A fear of pheromones (revisited)

October 3, 2013 | James Kohl

I’ve already mentioned that Chelo et al (2013) reported a nightmarish scenario on Friday the 13th of September that seems to have scared many evolutionary theorists into a haunting silence. The theorists are now figures in the shadows of their former vocal selves. Results from experiments on the model organism, C. elegans,  introduced a fear factor by refuting the theory of mutation-driven evolution. Mutations are not fixed in the genome, which means they can not be involved in natural selection. Haldane’s bastardization of Darwin’s theory was removed from further consideration by experiments that finally were designed and performed. (Isn’t biotechnology wonderful — if you’re not an evolutionary theorist, that is?)

Mutation-driven evolution never made any sense, anyway. Darwin’s ‘conditions of life’ clearly established the fact that organisms must eat, before they can develop into creatures that select for variations in other organisms.  Darwin made that clear even though he knew nothing about genetics.  Why did he feel he had to make it clear that all organisms must eat to evolve via reproduction? Could he somehow have predicted what other theorists might do with his theory? Perhaps Darwin was too polite to shout: “Hey, first they must eat; then reproduce!” Nevertheless, there should have been no need to tell anyone that ‘conditions of life’ are nutrient-dependent. We now know that ‘conditions of life’ are also pheromone-controlled because pheromones control reproduction.

Gidalevitz et al (2013) offer more evidence that refutes mutation-driven evolution by using what’s known about nutrient-dependent pheromone-controlled ‘conditions of life.’ They show that  “…natural variation shapes the susceptibility to proteotoxicity among genetically diverse but phenotypically normal individuals…” Their results from studies of genetic diversity and thermodynamically controlled protein folding on the same model organism, C. elegans, “…support the view that intrinsic aggregation propensity of the mutant disease-related proteins is not, by itself, sufficient to explain the disease onset and phenotypes.” Simply put, the thermodynamics of natural variation associated with organism-level thermoregulation is protective for some but not all individuals of the same species, which is why not all individuals of the same species have the same risk factors for diseases and their time of onset. Errors in protein folding and the onset of Alzheimer’s disease may not show up at all, but are clearly epigenetically effected by nutrient stress and social stress.

Of course, data from all experiments performed have continued to establish C. elegans as a potent model to study how nutrient-dependent pheromone-controlled natural variation in humans shapes the susceptibility to proteotoxicity among genetically diverse but phenotypically normal individuals.  The advantages of model organisms are clear in that context. We already know that nutrient-dependent pheromone-controlled rewiring of connectivity between C. elegans and P. Pacificus exemplifies how ecological, social, and neurogenic niche construction are involved in neuronal architecture that differentiates grazing behavior vs predatory behavior in these roundworms. The natural variation in their diet predictably results in differences in pheromone-controlled behavior.  The differences in behavior are predictable because the molecular mechanisms for nutrient-dependent pheromone-controlled adaptive evolution are conserved in species from microbes to man. That fact makes the concept of mutation-driven evolution seem foolish.  In mutations theory, nothing is unequivocally conserved, nothing is predictable, and mutations are not controlled by anything — except perhaps the natural genetic variation that enables adaptive evolution when mutations are not allowed to be permanently fixed in the DNA of any organized genome of any species on this planet.

If, as is clearly indicated, adaptive evolution is nutrient-dependent and pheromone-controlled, the fear factor is clearly the one that Lewis Thomas wrote about more than 40 years ago in “A Fear of Pheromones.”

 

 

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James Vaughn Kohl

James Vaughn Kohl

James Vaughn Kohl was the first to accurately conceptualize human pheromones, and began presenting his findings to the scientific community in 1992. He continues to present to, and publish for, diverse scientific and lay audiences, while constantly monitoring the scientific presses for new information that is relevant to the development of his initial and ongoing conceptualization of human pheromones.