Plenty of Room at the Bottom

Environmental selection is natural selection (2)

I believe that if you put enough biologically uniformed theorists in the same room, they will invent more theories to support the pseudoscientific nonsense they have touted in the past. See for example:

Environmental selection during the last ice age on the mother-to-infant transmission of vitamin D and fatty acids through breast milk


The synthesis presented here is a product of the American Association for the Advancement of Science’s 2017 annual meeting, as the ideas came together in the session entitled “Beringia and the Dispersal of Modern Humans to the Americas.”

Every aspect of every level of biophysically constrained food energy-dependent biologically-based cause and effect is placed back into the context of a ridiculous theory of human migration and evolution. The theory accurately attests to the link from one food energy-dependent base pair change to biodiversity in human populations via fixation of one amino acid substitution. But then, something goes horribly wrong.

The theory requires the fixation of the amino acid substitution to automagically occur in the context of the sun’s anti-entropic virucidal energy. The theory fails to mention the fact that the physiology of pheromone-controlled reproduction and the microRNA-mediated creation of all cell types in all living genera is required.

See for comparison: Anything published since the time I learned about the importance of microRNAs during the 2012 Society for Neuroscience annual meeting in New Orleans, LA.

From 2000/10/15 to 2012/10/15 microRNA Items: 1 to 20 of 19910

From 2012/10/15 to 2018/04/26 microRNA Items: 1 to 20 of 53458

The number of biologically informed serious scientists who have linked the energy-dependent creation of microRNAs to biophysically constrained viral latency and all biodiversity via the pheromone-controlled physiology of reproduction in bacteria continues to rapidly increase.

This begs the question: When will biologically uninformed science idiots stop attending meetings that facilitate their attempts to invent more ridiculous theories?


Environmental selection is natural selection

Environmental selection during the last ice age on the mother-to-infant transmission of vitamin D and fatty acids through breast milk was published on April 23, 2018

The ectodysplasin A receptor (EDAR) gene has a range of pleiotropic effects, including sweat gland density, incisor shoveling, and mammary gland ductal branching. The frequency of the human-specific EDAR V370A allele appears to be uniquely elevated in North and East Asian and New World populations due to a bout of positive selection likely to have occurred circa 20,000 y ago. The dental pleiotropic effects of this allele suggest an even higher occurrence among indigenous people in the Western Hemisphere before European colonization. We hypothesize that selection on EDAR V370A occurred in the Beringian refugium because it increases mammary ductal branching, and thereby may amplify the transfer of critical nutrients in vitamin D-deficient conditions to infants via mothers’ milk. This hypothesized selective context for EDAR V370A was likely intertwined with selection on the fatty acid desaturase (FADS) gene cluster because it is known to modulate lipid profiles transmitted to milk from a vitamin D-rich diet high in omega-3 fatty acids.

The authors placed my claims about the mouse-to-human model of the EDAR V370A variant back into the context of an evolutionary adaptation. They seem unwilling to accept the fact that the  EDAR V370A variant is a nutrient-dependent pheromone-controlled ecological adaptation in mice and in humans. It links energy-dependent changes from angstroms to ecosystems in all living genera via natural selection for energy-dependent codon optimality.
The EDAR V370A allele is also known as rs3827760, 1540T/C, 370A, or Val370Ala. It is a SNP in the ectodysplasin A receptor EDAR gene on chromosome 2.
See the author’s copy of my invited review of nutritional epigenetics, which was returned without review :
Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems (2014)

In the context of climate change and changes in diet, the story began with what probably was a nutrient-dependent base pair change and a variant epiallele that arose in a human population in what is now central China. Apparently, the effect of the epiallele was adaptive and it was manifested in the context of an effect on sweat, skin, hair, and teeth. In another mammal, such as the mouse, the effect on sweat, skin, hair, and teeth is probably due to a nutrient-dependent epigenetic effect on hormones responsible for the tweaking of immense gene networks that metabolize nutrients to pheromones. The pheromones appear to control the nutrient-dependent epigenetically-effected hormone-dependent organization and hormone-activation of reproductive sexual behavior in mammals such as mice and humans, but also in invertebrates and in microbes as previously indicated.

The ecological adaptations, which appear to be manifested in the human population are detailed in these two reports [162-163]. The ecological adaptations are likely to be nutrient-dependent and pheromone-controlled. If so, ecological variation probably leads to ecological, social, neurogenic, and socio-cognitive niche construction, which is manifested in increasing organismal complexity and species diversity. If not, there may be something as yet unknown about mutations and evolution that makes sense in the light of what is known about nutritional epigenetics and the molecular biology of species from microbes to man.

