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Nobel Prize winner HJ Muller, unwitting pioneer of genetic entropy theories

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hj muller

Muller received the Nobel Prize for “for the discovery that mutations can be induced by x-rays”. He studied the effects of mutation on populations, and indirectly spawned ideas which were elaborated in the book Genetic Entropy by Cornell geneticist John Sanford.

The theory of genetic entropy has the potential to overturn Darwinism on empirical grounds alone. Darwinism argues for inevitable progress, genetic entropy argues the opposite.

The thesis of genetic entropy can be explored by considering the amount of mutation in the human genome at present. Muller offers his thoughts:

it would in the end be far easier and more sensible to manufacture a complete man de novo, out of appropriately chosen raw materials, than to try to fashion into human form those pitiful relics which remained…

it is evident that the natural rate of mutation of man is so high, and his natural rate of reproduction so low, that not a great deal of margin is left for selection…

it becomes perfectly evident that the present number of children per couple cannot be great enough to allow selection to keep pace with a mutation rate of 0.1..if, to make matters worse, u should be anything like as high as 0.5…, our present reproductive practices would be utterly out of line with human requirements.

Hermann Muller quoted by John Sanford
Appendix 1, Genetic Entropy

“u” is the mutation rate. As John Sanford observes, Darwinian selection cannot keep pace with reality. Deterioration of the genome seems to be in evidence, and the efficacy of Darwinian mechanisms has been essentially falsified with respect to the human genome. Here is an excerpt of Sanford commenting on Muller’s work:

Muller calculated that the human fertility rate of that time (1950) could not deal with a mutation rate of 0.1. Since that time, we have learned that the mutation rate is a least 1,000-fold higher than he thought. Furthermore, fertility rates have declined sharply since then.

John Sanford

Walter ReMine was kind enough to point me to a more modern day version of Muller’s concerns: Why have we not died 100 times over? by Kondrashov (also from Cornell).

It is well known that when s, the selection coefficient against a deleterious mutation, is below 1/4 ~ Ne , where Ne is the effective population size, the expected frequency of this mutation is ~ 0.5, if forward and backward mutation rates are similar. Thus, if the genome size, G, in nucleotides substantially exceeds the Ne of the whole species, there is a dangerous range of selection coefficients, 1/ G less than s less than 1/4 N e . Mutations with s within this range are neutral enough to accumulate almost freely, but are still deleterious enough to make an impact at the level of the whole genome. In many vertebrates Ne ~ 10 , while G ~ 10 , so that the dangerous range includes more than four orders of magnitude. If substitutions at 10% of all nucleotide sites have selection coefficients within this range with the mean 10 , an average individual carries ~ 100 lethal equivalents. Some data suggest that a substantial fraction of nucleotides typical to a species may, indeed, be suboptimal.

Darwinian evolution doesn’t clean out all the bad in a population. Kondrashov’s observations discredit Darwin’s implicit claim of inevitable progess and the supposed survival of the fittest. The problem is that if genetic entropy is true, the ancestors are the fittest not the decendants. In that sense, the fittest don’t survive. To use Muller’s words, what remains in the end are not the fittest, but “pitiful relics”.

Kondrashov offers a supposed “fix” to the paradoxes so as to bolster Darwin’s failing theory. His fix is an appeal to “synergistic epsitasis”, but Sanford responds to this supposed “fix”:

one will encounter the term “synergistic epistasis”. When I first encountered this phrase I was very impressed. In fact, I was intimidated. It seemed to speak of a very deep understanding, a deep knowledge, which I did not possess. As I have seen it used more, and have understood these issues better, I believe I understand the term better. It is a sophisticated-sounding expression, signifying nothing. It has all the appearance of deliberate obfuscation. Literally translated, synergistic epistasis means “interactive interaction.”

Genetic Entropy by John C. Sanford is available at Amazon. I wrote a little bit about Sanford 2 years ago here: Respected Cornell geneticist rejects Darwinism.

