From Hydra to humans vs a Lakatosian research program

By: James V. Kohl | Published on: December 25, 2014

Imre Lakatos

Excerpt: “A Lakatosian research programme[8] is based on a hard core of theoretical assumptions that cannot be abandoned or altered without abandoning the programme altogether. More modest and specific theories that are formulated in order to explain evidence that threatens the ‘hard core’ are termed auxiliary hypotheses. Auxiliary hypotheses are considered expendable by the adherents of the research programme—they may be altered or abandoned as empirical discoveries require in order to ‘protect’ the ‘hard core’. Whereas Popper was generally read as hostile toward such ad hoc theoretical amendments, Lakatos argued that they can be progressive, i.e. productive, when they enhance the programme’s explanatory and/or predictive power, and that they are at least permissible until some better system of theories is devised and the research programme is replaced entirely. The difference between a progressive and a degenerative research programme lies, for Lakatos, in whether the recent changes to its auxiliary hypotheses have achieved this greater explanatory/predictive power or whether they have been made simply out of the necessity of offering some response in the face of new and troublesome evidence.”
My comment: The so-called “Modern Synthesis” has no explanatory and/or predictive power. Recent changes have removed the hard core of theoretical assumptions, which once led to claims about random mutations that somehow were linked from natural selection to the evolution of increasing organismal complexity. New and troublesome evidence continues to attest to the need to remove neo-Darwinian theories from any further consideration whatsoever in the context of what is known about biologically-based cause and effect.
For example, “The origin of our body axes” is epigenetically linked via nutrient-dependent RNA-directed DNA methylation and RNA-mediated amino acid substitutions to cell type differentiation via pheromone-controlled fixation of the amino acid substitutions and development of our central nervous system in this report: “In search of the origin of our brain
Science idiots must now link mutations to morphological phenotypes and to behavioral phenotypes during the development of biodiversity. They must start with asexual hydra and continue across all other species to primates.
Obviously, this will only be attempted by the biologically uninformed who will probably proclaim that the evolution of organismal complexity “just happens.” That’s what science journalist, Carl Zimmer left us with in his July 16, 2013 report on The Surprising Origins of Evolutionary Complexity.” “Others maintain that as random mutations arise, complexity emerges as a side effect, even without natural selection to help it along. Complexity, they say, is not purely the result of millions of years of fine-tuning through natural selection—the process that Richard Dawkins famously dubbed “the blind watchmaker.” To some extent, it just happens.”
Serious scientists continue to incorporate ridiculous theories in their reporting of results that refute the pseudoscientific nonsense of population geneticists. See: Sequential actions of β-catenin and Bmp pattern the oral nerve net in Nematostella vectensis. They are forced to claim they don’t understand the involvement of RNA-binding proteins, amino acid substitutions, and thermodynamic cycles of protein biosynthesis and degradation that link metabolic networks via  RNA-mediated events to genes and the control of cell type differentiation.
Alternatively, maybe they don’t understand that Feedback loops link odor and pheromone signaling with reproduction via bio-physical constraints on the chemistry of protein folding and conserved molecular mechanisms of cell type differentiation in all cells of all organisms of all genera. Perhaps they should start with a literature review. For example: Signaling Crosstalk: Integrating Nutrient Availability and Sex
Excerpt:“The mechanism by which one signaling pathway regulates a second provides insight into how cells integrate multiple stimuli to produce a coordinated response.” It is that coordinated response that these researchers seem unable to explain even after they have linked the epigenetically-effected morphological and behavioral phenotypes of species from Hydra to humans.
My comment: This molecular epigenetics of this coordinated response were included in our 1996 Hormones and Behavior review. From Fertilization to Adult Sexual Behavior. Nothing known about cell type differentiation has changed since we wrote: “Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans (Adler and Hajduk, 1994; de Bono, Zarkower, and Hodgkin, 1995; Ge, Zuo, and Manley, 1991; Green, 1991; Parkhurst and Meneely, 1994; Wilkins, 1995; Wolfner, 1988). That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.”
My comments to the Scientific American site: 
7/17/13 Darwin’s ‘conditions of life’ are nutrient-dependent. Nutrients metabolize to species specific pheromones that control reproduction in species from microbes to man via the same molecular mechanisms.
The epigenetic effects of food odors associated with nutrition and pheromones associated with socialization and with sexual reproduction are clearly responsible for linking the sensory environment directly to adaptive evolution sans consideration of mutation-driven evolution.
See for details: Nutrient-dependent/pheromone-controlled adaptive evolution: a model. Socioaffective Neuroscience & Psychology 2013, 3: 20553
The model includes examples of how a change in a single base pair results in an amino acid substitution that clearly links adaptive evolution, which has occurred during the past ~30,000 years in a human population in what is now central China, to the same molecular mechanisms in mice, other mammals, insects, nematodes, and microbes.
4/19/14 Ecological variation in nutrient availability and epigenetically-effected methylation is clearly the driver of ecological adaptations manifested in species diversity. If this had not already become clear to serious scientists, methylation would not be reported in the context of ‘Reconstructing the DNA Methylation Maps of the Neandertal and the Denisovan‘ (Instead, methylation is substituted for mutations and linked to epigenetic cause and effect.)
If nutrient-dependent pheromone-controlled ecological adaptations were not clearly responsible for species diversity, serious scientists might still claim that mutations somehow caused it, as they have claimed until recently. See: ‘A functional test of Neandertal and modern human mitochondrial targeting sequences. However, as serious scientists realized that there is no such thing as a fixed beneficial mutation, only evolutionary theorists continue to make claims based on the pseudoscience of population genetics.
It is unfortunate that pseudoscientists have influenced the ridiculous beliefs of so many people, because most of them can no longer grasp the scientific truth that life is nutrient-dependent and that the physiology of reproduction is controlled by pheromones in species from microbes to man. However, the fact that scientists like Svante Paabo have finally recognized the role of methylation is a sign that the next generation will be the one that dismisses mutation-initiated natural selection and/or mutation-driven evolution from any further consideration whatsoever.
Thus, there is still hope for scientific progress to be made by those who are not stuck with their opinions, while others examine the facts. See, for example, “Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems.”

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