More than four years later, biologically uninformed theorists have again tried to make natural selection something different than environmental selection. Nina G. Jablonski is one of the co-authors. I’m tempted to think that all the others also are biologically uninformed science idiots who cannot link physical and chemistry from subatomic particles to ecosystems via what organisms eat and the physiology of pheromone-controlled reproduction, which biophysically constrains viral latency in all living genera.
See also: microRNA and ADAR1 microRNA
For example:
Combinatory RNA-Sequencing Analyses Reveal a Dual Mode of Gene Regulation by ADAR1 in Gastric Cancer (April 25, 2018)
Virus-encoded miRNAs in Ebola virus disease (April 24, 2018)


RNA-mediated physics, chemistry, and molecular epigenetics (2)

9/16/15 This is an excellent introduction to speculation about how quantum mechanics might be linked from physics and chemistry to the conserved molecular mechanisms of epigenetically-effected biologically-based RNA-mediated cause and effect, which all serious scientists already know must link angstroms to ecosystems via the innate immune system, the physiology of reproduction, and supercoiled DNA.
The introduction to speculation may help you to explain why more scientific progress has not been made since 1944, when Schrodinger claimed:

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) — What is Life?

Schrodinger’s speculation linked what is now known about the anti-entropic virucidal energy of ultraviolet light from ecological variation to ecological adaptation in all living genera, Roger Penrose provided everyone with an important clue about life. He wrote:  “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?” Simply put, Penrose asked if pseudoscientists realize that all organisms must eat to reproduce because the physiology of reproduction is energy-dependent.
For comparison, antagonists Norman Freedus and Sean Ovis  attacked me and Tomi Aalto on the Epigenetic Control of Gene Expression FB group. My responses led Peter Mellow to ban me from participation.

Hi James, I just wanted to let you know that I have kicked and banned you from the Epigenetics discussion group for calling other people ‘fools’. Verbal abuse, even of this mild nature is inflammatory to constructive debate. Thank you for being a member. Take care.
My response: Thanks. If you had stopped the abuse as soon as it started, you would not have offended me enough to expose your group’s ignorance of energy-dependent cell type differentiation. You have lost one of your only supporters who has a 20 year record of publications on molecular epigenetics.

Follow-up: Norman Freedus and Sean Ovis are still participating after being warned. The moderators let their name calling and attacks on my credibility continue for several days, and then removed the content I posted. I cited published works that supported the model I am presenting at the forthcoming Genetics and Genomics virtual conference, next week.
I submitted the poster on 4/27/16 and have been overwhelmed by how much additional support for the representations I made has since come to my attention. Any time spent preparing even a poster session may cause others to also fall behind. I’m beginning to wonder if there is any point to trying to explain biologically-based cause and effect to anyone who still thinks in terms of mutations and evolution. If they are not thinking in terms of RNA-mediated amino acid substitutions that link angstroms to ecosystems via the physiology of reproduction and supercoiled DNA, they are at least a year behind the experimental evidence.
Some of the links below set the stage for examining other published works, but there may be much more information than others have previously considered. Clearly, the failure to consider biologically-based cause and effect must be the reason that neo-Darwinian theorists still exist. For example, look at the complexity of this ridiculous theory.

The Gonium pectorale genome demonstrates co-option of cell cycle regulation during the evolution of multicellularity


Multicellular organisms have independently evolved numerous times throughout the tree of life including plants, animals, fungi, cyanobacteria, amoeba, brown algae, red algae and green algae1, 2. In animals, multicellularity emerged 600–950 million years ago (Myr ago) correlating with a large expansion of genes encoding transcription factors, signalling pathways, and cell adhesion genes that were co-opted from their unicellular ancestors3, 4 Similarly, multicellular, terrestrial plants emerged ~750Myr ago correlating with an expansion of many signalling pathways present in their unicellular relatives5, 6.

Reported on 4/25/16 as: How and why single cell organisms evolved into multicellular life
Reported on 5/5/16 as: Pond scum and the gene pool: One critical gene in green algae responsible for multicellular evolution, understanding of cancer origin
The differences in these two reports on the same published article are difficult to explain. One critical gene is linked to multicellular evolution and cancer. Both reports attest to the facts in Nothing in Biology Makes Any Sense Except in the Light of Evolution (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 (p. 127).”

My comment: The theorists link the expansion of receptor-mediated signaling pathways to the evolution of multicellularity. They also link evolution from mutations to cancer. That explains why why all serious scientists are Combating Evolution to Fight Disease.

The evolutionary biologist Theodosius Dobzhansky famously noted that “nothing in biology makes sense except in the light of evolution,” but perhaps, too, “nothing in evolution makes sense except in the light of biology.” Although the latter might be an exaggeration, an important gap is being filled by molecular understanding of the genesis of variation that confers the ability to evolve.

