“…β-glucan possesses a significant immunostimulating activity in a wide variety of species, including earthworms, shrimp, fish, chicken, rats, rabbits, guinea pigs, sheep, pigs, cattle, and, last but not least, humans. Based on these results, it has been concluded that β-glucan represents a type of immunostimulanting molecule that is actively spanning full evolutionary spectrum. Some experiments also show that β-glucan can help even in the protection of plants. β-Glucan is therefore not only a biologically active polysaccharide with strong immunomodulating effects, but is also considered to be an evolutionary very old stimulant of a variety of defense immune reactions.”

My comment: Lenski’s group removed the context of neo-Darwinian ‘old stimulants’ and linked natural selection from codon usage to RNA-mediated protein folding biochemistry via the de novo creation of G protein-coupled receptors and the innate immune system, albeit apparently without the biophysically constrained links from the physiology of reproduction to supercoiled DNA.

In ‘Tempo and mode of genome evolution in a 50,000-generation experiment,‘ they cited:

8. Wichman, H. A., Badgett, M. R., Scott, L. A., Boulianne, C. M. & Bull, J. J. Different trajectories of parallel evolution during viral adaptation. Science 285, 422–424 (1999).

12. Kvitek, D. J. & Sherlock, G. Whole genome, whole population sequencing reveals that loss of signaling networks is the major adaptive strategy in a constant environment. PLoS Genet. 9, e1003972 (2013).

The two citations make it much more difficult to claim that evolution occurs across millions of years. Loss of receptor-mediated signaling networks is linked to viral latency via adaptation to viruses and virus-driven energy theft is linked to all pathology. Only nutrient energy-dependent microRNA flanking sequences link ecological variation to ecological adaptation via supercoiled DNA, which protects all organized genomes from virus-driven entropy.

Others have started to link my model of nutritional epigenetics and RNA-mediated cell type differentiation in their publications, albeit without a full understanding of why they have been forced to do that by the Laws of Physics, Basic Principles of Chemistry, and everything known to serious scientists who have linked energy-dependent changes from angstroms to ecosystems in all living genera.

My model: Nutrient-dependent/pheromone-controlled adaptive evolution: a model published on 6/14/13

8/6/13 Epigenetics: a new link between nutrition and cancer

9/17/13 Nutritional epigenomics: a portal to disease prevention

My invited review of nutritional epigenetics

4/11/14 Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems

Abstract excerpt:

This atoms to ecosystems model of ecological adaptations links nutrient-dependent epigenetic effects on base pairs and amino acid substitutions to pheromone-controlled changes in the microRNA / messenger RNA balance and chromosomal rearrangements. The nutrient-dependent pheromone-controlled changes are required for the thermodynamic regulation of intracellular signaling, which enables biophysically constrained nutrient-dependent protein folding; experience-dependent receptor-mediated behaviors, and organism-level thermoregulation in ever-changing ecological niches and social niches. Nutrient-dependent pheromone-controlled ecological, social, neurogenic and socio-cognitive niche construction are manifested in increasing organismal complexity in species from microbes to man.

My comment: Lynette R. Ferguson was one of two guest editors who requested my review of nutritional epigenetics for inclusion in the Special Issue Nutritional Epigenetics. My submission was returned without review, but her co-authored text and conclusion came from it.

See: 1/30/15 The Interaction between Epigenetics, Nutrition and the Development of Cancer


“…it is imperative to understand the implications of diet on epigenetic modifications, and the effect of those modifications on the development of cancer today and in future generations. Such an understanding and an appropriate resultant response would help decrease the level of risk in future generations.”

Abstract excerpt:

 The epigenetic modifications investigated include DNA methylation, histone modifications and the influence of microRNAs.

See also from Ferguson, Lynnette R. et al., (2015)

Genomic instability in human cancer: Molecular insights and opportunities for therapeutic attack and prevention through diet and nutrition

Abstract excerpt:

Genomic instability arises from many different pathways, such as telomere damage, centrosome amplification, epigenetic modifications, and DNA damage from endogenous and exogenous sources, and can be perpetuating, or limiting, through the induction of mutations or aneuploidy, both enabling and catastrophic.

My comment: Like others who are biologically uninformed, these researchers failed to mention anything about virus-driven energy theft. If I had mentioned anything more than this in my invited review, they would have undoubtedly also used that information without attribution.

For example, nutrient-dependent ecological niche construction leads to pheromone-controlled social niche construction via the nutrient-dependent pheromone-controlled physiology of reproduction. The nutrient-dependent origin of amino acid substitutions in viruses (Bedford et al., 2014; Gong, Suchard, Bloom, & Pascual, 2013; Kohio & Adamson, 2013; Yamada et al., 2010), which also are manifested in plant and animal interactions, exemplifies a continuum of biological plausibility and ecological validity in the context of Laws of Biology.

