Average child has 60 genetic mutations?

_{Denyse O'Leary

June 13, 2011

Darwinism, Genetics, Intelligent Design}

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From “We Are All Mutants: First Direct Whole-Genome Measure of Human Mutation Predicts 60 New Mutations in Each of Us,” (ScienceDaily, June 12, 2011), a study involving four adults and one child, we learn:

Each one of us receives approximately 60 new mutations in our genome from our parents. This striking value is reported in the first-ever direct measure of new mutations coming from mother and father in whole human genomes.[ … ]

Mutations that occur in sperm or egg cells will be ‘new’ mutations not seen in our parents.
Although most of our variety comes from reshuffling of genes from our parents, new mutations are the ultimate source from which new variation is drawn. Finding new mutations is extremely technically challenging as, on average, only 1 in every 100 million letters of DNA is altered each generation.

A surprise was the considerable variation in families, as to whether most mutations arose from the father or the mother. In theory, the father was favoured as a source of mutations because of “ the additional number of times that the genome needs to be copied to make a sperm, as opposed to an egg.”

Assuming the results hold up, what would they suggest about human evolution?

Comments

Bornagain, It's interesting how you and I switch from being adversaries to allies, depending on the subject matter, don't you think?Bruce David_{June 16, 2011
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Mung, If it is truly a random mutation within a functional sequence, such as a typo in a sentence, then you are clearly moving away from optimal functionality to sub-optimal functionality and are thus 'slightly detrimental'. If it is 'sub-functional or non-functional' energetic burden will increase and decrease fitness thus favoring removal by further mutation/selection. Notes; Astonishing DNA complexity update Excerpt: The untranslated regions (now called UTRs, rather than ‘junk’) are far more important than the translated regions (the genes), as measured by the number of DNA bases appearing in RNA transcripts. Genic regions are transcribed on average in five different overlapping and interleaved ways, while UTRs are transcribed on average in seven different overlapping and interleaved ways. Since there are about 33 times as many bases in UTRs than in genic regions, that makes the ‘junk’ about 50 times more active than the genes. http://creation.com/astonishing-dna-complexity-update also of interest; As former president of the French Academy of Sciences Pierre P. Grasse has stated: “What is the use of their unceasing mutations, if they do not change? In sum, the mutations of bacteria and viruses are merely hereditary fluctuations around a median position; a swing to the right, a swing to the left, but no final evolutionary effect.” Bacteria 'Invest' (Designed) Wisely to Survive Uncertain Times, Scientists Report - Dec. 2009 Excerpt: Essentially, variability of bacterial cells appears to match the variability in the environment, thereby increasing the chances of bacterial survival, http://www.sciencedaily.com/releases/2009/11/091102112102.htm It is also interesting to note that scientists have actually used a mechanism of 'excessive mutations' to help humans in their fight against pathogenic viruses, as the following articles clearly point out: GM Crops May Face Genetic Meltdown Excerpt: Error catastrophe occurs when high mutation rates give rise to so many deleterious mutations that they make the population go extinct. For example, foot and mouth disease virus treated with mutagens (base analogues fluorouracil and azacytidine) eventually become extinct [1]. Polio virus treated with the mutagenic drug ribavirin similarly went extinct [2]. http://www.i-sis.org.uk/meltdown.php Quasispecies Theory and the Behavior of RNA Viruses - July 2010 Excerpt: Many predictions of quasispecies theory run counter to traditional views of microbial behavior and evolution and have profound implications for our understanding of viral disease. ,,, it has been termed “mutational meltdown.” It is now clear that many RNA viruses replicate near the error threshold. Early studies with VSV showed that chemical mutagens generally reduced viral infectivity, and studies with poliovirus clearly demonstrated that mutagenic nucleoside analogs push viral populations to extinction [40]–[43]. The effect is dramatic—a 4-fold increase in mutation rate resulted in a 95% reduction in viral titer.,,, While mutation-independent activities have also been identified, it is clear that APOBEC-mediated lethal mutagenesis is a critical cellular defense against RNA viruses. The fact that these pathogens replicate close to the error threshold makes them particularly