My comment: Does anyone still take the claims about mutations and evolution seriously?  Dobzhansky probably was joking about the “light of evolution.” He knew that the anti-entropic energy of the sun was required to link ecological variation to ecological adaptation via amino acid substitutions. He may not have known the difference between an amino acid substitution and a mutation, but he certainly must have seen the light. Others are starting to see it, too.
See for example:  Micron-scale plasma membrane curvature is recognized by the septin cytoskeleton 4/6/16
reported on 4/28/16 as A cell senses its own curves
My comment: This links sensing and signaling to energy-dependent changes in cell types in all living genera via amino acid substitutions. Virus-driven energy theft prevents sensing and signaling by causing mutations that link the energy theft to amino acid substitutions in viruses.
See: Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution
Authors’ comment: The major antigenic changes of the influenza virus are primarily caused by a single amino acid near the receptor binding site.
My comment: Viruses don’t evolve. They steal energy and viruses adapt via amino acid substitutions that prevent the adaptations of the host to the virus. That is why every amino acid substitution matters in the context of Dobzhansky’s claims and in the context of all claims by serious scientists.
For example, see:  Every amino acid matters: essential contributions of histone variants to mammalian development and disease 3/11/14
My comment: That fact attests to the fact that all theories are not the same. See:  Status Anxiety: All ‘Theories’ Are Not the Same 5/3/16 That fact raises the question Suzan Mazur posed on 4/30/16 Does the “Extended Synthesis” Replace or Not Replace Neo-Darwinism? — What Has Templeton Funded?  I answered the question in a series of posts to her blog post, but after others complained, the discussion ended. That happens alot. People don’t like what I say, but they can’t explain any alternative.
No one seems willing to discuss facts like this: A microRNA switch regulates the rise in hypothalamic GnRH production before puberty 5/2/16. It was reported as Control of fertility: A new player identified. Expression of c-fos in the neurosecretory neurons that secrete gonadotropin releasing hormone (GnRH) is the obvious link from the epigenetic landscape to the physical landscape of supercoiled DNA via the immune system of all vertebrates. I mentioned that in my presentation, and cited articles for support. But also, expression of c-fos links gene activation to all cell type differentiation in all mammals via the microRNAome of bull sperm and microRNAs in human breast milk. The claim that microRNAs, or are they claiming the GnRH is a new player in fertility, is one that can be linked to medical errors as a cause of death in the US. Medical error third leading cause of death in US: study 5/3/16
Clearly, if you don’t know how the epigenetic landscape is linked to the physical landscape of DNA via energy-dependent RNA-mediated cell type differentiation, you’re more likely to make a mistake than someone who is biologically informed.
See also: Communicating Across Kingdoms?

Researchers pinpoint microRNAs that could play a role in how Wolbachia bacteria manipulate their arthropod hosts.

By Sandhya Sekar | December 15, 2014

My comment to the Scientist: 12/16/2014

“I am not sure that I would call this ‘communication,’ however,” he added, as the authors have in their paper.

I’m rather certain that no evolutionary theorist will recognize this as communication because they typically claim mutations can be linked to increasing organismal complexity. This work indirectly links mutations to perturbed protein folding, diseases, and disorders.
Works published by Leslie Vosshall’s group and by others have linked the epigenetic landscape to the physical landscape of DNA in the organized genomes of insects via experience-dependent  de novo creation of olfactory receptors. Their works link the epigenetically-effected microRNA/messenger RNA balance from RNA-directed DNA methylation and RNA-mediated amino acid substitutions to cell type differentiation via conserved molecular mechanisms in species from microbes to man.
The molecular mechanisms are nutrient-dependent and pheromone-controlled because the nutrient-dependent amino acid substitutions must be fixed in organized genomes via protein folding in the context of the species-specific physiology of reproduction. That fact links Darwin’s ‘conditions of life’ to cell type differentiation via examples provided in Nutrient-dependent/pheromone-controlled adaptive evolution: a model.
For supporting documentation that places the role of mutations in their proper perspective of pseudoscientific nonsense that began with de Vries definition of “mutation,” see: Amino Acid Residues Contributing to Function of the Heteromeric Insect Olfactory Receptor Complex ; orco mutant mosquitoes lose strong preference for humans and are not repelled by volatile DEET; and Evolution of mosquito preference for humans linked to an odorant receptor.
Those who accept definitions and try to link them to biologically-based behavior have done so without recognizing the role that feedback loops must play  in protein folding that links ecological variation to ecological adaptations. Instead, they claim mutations lead to the evolution of biodiversity, when serious scientists know that Feedback loops link odor and pheromone signaling with reproduction in species from microbes to man via conserved molecular mechanisms of communication. See also: Signaling Crosstalk: Integrating Nutrient Availability and Sex. Let’s stop the nonsense and call communication what it is, and recognize it for what it does.
Communication enables nutrient-dependent pheromone-controlled cell type differentiation via amino acid substitutions that control thermodynamic cycles of protein biosynthesis and degradation. Mutations perturb protein folding, which is why they are not beneficial and cannot lead to the evolution of increasing organismal complexity.