February 6, 2014 | James Kohl
- By Eric Reitan
My comment: Why isn’t the question: Does Francis Collins believe that mutation-driven evolution is responsible for Mosaic Copy Number Variation in Human Neurons? His answer could be compared to the answer I think I would get from an atheist. Do atheists believe that the human brain mutated into existence? Is there a model for that?
Excerpt: “Theists are in a kind of perpetual retreat as science continues to fill gaps that theists have insisted could only be filled by God.”
That opinion, like all opinions about theists, cannot be substantiated. Opinions like it should be viewed only in the context of the nonsensical ramblings that they obviously are. They can then be compared to what is known about conserved molecular mechanisms. For example, see:
“I’m trying to undo a mistake I made some years ago, and rethink the idea that the way to understand the mind is to take it apart into simpler minds and then take those apart into still simpler minds until you get down to minds that can be replaced by a machine…
The idea is basically right, but when I first conceived of it, I made a big mistake.” — Daniel Dennett
My comment on Dennett’s mistake and Collins’ belief.
It seems unlikely to me that anyone besides Collins could tell us what he believes. It is equally unlikely that anyone besides Dennett will admit that Dennett made a mistake. Why is someone else answering the question: Does NIH Head Francis Collins Believe in Intelligent Design?
If they think they are qualified to answer for Collins, perhaps they will next also answer for Dennett’s mistake and again be confidently wrong like Dennett was.
See also: Confidently wrong about evolutionRead more
February 1, 2014 | James Kohl
ecological adaptations reported in the context of evolutionary theory
Science 31 January 2014: Vol. 343 no. 6170 pp. 471-472
Excerpt: ”Finding traces of incipient speciation in human DNA is a stunning switch for biologists used to focusing on animals. “Seeing the signature of these rules of speciation in our own history is really amazing,” says speciation expert Daven Presgraves of the University of Rochester in New York.”
My comments to Science
1) (published 1/31/14): These results appear to conflict with previous reports of biologically plausible non-random experience-dependent receptor-mediated species divergence due to ecological variation and adaptations. At least two of those reports were co-authored by Dr. Akey.
The adaptations show up in nutrient-dependent pheromone-controlled differences in cell types, which appear to be due to alternative splicings of pre-mRNA and amino acid substitutions, and the adaptations also show up in chromosomal rearrangements like those recently reported in sparrows with different morphological and behavioral phenotypes (see Estrogen receptor α polymorphism in a species with alternative behavioral phenotypes).
The differences in sparrows appear to be consistent with vertebrate-wide nutrient-dependent pheromone-controlled adaptations like those in the mouse-to-human example detailed in Kamberov et al (2013) and Grossman et al (2013) where a base pair change and single amino acid substitution showed up as differences in skin and hair, but also in teeth and mammary tissue in a population that arose during the past ~30,000 years in what is now central China.
Submitted on Thu, 01/30/2014 – 20:31
2) (published 2/1/14)
“…DNA from a small number of Neandertal ancestors might have been swamped later by the sheer abundance of modern human DNA.”
“Swamped” is an interesting word choice. Dr. Akey is senior author of the article with an abstract that states: ” We estimate that approximately 73% of all protein-coding SNVs and approximately 86% of SNVs predicted to be
deleterious arose in the past 5,000–10,000 years.”
Creationists might take that to mean the “swamping” occurred after a flood of Biblical proportions, which appears to be somewhat consistent with Dobzhansky’s “Creationist” belief. Clearly, however, that’s only if you place
his stated belief into the context of a shorter time frame, which enabled rapid ecological adaptations to occur via the nutrient-dependent pheromone-controlled physiology of reproduction, changes in base pairs, amino
acid substitutions, and chromosomal rearrangements.
“I am a creationist and an evolutionist. Evolution is God’s, or Nature’s, method of Creation.” — Dobzhansky (1973) in “Nothing in Biology Makes Any Sense Except in the Light of Evolution”
Somewhat like Dobzhansky, perhaps, I have been overwhelmed by the amount of experimental evidence that suggests food is the ecological variable which is naturally selected. If so, the selection of nutrient-rich foods might lead to ”swamping” via ecological adaptations sans the theory of mutation-driven evolution.
Submitted on Sat, 02/01/2014 – 13:10
3) (published 2/2/14)
Adaptive changes during the past 10,000 to 5,000 years in genes associated with diet,immunity, skin pigmentation, and eye color were also recently reported in Olalde et al (2014):”Derived immune and ancestral pigmentation alleles in a 7,000-year-old Mesolithic European”.
