5th-6th Sept 2018 Dublin, Ireland

Nutrient-dependent pheromone-controlled feedback loops

Summary: The link from positive selection to one food energy-dependent base pair change and fixation of the mouse-model-to-human-specific EDAR V370A allele in populations on different continents attests to sympatric speciation at every level of examination that refutes the pseudoscientific nonsense of neo-Darwinian mutation-driven evolution.

Reported on 5/3/18 as: SWAT team of immune cells found in mother’s milk 


“There is a feedback loop,” says Yu. It’s known that some immune cells like leucocytes, another white blood cell that fights infection, increase in the milk in response to an infection in the baby.


…the largest immune cell population in breast milk is macrophages, which ILCs are known to direct. Macrophages, which literally means ‘big eaters,” are the largest of the white blood cells and much-better studied than ILCs. They are known for their ability to envelop unwanted items like bacteria, viruses…

Environmental selection during the last ice age on the mother-to-infant transmission of vitamin D and fatty acids through breast milk 4/23/18

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.

Reported as: Gene linked to breastfeeding may have boosted survival of earliest Americans (4/23/18)

…they carried a genetic mutation—revealed in ancient teeth—that boosted the development of milk ducts in women’s breasts, which may have helped nursing mothers pass more nutrients to their infants.

The obvious link from infant nutrition to healthy longevity was reported in the context of a ridiculous gene-centric theory of species survival. Gene-centric theories are all that pseudoscientists have left. They use them to hold back the scientific progress made by serious scientists like those who reported this:
Feedback loops link odor and pheromone signaling with reproduction (2005)

These results may reflect a strategy wherein GnRH neurons can modify diverse functions in order to coordinate the internal state of the animal and its behavior with reproduction in order to optimize reproductive success.

Alternative splicing of pre-mRNA

Diet-driven RNA interference and cancer prevention (3)

Excerpt: They claim to have found novel autoregulatory feedback loops that link changes in microRNAs to the alternative splicing factors SRSF1 and SRSF2.  Ectopic expression of SRSF1 can automagically repress the level of multiple microRNAs and SRSF2 can automagically upregulate miRNA expression.

The fact that a peer-reviewed work published in 2018 links autoregulatory feedback loops to automagically altered gene expression and apoptosis via alternative splicings of pre-mRNAs suggests it is time for all serious scientists to retire. The magic of pseudoscientists has prevailed for more than 2 decades.

See for comparison: In clinical trial, cream reduces squamous cell carcinoma risk

Results of a new randomized, double-blinded, controlled clinical trial in veterans showed a 75 percent reduction in the risk of needing surgery to treat a squamous cell carcinoma for a year after applying a skin cream for up to four weeks.

How Fluorouracil Works: (with my emphasis)

The ability of chemotherapy to kill cancer cells depends on its ability to halt cell division. Usually, the drugs work by damaging the RNA or DNA that tells the cell how to copy itself in division. If the cells are unable to divide, they die. The faster the cells are dividing, the more likely it is that chemotherapy will kill the cells, causing the tumor to shrink. They also induce cell suicide (self-death or apoptosis).

Chemotherapy drugs that affect cells only when they are dividing are called cell-cycle specific. Chemotherapy drugs that affect cells when they are at rest are called cell-cycle non-specific. The scheduling of chemotherapy is set based on the type of cells, rate at which they divide, and the time at which a given drug is likely to be effective. This is why chemotherapy is typically given in cycles.

Chemotherapy is most effective at killing cells that are rapidly dividing. Unfortunately, chemotherapy does not know the difference between the cancerous cells and the normal cells. The “normal” cells will grow back and be healthy but in the meantime, side effects occur. The “normal” cells most commonly affected by chemotherapy are the blood cells, the cells in the mouth, stomach and bowel, and the hair follicles; resulting in low blood counts, mouth sores, nausea, diarrhea, and/or hair loss. Different drugs may affect different parts of the body.

Fluoruracil belongs to the category of chemotherapy called antimetabolites. Antimetabolites are very similar to normal substances within the cell. When the cells incorporate these substances into the cellular metabolism, they are unable to divide. Antimetabolites are cell-cycle specific. They attack cells at very specific phases in the cycle. Antimetabolites are classified according to the substances with which they interfere. Fluoruracil is classified as a pyrimidine analog because it interferes with DNA and RNA synthesis by mimicking the building blocks necessary for synthesis.

The term antimetabolites is confusing. Metabolism is enzyme-dependent. Cell type differentiation is energy-dependent and the creation of microRNA links ATP to the creation of enzymes that metabolize food to the species-specific pheromones.
Pheromones biophysically constrain viral latency. That is how they prevent all pathology in the context of metabolism. Enzyme-dependent cycles of metabolism are the key to healthy longevity. Simply put, pheromones prevent the transgenerational epigenetic inheritance of nearly all viruses that have not been biophysically constrained by food energy-dependent metabolism.

Hardin, Hall and Rosbash (1990) put that fact into the perspective of Feedback of the Drosophila period gene product on circadian cycling of its messenger RNA levels. The feedback loops are food energy-dependent and biophysically constrained by naturally occurring RNA interference (i.e., natural selection for energy-dependent codon optimality). The feedback links the metabolism of food to pheromone-controlled biophysically constrained viral latency.

Rosbash shared the 2017 Nobel Prize in Chemistry, which attests to the fact that all serious scientists probably know how to prevent or to effectively treat cancer as a disorder of cyclic changes in the chemistry of energy-dependent RNA mediated cell type differentiation. Prevention should include limiting exposure to nutrient stress and/or social stress because stress alters microRNA-mediated alternative splicings that link food energy to the biophyiscally constrained chemistry of protein folding.

See: Microrna-mediated regulation of splicing factors SRSF1, SRSF2 and hnRNP A1 in context of their alternatively spliced 3’UTRs

The microRNAs targeting SRSF1 and SRSF2 are involved in a regulatory feedback loop. microRNAs miR-183-5p and miR-200c-3p that target SRSF2, affect the expression of genes involved in apoptotic regulation.

They claim to have found novel autoregulatory feedback loops that link changes in microRNAs to the alternative splicing factors SRSF1 and SRSF2.  Ectopic expression of SRSF1 can automagically repress the level of multiple microRNAs and SRSF2 can automagically upregulate miRNA expression.

The fact that a peer-reviewed work published in 2018 links autoregulatory feedback loops to automagically altered gene expression and apoptosis via alternative splicings of pre-mRNAs suggests it is time for all serious scientists to retire. The magic of pseudoscientists has prevailed for more than 2 decades.

See for comparison:

From Fertilization to Adult Sexual Behavior (1996)

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 [model organisms.]

See also:
Feedback loops link odor and pheromone signaling with reproduction (2005)
The feedback loops are food energy-dependent and biophysically constrained by the pheromone-controlled physiology of reproduction in species from microbes to humans.

Sarcasm alert: The treatment of automagically dysregulated apoptosis should probably begin with a change in diet.

Changes in diet have been linked from the energy-dependent creation of enzymes that specifically link an energy-dependent base pair change to microRNA-mediated DNA repair via fixation of an RNA-mediated amino acid substitution. The substitutions are linked to energy-dependent cell type differentiation and healthy longevity without the magic.

Just add food energy or the virus-driven theft of quantized energy to eliminate the term autoregulatory and you could prevent or effectively treat all virus-driven pathology. 

Energy-dependent RNA interference links the enzyme-dependent metabolism of food and drugs to cell type differentiation via feedback loops that link pheromones to biophysically constrained viral latency.

