Jay R. Feierman began his antagonism when we first met. At a poster presentation during a prestigious conference in 1995, I detailed all the aspects of my mammalian model. He asked “What about birds?”
He is the”bird-watching” moderator of the International Society for Human Ethology (ISHE) yahoo group who banned me from participation last year when I failed to answer a “yes” or “no” question about the role of RNA in cell type differentiation. Since then, his attacks on my model have been more subtle. Now, he realizes others are about to link all my claims to healthy longevity or virus-driven pathology. But Feierman still wants others to focus on his neo-Darwinian nonsense. For example, he posted this to the (ISHE) yahoo group earlier today.
1) Understanding how exactly the brain processes salience is a fundamental step to advance current associative learning theories. Verifiable predictive models could become crucial to understanding aberrant salience acquisition in stressful situations and pathological states like schizophrenia, obsessive-compulsive disorder, and addiction.
2) We adapted a mathematical model in order to predict the choice records from nine groups of mice trained with heterogeneous visual stimuli (Treviño et al., 2013).
3) The exact definitions for effective and acquired saliencies were relatively unimportant to us because there are multiple other ways in which they could be formulated.
My comment: Epigenetic effects on gene activation are not linked to affects on behavior by definitions or by mathematical models. They must be linked from energy-dependent hydrogen-atom transfer in DNA base pairs in solution to biophysically constrained cell type differentiation in the context of the RNA-mediated immune system and behavioral development during life history transitions.
The requirement for RNA-mediated effects, which are linked to affects on behavior is nutrient energy-dependent. The energy links the innate RNA-mediated immune system from epigenetic effects on hydrogen-atom transfer in DNA base pairs in solutions to affects on behavior via what is known about how supercoiled DNA is biophysically constrained by the chemistry of RNA-mediated protein folding.
Supercoiled DNA protects all organized genomes from virus-driven entropy. All associative learning in all contexts links chemotaxis from phototaxis to behavior via acquired salience that only arises in the context of the innate immune system.
Feierman’s nonsense will continue to cause more confusion until someone stops him. His claims are the claims of a fool who does not want to acknowledge what is well-known to others about RNA-mediated events that link ecological variation to ecological adaptations in all living genera via their physiology of reproduction.
Instead, he claims:
On 11/1/12: “Random mutations are the substrates upon which directional natural selection acts.”
On 2/16/13 : “Random gene mutation is the variance generator upon which natural selection operates.”
On 2/23/13: “…random genetic mutations generate the substrate upon which natural selection can act. Random genetic mutations create structural variations in protein enzymes…”
My comment: What is the basis for the pseudoscientific nonsense that Jay R. Feierman and others like him have been touting for many years?
On 6/14/13 I published: Nutrient-dependent/pheromone-controlled adaptive evolution: a model
On 6/14/13 Masatoshi Nei published: Mutation-Driven Evolution
…the largest contributor to the development of our personal preferences may be the unconscious epigenetic effects of food odors and pheromones on hormones that organize and activate behavior. If so, the model represented here is consistent with what is known about the epigenetic effects of ecologically important nutrients and pheromones on the adaptively evolved behavior of species from microbes to man. Minimally, this model can be compared to any other factual representations of epigenesis and epistasis for determination of the best scientific ‘fit’.
… 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 comment: You need only compare my conclusion to Nei’s textbook conclusions to determine whose model of adaptation is correct. If you try to put my model of ecological adaptation into neo-Darwinian nonsense, you end up looking as foolish as Feierman.
I wrote: Natural selection : “If you have variation, differential reproduction, and heredity, you will have evolution by natural selection as an outcome. It is as simple as that.” The variation is nutrient availability and nutrients metabolize to species-specific pheromones that control reproduction and heredity. Evolution by natural selection cannot be the outcome if something is not first selected. Selection is always for nutrients. It is as simple as that.
“It is very sad for me to see that when several different people on this group, all with doctorate degrees, tell you that you are not correct, you don’t consider that they might be telling you something helpful. Instead, you respond with arrogance and ignorance. I’ll add my voice to the other people on this group who have told you that you are not correct in terms of your understanding of what “variation” means in Darwinian biological evolution and what is doing the selecting. Variation is not nutrient availability and the something that is doing the selecting is not the individual organism. A feature of an educated person is to realize what they do not know. Sadly, you don’t know that you have an incorrect understanding Darwinian biological evolution. I think all of us are trying to be helpful to you. However, our efforts are in vain if you continue with arrogance and ignorance of this topic. All of us have areas of expertise. We have the potential to learn from one another. I’ve learned lots of very useful things from other members on this group. Any educated person should welcome constructive criticism. You are not an expert in everything. So, my advice is to listen and be open when other people are trying to be helpful to you and to help you correct some of what you are writing that is incorrect.”
My comment: Feierman is a retired physician who touts nothing but nonsense.
Religion and science are compatible, asserts psychiatrist Feierman (retired, U. of New Mexico; B.S., zoology) in introducing the new non-theological approach to the study of religion through neo- Darwinian disciplines including ethology (the biology of behavior), evolutionary psychology, and cognitive science.
“We are saying there is incontrovertible evidence that Alzheimer’s Disease has a dormant microbial component, and that this can be woken up by iron dysregulation. Removing this iron will slow down or prevent cognitive degeneration – we can’t keep ignoring all of the evidence,” Professor Douglas Kell said.
See also: Alzheimer’s, microRNAs, and olfaction
Excerpt: A Blood Test for Alzheimer’s? Circulating microRNAs could help doctors diagnose the neurodegenerative disease. By Jef Akst | July 30, 2013
My comment to The Scientist on this article:
In my model, the microRNA/messenger RNA balance is nutrient-dependent and pheromone-controlled. The epigenetic landscape becomes the physical landscape of DNA via the thermodynamics of intercellular signaling and intranuclear interactions. The result is nutrient-stress driven and social stress-driven alternative splicings that may initially benefit organism-level thermoregulation via creation of de novo olfactory receptor genes.
Increasing the number of olfactory receptor genes enables increased nutrient uptake. However, ongoing nutrient stress and/or social stress alter genetic predispositions for Alzheimer’s and other neurodegenerative diseases that until now have manifested themselves first in reduced olfactory acuity. This suggests to me that the role of the microRNAs might best be assessed in concert with smell testing to arrive more quickly at differential diagnoses in the future.
See also: Pheromones and the luteinizing hormone for inducing proliferation of neural stem cells and neurogenesis (2011)
My comment: Further delays in linking virus-driven energy theft to all pathology via microRNAs and olfaction will be caused by the failure to link nutritional epigenetics to treatments with pheromones that may prevent or lessen the severity of neurodegenerative diseases. If someone you love is suffering now from Alzheimer’s, thank someone like Jay R. Feierman or stop them from contributing to suffering by forcing them to explain their ridiculous ideas about how mutation-driven pathology can be linked to evolution in the context of anything known to serious scientists.
See also: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems
Nutrient-dependent epigenetic effects of vitamins appear to work in combinations with ions at the atomic level in ways that have not been fully considered in the context of ecological variables, nutrient metabolism and ecological adaptations. For example, phosphate is also important in ecological terms. In the context of systems biology, it is often a limiting nutrient in environments and its availability may govern the growth rate of organisms (Thomas et al., 2014). Furthermore, a recent report suggested that metabolites of phospholipids, which are present in cell membranes, may soon link clinical assays to early diagnosis and treatment of Alzheimer’s disease (Mapstone et al., 2014).