Nutrient-dependent pheromone-controlled niche construction (1700 words)
August 20, 2013 | James Kohl
On 3/12/13, I wrote: Random mutations are NOT the necessary contributing cause of Darwinian natural selection. Two reports attempt to convey that message: one on the head crest of pigeons, and another on beak morphology of finches. It is not a topic of debate in the scientific literature. Please attempt to support your opinions with data.
Natural selection is for nutrients. Nutrients metabolize to pheromones. Pheromones control reproduction. Adaptive evolution is nutrient-dependent and pheromone-controlled. Nutrient-dependent amino acid substitutions enable selection for phenotypic expression of social odors called pheromones in species from microbes to man.
“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.
If it is not that simple, someone needs to explain why they believe in a theory of mutation-driven evolution and detail how mutation-driven evolution occurs.
On 7/25/13, Jay R. Feierman wrote: 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.
ARROGANCE AND IGNORANCE?
When lab-grown organisms are fed the same food for many generations, their nutrient-dependent pheromone-controlled genetic diversity, which is naturally found in wild-type populations, is virtually eliminated. This fact is exemplified in a study that examined natural diversity in wild-type nematodes brought into the lab.
Researchers found that wild genotypes could be classified according to their food preferences and their collection site based on genotypic and transcriptome analyses. “The differences were also reflected in several fitness traits…” that incorporate differences in pH and osmotic pressure, as well as differences in chemical exposure, differences in temperature, and many other differences that probably influence genotypic and phenotype. Although the impact on fitness of most these differences cannot be assessed (e.g., in concert), in my model, the metabolism of nutrients to species-specific pheromones enables the selection of fitness traits that enable conspecifics to establish social niches in the ecological niches where they have found food.
Fitness assessment is made in the context of de novo creation of olfactory receptor genes, which enable ecological and social niche construction that leads to reproduction. In this context, olfactory/pheromonal input causes unicellular and multicellular organisms to respond to the presence of food odors, and it controls reproduction associated with successful nutrient acquisition.
Mutations are not involved in the ecological or the social niche construction that underlies species diversification via nutrient-dependent pheromone-controlled reproduction, which is why mutation-driven evolution must remain only a relatively simple theory. For example, in adaptive evolution via ecological and social niche construction in nematodes and in flies, the epigenetic effects of food odors and pheromones are also involved in neurogenic niche construction (Swarup et al., 2013; Bumbarger, Riebesell, Rödelsperger, & Sommer, 2013) — reviewed in Kohl (2013). Non-random niche construction may be a more difficult model to grasp than the simple theory of mutation-driven evolution. However, what is currently known about ecological, social, and neurogenic niche construction assures us that adaptive evolution requires nutrient-dependent pheromone-controlled ecological and social niche construction.
The requirement for controlled niche construction eliminates random mutations or any other type of “mutation” from any further consideration whatsoever in the context of evolutionary biology. Controlled niche construction should have eliminated the relatively simplistic concept of mutation-driven evolution from consideration long ago. Our adaptively evolved socio-cognitive niche construction should now enable us to think about how mutations might benefit species survival compared to the benefits of nutrient acquisition.
We should also be able to think about how mutations might be selected to enable species diversity like the selection of species-specific pheromones does. Unfortunately, many people were taught not to think of such things, and in the process of what they learned they were also taught to accept the theory of mutation-driven evolution — without question, as if it had any basis in biological facts. That’s why we now see that Physiology is rocking the foundations of evolutionary biology. It’s also why some people may wonder what took so long for evolutionary theorists to think about incorporating what’s known about the physiology of nutrient-dependent pheromone-controlled reproduction into what is known about evolutionary biology.
However, it is not only the evolutionary theorists who have taken too long to incorporate physiology into their opinions and their theories about the biology of behavior. Indeed, many human ethologists have also fallen prey to the same story-telling about mutation-driven evolution and natural selection by predation. Instead of it becoming easier to inform human ethologists, who are supposedly studying the biology of human behavior, it has become more difficult.
For example, despite our 2001 award-winning review article “Human Pheromones: “Integrating Neuroendocrinology and Ethology” by James V. Kohl*, Michaela Atzmueller, Bernhard Fink & Karl Grammer, the moderator of the International Society of Human Ethology’s yahoo group has refused to tether his opinions or any hypotheses about cause and effect to any biologically based discipline whatsoever. Indeed, on August 14, 2013, after the moderator, Jay R. Feierman posted a link to the article Stimulation of cell proliferation in the subventricular zone by synthetic murine pheromones, he refused to publish my comment on this excerpt from the article: “It might be that these pheromones stimulate the neural circuit that stimulates GnRH-expressing neurons (Boehm et al., 2005) in both females and males. The stimulation of GnRH neurons may, in females, increase the secretion of estrogen and induce them to come into estrus, and, in males, increase the secretion of testosterone, which promotes aggressive behaviors (Bronson and Desjardin, 1968; Davidson and Levine, 1972).”