Do not claim to have a logical philosophy if you cannot link the creation of the sun’s anti-entropic virucidal energy to every aspect of the biophysically constrained pheromone-controlled physiology of reproduction in species from microbes to human by starting with the obvious need to control viral replication in the ocean and linking the control to healthy longevity in modern human populations via fixation of RNA-mediated amino acid substitutions in all differentiated cell types.

See also: Metabolic Labeling and Profiling of Transfer RNAs Using Macroarrays

Transfer RNAs (tRNA) are abundant short non-coding RNA species that are typically 76 to 90 nucleotides in length. tRNAs are directly responsible for protein synthesis by translating codons in mRNA into amino acid sequences.

See also: Molecular mechanism of promoter opening by RNA polymerase III

RNA polymerase III (Pol III) and transcription factor IIIB (TFIIIB) assemble together on different promoter types to initiate the transcription of small, structured RNAs.

Nothing happens without the energy-dependent creation of the enzymes and the biophysically constrained viral latency that links the creation of G protein-coupled receptors to the functional structure of supercoiled DNA. The claims about molecular mechanisms of promoter opening appear to be deliberate attempts to obfuscate cause and effect.
Activation of G protein-coupled estrogen receptor signaling inhibits melanoma and improves response to immune checkpoint blockade

Female sex and history of prior pregnancies are associated with favorable melanoma outcomes. Here, we show that much of the melanoma protective effect likely results from estrogen signaling through the G protein-coupled estrogen receptor (GPER) on melanocytes. Selective GPER activation in primary melanocytes and melanoma cells induced long-term changes that maintained a more differentiated cell state as defined by increased expression of well-established melanocyte differentiation antigens, increased pigment production, decreased proliferative capacity, and decreased expression of the oncodriver and stem cell marker c-Myc. GPER signaling also rendered melanoma cells more vulnerable to immunotherapy. Systemically delivered GPER agonist was well tolerated, and cooperated with immune checkpoint blockade in melanoma-bearing mice to dramatically extend survival, with up to half of mice clearing their tumor. Complete responses were associated with immune memory that protected against tumor rechallenge. GPER may be a useful, pharmacologically accessible target for melanoma.

Sex-specific cell type differentiation links yeasts to primates via the nutrient-dependent pheromone-controlled physiology of reproduction that links the food energy-dependent structure and function of enzymes and G protein-coupled receptors to the biophysically constrained Structure and dynamics of GPCR signaling complexes, which are required to biophysically constrain viral latency in the context of effect of androgens and estrogens on difference in the cell type of males and females.
Any focus on G protein-coupled estrogen receptors compared to G protein-coupled androgen receptors  should be viewed with suspicion in the context of what has been known to all serious scientists about hormones and behavior since our Hormones and Behavior review of RNA-mediated cell type differentiation. From Fertilization to Adult Sexual Behavior (1996)
Simply put, the alternative splicings of pre-mRNAs, which are now called microRNAs, biophysically constrain energy-dependent viral latency and prevents the transgenerational epigenetic inheritance of nearly all virus-driven pathology until excess nutrient stress or social stress takes its toll on the innate immune system.
Eventually, our food energy-dependent RNA-mediated DNA repair fails, and the accumulation of viral microRNAs predicts the failure of cell type differentiation in the tissues that are required to sustain our physical health and mental health.

Cases of Cytosis

Narcissistic egomaniacal and deadly denial of autophagy

Summary: Viral latency is food energy-dependent and pheromone-controlled in the context of autophagy, which protects organisms from the virus-driven degradation of messenger RNA.

Workshop on Quantum Effects in Biological Systemshas established itself as an outstanding stage to present the research in the intersection of physics, chemistry and biology. This field has… established excitons in biology as the “must-talk-language” when describing the quantum effects in biological light-harvesting systems.

Pseudoscientists refuse to speak the “must-talk language” of biological light-harvesting systems. When was the last time you heard a theorist mention excitons?

Light-harvesting systems link the creation of the sun’s anti-entropic virucidal energy (Schrodinger’s negentropy, 1944 ) from the creation of food energy to the physiology of pheromone-controlled reproduction in all living genera via autophagy, which protects all organized genomes from virus-driven entropy.

See: Structural diversity of supercoiled DNA

…DNA supercoiling strongly affects DNA metabolism. Despite its importance, however, much about supercoiled DNA (positively supercoiled DNA, in particular) remains unknown. Here we use electron cryo-tomography together with biochemical analyses to investigate structures of individual purified DNA minicircle topoisomers with defined degrees of supercoiling. Our results reveal that each topoisomer, negative or positive, adopts a unique and surprisingly wide distribution of three-dimensional conformations. Moreover, we uncover striking differences in how the topoisomers handle torsional stress. As negative supercoiling increases, bases are increasingly exposed. Beyond a sharp supercoiling threshold, we also detect exposed bases in positively supercoiled DNA. Molecular dynamics simulations independently confirm the conformational heterogeneity and provide atomistic insight into the flexibility of supercoiled DNA. Our integrated approach reveals the three-dimensional structures of DNA that are essential for its function.

They linked energy-dependent changes in base pairs from supercoiled DNA to all biodiversity via cryo-ET, which helped to support their atomistic insight.

See for comparison: Structural Dynamics and Mechanochemical Coupling in DNA Gyrase

Gyrase… harnesses the free energy of ATP hydrolysis to perform mechanical work on DNA. The enzyme specifically introduces negative supercoiling in a process that must coordinate fuel consumption with DNA cleavage and religation and with numerous conformational changes in both the protein and DNA components of a large nucleoprotein complex.

Simply put, gyrase introduces the pathology of virus-driven negative supercoiling. Discussion with one of the co-authors, namely A.C. Parente, led me to make this claim in frustration:

No one who places “Plant Energy Biology” into the context of “Evolutionary Biology” will understand my model of the Mechanisms and Functional Diversity of Macromolecular Remodeling by ATP-Dependent Motors [autophagy]. It starts with the creation of energy and explains how virus-driven energy theft is linked to all pathology via conserved molecular mechanisms in species from microbes to humans. The mechanisms link energy-dependent changes in angstroms to ecosystems via what is known about autophagy. The energy is not destroyed. Viruses use it to replicate.

Parente, and other like her, have tried to present their findings in the context of evolution, which is why their experimental evidence makes no sense to serious scientists. Nothing except natural selection for energy-dependent codon optimality can link the energy-dependent physiology of pheromone-controlled reproduction from feedback loops to autophagy, which biophysically constrains viral latency.  Simply put, viral latency is food energy-dependent and pheromone-controlled.

Serious scientists have detailed that fact since 1994. See: [Pheromonal regulation of genetic processes: research on the house mouse (Mus musculus L.)]

A study of the influence of pheromone stressor(s) on proliferating germ and somatic cells was performed on laboratory lines of house mouse in the context of the physiological hypothesis of mutation process, proposed by M.E. Lobashev in 1947. Data from experiments are presented, and results obtained during last 10-15 years are discussed. The adaptive role of cytogenetic and other observed pheromonal effects is considered. The possible existence of interorganism systems of genetic regulation is discussed, the search for and study of which may help in more complete understanding of the regularities of functioning of genetic material.

See also: Combinatorial effects of odorants on mouse behavior

In summary, our findings indicate that the innate effect of an odorant on behavior can be context-dependent and subject to modification by other odorants. It is conceivable that signals derived from a single receptor can elicit innate behavioral attraction or aversion and involve hard-wired neural circuits. However, our studies indicate that these behavioral responses can be modulated by sensory inputs from other receptors via the interactions of signals derived from the different receptors within the brain. In short, innate behavioral output can be influenced by interactions within the brain among signals derived from different receptors in the nose.

