Are population geneticists serious scientists?

August 9, 2014 | James Kohl

Geneticists decry book on race and evolution

Excerpt 1): ‘…geneticists have crafted a joint response, concluding that “there is no support from the field of population genetics for Wade’s conjectures.” 

Excerpt 2): “…Wade charged that his critics were “indoctrinated in the social-science creed that prohibits any role for evolution in human affairs” and contended that the book’s central argument “has not been challenged by any serious scientist.”

My comment: Dobzhansky’s claims seem to be relevant.

From 1964 “…the only worthwhile biology is molecular biology. All else is “bird watching” or “butterfly collecting.” Bird watching and butterfly collecting are occupations manifestly unworthy of serious scientists!” http://icb.oxfordjournals.org/…

Are population geneticists “serious scientists?”

From 1973 “…the so-called alpha chains of hemoglobin have identical sequences of amino acids in man and the chimpanzee, but they differ in a single amino acid (out of 141) in the gorilla.” http://www.jstor.org/stable/44…

Do population geneticists know the difference that a single amino acid substitution makes?

See also: Natural Selection Promotes Antigenic Evolvability “…no mutational mechanism that is biased toward amino acid substitutions has been described.”http://dx.doi.org/10.1371%2Fjo…

Do population geneticists know how cell type differentiation occurs in species from microbes to man?

Until a mutational mechanism is discovered that might possibly somehow link mutation-initiated natural selection to the evolution of biodiversity, all we have to explain biophysically-constrained biologically-based biologically plausible cause and effect is facts. Have the facts been considered by population geneticists in the context of Darwin’s ecological approach to biodiversity: his ‘conditions of life?’

If Dobzhansky’s amino acid substitutions are nutrient-dependent (a fact?) and the physiology of reproduction is pheromone-controlled (a fact?), amino acid substitutions link Darwin’s ‘conditions of life’ from the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man via conserved molecular mechanisms.

The obvious link is from ecological variation (e.g., nutrient availability) to pheromone-controlled nutrient-dependent ecological adaptations. The adaptations are manifested in the morphological and behavioral phenotypes of all species in the context of reproduction that leads to nutrient-dependent amino acid substitutions and cell type differentiation. Cell type differentiation leads to biodiversity (e.g., without the pseudoscientific nonsense added to Darwin’s theory by population geneticists).

Finding support from population geneticists for the denigration of Wade’s approach is the politically correct, albeit academically irresponsible path of least resistance. Finding support from molecular biologists is unlikely because few are willing to become involved in any issue of racial differences.

However, if you ask a molecular biologist about why ecological adaptations seem to typically occur in the context of ecological variation, an explanation could be provided that is based on what is currently known. If you ask population geneticists why ecological variation appears to correlate with racial differences, they would need to explain to you why there is no such thing as a racial difference.

Population geneticists may not know that molecular biologists could explain to them why ecological variation, which leads to ecological adaptations via amino acid substitutions, appears to be manifested in morphological phenotypes that some people still refer to as racial differences. Molecular biologists may not know how to explain biologically-based cause and effect to population geneticists by substituting the term “ecological adaptation” for evolution.

Read more

A microRNA-mediated mechanism that is epigenetically inherited

August 8, 2014 | James Kohl

Pregnancy Stress Spans Generations

The stressors a female rat experiences during pregnancy can have repercussions for her granddaughters, a study shows.

By Anna Azvolinsky | August 7, 2014

Excerpt: “These changes could be the result of a microRNA (miRNA)-mediated mechanism, which may be epigenetically inherited across generations.”

My comment: 

There is currently no alternative explanation for these changes. However, a model of how nutrient-dependent pheromone-controlled amino acid substitutions link cell type differentiation (e.g., from the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man via conserved molecular mechanisms) explains how nutrient-dependent changes in the microRNA/messenger RNA balance cause effects on hormone-organized behaviors that also are affected by hormones.

Yes, it’s complicated! However, the link from ‘effect’ to ‘affect’ was explained in Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Bruce McEwen also focussed on the difference between  ‘effect’ and ‘affect’ in a correction to Brain on stress: How the social environment gets under the skin

Simply put, evolutionary theorists must realize that ecological variation and nutrient uptake are required for changes to the microRNA/messenger RNA balance. Those changes result in cell type differentiation via amino acid substitutions, which stabilize DNA in organized genomes. Until evolutionary theorists begin to think in terms of biophysically-constrained protein folding, they may continue to tout the pseudoscientific nonsense of mutation-initiated natural selection and the evolution of biodiversity.

