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Recent papers confirm that genetic entropy decreases fitness

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entropy illustrated

Over at Creation-Evolution Headlines, Dave Coppedge reports that two recent journal article’s have confirmed Cornell’s John Sanford’s “genetic entropy”: An accumulation of mutations always decreases fitness (contrary to neo-Darwinists’ hopes):

For mutations under epistasis to produce innovation, there must be a way for them to work together (synergistic epistasis). This is often assumed but has not been observed. Most experiments have shown beneficial mutations working against each other (antagonistic epistasis; see 12/14/2006), or causing even less fitness than if they acted alone (decompensatory epistasis; see 10/19/2004). In a new paper in Science,3 Khan et al, working with Richard Lenski [Michigan State], leader of the longest-running experiment on evolution of E. coli, found a law of diminishing returns with beneficial mutations due to negative epistasis.

Diminishing returns?

Like this, for example?: An increased number of spelling errors in a letter retyped in series by a number of different people does not add up to a new, better letter over time?

Coppedge also notes the way the science media handled the news, for example:

“The more mutations the researchers added, the more they interfered with each other,” was one of the “surprising” results.

Surprising to whom? Not to Dembski and other members of the No Free Lunch club.

Follow UD News for breaking news on the design controversy.

Comments
Joseph: beneficial mutations are more likely to accumulate than deleterious once. If dwarfism doesn't impair your probability of successful reproduction, than it isn't deleterious, but if it is, you are less likely to have descendents than your non-dwarf friend. So when an albino mutation comes along, it is more likely to happen in one of your friends descendents than in one of your own. However, if you have an allele that does enhance your probability of successful reproduction (makes you tall dark and handsome, perhaps) you are more likely to have descendents that your nerdy-looking friend. So when a smartness enhancing mutation comes along, it is more likely to happen in one of your descendents than in one of your nerdy-looking friend's descendents. That is why beneficial mutations tend to build, and deleterious mutations tend not to. However, if mutations are very frequent, and are mostly slightly, but not disastrously, deleterious, in a small population they may well build up, just by force of numbers.Elizabeth Liddle
June 13, 2011
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So, wrong on that point. Beneficial mutations accumulated.
from the article in science daily:
The more mutations the researchers added, the more they interfered with each other. It was as if the mutations got in each other's way as they all tried to accomplish the same thing. It was found that the beneficial mutations allowing the bacteria to increase in fitness didn't have a constant effect. The effect of their interactions depended on the presence of other mutations, which turned out to be overwhelmingly negative. "These results point us toward expecting to see the rate of a population's fitness declining over time even with the continual addition of new beneficial mutations," </strong
since the more complex the new function/feature the more mutations it takes, how can these complex functions/features evolve at all?tsmith
June 13, 2011
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DrREC, of course what you fail to mention, is that the 'beneficial' adaptations, taken from the Lenski study, were only 'more fit' in the sense of a 'stressed environment' that was different from the original 'normal' wild type environment, yet when the 'evolved' strain was compared to the parent wild type in the original 'normal' environment we find; 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 DrREC, why would you leave out this most important piece of the equation??? ================== 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.htmlbornagain77
June 13, 2011
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Elizabeth, My point is there isn't any evidence that mutations can accumulate in such a way- that is take all the polymorphisms you like and you still won't have anything resembling universal common ancestry. But you can get an albino dwarf with SCA. Also Dr Lee Spetner wrote "Not By Chance"- published in 1997- which explains the telic approach to mutations.Joseph
June 13, 2011
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Whoever posted this might have benefitted from reading the original papers. The conclusions are quite the opposite of this post. Post: "An accumulation of mutations always decreases fitness" Paper: "Adaptation......resulted in an average fitness increase after 600 generations of 66.8% " "These mutations together produced a fitness increase of ~30% relative to the ancestor....." So, wrong on that point. Beneficial mutations accumulated. What was observed is an increase in fitness that is less that that of the individual beneficial mutations summed (they don't totally work synergistically and independently). So, the 'net' fitness isn't equal to the 'gross'. The authors say: "In other words, epistasis acts as a drag that reduces the contribution of later beneficial mutations." Think of it this way-if you get a raise doubling your pay, your net income increases, but probably doesn't actually double due to increased taxes, etc. This is not to say your income didn't increase! Would you turn down the raise because gross doesn't equal net? Also, the negative epistasis wasn't universal! Summarizing the studies: "Thus, across these two distinct model systems 7 of 10 alleles consistently showed antagonism, whereas only 2 exhibited synergy." So all we can say is that adaptation more frequently shows negative epistasis than synergy. Which was predicted: "This tendency toward diminishing returns between beneficial mutations was predicted from trajectories of fitness increase and substitution rate (12) but had never been tested directly."DrREC
