November 4, 2012 | James Kohl
Society for the Scientific Study of Sexuality, Tampa, FL
Nov 8-11. Poster A-18 (Scheduled for presentation Nov 9)
Background:A detailed model explains how 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). That model is used to exemplify the effects of olfactory/pheromonal conditioning, which alters genetically predisposed, nutrient chemical -dependent, hormone-driven mammalian behavior and choices for pheromones that control reproduction via their effects on luteinizing hormone (Kohl, 1992).
Model: In this diagrammatic representation of the model [soon to be linked here], nutrient chemicals are metabolized to pheromones that condition behavior in precisely the same way that food odors condition behavior associated with food preferences. The epigenetic effects of olfactory/pheromonal input calibrate and standardize molecular mechanisms for genetically predisposed receptor-mediated changes in intracellular signaling and stochastic gene expression in gonadotropin releasing hormone (GnRH) neurosecretory neurons of brain tissue. For example: glucose (Roland & Moenter, 2011) and pheromones alter the secretion of GnRH and luteinizing hormone (LH). Parenthetically, a form of GnRH that is also linked to sexual orientation appears to control the feedback loops of developmental processes required for nutrient chemical ingestion, movement, reproduction, and the diversification of species from microbes to man.
Additional Considerations (not shown): The honeybee is an invertebrate model of adaptively evolved social behavior. 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. In the context of what has also been referred to as “biological embedding,” olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans. It is now clearer how an environmental drive evolved from that of nutrient chemical 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 such as LH, which has developmental affects on sexual behavior in nutrient chemical-dependent reproductively fit individuals across species of vertebrates.
This model of systems biology represents the conservation of bottom-up organization and top-down activation via:
1.Nutrient-dependent stress-induced and social stress-induced intracellular changes in the homeostatic balance of microRNA(miRNA) and messenger RNA (mRNA);
2.Intermolecular changes in DNA (genes);
3.Non-random experience-dependent stochastic variations in de novo gene expression for odor receptors;
4.The required gene-cell-tissue-organ-organ system pathway that links sensory input directly to gene activation in neurosecretory cells of the brain;
5.The required reciprocity that links gene expression to behavior that alters gene expression (i.e., from genes to behavior and back).
Conclusions: 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 also alter the development of the brain and behavior via the same molecular mechanisms. Those molecular mechanisms must be conserved across all species for adaptive evolution of the human brain and human behavior to occur (e.g., via properly timed reproductive sexual behavior of mammals). Note: In mammals, LH secretion is the measurable proxy for genetically predisposed differences in hypothalamic GnRH pulse frequency and amplitude and the downstream effects of GnRH on the HPG and HPA axes that provide feedback to the GnRH neuronal system, which is the central regulator of genetically predisposed nutrient chemical-dependent individual survival and pheromone-dependent species survival.
March 7, 2011 | jim
I have read this excellent book, but not yet had time to prepare a review because it arrived at the time I became extremely busy with other matters. For now, I can only again attest to the fact that:
Informed consumers who want to stay up-to-date may want to acquire the newly released 2nd edition of Rob van den Hurk’s book.
van den Hurk, R. (2011). Intraspecific chemical communication in vertebrates with special attention to sex pheromones. Zeist, The Netherlands, Pheromone Information Centre.
available for $45 or 35 euros (postage included)
paypal accepted through this account: email@example.com
August 11, 2014 | James Kohl
A short stretch of DNA is challenging what it means to be a species.
August 5, 2014
Excerpt: “Scientists have dubbed such regions of the genome “islands of speciation.” The persistence of such islands is a phenomenon that has been observed in a variety of organisms. Natural selection appears to put evolutionary pressure on these regions, which keeps both the genes and their corresponding traits distinct even in the face of interbreeding, while the rest of the genome can mix.”
My comment: Estrogen receptor α polymorphism in a species with alternative behavioral phenotypes details what appears to lie at the origin of species diversity in species from microbes to man in the context of these “islands of speciation.”
In their supporting information, the authors state: “The ZAL2 and ZAL2m alleles code for 597 amino acids, with two fixed differences driving a Val73Ile and Ala552Thr polymorphism in ZAL2m.” This links differences in parental feeding to nutrient-dependent pheromone-controlled amino acid substitutions that differentiate the cell types of all cells in all individuals of all species via conserved molecular mechanisms. Amino acid substitutions allow “islands of speciation” to emerge in the context of stabilized protein folding that is required for DNA to organize the genomes of what have consistently been referred to as different species.
For example, in the mouse-to-human model of cell type differentiation a valine to alanine substitution (similar to the one in the sparrows) differentiates the cell types of hair, teeth, sweat glands, and mammary tissue. See: Modeling Recent Human Evolution in Mice by Expression of a Selected EDAR Variant
However, when placed in to the context of chromosomal rearrangements in vertebrates, cause and effect is divorced from theories about mutation-initiated natural selection and the evolution of biodiversity. We can clearly see the differences between male mice and men, but we cannot see the similarities. Some evolutionary theorists hate to see such refutations of what they have offered as correlations based on observations and population genetics that this article politely states bastardized Darwin’s theory of evolution (with my emphasis below).
“Darwin, when he proved that species evolved, also proved there was no such thing as species,” said James Mallet….”
Population geneticists needed to show that species somehow evolved so they invented a theory of mutation-initiated natural selection and defined their terms before anyone realized that ecological variation leads to nutrient-dependent pheromone-controlled ecological adaptations via amino acid substitutions that link the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man.
