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Biologos, Venema and the Scientific Imagination

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Denis Venema wants to explain evolution to evangelical Christians because he doesn’t think it is understand sufficiently. But he asks us to use our imagination and avoids a carefully modelled defence of evolution. If that is the best Darwinists can do then is it any wonder that many of us reject it? See:
Venema Understanding Evolution: An Introduction to Populations and Speciation

Firstly, Venema follows the common evolutionary practice of presenting evidence for evolution by focussing upon the micro changes and then extrapolating without evidence to the macro evolutionary scale by assuming it happens by similar means. But the micro changes, such as that of his exampled stickleback fish, are simply uncontested even by young earth creationists, but what is contested is the belief that we can move from the small to the big without developing and modelling a credible pathway. Time and again evolutionists fail to deal with the problems, but simply make the switch from small to big thinking the flaws in their reasoning will not be noticed.

Venema though asks us to use our imagination to understand evolution. I find that wholly inadequate scientifically, especially when we can model such claims mathematically. And I wonder why such imaginary thinking has a right to be called science. He does though present claims that can be questioned scientifically; for instance believing that humanity evolved within a population size of roughly 10,000 people. So how should we model these claims?

Assuming 20 years for a generation and 6 million years from an ape-like ancestor to mankind would give 300,000 generations to achieve an evolutionary progression from an ape-like ancestor to man. As an aside, in that time only 3 billion individuals would have lived and died, a smaller number than the present human population alive today. Does he really expect us to believe that man could have arisen in so small a number of ancestors? Presumably we can look at the incidence of beneficial mutations in the present human population and ask whether sufficient beneficial mutations would have arisen and be compounded through 300,000 generations. I am afraid it doesn’t look good for evolution.

So down to modelling; we are led to believe that there is 1 percent difference between ape and man in the 3 billion base pairs of DNA, and if we use unrealistic assumptions then we might assume only 10 percent of DNA is coded with the rest considered ‘junk.’ But even 1 percent of 300 million is 3 million nucleotide differences between ape and man.

So we have to find 3 million base-pair beneficial mutational changes in 300,000 generations, or 10 per generation, both found and fixed in the population per generation. Is that possible? I challenge anyone to tell me it is adequate from what we know about the way the present day human population finds and fixes beneficial mutations, even for instance on a small island community of 10,000 people. It comes up against a number of problems.

Problem1. Haldane’s dilemma as discussed by ReMines in The Biotic Message and Sandford in Genetic Entropy (Refs below) (One might have thought these books would be at the top of Venema’s reading list considering his position). Anyway, as a simple overview of the claims of these books, in order for beneficial mutations to be fixed in the population we would need to pay a cost in terms of survivability of the mutated offspring against the un-mutated ones. Haldane thought it as high as 30 to 1, and higher vertebrates cannot hope to pay that cost. Haldane thought a cost of 0.1 per generation might be affordable and that it would take 300 generations to fix 1 beneficial mutation in a population. Venema’s population might then fix 1000 beneficial mutations in 6 million years; a little short of the 3 million required. 

Problem 2. We may also ask whether beneficial mutations actually provide any selective advantage to an organism. Sandford for instance has pointed out that beneficial mutations, when they rarely occur, are virtually invisible at the level of the phenotype anyway and so even Haldane’s 0.1 per generation looks unlikely.           

Problem 3. Harmful mutations are far more common than beneficial ones, perhaps as high as 1000 to 1. In order to weed out the harmful mutations evolution would have to proceed at a very slow rate indeed so that error catastrophe doesn’t occur in the population; a problem known today where small inbreeding populations are often on the verge of extinction. Furthermore, small populations do not have sufficient resources to find the necessary beneficial mutations, even though it makes it easier to spread the mutations that do occur through a population. A large population is more likely to find beneficial mutations, but work against their spread through the population due to the size.   

 So in summary, I would challenge Venema to respond seriously to the questions raised by Sandford and ReMine.

Sources: Walter ReMine’s The Biotic Message, St Paul, Minnesota: St Paul’s Science, pp. 208-236. Sanford, J (2005) Genetic Entropy and the Mystery of the Genome, New York: Elim Publ, especially pp.159-160, Haldane JBS (1957) ‘The Cost of Natural Selection,’ J. Genetics 55:511-24.