June 13, 2011
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Elizabeth, and you might like to reread the part where the mutation, you cited as 'beneficial', was actually found to be deleterious as far as the overall functional complexity of the protein was concerned.,,, But then being fair to the evidence was not your primary concern in the first place was it??? "The neo-Darwinians would like us to believe that large evolutionary changes can result from a series of small events if there are enough of them. But if these events all lose information they can’t be the steps in the kind of evolution the neo-Darwin theory is supposed to explain, no matter how many mutations there are. Whoever thinks macroevolution can be made by mutations that lose information is like the merchant who lost a little money on every sale but thought he could make it up on volume." Lee Spetner (Ph.D. Physics - MIT - Not By Chance) "The opportune appearance of mutations permitting animals and plants to meet their needs seems hard to believe. Yet the Darwinian theory is even more demanding: a single plant, a single animal would require thousands and thousands of lucky, appropriate events. Thus, miracles would become the rule: events with an infinitesimal probability could not fail to occur,,, There is no law against day dreaming, but science must not indulge in it." Pierre P. Grasse - past President of the French Academie des Sciences ============= Estimation of spontaneous genome-wide mutation rate parameters: whither beneficial mutations? (Thomas Bataillon) Abstract......It is argued that, although most if not all mutations detected in mutation accumulation experiments are deleterious, the question of the rate of favourable mutations (and their effects) is still a matter for debate. http://www.nature.com/hdy/journal/v84/n5/full/6887270a.html Distribution of fitness effects caused by random insertion mutations in Escherichia coli Excerpt: At least 80% of the mutations had a significant negative effect on fitness, whereas none of the mutations had a significant positive effect. http://www.springerlink.com/content/r37w1hrq5l0q3832/ “But in all the reading I’ve done in the life-sciences literature, I’ve never found a mutation that added information… All point mutations that have been studied on the molecular level turn out to reduce the genetic information and not increase it.” Lee Spetner - Ph.D. Physics - MIT - Not By Chance "Bergman (2004) has studied the topic of beneficial mutations. Among other things, he did a simple literature search via Biological Abstracts and Medline. He found 453,732 “mutation” hits, but among these only 186 mentioned the word “beneficial” (about 4 in 10,000). When those 186 references were reviewed, almost all the presumed “beneficial mutations” were only beneficial in a very narrow sense- but each mutation consistently involved loss of function changes-hence loss of information.” Sanford: Genetic Entropybornagain77
June 13, 2011
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@ uoflcard Thank you for your kind words :) You wrote:
That sounds great and makes perfect sense, except that there is a staggering lack of observed “beneficial” (i.e. complex-system-building) mutations.
Well, we need to get terminology a bit straighted here. In population genetic terms, a "beneficial" mutation is simply one that confers on the phenotype (i.e. the critter that bears it) a enhanced probability of reproductive success, usually considered relative to the allele it mutated from, although that gets complicated once an allele has been around for a while. So "beneficial" is not, in fact, defined as "complex-system-building". In fact, Darwin did not propose (and most biologists do not posit) that any single mutation was/is "complex-system-building", but rather, that complex systems must have been built up, incrementally, from new alleles that each conferred only a slight advantage (or perhaps neutral, or even slightly deleterious alleles that had only propagated through drift the population by drift). This is viewed, in some quarters, of course, as the Achilles heel of Darwinism. I don't think it is, but I think it's important to be clear what evolutionary theory is saying and what it is not. No evolutionary biologist would expect that any complex system appeared in a single mutation. Thus complex-systems, under evolutionary theory, have to be explained by incremental changes, not "hopeful monsters".
Also, I thought Darwinian evolution predicts that the most “fit” genomes will persist, regardless of whether they are better or worse than their predecessors, just as long as they’re better than their current competitors?
