Pseudoscientists ignore what serious scientists prove

By: James V. Kohl | Published on: August 15, 2016

Earlier today (8/14/16) I challenged a friend who stated that “scientists claim 65 million years of natural selection led from the demise of the dinosaurs to the evolution of humans.” I ineffectively tried to explain the difference between the claims of scientists, which are based on experimental evidence, and the claims of pseudoscientists, which are based on pseudoscientific nonsense.
Last week, this same friend asked where the energy comes from that is released when hydrogen atoms are split. How did it get into the atom?
He is asking questions that pseudoscientists do not ask, but he does not seem to know that their inability to answer is what makes them pseudoscientists. If they were serious scientists they would not make any unsubstantiated claims. They would supply experimental evidence of biologically-based cause and effect.
For example, Lenski’s group can’t answer any questions about energy-dependent biophysically constrained RNA-mediated cell type differentiation. The claims Lenski has touted are “…not strictly true…” because no experimental evidence linked them to the energy-dependent physiology of pheromone-controlled reproduction via codon usage and RNA-mediated protein folding chemistry, which is biophysically constrained by the ability of organisms to link receptor-mediated behavior to survival of their species. But Lenski’s group summarily dismisses that problem.
Tempo and mode of genome evolution in a 50,000-generation experiment (subscription required)
Excerpt: [section head] Evidence for Beneficial Mutations

… the expectation that synonymous substitutions—point mutations in protein-coding genes that do not affect the amino-acid sequence—are neutral and should therefore accumulate at a rate equal to the underlying mutation rate… is not strictly true owing to selection on codon usage, RNA folding, and other effects, but it is generally thought that such selection is extremely weak, affects only a small fraction of sites at risk for synonymous mutations, or both 36,37.

My comment: In their view, selection of food is extremely weak selection. This group just reasserted Lenski’s unsubstantiated claim about “Evidence for Beneficial Mutations.” All experimental evidence of biologically-based cause and effect links nutrient energy-dependent RNA-mediated amino acid substitutions to healthy longevity and all experimental evidence links virus-driven energy theft from mutations to all pathology.
See for comparison: Epigenetics and Genetics of Viral Latency

… viral latency is responsible for life-long pathogenesis and mortality risk…

My comment: Experimental evidence of biologically-based cause and effect supports claims about viral latency (biophysically constrained pathology) compared to viral persistence (active pathology) that are tractable across more that 20 years of published works by serious scientists.
For example, see:
2016 Codon identity regulates mRNA stability and translation efficiency during the maternal-to-zygotic transition
2015 Role of olfaction in Octopus vulgaris reproduction

Future work on O. vulgaris olfaction must also consider how animals acquire the odours detected by the olfactory organ and what kind of odour the olfactory organ perceives. The OL acting as control centre may be target organ for metabolic hormones such as leptin like and insulin like peptides, and olfactory organ could exert regulatory action on the OL via epigenetic effects of nutrients and pheromones on gene expression (Kohl, 2013; Elekonich and Robinson, 2000).

2013 Nutrient-dependent/pheromone-controlled adaptive evolution: a model
The record of publications that link the claims from 2015 Role of olfaction in Octopus vulgaris reproduction to everything known about codon usage and RNA-mediated protein folding chemistry includes:
2012 Sequential RNA degradation pathways provide a fail-safe mechanism to limit the accumulation of unspliced transcripts in Saccharomyces cerevisiae
2012 Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors
2011 Proofreading and spellchecking: A two-tier strategy for pre-mRNA splicing quality control
2010 microRNAs, the cell’s Nepenthe: clearing the past during the maternal-to-zygotic transition and cellular reprogramming
2005 Feedback loops link odor and pheromone signaling with reproduction
2005 Honey bees as a model for understanding mechanisms of life history transitions
2001 Human pheromones: integrating neuroendocrinology and ethology
2000 Organizational and activational effects of hormones on insect behavior
1996 From Fertilization to Adult Sexual Behavior
1992 Transfer RNA in Protein Synthesis
See also: Scholarly article for “codon identity” and “RNA stability” for comparison to this search on PubMed codon identity and RNA stability
See also: Schrodinger (1944) [the link opens the free pdf]

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)

See also: (2007) Visualizing the wonder of a living cell at 4.13 minutes

And these micro-machines really are at the heart of life. These micro-machines, which are the envy of nanotechnologists the world over, are self-directed, powerful, precise, accurate devices that are made out of strings of amino acids. And these micro-machines power how a cell moves. They power how a cell replicates. They power our hearts. They power our minds.

