Evolution’s Junk Science at the University of Maine

_{Cornelius Hunter

September 27, 2015

Intelligent Design}

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Thinking about taking CHY 431—Structure and Mechanism in Biological Chemistry next semester at the University of Maine? If so you likely will be fed junk evolutionary science like this page: Read more

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JoeCoder, I'm not a YEC and I take the empirical evidence of extreme molecular and morphological stasis in bacteria for millions upon millions of years at face value since it has been repeatedly checked and found to be robust. Moreover, I hold the ancient bacteria to directly falsify the claims of genetic drift and/or widespread genetic variability from Darwinists. It is a direct empirical falsification against the drift conjectures from Darwinists. That is as good as it gets in science. In science, direct empirical evidence trumps conjecture all the time. That is the way real science works. Yet, Darwinism is not real science since, among other things, its proponents will not accept falsification from this evidence nor will they accept falsification from multiple other lines of empirical evidence that directly contradict fundamental Darwinian claims. For instance:
Darwin's (failed) Predictions - Cornelius G. Hunter - 2015 This paper evaluates 23 fundamental (false) predictions of evolutionary theory from a wide range of different categories. The paper begins with a brief introduction to the nature of scientific predictions, and typical concerns evolutionists raise against investigating predictions of evolution. The paper next presents the individual predictions in seven categories: early evolution, evolutionary causes, molecular evolution, common descent, evolutionary phylogenies, evolutionary pathways, and behavior. Finally the conclusion summarizes these various predictions, their implications for evolution’s capacity to explain phenomena, and how they bear on evolutionist’s claims about their theory. *Introduction Why investigate evolution’s false predictions? Responses to common objections *Early evolution predictions The DNA code is not unique The cell’s fundamental molecules are universal *Evolutionary causes predictions Mutations are not adaptive Embryology and common descent Competition is greatest between neighbors *Molecular evolution predictions Protein evolution Histone proteins cannot tolerate much change The molecular clock keeps evolutionary time *Common descent predictions The pentadactyl pattern and common descent Serological tests reveal evolutionary relationships Biology is not lineage specific Similar species share similar genes MicroRNA *Evolutionary phylogenies predictions Genomic features are not sporadically distributed Gene and host phylogenies are congruent Gene phylogenies are congruent The species should form an evolutionary tree *Evolutionary pathways predictions Complex structures evolved from simpler structures Structures do not evolve before there is a need for them Functionally unconstrained DNA is not conserved Nature does not make leaps *Behavior Altruism Cell death *Conclusions What false predictions tell us about evolution https://sites.google.com/site/darwinspredictions/home Why investigate evolution’s false predictions? Excerpt: The predictions examined in this paper were selected according to several criteria. They cover a wide spectrum of evolutionary theory and are fundamental to the theory, reflecting major tenets of evolutionary thought. They were widely held by the consensus rather than reflecting one viewpoint of several competing viewpoints. Each prediction was a natural and fundamental expectation of the theory of evolution, and constituted mainstream evolutionary science. Furthermore, the selected predictions are not vague but rather are specific and can be objectively evaluated. They have been tested and evaluated and the outcome is not controversial or in question. And finally the predictions have implications for evolution’s (in)capacity to explain phenomena, as discussed in the conclusions. https://sites.google.com/site/darwinspredictions/why-investigate-evolution-s-false-predictions podcast - Dr. Cornelius Hunter: False Predictions of Darwinian Evolution, pt. 1 In this first podcast of a series, he discusses why he was inspired to pursue this work. http://www.discovery.org/multimedia/audio/2015/08/dr-cornelius-hunter-false-predications-of-darwinian-evolution-pt-1/ podcast - Dr. Cornelius Hunter: False Predictions of Darwinian Evolution, pt. 2 In this second podcast in a series, Dr. Hunter discusses the uniqueness of the DNA code and differences in fundamental molecules. http://www.discovery.org/multimedia/audio/2015/08/dr-cornelius-hunter-false-predictions-of-darwinian-evolution-pt-2/ podcast - Dr. Cornelius Hunter: False Predictions of Darwinian Evolution, pt. 3 In this third podcast of a series, Hunter discusses the prediction of Darwinian theory that mutations should not be adaptive but, instead, random, with respect to organisms' needs. Hunter contrasts this with what University of Chicago molecular biologist James Shapiro has shown about his model of natural genetic engineering. http://www.discovery.org/multimedia/audio/2015/08/dr-cornelius-hunter-false-predictions-of-darwinian-evolution-pt-3/ podcast - Dr. Cornelius Hunter: False Predictions of Darwinian Evolution, pt. 4 In this fourth and final podcast of the series, Dr. Hunter discusses evolution’s failed prediction that competition should be greatest between neighbors. http://www.discovery.org/multimedia/audio/2015/08/dr-cornelius-hunter-false-predictions-of-darwinian-evolution-pt-4/#more-30241
bornagain77_{September 28, 2015
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Things like the "ancient" modern bacteria, a limit on the survivability of lineages due to genetic entropy, and soft tissue and carbon-14 throughout the fossil record make me open minded to young life creation. But there's evidence against it too so I don't really know.
why the more of less discrete differences unless there is some kind of functional constraint in play?
