An evolutionary theory killer

How to create biologically uninformed theorists

Summary: On March 2, 2018, Philip C. Ball and Nick Lane started making claims about proton gradients. Their claims are based on my model of quantized energy as information. This post includes added support for what is known to all serious scientists about the light-activated endogenous substrates that link molecular epigenetics to RNA-mediated autophagy.
See first: Energy as information and constrained endogenous RNA interference (audio/visual aid 2017)

Feedback loops link quantized energy as information to biophysically constrained RNA-mediated protein folding chemistry. Light induced energy-dependent changes link angstroms to ecosystems from classical physics to chemistry/chirality and to molecular epigenetics/autophagy.

The National Microbiome Initiative links microbial quorum sensing to the physiology of reproduction via endogenous RNA interference and chromosomal rearrangements. The rearrangements link energy-dependent fixed amino acid substitutions to the Precision Medicine Initiative via genome wide inferences of natural selection.

This detailed representation of energy-dependent natural selection for codon optimality links biologically- based cause and effect from G protein-coupled receptors to RNA-mediated amino acid substitutions and the functional structure of supercoiled DNA. Energy-dependent polycombic ecological adaptations are manifested in supercoiled DNA. Chromosomal inheritance links the adaptations from morphological phenotypes to healthy longevity via behavioral phenotypes.

For contrast, virus-driven energy theft is the link from messenger RNA degradation to negative supercoiling, constraint breaking mutations, and hecatombic evolution. The viral hecatomb links transgenerational epigenetic inheritance from archaea to Zika virus-damaged DNA, which typically is repaired by endogenous RNA interference and fixation of RNA-mediated amino acid substitutions in organized genomes.

Added support for the light-activated molecular epigenetics of autophagy:
Light-powering Escherichia coli with proteorhodopsin (2007)

…we quantify the coupling between light-driven and respiratory proton currents… and show that light-driven pumping by PR can fully replace respiration as a cellular energy source in some environmental conditions.

Structure of the Deactive State of Mammalian Respiratory Complex I (2018)

…the deactive state arises when critical structural elements that form the ubiquinone-binding site become disordered, and we propose reactivation is induced when substrate binding to the NADH-reduced enzyme templates their reordering. Our structure both rationalizes biochemical data on the deactive state and offers new insights into its physiological and cellular roles.

Global collective motions in the mammalian and bacterial respiratory complex I (2018)

…we identify here transitions between experimentally resolved structures of the mammalian complex I as low-frequency collective motions of the enzyme, highlighting similarities and differences between the bacterial and mammalian enzymes. Despite the reduced complexity of the smaller bacterial enzyme, our results suggest that the global dynamics of complex I is overall conserved.

The conservation of light-powered functional structures and energy-dependent proton gradients link the deactive state in critical structures to the active state via the creation of enzymes in species from bacteria to mammals. The energy-dependent creation of the enzymes links metabolism of the energy (e.g., food energy) from pheromones to biophysically constrained viral latency in the context of the physiology of reproduction.
The pheromone-controlled physiology of reproduction in species from microbes to humans links our visual perception of energy and mass in the context of how ecological variation must be linked to energy-dependent ecological adaptations in all living genera.
See: Olfaction Warps Visual Time Perception

Our perception of the world builds upon dynamic inputs from multiple senses with different temporal resolutions, and is threaded with the passing of subjective time. How time is extracted from multisensory inputs is scantly known. Utilizing psychophysical testing and electroencephalography, we show in healthy human adults that odors modulate object visibility around critical flicker-fusion frequency (CFF)-the limit at which chromatic flickers become perceived as a stable color-and effectively alter CFF in a congruency-based manner, despite that they afford no clear environmental temporal information. The behavioral gain produced by a congruent relative to an incongruent odor is accompanied by elevated neural oscillatory power around the object’s flicker frequency in the right temporal region ~150-300 ms after object onset, and is not mediated by visual awareness. In parallel, odors bias the subjective duration of visual objects without affecting one’s temporal sensitivity. These findings point to a neuronal network in the right temporal cortex that executes flexible temporal filtering of upstream visual inputs based on olfactory information. Moreover, they collectively indicate that the very process of sensory integration at the stage of object processing twists time perception, hence casting new insights into the neural timing of multisensory events.

See also: Odors Alter Subjective Time Experience Author: Dr. ZHOU Wen’s Research Group Update time: 2017/05/15

The brain is not a timepiece. Whereas it is equipped with senses like vision, audition, touch, smell, and taste, it has no direct access to or measure of the physical time (unless you read from a clock). Rather, it constructs the subjective “time” of an event from the dynamic multisensory inputs associated with that event. Yet different senses come with different temporal precisions. For instance, when standing near an apple tree, you can detect the falling of an apple much better with your eyes or ears than the nose. How does the brain coordinate multisensory signals entering different brain regions with different temporal resolutions, and come up with the subjective time?