Metabolic and immunological challenges appear to be reflected in epigenetically-effected ecological adaptations. One adaptation appears to be the experience-dependent receptor-mediated ability to digest lactose.
That change and the other changes suggest an epigenetic effect of nutrient uptake was responsible for morphological and behavioral changes that could be sexually selected based on natural selection for food and its metabolism to species-specific pheromones that control the physiology of reproduction in species from microbes to man.
Submitted on Sat, 02/01/2014 – 22:35
I’ve also addressed a question posed in the context of the article.
4) published 2/3/14
In my model, the epigenetic effects of nutrient uptake and the metabolism of nutrients to species-specific pheromones link de novo creation of olfactory receptor genes in different cell types to infertility when spermatozoa are no longer able to “sniff out” an “egg” in invertebrates: Elekonich and Robinson (2000) and vertebrates: Diamond, Binstock and Kohl (1996).
If you look at the problem in the context of what we portrayed about the conserved molecular mechanisms at the advent of sexual reproduction in yeasts, you may see the continuum of ecological adaptations that began with
the nutrient-dependent pheromone-controlled chromosomal rearrangements that are required before sex chromosomes existed.
Submitted on Sun, 02/02/2014 – 14:34
In discussions elsewhere, I have asked that people address the perspective presented in the Science and Nature articles in the context of whatever opinion they have of how Mutation-driven evolution occurs.
Earlier, I provided this information in what has become an ongoing discussion of the topic: Where is the proof in pseudoscience?
See also: Diseases & disorders exemplify evolution
Note: As it becomes more difficult to deny that human ecological adaptations occurs via the conserved molecular mechanisms in species from microbes to man, Jay R. Feierman continues his attempts to prevent my model from being acknowledged by blocking many of my posts to the International Society for Human Ethology’s yahoo group. For example, yesterday he posted notice to the group of these publications: A game of thrones:Neural plasticity in mammalian social hierarchies (on social experience and neural plasticity) and Agency and Adaptation: New Directions in Evolutionary Anthropology (on phenotypic adaptation, cultural transmission, gene-culture coevolution, and niche construction.)
He did not post 7 of my submissions, one of which was about: Single-molecule tracking of the transcription cycle by sub-second RNA detection
Another submission was about The Makings of a Choosy Pathogen
The oomycete Phytophthora infestans is responsible for potato blight. A closely related pathogen afflicts the 4 o’clock flower. To assess why such similar pathogens are restricted to one host or the other, Dong et al. (p. 552; see the Perspective by Coaker) analyzed similar effectors from both pathogens. The results suggest that the host specialization that led to evolutionary divergence depends on reciprocal single–amino acid changes that tailor the pathogen effector to a specific host protease that is being disabled. Thus, small changes can open the door for a pathogen to jump to another species of host and, itself, diversify into another species of pathogen.
My comment: If evolutionary divergence resulted from single amino acid substitutions that were actually mutations, I would expect someone to explain how reciprocal mutations are involved in tailoring the required concurrent species-specific changes. Until then, the idea of concurrent reciprocal mutations in different species does not seem biologically plausible to me. Besides, I do not think that any experimental evidence supports the role of reciprocal mutations in ecological adaptations. Ecological variation leads to ecological adaptations via conserved molecular mechanisms in species from microbes to man, and that fact has been validated by experimental evidence. What biological facts have been included in theories of mutation-driven evolution? I’m only aware of the biological facts that have been excluded.
Researchers have moved quickly and are now examining biologically based cause and effect at levels from atoms to ecosystems. Feierman’s attempts to limit my dissemination of information that supports the model of cause and effect I have developed during the past few decades are as despicable as they have always been. The end result will be the same. Those who have continued to tout their nonsensical theories will be left behind, as they always have been when experimental evidence continues to support scientific progress and to expose the social pseuodoscience of theory.
Here is a recent 90 minute presentation about what is known at the atomic level of intracellular signaling.
Addendum (2/2/14): In his despicable ongoing attempts to deny me credit for my refutation of mutation-driven evolution, Feierman has since posted links to these articles:
Feierman’s behavior stems from our first encounter in 1995. After I explained the details of my model to him, he asked “What about birds?” I have since portrayed that question in the context of how much nonsense evolutionary theorists have incorporated into their beliefs about mutation-driven evolution during the past decades of scientific progress, which has shown that conserved molecular mechanisms are responsible for ecological adaptations in birds and every other species on the planet.
