Meaningful dialogue, anonymous fools and idiot minions

I use definitions to describe differences in behavior. I do not define biologically-based facts in attempts to make the definitions fit into the context of ridiculous theories about the development of behavior. I am not an idiot. An idiot is “…someone who acts in a self-defeating or significantly counterproductive way…. An idiot differs from a fool (who is unwise)…. the terms “idiot” and “idiocy” describe an extreme folly or stupidity, and its symptoms (foolish or stupid utterance or deed).”
Serious scientists may not know enough about other specialities to link biologically-based cause and effect across disciplines, but they are typically willing to learn. Idiots are too foolish to recognize that they need to learn about biologically-based cause and effect in the context of physics, chemistry, and conserved molecular mechanisms to avoid stupid utterances. For examples of stupid utterances, see the discussion of how species diverge.
For intelligent discussion of how species diverge see the comments on: Understanding and accounting for relational context is critical for social neuroscience
“…top-down causation is a key factor not just in the way the brain works but in broader contexts in biology and even physics.” — George F. R. Ellis
See also the comments by What does Ebola actually do?
This citation and quote will help to distinguish idiots from serious scientists:
Citation: The long non-coding RNA Dali is an epigenetic regulator of neural differentiation.
Quote: “…a single intergenic lncRNA controls the activity and methylation of genomically distal regulatory elements to modulate large-scale transcriptional programmes.”
An idiot would place the nutrient-dependent RNA-directed DNA methylation and RNA-mediated regulation of cell type differentiation into the context of mutations and/or natural selection. The idiot would try to make it appear that changes to DNA automagically lead to morphological and behavioral diversity manifested in the context of what they have been taught to believe is evolution.
A serious scientist would attempt to link top-down causation to bottom-up ecological variation. For example, serious scientists look for links between the epigenetic landscape and the physical landscape of DNA in the organized genomes of species from microbes to man. They include requirements for ecological adaptation, which is manifested in increasing complexity.
Nutrient uptake is the first requirement and metabolism of nutrients to species-specific pheromones that control the physiology of reproduction is the second requirement. Taken together, the two requirements are manifested in the diversity of morphological and behavioral phenotypes. Focus on the physics, chemistry, and conserved molecular mechanisms of cell type differentiation eliminates consideration of beneficial mutations that pseudoscientists think somehow link perturbed protein folding to increased organismal complexity. For comparison, nutrient-dependent amino acid substitutions stabilize protein folding, which is required for RNA-mediated regulation of cell type differentiation.
In mammals, The species-specific adaptation of milk to the nutritional requirements of the neonate may involve multiple processes, including the gain and loss of genes encoding the proteins, changes in expression levels of the proteins, and changes in composition of the proteins themselves.
The fact that these species-specific adaptations are nutrient-dependent and pheromone-controlled in the context of RNA-mediated amino acid substitutions has been obscured by the claims of wiki-idiots who tout theories about mutations that somehow link perturbed protein folding from ecological variation to nutrient-dependent ecological adaptations in marine and terrestrial mammals. Note, however, this wiki-idiot fact:None of the mutations so far identified have been shown to be causal for the lactase persistence allele, and it is thought that there are several more yet to be discovered.” No mutations have been found that link biologically-based cause and effect to nutrient-dependent RNA-directed DNA methylation and cell type differentiation via RNA-mediated amino acid substitutions in all mammals.
The idea that more mutations will be discovered and that they will be linked to lactase persistence in some human populations, but not others, is one that attests to the pseudoscientific nonsense of population genetics. Population geneticists invented neo-Darwinism and made Darwin’s ‘conditions of life’ appear to depend on mutations instead of nutrient uptake and pheromone-controlled reproduction.
[W]hat Haldane, Fisher, Sewell Wright, Hardy, Weinberg et al. did was invent…. The anglophone tradition was taught. I was taught, and so were my contemporaries, and so were the younger scientists. Evolution was defined as “changes in gene frequencies in natural populations.” The accumulation of genetic mutations was touted to be enough to change one species to another…. No, it wasn’t dishonesty. I think it was wish fulfillment and social momentum. Assumptions, made but not verified, were taught as fact. — Mazur (2014)
Clearly, many evolutionary biologists are among the other pseudoscientists who think mutations somehow lead to increasing organismal complexity. Even when all experimental evidence of biologically-based cause and effect links amino acid substitutions to cell type differentiation in all species, pseudoscientists continue their efforts to find mutations linked to lactase persistence.
See also: Using stable isotope biogeochemistry to study marine mammal ecology
Excerpt: “As different proteins contain distinct proportions of amino acids, differences in the protein composition among tissue types can yield dissimilar isotopic compositions irrespective of changes in diet”
Cited in Foote et al., (2013): “The differences in amino acid composition among different tissues can lead to large differences in trophic discrimination [38].”
See also: Ecological variation is the raw material by which natural selection can drive evolutionary divergence [1–4].
How can anyone miss the obvious link to terrestrial mammals from RNA-mediated amino acid substitutions and cell type differentiation in marine mammals? It has been reported since 1999 in a series of published works by many different authors. For example: John T. Caprio of Louisiana State University stated that the ability to identify molecules floating in the air is an adaptation of the original mechanism that enabled identification of amino acid-like chemicals soluble in water. See: How The Nose Knows: Research On Smell Boosted.
Why are evolutionary theorists only now beginning to tell others about the importance of social behavior? See: Darwin’s forgotten idea: The social essence of sexual selection How could they not realize that Feedback loops link odor and pheromone signaling with reproduction via conserved molecular mechanisms in species from microbes to man, which link social odors called pheromones from natural selection of food to sexual selection and species diversity?
See also: RNA-based Sex Determination?