My comment: The assembly of the micro-machines is energy-dependent. Virus-driven energy theft prevents the assembly of functional structures.
See also: Intrinsic limits to gene regulation by global crosstalk (2016)

We succeeded in relaxing many of our assumptions only to find that crosstalk constraints remain significant. This is because the major determinant of crosstalk is the binding site similarity S, which primarily depends on the typical mismatch energy and the length of the binding sites, L. Although crosstalk could be reduced by extending binding site length and/or augmenting the binding energy, both parameters are severely constrained by a combination of biophysical and evolutionary factors. The scale of the mismatch energy is set by the energetics of hydrogen bonds to ∼2–4 kBT, whereas the length of individual binding sites in eukaryotes appears strongly constrained by evolutionary considerations to ∼10 bp21,59,60. Moreover, the performance of complex regulatory schemes, which appear beneficial at first glance, is also limited by the explosion of possible non-cognate configurations that may lead to erroneous regulation. These constraints should apply universally, beyond the specific mechanisms we analysed in detail: any regulatory scheme operating at equilibrium, no matter how complex, faces a fundamental limit to its achievable error, for reasons that led Hopfield2 to propose kinetic proofreading.

See for comparison: What is life when it is not protected from virus driven entropy  (2016)
See also: Clathrin-coat disassembly illuminates the mechanisms of Hsp70 force generation, which was reported as: Tiny Impacts Help Keep Proteins Healthy

“This work was a tour de force, requiring the convergence of exceptional biochemical and molecular genetic skills with a deep understanding of the principles of physical chemistry,” commented Bruce Nicholson, Ph.D., the Chair of the Department of Biochemistry at the Health Science Center. “Such insights into the most basic aspects of protein chemistry and cell biology are often, as in this case, driven by a curiosity to find out how the molecular machines that drive our bodies work. But from these basic pursuits of scientific curiosity will often stem great benefits to human health.”

See for comparison: RNA-mediated physics, chemistry, and molecular epigenetics

Olfaction and the innate immune system link energy as information from the epigenetic landscape to the physical landscape of supercoiled DNA. The sun’s biological energy is the source of the information that links angstroms to ecosystems via physics, chemistry, and molecular epigenetics.

RNA-mediated protein folding chemistry and amino acid substitutions link the anti-entropic quantized energy of sunlight from the virucidal effects of ultraviolet (UV) light to healthy longevity via biophysically-constrained energy-dependent hydrogen-atom transfer in DNA base pairs in solution and cell type differentiation.

Biomarkers link energy-dependent differences in base pairs and amino acid substitutions to biosignatures across the healthy life span. RNA-mediated amino acid substitutions also reveal the increasing complexity of interactions among cell types as pathology progresses. For comparison, successful reproduction links energy from supercoiled DNA to protection of all organized genomes from virus-driven energy theft and pathology.

This model links the sun’s biological energy from top-down causation in microbes to the most recent model of bottom-up gene activation and cell type differentiation in vertebrates. Citations to extant literature provide examples of what is currently known about how ecological variation leads to biophysically constrained cell type differentiation in the context of nutritional epigenetics and Precision Medicine, which clearly link metabolic networks and genetic networks to pharmacogenomics.

My comment: I need not claim my work was the tour de force that Nicholson claims Sousa et al., (2016) work represents.  Until someone else links energy-dependent changes from angstroms to ecosystems via physics, chemistry, and molecular epigenetics, they will continue to offer only pieces of the energy-dependent puzzle that has already been put together by serious scientists.

See also: Structural diversity of supercoiled DNA


The structure of the B-form DNA double helix has been known for over 60 years1, yet DNA metabolism requires deviations, sometimes extreme, from this canonical form2, 3, 4. Studies of DNA are typically performed on short, linear DNA fragments that cannot be supercoiled; therefore our understanding of DNA is incomplete. In most organisms DNA is maintained in a negatively supercoiled (underwound) state. Positively supercoiled (overwound) DNA is transiently generated during DNA replication and transcription, and, if not promptly relaxed, inhibits these processes5.

My comment: Supercoiled DNA is not “generated” outside the context of metabolic networks linked to genetic networks, and supercoiled DNA has no function outside the context of thermodynamic cycles of protein biosynthesis and degradation, which are nutrient energy-dependent and controlled by the physiology of reproduction. Serious scientists have proved that!

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