Fortunately, serious scientists know that mutations perturb protein-folding, which means that mutations do not stabilize DNA in organized genomes. That’s why mutations cannot be linked from ecological variation to epigenetic effects on hormones that affect behavior manifested in increasing organismal complexity associated with morphological phenotypes.

Clearly, the evolutionary theorists can explain differences in morphological phenotypes that arise from mutations. But the fact that they cannot explain how mutations could effect hormones, which affect behavior, leaves some serious scientists wondering.

In the early 1990s, I began to wonder why the theorists were unable to think in terms of olfactory/pheromonal input, which we now know epigenetically effects hormones that obviously link ecological variation to ecological adaptations via affects on behavior. Recently, it has become clearer that evolutionary theorists cannot think about anything outside the context of mutation-initiated natural selection and the evolution of biodiversity.  Some of them are even attempting to re-invent their theories using the term “epimutation.”

I hope that serious scientists will stop that pseudoscientific nonsense before it becomes accepted as if it were based on any experimental evidence of biologically-based cause and effect whatsoever.  See for comparison: Nutrient-dependent/pheromone-controlled adaptive evolution: a model The model includes examples from different species that attest to facts about how amino acid substitutions link a microRNA-mediated mechanism that is epigenetically inherited from ecological variation to nutrient-dependent pheromone-controlled ecological adaptations, without any nonsense about mutation-driven evolution.

For contrast: Nei (2013) wrote: “…genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world.”

That’s nonsense! Ecological variation in the supply of nutrients leads to the nutrient-dependent pheromone-controlled physiology of reproduction and nutrient-dependent ecological adaptations manifested in the inherited morphological and behavioral phenotypes of species from microbes to man.

Read more

Something from no thing

August 7, 2014 | James Kohl

The Bridge From Nowhere

How is it possible to get something from nothing?

Excerpt: “Evolution has trained us to find causal patterns at any cost. As our ancestors wandered the African savanna, the ability to suss out effects from their causes marked a line between life and death. She ate that speckled mushroom and then fell ill.” 

My comment: Thank you for your explanation of how pattern recognition may be beneficial to serious scientists.

Creation enabled our nutrient-dependent ability to find causal patterns that cost us nothing. The fact that everything is connected to everything else is perfectly clear. It led some people to realize that eating some things can make us ill, which supports the claim that health and illness are nutrient-dependent. The fact that reproduction also is nutrient-dependent links what organisms eat to their species survival. 

We’ve since learned that “Feedback loops link odor and pheromone signaling with reproduction” via amino acid substitutions and cell type differentiation in species from microbes to man. Thus, anyone who believes that mutation-initiated natural selection led to the evolution of biodiversity — or that “Evolution has trained us…” to do anything — probably does not believe in causal patterns of biophysically-constrained biologically-based cause and effect that cost us nothing to believe in. For example, it costs nothing to believe light-harvesting functions link amino acid substitutions that differentiate cell types in plants and animals.

Similarly, it costs us nothing to believe that docosahexaenoic acid links the phrase “Let there be light!” to a quantum theory for its irreplaceable role in neural cell signaling via ecological variation that links quantum physics to quantum biology and ecological adaptations manifested in the increasing organismal complexity of brains.

Taken together, these facts suggest it costs us nothing to believe that ecological adaptations are manifested in the morphological and behavioral diversity of species from microbes to man via conserved molecular mechanisms that link the epigenetic landscape to the physical landscape of DNA in organized genomes.However, evolutionary theorists seem to somehow have not been trained to find causal patterns that molecular biologists have known about for more than 50 years. See for example: Biology, molecular and organismic  “Ingram and others found that hemoglobin S differs from A in the substitution of just a single amino acid, valine in place of glutamic acid in the beta chain of the hemoglobin molecule.”

Apparently, evolution has trained theorists to not find causal patterns at any cost. Evolutionary theorists linked the hemoglobin S variant from a mutation to natural selection and the evolution of human diversity with a theory that has never been substantiated by experimental evidence of biologically plausible cause and effect. Dobzhansky (1973), however, noted that “…the so-called alpha chains of hemoglobin have identical sequences of amino acids in man and the chimpanzee, but they differ in a single amino acid (out of 141) in the gorilla in “Nothing in Biology Makes Any Sense Except in the Light of Evolution.

It would be great if evolutionary theorists would look at pattern recognition from the perspective offered this article about something from no thing and recognize the pattern of biophysically-constrained biologically-based cause and effect. After all, it costs them nothing to believe in facts.

