Thesis 40

Thesis #40 – Experimental strategies for the study of aging that involve the introduction of novel mutations or increased levels of inbreeding will systematically impair the scientific study of aging, as they degrade and disrupt adaptation generally.


At this point, having got this far into the 55, my hope is that you are ready for the demolition work required to clear some space for the transformation of human aging.  This isn’t going to be pretty for the holdovers from twentieth century biology.  But just imagine how the Aristotelian physicists felt about the physicists who followed Galileo.

To this very day, cell and molecular biologists busily construct large-effect mutants using the Frankenstein technologies that are now available to them, including genetic engineering, cloning, and all the rest of it.  Characteristically, they do these things to haplessly inbred organisms that have been maintained with high levels of inbreeding in evolutionarily novel, if not seriously cruel, laboratory conditions.  This is The Island of Dr. Moreau of H.G. Wells industrialized on a massive scale, across thousands of laboratories throughout the industrial world.

I do not wish to suggest that this work is valueless.  Basic features of the molecular machinery of life have been worked out such methods.  Many of those who work on “the aging process” do so in the sincere, if misguided, hope that aging will prove to be a well-defined bit of molecular machinery, perhaps the progressive attenuation of telomeres at the tips of our chromosomes, as already mentioned.  Thus this type of experimental research is profitless when it is applied to the puzzles of aging, because aging is NOT a physiological process, as such.

Instead, because aging is solely an age-dependent pattern of failing adaptation in adults, it must be studied using methods that do not systematically degrade the adaptations of the organisms undergoing experiment.  Aging should not be studied using inbreeding, massive mutation, or teratogenesis (which means the induction of developmental monstrosity), whether that teratogenesis is achieved surgically or biochemically.  All of these interventions systematically degrade adaptation.  They will only adventitiously reveal much of the physiological or genetic underpinnings of adaptation.  I have already mentioned the best example of a Frankenstein experimental strategy that can reveal aspects of adaptation:  castration.  But such procedures chiefly reveal only one of the most elementary features of the evolutionary biology of adaptation, and thus aging:  the cost of reproduction.

But as a general rule, the best methods for studying aging will be the best methods for studying adaptation.  Here are some of the features of such research, at its best:  the use of outbred populations and cohorts when studying species that do not normally inbreed as part of their life-cycle; the careful examination of segregating genetic variation in such populations and cohorts, with respect to its abundance and its effects on the functional attributes of the organisms under study; forestalling developmental disasters, such as those of laboratory-induced teratogenesis.  In effect, these rules simply mean trying to study aging in organisms that are not being ill-used.

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