Yes, and this is a very important point (although, to nitpick, it's not that Darwinian evolution "predicts" this, so much as this is what the theory actually is - namely that adaptataion occurs because the alleles that persist will be those best at persisting!). However, you are absolutely right that under certain circumstances (for instance in small populations with very high mutation rates) the rate of deleterious allele production may be so high that although the most fit of each generation are those that pass on their alleles to the next generation, each generation also supplies its own new, bad alleles, and so the net fitness of the population still goes down. This is relatively easy to model, in fact, and there are even equations around that give the thresholds at which "mutational meltdown" becomes a problem. Only, sometimes it doesn't seem to when it should, which is an interesting puzzle :) I think my comments above also address your subsequent point, but I will make an additional point, which is that yes, again you are right, and because you are right, we can infer, that IF Darwinian evolution is broadly correct, then at least three things must be true: mutation rates cannot be so high as to swamp each new generation (effectively drowning out selection); at least some mutations must confer actual increased probability of reproduction; the system cannot be "brittle" - there must be a reasonable number of variants around any given allele that are more or less functional. In addition, there is an issue horizontal gene transfer, which is important (and achieved in sexually reproducing species by sexual reproduction) and helps to guard against genetic meltdown. oops gotta run, be back in a bit :) Cheers LizzieElizabeth Liddle
June 13, 2011
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ba77: there was no "excuse mongering" in my post! And you might like to re-read the part where I mentioned the Milano mutation.Elizabeth Liddle
June 13, 2011
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Joseph: I think there might be some confusion over the word "mutation". Many human genes have many polymorphisms, all of which function pretty well, but have slightly different phenotypic effects. The question is: where did those polymorphisms come from? Well, we have good ideas as to where some of them came from, because we know the kind of copying mechanisms that produce those variants, from repeated sections of code, to single nucleotide replacements, to recombination processes by which two parent alleles recombine to produce a new "child" allele. Are you suggesting that all but two of each set of human alleles are deleterious mutations? Because there is no reason to think so - they are just the variance that make us different from each other. Or are you suggesting that mutation is a specific, damaging process that can only result in deleterious alleles, and some other, perhaps Intelligent, process is responsible for the non-deleterious alleles? Because that isn't what the evidence suggests. The evidence suggests that most of what seem to be perfectly functional alleles have resulted from specific copying mechanisms that do not always result in the child allele being identical to either parent allele. It's possible of course that the kind of flexibility in the copying mechanisms was a deliberate design feature! But that wouldn't alter the fact that they are "mutations". Indeed, a better ID hypothesis, it seems to me, would be to posit that mutations are a deliberate design feature that enable populations to adapt (I think Behe's position may be near this one). But polymorphisms have to be explained somehow, and they seem, on the whole, to be pretty cool things.Elizabeth Liddle
June 13, 2011
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Elizabeth, First, let me say that I appreciate your attitude and tone, a refreshing change from most of what you hear in this debate. Second, let me say that I'm an engineer, not a biologist; I just happened to become interested when I was most of the way through engineering school. So correct me if I'm wrong about something that is a scientific fact From comment #1
Darwinian evolution does not predict that most mutations will be beneficial; it predicts that only neutral and beneficial mutations will persist. But the system can’t look ahead, so periods of relaxed selection can be followed by periods of drastic selection.
That sounds great and makes perfect sense, except that there is a staggering lack of observed "beneficial" (i.e. complex-system-building) mutations. Also, I thought Darwinian evolution predicts that the most "fit" genomes will persist, regardless of whether they are better or worse than their predecessors, just as long as they're better than their current competitors? From comment #3
Buildup of mutations without selection isn’t the same as buildup of those mutations that survive selection.
So if random mutation and natural selection is all that occurs in nature, and the vast majority of mutations are at least slightly harmful, aren't most selected mutations going to be at least slightly harmful, even during periods of "drastic selection"? And so even if there are system-building mutations (not yet verified?) that are then selected, these are tremendously out-numbered by the most-fit "slightly harmful" mutations. How does this eventually result in perfectly tuned, extremely complex systems? If I had to "evolve" a book using random mutation and selection with these mechanisms, starting with a coherent book, it seems like maybe I could change a few words, if I focused on them, but most of the book would go to pot. The other image that comes to mind is trying to solve a 10,000 x 10,000 x 10,000 Rubik's cube. You might be able to mutate/select and accumulate a few small patches of like-color squares, but to get the whole thing, or most of it, solved would take a heck of a lot of intelligence. Also from comment #3
