I’m not getting any responses to an attempt to discuss On epigenetics: We are not just our DNA. That suggests I should use the claims and my attempt to discuss them in a blog post. If no one else wants to discuss the links from atoms to ecosystems in the diagram above, at least there will be a record to show they ignored them, again.
For comparison: Watch paleoartist John Gurche’s vision of his own direct ancestry in under 2 minutes. Learn how he draws on fossil discoveries and forensic techniques to create transfixing reconstructions of long-lost human ancestors.
Yale University Press made this video to promote Shaping Humanity: How Science, Art, and Imagination Help Us Understand Our Origins in which paleoartist John Gurche uses fossils and forensics to create reconstructions of long-lost human ancestors.
See below: For contrast, researchers who report that an amino acid substitution linked to 180 disorders of cell type differentiation; to pathology; and to human facial characteristics are placing their findings into this misrepresentation of biologically-based cause and effect.
In outline: Newton and Laplace created a view of the world whose becoming is entirely entailed by “the laws”, plus the initial and boundary conditions. This view is in a deep sense not altered by quantum mechanics on at least some of its interpretations. In this world view, there can be no “true creativity”. All is already entailed from the start, for example, the Big Bang.
Few living scientists are as ambitious in their choice of problems as Stuart Kauffman. He is a polymath, with a degree in medicine and training in biochemistry, genetics, physics, philosophy and other fields.
… proposed that our scientific understanding of reality is radically incomplete, and that some sort of anti-entropy, order-generating force remains to be discovered.
My comment: Predictably, the anti-entropic force links atoms to ecosystems. Predictably, when it is rediscovered, it will embarrass anyone who has ignored Schrodinger’s claims about biologically-based cause and effect in “What is Life?”
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)
Porous systems are investigated using eigendecomposition of the Laplace matrix. Three parameters; tortuosity, surface-to-pore volume ratio and relaxation rate are derived from the eigenvalue spectrum of the Laplace matrix and connected to the parameters in the Padé approximation, an expression often used to describe the time-dependent diffusion coefficient in porous systems. The Padé length is identified for systems with large pore to connector volume ratio. The results are compared with simulations.
For comparison, see:
What is Life?: With Mind and Matter and Autobiographical Sketches (Canto Classics) Reprint Edition with forward by Roger Penrose who co-authored with George F.R. Ellis and Stephen Hawking
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?
My comment: Too often! How often do we hear about models like this: Nutrient-dependent/pheromone-controlled adaptive evolution: a model
Animal models are often used to model human physical and mental disorders. The honeybee already serves as a model organism for studying human immunity, disease resistance, allergic reaction, circadian rhythms, antibiotic resistance, the development of the brain and behavior, mental health, longevity, diseases of the X chromosome, learning and memory, as well as conditioned responses to sensory stimuli (Kohl, 2012).
For comparison see: Human brain networks function in connectome-specific harmonic waves
The dynamics of the oscillatory cortical networks is thought to emerge from the interplay of excitation; for instance mediated by glutamatergic principal cells, and inhibition; for instance mediated γ-aminobutyric acid GABAergic interneurons29.
Excitatory amino acids play a key role in both adaptive and deleterious effects of stressors on the brain, and dysregulated glutamate homeostasis has been associated with psychiatric and neurological disorders. Here, we elucidate mechanisms of epigenetic plasticity in the hippocampus in the interactions between a history of chronic stress and familiar and novel acute stressors that alter expression of anxiety- and depressive-like behaviors. We demonstrate that acute restraint and acute forced swim stressors induce differential effects on these behaviors in naive mice and in mice with a history of chronic-restraint stress (CRS). They reveal a key role for epigenetic up- and down-regulation of the putative presynaptic type 2 metabotropic glutamate (mGlu2) receptors and the postsynaptic NR1/NMDA receptors in the hippocampus and particularly in the dentate gyrus (DG), a region of active neurogenesis and a target of antidepressant treatment. We show changes in DG long-term potentiation (LTP) that parallel behavioral responses, with habituation to the same acute restraint stressor and sensitization to a novel forced-swim stressor. In WT mice after CRS and in unstressed mice with a BDNF loss-of-function allele (BDNF Val66Met), we show that the epigenetic activator of histone acetylation, P300, plays a pivotal role in the dynamic up- and down-regulation of mGlu2 in hippocampus via histone-3-lysine-27-acetylation (H3K27Ac) when acute stressors are applied. These hippocampal responses reveal a window of epigenetic plasticity that may be useful for treatment of disorders in which glutamatergic transmission is dysregulated.