See also my refutation of neo-Darwinian pseudoscientific nonsense: Nutrient-dependent/pheromone-controlled adaptive evolution: a model

See for comparison, on 7/25/13, psychiatrist Jay R. Feierman wrote:

“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.”

In my opinion, Jay R. Feierman goes far beyond the claims of other narcissistic egomaniacs, like Parente, who think they can use evolution as an explanation for all biophysically constrained biodiversity. Other egomaniacs also attempt to beat serious scientists into submission with ridiculous claims that the serious scientists do not understand Darwinian biological evolution. But see the 2009 and 2017 retractions of Jack Szostak’s claims about the evolution of amino acids. Please use the retractions to help stop the pseudoscientific nonsense touted by biologically uninformed theorists.

I am a medical laboratory scientist who knows that Darwin started with his food energy-dependent “conditions of life.” He presciently linked natural selection for energy-dependent codon optimality from the “conditions of life” to the physiology of pheromone-controlled reproduction and all biodiversity in every species he examined. He could have done no better if he knew anything about genetics and focused on one model organism of fixed amino acid substitutions, but that fact has changed.

See for example: Associative Mechanisms Allow for Social Learning and Cultural Transmission of String Pulling in an Insect

My comment: RNA-mediated associative mechanisms Posted by jvkohl on 14 Dec 2016 at 16:36 GMT

Two more articles have been reported that link the energy-dependent RNA-mediated supercoiling of DNA to all healthy longevity. The two articles also link virus-driven energy theft to negative supercoiling in bacteria and all pathology in species from archaea to humans via the transgenerational epigenetic inheritance of Zika virus-damaged DNA.

See: DNA Supercoiling Combats Environmental Challenges

See also: Honeybee memories: another piece of the Alzheimer’s puzzle?

The honeybee model organism links nutrient energy-dependent supercoiling to the pheromone-controlled physiology of reproduction in species from microbes to humans via the conserved molecular mechanisms that link autophagy to chromosomal rearrangements and all biodiversity. See the works of Nobel Laureates Thomas Hunt Morgan, Erwin Schrodinger, Linda Buck, Yoshinori Ohsumi, and Ben Feringa to help establish the facts about cell type differentiation in your future publications.

Competing interests declared: I own these domains: Pheromones.com, RNA-mediated.com and Autophagypro.com They are among others that I own and they collectively link what is currently known about energy-dependent cell type differentiation to all biodiversity via conserved molecular mechanisms.

With the launch of Autophagy.pro, I am considering the sale of the domain Autophagypro.com to someone with commercial interests.  Let the bidding begin, based on the claims of others with commercial interests who have failed to link pheromones to the prevention of pathology.
See for example: Pheromones and the luteinizing hormone for inducing proliferation of neural stem cells and neurogenesis
See also: Obligatory role of hypothalamic neuroestradiol during the estrogen-induced LH surge in female ovariectomized rhesus monkeys
reported as:  Estrogen discovery could shed new light on fertility problems

Estradiol builds in the bloodstream until it reaches a concentration that causes a surge of the hypothalamic and pituitary hormones, including one called luteinizing hormone, which in turn trigger an ovary to release an egg.

“It’s a feedback loop…

See also: Feedback loops link odor and pheromone signaling with reproduction
See also: Olfaction Warps Visual Time Perception

…we show in healthy human adults that odors modulate object visibility around critical flicker-fusion frequency (CFF)-the limit at which chromatic flickers become perceived as a stable color-and effectively alter CFF in a congruency-based manner, despite that they afford no clear environmental temporal information. The behavioral gain produced by a congruent relative to an incongruent odor is accompanied by elevated neural oscillatory power around the object’s flicker frequency in the right temporal region ~150-300 ms after object onset, and is not mediated by visual awareness. In parallel, odors bias the subjective duration of visual objects without affecting one’s temporal sensitivity. These findings point to a neuronal network in the right temporal cortex that executes flexible temporal filtering of upstream visual inputs based on olfactory information. Moreover, they collectively indicate that the very process of sensory integration at the stage of object processing twists time perception, hence casting new insights into the neural timing of multisensory events.

See also: Formulation and evaluation of anti-suicidal nasal spray of Thyrotropin releasing hormone
Re: The deadly denial of theorists who failed to examine the stress-linked activation of the death gene to glioblastoma.
See: Reduced expression of brain-enriched microRNAs in glioblastomas permits targeted regulation of a cell death gene
and A Concise Review of MicroRNA Exploring the Insights of MicroRNA Regulations in Bacterial, Viral and Metabolic Diseases 
Also, please note: I purchased the domain name: Subatomic.pro because the microRNA regulation of metabolic diseases links electrons to ecosystems in all living genera by protecting individuals and species from the degradation of their messenger RNA, which links mutations to all pathology.

See also: Combating Evolution to Fight Disease


The Light and Darkness of "Evolution 2.0"

The light of evolution in the oft-cited work by Dobzhansky (1973) is the energy from sunlight. The sun’s biological energy links its anti-entropic virucidal epigenetic effects to RNA-mediated amino acid substitutions that differentiate all cell types in all individuals of all living genera.
Excerpt from Dobzhansky (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: Viruses steal the energy that is required for nutrient-dependent RNA-mediated cell type differentiation in the context of RNA-mediated amino acid substitutions.
Authors’ comment on Koel et al., (2013): The major antigenic changes of the influenza virus are primarily caused by a single amino acid near the receptor binding site.
My comment: When a virus steals energy from a cell, it uses the energy to support viral replication, and viral replication perturbs nutrient-dependent cell type differentiation.
Excerpt from Taylor et al (2015):

After 96 hours of incubation of AR2 and Pf0-2x at room temperature on SMM, two breakout mutations were visible, conferring first slow (AR2S and Pf0-2xS) and then fast (AR2F and Pf0-2xF) spreading over the agar surface (Fig. 1A). The AR2F strain produces flagella, but we could not detect flagella in electron microscopy samples for AR2S (Fig. 1B). Genome resequencing revealed a single-nucleotide point mutation in ntrB in strain AR2S, causing an amino acid substitution within the PAS domain of the histidine kinase sensor NtrB [Thr97→Pro97 (T97P)] (13). The fast-spreading strain AR2F had acquired an additional point mutation in the σ54-dependent EBP gene ntrC, which alters an amino acid (R442C) within the DNA binding domain (Table 1 and table S2).

My comment: Collectively, three articles established the link from sunlight to RNA-mediated cell type differentiation via microRNAs and adhesion proteins linked to supercoiled DNA and chromosomal rearrangements in the context of the physiology of reproduction. But, they individually and collectively reported their findings in terms of mutations and evolution.
See for comparison: Feedback loops link odor and pheromone signaling with reproduction and What is Life?
My comment: An intelligent person need look no further than what is known about life in the context of the nutrient-dependent physiology of reproduction, which links all invertebrates to all vertebrates. After a brief review, they could still probably grasp the fact that supercoiled DNA protects organized genomes from virus-driven entropy. If an intelligent person did not look at the role of viruses, they might make the claims made by neo-Darwinian evolutionary theorists. That is why it is important to note that:

The entire evolution of the microbial world and the virus world, and the interaction between microbes and viruses and other life forms have been left out of the Modern Synthesis… — Eugene Koonin

See also: Who’s Invited to the Royal Society Evolution Paradigm Shift Meeting? – The Unofficial List

I was informed by the Royal Society science program office that there will be no formal presentations on viruses, per se, which seems peculiar considering viruses are now understood to be the biggest part of the biosphere, and a key reason for paradigm shift. Viruses and microbes — both organisms — were left out of the modern synthesis.

