Science vs nonsense (and scholarship): Comments approved 9/16/13 to 9/20/13

Addendum 9/27/13: Jay R. Feierman Moderator Yahoo Human-Ethology Group 9/26/13 wrote: “since James Kohl has not been posting on this group, I’ve not had to reject any submissions in almost a month.

My comment: Feierman was blocking nearly all my submissions, with the apparent approval of Wulf, and other ISHE members. I decided to contribute to discussions of science.  So far as I know, none of my submissions to “Science Magazine” have ever been blocked. All of the following submissions were approved within minutes of each other, despite the timing of the submissions.


In attempts to keep others abreast of integrative efforts to address science vs nonsense, I sometimes comment on articles in the top-tier journal “Science Magazine.”  Last week 5 comments were accepted. It was a record week for new scientific information, and I have never before commented 5 times in one week. Since a subscription is required to read my comments, I have posted them here. I should probably take the time to write another inclusive article about epigenetic effects on hormone-organized and hormone-activated invertebrate and vertebrate behavior that eliminate the entirety of mutations theory. But with the evidence that refutes mutations theory appearing daily in the articles written by others, by the time I complete yet another article, I will have fallen behind with my comments.

1. Your comment Submitted on Mon, 09/16/2013 – 16:40 on Safeguards for Cell Cooperation in Mouse Embryogenesis Shown by Genome-Wide Cheater Screen has been approved and is now live at,

Nei (author of Mutation-driven Evolution) said: (1) Mutation is the source of all genetic variation on which any form of evolution is dependent… (2) Natural selection is for saving advantageous mutations and eliminating harmful mutations. Selective advantage of the mutation is determined by the type of DNA change, and therefore natural selection is an evolutionary process initiated by mutation. It does not have any creative power in contrast to the statements made by some authors.” p 196.

I say that adaptive evolution is nutrient-dependent and pheromone-controlled via the de novo creation of olfactory receptor genes. Adaptive evolution is not exemplified in his representation of mutation-driven evolution because there is no de novo creation and no fixation of new alleles. There are only uncontrolled mutations, or those controlled from outside the realm of the physiology of reproduction, as if nutrient-dependent adaptive evolution could be controlled by predation instead of by the metabolism of the nutrients to species-specific pheromones that control reproduction in species from microbes to man.

2. Your [second] comment Submitted on Mon, 09/16/2013 – 18:56 on Safeguards for Cell Cooperation in Mouse Embryogenesis Shown by Genome-Wide Cheater Screen has been approved and is now live at,

Multicellular organisms “know” the difference between cooperating in the context of one of two ‘conditions of life’ (nutrient acquisition) and competing in the context of the other condition of life (reproduction). The simple explanation for their knowledge is self vs non-self recognition (via immune system function).

After the experiment that refuted mutation-driven evolution via fixation failure in nematodes was reported, it became clearer that nutrient-dependent species-specific sexually-dimorphic signals of fitness called pheromones cause adaptive evolution and its manifestation in flexible complexity. Simply put, olfactory/pheromonal input is the driving force behind adaptive evolution.

These authors also show they did not fail to consider the need for fixation.

Excerpt:“…the identification of olfactory receptors by our screen is not surprising, as the ability to cooperate with other cells must entail the ability to sense subtle changes in the microenvironment (indeed, chemotaxis proved to be an important component of the cooperative gene network in our analysis); this result is also in line with the so-called area-code hypothesis (27, 28).”

In my model, the de novo creation of olfactory receptor genes enables the epigenetic landscape to become the physical landscape of DNA via conserved nutrient-dependent pheromone-controlled molecular mechanisms. (The area code is assigned.) As is also exemplified in Drosophila and in the honeybee model organism: “The recently detailed mouse model (Li et al., 2013) builds on what is known about olfactory/pheromonal communication in species from microbes to man and incorporates works from mammals that elucidate the molecular mechanisms that are clearly involved.

Sex-dependent production of a mouse ‘chemosignal’ with incentive salience appears to have arisen de novo via coincident adaptive evolution that involves an obvious two-step synergy between commensal bacteria and a sex-dependent liver enzyme that metabolizes the nutrient chemical choline.”