Sackler Colloquium: Effects or AFFECTS on Behavior

Arthur M. Sackler Colloquium of the National Academy of Sciences,

Epigenetic Changes in the Developing Brain: Effects on Behavior,”

held March 28–29, 2014, at the National Academy of Sciences in Washington, DC. The complete program and video recordings of most presentations are available on the NAS website.
I reiterate: the title is: Epigenetic changes in the developing brain: Effects on behavior
I was taught that the epigenetic landscape must be linked to physical landscape of DNA in organized genomes of invertebrates and vertebrates via gene activation in hormone-secreting nerve cells of tissue in the brain.
I was taught that nothing but the gene, cell, tissue, organ, organ system pathway could link hormone-organization and hormone-activation from the sensory environment to AFFECTS on behavior.
The title of the Sackler Collogquia seems to suggest that experts on DNA methylation, histone chemistry, and the emerging field of non-coding RNAs may not know the difference between EFFECTS of sensory input on hormones and the AFFECTS of hormones on behavior.
That may be why some researchers still don’t understand the fact that “Feedback loops link odor and pheromone signaling with reproduction
Evolutionary theorists skip the feedback loops and claim that mutations somehow lead to evolved biodiversity. I find it impossible to believe in their theories.
I know that food odors epigenetically effect GnRH secretion and so do species-specific pheromones. The epigenetic effects on GnRH link the sensory environment to behavior in all vertebrates. Behavior is nutrient-dependent.
RNA-directed DNA methylation and RNA-mediated events link nutrient uptake to amino acid substitutions that differentiate cell types via changes in GnRH secretion and its downstream affects on species-specific behaviors and morphologies.
Was I taught to believe in pseudoscientific nonsense about the bio-physically constrained chemistry of protein folding and conserved molecular mechanisms that link epigenetic effects on hormones to affects on behavior? Alternatively, were you taught to believe in pseudoscientic nonsense that links mutations to morphological and behavioral phenotypes via evolution.
Bruce McEwen presented this talk as part of the National Academy of Sciences Sackler Colloquium Biological Embedding of Early Social Adversity: From Fruit Flies to Kindergartners held December 9-10, 2011 in Irvine, California.
See also with my emphasis: Thus, a future research goal should be to provide a neurobiological framework for understanding positive health, positive effect, and self-efficacy and self-esteem and how these components are biologically embedded in a nurturing environment by epigenetic influences, including effects on reactive alleles in the genome. CORRECTION: The authors note that on page 17184, right column, first paragraph, line 4, “effect” should instead appear as “affect.”
Gene Robinson presented this talk as part of the National Academy of Sciences Sackler Colloquium Biological Embedding of Early Social Adversity: From Fruit Flies to Kindergartners held December 9-10, 2011 in Irvine, California.
Other Sackler Colloquium videos: SacklerColloquia


Systems biology and memory disorders

Reversal of cognitive decline: A novel therapeutic program

Reported as:

Memory loss associated with Alzheimer’s reversed: Small trial succeeds using systems approach to memory disorders

News Article Excerpt:

(1) eliminating all simple carbohydrates, leading to a weight loss of 20 pounds;
(2) eliminating gluten and processed food from her diet, with increased vegetables, fruits, and non-farmed fish;
(3) to reduce stress, she began yoga;
(4) as a second measure to reduce the stress of her job, she began to meditate for 20 minutes twice per day;
(5) she took melatonin each night;
(6) she increased her sleep from 4-5 hours per night to 7-8 hours per night;
(7) she took methylcobalamin each day; ( Methylcobalamin (MeCbl), the activated form of vitamin B12)
(8) she took vitamin D3 each day;
(9) fish oil each day;
(10) CoQ10 each day;
(11) she optimized her oral hygiene using an electric flosser and electric toothbrush;
(12) following discussion with her primary care provider, she reinstated hormone replacement therapy that had been discontinued;
(13) she fasted for a minimum of 12 hours between dinner and breakfast, and for a minimum of three hours between dinner and bedtime;
(14) she exercised for a minimum of 30 minutes, 4-6 days per week.
Seven items are associated with nutrient uptake and five items are associated with stress reduction via exercise and sleep. Hormone replacement — for a total of 13 out of 14 items — also links the epigenetic landscape to the physical landscape of DNA in the organized genomes of all vertebrates via the same neuronal system.
The honeybee model organism can now be linked to epigenetically-effected human health and disease via the conserved molecular mechanisms of RNA-directed DNA methylation and RNA-mediated cell type differentiation. The link is the gonadotropin releasing hormone neuronal (GnRH) system. For example, Feedback loops link odor and pheromone signaling with reproduction via the GnRH neuronal system in mammals.
We linked the nutrient-dependent pheromone-controlled feedback loops across species from microbes to man via the conserved molecular mechanisms of cell type differentiation in our Hormones and Behavior review: From Fertilization to Adult Sexual Behavior.
Elekonich and Robinson (2000) “Organizational and activational effects of hormones on insect behavior” extended hormone-organized and hormone-activated behaviors to invertebrates and Elekonich and Roberts (2005) Honey bees as a model for understanding mechanisms of life history transitions extended our 1996 ‘microbes to man’ model to life history transitions in the honeybee.
In my 2012 review Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors, I noted that: “The honeybee already serves as a model organism for studying human immunity, disease resistance, allergic reaction, circadian rhythms, antibiotic resistance, the development of the brain and behavior, mental health, longevity, and diseases of the X chromosome (Honeybee Genome Sequencing Consortium, 2006). Included among these different aspects of eusocial species survival are learning and memory, as well as conditioned responses to sensory stimuli (Maleszka, 2008; Menzel, 1983).”
See: How Do We Answer Fools? Clearly, this new n=10 study, which has not been replicated, shows evolutionary theorists that — if honeybees had teeth — improved oral hygiene might be the most important intervention of all to help them avoid Alzheimer’s disease symptoms. Indeed, the theorists may even link their ideas about the evolution of pheromones to the evolution of teeth in predatory nematodes via mutations and/or natural selection, which they think somehow leads to the evolution of biodiversity.
For contrast, the 14 step intervention shows serious scientists how important it is to link the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man via conserved molecular mechanisms. Attempts to treat pathologies based on the pseudoscientific nonsense of evolutionary theories without considering their basis in nutrient-dependent pheromone-controlled cell type differentiation has led to 18 years of wasted research dollars that could have been better spent developing a model of biologically-based cell type differentiation, which is clearly involved in 13 of the 14 interventions listed above. See also: Pheromones and the luteinizing hormone for inducing proliferation of neural stem cells and neurogenesis.