The works on the white-throated sparrows have since exemplified cause and effect via the epigenetic effects of olfactory/pheromonal input on hormones that affect behavior in all vertebrates, such as crows, but also the invertebrates — like the butterflies mentioned here. Now, the theorists are scrambling to redefine their terms and refer to epigenetically-effected cell type differentiation in the context of epimutations, which are not fixed in the organized genomes, because no experimental evidence has shown that mutations are ever fixed in organized genomes.
If they ever were, there could be no such thing as the evolution of biodiversity because nutrient-dependent pheromone-controlled amino acid substitutions enable rapid changes to occur in organized genomes via chromosomal rearrangements. Mutations perturb the protein folding that’s required for the plasticity of changes that must accompany ecological changes manifested in chromosomal rearrangements, which makes mutation-driven evolution a ridiculously implausible theory. Fortunately, Israeli middle-schools now teach the theory of evolution in the context of what is known about ecological variation and how it leads to ecological adaptations manifested in the morphological and behavioral phenotype of species from microbes to man.
Indeed, there may be many researchers who were trained in Israel and do not believe in theories when it comes to what’s required for them to establish biologically-based cause and effect, which is experimental evidence of it, preferably in model organisms. See for example: Starvation-Induced Transgenerational Inheritance of Small RNAs in C. elegans. Clearly, what Darwin proved is that there is no such thing as a species in the context of fixation. At the same time, he showed that ‘conditions of life’ led to ecological adaptations, or to extinction.
Apparently, he knew from intuition and observations that organisms that do not eat do not mutate into other organisms; they starve to death. Surprisingly, evolutionary theorists may not have observed that, or do not think it is important enough to consider in the context of their stories.
August 11, 2014 | James Kohl
Scientists use the genome-editing technique to fix a disease-causing mutation in human cell lines.
August 5, 2014|
Excerpt 1): “β-thalassemia is caused by a mutation in the HBBgene, resulting in a severe hemoglobin deficiency.”
Excerpt 2): “One of the concerns with using CRISPR is that it has the potential to snip other, unintended sites in the genome.”
My comment: My concerns about using CRISPR are based on the likelihood that β-thalassemia results from nutrient-dependent amino acid substitutions that stabilize DNA in organized genomes. If so, using CRISPR will lead to genomic instability akin to using pharmaceuticals that alter protein folding and cell type differentiation that is nutrient-dependent and pheromone-controlled.
My comment to The Scientist appears below:
1) “The hemoglobinopathies, or Hb variants, are attributable to amino acid substitution(s) in either globin chain. Currently, 1,179 total hemoglobin variants have been characterized.2″
2)”Countries with the highest incidence of diabetes also tend to have high incidence of Hb variants in the population.14”
Correlations (don’t say it*) between amino acid substitutions that appear to differentiate the cell types of all cells in all individuals of all different species suggest the amino acid substitutions that differentiate cell types with hemoglobin variants and those that somehow contribute to diabetes also are nutrient-dependent.
However, the amino acid substitutions are not likely to become fixed in the absence of their effect on DNA stability in the organized genomes of species with circulatory systems that also produce pheromones, which control the physiology of reproduction in species from microbes to man.
For examples of other correlations in species with and without circulatory systems see: Nutrient-dependent/pheromone-controlled adaptive evolution: a model.
Is there a model of mutation-caused cell type differentiation via amino acid substitutions in species from yeasts to mammals? If not, my model may be the only model of biophysically-constrained biologically-based cause and effect that can be compared to correlations provided in the context of theories about how mutations and natural selection somehow led to the evolution of biodiversity.
* Don’t say that correlations are not causation unless you first attest to the fact that you have never thought in terms of Mutation-driven evolution without recognizing your unstated belief that correlations must be causation. If not, the theories about mutaitions are not biologically plausible theories.Read more
August 11, 2014 | James Kohl
Serbian government honored me by putting me on their 20 recently
In the context of nutritional epigenetics and “fitness,” small RNAs are clearly the drivers of ecological adaptations, which are globally manifested in affects on behavior associated with purchasing power.
Amir Siddiqui is an expert on fitness.
However, his size does not seem to matter in the context of biologically-based cause and effect linked from nutrition to epigenetic effects on hormones that affect behavior.
At the macroscopic level, appearances can be deceiving, even the appearance of faces on currency.
Amir Siddiqui is obviously big and healthy. But he may also know what others must remember. Nutrient-dependent microRNAs are the cause of everything, including our desire to eat more cheesecake (e.g., one of Amir’s favorites).
That fact was recently supported by experimental evidence reported as “The splicing modifiers reported here are orally bioavailable compounds that penetrate into all of the tissues we tested—including brain, spinal cord, and muscle—and consequently exert their action on SMN2 splicing in all cells of the body.” See:
Few others may understand what that means, but Amir exemplifies it. Across-species examples from model organisms are required. With examples they can see, others may better understand how the decisions we make about what to eat lead to nutrient-dependent changes in the microRNA/messenger RNA balance. Those changes lead from ecological variation to the amino acid substitutions that differentiate our cell types via the conserved molecular mechanisms that differentiate all the cell types of all individuals of all species from microbes to man.
Amir has a great sense of humor and his sense of humor is also an example of how people need not know anything about biophysical constraints and molecular mechanisms to understand what is obvious about nutritional epigenetics. We are what we eat!Read more