Master gene that makes mouse brain look human
Posted on June 1, 2013 by James Kohl.
Excerpt: “Researchers have now found a genetic mutation that causes mammalian neural tissue to expand and fold.”
My comment: There is no evidence that any genetic mutation causes mammalian neural tissue to expand and fold.
Excerpt: “The findings go against a common conception that “dumber species will have different genes” for brain development than more intelligent species, Borrell says. He adds that the mechanism could help explain how New World monkeys, with their small, smooth brains, could have evolved from an ancestor with a bigger and more folded brain. “It’s not a linear evolution from small, simple, smooth brains to large, gyrated brains.”
My comment: Small smooth brains that evolved from bigger more folded brains appear to represent regression, as occurs in blind cave fish and in murre-wing / penguin-flipper morphogenesis in flightless birds. Findings like these go against a common conception, and clarify the fact that it is a common misconception. As it has with eyes and wings, it has become clearer that non-linear ‘evolution from small, simple, smooth brains to large, gyrated brains‘ [and back] results from nutrient-dependent pheromone-controlled ecological, social, neurogenic, and socio-cognitive niche construction. In my model, for example, cause and effect is exemplified via focus on the molecular mechanisms of thermodynamic control of intracellular and intermolecular interactions, which enable organism-level thermoregulation common to species from microbes to man.
My model incorporates recent advances in mouse-to-human modeling of epigenetic effects of sensory input associated with nutrient uptake and with the metabolism of nutrients to species-specific pheromones shows that in only ~30,000 years a human population in Central China arose due to a single nutrient-dependent amino acid substitution. Adaptive evolution in a human population in only ~30,000 years is consistent with climate change and environmental determinants of microRNA/messenger RNA balance-regulation in plants. It is not consistent with mutations theory in the context of millions of years of evolution that somehow occurred.
For example, climate changes and nutrient-dependent changes led to starch production in leaves and diet-driven changes in the development of the brain and behavior of mammals due to differences in starch intake and its metabolism (e.g., in wolves and dogs). During about the same time (e.g., ~30,000 years) some reports indicate that Neandertals were somehow replaced by ‘modern’ humans. However, the possibility remains that nearly all the changes in the human genome that make us modern ‘humans’ have occurred during the past 5,000 years. “Of 1.15 million single-nucleotide variants found among more than 15,000 protein-encoding genes, 73% in arose the past 5,000 years…“
Mutations theory offers no explanation for any of the aforementioned cause and effect relationships. If there is some other theory with explanatory power in the context of what is now known about the molecular mechanisms of adaptive evolution, it could be compared to my model of nutrient-dependent pheromone-controlled adaptive evolution, and to evidence from a human population that arose during the past ~30,000 years in Central China.
I suspect that there is no theory and no other model with enough explanatory power to link the common molecular mechanisms of adaptive evolution in species from microbes to man to their nutrient-dependence and the control of reproduction by pheromones. I think that the lack of evidence to support another model angers those who have accepted the bastardization of Darwin’s theory with its original basis in ‘conditions of life’ that are clearly nutrient-dependent and pheromone-controlled.
Meanwhile, evidence for nutrient-dependent pheromone-controlled brain development continues to be ignored as noted in the context of Human Culture, an Evolutionary Force.
Excerpt: “People adapt genetically to sustained cultural changes, like new diets. And this interaction works more quickly than other selective forces, “leading some practitioners to argue that gene-culture co-evolution could be the dominant mode of human evolution,” Kevin N. Laland and colleagues wrote in the February issue of Nature Reviews Genetics.”
My comment: I wonder how much more obvious it will become that gene-culture co-evolution is the dominant mode of human evolution.
Excerpt: “…have argued for years that genes and culture were intertwined in shaping human evolution. “It wasn’t like we were despised, just kind of ignored…”
My comment: I wonder how much longer misrepresentations will continue and accurate representations of cause and effect will be ignored.
Excerpt: “The case of the EDAR gene shows how cautious biologists have to be in interpreting the signals of selection seen in the genome scans.”
My comment: The case of the EDAR gene show how cautious theorists should have been in promoting claims that mutations are somehow involved in adaptive evolution. Indeed, it is those theorists who should have been despised or ignored, since there is no evidence for mutation caused adaptive evolution. Thus, they are likely to remain angry because they cannot defend their theories.
In the context of facts, why would researchers who have focused on EDAR variants be ignored? The latest data from interdisciplinary research across species shows that the adaptive evolution of the human brain and behavior involves the same nutrient-dependent pheromone-controlled molecular mechanisms that are common in species from microbes to man. There is no longer even a vague suspicion that a genetic mutation causes mammalian neural tissue to expand and fold. Clearly, epigenetic effects of nutrients on EDAR variants and pheromone-controlled organism-level thermoregulation are involved, as is TRNP1. Theorists are left to contemplate why they thought in terms of adaptive evolution that was not nutrient-dependent and pheromone-controlled as the rest of the world laughs in the faces of their ignorance or confusion.
Retired medical laboratory scientist
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