Assorted notes, videos, and studies on Genetic Entropy (Deterioration of the genome):
Thermodynamic Argument Against Evolution - Thomas Kindell - video
Evolution Vs. Thermodynamics - Open System Refutation - Thomas Kindell - video
DNA Degeneration: Top Population Geneticists agree neo-Darwinism is not supported by the data – John Sanford - video
Mutations: Enemies of Evolution with Geneticist Dr John Sanford - video
Human evolution or extinction - video
Oxford University Admits Darwinism's Shaky Math Foundation - May 2011
Excerpt: However, mathematical population geneticists mainly deny that natural selection leads to optimization of any useful kind. This fifty-year old schism is intellectually damaging in itself, and has prevented improvements in our concept of what fitness is. - On a 2011 Job Description for a Mathematician, at Oxford, to 'fix' the persistent mathematical problems with neo-Darwinism within two years.
The next evolutionary synthesis: Jonathan BL Bard (2011)
Excerpt: We now know that there are at least 50 possible functions that DNA sequences can fulfill , that the networks for traits require many proteins and that they allow for considerable redundancy . The reality is that the evolutionary synthesis says nothing about any of this; for all its claim of being grounded in DNA and mutation, it is actually a theory based on phenotypic traits. This is not to say that the evolutionary synthesis is wrong, but that it is inadequate – it is really only half a theory!
Whale Evolution Vs. Population Genetics - Richard Sternberg PhD. in Evolutionary Biology - video
Waiting Longer for Two Mutations - Michael J. Behe
Excerpt: Citing malaria literature sources (White 2004) I had noted that the de novo appearance of chloroquine resistance in Plasmodium falciparum was an event of probability of 1 in 10^20. I then wrote that 'for humans to achieve a mutation like this by chance, we would have to wait 100 million times 10 million years' (1 quadrillion years)(Behe 2007) (because that is the extrapolated time that it would take to produce 10^20 humans). Durrett and Schmidt (2008, p. 1507) retort that my number ‘is 5 million times larger than the calculation we have just given’ using their model (which nonetheless "using their model" gives a prohibitively long waiting time of 216 million years). Their criticism compares apples to oranges. My figure of 10^20 is an empirical statistic from the literature; it is not, as their calculation is, a theoretical estimate from a population genetics model.
The next evolutionary synthesis: from Lamarck and Darwin to genomic variation and systems biology
Excerpt: If more than about three genes (nature unspecified) underpin a phenotype, the mathematics of population genetics, while qualitatively analyzable, requires too many unknown parameters to make quantitatively testable predictions . The inadequacy of this approach is demonstrated by illustrations of the molecular pathways that generates traits : the network underpinning something as simple as growth may have forty or fifty participating proteins whose production involves perhaps twice as many DNA sequences, if one includes enhancers, splice variants etc. Theoretical genetics simply cannot handle this level of complexity, let alone analyse the effects of mutation..
Evolution Vs Genetic Entropy - Andy McIntosh - video
Poly-Functional Complexity equals Poly-Constrained Complexity
“The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain - Michael Behe - December 2010
Excerpt: In its most recent issue The Quarterly Review of Biology has published a review by myself of laboratory evolution experiments of microbes going back four decades.,,, The gist of the paper is that so far the overwhelming number of adaptive (that is, helpful) mutations seen in laboratory evolution experiments are either loss or modification of function. Of course we had already known that the great majority of mutations that have a visible effect on an organism are deleterious. Now, surprisingly, it seems that even the great majority of helpful mutations degrade the genome to a greater or lesser extent.,,, I dub it “The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain.(that is a net 'fitness gain' within a 'stressed' environment i.e. remove the stress from the environment and the parent strain is always more 'fit')
Michael Behe: Challenging Darwin, One Peer-Reviewed Paper at a Time - December 2010
Where's the substantiating evidence for neo-Darwinism?