sensitive to slight increases in mutational load.,,, http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1001005#ppat-1001005-g003 Life Leads the Way to Invention - Feb. 2010 Excerpt: a cell is 10,000 times more energy-efficient than a transistor. “ In one second, a cell performs about 10 million energy-consuming chemical reactions, which altogether require about one picowatt (one millionth millionth of a watt) of power.” This and other amazing facts lead to an obvious conclusion: inventors ought to look to life for ideas.,,, Essentially, cells may be viewed as circuits that use molecules, ions, proteins and DNA instead of electrons and transistors. That analogy suggests that it should be possible to build electronic chips – what Sarpeshkar calls “cellular chemical computers” – that mimic chemical reactions very efficiently and on a very fast timescale. http://creationsafaris.com/crev201002.htm#20100226a Also of interest is that a cell apparently seems to be successfully designed along the very stringent guidelines laid out by Landauer's principle of 'reversible computation' in order to achieve such amazing energy efficiency, something man has yet to accomplish in any meaningful way for computers: Notes on Landauer’s principle, reversible computation, and Maxwell’s Demon - Charles H. Bennett Excerpt: Of course, in practice, almost all data processing is done on macroscopic apparatus, dissipating macroscopic amounts of energy far in excess of what would be required by Landauer’s principle. Nevertheless, some stages of biomolecular information processing, such as transcription of DNA to RNA, appear to be accomplished by chemical reactions that are reversible not only in principle but in practice.,,,, http://www.hep.princeton.edu/~mcdonald/examples/QM/bennett_shpmp_34_501_03.pdf etc.. etc... Well Mung, every measure I can find says that 'truly random' single point mutations will be slightly detrimental. Thus you are free to believe whatever you want, but as for myself, I will follow the evidence and it clearly indicates the premise is correct.bornagain77_{June 16, 2011
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Elizabeth, you state: "[Sanford] seems to think that the closer you get, from the deleterious end, to neutrality, the more mutations you find ('VSDMs'); then, without any justification, whether by argument or evidence, he assumes a cliff edge with virtually no mutations that are 'VSBMs'." This is simply not true. p. 24 of the paperback edition: "I have seen estimates of the ratio of deleterious-to-beneficial mutations which range from one thousand to one, up to one million to one. The best estimates seem to be one million to one (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)." On p. 25: "When it was discovered that certain forms of radiation and certain chemicals were powerful mutagenic agents, millions and millions of plants were mutgenized and screened for possible improvements...Vast numbers of mutants were produced and screened, collectively representing many billions of mutation events. A huge number of small, sterile, sick, deformed, aberrant plants were produced. However, from all this effort, almost no meaningful crop improvement resulted. The effort was for the most part an enormous failure. Why did this huge mutation/selection experiment fail...? It was because even with all those billions of mutations, there were no significant new beneficial mutations arising. The notable exceptions prove the point. For example, low phytate corn...The low phytate corn was created by nutagenizing corn, and then selecting for strains wherein the genetic machinery which directs phytic acid production had been damaged. Although the resulting mutant may be desired for a specific agricultural purpose, it was accomplished through net loss of information,...and the loss of biological function. Most of the other examples of successful mutation breeding are found within the area of ornamental plants. Examples of "useful" mutations...include sterility, dwarfing, mottled or variegated foliage, altered color patterns, or misshaped floral organs. And on p. 25: Bergman (2004)...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 consistently involved loss-of-function changes (hence loss of information). He was unable to find a single example of a mutation which unambiguously created new information. So I repeat my question, exactly how has Sanford “misunderstood his sources, and misread the data”?Bruce David_{June 16, 2011
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Mung, It is fairly hard to argue for ‘completely neutral’ mutations, for even mutations which ‘do nothing at all’ still require energy to replicate, and thus are a ‘slight burden’
I guess you got me there BA. But let me think. What if the mutation occurs as a result of the nucleotide being replicated?
