April 12, 2014 | James Kohl
Excerpt: “[The dietary intervention] is a general shift in what we’re feeding the cells to get them to do something different with their whole nutrient metabolism,” Friis noted. “There are signaling pathways that allow a cell to sense its environment and co-ordinate events to allow the cell to adapt to what’s going on. In this case, [cells are responding to] which nutrients are available.”
My comment: Dietary intervention (e.g., nutritional epigenetics) exemplifies what naturally occurs in the context of biophysically constrained ecological variations and natural selection for nutrient-dependent pheromone-controlled ecological adaptations. See : Signaling Crosstalk: Integrating Nutrient Availability and Sex. In yeasts, the “…Snf1-dependent pathway that senses limiting amounts of glucose acts on the mating pathway to reduce mating efficiency during times of nutrient stress. The mechanism by which one signaling pathway regulates a second provides insight into how cells integrate multiple stimuli to produce a coordinated response.”
Simply put, the coordinated response to nutrient stress (e.g., food availability) and social stress (e.g., the number of conspecifics requiring food) is controlled by the metabolism of nutrients (e.g., glucose) to species-specific pheromones that control the physiology of reproduction. See also: “The diverse social behaviors that are enabled by the functional flexibility of the secrete-and-sense circuits (Fig. 5C) may explain the frequent occurrence of this class of circuits in nature.”
Details of the systems biology that link nutrient stress and social stress from the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man have consistently been provided in the extant literature. However, the details have been placed into the context of evolutionary theory. Unfortunately, the misrepresentations of theory have been accepted despite the lack of experimental evidence that might otherwise have supported the claims made by evolutionary theorists. Thus, their unsupported claims have become popular — if only due to their simplicity.
We now know there are at least two ways that heritable variation can be generated by proteins, not DNA. Nutrient-dependent base pair flipping may result in spontaneous self-aggregating alternative splicings of pre-mRNA and alternative conformations of proteins that change a cell’s phenotype “… in an environmentally responsive manner with no change to DNA. The change is transmissible vertically, parent to offspring cell, as well as horizontally, to other cells in which the proteins come in contact. Another mechanism involves chaperones such as heat shock protein 90 (Hsp90), proteins that massage subideal (mutant) proteins into functional conformations but abandon their regular client proteins during heat and other stresses that destabilize proteins. This causes a stress-inducible release of phenotypic diversity, which may drive evolution (with phenotypes ultimately stabilized by subsequent genetic changes). Both of these molecular mechanisms of protein-based inheritance are major departures from the modern synthesis views of solely mutation-directed variation, solely genetic inheritance, and independence of the generation of variation from environmental conditions (Rosenberg & Queitsch, 2014, p. 1088).”
For contrast, the two ways that heritable variation can be generated by proteins involve the conserved molecular mechanisms of nutritional epigenetics, which means there is only one way to link biologically-based cause and effect to species diversity. For example, nutrient stress and social stress alter the seemingly futile thermodynamic cycles of protein biosynthesis and degradation. Epigenetic effects of olfactory/pheromonal input on heritable variation generated by proteins links biophysically-constrained conserved molecular mechanisms that enable ecological variations to result in ecological adaptations manifested in the stability of protein folding that is required for organism-level thermoregulation and species diversity. The ecological adaptations in protein-folding are manifested in species-specific morphological and behavioral phenotypes.
The idea that mutations could somehow result in morphological phenotypes, which were also somehow correlated with species-specific behavioral phenotypes, should be replaced with the facts of how food odors and pheromones epigenetically cause the species diversity that is manifested in ecological adaptations. Only the popularity of bastardized evolutionary theory can prevent accurate representations of cause and effect. However, now that the “…major departures from the modern synthesis views…” have been addressed by Rosenberg & Queitsch, 2014, others may be inclined to stop touting the pseudoscientific nonsense of evolutionary theory and begin to examine biological facts that have been established by experimental evidence in species from microbes to man.
Clearly, nutritional epigenetics and ecological adaptations make sense in the context of what is currently known about physics, chemistry, and molecular biology, which shows that nothing nothing about evolution makes sense. That explains why experimental evidence continues to support the detailed concept of “Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems” that dismisses current misrepresentations of evolutionary theory. Darwin’s theory can now be examined in the context of ‘conditions of life,’ which are nutrient-dependent and pheromone-controlled.