Lenski's e-coli - Analysis of Genetic Entropy
Excerpt: Mutants of E. coli obtained after 20,000 generations at 37°C were less “fit” than the wild-type strain when cultivated at either 20°C or 42°C. Other E. coli mutants obtained after 20,000 generations in medium where glucose was their sole catabolite tended to lose the ability to catabolize other carbohydrates. Such a reduction can be beneficially selected only as long as the organism remains in that constant environment. Ultimately, the genetic effect of these mutations is a loss of a function useful for one type of environment as a trade-off for adaptation to a different environment.
Genetic Entropy Confirmed (in Lenski's e-coli) - June 2011
Excerpt: No increases in adaptation or fitness were observed, and no explanation was offered for how neo-Darwinism could overcome the downward trend in fitness.
Mutations : when benefits level off - June 2011 - (Lenski's e-coli after 50,000 generations)
Excerpt: After having identified the first five beneficial mutations combined successively and spontaneously in the bacterial population, the scientists generated, from the ancestral bacterial strain, 32 mutant strains exhibiting all of the possible combinations of each of these five mutations. They then noted that the benefit linked to the simultaneous presence of five mutations was less than the sum of the individual benefits conferred by each mutation individually.
The evidence for the detrimental nature of mutations in humans is overwhelming for scientists have already cited over 100,000 mutational disorders.
Inside the Human Genome: A Case for Non-Intelligent Design - Pg. 57 By John C. Avise
Excerpt: "Another compilation of gene lesions responsible for inherited diseases is the web-based Human Gene Mutation Database (HGMD). Recent versions of HGMD describe more than 75,000 different disease causing mutations identified to date in Homo-sapiens."
I went to the mutation database website cited by John Avise and found this stated in 2009:
HGMD®: Now celebrating our 100,000 mutation milestone!
I really question their use of the word 'celebrating'. (Of note, apparently someone with a sense of decency has now removed the word 'celebrating')
"Mutations" by Dr. Gary Parker
Excerpt: human beings are now subject to over 3500 mutational disorders. (of note: this 3500 figure is cited from the late 1980's)
Human Evolution or Human Genetic Entropy? - Dr. John Sanford - video
This following study confirmed the detrimental mutation rate for humans, of 100 to 300 per generation, estimated by John Sanford in his book 'Genetic Entropy' in 2005:
Human mutation rate revealed: August 2009
Every time human DNA is passed from one generation to the next it accumulates 100–200 new mutations, according to a DNA-sequencing analysis of the Y chromosome. (Of note: this number is derived after "compensatory mutations")
This more recent study found a slightly lower figure:
We Are All Mutants: First Direct Whole-Genome Measure of Human Mutation Predicts 60 New Mutations in Each of Us - June 2011
This 'slightly detrimental' mutation rate of 100 to 200, or even 60, per generation is far greater than even what evolutionists agree is an acceptable mutation rate for an organism:
Beyond A 'Speed Limit' On Mutations, Species Risk Extinction
Excerpt: Shakhnovich's group found that for most organisms, including viruses and bacteria, an organism's rate of genome mutation must stay below 6 mutations per genome per generation to prevent the accumulation of too many potentially lethal changes in genetic material.
Human evolution or extinction (with Dr. John Sanford) - video
Genetic Entropy vs. Evolution - The Stark Reality - video
Contamination of the genome by very slightly deleterious mutations:
why have we not died 100 times over? Kondrashov A.S.
The Frailty of the Darwinian Hypothesis
"The net effect of genetic drift in such (vertebrate) populations is “to encourage the fixation of mildly deleterious mutations and discourage the promotion of beneficial mutations,”
Rate, molecular spectrum, and consequences of human mutation - Michael Lynch
Sanford’s pro-ID thesis supported by PNAS paper, read it and weep, literally - September 2010
Excerpt: Unfortunately, it has become increasingly clear that most of the mutation load is associated with mutations with very small effects distributed at unpredictable locations over the entire genome, rendering the prospects for long-term management of the human gene pool by genetic counseling highly unlikely for all but perhaps a few hundred key loci underlying debilitating monogenic genetic disorders (such as those focused on in the present study).