My comment: McEwen’s group does not link the ubiquitous mathematical framework referred to as the “eigendecomposition of the Laplace operator” to any theory. His group knows how heat, light, sound, electricity, magnetism, gravitation, and fluid mechanics predict human cortical activity. They may also know that hydrogen-atom transfer in DNA base pairs in solution must link atoms to ecosystems at the macroscopic scale via the circulating blood delivered to the brain.
So far as I know, Bruce McEwen has always used a model of nutrient-dependent epigenetically-effected biologically-based cause and effect to link ecological variation and ecological adaptation. His group now attests to the fact that the link can be one nutrient-dependent RNA-mediated amino acid substitution: BDNF Val66Met.
They have also linked what they know about BDNF Val66Met to what is known by others about COMT Val158Met and behavior during the life history transitions from adolescence to adulthood. The link is a functional single nucleotide polymorphism (SNP) in COMT (G-to-A base-pair substitution). The base-pair substitution leads to a methionine (Met) valine (Val) amino acid substitution at codons 108/158 (COMT Val158Met).
Carriers of the Met amino acid substitution are reported to have an allele that is linked to display of a fourfold decrease in enzymatic activity compared to Val allele carriers. The Met amino acid substitution is accompanied by increase of prefrontal DA activity (Lachman et al. 1996; Lotta et al. 1995). But, the link between the amino acid substitution, increased prefrontal DA activity and behavior is reported only as a link from an allele, as if a different gene was linked to differences in behavior outside the context of epigenetic effects on hormones that affect behavior.
See: Oppositional COMT Val158Met effects on resting state functional connectivity in adolescents and adults
…our findings are in line with a genetically-informed schizophrenia model derived from an orphan disease (Gothelf et al. 2005, 2013). In velo-cardiofacial syndrome (VCFS), a rare disorder with an increased risk of schizophrenia resulting from a microdeletion in 22q11.2, patients are known to lack one copy of COMT. In this patient group available evidence suggests that genotype effects of COMT Val158Met on cognitive performance are critically dependent on the maturational stage of the brain (Gothelf et al. 2005).
My comment: There is no mention that COMT Val158Met links an energy-dependent hydrogen-atom transfer of a DNA base pair in circulating blood to the amino acid substitution and the effect on hormones linked to the affect on behavior in the report. Instead they report their findings in the context of a gene linked from loss of one amino acid substitution to schizophrenia and to abnormal pharyngeal arch development that results in defective development of the parathyroid glands, thymus, and conotruncal region of the heart. Actually, I mentioned the 180 different disorders of cell type differentiation (above) because there are more than 180 different clinical features associated with velocardiofacial syndrome, with no single anomaly present in every patient. Some abnormalities are more common than others. Affected individuals may present with structural or functional palatal abnormalities, cardiac defects, unique facial characteristics, hypernasal speech, hypotonia, and defective thymic development. That means one energy-dependent base-pair change and one amino acid substitution was linked to all those morphological and behavioral phenotypes during life history transitions.
Cause and effect was reported as: Genes exhibit different behaviours in different stages of development
See my comment on that report:
The study highlights the dynamism of gene effects on brain function throughout the various stages of life such as adolescence or adulthood.
So does everything currently known about nutrient-dependent pheromone-controlled RNA-directed DNA methylation and cell type differentiation via RNA-mediated events and amino acid substitutions in species from microbes to man. See the following two references for information on the honeybee model organism.
Organizational and activational effects of hormones on insect behavior
Honey bees as a model for understanding mechanisms of life history transitions
For the link to conserved molecular epigenetics in mammals see: From Fertilization to Adult Sexual Behavior
Summary: These researchers know that they linked an energy-dependent base pair change to an amino acid substitution. They know that they linked one amino acid substitution to many different human morphological and behavioral phenotypes during life history transitions. Yet they reported their findings in the context of a gene-centric view of evolved phenotypic changes as if “Nature” made more than 180 mistakes associated with velocardiofacial syndrome, which also linked a gene to evolution.
