Evolution as a tinkerer?

By: James V. Kohl | Published on: February 10, 2014

The genetic origins of high-altitude adaptations in Tibetans

2/10/14 Excerpts with my emphasis
Excerpt 1: “Genetic adaptations for life at high elevations found in residents of the Tibetan plateau likely originated around 30,000 years ago …”
Excerpt 2: “The transfer of beneficial mutations between human populations and selective enrichment of these genes in descendent generations represents a novel mechanism for adaptation to new environments.”
Excerpt 3: “Unique to Tibetans are variants of the EGLN1 and EPAS1 genes, key genes in the oxygen homeostasis system at all altitudes. These variants were hypothesized to have evolved around 3,000 years ago, a date which conflicts with much older archaeological evidence of human settlement in Tibet.”
Excerpt 4: “…the team identified a population size split between Sherpa and lowland East Asians around 20,000 to 40,000 years ago, a range consistent with proposed archaeological, mitochondria DNA and Y chromosome evidence for an initial colonization of the Tibetan plateau around 30,000 years ago.”
Excerpt 5: “”This is a good example of evolution as a tinkerer,” said Cynthia Beall, PhD, professor of anthropology at Case Western Reserve University and co-author on the study.”
Excerpt 6: “”There is a strong possibility that these genes are adaptations to high altitude,” Di Rienzo adds.”
My comment: Ecological adaptations to high altitude are discussed as if variants of genes, which are associated with mitochondria DNA and Y chromosome evidence, evolved ~ 3,000 years ago in a population that colonized the Tibetan plateau ~ 30,000 years ago. Even if the reader started with the idea that  adaptations to high altitude must be ecological adaptations, it would be difficult to avoid the conclusion that beneficial mutations are naturally selected and transferred between human populations. Therefore, ecological factors are excluded and the mutations are an example of evolution as a tinkerer.
THAT’S AN INTERESTING HYPOTHESIS YOU HAVE THERE; IT WOULD BE A SHAME IF SOMEONE WERE TO TEST IT — Carl Sagan
The story in this article is an example of how the pseudoscience of evolutionary theory is presented as if it were supported by experimental evidence. The use of terms is confusing and the conclusion is framed in the context of how beneficial mutations are fixed via natural selection ~3000 years ago in a population that arose ~30,000 years ago and evolved via mutation-driven evolution.
An accurate representation of biologically based cause and effect challenges the story of mutation-initiated natural selection, but only after the story has been repeatedly told. During the past several decades the story has been told enough times to convince non-biologists that the straightforward Dobzahansky-Muller Incompatibility (DMI) proposal  associated with the null hypothesis of mutation-driven evolution has been accepted. That nonsensical proposal is unacceptable in the context of biological facts. That is, the DMI proposal in unacceptable to anyone who understands biology.
For example, the “HbVar database of hemoglobin variants and thalassemia mutations is one of the oldest and the most-appreciated locus-specific databases (LSDBs), not only from the globin but also from the wider genetic database community.”  There are 1182 hemoglobin variants that differentiate human cell types. There is no experimental evidence that suggests mutation-initiated natural selection is responsible for the differentiation of cell types in any species. All experimental evidence shows that ecological variation results in epigenetic effects that allow the epigenetic landscape to become the physical landscape of DNA in the organized genomes of species from microbes to man. Cause and effect has been repeated demonstrated in experiments that link ecological variation to the ecological, social, neurogenic, and socio-cognitive niche construction exemplified in species diversity as morphological and behavioral phenotypes. If an intelligent person looked only at hemoglobin variants in the α-like and β-like globin gene clusters and hemoglobinopathies, which are the most common single-gene genetic disorders in humans, they would not conclude that the variants lead to mutation-initiated natural selection. In the context of biological facts, the variants are clearly the result of differences in ecologies at different geographical locations that require the same nutrient-dependent pheromone-controlled ecological adaptations that are required in every other species on the planet that has not mutated into its existing morphological and behavioral phenotype.
 
 


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