A team at the Institute of Psychology at Chinese Academy of Sciences tackled this issue using odors and images. Specifically, Dr. Bin Zhou, the study’s lead author, and his colleagues examined whether odors could modulate one’s temporal sampling and subjective duration of visual objects. In their study, participants viewed two series of flickering isoluminant images in red and green (Figure 1A). One of the series contained opposite images of an apple or bananas; the other contained only images of red and green fields. When the images alternated at a frequency beyond 20 Hz, the participants started to have difficulty reporting which series contained an object. Indeed, for most people, chromatic flicker fusion frequency (CFF), the limit at which alternating colors become perceived as a stable fused color, falls somewhere between 20 and 25 Hz. Interestingly, the participants’ object detection accuracies around CFF were improved under the exposure of a congruent, as opposed to an incongruent, odor. In other words, the participants detected a rapidly flickering apple better when they smelled an apple odor rather than a banana odor, and vice versa (Figure 1B, left panel). In effect, the presence of a congruent odor facilitated the brain’s temporal sampling of a visual object and elevated its CFF (Figure 1B, right panel). Based on electrical activities recorded from the participants’ scalp, the researchers found that the integration between smell and vision strengthened the signals of the corresponding object in a brain region heavily implicated in object representations called the right temporal cortex, about 150-300 ms after object onset. They further showed that such integration lengthened one’s subjective duration of the corresponding object in a duration comparison task. The researchers concluded that subjective time is warped by the neural energy involved in representing multisensory inputs at subsecond scales.

Until Philip C. Ball mentioned that Nick Lane believed proton gradients came before the energy-dependent creation of RNA, I did not realize how little they knew about this link from differences in the energy of photons to consciousness.
See: What Affective Neuroscience Means for Science Of Consciousness (2013)

The coupling of the two circuits promotes an endogenous feedback that supports conscious processes. Within this framework, we present the defence that detailed study of both affective and cognitive processes, their interactions, as well of their respective brain networks, is necessary for a science of consciousness.

The coupling of the two circuits links differences in the energy of photons from the proton motive force to the light-activated endogenous feedback loops and Feedback loops link odor and pheromone signaling with reproduction.
It is extremely difficult for intelligent people to not link this experimental evidence to biophysically constrained viral latency in the context of reports that claim “Creatures’ Adaptability Begins with Their Sensors.”
But, see for comparison: David Attenborough on creationsim May, 2015

My comment on his nonsense: First steps to neutralizing Zika: How highly potent antibody neutralizes Zika infection discovered

This is framed within the context of energy-dependent changes in pH, which facilitate receptor-mediated entry of nutrients or viruses into specific cell types of species-specific tissues via stress-linked changes in hydrogen-atom transfer in DNA base pairs.

Virus-driven energy theft has been linked to all pathology in all living genera via the conserved molecular mechanisms of RNA-mediated polycombic protein folding chemistry compared to the hecatombic evolution of pathology manifested first in the differences between archaea and bacteria. Admitting that Carl Woese was wrong about the different domains of life is the first step towards understanding the difference between healthy longevity and the evolution of all virus-driven pathology.

Carl Woese was wrong

God did not create the viruses. He created the anti-entropic virucidal energy of sunlight, which protects all organized genomes from virus-driven entropy. Only the choices of our ancestors could have led to the increasing amout of virus-driven pathology during the past ~6000 years that pseudoscientists place into the context of millions of years of evolution. Then, they blame God, like these two pseudoscientists do. Darwin knew they would do that, which is why he insisted that others put conditions of life before natural selection. But they bastardized his theory anyway and taught their revision to anyone who was foolish enough to believe in it. It’s called the “Modern Synthesis” and was based on de Vries 1902 definition of “mutation.”

Celebrate Your Inner Virus

It is important that we understand the design present in viruses because God made them.

It is no wonder that Sir David Attenborough and many others like Philip C. Ball and Nick Lane are confused about the energy-dependent creation of healthy longevity and consciousness. Even some young earth creationists have failed to link the creation of the sun’s anti-entropic virucidal energy from changes in electrons to ecosystems via the proton motive force. That leaves every aspect of creation to be placed back into the context of ridiculous theories. The theories start with the virus-driven theft of quantized energy as information. The energy theft links mutations to all virus-driven pathology. The theft of quantized energy as information cannot be linked by serious scientists from beneficial mutations to the evolution of one species from another.
For comparison, pseudoscientists have no problem touting this confusing nonsense:
Sign of selection on mutation rate modifiers depends on population size (
1)  Genetic variation—the raw material for evolution—is ultimately generated by mutation.
2). …beneficial alleles never become deleterious and deleterious alleles never become beneficial.
Conclusion:

Whether these phenomena can be united in a single theoretical framework remains an open question that we are actively exploring. In any case, our results add to a growing appreciation of nonclassical population size dependence in evolution by natural selection (41, 42).

Funding for research that attempts to link natural selection to evolution via mutation-driven genetic variation should be used to link food odors and pheromones from the physiology of reproduction to biophysically constrained viral latency and ecological adaptations. It is time to stop creating more biologically uninformed theorists.

rp_levels-of-organization.jpg

The Aquatic Ape: New evidence?