RNA-directed DNA methylation and RNA-mediated events

Many colleagues and most of my antagonists seem to be unwilling to accept the fact that RNA-directed DNA methylation links the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man. Lack of acceptance appears to be due to the fact that they think mutations and natural selection link evolutionary events to biodiversity. There is no model for that, but they refuse to accept the fact that RNA-mediated events link ecological variation to ecological adaptations.There is a model for that!
The RNA-mediated events are nutrient-dependent because nutrients provide the methly groups required for DNA methylation. In my model, experience dependent odor exposure induces the de novo Creation of receptors that allow nutrients to enter the cell. For example, the Creation of olfactory receptor genes enables nutrient-uptake, which enables DNA methylation. The RNA-mediated events link DNA methylation from nutrient uptake to thermodynamic cycles of protein biosynthesis and degradation. Degradation of proteins links the byproducts of nutrient-dependent RNA-mediated events from DNA methylation and the metabolism of nutrients to the production of species-specific pheromones. Pheromones control the nutrient-dependent physiology of reproduction in species from microbes to man via the conserved molecular mechanisms I just detailed.
The links from physics and chemistry to the thermodynamics of RNA-directed DNA-methylation via RNA-mediated events that link the epigenetic landscape to protein folding that enables increasing organismal complexity via nutrient-dependent pheromone-controlled de novo gene Creation may be impossible to describe to those who are not familiar with physics, chemistry, and the molecular biology of biologically-based cause and effect. However, that is no excuse for anyone to continue to proceed with mathematical models of evolution that do not first address Darwin’s ‘conditions of life.’ Conditions of life are nutrient-dependent, no matter who first suggested they be considered before natural selection of anything else occurred for anything except food. Organisms without enough food due not mature or cannot attract a mate by producing nutrient-dependent pheromones. Thus, the pheromones that control reproduction fit into the context of conditions of life that lead to biodiversity. The fact that RNA-mediated events link nutrient-dependent amino acid substitutions to cell type differentiation in species from microbes to man and that fixation of the amino acid substitutions occurs only in the context of successful nutrient-dependent reproduction seems to be ignored by evolutionary theorists as if that fact — along with physics, chemistry, and molecular biology — could continue to be ignored.
Who is ignoring the facts?
Karl Grammer co-authored our award-winning 2001 review: Human pheromones: integrating neuroendocrinology and ethology He recently mentioned that he would publish a mathematical model of how pheromones influence behavior. This would be a counter-measure that might limit the successful defense of my model. He thinks my attempts to eliminate the theories of evolutionists and human ethologists from consideration are a waste of time. I think it is past time to provide serious scientists with experimental evidence of biologically-based cause and effect and require them to defend their ridiculous theories based on their mathematical models.
However, others have offered a relatively simply mathematical model of RNA-mediated events that links epigenetic effects of pheromones on hormones (neuroendocrinology) to the affects of hormones on behavior (ethology) via feedback loops. See: Mathematical model: microRNA and epigenetic regulation.
Now see: Maternal Methyl Supplemented Diets and Effects on Offspring Health “Lastly, methyl components may lead to tissue/cell-specific effects. Such differences would suggest that these diets might aide in disease prevention in select organs or tissues but also exacerbate disease risk in others.”
Now others can skip the physics, chemistry, and molecular biology. The link from the nutrient-dependent pheromone-controlled physiology of reproduction to tissue/cell-specific effects is clear in the context of what is known about Feedback loops link odor and pheromone signaling with reproduction and what is detailed in the mathematical model:  Interplay of microRNA and epigenetic regulation in the human regulatory network.
The maternal methyl supplementation report links epigenetic effects on cell type differentiation in tissues of organs in organ systems of organisms from ecological variation to the nutrient-dependent pheromone-controlled physiology of ecological adaptations via conserved molecular mechanisms of ecological, social, neurogenic, and socio-cognitive niche construction that I detailed in my model.
Ask Karl Grammer and other theorists who think they can mathematically model the complexities of biologically-based cause and effect that lead to tissue/cell-specific effects and affects on behavior in my model these two questions:
1) Why haven’t you told us what biologically-based evolutionary event links DNA methylation to the morphological and behavioral phenotypes you think somehow arose in the context of mutations, natural selection, and the evolution of biodiversity.
2) What makes you think you can mathematically model the interplay of microRNAs and epigenetic regulation of RNA-mediated biodiversity that clearly occurs in the context of amino acid substitutions that differentiate all cell types in all individuals of all species?
Other have claimed: “We cannot conceive of a global external factor that could cause, during this time, parallel evolution of amino acid compositions of proteins in 15 diverse taxa that represent all three domains of life and span a wide range of lifestyles and environments.” Jordan et al., (2005)
RNA-mediated events link nutrient-dependent pheromone-controlled cell type differentiation in every individual of every honeybee colony via conserved molecular mechanisms linked to cell type differentiation in all cells of all organisms of all species. See: Epigenomics and the concept of degeneracy in biological systems
“Feeding a complex diet known as royal jelly to a growing female larva inhibits global DNA methylation, increases levels of juvenile hormone and correlates with changes in gene expression, which result in the queen phenotype. In contrast, larvae fed less-nutritious worker jelly develop into functionally sterile short-lived worker bees. However, there are no specific ‘queen’ or ‘worker’ genes in the Apis genome. During the initial critical 96 h of larval growth, multiple sensory and secretory systems are involved in receiving, processing and conveying the nutritional information to multilevel, interlocked signaling pathways. The contrasting phenotypes result from threshold-based processes driven by metabolic fluxes, hormonal changes and differential methylation and expression of many genes [83]. All these components have the capacity to respond to environmental change, but their combined and coordinated action has evolved in honey bees as a powerful mechanism for reprograming the entire developmental trajectory with profound consequences for cellular and organismal phenotypes [82–85].”
The honeybee is the model organism that links conserved molecular mechanisms of biophysically-constrained biologically based cause and effect in species from microbes to man.
Does anyone seriously think they can mathematically model that, or anything else about RNA-mediated cell type differentiation. Do they think they can continue to make their mathematical models appear to be consistent with the pseudoscientific nonsense of evolutionary theory and human ethology? If so, perhaps Karl will have help in his efforts to continue to keep others from learning about how ecological variation leads to RNA-mediated ecological adaptations in species from microbes to man.
He’s been doing that since 2001, and it has become more difficult to continue doing so when all biological facts continue to attest to the pseudoscientific nonsense population geneticists used to invent and define neo-Darwinian evolutionary theory. But, I think there is little hope for him if he tries to continue to mathematically model anything that has not become established as a biological fact via experimental evidence of biologically-based cause and effect.