Comments
Bob decieves himself with this comment: “we now a have good handle on these problems” You know Bob your problem clearly is denial (and it ain’t a river in Egypt)! The first step in a person’s recovery is to be honest with themselves and admit that they got a problem in the first place. Come on Bob, you can do it, take that first step!! We will hold your hand and be with you buddy! You can make it Bob!! Just take that first step and take it one day at a time Buddy!
BA77, I understand your feelings here, but Bob OH is one of the few qualified critics still participating at UD. His participation is extremely valuable... You can come with me to PandasThumb some day and put your eagerness to wage battle to good use. I could use an enthusiastic wingman when I fly over to PT. But if Bob makes mistakes, or if we disagree, no need to rub it in. The problem with a discussion that include only pro-ID people is that there is a tendancy to overlook errors. We can be more assured of Sanford's case if we comb through the parts meticulously.... That said, let's give Bob and enthusiastic welcome to this discussion. Personally, I respect his courage and expertise in visiting here. Salvadorscordova
June 12, 2008
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Bob OH: 1. Muller’s Ratchet is only appropriate for asexual populations. Now, I know some Christian denominations give the impression they would like to ban sex, but that’s not a goer. Once you bring recombination into the picture, the argument breaks down.
For the reader's benefit, I sent Bob OH a copy of Sanford's book, and because Bob is a very gifted professional population geneticist, I felt his critique would be informative and valuable. I myself have stated there are things I would amend in Sanford's book.... I felt Bob would not miss any opportunity to point out Sanford's mistakes. :-) I love the open peer-review process. :-) That said, let's try to define what experiments and empirical observations would confirm or refute Sanford's thesis. With respect to Muller's ratchet, from the Appendix of Genetic Entropy
If we combine Muller's recognition of near-neutral (i.e. un-selectable) mutation, with his recognition of mutational advance, we see that no selection system can stop "Muller's Ratchet". Even in Sexual species page 166
Furthermore, if I'm not mistaken, mitochondrial DNA in human females, and the Y-chromosome in human males -- are ther limintations to recombination here? I think there is much not recombination from the male side [PT posted some issues about weak recombination from father's to mitochondrial DNA, but it's not much]. Although I have Sykes book on the Y-Chromosome, I don't have it handy. Help anyone. Furthermore, the u=0.1 relating to a reproduction rate of 2.4, does that assume 100% selection efficacy (the mutations are visible to selection)? Thanks.scordova
June 12, 2008
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1. Every time this subject is raised Darwinists respond with "but what about sexual recombination?". Unfortunately this is raised like a magic wand without any accompanying math COMBINED (as in, not just speculative scenarios that may or may not occur in nature regularly enough to effective) with empirical observations to justify that an overall downward trend is averted (notice I say "overall" since obviously there are exceptions). Is "Sally Otto’s talk at ESEB" available online? If not, at least we have Bob's own comments:
One of the big mysteries in evolutionary biology has been how sex evolved. John Maynard Smith pointed out in the 1960s that it really shouldn't have - there's a huge cost to any gene (because with sex it only has a 50% chance of being passed on), so a modifier that stops sex and have a 100% chance of being passed on will be fitter. Since then a lot of people have been worrying about this problem. In her plenary talk, Sally Otto talked about recent work that suggests we are close to a resolution of the problem. There have been a couple of explanations that have been around for some time. The first is that sex helps evolution because it breaks up bad combinations of genes, particularly when the disadvantages are magnified, so that the cost of carrying two bad genes is more than the cost of carrying one bad gene twice (technically this is called epistasis). This does give sex and advantage, but it's so small, and only occurs in limited and unlikely conditions. The second explanation is the Red Queen hypothesis, again. A species is being subjected to all sorts of attacks (pathogens, parasites etc.), which are co-evolving with them, so there is a constant arms race (this is the Red Queen bit). A species evolves defences, and sex can help combine them together, to increase the speed at which the species runs away from its enemies. This has some empirical support, but Otto showed that the theoretical results suggested it only worked under a narrow set of circumstances. She then introduced a third idea - to look at finite populations. All of the previous work she had presented had been done assuming infinite populations. But in a finite population gene combinations can be combined randomly by genetic drift, and also not every combination of genes will be present in the population. Sex can then work to combine gene combinations and give an advantage. Adding the Red Queen improves the advantage (and I suspect that any sort of environmental variation will give an advantage to sex, more work needs to be done etc.).
Sounds speculative... Let's assume these scenarios prevents or at least greatly slows a complete meltdown except in isolated cases. So genetic entropy may only kill off certain species but otherwise it's just a "trimming effect" where certain "unnecessary" features are lost (Sal's example of infrared vision in humans). But where is the evidence that such scenarios (by themselves without intelligently designed conservation/repair functionality) could maintain stasis long enough to allow for constructive beneficial mutations that lead to macroevolution in an indirect stepwise pathway? 