Thesis 23

Thesis #23 – Repairing all types of cumulative damage during the aging phase will provide at most partial amelioration for the problem of declining adaptation with age, because some of this decline will be due to failures of signaling and other features of gene regulation as a result of the de-tuning of adaptation with age.

The functioning of cells as complex as those of humans involves much more than the repetitious execution of the same biochemical processes over and over again.  Rather, our cells have elaborate networks of interaction among proteins and the nucleic acids involved in their synthesis.  Among the specific agents involved in these complex networks are transcription factors, proteins that affect the production of other proteins, sometimes on a vast scale, with one transcription factor affecting the production of hundreds of different types of protein.

This coordination of function by cells involves intracellular signaling cascades and other information-laden patterns of coordination.  In a sense, the human cell is a spectacularly complex hybrid analog-digital computer, where the digital components are provided by the nucleic acids, and the analog components are the proteins.  At ages when natural selection is acting with its full power, what our cells can accomplish is remarkable with respect to efficiency and precision.  But with an evolutionary view of health and function like the present one, as the forces of natural selection fade with adult age, the control of our cell functions is expected to deteriorate.  Thus, we can expect that some of our cells will become so dysfunctionally regulated with age as to turn malignant, losing self-inhibitory mechanisms, and degenerating into highly proliferative rogue cells that engender cancer, to give just one example.

It is not the case that, during aging, perfectly and perpetually attuned cells progressively lose function solely because of a substratum of damaged molecular components.  In addition to any such damage, the evolutionary genetic tuning required to sustain the signaling systems of the human cell will not be there at later ages.  Metaphorically, it is not just that the car is rusting; the driver is also falling asleep.  The cell genome is running out of information with which to sustain its role at later ages.  There are any number of metaphors that could be used here:  an actor who has run out of script; a videogame that hasn’t been properly programmed for its later “levels;” driving away from a city and having its radio stations fade out; and so on.

Thus, whatever damage we are able to repair at the level of cell, there will still be failures of function arising from progressively more severe failures of coordination among the complex networks that sustain cell functions.

This entry was posted in Complexity, Constraints, Theses and tagged , . Bookmark the permalink.