My comment: Why is a meeting that supposedly will address the evolution paradigm shift not going to include anyone who knows about virus-driven genomic entropy? Most serious scientists already know that …gradual mutation followed by selection has not, as a matter of fact, been demonstrated to be necessarily a cause of speciation.
That fact makes the motives of the meeting organizers increasingly suspicious. Clearly, the role of virus-driven genomic entropy msut be discussed in the context of a paradigm shift. The paradigm shift must also include what is known about nutrient-dependent RNA-mediated DNA repair. The nutrient-dependent repair mechanisms link metabolic networks to genetic networks in all living genera via the innate immune system.
See: Noncoding RNA –NORAD– Regulates Genomic Stability by Sequestering PUMILIO Proteins

Interestingly, it was recently reported that NORAD (LINC00657) is induced by hypoxia in human endothelial cells (Michalik et al., 2014), suggesting broader roles for NORAD in cellular stress responses. How NORAD influences the functional outputs of these and other stress response pathways, and the broader roles of NORAD in normal physiology and disease, represent important areas for future research.

My comment: The immune system is the interface between stress-related effects on cell types vs healthy longevity.  Stress-related proliferation of viruses links viral microRNAs to perturbed RNA-mediated protein biochemistry that is typically constrained by hydrogen-atom transfer in DNA base pairs. Constraint-breaking mutations show up quickly and are consistently linked to outcomes via changes in thermodynamic cycles of protein biosynthesis and degradation that can be measured via changes in the pH of human body fluids or via spectophotometry. Both types of measurements assess nutrient-energy theft by viruses.
See for example: Molecular requirements for a pandemic influenza virus: An acid-stable hemagglutinin protein

These studies link a fundamental property, activation energy of a fusion protein measured as its pH of activation (acid stability), to the ability of zoonotic influenza viruses to cause a human pandemic.

Reported as: Acid-sensitive molecular changes contribute to the emergence of pandemic influenza

“The hemagglutinin protein plays a central role in human flu pandemics, yet until now the molecular properties required for pandemic viruses have remained largely undefined,” Russell said. “Our findings suggested that one requirement for a pandemic influenza A virus was an acid-stabilized protein with an activation pH of 5.5 or less, which was sufficient to allow airborne human-to-human transmission at the start of the 2009 H1N1 pandemic.”

Koel et al., (2013) revisited: The major antigenic changes of the influenza virus are primarily caused by a single amino acid near the receptor binding site.
My comment: In the context of my model, virus-linked energy theft from specific cell types led to the stability of an acid-stabilized protein in the virus with an activation pH of 5.5 or less via a single amino acid, which allowed “…airborne human-to-human transmission at the start of the 2009 H1N1 pandemic.”
See also:  The Quest to End the Flu
My comment:

See also: “Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution”
The idea of biophysical constraints seems antithetical to the idea of nature somehow selecting mutations that cause amino acid substitutions. However, I am not a biophysicist or evolutionary theorist.
The problem may be my focus on nutrient-dependent receptor-mediated amino acid substitutions in species from bacteria to humans (non-viral organisms). Since I am not a virologist or physicist, I’m not sure that the laws of physics apply to viruses and their replication.
If they do, natural selection for random mutations is not likely to result in amino acid substitutions because the thermodynamics of changes in organism-level thermoregulation preclude such randomness. Stability of protein biosynthesis and degradation that probably depends on protein folding must somehow be controlled. Besides, I don’t know how random mutations in viruses could be naturally selected for inclusion in the human virome (or in the virome of any organism capable of thermoregulating its thermodynamic intercellular signaling).
If the Second Law of Thermodynamics does not apply to viruses, which means the chemical bonds that enable the amino acid substitutions can form at random and somehow be naturally selected, the details of biophysical constraints in this article seems out of place, since I do not think in terms of constrained random mutations and natural selection in mutation-driven evolution.
Hopefully, someone with a background in biophysics will address my confusion in case others are confused. In addition, I wonder if the consequences of understanding the evolutionary mechanisms that govern viruses extend to consequences important to understanding the evolution of species from bacteria to humans via constrained random mutations and natural selection?

The comment above was also published to the “Science Magazine” comments section, but it was removed and replaced with the authors’ comment. Obviously, they knew that anyone familiar with the laws of physics and chemistry of nutrient-dependent RNA-mediated protein folding would link virus-driven constraint breaking mutations to the antigenic change in the virus without claims about evolution.
Viruses don’t evolve! Antigenic changes don’t evolve! Proteins don’t evolve! Researchers must make it clearer that they know the difference between neo-Darwinian theory and facts about cell type differentiation. That is the only way serious scientists can avoid being removed from positions where their ignorance may cause a pandemic.

See also: It is not clear in any representation that a virus-driven change in a base pair could be linked from the theft of energy and perturbed hydrogen-atom transfer in DNA base pairs in solutuion to pathology. Although only one base pair change and one amino acid substitution may make a difference to the cell type, nutrient-dependent RNA-mediated healthy longevity is not placed into the context of one amino acid substitution linked to pH and spectophotometric assays of hydrogen ion concentration in body fluids. Thus, the accumulated knowledge fron every test that I ever performed during ~60,000 hours of testing in my career as a medical laboratory scientist is dismissed by the claims of evolutionary theorists.
However, the changes in hydrogen-atom transfer in DNA base pairs in solution have now been placed into the context of bacteria the move towards the light.
See: How slime can SEE where it’s going: Single-celled pond bacteria act like ‘microscopic eyeballs’ to sense light and move towards it
Light induced change in bacteria
Previous studies have shown Synechocysti contain photosensors and that they are able to perceive the position of a light source and move towards it – a phenomenon called phototaxis. This study showed how this process works. Bacteria moving towards a light is pictured
See also:
Comparative Proteomics Reveals Important Viral-Host Interactions in HCV-Infected Human Liver Cells
Theoretical investigation of hydrogen atom transfer in the cytosine-guanine base pair and its coupling with electronic rearrangement. Concerted vs stepwise mechanism
Wheeler’s delayed-choice gedanken experiment with a single atom
Effect of Methylation on the Properties of the H-Bridges in DNA. A Systematic Theoretical Study on the Couples of Base Pairs
Photoinduced amino–imino tautomerism of 2-aminopyridine in a low-temperature argon matrix
My comment: Even those who claim to be trying to reconcile the differences between theorists and creationists contribute to ongoing misunderstanding.
See: Darwinists Underestimate Nature. Creationists Underestimate God

You say that “We can produce new species at will and it happens all the time”.

My comment: February 7, 2016 at 7:21 am
Like many others, you seem to be confused about what can happen in the lab compared to what does not happen outside the lab.
For example: Re: “1) Hybrids, where Species 1 crossed with Species 2 gives you Species 3. ”

For comparison: Species of Drosophila


Hybrids of Drosophila pseudoobscutra and D. persirnilis are easily obtainable in the laboratory, but they are absent in localities where both species occur side by side (14).

See also: The Myopics of Darwinism, Dawkinsism and Blind Faith – Enter Evolution 2.0

My comments: Perry Marshall seems to be siding with those who think hybrids are proof that evolution may occur over millions of years, albeit without the pseudoscientific nonsense about mutations and natural selection.