Unexpectedly small effects of mutations in bacteria bring new perspectives - November 2010
Excerpt: Most mutations in the genes of the Salmonella bacterium have a surprisingly small negative impact on bacterial fitness. And this is the case regardless whether they lead to changes in the bacterial proteins or not.,,, using extremely sensitive growth measurements, doctoral candidate Peter Lind showed that most mutations reduced the rate of growth of bacteria by only 0.500 percent. No mutations completely disabled the function of the proteins, and very few had no impact at all. Even more surprising was the fact that mutations that do not change the protein sequence had negative effects similar to those of mutations that led to substitution of amino acids. A possible explanation is that most mutations may have their negative effect by altering mRNA structure, not proteins, as is commonly assumed.
To get around the problem of slightly detrimental mutations, that are below the power of Natural Selection to remove from the genome, Darwinists have tried to relabel the slightly detrimental mutations as 'neutral', but the fact is that if a mutation is 'just sitting there', not doing anything, then it is in reality placing a energetic burden on the cell and is not truly 'neutral' but is in fact slightly detrimental. Dr. Berlinski comments on the ad hoc 'neutral theory' of evolution here:
Majestic Ascent: Berlinski on Darwin on Trial - David Berlinski - November 2011
Excerpt: The publication in 1983 of Motoo Kimura's The Neutral Theory of Molecular Evolution consolidated ideas that Kimura had introduced in the late 1960s. On the molecular level, evolution is entirely stochastic, and if it proceeds at all, it proceeds by drift along a leaves-and-current model. Kimura's theories left the emergence of complex biological structures an enigma, but they played an important role in the local economy of belief. They allowed biologists to affirm that they welcomed responsible criticism. "A critique of neo-Darwinism," the Dutch biologist Gert Korthof boasted, "can be incorporated into neo-Darwinism if there is evidence and a good theory, which contributes to the progress of science."
By this standard, if the Archangel Gabriel were to accept personal responsibility for the Cambrian explosion, his views would be widely described as neo-Darwinian.
As well, the slow accumulation of 'slightly detrimental mutations' in humans, that is 'slightly detrimental mutations' which are far below the power of natural selection to remove from our genomes, is revealed by these following facts:
“When first cousins marry, their children have a reduction of life expectancy of nearly 10 years. Why is this? It is because inbreeding exposes the genetic mistakes within the genome (slightly detrimental recessive mutations) that have not yet had time to “come to the surface”. Inbreeding is like a sneak preview, or foreshadowing, of where we are going to be genetically as a whole as a species in the future. The reduced life expectancy of inbred children reflects the overall aging of the genome that has accumulated thus far, and reveals the hidden reservoir of genetic damage that have been accumulating in our genomes."
Sanford; Genetic Entropy; page 147
Children of incest - Journal of Pediatrics
Abstract: Twenty-nine children of brother-sister or father-daughter matings were studied. Twenty-one were ascertained because of the history of incest, eight because of signs or symptoms in the child. In the first group of 21 children, 12 had abnormalities, which were severe in nine (43%). In one of these the disorder was autosomal recessive. All eight of the group referred with signs or symptoms had abnormalities, three from recessive disorders. The high empiric risk for severe problems in the children of such close consanguineous matings should be borne in mind, as most of these infants are relinquished for adoption.
Using Computer Simulation to Understand Mutation Accumulation Dynamics and Genetic Load:
Excerpt: We apply a biologically realistic forward-time population genetics program to study human mutation accumulation under a wide-range of circumstances.,, Our numerical simulations consistently show that deleterious mutations accumulate linearly across a large portion of the relevant parameter space.
MENDEL’S ACCOUNTANT: J. SANFORD†, J. BAUMGARDNER‡, W. BREWER§, P. GIBSON¶, AND W. REMINE
Low-Quality Genes May Cause Mutational Meltdown: Deficiencies Compound Over Time - (Apr. 16, 2012)
Excerpt: To manipulate genetic quality, they introduced harmful mutations onto the fly's third chromosome. They then observed how the presence of these mutations affected the fitness of the second chromosome over 46 generations.
"Copies of chromosome two maintained in strains with poor-quality copies of chromosome three declined in fitness two to three times faster than those with good copies of chromosome three, suggesting that poor genetic quality elevates the mutation rate," said Sharp.