Point mutations may arise from spontaneous mutations that occur during DNA replication. - Point mutation
So it was already being copied anyways, and therefore there was no additional energy burden. Thus without more details on your part I find that argument unconvincing, to say the least.Mung_{June 16, 2011
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Getting Over the Code Delusion - From Junk to Living Organism - November 2010 Excerpt: So what’s going on? These puzzles turn out to be intimately related. As organisms rise on the evolutionary scale, they tend to have more “junk DNA.” Noncoding DNA accounts for some 10 percent of the genome in many one-celled organisms (i.e. 90% of single celled organisms are genetic coding regions), 75 percent in roundworms, and 98 percent in humans. The ironic suspicion became too obvious to ignore: maybe it’s precisely our “junk” that differentiates us from water fleas. Maybe what counts most is not so much the genes themselves as the way they are regulated and expressed. Noncoding DNA could provide the complex regulatory functions that direct genes toward service of the organism’s needs, including its developmental needs. That suspicion has now become standard doctrine — though a still much-too-simplistic doctrine if one stops there. For noncoding as well as coding DNA sequences continue unchanged throughout the organism’s entire trajectory of differentiation, from single cell to maturity. Lillie’s point therefore remains: it is hardly possible for an unchanging complex to explain an ordered developmental stream. Constant things cannot by themselves explain dynamic processes. http://www.thenewatlantis.com/publications/getting-over-the-code-delusionbornagain77_{June 16, 2011
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Mung, It is fairly hard to argue for 'completely neutral' mutations, for even mutations which 'do nothing at all' still require energy to replicate, and thus are a 'slight burden' Experimental Evolution of Gene Duplicates in a Bacterial Plasmid Model Excerpt: In a striking contradiction to our model, no such conditions were found. The fitness cost of carrying both plasmids increased dramatically as antibiotic levels were raised, and either the wild-type plasmid was lost or the cells did not grow. This study highlights the importance of the cost of duplicate genes and the quantitative nature of the tradeoff in the evolution of gene duplication through functional divergence. http://www.springerlink.com/content/vp471464014664w8/ The Extinction Dynamics of Bacterial Pseudogenes - Kuo and Ochman - August 2010 Excerpt: "Because all bacterial groups, as well as those Archaea examined, display a mutational pattern that is biased towards deletions and their haploid genomes would be more susceptible to dominant-negative effects that pseudogenes might impart, it is likely that the process of adaptive removal of pseudogenes is pervasive among prokaryotes." http://www.evolutionnews.org/2010/08/on_reductive_evolution_and_the037581.html Arriving At Intelligence Through The Corridors Of Reason (Part II) - April 2010 Excerpt: ,,, since junk DNA would put an unnecessary energetic burden on cells during the process of replication, it stands to reason that it would more likely be eliminated through selective pressures. https://uncommondescent.com/intelligent-design/arriving-at-intelligence-through-the-corridors-of-reason-part-ii/ How The Junk DNA Hypothesis Has Changed Since 1980 - Richard Sternberg - Oct. 2009 - Excellent Summary Excerpt: A surprising finding of ENCODE and other transcriptome projects is that almost every nucleotide of human (and mouse) chromosomes is transcribed in a regulated way. http://www.evolutionnews.org/2009/10/how_the_junk_dna_hypothesis_ha.html Non-coding RNAs and eukaryotic evolution - a personal view - John Mattick - May 2010 Excerpt: "But you certainly need to have a more complex regulatory framework to get to a more complex organism, and the astounding thing is that the only thing that does scale with complexity - because the number of genes does not - is the extent of the non-protein-coding genome." http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2905358/bornagain77_{June 16, 2011
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mung, page 23 of Genetic Entropybornagain77_{June 16, 2011
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Mung: it is NOT “well known that the majority of mutations are harmful”. It is fairly well-known that the vast majority of mutations are near-neutral.
And I thought I had a British sense of humor. :) I guess I've been fooling myself for a long time.Mung_{June 16, 2011
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Excerpt: Most mutations in the genes of the Salmonella bacterium have a surprisingly small negative impact on bacterial fitness.