2. Let's not forget, again, that high replicators like bacteria and viruses should avoid genetic entropy. Higher creatures with relatively low replication rates should be the focus of genetic entropy in the first place. UD has featured whole articles on the subject. https://uncommondescent.com/intelligent-design/genetic-entropy-and-malarial-parasite-pfalciparum/ 3. What if there are intensive repair mechanisms within "junk dna" that are only triggered in response to the accumulation of deleterious mutations? I'd presume a decent Designer would want to avoid long term degradation, which any good Designer would know would happen with a self-replicator. Kondrashov “Contamination of the genome by very slightly deleterious mutations: why have we not died 100 times over?” (1995, Journal of Theoretical Biology 175, 583-594). Suzanne Estes & Michael Lynch (2003), Evolution 57, 1022-1030. Abstract. Deleterious mutation accumulation has been implicated in many biological phenomena and as a potentially significant threat to human health and the persistence of small populations. The vast majority of mutations with effects on fitness are known to be deleterious in a given environment, and their accumulation results in mean population fitness decline. However, whether populations are capable of recovering from negative effects of prolonged genetic bottlenecks via beneficial or compensatory mutation accumulation has not previously been tested. To address this question, long-term mutation-accumulation lines of the nematode Caenorhabditis elegans, previously propagated as single individuals each generation, were maintained in large population sizes under competitive conditions. Fitness assays of these lines and comparison to parallel mutation-accumulation lines and the ancestral control show that, while the process of fitness restoration was incomplete for some lines, full recovery of mean fitness was achieved in fewer than 80 generations. Several lines of evidence indicate that this fitness restoration was at least partially driven by compensatory mutation accumulation rather than a result of a generic form of laboratory adaptation. This surprising result has broad implications for the influence of the mutational process on many issues in evolutionary and conservation biology. What if "compensatory mutation accumulation" is really repair mechanisms? That makes more sense than appealing to speculative scenarios. 4. Online searching... I know John has is own site with responses to critics but I can't find it again. Ran into this on Wikipedia that Sanford supposedly had peer reviewed last year:
Sanford, J.C., Baumgardner, J., Gibson, P., Brewer, W., ReMine, W. (2007). Using computer simulation to understand mutation accumulation dynamics and genetic load. In Shi et al. (Eds.), ICCS 2007, Part II, LNCS 4488 (pp.386-392), Springer-Verlag, Berlin, Heidelberg.
I couldn't find anyone discussing it online. http://www.jstor.org/pss/2410218 The abstract says it discusses mutational meltdown in relation to sexual species in the final section. Anyone know what it says?Patrick
June 12, 2008
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Bob Smirks: "please help me" Bob then takes a deep swig of hypothetical Darwinian fairtales, drunkenly, in false pride, slurs to me, "Explain to me how this 100 proof lie I am drinking tastes BA77".bornagain77
June 12, 2008
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BA77 - please help me. Explain the problems with the recent evolution of s^ex work. I assume you're familiar with it, otherwise you wouldn't be in a position to dismiss it. Would you?Bob O'H
June 12, 2008
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Jerry, What kind of junk have you been handed man? Ok, we got 270 million years of progressive loss of variability from the ancint lineage of trilobites, And you say "OH" this is predicted by evolution!?! Get a grip dude evolution can't forever be going on behind closed doors (smoke and mirrors more like it) I say the evidence fits perfectly to first principles of science and that evolution violates first principles of science and that unbiased examination of the evidence bears this out. By the way Jerry, What do you want Santa to bring you this year? (=))bornagain77
June 12, 2008
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Bob decieves himself with this comment: "we now a have good handle on these problems" You know Bob your problem clearly is denial (and it ain't a river in Egypt)! The first step in a person's recovery is to be honest with themselves and admit that they got a problem in the first place. Come on Bob, you can do it, take that first step!! We will hold your hand and be with you buddy! You can make it Bob!! Just take that first step and take it one day at a time Buddy!bornagain77
June 12, 2008
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bornagain77, you said "I’m sorry dude, if over 270 million years we do not see trilobites turn into something other than less variable trilobites, that is definitely not part of any proof of evolution, but clearly points to its fallacy and to Genetic Entropy’s validity," What you are describing is basic micro evolutionary processes which will narrow the gene pool due to environmental and isolation processes. This is not an example of genetic entropy but of natural selection processes and genetic drift processes operating over time which narrow gene pools. Genetic entropy does not narrow gene pools but supposedly creates a chaos within an increasingly more diverse gene pools but with an increasingly higher percentage of dysfunctional genetic elements. It predicts doom for every genome. Basic Darwinian processes, the genetic side, predicts a narrowing of the gene pool over time (what all your examples describe). As such there will be a limiting of the types of trilobites or other families, genera etc. one would expect to find as time marches on. Since this is what we see and what we would expect to see based on Darwinian processes, this evidence validates the Darwinian special theory. I suggest you read Denton. To counter this process the Darwinists predict that the isolated populations will grow in variety from mutations and thus produce new varieties and eventually new species which will eventually become classes, orders, families etc. Sanford says mutations will happen but what he also says is that it will be almost impossible for any positive mutations to show itself in the phenotype and thus be subject to selection. One of the problems I have with Sanford is how people here will describe the preserving of genetic elements over millions of years when Sanford says this cannot happen. This preservation argues against Sanford's ideas.jerry
June 12, 2008
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#19 bornagain77 "If you are saying a computing system in the genome to increase CSI is probable," It's precisely what I meant.kairos
June 12, 2008