Read more

Epimutations: Attacking pseudoscientific dogmas

August 6, 2014 | James Kohl

Our principle aim in the lab is to attack scientific dogmas.

Pseudoscientific dogma: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.”

My comment: I’ve tried to get along, REVISITED:  11 Simple Rules For Getting Along With Others “6. Avoid openly trying to reform people. Every man knows he is imperfect, but he doesn’t want someone else trying to correct his faults. If you want to improve a person, help him to embrace a higher working goal — a standard, an ideal — and he will do his own “making over” far more effectively than you can do it for him.” This suggestion does not seem to apply to evolutionary theorists who now substitute the term “epimutation” for amino acid substitutions and use sRNA rather than microRNA to avoid the obvious connection from the microRNA/messenger RNA balance to amino acid substitutions that differentiate the cell type of all cells of all individuals of all species.

See for example: Antifungal drug resistance evoked via RNAi-dependent epimutations.

Open reform of evolutionary theorists ridiculous perspectives  is required. Others must tell them enough is enough or they will continue to misrepresent biologically-based cause and effect and link disorder to the orderly increasing complexity of morphological and behavioral phenotypes. They want mutations and natural selection to be the link,  or epimutations to be the link, or whatever else they can think of to avoid admitting that they cannot think in terms of biologically-based cause and effect.

When will others be able to understand information like this:  “In Ostrinia moth species, substitution of a critical amino acid is sufficient to create a new pheromone blend (Lassance et al., 2013).

The problem for theorists appears to be a widely-touted example of what they think is natural selection via predation in fawn to pepper-colored moths.  The example is ridiculous and based on pseudoscientific nonsense, The moth larvae ate lead- and manganese-contaminated leaves that caused a nutrient-dependent pheromone-controlled color change. Thus, the color change was an ecological adaptation in the moths.

What about birds? Evolutionary theorists misrepresent the nutrient-dependent pheromone-controlled ecological adaptation in the moths. They tell people the nutrient-dependent pheromone-controlled ecological adaptation exemplifies mutation-initiated natural selection via predation. The color change, according to evolutionary theorists, occurred due to a mutation and the mutation was naturally selected because predatory birds could not see the pepper-colored moths on soot-covered trees as well as they could see the fawn-colored moths that had not mutated.

The fawn-colored moths that did not mutate suffered losses to their population via predation. Please change that ridiculous misrepresentation in your textbook if you are currently being taught to believe in the pseudoscientific nonsense of evolutionary theory. Do it now, before your biology teacher tries to get you to believe that the sickle cell hemoglobin variant that arose in populations where malaria was endemic, was due to a mutation that was naturally selected because it helped some human populations survive.

Hemoglobin variants are nutrient-dependent and pheromone-controlled like the variant that caused the change in the fawn to pepper-colored moths. That’s why the sickle-cell variant also is associated with skin pigmentation in some human populations. However, skin pigmentation involves a different variant that is associated with ingestion of fermented grains and milk products that supply additional sources of vitamin D, which is actually more like a sex steroid hormone than a vitamin.

The link from nutrient-uptake via microbes in the human gut that help to manufacture vitamin D leads to an amino acid substitution, which helped to stabilize the DNA in the organized genomes of human populations. The human populations developed lactose persistence via the nutrient-dependent change in an enzyme, which also helped the human populations to ecologically adapt to the presence of malarial parasites in their red blood cells. Their red blood cells did not mutate and the human populations were not naturally selected to evolve their morphological differences in sunny climates that changed the color of their skin.  That is not how ecological variation leads to ecological adaptations, which is via conserved molecular mechanisms in species from microbes to man.

All the changes can be attributed to ecological variation in a nutrient-dependent amino acid substitution that differentiated the cell types of human populations via their pheromone-controlled reproduction. That’s how ecological variation results in ecological adaptations in species from microbes to man.

The conserved molecular mechanisms that enable amino acid substitutions are the key to understanding what evolutionary theorists think is mutation-initiated natural selection that results in the evolution of biodiversity — in the moths and in human populations and in populations of other organisms.

Indeed, you might learn that evolutionary theorists believe just about everything Dobzhansky wrote in

1) “Nothing in Biology Makes Any Sense Except in the Light of Evolution” (1973) and in

2) “Biology, molecular and organismic” (1964)

What evolutionary theorists may not believe is that 50 years ago Dobzhansky (1964) wrote: “…the only worthwhile biology is molecular biology. All else is “bird watching” or “butterfly collecting.” Bird watching and butterfly collecting are occupations manifestly unworthy of serious scientists!”