The Genetic Decline of Humanity by Brian Thomas, M.S. *
Excerpt: Fossil human bones show that men were much stronger in the past. Neanderthals were ancient people who lived in caves ranging mostly from Europe to Israel. “One of the most characteristic features of the Neanderthals is the exaggerated massiveness of their trunk and limb bones. All of the preserved bones suggest a strength seldom attained by modern humans.”2
Anthropologist Peter McAllister researched fossil human footprints in Australia and found that whoever made those tracks had more speed than champion sprinter Usain Bolt.3 Also, European Paleolithic sites show that humans were larger then and have experienced a “marked decline in stature” from which they have not yet recovered.4
The GS (genetic selection) Principle - David L. Abel - 2009
Excerpt: Stunningly, information has been shown not to increase in the coding regions of DNA with evolution. Mutations do not produce increased information. Mira et al (65) showed that the amount of coding in DNA actually decreases with evolution of bacterial genomes, not increases. This paper parallels Petrov’s papers starting with (66) showing a net DNA loss with Drosophila evolution (67). Konopka (68) found strong evidence against the contention of Subba Rao et al (69, 70) that information increases with mutations. The information content of the coding regions in DNA does not tend to increase with evolution as hypothesized. Konopka also found Shannon complexity not to be a suitable indicator of evolutionary progress over a wide range of evolving genes. Konopka’s work applies Shannon theory to known functional text. Kok et al. (71) also found that information does not increase in DNA with evolution. As with Konopka, this finding is in the context of the change in mere Shannon uncertainty. The latter is a far more forgiving definition of information than that required for prescriptive information (PI) (21, 22, 33, 72). It is all the more significant that mutations do not program increased PI. Prescriptive information either instructs or directly produces formal function. No increase in Shannon or Prescriptive information occurs in duplication. What the above papers show is that not even variation of the duplication produces new information, not even Shannon “information.”
Experimental Evolution in Fruit Flies - October 2010
Excerpt: "This research really upends the dominant paradigm about how species evolve".,,, as stated in regards to the 35 year experimental failure to fixate a single beneficial mutation within fruit flies.
This following calculation by geneticist John Sanford for 'fixing' a beneficial mutation, or for creating a new gene, in humans, gives equally absurd numbers:
Dr. Sanford calculates it would take 12 million years to “fix” a single base pair mutation into a population. He further calculates that to create a gene with 1000 base pairs, it would take 12 million x 1000 or 12 billion years. This is obviously too slow to support the creation of the human genome containing 3 billion base pairs.
"I have seen estimates of the incidence of the ratio of deleterious-to-beneficial mutations which range from one in one thousand up to one in one million. The best estimates seem to be one in one million (Gerrish and Lenski, 1998). The actual rate of beneficial mutations is so extremely low as to thwart any actual measurement (Bataillon, 2000, Elena et al, 1998). Therefore, I cannot ...accurately represent how rare such beneficial mutations really are." (J.C. Sanford; Genetic Entropy page 24) - 2005
Estimation of spontaneous genome-wide mutation rate parameters: whither beneficial mutations? (Thomas Bataillon)
Abstract......It is argued that, although most if not all mutations detected in mutation accumulation experiments are deleterious, the question of the rate of favourable mutations (and their effects) is still a matter for debate.
Distribution of fitness effects caused by random insertion mutations in Escherichia coli
Excerpt: At least 80% of the mutations had a significant negative effect on fitness, whereas none of the mutations had a significant positive effect.
“But in all the reading I’ve done in the life-sciences literature, I’ve never found a mutation that added information… All point mutations that have been studied on the molecular level turn out to reduce the genetic information and not increase it.”