James V. Kohl says: January 26, 2016 at 3:24 pm
My 2012 Templeton Grant Proposal:

Nutrient chemicals are required to sustain life and for transgenerational epigenetic inheritance of biological populations. This fact is exemplified in the honeybee model organism and other model organisms. The nutrient chemicals cause receptor-mediated events. The receptor-mediated events allow nutrient chemicals to enter though the cell wall. Electrostatic changes then alter intracellular signaling as nutrient chemicals are metabolized to species-specific chemicals called pheromones.
The metabolism of nutrient chemicals to pheromones exemplifies the apparent design of biology. Bottom-up (genetically predisposed organization) and top-down reciprocity via sensory activation is what allows nutrient chemicals and pheromones to control survival of the species. The nutrient chemicals support individual fitness and the pheromones control reproduction. From the bottom up, their ability to control species survival is enabled by their epigenetic effects of nutrient chemicals that cause stochastic gene expression. Similarly, from the top down, pheromones epigenetically effect stochastic gene expression (in cells of organisms from microbes to man).
All extant organisms show a clear pattern of genetic predispositions that enable nutrient chemical-dependent and pheromone-dependent adaptive evolution via ecological, social, neurogenic, and socio-cognitive niche construction. Adaptive evolution is facilitated via the expression of new genes, including those that are important to the development of language abilities and human brain development.
The ability of cells containing genes to produce de novo genes does not seem to have developed via random mutations. Although gene expression is stochastic, organisms that choose the wrong nutrient chemicals are less reproductively fit and doomed to suffer and die. One organisms choice also may determine downstream down-stream epigenetic effects on other organisms that selfishly compete for life-sustaining nutrient chemicals in same ecological niche. Only when some level of cooperation is achieved can individuals or species survive in the same ecological niche, and species-specific pheromones ensure that two species do not share the same social niche.
Ecological and social niche construction collectively enabled evolved nutrient-dependent and pheromone-dependent neurogenic niche construction, which is exemplified in vertebrates by conservation of the GnRH molecule, and diversification of its receptor across 400 million years of adaptive evolution that first required nutrient-dependent and pheromone-dependent sexual reproduction in unicellular and multicellular organisms, with molecular origins as the alpha-mating pheromone in brewer’s/baker’s yeast.
The ecological and social niches constructed by one species that eats another exemplify how that advent of multicellularity and cooperation in different species enabled the cascade of diversity that is readily evidenced across Creation, as it always has been. When viewed from a model of complexity, Creation of the diversity of life does not appear to involve random events, but instead involves the common molecular biology of receptor-mediated events is species from microbes to man.
The concept that is extended is the epigenetic tweaking of immense gene networks in ‘superorganisms’ that ‘solve problems through the exchange and the selective cancellation and modification of signals. It is now clearer how an environmental drive probably evolved from that of food ingestion in unicellular organisms to that of socialization in insects. It is also clear that, in mammals, food odors and pheromones cause changes in hormones that have developmental affects on sexual behavior in nutrient-dependent, reproductively fit individuals across species of vertebrates.
Thus, simply put: “Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans.” And there is nothing random about that!

My comment: I did not receive the grant and as of 2/9/16, I had not received a response from Perry Marshall to my post, which addresses many of his claims. I held this blog post for several weeks to give Marshall and others a chance to respond to what is currently known to serious scientists about how physics, chemistry, and molecular epigenetics must be linked to healthy longevity or to virus-driven pathology.  Obviously, it is not only the neo-Darwinists and theoretical physicists who want to continue to ignore the obvious links from atoms to ecosystems via the sun’s anti-entropic energy.

Perry Marshall says:

February 9, 2016 at 3:39 pm

No argument that living things use sunlight in processing of information.Show me a non-living thing that turns sunlight or chemicals into code and then we’ll have something to talk about. Thus far nothing you have presented so far meets the specification of the prize.

James V. Kohl says:

February 9, 2016 at 5:51 pm
Thanks. I think others can see what is happening with the specifications of the prize.
From page 206 of “Evoluton 2.0.”
You wrote: “But I could find no formula or transformation that turns matter or energy into information. This is precisely what the Evolution 2.0 Prize seeks to discover.”
Sunlight is the energy that links information to matter. Now it’s not a formula that you want; it’s an example of a non-living thing that links sunlight from quantum physics to the chemistry of protein folding via the de novo creation of nucleic acids.
Why not simply admit that you will not accept any accurate representation of biological facts that link the de novo creation of nucleic acids (the code) to all RNA-mediated biodiversity. You’re stuck with your claims about hybrids and Shapiro’s nonsense.
Addendum: Shapiro’s nonsense was published as Evolution: A View from the 21st Century
Excerpt: Proteins operate as conditional microprocessors in regulatory circuits.
Excerpt: The concept of most proteins as systems of domains exemplifies the new combinatorial thinking frequently emphasized in this book. It makes good sense a priori to expect that a protein will make a successful functional change by acquiring an existing intact binding or catalytic capability. Intuitively, this has a far higher probability of proving effective than does a random process of changing one amino acid at a time and gradually selecting modest improvements in catalysis or binding specificity.
My comment: The processes that link RNA-mediated amino acid substitutions to cell type differentiation in all living genera via the physiology of reproduction are nutrient-dependent. They are not random processes that change amino acids one at a time. The processes link atoms to ecosystems via hydrogen-atom transfer in DNA base pairs in solution in the context of microRNAs, adhesion proteins, DNA repair, and the stability of organized genomes that links supercoiled DNA to protection against virus-driven entropy.
Shapiro’s book (2011) and Nei’s book (2013) Mutation-Driven Evolution were more than a decade past their due dates. As is common with all textbooks, by the time they are published, new information makes them increasingly worthless to anyone who needs to learn more about what is known to serious scientists. For that knowledge, you must follow the extant literature and try to keep up. Good luck catching up before you try to keep up with what is being published on the role of microRNAs in cell type differentiation.
See, for example: Items: 1 to 20 of 47233

Perry Marshall says:

February 9, 2016 at 9:45 pm

James, if you think you have a solution then fill out a proper prize submission and show that you have met the specification.
My comment: Perry Marshall removed my response. I asked where to find the prize submission form and asked again about the Non-Disclosure Agreement (NDA), which he claims is not yet available. He contacted me via email. He claimed that he would send the submission form and asked me to be patient while waiting for the NDA. It seems clear to me that the prize is part of a scam. One that provides an opportunity for Perry Marshall to market his book with his opinions about how biologically-based cause and effect are linked to nutrient-dependent biodiversity. But, as every serious scientist knows, Perry Marshall’s opinions are worth no more than the opinions of others who are biologically uninformed.

James V. Kohl says:

Your comment is awaiting moderation.

February 10, 2016 at 2:30 am

Thanks. I’m disgusted by your claims and the missing “proper prize submission” form, and the unavailable non-disclosure agreement.
The delay has left others with the opportunity to move forward with publications that address your questions in the context of the same experimental evidence I intended to provide several weeks ago.
You should have admitted that the forms weren’t available, so that everyone would be aware of the delay you caused in my attempt to win the prize.

Feedback loops link insects to human brains

Ants Swarm Like Brains Think

A neuroscientist studies ant colonies to understand feedback in the brain.

By Carrie Arnold Illustration by Jonathon Rosen April 23, 2015

Excerpt 1: “The behavior of each individual in the group is set by the rate at which it meets other ants and a set of basic rules. Its behavior alters that of its neighbors, which in turn affects the original ant, in a classic example of feedback. The result is astonishing, complex behavior.”

Excerpt 2): “Feedback loops are everywhere on every level. They allow the system to realize that what it used to be doing isn’t working any more, and to try something new.”