All serious scientists would ask at least two questions:
- What prevents the mistakes from causing extinction of a species that accumulates mutations during the life history transitions?
- How could primate ancestors mutate and become individuals that somehow established a population of ecologically adapted modern humans?
Dobzhansky (1973) claimed that “…the so-called alpha chains of hemoglobin have identical sequences of amino acids in man and the chimpanzee, but they differ in a single amino acid (out of 141) in the gorilla ( p. 127)”
Can that claim be placed into the context of transgenerational epigenetic inheritance by what is known or suspected about how the Zika virus might be linked to craniofacial morphology and to brain development, which is probably linked to behavior during life history transitions of all invertebrates and vertebrates. What is the best approach to take in attempts to discuss the claims of neo-Darwinian theorists, other theorists, or serious scientists who know how to link physics and chemistry to the conserved molecular mechanisms of nutrient-dependent RNA-mediated cell type differentiation? I’ve tried everything I can think of to help with potential discussions.
Thanks. It is not so much what I have shown. It is the details of biophysically constrained links from atoms to ecosystems, which are perturbed by viruses.
Ecker (from the human genome project) is senior author of a published work with this line as the first line in the abstract.
“RNA silencing at the transcriptional and posttranscriptional levels regulates endogenous gene expression, controls invading transposable elements (TEs), and protects the cell against viruses.”
What I have shown links quantum physics to the de novo creation of genes. What you have shown is that DNA repair mechanisms are required to maintain the virus-perturbed code.
I have shown how RNA-mediated DNA repair occurs in the context of an atoms to ecosystems model. You are still discussing randomness and evolution with people who know nothing about nutrient energy-dependent cell type differentiation.
It may not be possible for them to move forward, but you have the attention of a few other serious scientists who can link your claims across all living genera by what is currently known.
In my opinion, you are excluding their input by not allowing the first part of my submission to be included in the context of the prize.
Thank you for allowing the link to my invited review of nutritional epigenetics. If you include it as part 1 of the prize submission, perhaps others will see why the review was invited, and why the submission was returned without review.
Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems
No one from any camp wants someone like you or like me to destroy their theories. And, no one else from outside those camps will risk their wrath — as you have been told.
Why are you concerned about accepting the review as part 1 of the 2 part submission that will link hydrogen-atom transport in DNA base pairs to cell type differentiation that is perturbed by viruses?
It’s just part 1 of the submission. Perhaps part 2 will be unnecessary, or meaningless. But if you exclude part 1 because of the complexity, no one gets to part 2 who isn’t already nearly there.
And the works of others who are nearly there will not be integrated into the representations made in your book.
Thanks. I have demonstrated the well-known need for an anti-entropic force, which must be linked from Schrodinger’s claims to Stuart Kauffman’s claims. I have detailed the links from the anti-entropic force to RNA-mediated DNA repair at a time when Kauffman and Sheldrake are not discussing Lipton’s works and you are not discussing the works that refute Shapiro’s theories.
You have led many others to a point where they can dismiss “Evolution 2.0” as nothing more than another opinion. That’s what folks like PZ Myers want them to do, and that’s why he attacked me for my accurate representation of chromosomal rearrangements.
Others have linked the anti-entropic force from microbes in the guts of octopuses to chromosomal rearrangements and to human cognition via the conserved molecular mechanisms I have helped to detail during the past 20 years.
Simply put, you’re still trying to address the ridiculous claims of people like PZ Myers when it’s time to dismiss their nonsense and move forward using experimental evidence of biologically- based cause and effect.
For example: Feedback from Network States Generates Variability in a Probabilistic Olfactory Circuit and Feedback loops link odor and pheromone signaling with reproduction are ‘cut from the same cloth.’
The metaphorical cloth emerged in the context of Dobzhansky’s “light of evolution,” which turned out to be the light that linked ecological variation to ecological adaptation in all living genera via nutrient-dependent RNA-mediated cell type differentiation in the context of the physiology of reproduction in all living genera.
I gave up on attempts to discuss anything on Perry Marshall’s sites. Clearly, he does not want to start with nutrient-dependent RNA-mediated protein folding chemistry in an attempt to link what is known to serious scientists to his revision of Darwin’s works.