Lee Spetner - Ph.D. Physics - MIT - Not By Chance
John Sanford writes in “Genetic Entropy & the Mystery of the Genome”: “Bergman (2004) has studied the topic of beneficial mutations. Among other things, he did a simple literature search via Biological Abstracts and Medline. He found 453,732 ‘mutation’ hits, but among these only 186 mentioned the word ‘beneficial’ (about 4 in 10,000). When those 186 references were reviewed, almost all the presumed ‘beneficial mutations’ were only beneficial in a very narrow sense–but each mutation consistently involved loss of function changes–hence loss of information. While it is almost universally accepted that beneficial (information creating) mutations must occur, this belief seems to be based upon uncritical acceptance of RM/NS, rather than upon any actual evidence. I do not doubt there are beneficial mutations as evidenced by rapid adaptation yet I contest the fact that they build meaningful information in the genome instead of degrade preexisting information in the genome.” (pp. 26-27)
“Mutations, in summary, tend to induce sickness, death, or deficiencies. No evidence in the vast literature of heredity change shows unambiguous evidence that random mutation itself, even with geographical isolation of populations leads to speciation.”
Lynn Margulis - Acquiring Genomes , p. 29.
“But there is no evidence that DNA mutations can provide the sorts of variation needed for evolution… There is no evidence for beneficial mutations at the level of macroevolution, but there is also no evidence at the level of what is commonly regarded as microevolution.”
Jonathan Wells (PhD. - Molecular Biology)
"Of carefully studied mutations, most have been found to be harmful to organisms, and most of the remainder seem to have neither positive nor negative effect. Mutations that are actually beneficial are extraordinarily rare and involve insignificant changes. Mutations seem to be much more degenerative than constructive…"
Kurt Wise, paleontologist (2002, p.163)
"The neo-Darwinians would like us to believe that large evolutionary changes can result from a series of small events if there are enough of them. But if these events all lose information they can’t be the steps in the kind of evolution the neo-Darwin theory is supposed to explain, no matter how many mutations there are. Whoever thinks macroevolution can be made by mutations that lose information is like the merchant who lost a little money on every sale but thought he could make it up on volume."
Lee Spetner (Ph.D. Physics - MIT - Not By Chance)
"The opportune appearance of mutations permitting animals and plants to meet their needs seems hard to believe. Yet the Darwinian theory is even more demanding: a single plant, a single animal would require thousands and thousands of lucky, appropriate events. Thus, miracles would become the rule: events with an infinitesimal probability could not fail to occur,,, There is no law against day dreaming, but science must not indulge in it."
Pierre P. Grasse - past President of the French Academie des Sciences
Mutations: evolution’s engine becomes evolution’s end! - Article Highlighting The Technical Points Of Genetic Entropy
Excerpt: recent discoveries show that mutations interfere with all molecular machinery. Life’s error correction, avoidance and repair mechanisms themselves suffer the same damage and decay. The consequence is that all multicellular life on earth is undergoing inexorable genome decay.
Darwin Was Wrong: A Study in Probabilities
"To propose and argue that mutations even in tandem with 'natural selection' are the root-causes for 6,000,000 viable, enormously complex species, is to mock logic, deny the weight of evidence, and reject the fundamentals of mathematical probability."
Cohen, I.L. (1984) -
Dr. David Berlinski: Random Mutations – video
Random Mutations Destroy Information - Perry Marshall - video
Random Mutation Generator
All Well Studied Mutations Reduce Genetic Information - Dr. Georgia Purdom - video
No Beneficial Mutations - Not By Chance - Evolution: Theory In Crisis - Lee Spetner - Michael Denton - video
“Mutations are rare phenomena, and a simultaneous change of even two amino acid residues in one protein is totally unlikely. One could think, for instance, that by constantly changing amino acids one by one, it will eventually be possible to change the entire sequence substantially… These minor changes, however, are bound to eventually result in a situation in which the enzyme has ceased to perform its previous function but has not yet begun its ‘new duties’. It is at this point it will be destroyed - along with the organism carrying it.” Maxim D. Frank-Kamenetski, Unraveling DNA, 1997, p. 72. (Professor at Brown U. Center for Advanced Biotechnology and Biomedical Engineering)
Evolution Cartoon - Waiting For That Beneficial Mutation - video