Assuming I'm understanding what you're talking about, I think everyone agrees that certain sequences of cytochrome C are constrained. Whatever deleted those sequences didn't live to tell about it. If mitochondrial genes had no constraints there would be no such things as mitochondrial diseases.JoeCoder_{September 28, 2015
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JoeCoder, My first impression is that the sequences should blend even past the point where every spot has been mutated if the positions were truly random as Darwinism holds, and should not form 'islands' as they do. i.e. why the more of less discrete differences unless there is some kind of functional constraint in play? Moreover, as to the Darwinian presupposition that sequences vary widely over deep time, the empirical evidence simply does not support that Darwinian presupposition:
The Paradox of the "Ancient" (250 Million Year Old) Bacterium Which Contains "Modern" Protein-Coding Genes: “Almost without exception, bacteria isolated from ancient material have proven to closely resemble modern bacteria at both morphological and molecular levels.” Heather Maughan*, C. William Birky Jr., Wayne L. Nicholson, William D. Rosenzweig§ and Russell H. Vreeland ; http://mbe.oxfordjournals.org/cgi/content/full/19/9/1637
These following studies, by Dr. Cano on ancient bacteria, preceded Dr. Vreeland's work:
“Raul J. Cano and Monica K. Borucki discovered the bacteria preserved within the abdomens of insects encased in pieces of amber. In the last 4 years, they have revived more than 1,000 types of bacteria and microorganisms — some dating back as far as 135 million years ago, during the age of the dinosaurs.,,, In October 2000, another research group used many of the techniques developed by Cano’s lab to revive 250-million-year-old bacteria from spores trapped in salt crystals. With this additional evidence, it now seems that the “impossible” is true.” http://www.physicsforums.com/showthread.php?t=281961 Revival and identification of bacterial spores in 25- to 40-million-year-old Dominican amber Dr. Cano and his former graduate student Dr. Monica K. Borucki said that they had found slight but significant differences between the DNA of the ancient, 25-40 million year old amber-sealed Bacillus sphaericus and that of its modern counterpart, (thus ruling out that it is a modern contaminant, yet at the same time confounding materialists, since the change is not nearly as great as evolution's 'genetic drift' theory requires.) http://www.sciencemag.org/cgi/content/abstract/268/5213/1060
In reply to a personal e-mail from myself, Dr. Cano commented on the 'Fitness Test' I had asked him about:
Dr. Cano stated: "We performed such a test, a long time ago, using a panel of substrates (the old gram positive biolog panel) on B. sphaericus. From the results we surmised that the putative "ancient" B. sphaericus isolate was capable of utilizing a broader scope of substrates. Additionally, we looked at the fatty acid profile and here, again, the profiles were similar but more diverse in the amber isolate.": Fitness test which compared ancient amber sealed bacteria to its modern day descendants, RJ Cano and MK Borucki
Thus, the most solid evidence available for the most ancient DNA scientists are able to find does not support evolution happening on the molecular level of bacteria. In fact, according to the fitness test of Dr. Cano, the change witnessed in bacteria conforms to the exact opposite, Genetic Entropy; a loss of functional information/complexity, since fewer substrates and fatty acids are utilized by the modern strains. Considering the intricate level of protein machinery it takes to utilize individual molecules within a substrate, we are talking an impressive loss of protein complexity, and thus loss of functional information, from the ancient amber sealed bacteria. Here is a revisit of the 'Fitness Test'
Is Antibiotic Resistance evidence for evolution? - 'Fitness Test' – video https://www.youtube.com/watch?v=rYaU4moNEBU
As well Joe, I really question whether the mutations on your citation are truly random as the researchers presuppose they are or whether the mutations are being implemented by the molecular machinery of the cell in some kind of top down designed fashion that we are not yet fully aware of:
"It is difficult (if not impossible) to find a genome change operator that is truly random in its action within the DNA of the cell where it works' James Shapiro - Evolution: A View From The 21st Century - (Page 82)
From the Design perspective, I would expect mitochondrial DNA to have a similar level of 'directed mutations' occurring to it as does happen to regular DNA.
