The death of human ethology via ecology

By: James V. Kohl | Published on: May 3, 2017

Nutrient-dependent/pheromone-controlled adaptive evolution: a model Open access publication on June 14, 2013
Mutation-driven evolution also published on June 14, 2013
Variable habitat conditions drive species covariation in the human microbiota Open access publication on April 27, 2017

…we found that genetically related species respond to fluctuating habitat conditions in the same way, implying that they occupy similar ecological niches. Thus, current taxonomic groupings of bacteria are largely sufficient for explaining cross-sectional correlations in relative species abundances over the healthy human population. This result is not at odds with high rates of HGT; it simply implies ecologically derived constraints on evolution.

Reported on April 27, 2017 as: Resource availability drives person-to-person variations in microbes living in the body

Ecological model reveals relationships between resource availability and microbe species abundance

Historical perspective: “What is Life?” (1944)

Indeed, in the case of higher animals we know the kind of orderliness they feed upon well enough, viz. the extremely well-ordered state of matter in more or less complicated organic compounds, which serve them as foodstuffs. After utilizing it they return it in a very much degraded form -not entirely degraded, however, for plants can still make use of it. (These, of course, have their most power supply of ‘negative entropy’ the sunlight.) (pp. 73 and 74)

From the forward to the reprint edition of “What is Life?” (1944)

How often do we still hear that quantum effects can have little relevance in the study of biology, or even that we eat food in order to gain energy? — Roger Penrose August 8, 1991

All current extant literature attests only to the obvious role of ecological variation and food energy as information, which enables the ecological adaptations manifested in species diversity via the physiology of biophysically constrained pheromone-controlled reproduction. Nutrient energy-dependent changes in the microRNA/messenger RNA balance protect supercoiled DNA from virus-driven energy theft and the degradation of messenger RNA, which links mutations to all pathology. All serious scientists are now aware of these facts, but pseudoscientists are not convinced.
See for example:
7/24/13 James V. Kohl: “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.
Despite the facts expressed by Schrodinger and emphasized by Penrose as well as my claim (above), neo-Darwinian theorists still seem willing to accept the claims of biologically uninformed science idiots, such as this one:
Jay R. Feierman: 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 [of] Darwinian biological evolution.
Jay R. Feierman: I am absolutely certain that if you showed this statement to any professor of biology or genetics in any accredited university anywhere in the world that 100% of them would say that “Random mutations are the substrate upon which directional natural selection acts” is a correct and true statement.
See for comparison:
Foote et al (2013)“Ecological variation is the raw material by which natural selection can drive evolutionary divergence [1–4].
Chung et al (2014) “…ecological divergence and mate choice may produce reproductive isolation and speciation….
Plucain  et al (2014) “Ecological opportunities promote population divergence into coexisting lineages.
The pseudoscientific nonsense touted on this Yahoo group has not ended.

Human ethology is the study of the biology of human behavior, including the behavior’s phylogeny (evolutionary history), ontogeny (development), proximate causes, and adaptiveness (survival value). Postings relevant to these topics will be accepted.

Sonny Williams wrote:
Re: For the sake of all humanity, please ignore the shrill, uninformed cries of creationists and other types of supernaturalists.  Instead, talk to a regulatory geneticist.
I responded with a comment about the game: Cytosis: A Cell Biology Board Game

See: msg 86257

James Gray: Jay, I hope you can say that you missed the threat in this quote from Kohl. “What game will you be playing until your career as a researcher or philosopher or your life as as biologically uninformed atheist ends at the hands of those who are biologically informed young earth creationists?”

I know only two people who would take my comment about the game Cytosis, and perceive it as a threat that they would be killed by young earth creationists. James Gray is one; here is the other one:

Sonny Williams: Thanks for catching this, James…and warning me.  I consider Kohl a personal threat and think it is time he be banned from the group.

So far as I know, I am the only participant in the group that has published an award-winning review of human ethology.
See: Human pheromones: integrating neuroendocrinology and ethology (2001)
See also: msg 86274

Excerpt: “Scientific advisers to President Obama warn that the U.S. urgently needs a new biodefense strategy and should regularly brief President-elect Donald Trump on the dangers posed by new technologies like CRISPR, gene therapy, and synthetic DNA, which they say could be coöpted by terrorists.”

It will be interesting to see whether or not Sonny Williams and/or James Gray will claim that I threatened they would be killed by terrorists.
In any case, the regulatory geneticist Giacomo Cavalli and others have finally brought forth their claims about Stable Polycomb-dependent transgenerational inheritance of chromatin states in Drosophila
The claims were reported as: We are more than our DNA: Discovering a new mechanism of epigenetic inheritance

Cavalli and his team at the Institute of Human Genetics (University of Montpellier / CNRS) are the first to show that regulation of gene position can lead to transgenerational inheritance.