...Advantageous anatomical mutations are never observed. The four-winged fruit fly is a case in point: The second set of wings lacks flight muscles, so the useless appendages interfere with flying and mating, and the mutant fly cannot survive long outside the laboratory. Similar mutations in other genes also produce various anatomical deformations, but they are harmful, too. In 1963, Harvard evolutionary biologist Ernst Mayr wrote that the resulting mutants “are such evident freaks that these monsters can be designated only as ‘hopeless.’ They are so utterly unbalanced that they would not have the slightest chance of escaping elimination through natural selection." -
"A Dutch zoologist, J.J. Duyvene de Wit, clearly demonstrated that the process of speciation (such as the appearance of many varieties of dogs and cats) is inevitably bound up with genetic depletion as a result of natural selection. When this scientifically established fact is applied to the question of whether man could have evolved from ape-like animals,'.. the transformist concept of progressive evolution is pierced in its very vitals.' The reason for this, J.J. Duyvene de Wit went on to explain, is that the whole process of evolution from animal to man " ' . . would have to run against the gradient of genetic depletion. That is to say, . . man )should possess] a smaller gene-potential than his animal ancestors! [I] Here, the impressive absurdity becomes clear in which the transformist doctrine [the theory of evolution] entangles itself when, in flat contradiction to the factual scientific evidence, it dogmatically asserts that man has evolved from the animal kingdom!" —Op. cit., pp. 129-130. [Italics his; quotations from *J.J. Duyvene de Wit, A New Critique of the Transformist Principle in Evolutionary Biology (1965), p. 56,57.]
Stephen Meyer - Functional Proteins And Information For Body Plans - video
Dr. Stephen Meyer comments at the end of the preceding video,,,
‘Now one more problem as far as the generation of information. It turns out that you don’t only need information to build genes and proteins, it turns out to build Body-Plans you need higher levels of information; Higher order assembly instructions. DNA codes for the building of proteins, but proteins must be arranged into distinctive circuitry to form distinctive cell types. Cell types have to be arranged into tissues. Tissues have to be arranged into organs. Organs and tissues must be specifically arranged to generate whole new Body-Plans, distinctive arrangements of those body parts. We now know that DNA alone is not responsible for those higher orders of organization. DNA codes for proteins, but by itself it does insure that proteins, cell types, tissues, organs, will all be arranged in the body. And what that means is that the Body-Plan morphogenesis, as it is called, depends upon information that is not encoded on DNA. Which means you can mutate DNA indefinitely. 80 million years, 100 million years, til the cows come home. It doesn’t matter, because in the best case you are just going to find a new protein some place out there in that vast combinatorial sequence space. You are not, by mutating DNA alone, going to generate higher order structures that are necessary to building a body plan. So what we can conclude from that is that the neo-Darwinian mechanism is grossly inadequate to explain the origin of information necessary to build new genes and proteins, and it is also grossly inadequate to explain the origination of novel biological form.’ - Stephen Meyer - (excerpt taken from Meyer/Sternberg vs. Shermer/Prothero debate - 2009)
Epigenetics and the "Piano" Metaphor - January 2012
Excerpt: And this is only the construction of proteins we're talking about. It leaves out of the picture entirely the higher-level components -- tissues, organs, the whole body plan that draws all the lower-level stuff together into a coherent, functioning form. What we should really be talking about is not a lone piano but a vast orchestra under the directing guidance of an unknown conductor fulfilling an artistic vision, organizing and transcending the music of the assembly of individual players.
A review of The Edge of Evolution: The Search for the Limits of Darwinism
The numbers of Plasmodium and HIV in the last 50 years greatly exceeds the total number of mammals since their supposed evolutionary origin (several hundred million years ago), yet little has been achieved by evolution. This suggests that mammals could have "invented" little in their time frame. Behe: ‘Our experience with HIV gives good reason to think that Darwinism doesn’t do much—even with billions of years and all the cells in that world at its disposal’ (p. 155).
Thus, the actual rate for 'truly' beneficial mutations, which would account for the staggering machine-like complexity we see in life, is far in excess of one-hundred-billion-billion mutational events. So this one in a thousand, to one in a million, number for 'truly' beneficial mutations is actually far, far, too generous for an estimate for evolutionists to use as an estimate for beneficial mutations.
