Thesis 38

Thesis #38 – Some environmentally-induced variation in patterns of aging reflects the impact of selectively-favored patterns of life-history plasticity, but some environmental variation in aging does not reflect adaptive plasticity, such as that due to novel environments.

An important distinction needs to be drawn, in light of the findings just mentioned.  This distinction revolves around differences in the ways environments impinge on aging.

When aging in mammals or insects responds to reduced nutritional levels, in at least some cases these responses reflect selectively favored forms of plasticity.  Drosophila, the fruit flies that I work with, have a number of molecular signaling mechanisms which regulate reproduction and other aspects of their metabolism in response to diet.  This is not to claim that there aren’t direct effects of nutritional changes on fertility, physiologically.  There certainly are:  if an animal doesn’t have the fats, amino acids, and other substances required to build eggs, then those eggs won’t be made, and that animal won’t reproduce.  But there are also well-known signaling pathways involved, such as those that involve genes like sirtuins and the daf loci.  Such signaling pathways produce adaptive plasticity, plasticity which on average enhanced Darwinian fitness in the evolutionary past of these populations.

But other forms of physiological change, and thus resultant changes in patterns of aging, do not necessarily involve either adaptive plasticity or allocation of nutrients.  These changes in aging patterns arise from animals being exposed to compounds that they may lack useful responses to, compounds that do not engender well-defined or well-regulated physiological responses.  The point is that evolutionary novelty can place animals in settings for which they simply lack the adaptations required to cope.

This is what humans are now doing to many animal and plant species, including ourselves.  Our chemists, both pharmaceutical and industrial, are rapidly developing and releasing chemical compounds which are largely or completely novel.  Such novel compounds establish environments, and concomitant physiological effects, that evolution by natural selection has not molded contemporary living species to cope with.  Under such evolutionarily novel conditions, our bodies do not have the physiological or even anatomical equipment to function with high levels of fitness.  That is, industrial foods, cleaning products, fabrics, and the like can be expected to systematically degrade our function, when everything else is equal.

An important exception to the problematic nature of pathological novelty is when such evolutionarily novel compounds are used against our disease organisms, be they viral, bacterial, or fungal.  Hitting bacteria with a new antibiotic can stop them from damaging, or even killing, us during the course of bacterial infections.  Likewise for antiviral and antifungal compounds.  Indeed, the two tasks that pharmaceuticals are best at are:  (i) killing things, most usefully our infectious agents; and (ii) knocking out basic physiological functions, such as pain sensation, consciousness, mucous production, or defecation.  That is, pharmaceuticals are often effective at shutting down the sensitive networks that sustain life-forms, be they the networks of our pathogens or ourselves.

This entry was posted in Aging, Complexity, Context, Environments, Physiology, The New Science, The Science, Theses and tagged , . Bookmark the permalink.