My comment: See also: The Brain Is Broadly Wired for Reproduction and Feedback loops link odor and pheromone signaling with reproduction

In his comment on this article, Roy Niles claims that he has explained how purposeful systems evolved in bees, ants, and other species. Nothing with any explanatory power has come from him so far. His claim that “…each and all of the ants are born to fit within a hierarchy…” is more pseudoscientific nonsense.
In my model, nutrient-dependent RNA-mediated amino acid substitutions link ecological variation to ecological adaptations without ridiculous theories about “evolved” purposeful systems. For example, nutrient-dependent metabolic networks and genetic networks are linked via pheromones that control the physiology of reproduction and fixation of the amino acid substitutions.
See: Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors
Excerpt: Conditioned hormonal and behavioral responses to odors associated with food selection and conspecifics in mammals require something like the collective ‘neural networks’ of beehives. Philosophically and metaphorically, these neural networks extend to mammalian brains. The concept that is extended is the epigenetic tweaking of immense gene networks in ‘superorganisms’ (Lockett, Kucharski, & Maleszka, 2012) that ‘solve problems through the exchange and the selective cancellation and modification of signals (Bear, 2004, p. 330)’. It is now clearer how an environmental drive probably evolved from that of food ingestion in unicellular organisms to that of socialization in insects.
See also: Nutrient-dependent/pheromone-controlled adaptive evolution: a model
Conclusion: “Minimally, this model can be compared to any other factual representations of epigenesis and epistasis for determination of the best scientific ‘fit’.”
Roger Gorski and JV Kohl 1995 05

Mutisensory integration: watching the paradigm shift

Multisensory integration and causal inference in the brain
Excerpt (with my emphasis):  It is largely unknown how the brain implements prior knowledge and expectations. Various mechanisms have been proposed such as spontaneous activity (Berkes et al., 2011), the fraction of neurons encoding a particular feature (Girshick et al., 2011), their response gain and tuning curves or connectivity and top-down projections from higher order areas (Rao and Ballard, 1999).”
My comment: The brain implements prior knowledge and expectations through nutrient-dependent pheromone-controlled feedback loops linked to RNA-mediated chromatin loops and protein folding.
Feedback from Network States Generates Variability in a Probabilistic Olfactory Circuit
Excerpt: “The integration of sensory information with network states may represent a general mechanism for generating variability in behavior.”
The integration is nutrient-dependent. Integration links the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man via the biophysically constrained chemistry of nutrient-dependent RNA-mediated amino acid substitutions. The substitutions are fixed via the biophysically constrained physiology, which links the RNA-mediated chemistry of protein folding to of nutrient-dependent reproduction via metabolic networks and genetic networks. For example, in vertebrates, the importance of the  GnRH-controlled link to metabolic networks and genetic networks has been exquisitely detailed. Only one nutrient-dependent amino acid substitution in the GnRH decapeptide is required to link differences in many different species.

Evolution of gonadotropin-releasing hormone (GnRH) structure and its receptor

Excerpt: “When the chiral amino acid (Ala) in position six of Ciona I GnRH was substituted with the achiral glycine or with d-Ala, which enhances the type II’ β-turn conformation, there was a marked increase in the binding affinity of the peptides at the vertebrate GnRH receptor (Barran et al., 2005).”

See also: Evolution of Constrained Gonadotropin-releasing Hormone Ligand Conformation and Receptor Selectivity

Excerpt: “These findings indicate that the substitution of glycine for a chiral amino acid in GnRH during evolution allows a more constrained conformation for receptor binding and that this subtle single amino acid substitution in a site remote from the ligand functional domains has marked effects on its structure and activity.”

My comment: Glycine is the “simplest” amino acid. The “R group” is a hydrogen atom, which is why glycine is not a chiral compound. That means there is no such thing as L-glycine or D-glycine. For comparison,  other natural amino acids are chiral.  Most amino acids are L and sugars are D.

Some evolutionary theorists seem to think that glycine formed spontaneously from acetate or glycerol, which also suggests that a deep space astronomical “accident” led to the presence of L-amino acids instead of D-amino acids. See: Enrichment of the amino acid l-isovaline by aqueous alteration on CI and CM meteorite parent bodies

Excerpt: “…amino acids delivered by asteroids, comets, and their fragments would have biased the Earth’s prebiotic organic inventory with left-handed molecules before the origin of life.”

Theorists who are unable to link our sun’s anti-entropic energy to the origin of life via the de novo creation of amino acid substitutions have also proposed other ridiculous theories that fail to link nutrient-dependent amino acid substitutions to cell type differentiation via what is currently known about the physiology of reproduction, fixation of amino acid substitutions, and cell type differentiation.

Watching a paradigm shift in neuroscience

Excerpt (with my emphasis): “…the variability provided by the feedback connections dominate an adaptive feature of the behavior, its variability. This work adds C. elegans to the elongating list of animals, whose nervous systems are organized such that ongoing activity is modulated by external stimuli. It seems, in such nervous systems, even a numerically small feedback component provides a fundamental contribution to the overall architecture. What does this mean for brains whose anatomy appears to be dominated by feedback loops?”

My answer: That was a rhetorical question. Bjorn Brembs knows what it means. It means that anyone who denies what is known about nutrient-dependent pheromone-controlled feedback loops in species from microbes to man will continue to look even more foolish to serious scientists.

See for example: Nutrient-dependent/pheromone-controlled adaptive evolution: a model.

Excerpt: “For instance, ‘our experiments suggest that excitatory odor responses are transiently suppressed (in terms of overall firing rates), but more complex temporal shaping of responses may occur because of interplay of intrinsic properties, sensory drive, and the feedback activity’ (Markopoulos, Rokni, Gire, & Murthy, 2012, p. 1186). In context, this was suggested in ‘Feedback loops link odor and pheromone signaling with reproduction’ (Boehm, Zou, & Buck, 2005).”

My comment: Since the time that 2004 Nobel Laureate, Linda Buck co-authored (Boehm, Zou, & Buck, 2005), the link from odor and pheromone signaling via the feedback loops linked to reproduction has been clearly established. Nutrient-dependent RNA-directed DNA methylation and RNA-mediated amino acid substitutions differentiate all cell types in all individuals of all species. In species from microbes to man, for example,  fixation of the amino acid substitutions occurs in the context of the nutrient-dependent pheromone-controlled physiology of reproduction.

The physiology of reproduction in animals is linked to the physiology of reproduction in plants via the anti-entropic biological energy of the sun and the light-induced de novo creation of amino acids.

See: Common origins of RNA, protein and lipid precursors in a cyanosulfidic protometabolism

Excerpt: “Rather than invoking fundamentally different scenarios and chemistries for the syntheses of the molecular components of informational, compartment-forming and metabolic subsystems, and then concluding that one or other subsystem must have come first, we describe a scenario in which variations on a chemical homologation theme result in the components of all three subsystems being produced and then blended together.”

My comment: Before anything is produced or blended together, the sun’s biological energy must start the chemical reactions that lead to the de novo creation of amino acids. In several other blog posts, I have linked viral microRNA suppression by nutrient-dependent microRNAs from entropic elasticity to increasing organimal complexity via the biophysically constrained chemistry of nutrient-dependent RNA-mediated protein folding, whether it occurs in the context of photosynthesis or nutrient uptake, including DNA uptake, from heterospecifics.

A recent report links nutrient-dependent microRNAs from protein biosynthesis and degradation to memory, albeit with no mention of the link from microRNAs to amino acid substitutions that differentiate cell types in the brain. The report is slightly misleading, but see: miR-26a and miR-384-5p are required for LTP maintenance and spine enlargement

Excerpt (with my emphasis): “Protein synthesis is also required for other forms of synaptic plasticity, such as long-term synaptic depression (LTD), which leads to decreases in synaptic strength. The unique changes in synapses that occur during each type of synaptic plasticity cannot be accounted for by global upregulation of translation. Indeed, translation of selective messenger RNAs (mRNAs) has been implicated in synaptic plasticity5. For instance, after LTP is induced, Ca2þ/calmodulin-dependent protein kinases II (CaMKII) promotes phosphorylation of cytoplasmic polyadenylation element (CPE)-binding protein, which in turn stimulates the polyadenylation and translation initiation of mRNAs containing CPE7,8. However, little is yet known about the mechanisms of gene-specific regulation of translation and about which genes are translated during LTP.”

