A Q&A on randomness and God’s providence
…the main goal is to really put together a collection of scholarly studies of these issues: physicists, biologists, mathematicians, statisticians, philosophers and theologians.
replaced: Randomness and Divine Providence
Supported by the John Templeton Foundation
Submission deadline: October 1, 2012
Excerpt 1) This initiative seeks proposals from scientists, philosophers, theologians, and interdisciplinary teams of scholars who are interested in exploring the relationship between randomness and divine providence.
Excerpt 2) Based on the letters of intent, some applicants will be invited to submit a full proposal which will explain the project in greater detail.
Accepted Project Submissions changed to promote “Mathematics & Statistics”
My submission (not accepted)
Nutrient chemicals are required to sustain life and for transgenerational epigenetic inheritance of biological populations. This fact is exemplified in the honeybee model organism and other model organisms. The nutrient chemicals cause receptor-mediated events. The receptor-mediated events allow nutrient chemicals to enter though the cell wall. Electrostatic changes then alter intracellular signaling as nutrient chemicals are metabolized to species-specific chemicals called pheromones.
The metabolism of nutrient chemicals to pheromones exemplifies the apparent design of biology. Bottom-up (genetically predisposed organization) and top-down reciprocity via sensory activation is what allows nutrient chemicals and pheromones to control survival of the species. The nutrient chemicals support individual fitness and the pheromones control reproduction. From the bottom up, their ability to control species survival is enabled by their epigenetic effects of nutrient chemicals that cause stochastic gene expression. Similarly, from the top down, pheromones epigenetically effect stochastic gene expression (in cells of organisms from microbes to man).
All extant organisms show a clear pattern of genetic predispositions that enable nutrient chemical-dependent and pheromone-dependent adaptive evolution via ecological, social, neurogenic, and socio-cognitive niche construction. Adaptive evolution is facilitated via the expression of new genes, including those that are important to the development of language abilities and human brain development.
The ability of cells containing genes to produce de novo genes does not seem to have developed via random mutations. Although gene expression is stochastic, organisms that choose the wrong nutrient chemicals are less reproductively fit and doomed to suffer and die. One organisms choice also may determine downstream down-stream epigenetic effects on other organisms that selfishly compete for life-sustaining nutrient chemicals in same ecological niche. Only when some level of cooperation is achieved can individuals or species survive in the same ecological niche, and species-specific pheromones ensure that two species do not share the same social niche.
Ecological and social niche construction collectively enabled evolved nutrient-dependent and pheromone-dependent neurogenic niche construction, which is exemplified in vertebrates by conservation of the GnRH molecule, and diversification of its receptor across 400 million years of adaptive evolution that first required nutrient-dependent and pheromone-dependent sexual reproduction in unicellular and multicellular organisms, with molecular origins as the alpha-mating pheromone in brewer’s/baker’s yeast.
The ecological and social niches constructed by one species that eats another exemplify how that advent of multicellularity and cooperation in different species enabled the cascade of diversity that is readily evidenced across Creation, as it always has been. When viewed from a model of complexity, Creation of the diversity of life does not appear to involve random events, but instead involves the common molecular biology of receptor-mediated events is species from microbes to man.
The concept that is extended is the epigenetic tweaking of immense gene networks in ‘superorganisms’ that ‘solve problems through the exchange and the selective cancellation and modification of signals. It is now clearer how an environmental drive probably evolved from that of food ingestion in unicellular organisms to that of socialization in insects. It is also clear that, in mammals, food odors and pheromones cause changes in hormones that have developmental affects on sexual behavior in nutrient-dependent, reproductively fit individuals across species of vertebrates.
Thus, simply put: “Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans.” And there is nothing random about that!
My comment: I should have known better than to submit a proposal to explain non-randomness to a group of theologians who clearly intended to keep trying to support neo-Darwnian evolution. I suspected they simply did not know that their was nothing random about creation. Since then, Eugene Koonin has admitted that:
It will be interesting to see how much progress is made by theistic evolutionists who do not understand the fact that Koonin just changed everything that has ever been claimed by theorists. Until further experimental evidence of biologically-based cause and effect includes the role of viruses, the link from viral microRNAs and entropic elasticity to genomic entropy may still be placed before the anti-entropic epigenetic effect of the sun’s biological energy on cell type differentiation of all cells in all individuals of all living genera via their physiology of reproduction. The physiology of reproduction links ecological variation to ecological adaptation via the conserved molecular mechanisms of RNA-mediated gene duplication and RNA-mediated amino acid substitutions that link metabolic networks to the stability of genetic networks in organized genomes.
Koonin admits that the new understanding of evolution must include something that happened “..before the emergence of cells.” How much longer do you think it will be until the Templeton Foundation begins funding research that links virus-perturbed protein folding to pathology after the creation of the first cell? I think the distribution of funding should have changed in 2005, when senior author Koonin claimed:
Excerpt:
Does anyone else not agree that creation must have preceded the emergence of the last universal common ancestor of all extant organisms and that is precisely what Dobzhansky (1973) implied when he wrote:
If you agree that this attests to the fact that the creation of different species did not randomly occur, you may not be funded by the Templeton Foundation. However, if you can provide experimental evidence to support your claims about Randomness and Divine Providence, your 7-figure prize awaits.
See: Evolution 2.0: Breaking the Deadlock Between Darwin and Design
Before your attempt to win the prize, however, you might wish to see “The Darwin Code: Intelligent Design without God.” Greg Bear is another non-biologist who, like Perry Marshall, included the role that viruses play in the creation of new species beginning with his 1985 book publication of “Blood Music.”
Dr. Kwang Jeon wrote:
It is amazing that Perry Marshall, a non-biologist marketing expert, can make anyone else think that he knows what is known to serious scientists about energy-dependent biophysically constrained pheromone-controlled RNA-mediated cell type differentiation.
See for comparison RNA-mediated.com
See also:
