Target Trial Emulation: The Bridge Between RCTs and Real-World Data
You can't randomize everything. But you can emulate it. Here's how — and where it breaks.
Where correlation ends and causation begins. Exploring causal inference across cardiovascular disease, dermatology, genomics, and the boundaries of what observational data can teach us.
A single pill combining an antihypertensive, a statin, and aspirin. Elegant in concept, messy in real-world evidence. My dissertation uses target trial emulation on 24,788 participants from the All of Us Research Platform to untangle what happens when we move from controlled trials to the chaos of actual patient lives. The results from parametric G-formula, Dynamic Bayesian Networks, and standard regression don't just differ — they tell fundamentally different stories about who benefits and who doesn't.
You can't randomize everything. But you can emulate it. Here's how — and where it breaks.
Three in ten psoriasis patients don't respond to biologics. Prediction models tell us who. But only causal models tell us why — and what to do about it.
Same data, same question, different causal architectures. When they converge, you celebrate. When they diverge, that's where the real science begins.
I was a PI on the Phase III dupilumab trials. Eight years later, my PhD is about what RCTs can't tell us. Here's what changed my mind.
Directed Acyclic Graphs are the lingua franca of causal inference. But drawing the wrong arrow can be worse than drawing none at all.
New posts on causal inference, genomics, and the messy space between correlation and causation. No spam. Just science.