The foundational rule of Genetic Entropy for biology, which can draw its foundation in science from the twin pillars of the Second Law of Thermodynamics and from the Law of Conservation of Information (Dembski, Marks, Abel), can be stated something like this:
"All beneficial adaptations away from a parent species for a sub-species, which increase fitness to a particular environment, will always come at a loss of the optimal functional information that was originally created in the parent species genome."
A. L. Hughes's New Non-Darwinian Mechanism of Adaption Was Discovered and Published in Detail by an ID Geneticist 25 Years Ago - Wolf-Ekkehard Lönnig - December 2011
Excerpt: The original species had a greater genetic potential to adapt to all possible environments. In the course of time this broad capacity for adaptation has been steadily reduced in the respective habitats by the accumulation of slightly deleterious alleles (as well as total losses of genetic functions redundant for a habitat), with the exception, of course, of that part which was necessary for coping with a species' particular environment....By mutative reduction of the genetic potential, modifications became "heritable". -- As strange as it may at first sound, however, this has nothing to do with the inheritance of acquired characteristics. For the characteristics were not acquired evolutionarily, but existed from the very beginning due to the greater adaptability. In many species only the genetic functions necessary for coping with the corresponding environment have been preserved from this adaptability potential. The "remainder" has been lost by mutations (accumulation of slightly disadvantageous alleles) -- in the formation of secondary species.
Moreover, on top of all this, as if this wasn't bad enough, it is found that the overwhelming majority of changes, mutations, in genomes are 'non-random' mutations, as is required by the standard neo-Darwinian theory (i.e. 'Random" Variation and Natural Selection).
Revisiting the Central Dogma in the 21st Century - James A. Shapiro - 2009
Excerpt (Page 12): Underlying the central dogma and conventional views of genome evolution was the idea that the genome is a stable structure that changes rarely and accidentally by chemical fluctuations (106) or replication errors. This view has had to change with the realization that maintenance of genome stability is an active cellular function and the discovery of numerous dedicated biochemical systems for restructuring DNA molecules.(107–110) Genetic change is almost always the result of cellular action on the genome. These natural processes are analogous to human genetic engineering,,, (Page 14) Genome change arises as a consequence of natural genetic engineering, not from accidents. Replication errors and DNA damage are subject to cell surveillance and correction. When DNA damage correction does produce novel genetic structures, natural genetic engineering functions, such as mutator polymerases and nonhomologous end-joining complexes, are involved. Realizing that DNA change is a biochemical process means that it is subject to regulation like other cellular activities. Thus, we expect to see genome change occurring in response to different stimuli (Table 1) and operating nonrandomly throughout the genome, guided by various types of intermolecular contacts (Table 1 of Ref. 112).
Is Antibiotic Resistance evidence for evolution? - 'The Fitness Test' - video
The Genetic Selection (GS) Principle - David L. Abel
Abstract. The GS (Genetic Selection) Principle states that biological selection must occur at the nucleotide-sequencing molecular-genetic level of 3’5′ phosphodiester bond formation. After-the-fact differential survival and reproduction of already-programmed, already-living phenotypic organisms (natural selection) does not explain polynucleotide sequence prescription and coding. All life forms depend upon exceedingly-optimized genetic algorithms. Biological control requires selection of particular physicodynamically indeterminate configurable switch settings to achieve potential function. This occurs largely at the level of nucleotide selection, prior to the realization of any isolated or integrated biofunction. Each selection of a nucleotide corresponds to a quaternary (four-way) switch setting. Formal logic gates must be set initially that will only later determine folding and binding function through minimum Gibbs-free energy sinks. The fittest living organisms cannot be favored until they are first programmed and computed. The GS Principle distinguishes selection of existing function (undirected natural selection) from selection for potential function (formal selection at decision nodes, logic gates and configurable switch settings).
Don Patton - Entropy, Information, and The 'Deteriorating' Fossil Record - video
Falsification Of Neo-Darwinism by Quantum Entanglement/Information
Does Quantum Biology Support A Quantum Soul? – Stuart Hameroff - video (notes in description)
Intelligent Design - The Anthropic Hypothesis
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