I could simply say this means we are what we eat and the metabolism of what we eat to species-specific pheromones tells other organisms who and what we are. The ability to communicate in this manner is due to experience-dependent de novo creation of olfactory receptor genes via conserved molecular mechanisms in all species.

Experimental evidence is already available in the context of amino acid substitutions that cause variable pheromone production

3. Your comment Submitted on Fri, 09/20/2013 – 09:12 on Growing Pains has been approved and is now live at,

It seems to me that nutrient stress and social stress epigenetically effect the regulation of gonadotropin releasing hormone (GnRH) pulse frequency, which integrates all sensory input from the environment via the hypothalamic-pituitary-gonadal-adrenal (HPGA) axis. The epigenetic effect of glucose uptake could thus be linked to height, and the epigenetic effect of too much glucose could thus be linked to diabetes via the same model of nutrient-dependent pheromone-controlled adaptive evolution in which nutrient stress and social stress are not associated with adaptations but are associated with diseases and disorders.

4. Your comment Submitted on Fri, 09/20/2013 – 09:44 on Be Honest has been approved and is now live at,

Honest signals, which provide feedback between a signal, its bearer, and recipients are nutrient-dependent in species from microbes to man. Reproduction is pheromone-controlled. This means the honest signals are not
visual signals except via the association of visually ‘perceived’ phenotype with the epigenetic effects of nutrients and pheromones on hormone-organized and hormone-activated adaptive evolution in vertebrates and invertebrates that keep the signal, and the signaler, honest (via feedback loops).

The honeybee is the model organism that exemplifies invertebrate nutrient-dependent pheromone-controlled hormone-organized and hormone-activated adaptive evolution. Non-visual signal-dependent cause and effect in vertebrates like mammals occurs via nutrient-dependent amino acid substitutions that exemplify how the epigenetic landscape becomes the physical landscape of DNA in the organized genomes of all species via alternative splicings.

Confusion about the role of plumage color and honest signals in birds has been reduced by a recent report in “Animal Behavior” by Danielle Whittaker’s group. The title is “Bird odour predicts reproductive success.”

5. Your comment Submitted on Fri, 09/20/2013 – 18:36 on When Prior Belief Trumps Scholarship has been approved and is now live at,

Excerpt: “As Meyer points out, he is not a biologist; so perhaps he could be excused for basing his scientific arguments on an outdated understanding of morphogenesis.”

Until a week ago, when the results of an experiment that might have provided proof of mutation-driven evolution, but didn’t, morphogenesis seemed to be understood largely in terms of mutations theory. See, “An experimental test on the probability of extinction of new genetic variants.”

How will evolutionary theorists explain morphogenesis this week? Mutations are not fixed in the genome of nematodes, and no other experiments have ever been done to show that mutations are fixed in the DNA of an organized genome in any species.

That might not be a big problem for those who continue to believe in evolution, but without its mutation-driven characterization in the context of morphogenesis, the reality of adaptive evolution becomes clearer.

It is nutrient-dependent, of course. But the nutrients metabolize to species-specific pheromones that control reproduction, which eliminates mutations theory in its entirety. Adaptive evolution is nutrient-dependent and the molecular mechanisms of reproduction are pheromone-controlled in species from microbes to man.

Can anyone be excused for not realizing that? Even Darwin noted that ‘conditions of life’ must be considered before natural selection can be. ‘Conditions of life’ appear to have always been nutrient-dependent and pheromone-controlled, but no scientific evidence suggests any basis for statements about mutations and evolution.

Thus, if I were Dr. Marshall, I wouldn’t complain about someone else’s scholarship being trumped by prior belief, unless I never believed that mutations played a role in evolution. That belief exemplifies a lack of scholarship.


P.S. It is remarkable that the president of the ISHE urged me “…to respect the rules of our disciplines and of scholarly conduct.” I prefer to contribute to scientific advances, instead. Too many logical fallacies have been integrated into what may be considered by others to be scholarly conduct when it is actually just academic suppression of new ideas and fully detailed models of cause and effect that make some scholars look like fools. What kind of moderator gleefully writes: “I was rejecting several of his submissions a day for a month or more before he stopped submitting to this group” about an ISHE member who co-authored the award-winning 2001 Neuroendocrinology Letters review: Human pheromones: integrating neuroendocrinology and ethology. Why would the president of the ISHE support such nonsense?


Author: James Kohl

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