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Kairos you stated: "As I’ve already stated in another thread I’m not convinced that CSI cannot grow, provided that we have the action of a very complex computing system (which in turn is surely out of the possibility of RM+NS)." If you are saying a computing system in the genome to increase CSI is probable, I completely disagree that any material computer in the genome can ever increase CSI and miss our present level of scutiny. One problem that comes immediately to mind is the search space is simply far too vast and would require to much memory Even our present super computers are swamped by single proteins: In the year 2000 IBM announced the development of a new super-computer, called Blue Gene, that is 500 times faster than any supercomputer built up until that time. It took 4-5 years to build. Blue Gene stands about six feet high, and occupies a floor space of 40 feet by 40 feet. It cost $100 million to build. It was built specifically to better enable computer simulations of molecular biology. The computer performs one quadrillion (one million billion) computations per second. Despite its speed, it is estimated it will take one entire year for it to analyze the mechanism by which JUST ONE “simple” protein will fold onto itself from its one-dimensional starting point to its final three-dimensional shape. "Blue Gene's final product, due in four or five years, will be able to "fold" a protein made of 300 amino acids, but that job will take an entire year of full-time computing." Paul Horn, senior vice president of IBM research, September 21, 2000 http://www.news.com/2100-1001-233954.html As well Dr. Gitt in His book "In The Begining Was Information" states; “There is no known law of nature, no known process and no known sequence of events which can cause information to originate by itself in matter.” Werner Gitt, “In the Beginning was Information”, 1997, p. 106. (Dr. Gitt was the Director at the German Federal Institute of Physics and Technology) His challenge to scientifically falsify this statement has remained unanswered since first published. I don't know how big the "ultimate computer" would have to be to figure out appropriate proteins for shape space, genetic codes and the multitude of required related hardware, but I am sure that such a sophisticated computer program would undoubtedly reveal itself in the genetic code, and would not be hidden for very long from our ever probing scientific eyes.bornagain77
June 12, 2008
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#3 bornagain77 Despite Dr. Sanford’s unwarranted extrapolation to a YEC, the Genetic Entropy principle is still valid for biology from all empirical evidences that I can gather, But this is my overall opinion too (with some doubt thta I'll explain below. When I wrote: "Unfortunately in this way also all the valid concepts against NDE put in the field by Sanford are discarded as result of YEC ideas" I forgot to add "discarded by most scientists who don't want (or don't have time) to read about". "and meshes extremely well with Dr Dembski’s work on “Conservation of Information”. As I've already stated in another thread I'm not convinced that CSI cannot grow, provided that we have the action of a very complex computing system (which in turn is surely out of the possibility of RM+NS). Instead, I have some doubts about the significance of GE (which I think does exist anyway) in evolution concern the possibility that DNA could actually contain very sophisticated (and so far unknown) feedback mechanisms to keep under control DNA degradation. If this should be the case, we would have another major evidence for IDkairos
June 12, 2008
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Just a couple of comments: 1. Muller's Ratchet is only appropriate for asexual populations. Now, I know some Christian denominations give the impression they would like to ban sex, but that's not a goer. Once you bring recombination into the picture, the argument breaks down. 2. I'm reading Sanford's book at the moment, and I'm not impressed with it (hey, would you expect anything else? :-)). I intend to blog on it when I've finished, but some parts are simply wrong (he ignores Fisher's work, for example). I also keep on thinking "yes, but show us the maths" - it's all arm-waving, with no real meat. 3. We have moved on since 1995 - I intend to dig into the literature later (as part of my review of Sanford). My impression from Sally Otto's talk at ESEB last year is that we now a have good handle on these problems, but I would need to read up on it. It comes back to sex again.Bob O'H
June 12, 2008
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Jerry, I'm sorry dude, if over 270 million years we do not see trilobites turn into something other than less variable trilobites, that is definitely not part of any proof of evolution, but clearly points to its falacy and to Genetic Entropy's validity, If you deny this is true you are ignoring clear evidence and obfuscating what is required for evolution to be proven true. The trilobites should definitely show some mighty powerful evolutionary fireworks in 270 million years!! Man their should have been trilobites turning into completely different phyla in that amount of time!!!! You are lying to me and to yourself if you actually think Darwinian theory predicts this loss of variability!! If you truly do believe evolution should predict this and that is truly what should happen for trilobites over 270 million years then you are as gullible as a small child who believes in Santa Clause!bornagain77
June 11, 2008
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scordove, Here is some information for ancient bacteria that seems to conform Genetic Entropy: ..... gpuccio and I could find no “fitness test” in Vreeland’s or Cano’s ancient bacteria work, so I wrote Dr. Cano, the researcher of the 25-40 million year old “amber” bacteria and he wrote back saying this: We performed such a test, a long time ago, using a panel of substrates (the old gram positive biolog panel) on B. sphaericus. From the results we surmised that the putative “ancient” B. sphaericus isolate was capable of utilizing a broader scope of substrates. Additionally, we looked at the fatty acid profile and here, again, the profiles were similar but more diverse in the amber isolate. No antimicrobial panel was used. This is all the data we have and if you want specifics I’ll have to dig through my old notebooks. But it’s there somewhere. Take care Raul Yet when I wrote back asking for more specifics, I received no further reply from him other than for him to say that he was “undecided” as to whether the evidence indicated a gain or loss in complexity for the modern bacteria. I guess he gathered that I was an ID proponent and did not want to get involved (probably ghosts of EXPELLED scared him) But even in this simple test he performed, a narrowing of abilities is shown for the ancient bacteria. This pattern of "narrowing" holds anywhere and everywhere I look, I can never find an increase of complexity for any "sub-speciation" events. It seems the best RM/NS can do is sift prreexisting information into narrower channels. Thus conforming to Genetic Entropy.bornagain77
June 11, 2008