Note: All but one of the reviewers who were invited to review my invited submission refused to review “Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems.” The article on dietary intervention and two articles on on 1) and 2) link nutrient stress and social stress to ecological adaptations via conserved molecular mechanisms of protein folding. The only comment on my review was that it was not focused and self-aggrandizing.Read more
April 11, 2014 | James Kohl
Excerpted from the Society for Behavioral Neuroendocrinology Announcement 4/11/14
RP Michael, who was born in London in 1924, died peacefully in his sleep in Atlanta on January 5, 2014.
My comment: Dr. Michael was one of the first to recognize the likelihood that women produced pheromones, and he patented the idea in 1972. For example, as cited in Human Pheromones: Releasers or Primers Fact or Myth:
1) Michael, R.P. 1972. Fragrance blends based on the fatty acids and their employment in pharmaceutical products and in cosmetic products French patent # 2124399.
See also, in the article by George Preti and Charles Wysocki (2000):
2) Michael, R.P. & Keverne, E.B. 1970. Primate sex pheromones of vaginal origin. Nature, 218, 964-966.
3) Michael, R.P., Keverne, E.B. & Bonsall, R.W. 1971. Pheromones: Isolation of male sex attractants from a female primate. Science, 172, 964-966.
Now see: Are Human Pheromones Real?
“They don’t have any history in the biomedical literature—they just fell out of the sky,” says olfactory neuroscientist Charles Wysocki, also of Monell.
Wysocki has cited works that might well have been included in a recent report by other researchers at Monell. Detecting Fat Content of Food from a Distance: Olfactory-Based Fat Discrimination in Humans. “…this is not a learned ability or dependent on nutritional traits. The demonstration that humans have a functional olfactory system specific for detecting levels of fat content warrant further explorations into this mechanism given its potential to aid in a general reduction of our fat intake.”
Others might make the connection between our ability to detect fat in food odors and our ability to detect the metabolism of fat to fatty acids, which were initially referred to as copulins before they were offered as the first example of putative human pheromones. Clearly, there is a history in the biomedical literature that tentatively linked food odors and pheromones to sex differences in behavior. Unfortunately, RP Michael died before publication of the article that linked the human perception of food odors to theories of the human perception of pheromones based on his works. However, he did not live to see the comments of human pheromone-deniers, who successfully pushed his works aside for more than 40 years.
See also: Putative Human Pheromones Increase Women’s Observed Flirtatious Behaviors and Ratings of Attraction (2009). Abstracts book opens here: http://www.achems.org/files/public/2009ABSTRACTSFINAL.pdf Excerpt: “Mammalian conditioning paradigms suggest that androstenol conditions hormonal effects in women that are unconsciously associated with the potential behavioral affects of androsterone. We evaluated individual video-taped fifteen-minute interactions of fourteen ovulatory-phase women during a cooperative task. During the task, our male accomplice wore either a standardized androstenol / androsterone mixture diluted in propylene glycol, or just the diluent (i.e., propylene glycol). Sandalwood odor was added to the mixture and to the propylene glycol to keep our accomplice blind to his condition. Women were more likely to display flirtatious behaviors when our accomplice was wearing the mixture than when he wore the diluent (t(12) = 4.38, p <.01; IRR: r =.914, p = .01). Specifically, they were more likely to make eye contact with our accomplice (t(12) = 3.43, p = .01; IRR: r = .964, p = .01) and they laughed more during the interaction (t(12) = 5.20, p <.01; IRR: r = .810, p = .01). There was no significant effect of the mixture in the women’s rating of our accomplice as being more intelligent, more comfortable to be around, funnier, more “good-looking,” or in having our accomplice as a task partner again. However, when our accomplice was wearing the mixture, the women rated themselves as being more attracted to him (t(12) = 2.786, p = .016). Our results suggest that combining the known hormonal effects of androstenol (e.g., on luteinizing hormone) and the possible behavioral affects of androsterone extends non-human animal models of olfactory/pheromonal communication to humans. Our disclosed mixture may help to better characterize species-specific human pheromones.
Based on RP Michael’s works, it makes no sense for anyone to be the first to patent human pheromones. It would be akin to patenting food odors, which epigenetically effect the same neuronal systems of all mammals just like pheromones do. But it makes no sense for researchers to claim that human pheromones or that food odors “…don’t have any history in the biomedical literature—they just fell out of the sky…” Obviously, the history of olfactory/pheromonal input that epigenetically effects the hormones that affect behavior is well-established in the biomedical literature. The idea that human pheromones affect human behavior did not just fall out of the sky. It came from examples of cause and effect in many different species, just like the idea that food odors affect human behavior came from examples of cause and effect in many different species.
