details of the argument. The essential point is that I [K] is a splitting cri-
terion under these theorems, and thus partakes of the homology with free
energy density we have invoked above.
Activation of universality class tuning, our version of the mutator, then
becomes itself a punctuated event in response to increasing linkage between
organism and externally imposed selection or other pressure.
To reiterate slightly, Thaler [48] has suggested that the mutagenic ef-
fects associated with a cell sensing its environment and history could be as
exquisitely regulated as transcription. Our invocation of the Rate Distortion
or Joint Asymptotic Equipartition Theorems in address of the mutator neces-
sarily means that mutational variation comes to significantly reflect the gram-
mar, syntax, and higher order structures of the embedding processes. This
involves far more than a simple ‘colored noise’ - stochastic excursions about
a deterministic ‘spine’ - and most certainly implies the need for exquisite
regulation. We have thus provided a deep information theory argument for
Thaler’s speculation.
In the same paper Thaler further argues that the immune system provides
an example of a biological system which ignores conceptual boundaries be-
tween development and evolution. Elsewhere [53, 56] we explore the immune
system from I.R. Cohen’s information theory perspective on immune cogni-
tion. While evolutionary phenomena are not cognitive in the sense of the
immune system, they may still significantly interact with development. The
very reproductive mechanisms of a cell, organism, or organization may be-
come closely coupled with structured external selection pressure in a manner
recognizably analogous to ‘ordinary’ punctuated evolution.
Thaler [48] specifically examines the meaning of the mutator for the bi-
ology of cancer, which, like the immune system it defies, is seen as involving
both development and evolution. In our version of the mechanism, the sud-
den phase transition-like change in the mutual information I [K] at KC might
represent an initiating event, while subsequent closely linked paths that lead
to malignancy could be considered a series of promoting phase transitions. In
reality, there would seem to be a single, undifferentiated, interlinked process
representing the staged failure of a cellular cognitive control strategy which
can itself become convoluted with systems of structured external stressors
affecting the mutator. We expand on this point:
Various authors have argued for ‘non-reductionist’ approaches to tumori-
genesis (e.g.[6, 50]), including psychosocial stressors as inherent to the process
[21]. What is clear is that, once a mutation has occurred, multiple systems
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