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). http://shapiro.bsd.uchicago.edu/Shapiro2009.AnnNYAcadSciMS.RevisitingCentral%20Dogma.pdf
bornagain77_{September 28, 2015
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@Virgil Cain @15 I full agree that generation time is one complicating factor. Number of cell divisions per generation also affects mutation rate. And number of offspring and total genome size also affect the strength of selection. There are many differences between fish and horses and I don't think anybody really knows whether they cancel each other out or not. Just the hazards of molecular clocks. I don't think we can test saturation without being around for millions of years, but see my previous comment about why it should be inevitable.JoeCoder_{September 28, 2015
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BA77 wrote:
And your real time empirical evidence for your claim of Genetic saturation is where exactly?

Your empirical evidence that molecular clock saturation is anything other than a figment of your imagination is what exactly?
1. In humans, mitochondrial genomes are observed to mutate at a rate of something like 1.2 * 10^-6 per base pair per year.. Older studies not based on phylogeny instead of direct measurements estimated the rate to be ~20 to 50 times slower, but now we know those were faulty. These are all much faster than nuclear genome mutation rates. 2. That means after about 10^6, or a million years, every allowable site on a mitochondrial gene like cytochrome c has mutated about once, and now they're starting to mutate more than once. You measure ages by calculating differences, but once ever allowable site has mutated your clock has reached its max age. That's full saturation. Given enough time and mutation it's inevitable. Although selection may slow it somewhat on non-neutral sequences. 3. Therefore it's meaningless to use mitochondrial clocks to measure multiple millions of years. From your sources above, I expect Michael Behe, Doug Axe, Ann Gauger, Stephen Meyer, Paul Giem and John Sanford would likely agree. 4. Above you said, "according to evolutionary theory, one would expect the cytochrome C of a bacterium to be closer to the cytochrome C of a tuna (fish) than a horse" But no--we're way past saturation point so we should expect meaningless readings.according to evolutionary theory, one would expect the cytochrome C of a bacterium to be closer to the cytochrome C of a tuna (fish) than a horse.JoeCoder_{September 28, 2015
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And your real time empirical evidence for your claim of Genetic saturation is where exactly? Anybody can make up a just so story about sequences. Proving your imaginary claim is another thing all together. You do understand what real time empirical evidence is don't you? Hint, your imagination is not it! The following might give you a clue as to what actual empirical evidence looks like:
“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. http://behe.uncommondescent.com/2010/12/the-first-rule-of-adaptive-evolution/ Michael Behe talks about the preceding paper in this following podcast: Michael Behe: Challenging Darwin, One Peer-Reviewed Paper at a Time – December 2010 http://intelligentdesign.podomatic.com/player/web/2010-12-23T11_53_46-08_00 Biological Information - Loss-of-Function Mutations by Paul Giem 2015 - video (Behe - Loss of function mutations are far more likely to fix in a population than gain of function mutations) https://www.youtube.com/watch?v=hzD3hhvepK8&index=20&list=PLHDSWJBW3DNUUhiC9VwPnhl-ymuObyTWJ Response to John Wise – October 2010 Excerpt: A technique called “saturation mutagenesis”1,2 has been used to produce every possible developmental mutation in fruit flies (Drosophila melanogaster),3,4,5 roundworms (Caenorhabditis elegans),6,7 and zebrafish (Danio rerio),8,9,10 and the same technique is now being applied to mice (Mus musculus).11,12 None of the evidence from these and numerous other studies of developmental mutations supports the neo-Darwinian dogma that DNA mutations can lead to new organs or body plans–because none of the observed developmental mutations benefit the organism. http://www.evolutionnews.org/2010/10/response_to_john_wise038811.html Experimental Evolution in Fruit Flies (35 years of trying to force fruit flies to evolve in the laboratory fails, spectacularly) - October 2010 Excerpt: "Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles.,,, "This research really upends the dominant paradigm about how species evolve," said ecology and evolutionary biology professor Anthony Long, the primary investigator. http://www.arn.org/blogs/index.php/literature/2010/10/07/experimental_evolution_in_fruit_flies
bornagain77_{September 28, 2015
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bornagain77: mmmm You didn't corrected your first strawman before starting on your second. Genetic saturation http://www.isogg.org/wiki/SaturationZachriel_{September 28, 2015
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"It’s basic arithmetic." mmmm, in so far as math can be applied to the imaginary claims of Darwinian evolution, math consistently shows us that Darwinian evolution is astronomically unlikely:
HISTORY OF EVOLUTIONARY THEORY – WISTAR DESTROYS EVOLUTION Excerpt: A number of mathematicians, familiar with the biological problems, spoke at that 1966 Wistar Institute,, For example, Murray Eden showed that it would be impossible for even a single ordered pair of genes to be produced by DNA mutations in the bacteria, E. coli,—with 5 billion years in which to produce it! His estimate was based on 5 trillion tons of the bacteria covering the planet to a depth of nearly an inch during that 5 billion years. He then explained that,, E. coli contain(s) over a trillion (10^12) bits of data. That is the number 10 followed by 12 zeros. *Eden then showed the mathematical impossibility of protein forming by chance. http://www.pathlights.com/ce_encyclopedia/Encyclopedia/20hist12.htm Darwin's Doubt - Chapter 12 - Complex Adaptations and the Neo-Darwinian Math - Dr. Paul Giem - video http://www.youtube.com/watch?v=ZFY7oKc34qs&list=SPHDSWJBW3DNUaMy2xdaup5ROw3u0_mK8t&index=7 Biological Information - Overlapping Codes 10-25-2014 by Paul Giem - video https://www.youtube.com/watch?v=OytcYD5791k&index=4&list=PLHDSWJBW3DNUUhiC9VwPnhl-ymuObyTWJ See also Mendel's Accountant and Haldane's Ratchet: John Sanford and company
Darwinism is impossible, "It’s basic arithmetic."bornagain77_{September 28, 2015
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bornagain77: Zachriel, mmmmm, I asked for empirical evidence that your claim for Darwinian evolution (particularly molecular clocks) was true and was not a figment of your imagination. We didn't make a claim about evolution, but that you posted a strawman argument based on your misunderstanding of evolution. Genetic saturation is posited to occur when enough time has passed that new mutations are likely to occur on already mutated sites. If the region is short, or the rate of evolution is high, then saturation occurs in less time. It's basic arithmetic.Zachriel_{September 28, 2015
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Zachriel, mmmmm, I asked for empirical evidence that your claim for Darwinian evolution (particularly molecular clocks) was true and was not a figment of your imagination. I've listed some of my evidence against it being true already. As to an imaginary hypothesis predicting anything, well I guess you can predict as many fluffy pink unicorns dancing on rainbows as you need to as long as you are not constrained by the trifling details of what reality actually says is possible for your hypothesis. And exactly why are you not concerned by your blatant lack of integrity in all this? In your refusal to deal honestly with the consistent empirical failings of your 'theory'? It is simply insane for you to continually go on like this as if you had a case to make in the first place.bornagain77_{September 28, 2015
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bornagain77: And your empirical evidence that molecular clock saturation is anything other than a figment of your imagination is what exactly? The argument you presented was that the hypothesis predicts A, but we see B, while the actual hypothesis predicts B.Zachriel_{September 28, 2015
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And your empirical evidence that molecular clock saturation is anything other than a figment of your imagination is what exactly? I've already listed empirical evidence that goes directly against your entire concept of a molecular clock: https://uncommondescent.com/intelligent-design/evolutions-junk-science-at-the-university-of-maine/#comment-581485 Moreover, my argument is not based on the assumption of the supposed evolution of cytochrome C simply because there is no empirical evidence whatsoever that the origin or evolution of cytochrome C is even remotely possible by unguided material processes. Indeed, my argument is based on the assumption of the Intelligent Design of cytochrome C. You do realize that empirical science is based on real time experimental evidence and not on imagination don't you?
“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” Maxim D. Frank-Kamenetski, Unraveling DNA, 1997, p. 72. (Professor at Brown U. Center for Advanced Biotechnology and Biomedical Engineering) Stability effects of mutations and protein evolvability. October 2009 Excerpt: The accepted paradigm that proteins can tolerate nearly any amino acid substitution has been replaced by the view that the deleterious effects of mutations, and especially their tendency to undermine the thermodynamic and kinetic stability of protein, is a major constraint on protein evolvability,, http://www.ncbi.nlm.nih.gov/pubmed/19765975 Extreme functional sensitivity to conservative amino acid changes on enzyme exteriors - Doug Axe Excerpt: Contrary to the prevalent view, then, enzyme function places severe constraints on residue identities at positions showing evolutionary variability, and at exterior non-active-site positions, in particular. http://nsmserver2.fullerton.edu/departments/chemistry/evolution_creation/web/AxeProteinEvolution.pdf Darwin's God: Post Synaptic Proteins Intolerant of Change - December 2010 Excerpt: Not only is there scant evidence of intermediate designs leading to the known proteins, but the evidence we do have is that these proteins do not tolerate change. http://darwins-god.blogspot.com/2010/12/post-synaptic-proteins-intolerant-of.html "Biologist Douglas Axe on Evolution's (non) Ability to Produce New (Protein) Functions " - video Quote: It turns out once you get above the number six [changes in amino acids] -- and even at lower numbers actually -- but once you get above the number six you can pretty decisively rule out an evolutionary transition because it would take far more time than there is on planet Earth and larger populations than there are on planet Earth. https://www.youtube.com/watch?v=8ZiLsXO-dYo
In fact the Ribosome, which makes the myriad of different, yet specific, types of proteins found in life, is found to be severely intolerant to any random mutations occurring to proteins.
