I guess there’s two different paths this was pushing along, the first was that “time” doesn’t really exist like we perceive it or talk about it in most physics models, it’s a property we derive from causality. And we like causality because it appears, thus far, to be an inviolable universal constant. Rather than “time”, IMO describing specific “time-space” reference frames as “sequence” frames kind of makes it easier to imagine how each of the properties of “time and space” can “distort” relative to each other and still be conceptually the same thing. Because there is a “global maximum” for each frame, stretching one property reduces the others proportionate to that maximum.
This pattern of “global maximum” (and “global minimum”) repeats throughout “higher order” constructs, up through the chemistry and biology path.
So the conceit is that rather than just a single perception of time, we perceive it on multiple levels, which is integrated just like our millions of visual sensors integrate multiple levels of information into a cogent presentation (e.g. first order neuron intensities, which get mapped into objects, which get mapped into “motive/prediction” streams).
I guess it’s not a terribly intuitive concept which is why it got abandoned at this stage, but individual cells speed up or slow down metabolic processes as a function of how active their external environment is. This rate of metabolic response is analogous to the “cellular perception of time”, and is one of the bits of information that gets transmitted via RNA. Using that planarian model, every single cell must transmit some type of “sequence timing” to help newly formed cells synchronize against the existing cells metabolic “timings”.
We can observe cellular rates changing based on information, and the current popular thesis is that “aging” as a whole is sensitivity (or lack of sensitivity) to those external timing updates (see Loss of epigenetic information as a cause of mammalian aging). If we think of these RNA/protein/peptide signals as metabolic state synchronizers instead of assuming that each has a specific universal function (e.g. this RNA at this vessicle causes this result), we can begin to view intra-cellular and inter-cellular communication as more a constant barrage of “speed up” and “slow down” signals to various processes.
This carries to the higher level abstractions in our cognitive maps, on a couple of levels.
First, the more sensitivity to specific speed up and slow down signals we have, the faster or slower the organism “perceives” time. Switching to humans specifically, we have a low burden of epigenetic information. A year feels like forever (generally) when you are two because we don’t have much synchronized epigenetic information. It takes uh… time… for the specific RNA encoding a bit of epigenetic information to be transferred to enough cells to create a stable representation of the information.
As humans age, intercellular communication gets a bit more efficient because they can start binding “existing RNA + specific peptide” equals a discrete information representation, and between local groups of cells (this is where astrocytes come in heavy) they can cut down energy use by just sending a protein/peptide signal since all the local group cells will be using the same base RNA representation. This also starts speeding up our “time perception” because each particular astrocyte starts getting activated more often as a function of how many sub representations we’ve bound to a particular (nc?)RNA sequence. Finally, when astrocytic function starts breaking down near the end of the lifespan, general perception of time starts slowing down again as the metabolic ability to pump out the necessary signalling peptides lowers overall map activation in local groups of cells.
This conceit of activation rate and current density of signalling carries up to our stream level/top level perception of time. States which present high levels of information writing “speed up” the perception of time because the hippocampal/DCN nuclei are pushing higher levels of writes, these writes on the map level are represented by higher levels of protein/peptide transmission, these writes on the cellular level are specific metabolic activations of stored epigenetic information, and underlying that are the chemical/energetic min/max the system is designed for.
This is off the top of my head with my kids going nuts, so if something doesn’t make sense please ask because it probably doesn’t make sense and I can try to clarify.
edit: Yeah, that was less coherent, didn’t get the whole “cells can only do so much at a time” angle in there clearly enough, there’s a min/max metabolic state for cells, which is just as rigid as our universal constants that was meant to tie the two conceits together.