For comparison, the excerpt is from Genomic instability in human cancer: Molecular insights and opportunities for therapeutic attack and prevention through diet and nutrition:

“…vitamins, minerals, and antioxidants, such as vitamin D, vitamin B, selenium, and carotenoids, as well as nutraceuticals, such as resveratrol, have shown remarkable plasticity in elucidating antitumor responses. In addition to alleviating genomic instability, these compounds are known to inhibit proliferative signaling [353], [354], [355], attenuate oncogenic metabolism [268], [338], [364], [383], [384], [385], [386], and block inflammation [354], [391], [392], [393], [394], [395], [396], [397], [398], [399], [400], [401], [402], [403], [404].

My comment: What does Genomic instability in human cancer: Molecular insights and opportunities for therapeutic attack and prevention through diet and nutrition tell us about the cause of the proliferative signaling, which has been linked to all pathology?

Others have since linked virus-driven energy theft to oncogenic metabolism, but they seem very unsure of how to link angstroms to ecosystems in all living genera.

See: The Evolution of Epigenetics: From Prokaryotes to Humans and Its Biological Consequences


The virus reprograms the host’s epigenetic machinery, which permanently affects the host cells.94 One study has demonstrated that cells that have been exposed to EBV experience hypermethylation at CpG islands when compared to cells that have not been exposed to the virus.94 Some of these methylations affect the transcription of genes, which may increase the tumorigenic capabilities of the host cells and lead to the development of cancer.

 See for comparison to their video representation (below):

Like many other groups, this one is stuck with neo-Darwinian theories, which means they must place their claims into the context of pseudoscientific nonsense. They have discovered nothing new about energy-dependent cell type differentiation or virus-driven energy theft, which already has been linked to all pathology.

For comparison to what the future holds for researcher in this group, see:  A comparative perspective on epigenetics


She also reviews how olfactory imprinting can be inherited epigenetically by subsequent generations – although the mechanism of transmission is yet to be determined.

Excerpt from the conclusion: 

Hoppeler says, ‘I really hope that the awareness of the possibility that epigenetic mechanisms modify the situation of a species under certain conditions is providing a better understanding of how a phenotype can be morphed and may morph over several generations’.

My comment: Any researcher who continues to make claims about evolution across more than several generations is stuck with the horrid failure of ridiculous attempts to link the 1902 definition of “mutation” to assumptions about how many accumulated mutations might be required for one species to evolve into another. Researchers like that are evolutionary dead-ends.

None of their ridiculous claims will be known to serious scientists of the future. For example, in only one generation, Richard Lenski — who was reported to be The Man Who Bottled Evolution — has been caught holding experimental evidence of how ecological variation is linked to ecological adaptation in all living genera via their nutrient energy-dependent physiology of reproduction, and supercoiled DNA.

The supercoiled DNA protects all living genera from virus-driven pathology and genomic entropy. But Pennisi, reporting in Science, starts with the headline: “Richard Lenski’s 25-year experiment in bacterial evolution shows no signs of running out of surprises about how mutation and selection shape living things.”

SURPRISE! The bacteria never evolved. They adapted. There was no mutation and selection. There was only selection for energy-dependent codon usage in the context of RNA-mediated cell type differentiation, which links ecological variation to biophysically constrained ecological adaptation via protein folding chemistry and DNA repair. Virus-driven energy theft prevents DNA repair.

See also: Repair of traumatized mammalian hair cells via sea anemone repair proteins


The results of this study suggest that at least some of the subcellular mechanisms by which damaged hair bundles are repaired were conserved in evolution.

My comment: How does DNA repair occur in the context of “evolution?”

Reported as: Sea anemone proteins repair damaged mouse cochlear hair cells


…mice produce many proteins that are closely related to the sea anemone repair proteins, suggesting that it may be possible to mobilise the same repair mechanisms in mammals with damaged hearing. Watson hopes that this ground-breaking discovery will eventually lead to a treatment for patients with hearing loss. However, he acknowledges that this research is in its infancy and is keen to discover the mechanism that could eventually allow sea anemones to restore our hearing.

My comment: Research that links energy-dependent RNA-mediated DNA repair to viral latency is not in its infancy and it does not link conserved molecular mechanisms of biophysically constrained protein folding chemistry to “evolution.” All experimental evidence of biologically-based cause and effect links energy-dependent changes from angstroms to ecosystems and virus-driven energy theft to all pathology in the context of ecological variation and ecological adaptation. If you let them, theorists will continue to claim that serious scientists do not know how to link cause and effect from the innate immune system to supercoiled DNA in all cell types of all individuals of all living genera.

See also: A comparative perspective on epigenetics


She also reviews how olfactory imprinting can be inherited epigenetically by subsequent generations – although the mechanism of transmission is yet to be determined.

My comment: The molecular mechanisms of biophysically constrained RNA-mediated protein folding chemistry were detailed in From Fertilization to Adult Sexual Behavior.  See our section on molecular epigenetics and tell theorists to stop pretending they don’t know how to link ecological variation to ecological adaptation except via the magic of “evolution.”

See also: Feedback loops link odor and pheromone signaling with reproduction

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