I agree that the evidence shows that most mutations are harmful, and that in a period of “relaxed selection” mutations that would be harmful in a period of more stringent selection will tend to build up, and that this can be a problem (e.g. Giant Pandas). It’s especially a problem with very small populations, or once a population gets very small. Indeed it’s part of the process of extinction, which we know occurs with great frequency.
That seems to beg the question of what happened at the beginning of life or maybe also the beginning of "branches" when populations were very small. How did these flourish when small populations that we observe struggle tremendously?uoflcard
June 13, 2011
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Elizabeth, ignoring your blatant 'excuse mongering' in the main of your post, let's just look at your cited claim for a beneficial mutation: Site #1)The Milano Mutation: A Rare Protein Mutation Offers New Hope for Heart Disease Patients1 Site #2)‘Defective’ but beneficial gene may bring about novel ways to clear arterial plaque buildup2 I have checked these, and they work as of Feb 04, 2003. Thanks for the good communication. In Christ, J.R. It would appear that the questioner is under the mistaken impression that beneficial mutations are a problem for creationists. Some creationists make this unfortunate error. The mutations Q&A section of our Web site clearly teaches that the issue is not whether the mutation is beneficial but if it adds new genetic information (specified complexity). So it would have been clear that the A-I Milano mutation is not evidence for microbe-to-man evolution. What has happened? One amino acid has been replaced with a cysteine residue in a protein that normally assembles high density lipoproteins (HDLs), which are involved in removing ‘bad’ cholesterol from arteries. The mutant form of the protein is less effective at what it is supposed to do, but it does act as an antioxidant, which seems to prevent atherosclerosis (hardening of arteries). In fact, because of the added -SH on the cysteine, 70% of the proteins manufactured bind together in pairs (called dimers), restricting their usefulness. The 30% remaining do the job as an antioxidant. Because the protein is cleverly designed to target ‘hot spots’ in arteries and this targeting is preserved in the mutant form, the antioxidant activity is delivered to the same sites as the cholesterol-transporting HDLs. In other words, specificity of the antioxidant activity (for lipids) does not lie with the mutation itself, but with the protein structure, which already existed, in which the mutation occurred. The specificity already existed in the wild-type A-I protein before the mutation occurred. Now in gaining an anti-oxidant activity, the protein has lost a lot of activity for making HDLs. So the mutant protein has sacrificed specificity. Since antioxidant activity is not a very specific activity (a great variety of simple chemicals will act as antioxidants), it would seem that the result of this mutation has been a net loss of specificity, or, in other words, information. This is exactly as we would expect with a random change. http://creation.com/a-i-milano-mutationevidence-for-evolution Elizabeth, perhaps you would like to look for another 'beneficial' mutation???bornagain77
June 13, 2011
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ba77: it's very difficult to know whether a new allele is beneficial or deleterious, especially if the effect is slight. They can usually only be detected statistically. And remember that "beneficial" and "deleterious", in the population genetics sense, are only meaningful in relation to the current environment. What is beneficial in one environment may be neutral or deleterious in the next, and vice versa. But, since you ask: http://www.lbl.gov/Science-Articles/Archive/LSD-Milano-Bielicki.html The vast majority of mutations are near-neutral in any given environment. This is an unusual one in conferring a clear benefit to the individual. Whether it will actually "be selected" or not, remains unclear, though. That will depend on whether it confers a reproductive advantage. It may not. On the other hand there is some evidence that women's access to fertility control may be resulting in extended fertility, which would make sense; as women postpone child-bearing, women bearing alleles (whether new or existing) that tend to result in later menopause are more likely to have children than those bearing alleles that promote earlier menopause earlier. The former will therefore tend to increase in prevalence, and there is some evidence that they are doing so. It may be a good example of alleles that were slightly deleterious becoming advantageous, and vice versa. I'll try to look out the source (can't find it right now).Elizabeth Liddle
June 13, 2011
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There still isn't any evidence that any amount of accumulated mutations can do what the theory of evolution requires for universal common descent. Accumulated mutations gets you an albino dwarf with sickle-cell anemia. Just sayin'...Joseph
June 13, 2011
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I don't think it's correct to say that it decreases fitness. It's the rate of fitness increase that is slowed. Which contrasts with work doing this sort of study of interactions for mutations all in the same protein - there they interact violently, sometimes being good or bad, and there have been no apparent trends between benefit of a mutation and how good you were before it arrived.anaruiz
June 13, 2011
