- Home: Cardiology: December 18, 2013
Going against the flow: Halting atherosclerosis by targeting micro RNA
Excerpt 1: “…the master controller comes from a source that scientists had thought was leftover garbage. It is a micro RNA molecule, which comes from an unused template that remains after punching out ribosomes –– workhorse protein factories found in all cells.”
Excerpt 2: “This is one of the most abundant streams of RNA that cells produce, and it turns out to be the source for a molecule that controls atherosclerosis,” Jo says. “Why did nature do it that way? I don’t think we know yet.”
My comment: The questions we ask determine how they are answered. If you ask an evolutionary theorist why nature did anything, you will probably get an answer based on the theory of mutation-initiated natural selection. If you ask an evolutionary theorist what was naturally selected, or how adaptations resulted from mutations that were selected, you will get a response that includes only unintelligible nonsense. Simply put, evolutionary theorists have no idea how natural selection works, or why mutations that typically cause diseases and disorders might be beneficial in the context of natural selection.
Unfortunately, evolutionary theorists have influenced the questions that scientists ask. Fortunately, experimental evidence reported in The atypical mechanosensitive microRNA-712 derived from pre-ribosomal RNA induces endothelial inflammation and atherosclerosis helps to detail how ecological variation and conserved molecular mechanisms contribute to the adaptive differentiation of cell types, individuals, and species. What we referred to in our 1996 review article as the small intranuclear proteins that participate in generating alternative splicings that contribute to contribute to sexual differentiation can now be viewed in the context of how microRNAs differentiate all cell types in all individuals of all species, not just the cell types that are sexually differentiated.
We now know that ecological variation determines which microRNAs are most critically involved in the global differentiation of cell types via the epigenetic effects of nutrients. For example, experimental evidence reported last year indicated a role for plant microRNAs as a bridge between diet and gene expression in animals via the post-transcriptional silencing of mRNA translation. Simply put, scientists provided evidence of how a specific mechanism of post-transcriptional silencing of mRNA translation allows ecological variation to alter our phenotype. That experimental evidence put the burden of proof on evolutionary theorists to provide experimental evidence that supports mutation-initiated natural selection. Instead of attempting to support their theories with experimental evidence, some theorists attempted to eliminate natural selection from mutation-initiated natural selection and continue touting mutation-driven evolution as if there were experimental evidence that supported the revision to their theory.
Meanwhile, a team of scientists finally performed experiments on a model organism that clearly showed that mutations are not fixed in the genome. The researchers concluded that “ …the development of more general theoretical models explaining the fate of new alleles across long evolutionary timescales…” was required. The response by evolutionary theorists to the results of their experiment was predictable. Theorists continue to claim that mutations occur, which is obvious. But they also continue to claim that classical theories of population genetics, not experimental evidence of biologically-based cause and effect, is all that’s required to support their claims of mutation-driven evolution.
What’s worse is that the moderator of the International Society of Human Ethology’s yahoo group wrote that: I am absolutely certain that if you showed this statement to any professor of biology or genetics in any accredited university anywhere in the world that 100% of them would say that “Random mutations are the substrate upon which directional natural selection acts” is a correct and true statement. Clearly, there are many others, like Jay R. Feierman, who think their claims of mutation-initiated natural selection are supported by experimental evidence.
They are wrong. What they believe in is not based on any experimental evidence. Their beliefs are based on their observations and theorists have continued to tout theories based on observations for nearly 40 years after Dobzhansky (1964) compared them to bird-watchers and butterfly collectors. At the time, Dobzhansky also wrote this: “Self-reproduction plus mutation make possible natural selection. Natural selection makes possible evolution.” However, I’m certain that given the accumulation of evidence from molecular biology that he would now agree it has since become perfectly clear that “Ecological variation is the raw material by which natural selection can drive evolutionary divergence [1–4].”
Indeed, the most recent experimental evidence shows that “miR-712 may also be transferred to blood” which is how it epigenetically effects leukocytes and the cell types of arteries via the migration of vascular smooth muscle cells with results in a multitude of pro-atherogenic changes. Thus, the authors claim that “Targeting these mechanosensitive ‘athero-miRs’ such as miR-712 and miR-205 may provide a new treatment paradigm in atherosclerosis.”