Then, in 1973, he noted “… the so-called alpha chains of hemoglobin have identical sequences of amino acids in man and the chimpanzee, but they differ in a single amino acid (out of 141) in the gorilla.” At the same time he proclaimed, “It is wrong to hold creation and evolution as mutually exclusive alternatives. I am a creationist and an evolutionist.”

Today, we know that his claim to be an evolutionist was based on the theory that mutations and natural selection led to the evolution of biodiversity. Since we also know how ecological variation led to nutrient-dependent pheromone-controlled ecological adaptations in moths and humans, it is much clearer that amino acid substitutions lead to the de novo creation of olfactory receptor genes in moths and humans that facilitate cell type differentiation in all the cells of all individuals of all populations, which results in all biodiversity in species from microbes to man.

Read more

Order and disorder: Ecological adaptations not mutations

August 2, 2014 | James Kohl

In the context of order and disorder that includes what is known about quantum physics and light-induced amino acid substitutions in plants and animals, as well as the control of the functional rearrangement of influenza hemagglutinin, I’m beginning to see even more confusion/obfuscation enter the picture of biophysically-constrained ecological adaptations.

The nutrient-dependent ecological adaptations are now being put into the context of mutation-initiated natural selection and the evolution of biodiversity (i.e., “Evolution for Dummies”).

ECOLOGICAL ADAPTATIONS (not mutations)

Nutrient-dependent changes in the microRNA/messenger RNA balance are readily linked from ecological variation to ecological adaptations via conserved molecular mechanisms that eliminate mutation-initiated natural selection and evolution from consideration. However, since no experimental evidence of biologically-based cause and effect has shown that mutations are ever fixed in the organized genomes of any population of any species, researchers now refer to the amino acid substitutions that are fixed in the genome as if they were epimutations (translation: epigenetically-effected mutations).

For example, in this article about epimutations, microRNAs also are referred to as small RNAs and labeled sRNAs with this mention of what a small RNA is. “Most of these sRNAs average 21–24 nucleotides in length…”

A microRNA (abbreviated miRNA) is a small non-coding RNA molecule (containing about 22 nucleotides). Thus, the quantum leap from biophysically constrainted light-induced amino acid substitutions to the nutrient-dependent microRNA/messenger RNA balance that controls genome stability via epigenetically-effected amino acid substitutions is replaced with the concept of epigenetically-effected mutations, which are called epimutuations.

By mixing the theory of mutation-initiated natural selection and the evolution of biodiversity with biological facts about how ecological variation leads to epigenetically-effected ecological adaptations manifested in biodiversity, the senior author of the “epimutations” article sets the stage for his claim to be “the first” to find something new and important.

It could be like the discovery of other molecular phenomena like introns or microRNAs, where it all began with just one example,” said Heitman. “We think this discovery may turn out to be generalized fairly quickly.

What discovery? They link nutrient-dependent microRNAs from ecological variation to ecological adaptations in the context of conserved molecular mechanisms in species from microbes to man.

The researchers think these epimutations could be employed in a variety of situations, enabling an organism to adapt to an unfavorable environment and then adapt again when conditions improve.

DISCOVER THIS!

Nutrient-dependent epigenetically-effected alternative splicings of pre-mRNA, which can be called microRNAs or sRNAs result in amino acid substitutions that enable organisms to adapt to ecological change. When the supply of nutrients is reduced, starvation causes experience-dependent creation of receptors that enable nutrient uptake from a novel source.

If a novel source cannot be used, the pheromone-controlled physiology of nutrient-dependent reproduction leads to death of individuals and may lead to the extinction of any species that could not ecologically adapt via experience dependent de novo creation of receptors that let nutrients into the cell. The species in which de novo creation of receptors does not occur quickly enough do not mutate into another species that was somehow naturally selected to “evolve.”

Ideas about epimutations that include what is known about sRNAs but ignore facts about the nutrient-dependent microRNA/messenger RNA balance, amino acid substitutions, and epigenetically-effected morphological and behavioral diversity will make it possible for evolutionary theorists to continue touting their nonsense about mutation-initiated natural selection until serious scientists say ENOUGH!

In the context of order and disorder, some researchers have already said this. I’m not the only one who has had ENOUGH of the pseudoscientific nonsense from population geneticists.

[W]hat Haldane, Fisher, Sewell Wright, Hardy, Weinberg et al. did was invent…. The anglophone tradition was taught. I was taught, and so were my contemporaries, and so were the younger scientists. Evolution was defined as “changes in gene frequencies in natural populations.” The accumulation of genetic mutations was touted to be enough to change one species to another…. No, it wasn’t dishonesty. I think it was wish fulfillment and social momentum. Assumptions, made but not verified, were taught as fact.