Comments
DrREC, you are the one who said DEMONSTRATE, I merely exposed you for being a liar once again to cover up the fact you have ZERO evidence!bornagain77
September 16, 2011
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The query wasn't limited to natural processes. It was for the origination of a novel protein by 'Darwinian' processes. Recombination and mutagenesis coupled with selection made novel proteins.DrREC
September 16, 2011
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DrREC, why don't you use the Lenski Long Term Experiment to DEMONSTRATE what almighty neo-Darwinism can do??? Oh that's right Lenski's e-coli support the opposite conclusion!bornagain77
September 16, 2011
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LOL, so now we're down to direct observation, and the rejection of inference. Have you observed design, or is it an inference?DrREC
September 16, 2011
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So neo-Darwinian evolution practices,,, Strategy and success for the directed evolution of enzymes Calling a AMC Gremlim a formula one race car does not make the it true DrREC, But alas truth is not what you are interested in is it???bornagain77
September 16, 2011
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DrREC you claim: 'The first two demonstrate the generation of novel, functional proteins by mutation and recombination of previously non-coding regions.' Excuse me, they infer relationship from sequences and definitely do not DEMONSTRATE the novel proteins arising!!!bornagain77
September 16, 2011
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" ‘intelligently’ direct the experiment" No, they don't design the outcome. They generate variation with mutation and recombination, and select for results. How is this not analogous to natural selection?DrREC
September 16, 2011
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DrREC, you got to be kidding, do you actually think your last paper that you cited is neo-Darwinian in the least. Those guys are using every bit of knowledge and ingenuity they got to 'intelligently' direct the experiment. Perhaps you don't consider the experimenters intelligent since they are merely accidental by-products of Darwinism and thus it is okay for them to interfere with neo-Darwinian processes as much as they wany?? :) But as for myself, I see a very heavy thumb on the scale for your supposed evidence that testifies all the more clearly of the poverty of your evidential base since you have had to resort to such shenanigans!bornagain77
September 16, 2011
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"Why DrREC, so all you have to do to prove your point is say that Protein a evolved from protein b??? Why that is just special DrREC! Perhaps you could sooth my doubts and actually physically demonstrate the origination of a new protein from a old protein and establish your theory/religion as at least scientifically plausible???" I'm sorry, I find this rant awfully incoherent, and I don't understand why my previous references are insufficient to answer your query. The first two demonstrate the generation of novel, functional proteins by mutation and recombination of previously non-coding regions. The last demonstrates the directed evolution of novel activities (taking activity/protein a and evolving it into activity/protein b, where b doesn't exist in nature, by 'Darwinian' processes-mutation and recombination acted on by selection.DrREC
September 16, 2011
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BA77, they aren't limited in red blood cell production. Read the article: "What's unique about Tibetans is they don't develop high red blood cells counts" Which is a good thing. Google polycythemia and thrombosis if you don't believe me. Increased blood viscosity risks clots, spleen damage, etc. They have heathy hematocrit values--not exactly a loss of information, or deleterious mutation. What is remarkable is they harbor adaptive mutations to a number of genes, that allow them, without cranking out massive numbers of red blood cells, to survive at elevation. These are gain-of-function mutations, despite your blustering otherwise. Many more recent publications: http://scholar.google.com/scholar?hl=en&q=tibetan+altitude+adaptation&as_sdt=0%2C7&as_ylo=2011&as_vis=1DrREC
September 16, 2011
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Why DrREC, so all you have to do to prove your point is say that Protein a evolved from protein b??? Why that is just special DrREC! Perhaps you could sooth my doubts and actually physically demonstrate the origination of a new protein from a old protein and establish your theory/religion as at least scientifically plausible???