The Ribosome: Perfectionist Protein-maker Trashes Errors Excerpt: The enzyme machine that translates a cell's DNA code into the proteins of life is nothing if not an editorial perfectionist...the ribosome exerts far tighter quality control than anyone ever suspected over its precious protein products... To their further surprise, the ribosome lets go of error-laden proteins 10,000 times faster than it would normally release error-free proteins, a rate of destruction that Green says is "shocking" and reveals just how much of a stickler the ribosome is about high-fidelity protein synthesis. http://www.sciencedaily.com/releases/2009/01/090107134529.htm
And exactly how is the unguided Darwinian evolution of new life forms suppose to 'randomly' occur if it is prevented from 'randomly' occurring to proteins in the first place? Moreover, amino acid positions in a protein are found to be interdependent to other amino acid positions in the protein, i.e. (context dependency), thus exponentially exasperating the problem for neo-Darwinists:
(A Reply To PZ Myers) Estimating the Probability of Functional Biological Proteins? Kirk Durston , Ph.D. Biophysics - 2012 Excerpt (Page 4): The Probabilities Get Worse This measure of functional information (for the RecA protein) is good as a first pass estimate, but the situation is actually far worse for an evolutionary search. In the method described above and as noted in our paper, each site in an amino acid protein sequence is assumed to be independent of all other sites in the sequence. In reality, we know that this is not the case. There are numerous sites in the sequence that are mutually interdependent, (i.e. context dependent), with other sites somewhere else in the sequence. A more recent paper shows how these interdependencies can be located within multiple sequence alignments.[6] These interdependencies greatly reduce the number of possible functional protein sequences by many orders of magnitude which, in turn, reduce the probabilities by many orders of magnitude as well. In other words, the numbers we obtained for RecA above are exceedingly generous; the actual situation is far worse for an evolutionary search. http://powertochange.com/wp-content/uploads/2012/11/Devious-Distortions-Durston-or-Myers_.pdf
Moreover, context dependency is found on several different levels within the protein:
"Why Proteins Aren't Easily Recombined, Part 2" - Ann Gauger - May 2012 Excerpt: "So we have context-dependent effects on protein function at the level of primary sequence, secondary structure, and tertiary (domain-level) structure. This does not bode well for successful, random recombination of bits of sequence into functional, stable protein folds, or even for domain-level recombinations where significant interaction is required." http://www.biologicinstitute.org/post/23170843182/why-proteins-arent-easily-recombined-part-2
And the evidence goes on and on and on like this. Never getting any better for Darwinists. As I said before, neo-Darwinists have no empirical evidence whatsoever for their claims! All they have is imaginary just so stories!bornagain77_{September 28, 2015
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JoeCoder:
If we assume common descent, horses and tuna are both separated from bacteria by the same amount of time.
Generations is the key and time is only part of that.
Why should one be more divergent than the other?
OK, assuming common descent and the sequence prokaryotes-> single-celled eukaryotes->multicellular euks-> ...->fish->amphibian->reptile->mammal, then fish, ie tuna, should have a sequence to reflect that. (Yes I know the tuna of today are just as evolved as the mammals of today. That is why it is dumb to look at bacteria of today and assume some ancient strains had similar genetic makeup- "those genes were conserved cuz the bacteria of today have them and so do extant metazoans x.y and z")
1. Even if evolution by unguided common descent is true, a cytochrome molecular clock is expected to become fully saturated, or “max out” before you get to hundreds of millions of years.
How can we test that?Virgil Cain_{September 28, 2015
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bornagain77: How so? Because you posted an argument based on evolution of cytochrome C which ignored saturation.Zachriel_{September 28, 2015
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Zachriel you claim: "the deduction is faulty" How so? You, as an atheistic neo-Darwinist, have no evidence whatsoever that unguided material processes can create proteins nor even modify proteins to any significant degree. Thus why should your Darwinian just so stories even be given the time of day as to explaining the non-blended 'islands of functionality' witnessed for Cytochrome C? When I worked in a chemical factory as an Instrumentation technician, if I told my boss that I had a hypothesis as to what the measurement of such and such parameter was and not an actually measurement for it, I would have been fired on the spot for not giving him an accurate measurement for the parameter that he had requested at the time he had requested it. But when I request empirical evidence from Darwinists for their claims all I ever get are just so stories and never any real time empirical evidence. If Darwinists worked at a chemical factory and practiced science as they currently do, they would all rightly be fired. So why are Darwinists given a free ride in regards to hard science? Why do you yourself not demand more integrity from yourself and other Darwinists in regards to the science at hand?bornagain77_{September 28, 2015
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Not sure the purpose of your post...
