We were asking
Does the topology response at q48 represent genuine fission or an earlier susceptibility in the body's surface layer?
A q48 causal-order effect increased thresholded component counts, but the extra pieces were mostly tiny, mid-density peripheral structures rather than macroscopic daughters.
Does the topology response at q48 represent genuine fission or an earlier susceptibility in the body's surface layer?
The signal vanished when components had to carry even a small fraction of total mass, so the experiment found density-specific fraying rather than a rise in daughter incidence.
Can a surface-targeted intervention amplify that susceptibility until material partitions into persistent daughters?