A radical new holistic view of health based on cooperation and disease based on competition September 16, 2013
Excerpt: “Their unique approach is backed by experimental evidence.”
My comment: Multicellular organisms tend to cooperate in the context of nutrient acquisition but are less likely to cooperate in the context of sexual reproduction via mate acquisition. They seem to know the difference between cooperating in the context of one of two ‘conditions of life’ (i.e., nutrient acquisition) and competing in the context of the other condition of life (i.e., reproduction). These ‘conditions of life’ are drawn from Darwin’s works.
The simple explanation for the difference between cooperating and competing is self vs non-self recognition (via immune system function).
After the experiment that refuted mutation-driven evolution (e.g., in nematodes) was reported, how could it not become perfectly clear that nutrient-dependent species-specific sexually-dimorphic signals of fitness called pheromones cause adaptive evolution and its manifestation in complexity? Why is it not yet clear that olfactory/pheromonal input is the driving force behind adaptive evolution?
What did everyone else think enabled the epigenetic landscape to to become the physical landscape of DNA in the organized genomes of species from microbes to man? Did anyone consider the need for fixation of new alleles, or did most people think it just automagically happened? No, not everyone thought that, and not everyone failed to consider the need for fixation. See, for example: Safeguards for Cell Cooperation in Mouse Embryogenesis Shown by Genome-Wide Cheater Screen [subscription required
Article excerpt: “…the identification of olfactory receptors by our screen is not surprising, as the ability to cooperate with other cells must entail the ability to sense subtle changes in the microenvironment (indeed, chemotaxis proved to be an important component of the cooperative gene network in our analysis); this result is also in line with the so-called area-code hypothesis (27, 28).”
My comment: In my model, the de novo creation of olfactory receptor genes enables the epigenetic landscape to become the physical landscape of DNA via conserved nutrient-dependent pheromone-controlled molecular mechanisms. As exemplified in the honeybee model organism: “The recently detailed mouse model (Li et al., 2013) builds on what is known about olfactory/pheromonal communication in species from microbes to man and incorporates works from mammals that elucidate the molecular mechanisms that are clearly involved. Sex-dependent production of a mouse ‘chemosignal’ with incentive salience appears to have arisen de novo via coincident adaptive evolution that involves an obvious two-step synergy between commensal bacteria and a sex-dependent liver enzyme that metabolizes the nutrient chemical choline.”
Perhaps I should have simply said this means we are what we eat and the metabolism of what we eat to species-specific pheromones tells other organisms who and what we (and whether or not to eat us). The ability to communicate in this manner is due to experience-dependent de novo creation of olfactory receptor genes via conserved molecular mechanisms in all species. Experimental evidence is already available in the context of nutrient-dependent amino acid substitutions that cause species specific differences in pheromone production that control nutrient-dependent reproduction. Unfortunately, that wide body of experimental evidence has been virtually ignored.