That goes for all of your posts, ZachrielVirgil Cain_{September 28, 2015
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bornagain77: Speculating about nuances in Darwinian just so stories is apparently not my forte since my eyes glazed over when I read your post. All I know is that Darwinists have no real time empirical evidence, that I know of, to back up their claims. Not sure the purpose of your post then. The original post takes the hypothesis and then tries to deduce the entailments. As JoeCoder points out, the deduction is faulty.Zachriel_{September 28, 2015
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JoeCoder, whatever. Speculating about nuances in Darwinian just so stories is apparently not my forte since my eyes glazed over when I read your post. All I know is that Darwinists have no real time empirical evidence, that I know of, to back up their claims. That is all that matters in my book. If you know of real time empirical evidence to the contrary, I would be happy to discuss that. Barring that I think that, overall, we may be on the same page.bornagain77_{September 27, 2015
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Common ancestry is perhaps the most critical assumption of molecular clocks, and if it's wrong then molecular clock readings will be all over the map. And they are. But contrary to your long list of citations that's not what we're discussing here. My point is that even if that were not the case, a cytochrome c molecular clock would still fail because it eventually reaches saturation, where the only thing left to mutate are the conserved sequences. And if you do that your population dies. So: 1. Even if evolution by unguided common descent is true, a cytochrome molecular clock is expected to become fully saturated, or "max out" before you get to hundreds of millions of years. 2. Yet you're pointing to how it gives erroneous divergences for ages of hundreds of millions and even billions of years, and saying that means evolution is wrong. Unless you disagree with the idea of conserved sequences and saturation, and think most letters in a cytochrome c gene can mutate without consequence?JoeCoder_{September 27, 2015
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JoeCoder, the cytochrome C 'isolated' sequence divergence, i.e. not 'blended', more parsimoniously fits the Design model of the Designer reusing the design specifically tweaked for the particular creature. This is especially true considering the abject poverty of any supporting empirical evidence for Darwinian presuppositions. i.e. Empirical evidence or Just so stories, Which one carries the weight in science? Moreover, the molecular clock conjecture of Darwinists is, as far as empirical evidence itself is concerned, dead:
Fudging Evolution to Avoid Falsification - March 12, 2015 Evolutionary theory follows Finagle’s Rule #4: “Draw your curves, then plot your data.” Excerpt: “The fact that the clock is so uncertain is very problematic for us,” David Reich of Harvard said at a recent meeting where no consensus was reached. “It means that the dates we get out of genetics are really quite embarrassingly bad and uncertain.” The solution for some has been to invoke “rate heterogeneity”: mutations rates that speed up or slow down as needed to keep the theory intact. - http://crev.info/2015/03/fudging-evolution/ Evolution Makes No Sense on This Molecular Clock Problem - Cornelius Hunter - June 15, 2015 Excerpt: The theory-laden measurements are based on evolutionary theory. The theory-neutral measurements do not entail evolutionary thinking. In other words, making measurements based on evolutionary theory leads to problems. The resulting DNA mutation rates are not even close to what we can measure more directly, free from theoretical assumptions. As is often the case, these discrepancies between the evidence and the theory leave evolutionists unsure and of differing opinions. As one evolutionist admitted: "The fact that the clock is so uncertain is very problematic for us, It means that the dates we get out of genetics are really quite embarrassingly bad and uncertain." http://darwins-god.blogspot.com/2015/06/evolution-makes-no-sense-on-this.html Paper Suggests Catch 22: Neo-Darwinism Faces Either a Massive Molecular Clock Misfire, or a Major Biogeographical Conundrum - Casey Luskin December 20, 2014 http://www.evolutionnews.org/2014/12/paper_suggests_092171.html
Also see Meyer's book 'Darwin's Doubt' for a more thorough critique of molecular clocks. Here is a short review:
Review: Darwin's Doubt: - Rich Deem Molecular Clock: Based upon the concept of a molecular clock in the genetic sequences of key genes of Cambrian ancestors, scientists have attempted to calculate the time at which these hypothetical ancestors must have evolved. Since the fossil record failed to demonstrate these pre-Cambrian ancestors, scientists had hoped to raise doubt on the brevity of the Cambrian explosion. Calculations based upon a molecular clock showed that these hypothetical ancestors must have arisen a billion or more years ago (half a billion before the Cambrian explosion). However, there isn't even a hint of multicellularity that far back, even though we can find fossil evidence of single-celled organisms as far back as 3.5 billion years ago. Molecular clocks based upon different proteins in different studies produce divergence dates that vary by more than 1 billion years. Hence, the accuracy of such studies must be questioned. http://www.godandscience.org/evolution/darwins_doubt.html
The following paper reveals that the assumption of the molecular clock is a philosophical, not empirical, assumption of Darwinists:
Do Molecular Clocks Run at All? A Critique of Molecular Systematics - Jeffrey H. Schwartz, Bruno Maresca Abstract: Although molecular systematists may use the terminology of cladism, claiming that the reconstruction of phylogenetic relationships is based on shared derived states (synapomorphies), the latter is not the case. Rather, molecular systematics is (largely) based on the assumption, first clearly articulated by Zuckerkandl and Pauling (1962), that degree of overall similarity reflects degree of relatedness. This assumption derives from interpreting molecular similarity (or dissimilarity) between taxa in the context of a Darwinian model of continual and gradual change. Review of the history of molecular systematics and its claims in the context of molecular biology reveals that there is no basis for the “molecular assumption.”.. For historians and philosophers of science the questions that arise are how belief in the infallibility of molecular data for reconstructing evolutionary relationships emerged, and how this belief became so central … http://www.pitt.edu/~jhs/articles/Schwartz&Maresca_Mol_clocks.pdf