When they learn that they have provided experimental evidence that supports a model of how …the epigenetic ‘tweaking’ of the immense gene networks… occurs via exposure to nutrient chemicals and pheromones, they may make broader-claims for new treatments of other diseases and disorders linked to nutrient stress and social stress (i.e., all of them) via conserved molecular mechanisms of adaptations in species from microbes to man. Hopefully, they will not continue to say things like: “Why did nature do it that way? I don’t think we know yet.” They may not accept the fact that God did it that way, but they should be less likely to accept the claim that mutation-initiated natural selection somehow did it.
Evangelism
The accumulation of experimental evidence led me to write, on 7/24/13: Natural selection [Excerpted from the Berkeley page on Understanding evolution]: “If you have variation, differential reproduction, and heredity, you will have evolution by natural selection as an outcome. It is as simple as that.”
The variation is nutrient availability and nutrients metabolize to species-specific pheromones that control reproduction and heredity. Evolution by natural selection cannot be the outcome if something is not first selected. Selection is always for nutrients. It is as simple as that. — JV Kohl
Perspectives for the future:
After Feierman’s anti-religion posts to the human ethology group during the past week, and after he blocked all of my responses to his nonsensical misrepresentations of biological facts, he also blocked my comment on this article. He provided a link to: Is Evangelism Going Out of Style?
Excerpt: “…evangelicals also have among the highest rates of failure in follow-through from conviction to action when it comes to sharing their faith. Nearly one-third (31%) believe they should evangelize, but have not done so—at least within the past year.”
My comment: There are different forms of evangelism. See, for example page 254 from the 2005 Nutrient Reference Values for Australia and New Zealand Including Recommended Dietary Intakes (the link below opens the full text pdf)
The late MG Hardinge’s academic legacy extends his medical evangelism across more than 60 years. However, he did not answer any questions about why nature used ecological variation as its means to enable adaptations in species from microbes to man, which is obviously how adaptations occur. His evangelical approach attests to how our Creator God used nutrient uptake to epigenetically effect the conserved molecular mechanisms that enable species diversity via what we now know is the nutrient-dependent pheromone-controlled physiology of reproduction.
Until today, we have seen some scientists and many theorists go against the flow of any experimental evidence that might support the beliefs of people who they label “Creationists”. However, we have also seen the experimental evidence of conserved molecular mechanisms manifested in health and disease in species from microbes to man. The experimental evidence continues to make it more difficult to take the claims of any “theorist” seriously. Thus, it appears the medical evangelists, like Hardinge, are correct — unless there is any experimental evidence that suggests they are not.
Note: The experimental evidence that showed mutations are not fixed in the genome of a model organism, the nematode C. elegans: An experimental test on the probability of extinction of new genetic variants was published in the same journal that published this article The atypical mechanosensitive microRNA-712 derived from pre-ribosomal RNA induces endothelial inflammation and atherosclerosis. Taken together, both articles show that “…the epigenetic ‘tweaking’ of the immense gene networks that occurs via exposure to nutrient chemicals and pheromones can now be modeled in the context of the microRNA/messenger RNA balance, receptor-mediated intracellular signaling, and the stochastic gene expression required for nutrient-dependent pheromone-controlled adaptive evolution.” Thus, the journal “Nature Communications” is helping to show everyone that “nature” communicates with food odors and pheromones. That makes “nature” another part of God’s Creation that can be readily observed.
For example, in my model “Differences in the behavior of nematodes are determined by nutrient-dependent rewiring of their primitive nervous system (Bumbarger et al., 2013). Species incompatibilities in nematodes are associated with cysteine-to-alanine substitutions (Wilson et al., 2011), which may alter nutrient-dependent pheromone production.” Physical evidence of de novo Creation of teeth in predatory nematodes may still be misrepresented as the result of millions of years of accumulated mutations, but no one who understands the basic prinicples of biology or levels of biological orgnanization required to link sensory cause to genetically predisposed ecological, social, neurogenic, and socio-cognitive niche construction is likely to link adaptations to mutations much less to mutation-driven evolution.
James V. Kohl detailedl how quantized energy-dependent microRNA biogenesis links the pheromone-controlled physiology of reproduction to biophysically constrained viral latency and healthy longevity. Links from what organisms eat to the enzyme-dependent metabolism of food also link metabolic networks to microRNA-mediated genetic networks in the context of RNA interference. Drug therapies alter RNA interference by altering cell type differentiation in all cells of all individuals of all species. For comparison, during the past 26 years, Kohl has detailed how the chemistry of protein folding is biophysically constrained at every level of biological organization by conserved molecular mechanisms.