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bornagain77, Everything you wrote in response to my observation is explainable by current theories of genetics. In other words it is the basic micro evolutionary part of the modern synthesis or what Denton calls Darwin's special theory. I believe you are confusing narrowing of the gene pool through isolation and environmental pressures with deterioration of the genome through mutation. The latter expands the gene pool while the former narrows it. All your examples are narrowing of the gene pool through basic Darwinian processes. According to Sanford, the expansion of the gene pool is harmful because none or few of the mutations are useful and eventually through accumulation lead to a malfunction of the organism. The only problem is that we do not see this malfunction in the world. According to some of Sanford's charts we should be seeing big time problems with many genomes. But we do not see any so by logic that invalidates the assumptions on which the charts are based.jerry
June 11, 2008
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scordova, John Sanford has a simulation program for modeling genetic change over time called Mendel's Accountant. You can get more information and a link to a free download at http://mendelsaccountant.info/ . The program requires Apache Server and Perl and will run within a browser on your PC or Mac. I'm interested to know what you think about it since I'm not qualified to judge. I can point you to resources for installing and configuring Apache and Perl if you need it.bb
June 11, 2008
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Jerry wrote: Nor have I ever seen any reports from any other part of the world about extinctions being caused by genomic factors.
One does not need extinction to demonstrate genetic entropy. Reductive evolution is loss of function. So powerful has the mindset been of upward Darwinian progress that malfunctioning "pitiful relics" have been mis-interpreted as pre-cursors, ancestors, or transitionals, when in fact they were once-fully functional species that became victims of gentic entropy. Darwinist made false claims about supposed pre-coursors and transitionsal which were nothing of the sort but rather victims of destructive evolution. See: Cautionary Tales
Darwin, for example, suggested that the simple swim bladder had been converted into lungs (1859, 190-1), but today we know that swim bladders are actually simplified lungs (see Gould's essay in Eight Little Piggies for a lucid account). In this essay I will review various cases in which simplicity has been erroneously equated with primitiveness. In neither of these cases did Darwinism raise any doubts about the result, and probably played a big role in its acceptance. .... Microsporidia Consider the Microsporidia, part of the taxon Archezoa, thought to be a remnant of primitive eukaryotes (Keeling 1998). Eukaryotes are characterized by a number of features, including their mitochondria, and when a number of organisms lacking mitochondria were discovered, they were naturally regarded as representing a primitive, pre-mitochondrian state. In addition to mitochondria, the Microsporidia also lacks peroxisomes, Golgi bodies, and even cilia. Furthermore, their ribosomes were the same size as those found in bacteria. To top it all off, the basic prediction of the pre-mitochondrian Micropiridia hypothesis was fulfilled: Initial molecular phylogenies placed it at the root of the eukaryotic tree, branching off earlier than the mitochondria-bearing members (Vossbrinck et al. 1987). Surely, a beautiful example of a Darwinian hypothesis being tested and confirmed by the data? Well, things soon began to get a little more complicated. You see, Microporidia are parasites, and parasites are known to experience streamlining selection. The possibility that their simplicity was simply the result of a secondary reduction became very real with the discovery that they possessed an insertion shared only by animals and fungi (Kamaishi et al. 1996), and later phylogenies based on tubulins supported a relationship with fungi (Edlind et al. 1996; Keeling & Doolittle 1996). The final nail in the coffin was the discovery that Microporidia contained genes from mitochondria, indicating that they once possessed them, but subsequently lost them (Germot, Philippe & Le Guyader 1997; Hirt et al. 1997). Placozoa Represented by a single species, Trichoplax adhaerens, scraped off the glass wall of an aquarium in an Austrian laboratory in 1883, Placozoa is one of the more remarkable of the metazoan phyla. They have less DNA than any other animal, and with their only four cell types (sponges, in comparison, has 10-20 different types) they are considered the morphologically most simple animals (Grell and Ruthmann 1991). Consequently, they were placed on the basal branches of phylogenies, with Eumetazoa as a sister group (Zrzavý et al. 1998; Peterson & Eernisse 2001). As two researchers recently remarked, "Trichoplax adhaerens represents the morphologically most simply organized multicellular animal known, and thus has often been seen as the "living ancestor" of all metazoans." (Ender & Schierwater 2003, 130). This view, however, is in conflict with the molecular data, which consistently places Placozoans among the more derived metazoans (Abouheif, Zardoya, & Meyer 1998; Collins 1998, 2002; Kim, Kim, & Cunningham 1999; Peterson & Eernisse 2001). If this is the case, Placozoa must have undergone an extreme degree of reducing selection, losing such non-trivial features as "specialized muscle cells, nerve cells, and a fixed anteroposterior axis" (Jenner 2004, 374). The type III secretory system The eubacterial flagellum has been cited as an obstacle to Darwinian evolution (Denton 1985; Behe 1996). In response to this, many Darwinists, primarily writing on internet discussion boards, have raised the type III secretory system as illustrating a step in the evolution of the flagellum. The secretory system is employed by bacteria for transporting proteins into other cells, which can either harm the receiver or establish a mutualistic symbiosis, as in Rhizobium and legumes, where the bacteria provides the plant with nitrogen, while the plant supplies nutritients. The secretory system has substantial homologues with the flagellum (Hueck 1998), and some critics imagine the simple secretory system as a precursor to the more complex flagellum. This, however, is at odds with the concensus of the scientific community, which is that it was the secretory system that evolved from the flagellum, not the other way around (e.g. Stephens & Shapiro 1996; Macnab 1999; Nguyen 2000), though see Gohpna, Ron & Graur (2003) for a dissenting opinion and Saier (2004) for a response. Contrary to acting as a "steppping stone" in the evolution of flagella, the secretory system is the result of reducing selection, a common fate for organisms living in close symbiotic relationships (Andersson & Andersson 1999).