April 11, 2014 | James Kohl
Excerpt 1): ” …the “bird flu” virus has yet to evolve a means of spreading easily among people.”
Excerpt 2): “While the new study suggests the mutations needed are relatively few, it remains unclear whether they’re likely to happen outside the laboratory.”
My comment: Nutrient-dependent amino acid substitutions underlie change in the virulence of H1N1 . When the substitutions are reported in H5N1 as if they were mutations: ‘…we examine pairwise relationships between viruses and observe a correlation between amino acid mutations and antigenic distance…” biologically-based cause and effect is eliminated from any further consideration.
No mutations outside the lab occur, but laboratory researchers proceed to determine how to cause mutations. This leads to development of ineffective treatments with serious side effects.
This brings the ever-present role of evolutionary theory into the picture of molecular medicine, which requires that research proceed based on biological facts. If no mutations outside the lab occur, evolutionary theory should not be brought into the lab. Only wasted efforts from money better spent elsewhere will result from theoretical nonsense.
Excerpt: “It also claimed that the drug had a number of side-effects, including nausea, headaches, psychiatric events, kidney problems and hyperglycaemia.”
My comment: Amy Adamson and Hinissan Kohio showed that flu infection is linked to glucose metabolism in mammalian cells. That fact suggests that the side-effects of Tamiflu may be linked to altered glucose metabolism by the virus. Thus, nutritional epigenetics probably holds more promise than does evolutionary theory in the context of effective treatments with fewer reported instances of side effects.Read more
April 5, 2014 | James Kohl
Note: All linked articles are available for free.
Interactions with Combined Chemical Cues Inform Harvester Ant Foragers’ Decisions to Leave the Nest in Search of Food, was coauthored by DM Gordon (2013) who also wrote the recently published monograph The Ecology of Collective Behavior.
Excerpt 1 from Gordon (2014): “Similar patterns of interaction, such as network motifs and feedback loops, are used in many natural collective processes, probably because they have evolved independently under similar pressures. Here I consider how three environmental constraints may shape the evolution of collective behavior: the patchiness of resources [e.g., nutrients], the operating costs of maintaining the interaction network that produces collective behavior [e,g., metabolism], and the threat of rupture of the network [e.g., failure to reproduce]. The ants are a large and successful taxon that have evolved in very diverse environments. Examples from ants provide a starting point for examining more generally the fit between the particular pattern of interaction that regulates activity, and the environment in which it functions.”
My comment: In Kohl (2012), I wrote: “Insect species exemplify one starting point along an evolutionary continuum from microbes to humans that epigenetically links food odors and social odors to multisensory integration and behavior.”
Excerpt 2 from Gordon (2014): “Both theoretical and empirical work are needed to investigate this fit, and to move toward a general understanding of the evolution of collective behavior. An ecological perspective can bring together current work in the investigation of diverse complex systems.”
My comment: In Kohl (2013) I wrote: “Minimally, this model can be compared to any other factual representations of epigenesis and epistasis for determination of the best scientific ‘fit’.”
Although Gordon and I appear to be interested in detailing the ecology of collective behavior, she is still attempting to frame the ant model in the context of evolution of collective behavior. To her credit, however, the title of her most recent article correctly represents biologically-based cause and effect. Simply put, we both appear to know that ecological variation is manifested in ecological adaptations, which include adaptations in behavior. And we both appear to know that behavior does not evolve.
Anyone who is interested in linking ecology to collective behavior can quickly learn about the role that food odors and pheromones play in ecological adaptations of morphological and behavioral phenotypes. Moving forward from ants (Gordon’s model organism) or honeybees (my model organism) to humans, others can also learn why evolutionary theory is being dismissed as mere speculation in Neanderthal ancestry drives evolution of lipid catabolism in contemporary Europeans.
In the prestigious journal Nature Communications, these authors claim: “It is appealing to speculate that genetic variants affecting lipid catabolism in modern Europeans were acquired by modern human ancestors through genetic flow from Neanderthals, and then spread rapidly though the ancestral population by means of positive selection.” In the absence of experimental evidence, their speculation loses its appeal. Experimental evidence shows what happens when ecological factors are considered in the context of natural genetic engineering and species diversity. In the authors’s words, it becomes clear that “…genetic variants provided an adaptive advantage to both Neanderthal and human populations in the conditions of prehistoric Europe.”
