Putting the theory before the data: Is “massive modularity” a necessary foundation of evolutionary psychology?

Excerpt 1) “Anyone who attends HBES, EHBEA, ISHE or any of the other conferences dedicated to the approach will discover that new fields of study are constantly being approached through the lens of evolutionary theory.”

Excerpt 2) “There is little to be gained by prematurely formalising the foundations of the field – putting the theory before the data – particularly if those foundations later turn out to be shaky.”

My comment: This report cites a presentation by John Richer made at the ISHE Summer Institute where I presented a poster.

Published Abstract: “Chemical ecology drives adaptive evolution via 1) ecological niche construction, 2) social niche construction, 3) neurogenic niche construction, and 4) socio-cognitive niche construction (Kohl, 2012). Nutrients are metabolized to pheromones that condition effects on hormones that affect behavior in the same way that food odors condition behavior associated with food preferences. For example: glucose (Roland and Moenter, 2011) and pheromones alter the secretion of gonadotropin releasing hormone (GnRH) and luteinizing hormone (LH). Across species comparisons of epigenetic effects on genetically predisposed nutrient-dependent and hormone-driven invertebrate and vertebrate social and sexual behavior indicate that human pheromones alter the development of the brain and behavior via the same molecular mechanisms (Krubitzer & Seelke, 2012), which are conserved across all species.”

See also the article by Burke (2014) and my comments at Why isn’t everyone an evolutionary psychologist?

Anyone who is now, or has ever considered becoming an evolutionary psychologist, can consider this fact in the context of how Ian Stephen presents it.

Excerpt 3) “While the sociological or cultural model is assumed to be true unless proven false beyond any possible doubt, the biological model is assumed to be false unless evidence is completely unassailable in their support.”

My comment: Nutrient-dependent/pheromone-controlled adaptive evolution: a model was published ~2 months before my ISHE presentation. The 5.5 minute video is here and the poster of Nutrient-dependent / Pheromone-controlled adaptive evolution: (a mammalian model of thermodynamics and organism-level thermoregulation) is here. From the description: This model refutes a book-length revision of a theory: ‘Mutation-driven evolution

That book was published on the same day as my journal article. The book concludes: “…genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world. In this view of evolution there is no need of considering teleological elements.” My article concludes: Minimally, this model can be compared to any other factual representations of epigenesis and epistasis for determination of the best scientific ‘fit’.

No serious scientist has compared my detailed model of RNA-mediated events and amino acid substitutions that lead from ecological variation to ecological adaptations manifested in all cell types of all individuals of all species to Nei’s theory about constraint-breaking mutation and biodiversity. The model has, however, been repeatedly attacked by evolutionary theorists. For example, see: Criticisms of the nutrient-dependent pheromone-controlled evolutionary model.

“James Kohl presents an unsupported challenge to modern evolutionary theory and misrepresentations of established scientific terms and others’ research. It was a mistake to let such a sloppy review through to be published.”

Clearly, Ian Stephen has correctly portrayed the problem common to theorists, especially among those who attend HBES, EHBEA, or ISHE conferences. Many of them attack details of biophysically-constrained biologically-based RNA-mediated events that link cause and effect to the morphological and behavioral phenotypes of all species via conserved molecular mechanisms. They claim that biologically-based evolutionary events, which have not been described, support their theories about mutations and natural selection, or whatever else they have been taught to believe links ecological variation to biodiversity in species from microbes to man.

When challenged to provide experimental evidence of biologically-based cause and effect, theorists tend to cite works published by researchers who already believe in the pseudoscientific nonsense touted by population geneticists in articles that link nutrient-dependent gene duplication to changes in morphology that theorists appear to think somehow evolved outside the constraints of the species-specific pheromone-controlled physiology of reproduction that enables population-wide fixation of the nutrient-dependent amino acid substitutions that differentiate all cell types in all species. For example: “…the so-called alpha chains of hemoglobin have identical sequences of amino acids in man and the chimpanzee, but they differ in a single amino acid (out of 141) in the gorilla.” (Dobzhansky, 1973)

See also: Combating Evolution to Fight Disease with my comments and RNA and dynamic nuclear organization with my comment.

Note: Publication of Nutrient-dependent/pheromone-controlled adaptive evolution: a model led to an editor’s request for my submission of a review on nutritional epigenetics. The invited review was rejected when reviewers refused to review it. When I submitted it to another journal, the editor rejected it because he did not want his journal to be involved in any controversy involving evolutionary theory. There’s no controversy, just facts — clearly represented in:

Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems

Abstract: This atoms to ecosystems model of ecological adaptations links nutrient-dependent epigenetic effects on base pairs and amino acid substitutions to pheromone-controlled changes in the microRNA / messenger RNA balance and chromosomal rearrangements. The nutrient-dependent pheromone-controlled changes are required for the thermodynamic regulation of intracellular signaling, which enables biophysically constrained nutrient-dependent protein folding; experience-dependent receptor-mediated behaviors, and organism-level thermoregulation in ever-changing ecological niches and social niches. Nutrient-dependent pheromone-controlled ecological, social, neurogenic and socio-cognitive niche construction are manifested in increasing organismal complexity in species from microbes to man. Species diversity is a biologically-based nutrient-dependent morphological fact and species-specific pheromones control the physiology of reproduction. The reciprocal relationships of species-typical nutrient-dependent morphological and behavioral diversity are enabled by pheromone-controlled reproduction. Ecological variations and biophysically constrained natural selection of nutrients cause the behaviors that enable ecological adaptations. Species diversity is ecologically validated proof-of-concept. Ideas from population genetics, which exclude ecological factors, are integrated with an experimental evidence-based approach that establishes what is currently known. This is known: Olfactory/pheromonal input links food odors and social odors from the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man during their development.

 

 

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