In our review, we wrote: “…our discourse on affect, which includes the effect of human pheromones on hormones like GnRH, and thus on behavior, is the concept that affect is conditioned in the presence of other sensory input.” Indeed, we included the following statement: “It seems likely that odor-induced, GnRH-directed conditioning of human LH release may be used to evoke functional changes in the mammalian neuroendocrine pathways that mediate the release of T [testosterone] and E [estrogen], with or without visual awareness of any associated stimuli.”
The authors of Stimulation of cell proliferation in the subventricular zone by synthetic murine pheromones also wrote that “The ability of pheromones to act via sex horomones [sic] to promote cell proliferation/neurogenesis is an area that merits further investigation.” I was flabbergasted, since I had been investigating that for more than two decades, and incorporated that fact into my model when it was first presented at a scientific forum in1992 with the tentative title: Luteinizing hormone (LH): The Link Between Sex and the Sense of Smell? I later reported on the 2011 patent titled: Pheromones and the luteinizing hormone for inducing proliferation of neural stem cells and neurogenesis.
Tired of being ignored, I complained to the president of ISHE about Feierman’s suppression of accurate representations of cause and effect, but only after he commented that ISHE was HBES (the Human Behavioral and Evolution Society) “lite”. Feierman wrote: “… there is very little difference between the types of papers presented at HBES and ISHE. In many ways, ISHE is “HBES Lite,”…” In 2010, I presented “Human Pheromones: Linking Neuroendocrinology and Ethology (revisited)” at the ISHE annual meeting. I had abandoned all hope that members of HBES would ever include what is known about the biological basis of behavior in their stories about its evolution after a presentation on human pheromones I made in1999, which was accompanied by a poster session of my model, at their annual meeting. The president of ISHE responded to my complaint in the context of “Problems created by J. Kohl.”
What problems? Here’s a clue from the current president of ISHE: The beauty of our science is that we are gradually coming closer to the truth. The horror of science is that it consistently and very gradually comes closer to the truth only after propagating lies for many decades, including the past two decades after my first presentation on the link between sex and the sense of smell, and subsequent publication of our 1996 Hormones and Behavior review article From Fertilization to Adult Sexual Behavior in which we may have been the first to introduce information on molecular epigenetics in that context (e.g., of GnRH-modulated behavioral development).
“Yet another kind of epigenetic imprinting occurs in species as diverse as yeast, Drosophila, mice, and humans and is based upon small DNA-binding proteins called “chromo domain” proteins, e.g., polycomb. These proteins affect chromatin structure, often in telomeric regions, and thereby affect transcription and silencing of various genes (Saunders, Chue, Goebl, Craig, Clark, Powers, Eissenberg, Elgin, Rothfield, and Earnshaw, 1993; Singh, Miller, Pearce, Kothary, Burton, Paro, James, and Gaunt, 1991; Trofatter, Long, Murrell, Stotler, Gusella, and Buckler, 1995). 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.”
In the past 16 years, since publication of the review article quoted above, alternative splicings of otherwise identical genes have taken center stage in the context of explaining all behaviors required for species survival and for adaptive evolution. On August 14, 2013, comments from the ISHE yahoo group moderator changed from his oft-repeated regurgitation of scientifically unsupported opinion: “Random mutations are the substrates upon which directional natural selection acts.” The change was to to “mutations are A substrate upon which natural selection acts.” This change was in a response to a complaint about my “inane creationist views on evolution“. Neither the ‘Sonny’ Williams, who is my constant antagonist, nor anyone participating in the ISHE group’s discussions has provided any scientific evidence that refutes what I’ve been presenting and publishing during the past two decades. Instead, like Feierman, they tout random mutations theory and Williams has gone so far as to say that “One of the most egregiously incorrect statements that Mr. Kohl consistently repeats is that all life shares the same molecular processes. That is absurd.” Returning to the newest report on nutrient-dependent pheromone-controlled adaptive evolution in nematodes, I will add that Williams also wrote: In this regard, it is worth noting that experiments in C. elegans reveal that transgenerationally inherited epigenomes slowly but surely “disappear;” this is, more and more individuals in each generation revert to the original epigenome.
Can you guess who is even less informed about the biology of behavior than the moderator of the ISHE yahoo group? Are you more informed? If not, read A post-genomic view of behavioral development and adaptation to the environment by ISHE(2013) Summer Institute presenters Peter LaFreniere and Kevin MacDonald. Then scan Gene-environment and protein degradation signatures characterize genomic and phenotypic diversity in wild Caenorhabditis elegans populations. If, after reading those two published works or anything that I have published, you continue to think that mutations are substrates on which natural selection acts, you need never read anything from the current literature again. You will be stuck in the past, along with others who refuse to acknowledge that adaptive evolution is nutrient-dependent and pheromone-controlled in species from microbes to man.