See: Full of Hot Air by Stephen J. Gould:
lungs must have evolved from swim bladders right? Wrong, dead wrong. Swim bladders evolved from lungs. Stephen J. Gould
scordova
June 11, 2008
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Nor have I ever seen any reports from any other part of the world about extinctions being caused by genomic factors.
Genetic Entropy does not necessarily imply immediate extinction.... In any case, see: Mutational Meltdown for micro examples of genetic entropy. It appears the principles ought to be partially scalable to large populations, except larger populations serve to slow the meltdown... Since we're mentioning Muller, here is a passing reference: Muller's Ratchet and Mutational Meltdown Also Muller's Ratchet and Compensatory Mutation:
Evolutionary theory predicts that mutational decay is inevitable for small asexual populations, provided deleterious mutation rates are high enough. Such populations are expected to experience the effects of Muller's Ratchet [1,2] where the most-fit class of individuals is lost at some rate due to chance alone, leaving the second-best class to ultimately suffer the same fate, and so on, leading to a gradual decline in mean fitness. The mutational meltdown theory [3,4] built upon Muller's Ratchet to predict a synergism between mutation and genetic drift in promoting the extinction of small asexual populations that are at the end of a long genomic decay process. Regardless of reproductive mode, mitochondrial genomes from most animal species are expected to be particularly sensitive to Muller's Ratchet due to their uniparental inheritance, high mutation rates and lack of effective recombination [3,5,6]. The genomic decay effects of Muller's Ratchet have been observed in laboratory evolution experiments with abiotic RNA molecules [7], biotic RNA viruses [8], bacteria [9] and yeast [10]. Indirect evidence for the effects of Muller's Ratchet in nature has resulted from studies on the long-term effects of reduced population sizes on genetic diversity and fitness in amphibians [11], greater prairie chickens [12,13] and New Zealand avifauna [14]. Molecular evidence for Muller's Ratchet has resulted from analyses of deleterious tRNA gene structures encoded by mitochondrial genomes [15] and analyses of Drosophila sex chromosome evolution [16]. However, direct knowledge on the susceptibilities of natural populations to Muller's Ratchet and the molecular mechanisms underlying this process remain enigmatic.
scordova
June 11, 2008
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Jerry you stated: "His claims as to the results of the genetic entropy process seem outlandish which means if they are not validated with real world data (deteriorating genomes), then the rest of his arguments are suspect." I have a comment that is stuck in moderation that list several lines of evidence supporting Sanford's overall claim for the principle of GEbornagain77
June 11, 2008
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I've read most of Sanford's book and have no way to evaluate it. A lot of his arguments sounds reasonable but I have no way to judge them. His claims as to the results of the genetic entropy process seem outlandish which means if they are not validated with real world data (deteriorating genomes), then the rest of his arguments are suspect. As I have said before, the bugs and weeds in my area are reproducing just fine and there does not seem to be any evidence of any extinctions going on or a lack of heartiness. Nor have I ever seen any reports from any other part of the world about extinctions being caused by genomic factors. It is only a matter of time before multiple members of the same species are compared and then there will be a whole new world to explore including whether Sanford's ideas have any validity.jerry
June 11, 2008
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When it becomes apparent Darwinists can't argue for the survival of the fittest, Darwinists have to restate Darwin's theory as survival of the sickest. See this 2008 NY Time Best seller: Survival of the Sickest A Medical Maverick Discovers Why We Need Disease. [so much for bad design arguments, a Darwinist defends disease and misery]
Was diabetes evolution's response to the last Ice Age? Did a deadly genetic disease help our ancestors survive the bubonic plagues of Europe? Will a visit to the tanning salon help lower your cholesterol? Why do we age? ... This revelatory book explains how, especially when you take the evolutionary long-view, many diseases are really complicated blessings, not simple curses. Survival of the Sickest answers the riddles behind many diseases that seem to be inexplicably wired into our genetic code, starting with the biggest riddle of them all: If natural selection is supposed to get rid of harmful genetic traits, why are hereditary diseases so common?
The obvious answer to the author's question seems to have escaped him: Darwinian selection doesn't work very well!!! Instead he spins a story that's supported by circular reasoning, not empirical evidence. So to defend against the evident genetic deterioration, Darwinists try to establish selective stories to justify the deterioration. But these selective stories fail under empirical scrutiny. See: Darwinist chastised for spinning just so stories, but he still brings home the bacon.
Indeed, after 50 years of investigation, we can’t convincingly demonstrate selection for most of the red-blood-cell diseases,
PS just for kicks, in the link on the just so stories:
Europeans resist “mad cow disease” because their ancestors were selected for cannibalism….Jews were selected for higher intelligence than other peoples because of the calculational demands of money-lending…
scordova
June 11, 2008
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Off Topic Video: The Dawkins Delusion http://www.godtube.com/view_video.php?viewkey=4bd18ca563993206f766bornagain77
June 11, 2008