bornagain77_{September 27, 2015
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BA77: I'm a creationist so most of your arguments don't apply to me. But to critique a theory (incl. evolutionary theory) it is useful to do so within the model it's presented. I think John Sanford's genetic entropy argument likely prevents lineages from having persisted for millions of years at all. But I do not think your points about cytochrome C comparisons are evidence against evolutionary theory in themselves. Sanford's model show that it's primarily nearly-neutral / slightly-deleterious mutations that accumulate. So if mutating the remaining ~65% of cytochrome C is strongly deleterious, than any organism mutating those will die, while the remainder of the population will instead accumulate slightly deleterious mutations elsewhere--likely mostly in the nuclear genome. This is not a just so story. It's supported by the conserved sequences we see in cytochrome C among all organisms. That means whatever past organisms mutated those letters didn't live to tell about it. So ignoring the other problems with evolutionary theory, we would expect full mitochondrial clock saturation after a while, and all lineages stalling at more or less the same clock reading.JoeCoder_{September 27, 2015
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Joe Coder you state: "Meaning that it cannot diverge further than about 65% because selection prevents it?" How convenient. Just so stories explain everything huh? Small Problem, selection cannot see to the molecular level. i.e. Princess and the pea paradox, J. C. Sanford, Genetic Entropy. Selection is far more impotent than Darwinists let on. Moreover, why is it that the fossil record shows extreme stasis of form once a particular form appears in the fossil record but Darwinists presuppose that the sequences within that form are continually diverging. It is unparsimonious to presuppose that both shape of a type of species to be reducible to specific sequences (which they are not by the way) and also that the sequences are diverging. Anyways, it is all just so story telling anyway since, as Dr. Hunter pointed out, you have no real time empirical evidence that any of your conjectures for the origin and transformation of proteins are possiblebornagain77_{September 27, 2015
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Moreso, perhaps the molecular clock becomes fully saturated in the time since the bacteria / vertebrate divergence, and the time since the tuna / horse divergence? Meaning that it cannot diverge further than about 65% because selection prevents it? Also I completely messed up my blockquotes in my previous comment.JoeCoder_{September 27, 2015
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no blending? how convenient! see pages 281-287, "Evolution: A Theory In Crisis", for a more thorough critique of the 'isolation' problem also see Molecular Clocks: Michael Denton continues to be vindicated https://uncommondescent.com/intelligent-design/molecular-clocks-michael-denton-continues-to-be-vindicated/ etc.. etc.. Moreover, it is now known that the 3-D 'form/shape' of an organism is not even reducible to sequential information on DNA and/or proteins as is presupposed in Darwinism (J. Wells, S. Meyer). As well, the genetic evidence is far more troublesome now for Darwinists than it was known to be when Denton wrote his book in the 1980s:
Logged Out - Scientists Can't Find Darwin's "Tree of Life" Anywhere in Nature by Casey Luskin - Winter 2013 Excerpt: the (fossil) record shows that major groups of animals appeared abruptly, without direct evolutionary precursors. Because biogeography and fossils have failed to bolster common descent, many evolutionary scientists have turned to molecules—the nucleotide and amino acid sequences of genes and proteins—to establish a phylogenetic tree of life showing the evolutionary relationships between all living organisms.,,, Many papers have noted the prevalence of contradictory molecule-based phylogenetic trees. For instance: • A 1998 paper in Genome Research observed that "different proteins generate different phylogenetic tree[s]."6 • A 2009 paper in Trends in Ecology and Evolution acknowledged that "evolutionary trees from different genes often have conflicting branching patterns."7 • A 2013 paper in Trends in Genetics reported that "the more we learn about genomes the less tree-like we find their evolutionary history to be."8 Perhaps the most candid discussion of the problem came in a 2009 review article in New Scientist titled "Why Darwin Was Wrong about the Tree of Life."9 The author quoted researcher Eric Bapteste explaining that "the holy grail was to build a tree of life," but "today that project lies in tatters, torn to pieces by an onslaught of negative evidence." According to the article, "many biologists now argue that the tree concept is obsolete and needs to be discarded.",,, Syvanen succinctly summarized the problem: "We've just annihilated the tree of life. It's not a tree any more, it's a different topology entirely. What would Darwin have made of that?" ,,, "battles between molecules and morphology are being fought across the entire tree of life," leaving readers with a stark assessment: "Evolutionary trees constructed by studying biological molecules often don't resemble those drawn up from morphology."10,,, A 2012 paper noted that "phylogenetic conflict is common, and [is] frequently the norm rather than the exception," since "incongruence between phylogenies derived from morphological versus molecular analyses, and between trees based on different subsets of molecular sequences has become pervasive as datasets have expanded rapidly in both characters and species."12,,, http://www.salvomag.com/new/articles/salvo27/logged-out.php podcast - Molecular Data Wreak Havoc on (Darwin's) Tree of Life - Casey Luskin - March 2014 http://intelligentdesign.podomatic.com/entry/2014-03-14T16_17_31-07_00
bornagain77_{September 27, 2015
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[Denton] left it to the reader to realize that, according to evolutionary theory, one would expect the cytochrome C of a bacterium to be closer to the cytochrome C of a tuna (fish) than a horse (mammal).