What percentage of mutations are in the genes?Mung_{June 16, 2011
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Elizabeth you state: 'While there is reason to assume that in a well-adapted population, more of those near-neutral mutations will be deleterious than beneficial, the opposite will tend to be true in a population that is undergoing environmental change.' This is a false statement! It is true that in constant environment there have never been observed any mutations that were 'beneficial', Testing Evolution in the Lab With Biologic Institute's Ann Gauger - podcast with link to peer-reviewed paper Excerpt: Dr. Gauger experimentally tested two-step adaptive paths that should have been within easy reach for bacterial populations. Listen in and learn what Dr. Gauger was surprised to find as she discusses the implications of these experiments for Darwinian evolution. Dr. Gauger's paper, "Reductive Evolution Can Prevent Populations from Taking Simple Adaptive Paths to High Fitness,". http://intelligentdesign.podomatic.com/entry/2010-05-10T15_24_13-07_00 Is Antibiotic Resistance evidence for evolution? - 'The Fitness Test' - video http://www.metacafe.com/watch/3995248 ,,,yet contrary to the claim of Elizabeth that most mutations will not be slightly detrimental when an environment is 'stressed' (changed in her words), the fact is that very few mutations help to generate a beneficial adaptations in a 'stressed environment',,, Michael Behe, The Edge of Evolution, pg. 162 Swine Flu, Viruses, and the Edge of Evolution "Indeed, the work on malaria and AIDS demonstrates that after all possible unintelligent processes in the cell--both ones we've discovered so far and ones we haven't--at best extremely limited benefit, since no such process was able to do much of anything. It's critical to notice that no artificial limitations were placed on the kinds of mutations or processes the microorganisms could undergo in nature. Nothing--neither point mutation, deletion, insertion, gene duplication, transposition, genome duplication, self-organization nor any other process yet undiscovered--was of much use." http://www.evolutionnews.org/2009/05/swine_flu_viruses_and_the_edge.html ,,,Moreover these beneficial adaptations all, for the vast majority of times, come at a loss of functional information/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', without several rounds of 'compensatory mutations' for the 'more evolved strain') http://behe.uncommondescent.com/2010/12/the-first-rule-of-adaptive-evolution/bornagain77_{June 16, 2011
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Mung: it is NOT "well known that the majority of mutations are harmful". It is fairly well-known that the vast majority of mutations are near-neutral. While there is reason to assume that in a well-adapted population, more of those near-neutral mutations will be deleterious than beneficial, the opposite will tend to be true in a population that is undergoing environmental change. This is one of a number of points that Sanford does not consider, and is crucial. In fact he seems to think that the closer you get, from the deleterious end, to neutrality, the more mutations you find ("VSDMs"); then, without any justification, whether by argument or evidence, he assumes a cliff edge with virtually no mutations that are "VSBMs". This is an actual mistake, and his entire argument fails because of it.Elizabeth Liddle_{June 16, 2011
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'I wonder where on earth I got the idea that the vast majority of genetic mutations don’t have any effect at all,' note: 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. http://www.physorg.com/news/2010-11-unexpectedly-small-effects-mutations-bacteria.htmlbornagain77_{June 16, 2011
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... it is well known that the vast majority of genetic mutations are harmful.