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Here are some references that point to Genetic Entropy: The current state of science has humans migrating out of Africa 50,000 years ago. It is currently proven that the current African populations have more diversity of Genetic information than any other race of humans. Tishkoff; Andrew Clark, Penn State; Kenneth Kidd, Yale University; Giovanni Destro-Bisol, University “La Sapienza,” Rome, and Himla Soodyall and Trefor Jenkins, WITS University, South Africa, looked at three locations on DNA samples from 13 to 18 populations in Africa and 30 to 45 populations in the remainder of the world. “We found an enormous amount of diversity within and between the African populations, and we found much less diversity in non-African populations,” Tishkoff told attendees today (Jan. 22) at the annual meeting of the American Association for the Advancement of Science in Anaheim. “Only a small subset of the diversity in Africa is found in Europe and the Middle East, and an even narrower set is found in American Indians.” In this study for ancient Austrailian DNA we have clear evidence of Genetic Entropy being obeyed!: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=33358 Of special note: Adcock et al. (7) clearly demonstrate the actual extinction of an ancient mtDNA lineage belonging to an anatomically modern human, because this lineage is not found in living Australians. Although the fossil evidence provides evidence of the continuity of modern humans over the past 60,000 years, the ancient mtDNA clearly does not, providing an excellent example of why the history of any particular locus or DNA sequence does not necessarily represent the history of a population. Adcock et al.’s (7 And this analysis of the preceding study http://www.godandscience.org/evolution/multiregional.html points out that the range of the 40,000 year old mtDNA is within the range of modern humans. and this excellent study of trilobites over 270 million years; http://www.terradaily.com/reports/The_Cambrian_Many_Forms_999.html excerpt: He focused on actively evolving characteristics. The trilobite head alone, for example, displays many such characteristics. These include differences in ornamentation, number and placement of spines, and the shape of head segments. His findings: Overall, approximately 35 percent of the 982 trilobite species exhibited some variation in some aspect of their appearance that was evolving. But more than 70 percent of early and middle Cambrian species exhibited variation, while only 13 percent of later trilobite species did so. “There’s hardly any variation in the post-Cambrian,” he said. “Even the presence or absence or the kind of ornamentation on the head shield varies within these Cambrian trilobites and doesn’t vary in the post-Cambrian trilobites.” and this study confirming the "parent species" of sheep have a robust genetic code when compared to their "sub-species": Single male and female sheep maintain genetic diversity.A mouflon population, bred over dozens of generations from a single male and female pair transplanted to Haute Island from a Parisian zoo, has maintained the genetic diversity of its founding parents. This finding challenges the widely accepted theory of genetic drift, which states the genetic diversity of an inbred population will decrease over time. "What is amazing is that models of genetic drift predict the genetic diversity of these animals should have been lost over time, but we've found that it has been maintained," said Dr. David Coltman, an evolutionary geneticist at the University of Alberta. http://www.sciencedaily.com/releases/2007/03/070309103157.htm and this for dogs: Here is a Paper that has confirmation of dogs and grey wolves staying within principle of Genetic Entropy. http://jhered.oxfordjournals.org/cgi/reprint/90/1/71.pdf of special note: Some sequences found in dogs were identical to those in wolves… The sequence divergence within dogs was surprisingly large: the mean sequence divergence in dogs 2.06 + or - 0.07% was almost identical to the 2.10 + or - 0.04% (sequence divergence) found within wolves. (notice that sequence divergence is slightly smaller for the population of dogs than for the population of wolves) Coupled with the diverse morphology of domesticated dogs and known hazards of dog breeding, this evidence strongly indicates “front loaded adaptations” at a loss of information from parent species. Thus, this is genetic confirmation of the principle of Genetic Entropy for dogs from wolves! Of special note for the Mexican hairless dog (chihuahas); many founder halotypes were likely lost because of "genetic drift" The gene that determines hairlessness is dominant but lethal when homozygous. Thus clearly the "mutation" that causes hairlessness is not a gain in information. This following paper is more recent and more concrete in establishing the principle of Genetic Entropy for dogs/wolves: Origin of dogs traced http://news.bbc.co.uk/2/hi/science/nature/2498669.stm of special note: Their findings, reported in the journal Science, point to the existence of probably three founding females - the so-called "Eves" of the dog world. They conclude that intensive breeding by humans over the last 500 years - not different genetic origins - is responsible for the dramatic differences in appearance among modern dogs. and the paper itself: http://www.sciencemag.org/cgi/content/abstract/298/5598/1610?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=%28Peter+AND+Savolainen+AND+science+AND+old+AND+world+AND+dogs%29&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT Genetic Evidence for an East Asian Origin of Domestic Dogs Peter Savolainen,1* Ya-ping Zhang,2 Jing Luo,2dagger Joakim Lundeberg,1 Thomas Leitner3 The origin of the domestic dog from wolves has been established, but the number of founding events, as well as where and when these occurred, is not known. To address these questions, we examined the mitochondrial DNA (mtDNA) sequence variation among 654 domestic dogs representing all major dog populations worldwide. Although our data indicate several maternal origins from wolf, >95% of all sequences belonged to three phylogenetic groups universally represented at similar frequencies, suggesting a common origin from a single gene pool for all dog populations. A larger genetic variation in East Asia than in other regions and the pattern of phylogeographic variation suggest an East Asian origin for the domestic dog, ~15,000 years ago. How did they trace the lineages? They traced it by the loss of genetic variation (the loss of "front" loaded CSI information). as well as trees staying within genetic entropy: At one of the few petrified forests that sports ginkgo wood, I was told by the naturalist that ginkgos are old in the fossil record—they date from the Permian back when trees were first “invented”. She said that there are a number of species of fossilized Ginkgoaceae, yet Ginkgo biloba, is the only species left alive today. Even Allen MacNeill agrees with this: "As Niles Eldredge and Stephen Jay Gould pointed out almost three decades ago, the general pattern for the evolution of diversity (as shown by the fossil record) follows precisely this pattern: a burst of rapid diversity following a major ecological change, and then a gradual decline in diversity over relatively long periods of time." Allen MacNeill PhD (teaches evolution) and this following study is interesting because it shows ancient (parent) species of