All genetic variants are nutrient-dependent — even those that arise due to mutations. Similarly, species diversity is nutrient-dependent. No speculation is required, because diversity in populations is controlled by the metabolism of nutrients to species-specific pheromones in species from microbes to man.
Ants and honeybees are model organisms that attest to the facts of how ecological variation results in ecological adaptations via species-specific behaviors associated with ecological variation in nutrient availability. That is why the example of a nutrient-dependent single base pair change and single amino acid substitution in a modern human population, which supposedly arose in what is now central China during the past ~30K years, is such a powerful example of biologically-based cause and effect. It links the conserved molecular mechanisms of ecologically adapted nutrient-dependent pheromone-controlled insect behavior to ecologically adapted human behaviors via a mammalian model.
For example, the mouse model of ecological adaptations, which experimental evidence shows occur via the same amino acid substitution in humans, provides experimental evidence that differences in sweat, teeth, mammary tissue and hair can be linked to the pheromone-controlled physiology of reproduction. That experimental evidence links food odors and pheromones to the ecology of collective behavior in ants, other invertebrates (e.g., honeybees) and the conserved molecular mechanisms of species diversity in all other species from microbes to man.
Now that others are revealing what is known about nutrient-dependent biologically-based cause and effect in articles like Neanderthal ancestry drives evolution of lipid catabolism in contemporary Europeans, it won’t be long until they also admit that the link from ecological variation to human behavior exemplifies ecological adaptation not evolution. Lipid catabolism is obviously nutrient dependent. If lipids aren’t ingested they cannot be catabolized. The first step is to clearly admit to speculation about evolution. Next, others can begin to link what is known about ecological variation and ecological adaptation to nutrient-dependent pheromone-controlled adaptations. The speculation about evolution can then be eliminated from any further consideration whatsoever via experimental evidence of nutrient-dependent pheromone-controlled ecological adaptations. Clearly there is no evolution involved. Once everyone realizes that, serious scientists can begin to help others determine how long it take for ecological adaptations that result in species diversity to sweep through populations of organisms that once were thought to mutate and evolve into other species.
I suspect, but cannot prove, that the changes in the human population that arose in what is now central China took only 10,000 years at most. Indeed, one report indicated that 500 species of fish arose during 15,000 years, which suggests that evolutionary theorists may have other admissions to make about their speculations.
April 4, 2014 | James Kohl
The latest experimental evidence of biological facts was incorporated in Nutrient-dependent/pheromone-controlled adaptive evolution: a model. I think it was largely because of what the late Carl Sagan said about literacy and nutrition that participants on the Neuroanthropology Interest Group FB page have come to see problems with what Neil deGrasse Tyson is now claiming about evolution. For example, the common claim that ‘Evolution is well-established by evidence’ was something the new Cosmos covered in its second episode.”
What we were told was well-established by evidence is now accurately portrayed as appealing speculation.
1) Appealing speculation: “It is appealing to speculate that genetic variants affecting lipid catabolism in modern Europeans were acquired by modern human ancestors through genetic flow from Neanderthals, and then spread rapidly though the ancestral population by means of positive selection.”
The appealing speculation can now be compared to biological facts.
2) Biological facts: “…our results indicate that this massive developmental remodeling of the human cortex, which affects hundreds of genes, might be driven by expression changes of only a few key regulators, such as microRNAs.”
I asked: Does anyone think that positive selection for genetic variants affecting lipid catabolism is a biologically plausible explanation? In my model, for comparison, the variants arise due to ecological variation that results in ecological adaptations.
2) MicroRNA-Driven Developmental Remodeling in the Brain Distinguishes Humans from Other Primates take the claim that ‘evolution is well-established by evidence’ from being a questionable claim to being a blatant misrepresentation of biological facts.
Do biological facts make any difference in the context of what people believe? See for example:
The question arises, given these biological facts, why do people still believe that evolution is well-established by evidence? The only experimental evidence of biologically based cause and effect shows that species diversity results from ecological adaptations. For example, cancer (see #4 above) does not cause species diversity. But what difference does that fact make?
Tuesday, Sep 17, 2013 08:43 AM EST
Forget the dream that education, scientific evidence or reason can help people make good decisions
Marty Kaplan, Alternet
Excerpt: “The power of emotion over reason isn’t a bug in our human operating systems, it’s a feature.”Read more