(9)
where splitting criterion is given by
I(Y1;Y2|Y3) ≡
H(Y3)+H(Y1|Y3)+H(Y2|Y3)-H(Y1,Y2,Y3)
We can then examine mixed cognitive/adaptive phase transitions anal-
ogous to learning plateaus [57] in the splitting criterion I(Y1, Y2|Y3), which
characterizes the synergistic interaction between structured psychosocial stress,
the CMC, and the tumor’s adaptive mutator. These transitions delineate the
various stages of tumorigenesis, which are embodied in the slowly varying
‘piecewise adiabatically memoryless ergodic’ phase between transitions.
Discussion and conclusions
We have applied an elaborate mathematical modeling strategy to the
problem of disparities in occurrence and progression of certain cancers be-
tween powerful and marginal subgroups. As the ecologist E.C. Pielou has
argued [40, p. 106], a severe methodological limit to any such approach is
that mathematical models do not create new knowledge, they create new
speculation, even when they appear to fit available data quite well. Their
often considerable utility lies almost entirely in raising questions for subse-
quent empirical study, which, in a scientific context, is the only true source
of new knowledge.
The speculations emerging from our model are of some interest.
We have expressed tumorigenesis in terms of a synergistic linkage of a
‘language’ of structured external stress with the adaptive mutator and its
opposing cognitive process, mutation control.
Raised rates of cellular mutation which quite literally reflect biocultural
selection pressure through Ademi’s distorted mirror do not fit a cognitive
paradigm: The adaptive mutator may propose, but selection disposes. How-
ever, the effect of structured stress on both the mutator and on mutation con-
trol, which itself constitutes the selection pressure facing a clone of mutated
cells, connects the mechanisms. Subsequent multiple evolutionary ‘learning
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