Gah. I wonder where on earth I got the idea that the vast majority of genetic mutations don't have any effect at all, and therefore are neither beneficial nor harmful. I guess I need to read more Sanford!Mung_{June 16, 2011
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Elizabeth, You said in #7, "In my view, he bases his case on a serious misreading of the literature he cites (Kondrashov and Kimura especially)...But as far as I can see, he simply gets his numbers wrong, and also ignore many factors that counter his case, as well as important data." But when Bornagain77 comments, "Funny Elizabeth that you never present any actual evidence to counter the principle of Genetic Entropy, but merely your ‘interpretation'”, you reply, "The main evidence, ba77, is that plenty of species are thriving. If Genetic Entropy was true, all populations would be decreasing. They aren’t." And a little later, "The fact that species are thriving means that Sanford is incorrect. That’s all." Then when uoflcard in #12 and I in #33 point out that the existence of thriving species does not invalidate Sanford's thesis, you return in #34 to your original contention, which you sidestepped in response to BA77: "I think Sanford is actually wrong in his analysis that Genetic Entropy is inevitable under evolutionary theory. I think he has misunderstood his sources, and misread the data." Now my reading of Sanford is that he takes known rates of mutation coupled with the ratios of those that are beneficial to those that are harmful along with the proportion of those that are selectable in multicellular organisms (based on the work of population geneticists) and concludes, using those numbers, that the genomes of all multicellular organisms are slowly degrading as mildly harmful mutations accumulate in generation after generation. He also concludes that this accumulation of harmful mutations eventually results in species extinction, a process that takes roughly several million years, the typical length of time that occurs between the introduction of a species into the fossil record and its sudden disappearance. If your contention is that Sanford "has misunderstood his sources, and misread the data," could you please be more specific and tell us exactly what his errors are? And BTW, the OP DOES support Sanford's thesis, since it is well known that the vast majority of genetic mutations are harmful.Bruce David_{June 16, 2011
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However, we know that large numbers of genes have many polymorphisms...
Is this something predicted by Darwinian theory? Shouldn't we see the exact opposite of this, if Darwinian theory is correct?Mung_{June 15, 2011
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Elizabeth you state: 'I’d also point out that we do not know that VSDMs outnumber VSBMs. They may do, but there is no reason to think that VSBMs are particularly rare.' No Elizabeth, DO NOT use WE!!! YOU DO NOT KNOW!!! Mutation Studies, Videos, And Quotes http://docs.google.com/Doc?docid=0AYmaSrBPNEmGZGM4ejY3d3pfMjZjZnM5M21mZgbornagain77_{June 15, 2011
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Elizabeth, yes the OP does when taken in context (which you are loathe to do), and as to prime example of your extreme bias in 'interpretation of evidence' you state: 'However, if you want evidence for beneficial mutatations, check out the Lenski studies referenced in another recent OP here.' HMMM Elizabeth, it seems those 5 'beneficial mutations', when taken singly, are only beneficial in a very select reading of 'beneficial'; Michael Behe's Quarterly Review of Biology Paper Critiques Richard Lenski's E. Coli Evolution Experiments - December 2010 Excerpt: After reviewing the results of Lenski's research, Behe concludes that the observed adaptive mutations all entail either loss or modification--but not gain--of Functional Coding ElemenTs (FCTs) http://www.evolutionnews.org/2010/12/michael_behes_quarterly_review041221.html 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. http://www.answersingenesis.org/articles/aid/v4/n1/beneficial-mutations-in-bacteria Thus Elizabeth you have no evidence for 'truly beneficial mutations' in the Lenski study you cited; but to make matters much worse for you, the whole point of the Lenski paper was to point out that the 'beneficial mutations', you were hoping to contort to be evidence for your neo-Darwinian worldview, are no longer beneficial, even in the narrow sense, when the mutations are present all together!!! Thus Elizabeth even though the evidence is very clear, once again you have severely twisted to meet your 'Cleopatra' (Queen of Denial) criteria for being evidence for your position. Truly a rabbit hole of illusion Elizabeth!!!bornagain77_{June 15, 2011
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Well, no, ba77, the OP doesn't provide such evidence. It actually suggests that a rather low rate of mutation, although this is probably because it excludes mutations that arise during recombination. It says nothing about the distribution of those mutation on the scale of deleterious-beneficial, and, as Mung points out, the number that hit a useful allele may be very small. However, we know that large numbers of genes have many polymorphisms, and those must have come from somewhere. The OP suggests one route, together with the interesting possibility that mutation rate itself may be heritable. However, if you want evidence for beneficial mutatations, check out the Lenski studies referenced in another recent OP here. I'd also point out that we do not know that VSDMs outnumber VSBMs. They may do, but there is no reason to think that VSBMs are particularly rare.Elizabeth Liddle_{June 15, 2011
