simulations and an application to two randomized trials of a monoclonal neutralizing antibody for HIV-1 prevention: HVTN 704/HPTN 085 (cisgender men and transgender persons in the Americas and Switzerland) and HVTN 703/HPTN 081 (women in sub-Saharan Africa). The results highlight the potential of our approaches to efficiently estimate causal effects while addressing heterogeneity across data sources and adhering to privacy and robustness constraints.