Dollo’s law, the symmetry of time, and the edge of evolution - Michael Behe - Oct 2009 Excerpt: Nature has recently published an interesting paper which places severe limits on Darwinian evolution.,,, A time-symmetric Dollo’s law turns the notion of “pre-adaptation” on its head. The law instead predicts something like “pre-sequestration”, where proteins that are currently being used for one complex purpose are very unlikely to be available for either reversion to past functions or future alternative uses. http://www.evolutionnews.org/2009/10/dollos_law_the_symmetry_of_tim.html Severe Limits to Darwinian Evolution: - Michael Behe - Oct. 2009 Excerpt: The immediate, obvious implication is that the 2009 results render problematic even pretty small changes in structure/function for all proteins — not just the ones he worked on.,,,Thanks to Thornton’s impressive work, we can now see that the limits to Darwinian evolution are more severe than even I had supposed. http://www.evolutionnews.org/2009/10/severe_limits_to_darwinian_evo.html#more 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 The Evolutionary Accessibility of New Enzyme Functions: A Case Study from the Biotin Pathway - Ann K. Gauger and Douglas D. Axe - April 2011 Excerpt: We infer from the mutants examined that successful functional conversion would in this case require seven or more nucleotide substitutions. But evolutionary innovations requiring that many changes would be extraordinarily rare, becoming probable only on timescales much longer than the age of life on earth. http://bio-complexity.org/ojs/index.php/main/article/view/BIO-C.2011.1/BIO-C.2011.1 When Theory and Experiment Collide — April 16th, 2011 by Douglas Axe Excerpt: Based on our experimental observations and on calculations we made using a published population model [3], we estimated that Darwin’s mechanism would need a truly staggering amount of time—a trillion trillion years or more—to accomplish the seemingly subtle change in enzyme function that we studied. http://biologicinstitute.org/2011/04/16/when-theory-and-experiment-collide/ “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) "A problem with the evolution of proteins having new shapes is that proteins are highly constrained, and producing a functional protein from a functional protein having a significantly different shape would typically require many mutations of the gene producing the protein. All the proteins produced during this transition would not be functional, that is, they would not be beneficial to the organism, or possibly they would still have their original function but not confer any advantage to the organism. It turns out that this scenario has severe mathematical problems that call the theory of evolution into question. Unless these problems can be overcome, the theory of evolution is in trouble." Problems in Protein Evolution: http://www.cs.unc.edu/~plaisted/ce/blocked.html 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
bornagain77
September 16, 2011
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This following article, which has a direct bearing on the 98.8% genetic similarity myth, shows that over 1000 'ORFan' genes, that are completely unique to humans and not found in any other species, and that very well may directly code for proteins, were stripped from the 20,500 gene count of humans simply because the evolutionary scientists could not find corresponding genes in primates. In other words evolution, of humans from primates, was assumed to be true in the first place and then the genetic evidence was directly molded to fit in accord with their unproven assumption. It would be hard to find a more biased and unfair example of practicing science!
Human Gene Count Tumbles Again - 2008 Excerpt: Scientists on the hunt for typical genes — that is, the ones that encode proteins — have traditionally set their sights on so-called open reading frames, which are long stretches of 300 or more nucleotides, or “letters” of DNA, bookended by genetic start and stop signals.,,,, The researchers considered genes to be valid if and only if similar sequences could be found in other mammals – namely, mouse and dog. Applying this technique to nearly 22,000 genes in the Ensembl gene catalog, the analysis revealed 1,177 “orphan” DNA sequences. These orphans looked like proteins because of their open reading frames, but were not found in either the mouse or dog genomes. Although this was strong evidence that the sequences were not true protein-coding genes, it was not quite convincing enough to justify their removal from the human gene catalogs. Two other scenarios could, in fact, explain their absence from other mammalian genomes. For instance, the genes could be unique among primates, new inventions that appeared after the divergence of mouse and dog ancestors from primate ancestors. Alternatively, the genes could have been more ancient creations — present in a common mammalian ancestor — that were lost in mouse and dog lineages yet retained in humans. If either of these possibilities were true, then the orphan genes should appear in other primate genomes, in addition to our own. To explore this, the researchers compared the orphan sequences to the DNA of two primate cousins, chimpanzees and macaques. After careful genomic comparisons, the orphan genes were found to be true to their name — they were absent from both primate genomes. http://www.sciencedaily.com/releases/2008/01/080113161406.htm