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Elizabeth, since evidence, and even this very OP, has presented actual evidence to you that you are wrong and Genetic Entropy is true, perhaps you would care to present actual evidence (for truly beneficial mutations, genome plasticity and extreme genome management for the overwhelming majority of slightly deleterious mutations that do occur) instead of just your opinion/thinking, that you are not wrong???bornagain77_{June 15, 2011
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Mung, we seem to be having serious communication difficulties here. I accept a substantial portion of the liability but not the full portion; clearly there is a level of distrust on your part of me that will have to be overcome before we can do much better. So I will make three points, make of them what you will; I will try to be unambiguous, but may not succeed: 1. I think Sanford is actually wrong in his analysis that Genetic Entropy is inevitable under evolutionary theory. I think he has misunderstood his sources, and misread the data. 2. I think (though conceivably I could have misunderstood him) that his own position is that the most likely scenario is that mankind was created perfect in the Garden of Eden a few thousand years ago, and our genomes have been deteriorating inevitably since then. 3. He offers the alternative that our genomes are not inevitably deteriorating, but that if so, there must be some natural or supernatural force stopping them, because otherwise that's what the science (including Darwinism) predicts. My position is that science predicts this only in very particular circumstances, and that even there, there are natural forces that tend to stop it happening, so no supernatural prevention system need be invoked or inferred. As for the thesis of his book: my reading of it is that our genomes are inevitably deteriorating, hence the title. He does not offer a natural alternative in his book (though he does tell us to put our hope in Jesus Christ). If something is inevitably deteriorating, the corollary is that it started in a much nearer-perfect, if not perfect, state, and the time line he suggests is a few thousand years. This conforms with his YEC position, and I see no reason to think it is not the corollary he himself draws, especially as he, as I read it, confirmed it in his email to me. If I've misunderstood him, so be it. You are correct that I overlooked the word "natural" in his email, and I'm encouraged, in a way, that he allows for such a possibility. However, I don't think it is even required (at least to the extent he implies), as I think his concept of Genetic Entropy is actually an error. I think this because I have read the papers he cites and I don't think they lead to the conclusions he draws. In peace LizzieElizabeth Liddle_{June 15, 2011
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Lizzy, Re. #26: Well, nice talking with you, too. You may call me Bruce if you like. I must say, though, that you have basically sidestepped my point, which is that major modifications to any complex system of whatever nature (be they biological or otherwise) cannot be accomplished through a series small incremental steps if there is a requirement that the system continue to function after each such step. This is because a complex system is composed of many parts that fit together and interact both spatially and temporally in ways that depend on each other. I refer you again to the example I invoked in #15 of the impossibility of evolving an avian lung from a bellows lung. If you try to do this in small steps, the intermediate stages don't work and would be fatal to the organism. Therefore, if it happened in a Darwinian way, it must have happened all at once (ie., saltationally). However, absent engineering input from an intelligent agent, such an emergence of a radically new organism in one fell swoop is effectively impossible, given the probabilities. Regarding the ongoing discussion around Sanford's book, when you say that Sanford's thesis is invalidated by the fact that there are "thriving species" alive today, you have again missed the point, which is that EITHER Darwinism is correct OR Sanford is, but not both. If Sanford is correct then this implies that currently "thriving" species were introduced by some means complete with perfect (ie., non-degraded) genomes within the last several million years (the typical length of time that a species exists in the fossil record). We observe them thriving today simply because their genomes have not yet had time to degrade to the point of non-viability. This includes us, by the way. In short, the current existence of thriving species does not, in and of itself, invalidate Sanford.Bruce David_{June 14, 2011
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Elizabeth Liddle:
I am certainly prone to errors, but I do not lie.
Elizabeth. What sort of error was it? Did you simply not read what he wrote? Are you just so locked into a certain perception of Sanford that you are blinded to what he actually says? You misrepresented Sanford, not just once, but twice. Not only did he write, natural OR supernatural, but he also clearly stated that he accepts neither of those.