See for comparison: From Fertilization to Adult Sexual Behavior (1996)

Molecular distance. As measured in centimorgans, human and other species’ male and female chromosomes, including the autosomes, tend to have different lengths in various segments. To some extent, this suggests a correlation with physical distance but instead the differing lengths are based upon rates of recombination; although sections of most female chromosomes are longer than their homologous counterparts in male chromosomes, in some segments of various chromosomes opposite length-difference occurs, with males having larger centimorgan values than females in those regions (Lawrence, Collins, Keats, Hulten, and Morton, 1993; Murray, Buetow, Weber, Ludwigsen, Scherpbier-Heddema, Manion, Quillen, Sheffield, Sunden, and Duyk, 1994; Straub, Speer, Luo, Rojas, Overhauser, Ott, and Gilliam, 1993). While ramifications of these centimorgan sexual dimorphisms are not yet clearly established, in recent years cis- and trans-acting factors contributing to these recombination length differences have been reported for a specific part of the murine major histocompatibility complex (MHC) (Shiroishi, Sagai, Hanzawa, Gotoh, and Moriwaki, 1991).

See also:

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.

Anyone who claims they are the first to link the nutrient energy-dependent stability of polycombiic ecological adaptation via the transgenerational inheritance of chromatin states should be viewed with suspicion. Chromosomal inheritance was first linked to the transgenerational epigenetic inheritance of chromatin states by Thomas Hunt Morgan, who won the 1933 Nobel Prize in Physiology or Medicine for his works.
With all due respect Giacomo Cavalli may have come in third with publication in 2007 of  Combinatorial epigenetics, “junk DNA”, and the evolution of complex organisms.

The imposition at a distance of new chromatin structures with regulatory impact can occur in cis as well as in trans, and is examined as intrachromosomally spreading teleregulation and interchromosomal “gene kissing”. The chances for two or more particular epigenetically determined regulatory trends to occur together in a cell are increased thanks to the proposed low specificity requirements for most of the pertinent sequence changes in intergenic and intronic DNA or in the distribution of middle repetitive sequences that have teleregulatory impact. Inheritable epigenetic changes (“epimutations”) with effects at a distance would then perdure over the number of generations required for “assimilation” of the several regulatory novelties through the occurrence and selection, gene by gene, of specific classical mutations. These mutations would have effects similar to the epigenetic effects, yet would provide stability and penetrance. The described epigenetic/genetic partnership may well at times have opened the way toward certain complex new functions. Thus, the presence of “junk DNA”, through co-determining the (higher or lower) order and the variants of chromatin structure with regulatory effects at a distance, might make an important contribution to the evolution of complex organisms.

I mayt never know if Giacomo Cavalli come in third with representations of intrachromosomally spreading teleregulation and interchromosomal “gene kissing” It is hard to evaluate his works, since he placed his finding into the context of epimutations and evolution via “junk DNA.”
For comparison, young earth creationists have been addressing the nonsense about “junk DNA” during the past two months.
See for instance: Major Evolutionary Blunders: Evolutionists Strike Out with Imaginary Junk DNA, Part 1

Scientists whose analysis is constrained to fit evolutionary theory will not see a brain, a digestive system, and other complicated biological phenomena as designed things but rather as conglomerations of parts cobbled together by nature. “We’re all here because of mutations,” claims molecular neuroscience professor Jernej Ule, who adds:

But most random mutations actually disrupt the functions of our genes and so are a common source of genetic diseases….How does nature resolve this conflict?…We’ve known for decades that evolution needs to tinker with genetic elements so they can accumulate mutations while minimising [sic] disruption to the fitness of a species.4

See also: Major Evolutionary Blunders: Evolutionists Strike Out with Imaginary Junk DNA, Part 2

I think this will come to be a classic story of orthodoxy derailing objective analysis of the facts, in this case for a quarter of a century….The failure to recognize the full implications of this [important parallel information derived from non-coding DNA] may well go down as one of the biggest mistakes in the history of molecular biology

For more information on parallel information, which appears to be linked to non-coding DNA see: A universal trend of amino acid gain and loss in protein evolution

We cannot conceive of a global external factor that could cause, during this time, parallel evolution of amino acid compositions of proteins in 15 diverse taxa that represent all three domains of life and span a wide range of lifestyles and environments. Thus, currently, the most plausible hypothesis is that we are observing a universal, intrinsic trend that emerged before the last universal common ancestor of all extant organisms.

See also: The death of human ethology via ecology (2)

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