The sheer, and blatant, shoddiness of the science of the preceding study should give everyone who reads it severe pause whenever, in the future, someone tells them that genetic studies have proven evolution to be true. This following site has a brief discussion on the biased methodology of the preceding study: https://uncommondescent.com/intelligent-design/proteins-fold-as-darwin-crumbles/#comment-358505 If the authors of the preceding study were to have actually tried to see if the over 1000 unique ORFan genes of humans may actually encode for proteins, instead of just written them off because they were not found in other supposedly related species, they would have found that there is ample reason to believe that they may very well encode for biologically important proteins:
A survey of orphan enzyme activities Abstract: We demonstrate that for ~80% of sampled orphans, the absence of sequence data is bona fide. Our analyses further substantiate the notion that many of these (orfan) enzyme activities play biologically important roles. http://www.biomedcentral.com/1471-2105/8/244 Dr. Howard Ochman - Dept. of Biochemistry at the University of Arizona Excerpt of Proposal: The aims of this proposal are to investigate this enigmatic class of genes by elucidating the source and functions of “ORFans”, i.e., sequences within a genome that encode proteins having no homology (and often no structural similarity) to proteins in any other genome. Moreover, the uniqueness of ORFan genes prohibits use of any of homology-based methods that have traditionally been employed to establish gene function.,,, Although it has been hypothesized that ORFans might represent non-coding regions rather than actual genes, we have recently established that the vast majority that ORFans present in the E. coli genome are under selective constraints and encode functional proteins. https://uncommondescent.com/intelligent-design/proteins-fold-as-darwin-crumbles/comment-page-5/#comment-358868
In fact it turns out that the authors of the 'kick the ORFans out in the street' paper actually did know that there was unbiased evidence strongly indicating the ORFan genes encoded proteins but chose to ignore it in favor of their preconceived evolutionary bias: https://uncommondescent.com/intelligent-design/proteins-fold-as-darwin-crumbles/comment-page-4/#comment-358547 Moreover the 'anomaly' of unique ORFan genes is found in every new genome sequenced:
Widespread ORFan Genes Challenge Common Descent – Paul Nelson – video with references to literature http://www.vimeo.com/17135166
As well, completely contrary to evolutionary thought, these 'new' ORFan genes are found to be just as essential as 'old' genes for maintaining life:
Age doesn't matter: New genes are as essential as ancient ones - December 2010 Excerpt: "A new gene is as essential as any other gene; the importance of a gene is independent of its age," said Manyuan Long, PhD, Professor of Ecology & Evolution and senior author of the paper. "New genes are no longer just vinegar, they are now equally likely to be butter and bread. We were shocked." http://www.sciencedaily.com/releases/2010/12/101216142523.htm New genes in Drosophila quickly become essential. - December 2010 Excerpt: The proportion of genes that are essential is similar in every evolutionary age group that we examined. Under constitutive silencing of these young essential genes, lethality was high in the pupal (later) stage and (but was) also found in the larval (early) stages. http://www.sciencemag.org/content/330/6011/1682.abstract
of related interest:
Study Reports a Whopping "23% of Our Genome" Contradicts Standard Human-Ape Evolutionary Phylogeny - Casey Luskin - June 2011 Excerpt: For about 23% of our genome, we share no immediate genetic ancestry with our closest living relative, the chimpanzee. This encompasses genes and exons to the same extent as intergenic regions. We conclude that about 1/3 of our genes started to evolve as human-specific lineages before the differentiation of human, chimps, and gorillas took place. (of note; 1/3 of our genes is equal to about 7000 genes that we do not share with chimpanzees) http://www.evolutionnews.org/2011/06/study_reports_a_whopping_23_of047041.html
bornagain77
September 16, 2011