The most obvious conclusion would be a Biblical view of history, however the alternative would be to hypothesize that there are other forces (natural or supernatural), which help out mutation/selection. I personally hold the first view, but for those who find this too hard to believe, they are forced to choose the second view.
Seriously. He presents two alternative views and says he holds the first, which he calls "a Biblical view of history."
I am happy to substitute the word corollary.
What then do you now say is the thesis of his book?Mung_{June 14, 2011
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bornagain77@30:
Bull Elizabeth...
Where are the tone police?Pedant_{June 14, 2011
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Bull Elizabeth, your evidence that Genetic Entropy is not a real concern, is the same evidence I can use to show that God initially created each lifeform on Earth!!! WEhereas real evidence is simply Denied or rationalized away. You are not fair with the evidence in the least!!!bornagain77_{June 14, 2011
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Well, the thing is, ba77, that I tend to find the evidence you offer as unpersuasive as you find the evidence I offer you! So just telling me that I'm in denial, isn't going to help much, I'm afraid. As I see it, there is persuasive evidence for my position, and I would be "in denial" if I didn't acknowledge it. But I also acknowledge that that evidence does not persuade you, and I appreciate your efforts.Elizabeth Liddle_{June 14, 2011
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Elizabeth, you state: 'Yes, I know that embryological development is not Darwinian evolution; however the two are extremely closely linked, and must be, as the genes that control development are inherited.' ,,,But, contrary to your 'decree', the evidence states: The mouse is not enough - February 2011 Excerpt: Richard Behringer, who studies mammalian embryogenesis at the MD Anderson Cancer Center in Texas said, “There is no ‘correct’ system. Each species is unique and uses its own tailored mechanisms to achieve development. By only studying one species (eg, the mouse), naive scientists believe that it represents all mammals.” http://www.the-scientist.com/news/display/57986/ Marsupial Embryos Challenge Common Ancestry – Casey Luskin - audio podcast http://intelligentdesign.podomatic.com/entry/2011-02-09T16_33_21-08_00 A Primer on the Tree of Life (Part 4) Excerpt: "In sharks, for example, the gut develops from cells in the roof of the embryonic cavity. In lampreys, the gut develops from cells on the floor of the cavity. And in frogs, the gut develops from cells from both the roof and the floor of the embryonic cavity. This discovery—that homologous structures can be produced by different developmental pathways—contradicts what we would expect to find if all vertebrates share a common ancestor. - Explore Evolution http://www.evolutionnews.org/2009/05/a_primer_on_the_tree_of_life_p_3.html#more Neo-Darwinism's Gene Homology Problem - video http://www.youtube.com/watch?v=_6P6bXA50c0 Icons of Evolution 10th Anniversary: Haeckel's Embryos - January 2011 - video http://www.youtube.com/watch?v=W0kHPw3LaG8 Haeckel's Bogus Embryo Drawings - The faked drawings compared to actual pictures http://www.newworldencyclopedia.org/entry/Image:Ontogeny2.jpg Actual Embryo photos; http://www.intelldesign.com/wp-content/uploads/2008/12/richardson-embryos1-1024x385.jpg There is no highly conserved embryonic stage in the vertebrates: - Richardson MK - 1997 Excerpt: Contrary to recent claims that all vertebrate embryos pass through a stage when they are the same size, we find a greater than 10-fold variation in greatest length at the tailbud stage. Our survey seriously undermines the credibility of Haeckel's drawings, http://www.ncbi.nlm.nih.gov/pubmed/9278154 Current Textbooks Misuse Embryology to Argue for Evolution - June 2010 http://www.evolutionnews.org/2010/06/current_textbooks_misuse_embry035751.htmlbornagain77_{June 14, 2011
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Elizabeth, you never present any real evidence for your position, as uoflcard so clearly called you on. But when real evidence is presented against you you just deny that it matters. THAT Elizabeth IS DENIALISM!!! notes: 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 this following fact: “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 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. http://www.jpeds.com/article/S0022-3476%2882%2980347-8/abstract ,,,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: HGMD®: Now celebrating our 100,000 mutation milestone! http://www.biobase-international.com/pages/index.php?id=hgmddatabase Even if a truly beneficial random mutation/variation event to the DNA ever did occur, ignoring the fact that that the DNA doesn't solely control encoding for body plans, the 