If we assume common descent, horses and tuna are both separated from bacteria by the same amount of time. Why should one be more divergent than the other?
JoeCoder_{September 27, 2015
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The serendipity is astonishing. Miraculous, even. I wonder if they will be taught that chemistry is not reducible to physics.Mung_{September 27, 2015
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Cytochrome C Excerpt: If the existence of cytochrome C in “higher forms” of animals is the result of evolution from a common ancestor, then one would expect to see a logical progression. That is, the cytochrome C of an invertebrate (like a worm) would be slightly different from a bacteria. A “primitive” vertebrate (like a fish) would have those same differences, plus a few more. As you progress along the presumed evolutionary path to amphibians, reptiles, mammals, primates, ending with humans, you should see the changes in cytochrome C accumulate. On the other hand, if cytochrome C is a commonly used component employed by a designer, you will not see that logical progression. You will just see minor differences which optimize cytochrome C for that kind of creature.,,, There is a way to distinguish evolution from design at the molecular level. Molecular biologist Michael Denton examined the molecular evidence in detail. He said,,,
",,,Where the fossils had failed and morphological considerations were at best only ambiguous, perhaps this new field of comparative biochemistry might at last provide objective evidence of sequence and of the connecting links which had been so long sought by evolutionary biologists. However, as more protein sequences began to accumulate during the 1960s, it became increasingly apparent that the molecules were not going to provide any evidence of sequential arrangements in nature, but were rather going to reaffirm the traditional view that the system of nature conforms fundamentally to a highly ordered hierarchic scheme from which all direct evidence for evolution is emphatically absent.",,
Dr. Denton then produced several tables and diagrams that show this. He showed, for example, that the cytochrome C in bacteria is 64% different from horses and pigeons, 65% different from tuna and silkmoths, 66% different from wheat, and 69% different from yeast. 2 He left it to the reader to realize that, according to evolutionary theory, one would expect the cytochrome C of a bacterium to be closer to the cytochrome C of a tuna (fish) than a horse (mammal). Furthermore, the horse should have the same mutations as the tuna, plus a few more. This is not what the molecular data shows.,,, Dr. Denton’s Figure 12.1, “The Cytochromes Percent Sequence Difference Matrix” 3, is an abridged version of the 1972 Dayhoff Atlas of Protein Structure and Function Matrix of nearly 1089 entries showing the percent difference between 33 species. Denton’s abridged matrix shows that molecular biologists can easily recognize which cytochrome C sample came from a fish and which came from a mammal.
"However, the most striking feature of the matrix is that every identifiable subclass is isolated and distinct. Every sequence can be unambiguously assigned to a particular subclass. No sequence or group of sequences can be designated as intermediate with respect to other groups. All the sequences of each subclass are equally isolated from the members of another group. Transitional or intermediate classes are completely absent from the matrix. 4"
If evolution were true, and creatures gradually evolved from one to another, there should be intermediate forms. Intermediate forms should be found in living creatures, in the fossil record, and in proteins. It should, in at least some cases, be hard to classify things because the boundaries are blurred. (But the boundaries are distinct as would be expected under the Design presupposition) http://scienceagainstevolution.info/v7i10f.htm
of supplemental interest
Transitional Metals And Cytochrome C oxidase - Michael Denton - Nature's Destiny (Page 204) http://books.google.com/books?id=CdYpDRY0Z6oC&pg=PA203&lpg
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