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"DrREC, do you want to show ANY evidence that just one gene and/or protein can arise by neo-Darwinian processes?" Recent de novo origin of human protein-coding genes http://genome.cshlp.org/content/early/2009/08/31/gr.095026.109 Evolution of novel genes. http://www.ncbi.nlm.nih.gov/pubmed/11682312 Strategy and success for the directed evolution of enzymes. http://www.ncbi.nlm.nih.gov/pubmed/21684150 "......including examples of catalytic activity for which there is no precedent in nature"DrREC
September 16, 2011
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DrREC, do you want to show ANY evidence that just one gene and/or protein can arise by neo-Darwinian processes? Could Chance Arrange the Code for (Just) One Gene? "our minds cannot grasp such an extremely small probability as that involved in the accidental arranging of even one gene (10^-236)." http://www.creationsafaris.com/epoi_c10.htm "Estimating the Prevalence of Protein Sequences Adopting Functional Enzyme Folds” 2004: - Doug Axe ,,,this implies the overall prevalence of sequences performing a specific function by any domain-sized fold may be as low as 1 in 10^77, adding to the body of evidence that functional folds require highly extraordinary sequences." http://www.mendeley.com/research/estimating-the-prevalence-of-protein-sequences-adopting-functional-enzyme-folds/bornagain77
September 16, 2011
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DrREC actually, to show you for the inflexible/dishonest neo-Darwinian dogmatist that you truly are (which I enjoy doing by the way), here is the clear evidence, in the Himalayan oxygen mutation, that throws up a huge red flag on such mutations being considered truly random mutations, as is required by neo-Darwinism (your religion), and clearly points to the fact that they should in fact be considered 'designed/calculated' mutations arising 'rapidly' from the regulatory epigentic information controlling the DNA:
neo-Darwinism presupposes that the 'beneficial mutations' which conferred the advantage for Tibetans to live at high altitudes was completely random, yet when looked at from the point of population genetics, the evidence gives every indication that the 'beneficial mutations' were not random at all but were in fact 'programmed' mutations: Another Darwinian “Prediction” Bites the Dust - PaV - August 2010 Excerpt: this means the probability of all three sites changing “at once” (6.25 X 10^-9)^2 = approx. 4 X 10^-17 specific bp change/ yr. IOW (In Other Words), for that size population, and this is a very reasonable guess for size, it would take almost twice the life of the universe for them to take place “at once”. Thus, the invocation of “randomness” in this whole process is pure nonsense. We’re dealing with some kind of programmed response if, in fact, “polygenic selection” is taking place. And, that, of course, means design. https://uncommondescent.com/intelligent-design/another-darwinian-prediction-bites-the-dust/#more-14516
Further notes:
Recently new supposedly 'beneficial mutations' were found in Tibetans that have allowed them to survive in extremely high altitudes, with less oxygen. Yet once again the new supposedly 'beneficial mutations' are actually found to be 'slightly detrimental' because they in fact result in a limit on the red cell blood count for Tibetans: Tibetans Developed Genes to Help Them Adapt to Life at High Elevations - May 2010 Excerpt: "What's unique about Tibetans is they don't develop high red blood cells counts," http://www.sciencedaily.com/releases/2010/05/100513143453.htm Yet high red blood cell counts are actually found to be good,, Extremely fit individuals may have higher values—significantly more red cells in their bodies and significantly more oxygen-carrying capacity—but still maintain normal hematocrit values. http://wiki.medpedia.com/Red_Blood_Cells ,,,Thus they were actually incorrect to imply that a limit on red blood cell counts in Tibetans is 'beneficial',,, Thus this is clearly another example of a loss of overall functional information, and fitness, for the human genome, since, on the molecular level, nothing was gained but something was lost. This following article goes into more detail and points out many other inconsistencies with the Tibetan mutations that evaporate any claim for evidence of a 'truly' beneficial mutation: Tibetans Evolved Altitude Tolerance in 3,000 Years? - July 2010 http://www.creationsafaris.com/crev201007.htm#20100703a
bornagain77
September 16, 2011
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Anyone want to show calculations that the number of mutations between humans and chimps is impossible? Anyone want to defend the claim in the original post that there must be a whopping number of beneficial mutations?DrREC
September 16, 2011
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"much less can the mutations be claimed as purely random mutations and not, in fact, be claimed as ‘calculated’ mutations)" Haha...there it is. Show BA77 evidence of a gain-of-information mutation, and guess what, it is designed. How was this detected, how do you discern it from natural processes? Doesn't matter-because design is just something you can tack onto any observation. It is unfalsifiable in this sense. See something evolve-thats just design unfolding. Which is fine as a personal belief. It is also more simply called theistic evolution. It isn't much of a science.DrREC