'beneficial mutation' would still be of absolutely no use for a Darwinian scenario because the mutation would be swallowed in the vast ocean of slightly detrimental mutations which are far below the culling power of natural selection to remove from a genome. these following studies make this point clear: Contamination of the genome by very slightly deleterious mutations: why have we not died 100 times over? Kondrashov A.S. http://www.ingentaconnect.com/content/ap/jt/1995/00000175/00000004/art00167 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,” http://www.evolutionnews.org/2009/07/the_frailty_of_the_darwinian_h.html#more High genomic deleterious mutation rates in hominids Excerpt: Furthermore, the level of selective constraint in hominid protein-coding sequences is atypically (unusually) low. A large number of slightly deleterious mutations may therefore have become fixed in hominid lineages. http://www.nature.com/nature/journal/v397/n6717/abs/397344a0.html High Frequency of Cryptic Deleterious Mutations in Caenorhabditis elegans ( Esther K. Davies, Andrew D. Peters, Peter D. Keightley) "In fitness assays, only about 4 percent of the deleterious mutations fixed in each line were detectable. The remaining 96 percent, though cryptic, are significant for mutation load...the presence of a large class of mildly deleterious mutations can never be ruled out." http://www.sciencemag.org/cgi/content/abstract/285/5434/1748 All life eventually succumbs to the effects of Genetic Entropy, but humans are especially vulnerable. As This following study reveals: 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). https://uncommondescent.com/darwinism/sanfords-pro-id-thesis-supported-by-pnas-paper-read-it-and-weep-literally/bornagain77_{June 14, 2011
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Bruce David @ 15
The process of embryological development is not Darwinian evolution, it is the process by which an organism is built in the natural world.
Yes, I know that embryological development is not Darwinian evolution; however the two are extremely closely linked, and must be, as the genes that control development are inherited.
Darwinian evolution requires that each incremental step result in a functioning organism. The intermediate steps in embryological development do not result in functioning (that is, viable) organisms. They will not survive on their own until they are ready to hatch or be born.
This is not always true, and it is also a somewhat narrow view of development. More to the point, it's not terribly relevant to the point I was making! Which is that at all stages of an organism's life it has to function as an organism (whether "on its own" or not), whereas a jet fighter does not have to function at all until it is ready for use. This means that the "design" (with or without scare quotes) of a living organism has to ensure that it is viable during the assembly process itself. And so, rather than bits being bolted on as required, development involves the differential expression of genes that result in the differentiation of cells and the deformation of the developing organism into intermediate morphologies. So any account of the way that genes account for development has to account for this step-wise expression in response to cell signalling, in other words for the way that genes are switched on and off throughout development (and indeed throughout life). So the entire functioning of an organism is much more, well, organic than a human-built artefact, so that a slight tweak to a regulatory gene here, and a slight tweak to a protein there can have smooth, but sometimes substantial, effects on the developing and functioning organism. Biological things, unlike human engineered things, grow, develop and breed, remaining viable at all times despite all these processes being step-wise. Biological processes lend themselves to this, while human engineering doesn't, which is why I find the argument that what is true in the one must be true in the other unpersuasive :) Anyway, nice to talk to you. Cheers LizzieElizabeth Liddle_{June 14, 2011
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bornagain77: I have simply read the papers quoted in the OP. I'm not "in denial" - I'm simply reporting what they found. It's a shame they are behind a paywall, but fortunately the abstracts are online, and the content is fairly clear from the abstracts.Elizabeth Liddle_{June 14, 2011
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Mung wrote:
But, unfortunately, you failed to resolve the matter in dispute, which was whether it was the thesis of his book that humans were created perfect approx 10,000 years ago, etc. From his response, I would say that at best that is a corollary, rather than the thesis of the book.
I am happy to substitute the word corollary.Elizabeth Liddle_{June 14, 2011
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