If you’ve had ENOUGH of this pseudoscientific nonsense, and want to learn more about biological facts, you may also want to learn more about why Israeli middle schools are now teaching the theory of evolution.  They appear to be using it as an example of pseudoscientific nonsense that can be compared to what is known about ecological variation and how the disorder or variation leads to well-ordered de novo creation of olfactory receptor genes via nutrient-dependent amino acid substitutions that stabilize DNA in the organized genomes of species from microbes to man.

When will other school systems begin teaching students about the differences between ridiculous theories and biological facts about biophysically-constrained ecological adaptations are manifested in biodiversity?

Earlier today I received the reprint of an article published by serious scientists in the prestigious journal Cell: Starvation-Induced Transgenerational Inheritance of Small RNAs in C. elegans. After I read more about the starvation-induced link to cell type differentiation in C. elegans, I was not surprised to see the stated goal of Oded Rechavi’s lab in Israel:

Our principle aim in the lab is to attack scientific dogmas.

Finally, serious scientists are no longer willing to wait for evolutionary theorists to start learning about biology. Like a few others, the Rechavi lab researchers are attacking the pseudoscientific nonsense of mutation-initiated natural selection and the evolution of biodiversity.

How much clearer can it be that starving nematodes must adapt to ecological changes or their species becomes extinct. How much clearer can it be that ecological variation in the diet of nematodes is what causes nutrient-dependent amino acid substitutions that differentiate the pheromone-controlled cell types of different nematode species? In a news release published on January 13, 2013, Ralf Sommer said: “The patterns of synaptic connections perfectly mirror the fundamental differences in the feeding behaviours of P. pacificus and C. elegans.”

P. pacificus is a nematode species with teeth; C. elegans is a nematode species without teeth. The neuronal networks of the two species are wired differently and their nutrient-dependent pheromone-controlled reproduction is the most obvious cause of their differences in morphology and differences in their behavior.

No experimental evidence suggests that one species of nematode mutated into another. In fact, experimental evidence from C. elegans already has shown that mutations are not fixed in the DNA of the C. elegans organized genome. That finding “…set the stage for the development of more general theoretical models explaining the fate of new alleles…” but without fixed mutations in DNA, no model can explain the fate of new alleles in the context of natural selection that leads to the evolution of biodiversity. Mutations that are not fixed cannot be “naturally selected” and the result of the mutations cannot be evolutionary diversity.

Evolutionary theorists must invent new terms that can be used to describe how biodiversity arises, and some of them have decided to invent the term “epimutation” and attempt to explain how nutrient-dependent epigenetic changes in the organized DNA of species from microbes to man lead to the evolution of biodiversity. Shall serious scientists wish them luck with the invention of their new theories about epimutations and the evolution of biodiversity? Or will serious scientists mount an unending attack on the pseudoscientific nonsense of theorists and begin to make scientific progress that can more rapidly be made if people aren’t taught to believe in a ridiculous theory instead of biological facts about how ecological variation results in ecological adaptations? I hope that my published and unpublished works make it clear that I prefer the Rechavi lab’s attack strategy.

Nutrient-dependent/pheromone-controlled adaptive evolution: a model

and

Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems

“This atoms to ecosystems model of ecological adaptations links nutrient-dependent epigenetic effects on base pairs and amino acid substitutions to pheromone-controlled changes in the microRNA / messenger RNA balance and chromosomal rearrangements. The nutrient-dependent pheromone-controlled changes are required for the thermodynamic regulation of intracellular signaling, which enables biophysically constrained nutrient-dependent protein folding; experience-dependent receptor-mediated behaviors, and organism-level thermoregulation in ever-changing ecological niches and social niches. Nutrient-dependent pheromone-controlled ecological, social, neurogenic and socio-cognitive niche construction are manifested in increasing organismal complexity in species from microbes to man. Species diversity is a biologically-based nutrient-dependent morphological fact and species-specific pheromones control the physiology of reproduction. The reciprocal relationships of species-typical nutrient-dependent morphological and behavioral diversity are enabled by pheromone-controlled reproduction. Ecological variations and biophysically constrained natural selection of nutrients cause the behaviors that enable ecological adaptations. Species diversity is ecologically validated proof-of-concept. Ideas from population genetics, which exclude ecological factors, are integrated with an experimental evidence-based approach that establishes what is currently known. This is known: Olfactory/pheromonal input links food odors and social odors from the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man during their development.”

Read more
Page 2 of 21012345...102030...Last »