The Waterside Ape

In 1960, the eminent Oxford marine biologist Sir Alister Hardy proposed a revolutionary idea: that our human ancestors had not started their existence on the wide savannahs of Africa, but had become accustomed to living alongside water – swimming and diving in the shallows, collecting the abundant food, and learning to use language and fashion tools. Hardy asserted that this adaptation to living at the waterside –whether by rivers and pools or by the ocean – would also account for a whole range of peculiarities about the human form, including the layers of fat beneath the skin, the relative lack of body hair, the development of language and speech, and what he called our “runaway brains”.

Perhaps surprisingly, it was a screenwriter rather than a scientist, Elaine Morgan, who took up Hardy’s theory and, for over 40 years, progressively refined the evidence for the idea. Most mainstream paleo-anthropologists ridiculed and rejected the Hardy-Morgan thesis for decades, but some influential scientists asked for the proposal to be approached with an open mind.

Sir David Attenborough first considered the controversial theory on Radio 4 in 2004, and in this new two-part series, he brings listeners up-to-date with the story and the evidence put forward since then – for both the hypothesis and also for its continuing detractors. Back in 2004, Sir David asked Elaine Morgan how long it would take for the aquatic adaptation theory to become a mainstream account of human origins. She answered: “I’ll give it ten years.” As the programme reviews the new evidence, has she been proved right?

Presenter/Sir David Attenborough, Producer/Richard Collins for Pier Productions

Re: As we review the new evidence, has she been proved right?

My comment: No experimental evidence of biologically-based cause and effect ever suggested that Elaine Morgan was wrong.  She accurately predicted that 2014 would be the year in which she was proved right. As far as I know, she was predictably right.
See this 2014 invited review of nutritional epigenetics (and energy-dependent RNA-mediated cell type differentiation):

Nutrient-dependent pheromone-controlled ecological adaptations: from atoms to ecosystems

The invited review was requested by guest editors for a special issue of “Nutrients.” The reason for the request was clear.
In Nutrient-dependent/pheromone-controlled adaptive evolution: a model (2013), I concluded:

…the largest contributor to the development of our personal preferences may be the unconscious epigenetic effects of food odors and pheromones on hormones that organize and activate behavior. If so, the model represented here is consistent with what is known about the epigenetic effects of ecologically important nutrients and pheromones on the adaptively evolved behavior of species from microbes to man. Minimally, this model can be compared to any other factual representations of epigenesis and epistasis for determination of the best scientific ‘fit’.

My 2014 invited review was returned without review. No factual representations of epigenesis and epistasis have been offered for comparison to the ridiculous claims of theorists. For example:
In Mutation-Driven Evolution, which was published on the same day as my 2013 review, Masatoshi Nei concluded:

…genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world. In this view of evolution there is no need of considering teleological elements.

In my model, and in the context of Elaine Morgan’s claims, viral latency is biophysically constrained by the nutrient energy-dependent physiology of reproduction in all living genera.
See also: Epigenetics and Genetics of Viral Latency

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

For brief reviews of Elaine Morgan’s claims, see:

I do not believe any experimental evidence of energy-dependent biologically-based cause and effect suggests that we evolved from any other species. I suspect that Sir David Attenborough will not be the first to consider my model in the context of his review of Darwinian and/or neo-Darwinian theories. There is too much known to serious scientists about energy-dependent RNA-mediated cell type differentiation to reach any other conclusion than the one reached by Paul M. Lieberman in Epigenetics and Genetics of Viral Latency.
I reiterate:

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

See for comparison:

See also:

The idea that Elaine Morgan can be proved right without proving that Darwian and neo-Darwinian theories are overwhelmingly wrong is an idea that should have been considered during the past 40 years. Instead, consideration of the claims made by theorists have left theorists with nothing more than their ridiculous theories.
See for comparison: Structural diversity of supercoiled DNA, Glucose Tightly Controls Morphological and Functional Properties of Astrocytes,
Tight DNA packaging protects against ‘jumping genes,’ potential cellular destruction Thanks to Teresa Binstock for bringing this article about supercoiled DNA to my attention.
“Tight DNA packaging” and “tightly coiled DNA” are terms used to obfuscate the facts about supercoiled DNA that have already linked viral latency to all pathology.
Supercoiled DNA protects the organized genomes of all living genera from virus-driven entropy. That fact has been the focus of my efforts here and at RNA-mediated.com
Why is Teresa Binstock — co-author of our 1996 Hormones and Behavior review — the only one who seems to be following the literature on RNA-mediated cell type differentiation?

See also: Systematic chemical screening identifies potential antimalarials with new mechanism of action

When Schreiber’s team looked for compounds that met both criteria – displaying a novel mechanism of action and activity during all three disease stages – a series of compounds stood out. All of them acted on the same target, phenylalanyl-tRNA synthetase, a complex enzyme that contributes to protein synthesis. When they tested the compounds in mice, it eradicated the malaria parasites during all three stages of the disease.

Cause and effective treatment are RNA-mediated via links from metabolic networks to genetic networks across species.