September 16, 2011
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Semi OT:, In this podcast, Casey Luskin thoroughly debunks the hype surrounding the newest missing link, Australopithecus sediba. Starting a little after the 7:00 minute mark on the podcast, he quotes from several leading paleontologists in the field who express deep skepticism for the grandiose claims being made in media headlines about its status as irrefutable proof of a 'missing link' for human evolution: Recently Reported Fossil is Old News: Media Hype & the Upcoming Election http://intelligentdesign.podomatic.com/entry/2011-09-16T12_16_16-07_00bornagain77
September 16, 2011
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One day there was a single celled organism splooshing around all by itself having all sorts of fun. It was the only life in the whole universe. I cant tell you how it got there. He was lonely so he turned into two organisms. I cant tell you how. He wished he could turn into a bird and fly in the sky so he did. Don't worry its not magic coz it took a real long time for him to do it. Wow! thank you imagination I now understand the theory of evolution.Mytheos
September 16, 2011
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Initially it may have seemed the more "scientific" option to be a naturalist. However as soon as the naturalist endeavors to defend their belief they are constantly defying "science" at every turn. How can a "scientist" look at a whole system that is slowly by short and sure steps degrading, go and tell the world that it is evolving? Imagination is key I suspect.Mytheos
September 16, 2011
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If it's one thing I hate with a passion its the low probability but great amount of time argument. If everyone is honest we will realize that this is a very difficult problem where small mistakes in measured rates have great consequences. Two examples from basic math The harmonic sequence 1/1 + 1/2 + 1/3 + 1/4 .... so many terms , but each gets smaller. What is the answer? - it never stops growing and can be shown to be infinite ( or more technically, non-convergent.( A power series 9/10 + 9/10^2 + 9 /10^3 + 9/10^4... This again has an infinite number of terms, but it not only converges but has a recognizable answer. It is the number that is usually written 1. ( one ). In order to make real quantitative arguments about probabilities or sequences involving a large number of trials with small probability, you have to know the detailed quantities to incredible precision. Hand waving arguments which move from micro evolution to macro evolution are just so much garbage.JDH
September 15, 2011
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Moreover, neo-Darwinism is simply at a complete loss to explain the beauty of this: Standing Ovation! Jackie Evancho WOW's Audience! - Inspirational Videos http://www.godtube.com/watch/?v=KK67Y7NXbornagain77
September 15, 2011
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To show how grossly misleading neo-Darwinists can be about population genetics, on the web and to the general public, here is the neo-Darwinists very own population genetics model applied to the hypothetical scenario for whale evolution;
Whale Evolution Vs. Population Genetics - Richard Sternberg PhD. in Evolutionary Biology - video http://www.metacafe.com/watch/4165203 referenced paper in preceding 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. http://www.discovery.org/a/9461
Moreover, despite what DrREC, and other neo-Darwinists on the web may say, the fact that there are severe problems in the mathematical population genetics model of neo-Darwinists is readily admitted by many of the population geneticists themselves:
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. http://www.evolutionnews.org/2011/05/oxford_university_admits_darwi046351.html
But, of personal note, when considering the multiple overlapping layers of coding in the genome,,,