cichlids exhibiting rapid adaptation while younger sub-species don't change at all i.e. they "ran out" of front loaded information. African cichlid fish: a model system in adaptive radiation research http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1635482 of special note: Interestingly, ecological opportunity (the availability of an unoccupied adaptive zone), though explaining rates of diversification in radiating lineages, is alone not sufficient to predict whether a radiation occurs. The available data suggest that the propensity to undergo adaptive radiation in lakes evolved sequentially along one branch in the phylogenetic tree of African cichlids, but is completely absent in other lineages. Instead of attributing the propensity for intralacustrine speciation to morphological or behavioural innovations, it is tempting to speculate that the propensity is explained by genomic properties that reflect a history of repeated episodes of lacustrine radiation: the propensity to radiate was significantly higher in lineages whose precursors emerged from more ancient adaptive radiations than in other lineages. As well it should be noted that the ancient lineages of cichlids upon closer examination had something like 7 different types of photoreceptor cells while all younger species had lost the use of some, Once again staying within the principle of genetic entropy. I have a few more studies I've collected but these studies should be enough to drive home the point that Genetic Entropy has stunning empirical evidence backing it up.bornagain77
June 11, 2008
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I do not agree with everything in Sanford's book, but I think the topic is worthy of exploration, and if he (and Muller) are fundamentally right, this will be significant to medical science... Will the scientific communty be willing to consider the possibility of gentic entropy or will they close their eyes because Sanford's work leads to numerous uncomfortable conclusions. Oxford geneticist Bryan Sykes independently arrived at a comparable conclusion in the book Adam's Curse, but unfortunately Sykes gave little in the way of published calculations! I personally have been curious if human beings had infra-red vision once upon a time, and then slowly lost it. There is a growing spread of myopia (possibly genetic, not just environmental), so it stands to reason other functions have died including infra-red vision. One of UD's commercial sponsors, a graduate of Johns Hopkins and author of The Days of Peleg (see sidebar) offers this here: Days of Peleg:
This Neanderthal cave is north of Les Ezies, and runs more than seven miles underground. Engravings and drawings cover the walls, and visitors can view them while riding the little tourist train that runs much of the distance. Somehow this artwork was done without conventional light (i.e. smoky flames or torches) since the walls at the time of its 'discovery' were clean and untarnished or "white crystalline". "Experts" suggest that Neanderthals must have used "smokeless fat" for their torches to explain this. One alternative is Infra-red vision in early humans. During WWII, some soldiers were given high doses of Vitamin A in a special diet, and over a period of time, many developed infra-red acuity. However, the actual diet was harmful, and it was discontinued in favor of the newly developed 'snooperscope'. Also, people who are totally color-blind, often report being able to see infra-red.
I do not necessarily think most Junk DNA is functional today. I would argue that maybe large sections of junk DNA USED TO BE functional, but now we have lots of broken parts, or dare I say, "pitiful relics".scordova
June 11, 2008
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Kairos, Despite Dr. Sanford's unwarranted extrapolation to a YEC, the Genetic Entropy principle is still valid for biology from all empirical evidences that I can gather, and meshes extremely well with Dr Dembski's work on "Conservation of Information". The only missing piece I found need of was provided in Dr. Spetner's book "Not By Chance" http://www.amazon.com/Not-Chance-Shattering-Modern-Evolution/dp/1880582244 In Chapter 7 Spetner puts forward a case for non-random variation and in Chapter 8 gives us his alternative to evolution what he calls the NREH (Non Random Evolutionary Hypothesis) This Non-Random Evolutionary Hypothesis, is needed to explain rapid adaptations (all of which lose CSI from a "parent species"). NREH added to CSI and genetic Entropy helps explain that there are many adaptations in the literature that cannot be explained by purely evolutionary processes, so it becomes apparent that the environment is in fact triggering a front loaded mutation search, which will in short time find the correct mutation (while decreasing CSI and staying within first principles).bornagain77
June 11, 2008
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#1 DaveScot "Sanford chose to quote a wildly high mutation rate so he could compress the extinction time from millions to thousands of years and thus ignore the fossil record in favor of a young earth interpretation of the bible." I too had the same reaction after reading GE book. Unfortunately in this way also all the valid concepts against NDE put in the field by Sanford are discarded as result of YEC ideaskairos
June 11, 2008
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I read Sanford's book last year. The only real problem I had with it was the baseline mutation rate he chose which was at least one or more orders of magnitude higher than what is usually given. I agree that genetic entropy alone should cause higher animal species to become extinct after a period of millions of years with the commonly given mutation rate. Sanford chose to quote a wildly high mutation rate so he could compress the extinction time from millions to thousands of years and thus ignore the fossil record in favor of a young earth interpretation of the bible. Too bad. It's otherwise quite credible. I was extremely disappointed when I discovered what he'd done as genetic entropy as a major cause of extinction was apparent to me long before I read Sanford or Haldane or anyone else who'd touched on the problem with RM+NS in a similar way. It's just common sense and fits quite well with the fossil record. The interesting question is what allowed some lucky few germ lines in higher animals to escape genetic entropy such that their line has been able to persist for hundreds of millions of years. Front loading, among other hypothetical intelligent design frameworks, offers an answer to that. I've yet to see any non-design explanation that adequately addresses the genetic entropy problem.DaveScot
June 11, 2008
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