Does anyone else still think it is likely to be mutations that are naturally selected to result in the evolution of neuronal cell types and the single neuron dynamics of computations that enabled nutrient-dependent pheromone-controlled what is now portrayed as the evolution of ectodermal patterning? Is there a model for that?
February 5, 2014 | James Kohl
Excerpt: “How can it be that so many influential, powerful, wealthy, in-the-public people can be so confidently wrong about evolutionary biology? How did that happen? Why does it happen? Why does it persist? It really is a bit of a puzzle if you think about how they’d be embarrassed not to know that the world is round.”
My comment: Why aren’t evolutionary theorists embarrassed by the biological facts that have come from the past few decade’s-worth of works by serious scientists? It’s difficult for me to see someone reference David Haig’s work and then take it out of the context of nutrient-dependent pheromone-controlled epigenetic imprinting and mosaic copy number variation in human neurons.
Therefore, while it’s great to see someone admit that they’ve been wrong about how theorists first conceptualized the brain, it’s past time to look at the experimental evidence that links the epigenetic landscape to the physical landscape of DNA in the organized genome of every organism on the planet. The experimental evidence attests to ecological variation and the biologically-based cause of adaptations, which explains why the theorists are wrong, and why “…so many influential, powerful, wealthy, in-the-public people can be so confidently…” RIGHT — and continue to ignore the ridiculous theorists until they provide experimental evidence of cause and effect in the model organisms that have been the basis of scientific progress.
See for example: Mosaic Copy Number Variation in Human Neurons with my comments, which were published on the Science Magazine site:
My comment: 1) Re: Aplysia. Why not nematodes?
“High-throughput imaging of neuronal activity in Caenorhabditis elegans”http://www.pnas.org/content/110/45/E4266.full
The article helps to elucidate the conserved molecular epigenetics of cause and effect in a model organism of ecological, social, and neurogenic niche construction sans mutations theory.
Altered transcription can be associated with minimal variability in epigenetic landscapes that results in neurons with different genomes and distinct molecular phenotypes.
Effects of olfactory/pheromonal input appear to directly link the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man. In nematodes, conserved molecular mechanisms now link pulsing food odors and observed responses to the pulsatile secretion of gonadotropin releasing hormone (GnRH) in vertebrates. GnRH pulses links the epigenetic effects of food odors and pheromones to human behavior via systems biology and the ability of pulses to integrate information and rapidly transmit it throughout neuronal networks.
We can better understand the development of subtle differences in human behavior that are genetically predisposed and epigenetically effected. This will help us distinguish between genetic predisposition (nature) and effects of the sensory environment (nurture)during behavioral development.
The advantage is that we can also avoid attributing differences to mutations-initiated natural selection or to mutation-driven evolution by using what is known about biologically based cause and effect.
My comment: 2) The neuronal copy number variation (CNV) can be traced to its origins in yeasts, when epigenetically-effected CNVs enable self vs non-self recognition at the advent of immune system function and sexual reproduction, albeit sans neurons.
Olfactory/pheromonal input is subsequently associated with alternative splicings that link the epigenetic ‘landscape” to the physical landscape of DNA in the organized genome of species from microbes to man via CNVs and other variants. During adaptive evolution the CNVs in neurons are directly linked from olfactory/pheromonal input via ecological, social, neurogenic, and socio-cognitive niche construction. For example, neuronal niche construction in nematodes proceeds across species via conserved molecular mechanisms required for the thermodynamics of seemingly futile nutrient-dependent cycles of protein synthesis and degradation to species-specific pheromones. Pheromones control the physiology of reproduction and help to control nutrient-dependent organism-level thermoregulation.
In a mammal, see for example: “Odorant receptor gene choice and axonal wiring in mice with deletion mutations in the odorant receptor gene SR1.” However, see also my ISHE Summer Institute poster session uploaded to figshare: Nutrient-dependent / Pheromone-controlled adaptive evolution: (a mammalian model of thermodynamics and organism-level thermoregulation). I included details that eliminate mutations from further consideration in adaptive evolution. To do that I used examples from nematodes, insects, other mammals, and a human population that arose in what is now central China during the past ~30,000 years.