My comment: Their claim that “little is yet known” can be placed into the context of what is known to others. The microRNA/messenger RNA balance links ecological variation to nutrient-dependent protein biosynthesis via amino acid substitutions that stabilize protein folding in the organized genomes of all genera. See: Context-specific microRNA function in developmental complexity

Excerpt: Overwhelming evidence is also now accumulating to support hypotheses for miRNA and other small non-coding RNA molecules in autocrine, paracrine, and exocrine signalling events (Dinger et al., 2008). For example, miRNAs have been shown to exist in 50–100 nm diameter vesicles known as exosomes, which are secreted by a variety of cell types and tissues, and have been found to be involved in processes such as cancer (Lotvall and Valadi, 2007; Skog et al., 2008). Importantly, miRNAs from these vesicles can even be taken up into recipient cells to mediate silencing effects (Kosaka et al., 2010). Interestingly, the plant miR-168—highly expressed in rice—has also recently been shown to be present in human blood plasma (Zhang et al., 2011). This investigation also revealed plant miRNA to be stable in cooked foods, with dietary consumption of plant material resulting in exogenous plant miRNAs being absorbed into the bloodstream of mice from the gastrointestinal tract. Plant miR-168 was even shown to regulate the expression levels of target genes in the liver such as LDLRAP1 (low-density lipoprotein receptor adapter protein 1), resulting in decreased LDL removal from blood plasma in mice. Indeed, such a significant discovery revolutionizes the complexity with which miRNAs are considered to function in mammals throughout various developmental and pathophysiological processes.

My comment: The anti-entropic energy of the sun is linked to nutrient-dependent microRNAs that repair DNA damage. The damage done by viral microRNAs links entropic elasticity to the RNA-mediated protein biosynthesis and degradation required for epigenesis and epistasis. The link from DNA damage repair may be the most important consideration given the obvious atoms to ecosystems connection to cell type differentiation via amino acid substitutions.

The paradigm shift in neuroscience that links top-down causation to biodiversity via cell type differentiation has left theoretical physicists with nothing to contribute to scientific progress. Instead, they are forced to invent more ridiculous theories. For example, in response to what is currently known to serious scientists about light-induced de novo creation of amino acids and biologically-based cause and effect manifested in cell type differentiation linked to amino acid substitutions, theorists have asserted that information transmission can occur without the transmission of energy.

See: Photon ‘afterglow’ could transmit information without transmitting energy
Excerpt: “…up until now, it has been believed that real quanta, such as real photons of light, are the only carriers of information from the early Universe.”
See also: Attempts to exempt speculative theories of the Universe from experimental verification undermine science, argue George Ellis and Joe Silk.
I asked: Has everyone decided to ignore that fact? There is a clear link from the light-induced de novo creation of amino acids to their anti-entropic epigenetic effect on cell type differentiation in plants and animals. Simply put, cell type differentiation is controlled by the biophysically constrained chemistry of RNA-mediated amino acid substitutions and protein folding.
Inventing a theory of information transfer that occurs without energy transfer is required because serious scientists have focused on the fact that “Life is physics and chemistry and communication” That means pseudoscientists are forced to fight against the facts by inventing new theories that disassociate energy and information.But see: Scientific method: Defend the integrity of physics The discussion of information transfer without transmitting energy ignores that fact that Life is physics and chemistry and communication. See also: What is Life?: With Mind and Matter and Autobiographical Sketches
Excerpt (with my emphasis): “…a very small number of individuals, say two or three in tens of thousands, turn up with small but ‘jump-like’ changes, the expression ‘jump-like’ not meaning that the change is so very considerable, but that there is a discontinuity inasmuch as there are no intermediate forms between the unchanged and the few changed. De Vries called that a mutation. The significant fact is the discontinuity. It reminds a physicist of quantum theory -no intermediate energies occurring between two neighbouring energy levels. He would be inclined to call de Vries’s mutation theory, figuratively, the quantum theory of biology. We shall see later that this is much more than figurative. The mutations are actually due to quantum jumps in the gene molecule”(p. 33-34).
My comment: Theoretical physicists must now break the link between energy and information or change the definition of “mutation.” That fact helps to explain why two theorists recently discussed changing the definition of evolution. See: Beyond Genetic Evolution. A Conversation With Eva Jablonka
Excerpt 1 with my emphasis) “Types do not have to be genotypes, they can be epigenotypes, behavioral types,  symbolic types. If we agree on that broad definition,  I don’t see why change over time with respect to them is not evolution. Symbolic evolution is a very different type of evolution,  among other things it is a developmental  system that can direct its own evolution. But this does not make it non-evolutionary.”
Excerpt 2) “This is a good opportunity to move to the second dimension of evolution, epigenetics. Now we do have mechanisms, and we can begin to understand how epigenetics counts as an inheritance system.”

Regarding Excerpt 1):  “I don’t see why change over time with respect to them is not evolution.”

See: Sulfur-cycling fossil bacteria from the 1.8-Ga Duck Creek Formation provide promising evidence of evolution’s null hypothesis.
No change occurred in microbes during 1.8 billion years.
See also: Evolutionary resurrection of flagellar motility via rewiring of the nitrogen regulation system. 
Genetically modified bacteria re-evolved their missing flagella “over-the-weekend.”
Claims that “evolution” did not occur in 1.8 billion years but it occurred in 4 days do not support use of the definition of evolution as “…change over time…” or a change to “symbolic evolution”(e.g., “…a developmental  system that can direct its own evolution.”) Developmental systems in all organisms are nutrient-dependent and they do not direct their own evolution. Organisms and species either find enough food to eat or they die and become extinct.

Regarding Excerpt 2): “…the second dimension of evolution, epigenetics.” 

