Matched burden
Fault count, intensity, dwell time, treated fraction and target engagement are equivalent.
COV‑AGE
Can two aged tissues with the same total amount of damage have different function solely because the damage is arranged and correlated differently?
The idea in plain language
If total burden is held constant and function still changes, the geometry of failure may be a causal variable. If function does not change, the central Project 150 theory loses its reason to exist.
This is deliberately an experiment against the hypothesis—not a search for a favourable biomarker and not an attempt to confirm it at any cost.
Contained geometryFaults remain locally isolatable
Correlated geometryEvery module shares the fault mode
Experimental logic
The experiment is interpretable only if burden matching, temporal order and independent replication succeed.
Fault count, intensity, dwell time, treated fraction and target engagement are equivalent.
A cell-state fault and a niche fault must show the same direction.
Covariance and propagation must change before durable function.
Force, barrier recovery, mobility, reserve and pathology outrank clocks.
Cancer, infection, clonal expansion, frailty and impaired healing can negate benefit.
Matched arms
Procedure and imaging control
Same burden concentrated in isolatable regions
Same burden dispersed without organised topology
Common-mode coverage across every module
Same cumulative exposure with temporal independence
Context only; not the therapeutic target
Primary outcomes
In situ specific force, fatigue resistance and recovery—not grip alone.
Barrier recovery, tensile integrity, wound closure and blinded pathology.
Gait, spontaneous activity, cardiorespiratory reserve and challenge recovery.
Common-mode fraction, propagation radius and modularity at matched mean burden.
Preregistered failure
Covariance changes substantially at matched burden, but hard function does not.
The pattern effect appears in only one fault class or reverses without a prespecified mechanism.
Cell composition, perfusion, clonality or a single pathway explains the result better.
The architecture changes after function, not before it.
Any gain is offset by cancer, infection, frailty or impaired healing.
The result fails across sex, site or a second genetic model.