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further note: 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 I really question their use of the word 'celebrating'. This following study confirmed the detrimental mutation rate for humans, of 100 to 300 per generation, estimated by John Sanford in his book 'Genetic Entropy' in 2005: Human mutation rate revealed: August 2009 Every time human DNA is passed from one generation to the next it accumulates 100–200 new mutations, according to a DNA-sequencing analysis of the Y chromosome. (Of note: this number is derived after "compensatory mutations") http://www.nature.com/news/2009/090827/full/news.2009.864.html This 'slightly detrimental' mutation rate of 100 to 200 per generation is far greater than even what evolutionists agree is an acceptable mutation rate for an organism: Beyond A 'Speed Limit' On Mutations, Species Risk Extinction Excerpt: Shakhnovich's group found that for most organisms, including viruses and bacteria, an organism's rate of genome mutation must stay below 6 mutations per genome per generation to prevent the accumulation of too many potentially lethal changes in genetic material. http://www.sciencedaily.com/releases/2007/10/071001172753.htm 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/ As well, the slow accumulation of 'slightly detrimental mutations' in humans, that is 'slightly detrimental mutations' which are far below the power of natural selection to remove from our genomes, is revealed by 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 147bornagain77
June 13, 2011
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Elizabeth as to this statement of yours: 'it predicts that only neutral and beneficial mutations will persist.' AHH, the elusive, shy and docile, beneficial mutation. Have you, by chance :) , located an unambiguous 'beneficial mutation', so that we might know if they really and truly exist? “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') http://behe.uncommondescent.com/2010/12/the-first-rule-of-adaptive-evolution/ Michael Behe's Amazon Blog - October 2007 Excerpt: As I showed for mutations that help in the human fight against malaria, many beneficial mutations actually are the result of breaking or degrading a gene. Since there are so many ways to break or degrade a gene, those sorts of beneficial mutations can happen relatively quickly. For example, there are hundreds of different mutations that degrade an enzyme abbreviated G6PD, which actually confers some resistance to malaria. Those certainly are beneficial in the circumstances. The big problem for evolution, however, is not to degrade genes (Darwinian random mutations can do that very well!) but to make the coherent, constructive changes needed to build new systems. http://behe.uncommondescent.com/page/6/ Richard Dawkins’ The Greatest Show on Earth Shies Away from Intelligent Design but Unwittingly Vindicates Michael Behe - Oct. 2009 Excerpt: The rarity of chloroquine resistance is not in question. In fact, Behe’s statistic that it occurs only once in every 10^20 cases was derived from public health statistical data, published by an authority in the Journal of Clinical Investigation. The extreme rareness of chloroquine resistance is not a negotiable data point; it is an observed fact. http://www.evolutionnews.org/2009/10/richard_dawkins_the_greatest_s.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 Moreover Elizabeth, Genetic Entropy, besides being based on the fact that all known mutations are detrimental, is also primarily based on the fact that the vast majority of mutations are 'slightly detrimental' and are thus far below the power of natural selection to remove from a genome before they spread throughout the entire population: 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.html Evolution Vs Genetic Entropy - Andy McIntosh - video http://www.metacafe.com/watch/4028086bornagain77
June 13, 2011
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No, I'm not saying that at all :) I agree that the evidence shows that most mutations are harmful, and that in a period of "relaxed selection" mutations that would be harmful in a period of more stringent selection will tend to build up, and that this can be a problem (e.g. Giant Pandas). It's especially a problem with very small populations, or once a population gets very small. Indeed it's part of the process of extinction, which we know occurs with great frequency. So I'm not clear what evidence you think I'm ignoring :) All I'm saying is that it's not "contrary to neo-Darwinists’ hopes". Buildup of mutations without selection isn't the same as buildup of those mutations that survive selection. Anyway, gotta love you and leave you for a bit :) Cheers LizzieElizabeth Liddle
June 13, 2011
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Elizabeth, basically you are saying, No matter what the evidence says, I will make up any 'just so' I can story so that I can maintain my blind faith in neo-Darwinism.bornagain77
June 13, 2011
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Yes, accumulation of mutations during a period where few mutations result in reduced probability of reproduction will tend to decrease fitness in the long term when that period comes to an end, but as they can only accumulate when those selection pressures are relaxed, they are likely to be purged when the very conditions in which they actually reduce fitness come to pass. Which may not happen. Darwinian evolution does not predict that most mutations will be beneficial; it predicts that only neutral and beneficial mutations will persist. But the system can't look ahead, so periods of relaxed selection can be followed by periods of drastic selection. Which is the problem faced by Giant Pandas right now.Elizabeth Liddle
June 13, 2011
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