The MicroRNAome Strikes Back: A Sokalian hoax (7)

Let food be thy medicine and medicine be thy food?

His claim can now been considered in the context of molecular epigenetics and works by others such as:
St. Paul; Darwin; Sinclair Lewis (1925); Schroedinger (1944); Karlson and Luscher (1959); McEwen with Fritz (1959); McEwen et al.,  (1964); Dobzhansky (1964); Frohlich (1968); Dobzhansky (1973); Daev (1994); Kohl and Francoeur (1995); Diamond, Binstock and Kohl (1996); Nonomura (2018); Kong et al., (2018); and Chen et al (2018)
In thousands of publications, individually and collectively, these people and groups have pitted experimental evidence of biophysically constrained energy-dependent viral latency against the claims of those who tout entropy as an explanation for mutation-driven evolution via natural selection of something besides food.
See for comparison: Evaluation of Preexisting Anti-Hemagglutinin Stalk Antibody as a Correlate of Protection in a Healthy Volunteer Challenge with Influenza A/H1N1pdm Virus
Reported as: Flu infection study increases understanding of natural immunity 

The head region of HA is constantly changing, which is why influenza vaccine strains must be updated each year. The HA stem region, however, is less susceptible to change, making it a potential target for novel vaccines aimed at broader, more durable protection.

Reported as: You Are Shaped by the Genes You Inherit. And Maybe by Those You Don’t (by Carl Zimmer)
Kong et al., (2018) removed a beneficial mutation from consideration as a link to evolution and there is no mention of evolution in the context of the transgenerational epigenetic inheritance of behavioral phenotypes. That makes sense to serious scientists who known that behavior is experience-dependent and receptor-mediated.
That may explaine why the authors of the journal article changed the focus to epigenetic effects of nutrition on behavioral phenotypes with no mention of evolution. Then, Carl Zimmer changed his focus to claims about genetic nurture.

…genetic nurture is ultimately due to genetic variation in the population and is mediated by the environment that parents create for their children.

The only mention of mutation is in the context of a citation to Loss-of-function mutations in SLC30A8 protect against type 2 diabetes (2014).
Was Carl Zimmer forced to abandon his past nonsense and report the differences as variants in human populations? Perhaps we will learn more about the variants from other journalists.
See for instance, the nonsense about the beneficial mutation was reported by Gina Kolata in the New York Times as Rare Mutation Kills Off Gene Responsible for Diabetes (2014)

This is the first time in diabetes research that a mutation that destroys a gene has proved beneficial, noted Louis Philipson, director of the Kovler Diabetes Center at the University of Chicago. For drug development, he said, “that is very powerful.” the same mutation that protects people from diabetes, by destroying one copy of the gene, known as ZnT8, has the opposite effect in some strains of mice. Destroying that gene actually causes diabetes in the animals.

The ability of pseudoscientists and journalists who promote “Big Pharma” (or something else undisclosed) to obfuscate what is known to serious scientists about the nutrient-dependent pheromone-controlled physiology of reproduction in species from microbes to humans has become perfectly clear.
See for instance: The rate of meiotic gene conversion varies by sex and age (2016)

Meiotic recombination involves a combination of gene conversion and crossover events that, along with mutations, produce germline genetic diversity.

The molecular mechanisms of recombination and genetic diversity have been the focus of serious scientists ever since Darwin presciently placed them into the context of his “conditions of life.”
The only link from mutations to germline genetic diversity still requires serious scientists to start with the creation of the sun’s anti-entropic virucidal energy and link Darwin’s “conditions of life”  it from the physiology of pheromone-controlled reproduction to all biodiversity on Earth in the context of biophysically constrained viral latency via the creation of RNA-mediated amino acid substitutions that differentiate the cell types of all individuals of all living genera.
See for example: Skin microbiota–host interactions  (2018)

The skin is a complex and dynamic ecosystem that is inhabited by bacteria, archaea, fungi and viruses. These microbes—collectively referred to as the skin microbiota—are fundamental to skin physiology and immunity. Interactions between skin microbes and the host can fall anywhere along the continuum between mutualism and pathogenicity. In this Review, we highlight how host–microbe interactions depend heavily on context, including the state of immune activation, host genetic predisposition, barrier status, microbe localization, and microbe–microbe interactions. We focus on how context shapes the complex dialogue between skin microbes and the host, and the consequences of this dialogue for health and disease.‏

The continuum between mutualism and pathogenicity is food energy-dependent an the physiology of reproduction biophysically  constrains viral latency. That fact has been placed into the context of differences in the membrane construction of bacteria that vary in the context of links from quantized energy as information to quantum souls.
See for instance: Promises and Challenges in Continuous Tracking Utilizing Amino Acids in Skin Secretions for Active Multi-Factor Biometric Authentication for Cybersecurity 

See also: Soil bacteria, bulls, cows, microRNAs, and mammary glands

No experimental evidence of biologically-based cause and effect links anything to the evolution of anything else. Quantum physics links the de novo creation of olfactory receptor genes to all biologically-based cause and effect. All experimental evidence links the sun’s biological energy from top-down causation to biophysically constrained RNA-mediated protein folding chemistry via amino acid substitutions in organized genomes, which link behavior and supercoiled DNA to protection from virus-driven energy theft and genomic entropy.