Scientists Discover Parallel Codes In Genes Excerpt: Their work,,, shows that the genetic code -- used by organisms as diverse as reef coral, termites, and humans -- is nearly optimal for encoding signals of any length in parallel to sequences that code for proteins. http://www.sciencedaily.com/releases/2007/02/070208230116.htm There also appears to be extensive sequence dependent three-dimensional organization within chromosomes and the whole nucleus (Manuelides, 1990; Gardiner, 1995; Flam, 1994). Trifonov (1989), has shown that probably all DNA sequences in the genome encrypt multiple “codes” (up to 12 codes). Dr. John Sanford; Genetic Entropy 2005 DNA - Evolution Vs. Polyfuctionality - video http://www.metacafe.com/watch/4614519 Scientists Map All Mammalian Gene Interactions – August 2010 Excerpt: Mammals, including humans, have roughly 20,000 different genes.,,, They found a network of more than 7 million interactions encompassing essentially every one of the genes in the mammalian genome. http://www.sciencedaily.com/releases/2010/08/100809142044.htm 3-D Structure Of Human Genome: Fractal Globule Architecture Packs Two Meters Of DNA Into Each Cell - Oct. 2009 Excerpt: the information density in the nucleus is trillions of times higher than on a computer chip -- while avoiding the knots and tangles that might interfere with the cell's ability to read its own genome. Moreover, the DNA can easily unfold and refold during gene activation, gene repression, and cell replication. http://www.sciencedaily.com/releases/2009/10/091008142957.htm
,,,I simply find that it is beyond ludicrous to even begin to entertain the thought that this level of unmatched functional integrated information was put together by mutations filtered by differential death. But alas, as Dr. Hunter says, ,,, Religion drives science and it matters!bornagain77
September 15, 2011
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Instead of DrREC's grossly misleading hypothetical scenarios for the neo-Darwinian evolution of humans, let's look at some actual evidence and see what reality itself is telling us about the plausibility of neo-Darwinian evolution of humans. First no neo-Darwinists seems be able to show me ANY beneficial mutations, in humans (or anything else for that matter), that will withstand scrutiny, (Lactase persistence, and Himilaya high altitude/low oxygen tolerance mutations, in humans, both fail scrutiny for functional information generation, much less can the mutations be claimed as purely random mutations and not, in fact, be claimed as 'calculated' mutations), Yet the evidence for detrimental mutations in humans is simply overwhelming:
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:
HGMD®: Now celebrating our 100,000 mutation milestone! http://www.biobase-international.com/pages/index.php?id=hgmddatabase
I really question their use of the word 'celebrating'. Using real world parameters, here is the correct model for what is actually going on with genomes:
Evolution Vs Genetic Entropy - video http://www.metacafe.com/watch/4028086/ Genetic Entropy vs. Evolution - The Stark Reality - video http://vimeo.com/24870022 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. http://bioinformatics.cau.edu.cn/lecture/chinaproof.pdf MENDEL’S ACCOUNTANT: J. SANFORD†, J. BAUMGARDNER‡, W. BREWER§, P. GIBSON¶, AND W. REMINE http://mendelsaccount.sourceforge.net http://www.scpe.org/vols/vol08/no2/SCPE_8_2_02.pdf
Here is a pretty accurate measure for the detrimental mutation rate in humans.
We Are All Mutants: First Direct Whole-Genome Measure of Human Mutation Predicts 60 New Mutations in Each of Us - June 2011 http://www.sciencedaily.com/releases/2011/06/110613012758.htm
This 'slightly detrimental' mutation rate of 60, per generation is far greater than even what neo-Darwinists agree is a 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. http://www.sciencedaily.com/releases/2007/10/071001172753.htm
etc.. etc.. etc..bornagain77
September 15, 2011
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I chuckled at this one. You lead with:"Denis Venema wants to explain evolution to evangelical Christians because he doesn’t think it is understand sufficiently" and as if to prove his point, you proceed to butcher the topic. Your assumptions: 1) 10 percent of DNA is coded with the rest considered ‘junk.’ (way high) 2) 3 million base-pair beneficial mutational changes (Beneficial???) Could you explain your logic on these mutations ALL being beneficial? Really, I'm curious. Do you think only beneficial mutations can fix? In contrast to your approach, let's just take the simplest route, and say that on average, the across the genome mutations are neutral. Under neutral selection, the rate of fixation for a mutation not subject to selection is the rate of introduction of such mutations. A low estimate is ~1.1×10?8 per site per generation. Times 3 billion sites, 300,000 generations, 2 lineages, we're at 19.8 million, or 1.51%. Not bad. Of course, functional sites show purifying selection, so fewer mutations get fixed there then elsewhere, and open reading frames end up showing ~99.5%+ identity-that is, about 30% of human and chimp proteins having identical amino acid sequences, and the remainder having one or two differences. Are even all these beneficial? Probably not. Some of those tested seem to do little functionally. Many are nearly synonymous, substituting a very similar amino acid. By the way, this difference is only about 10 times the difference between any two humans, if I recall correctly. Haldane's dilemma has been dealt with extensively elsewhere.DrREC
September 15, 2011
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