Conserved molecular mechanisms of epigenetically-effected biophysically constrained nutrient-dependent pheromone-controlled RNA-directed DNA methylation and events link the RNA-mediated chemistry of protein folding to cell type differentiation in species from microbes to humans. The conserved molecular mechanisms show how the epigenetic landscape becomes the physical landscape of DNA in organized genomes without use of any definition of “mutation” or any definition of “evolution.”
The conserved molecular mechanisms link top-down causation to biologically-based cause and effect without the pseudoscientific nonsense of definitions and assumptions. Serious scientists don’t care how long anyone thinks it might take for mutations to lead to the evolution of a new species.
Mutations perturb protein folding. They cannot lead to the evolution of a new species. Loss of function mutations are linked to genes that are no longer needed, not to the de novo creation of new genes.  Thus, no loss of function in microbes that are supposedly 1.8 billion years-old can be compared to the gain of the bacterial flagellum “over-the-weekend.” Watch your clock, or set your timer. If you look again at a microbe that supposedly “re-evolved” its flagellum, and you see the flagellum, you need not reset your clock to 1.8 billion years.
Gaining the functional flagellum was linked from nutrient-dependent amino acid substitutions to pheromone-controlled cell type differentiation of a complex structure. No loss of function in 1.8 billion years could be linked to the absence of light-induced amino acid substitutions in bacteria that live the bottom of the sea floor.
Understanding how viral microRNAs and nutrient-dependent microRNAs are linked from the microRNA/messenger RNA balance to nutrient-dependent RNA-mediated cell type differentiation via the physiology of reproduction is obviously important to understanding how metabolic networks and genetic networks interact in the context of the epigenetic landscape. But see: New insight into how proteins find their DNA binding sites in the genome.
Excerpt: Rohs and colleagues found that introducing shape-recognizing amino acids from one transcription factor to another swapped binding specificities between Hox proteins.
My comment: This suggests the need for a model of RNA-mediated cell type differentiation that links nutrient-dependent molecular epigenetics from genome positioning and timings and molecular distance via amino acids, which also suggests that the gene-centric approach by evolutionary theorists has been a waste of time, money, effort, and careers. If so, that fact helps to explain why serious scientists are Combating Evolution to Fight Disease.
See my comments on that article to the “Science Magazine site
3/7/14 Darwin probably anticipated the insemination of population genetics that led to the bastardization of his detailed observations in the “Modern Synthesis.” He politely insisted that ‘conditions of life’ be considered before natural selection.
There are two ‘conditions of life.’ It is nutrient-dependent and pheromone-controlled. Rosenberg and Queitsch now note the work with Dobzhansky’s rarely acknowledged claim: “I am a creationist and an evolutionist.” They also declare the need for “Deep understanding of the mechanisms that generate variation at the molecular level…”
Deep understanding of the ‘conditions of life’ does not come from theory.
Problems with the “modern synthesis” now lead us back to the facts about biologically-based cause and effect that Darwin and Dobzhansky approached with humility, which are the same biological facts that evolutionists approached with ignorance about behavioral affects and the arrogance that accompanies that ignorance. Rosenberg and Queitsch echo the sentiments of those who have been subjected to academic suppression.
Clearly, however, “nothing in evolution makes sense except in the light of biology” is not an exaggeration. It is a common sense statement about the biologically plausible genesis of functional cell types. Population genetics and evolutionary theories abandoned the biophysical constraints of ecological variation and the physiology of reproduction, which enable epigenetically-effected nutrient-dependent pheromone-controlled receptor-mediated ecological adaptations and species diversity via the complexities of protein folding and niche construction.
It’s time for biophysicists to tell theorists and pathologists how to differentiate between theories about the genesis of different cell types and the biological facts about the nutrient-dependent pheromone-controlled ecological adaptations that enable the genesis of different cell types in individuals of different species. Simply put, it’s time to stop trying to explain ecological adaptations in the context of mutations and evolution.
7/15/14 Re: “Molecular biology and evolutionary biology have been separate disciplines and scientific cultures: The former is mechanistic and focused on molecules; the latter is theoretical and focused on populations.”
Now see: A mechanistic link between gene regulation and genome architecture in mammalian developmenthttp://www.sciencedirect.com/science/article/pii/S0959437X14000495 for the refutation of neo-Darwinian pseudoscientific nonsense.Experimental evidence of biologically-based cause and effect does not support ideas about mutations, natural selection, and the evolution of biodiversity.Experimental evidence of biologically-based cause and effect supports the fact that ecological variation leads to nutrient-dependent pheromone-controlled ecological adaptations in species from microbes to man via conserved molecular mechanisms.
9/7/14 Re:”…the driver of evolution is not mutations or variation but selection, be it natural, artificial, kin or sexual selection. Mutation is but one of the factors that contribute to variation.”I thought Robert Frye knew better than that, because he attended a 1993 symposium I organized and my 2007 Reiss Plenary session of The Mind’s Eyes: Modeling the Development of Diverse Sexual Preferences.Perhaps this is a different Robert Frye or one who thinks that sexual orientation arises via mutations and natural selection in human males but via nutrient-dependent pheromone-controlled cell type differentiation in yeasts as we reported in our 1996 Hormones and Behavior review. From Fertilization to Adult Sexual Behavior
http://www.hawaii.edu/PCSS/biblio/articles/1961to1999/1996-from-fertiliz… “Parenthetically it is interesting to note even the yeast Saccharomyces cerevisiae has a gene-based equivalent of sexual orientation (i.e., a-factor and alpha-factor physiologies). These differences arise from different epigenetic modifications of an otherwise identical MAT locus…”Robert: What about Anne’s rams. Are they among the selected mutants that you think may have evolved their exclusive homosexual orientation?
9/13/14 “An alternative theory proposes environmentally induced change in an organism’s behavior as the starting point (1), and “phenotypic plasticity” that is inherited across generations through an unspecified process of “genetic assimilation” (2).” http://www.sciencemag.org/content/332/6034/1161.short
This is now more than merely an alternative theory of genetic assimilation. It links transgenerational epigenetic effects from nutrient uptake and RNA-mediated events to amino acid substitutions that differentiate the cell types of all cells in all individuals of all organisms.
See, for example: Starvation-Induced Transgenerational Inheritance of Small RNAs in C. elegans http://www.cell.com/cell/abstract/S0092-8674(14)00806-XThe nutrient stress-induced RNA-mediated events, which link the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man, also link morphological and behavioral diversity via conserved molecular mechanisms exemplified in the context of biologically plausible ecological speciation in nematodes.
See: System-wide Rewiring Underlies Behavioral Differences in Predatory and Bacterial-Feeding Nematodes http://linkinghub.elsevier.com/retrieve/pii/S0092867412015000
A difference in their feeding behavior and in the anatomy of their mouth parts is linked from nutrient-dependent pheromone-controlled feedback loops to ecological, social, and neurogenic niche construction. The change in focus from mutations, natural selection, and the evolution of biodiversity via unknown evolutionary events to nutrient-dependent pheromone-controlled RNA-mediated events that differentiate cell types may be required for others to realize the difference between evolutionary theories and biologically-based facts about RNA-mediated events.RNA-mediated events are biophysically constrained, which means they are a biologically plausible way to link the physics and chemistry of protein folding to increasing organismal complexity via molecular biology. RNA-mediated events can also be compared to any unknown evolutionary events that might arise in the context of an alternative theory about constraint-breaking mutations, or other theories that include no mention of RNA-mediated events.
For a model of RNA-mediated cell type differentiation that links nutrient-dependent molecular epigenetics to genome positioning and timings and to molecular distance see From Fertilization to Adult Sexual Behavior.For the link from RNA-mediated cell type differentiation via amino acid substitutions in species from microbes to humans see Nutrient-dependent/pheromone-controlled adaptive evolution: a model.
For the link from atoms to ecosystems in all genera, see: Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems


Memory of repression and memory of behavior (2)

Mutations that become so common that they affect more than 1% of a population are called polymorphisms (for example, the human blood types A, B, AB, and O).

The claim that human blood types are mutations should be supported with experimental evidence of biologically-based cause and effect. Ask your professor, “What evolutionary event linked the mutation to natural selection and the evolution of human blood types?
How did nutrient-dependent cell type differentiation become mutation-initiated cell type differentiation, when it is nutrient-dependent, receptor-mediated in human blood cells, and pheromone-controlled by RNA-mediated events in species from microbes to all other primates?”
Tell your professor to stop touting the pseudoscientific nonsense of evolutionary theory and learn about RNA-mediated events that link nutrient uptake to cell type differentiation, which is controlled by feedback loops. The feedback loops link food odors and pheromones to reproduction in species from microbes to man, according to at least one Nobel Laureate and her co-authors.
The basics of cell type nutrient-dependent pheromone-controlled cell type differentiation are detailed in less than 2 minutes in this video.

Additional complexity is included in this 5.5 minute video from my last presentation. Examples of ecological speciation from nematodes to primates may help others who are Combating Evolution to Fight Disease.