Non-random experience-dependent adaptive evolution appears to occur due to a thermodynamically controlled single base pair change and nutrient-dependent amino acid substitution best exemplified in the mouse model via what is neuroscientifically known about nutrient-dependent pheromone-controlled reproduction, which establishes the role of neuronal CNVs.Read more
February 5, 2014 | James Kohl
After the debate, I commented:
Ecological variation and nutrient-dependent life controlled by the metabolism of nutrients to species-specific pheromones that control the physiology of reproduction has replaced mutation-driven evolution in the context of a biologically plausible ecologically valid model for the Creation of new genes and organismal complexity.
The number of different proteins in different cell types of individuals in different species has established the obvious fact that the proteins did not result from mutations because mutations perturb protein folding. Most biology teachers still teach students that mutation-initiated natural selection is the cause of evolution.
It would have been great to hear either speaker address what is currently known about the conserved molecular mechanisms of species diversity that should long ago have eliminated mutation-driven evolution from any further consideration whatsoever.
“Our central finding, that fitness epistasis is widespread within natural populations, indicates that the raw material to drive reproductive isolation is segregating contemporaneously within species and does not necessarily require, as proposed by the DMI model 22, the emergence of genetically incompatible mutations independently derived and fixed in allopatric lineages 23.”
Someone sarcastically complained that they didn’t understand my comment, so I added this:
For example see:
YES is the biologically plausible and ecologically validated answer in species from microbes to man. From a Creationist perspective, “Yes” is the correct answer in the context of all plant and animal interactions because the molecular mechanisms of epigenetic cause and effect are conserved.
Plant life and animal life have common features at the cellular level. Biological Laws do more than suggest that ecological variation in nutrient availability leads to ecological adaptations. For comparison, “mutation-driven evolution” violates Laws of Biology, which biophysically constrain mutations that perturb the protein-folding required for increased organismal complexity (i.e., God’s Creation).
I think I could make a case for evolutionary theorists breaking the Laws of Biology with their theories, but doubt they will be prosecuted or persecuted for doing so. Similarly, Carl Zimmer will probably get away with presenting my life’s work in little quips like: “Do they lure the hummingbirds with special odors?” — after touting evolutionary theory for decades in everything he has written.
Suddenly, for Zimmer, special odors may be involved — as if food odors and social odors had not always been involved in Darwin’s ‘conditions of life,’ which reflect that every organism across God’s Creation must eat and reproduce — not merely mutate into another species to fit the evolutionary theorist’s limited perspectives.Read more
January 31, 2014 | James Kohl
- 29 January 2014 by John Cryan and Timothy Dinan [subscription required to read full article]
Excerpt: The bacterium Lactobacillus rhamnosus, which is used in dairy products, has potent anti-anxiety effects in animals, and works by changing the expression of GABA receptors in the brain.
My comment: Kohl, K.D. (2012) Diversity and function of the avian gut microbiota links what is known about mammals to other vertebrates (birds) and to insects (bees) via conserved molecular mechanisms in species from microbes to man (and Kohl’s Laws of Biology — i.e., nutrient-dependent, pheromone-controlled, receptor-mediated, experience-dependent ecological adaptations).
See also my comments and the comments by Dr. Charles Bailey (psychiatrist) on: The evolutionary and genetic origins of consciousness in the Cambrian Period over 500 million years ago
If you still think that Kohl’s Laws of Biology do not apply across species, see Amino acid enrichment and compositional changes among mammalian milk proteins and the resulting nutritional consequences, but do not take seriously the claim that “…milk proteins may have adapted to the species-specific nutritional needs of the neonate.” That claim is associated with evolutionary theory, which suggests that mutations cause beneficial adaptations (in proteins).
Proteins do not adapt; organisms adapt. The fact that organisms adapt is clear in all mammals because amino acid substitutions can also be detected by adult humans. We have the ability to detect differences in fat concentrations in milk via our sense of smell: Detecting Fat Content of Food from a Distance: Olfactory-Based Fat Discrimination in Humans.
If we did not share the conserved molecular mechanisms that enable the ability of all mammals to detect these differences, the epigenetic landscape could not become the physical landscape of our DNA via the conserved molecular mechanisms of species from microbes to man. Our detection abilities would have had to mutate into existence via mutations in amino acids in milk and concurrent mutations in our olfactory receptor genes, and their is no model for that. Mutation-driven evolution is a ridiculous theory that is the basis for touting such nonsense! There is no experimental evidence to support that theory, yet as you have just learned there is overwhelming experimental evidence to support Kohl’s Laws of Biology and the nutrient-dependent pheromone-controlled de novo Creation of genes that links olfactory/pheromonal input to genetically predisposed behavior in species from microbes to man.