We’ve spent four decades arguing over a simple binary: is the human body a car rusting in the rain, or a high-performance engine that can't find its "off" switch? On one side, you’ve got Error Accumulation. On the other, Hyperfunction.

The Epigenetic Drift camp suggests molecular noise just keeps piling up until the signal-to-noise ratio hits zero. It’s a tidy, democratic view of decay, but it fails the reality test. If aging were truly a matter of random noise, human senescence wouldn't be so predictable. We’d see a much wider distribution of natural lifespans. By sheer luck, someone should’ve drifted their way to 200 years old by now.

This is why the Developmental Overshoot hypothesis is likely where the field is headed. This isn't about simple "wear and tear." It’s the realization that the pathways—mTOR, TGF-beta, Wnt—responsible for building our skeletons and wiring our brains simply don't know how to stop. They keep pushing, eventually turning maturation into hypertrophic exhaustion. We don't just fade away; we over-express ourselves into the grave.

The Overshoot model explains why caloric restriction and rapamycin work across such diverse species. These interventions aren't "fixing" damage. They’re just lowering the volume on a signal that’s turned toxic.

Currently, billions are flowing into "cleaning up the mess" via senolytics and debris clearance. That’s just mopping the floor while the tap is still running at full blast. We need a serious shift toward re-tuning somatic setpoints. If we don't move from "damage repair" to "program modulation," we’re just building expensive mops for a house that's still flooding.

We need to find the governor switches for these pathways. It isn't enough to find more inhibitors; we need a way to tell the genome that the construction phase is over and the maintenance phase must begin. Who’s actually working on that?