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

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.

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

  1. 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.

  2. #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 ideas

  3. 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-Chan.....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).

  4. 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”.

  5. 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.g.....rtid=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/e.....ional.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/repo.....s_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/re.....103157.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.o.....0/1/71.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/sci.....498669.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/.....type=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.g.....id=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.

  6. Off Topic Video:

    The Dawkins Delusion

    http://www.godtube.com/view_vi.....993206f766

  7. 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…

  8. 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.

  9. 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 GE

  10. 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.

  11. 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

  12. 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.

  13. 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.

  14. 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.

  15. 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!

  16. 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.

  17. #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 ID

  18. 18

    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.

  19. #19 bornagain77

    “If you are saying a computing system in the genome to increase CSI is probable,”

    It’s precisely what I meant.

  20. 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.

  21. 21

    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!

  22. 22

    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? (=))

  23. 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?

  24. 24

    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″.

  25. 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.

    http://www.uncommondescent.com.....alciparum/

    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?

  26. 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.

  27. 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.

    Salvador

  28. [note: correction to above post]

    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
    Genetic Entropy

  29. 29

    Salvador,
    You are right, And I apologize to you Bob for my being a bit to witty in my responses to you. You are indeed a valuable counter-balance to debate with.

  30. bornagain77,

    I suggest you tone down your rhetoric. If for example it turns out I am right then you will look foolish with some of your comments.

    You don’t seem to understand how micro evolution works and what are the basic tenets of it and where are the weak points of the Darwinian paradigm in total. It is not on the genetic side which is where your examples are from. Genetics predicts all the things you are bringing up. The weakness of the Darwinian paradigm has always been on the creation of new meaningful variation which is why the trilobites gene pool became narrower and narrower. That is what the Edge of Evolution is all about.

  31. bb wrote:

    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 and configuring Apache and Perl if you need it.

    That would be wonderful. Thank you for bringing this to my attention…

    I’ll be meeting with Walter ReMine this month, and hope to see John Sanford in August at the ICC2008 conference.

    This really should be project that non-ID folk should be interested in since it deals with issues relevant to medical science.

    The major party on the non-ID side that has done independent work on the topic is Oxford Geneticist Bryan Sykes and friends. Sykes authored Adam’s Curse:

    Sykes concludes by noting that, as evidenced by declining sperm counts and high percentages of abnormal sperm, among other variables, the Y chromosome is a genetic mess and is deteriorating so quickly that men could become extinct.

    Sykes gives the human race 100,000 years….

    Some other geneticists have a grim view for humainity’s genes (but for very different reasons).

    See: JohnJoe McFadden Our Genes are Doomed.

  32. Jerry;
    As I have seen numerous times, Darwinism can predict anything and can be falsified by absolutely nothing, thus it totally useless as theory of biological origins, (Useless except as it is used as a foil to refine the proper ID ). Whereas Genetic Entropy/ID also predicts the same pattern a loss of variety and Genetic diversity and can be falsified by showing sub-species that have greater potential diversity than the parent strain. Even in the recently touted acquired citrate ability of E-coli. I can surmise that it came at a loss of CSI and this can probably be verified by testing for the range of substrates that are utilized by each strain. Regardless, the fact that the mutant strain of E-coli will soon be out-competed by the Parent strain in the original environment clearly shows that the bacteria have not passed the threshold of complexity generation necessary to prove evolution true. Thus it goes on and on Jerry, evolutionists forever chasing their tail in a circle trying to find the elusive conclusive piece of evidence that will vindicate their theory, all the while the public is misled into thinking evolutionary theory has been proved true repeatedly. NO, Jerry, come to think of it, after 150 + years of evolutionists failing to provide conclusive evidence I am not worried in the least that evolution will suddenly be proved right.

  33. The weakness of the Darwinian paradigm has always been on the creation of new meaningful variation

    Well, it appears there are more weakness, and the weakness in question is that ability of Darwinian Selection to weed out the bad. Furthermore, this aspect is emprically testable….

    The original Darwinian paradigm (as stated by Darwin himself):

    Natural Selection is daily and hourly scrutinising, throughout the world, the slightest variations; rejecting those that are bad, preserving and adding up all that are good.

    C.DARWIN sixth edition Origin of Species — Ch#4 Natural Selection

    We know that standard genetics has absolutely refuted this utopian view of selection. Darwinian selection does not hourly weed out the bad nor preserve ALL that is good.

    At issue is the search for evidence for how poorly Darwinian selection is unable to weed out the bad in the current day. Notice I try to refrain from the phrase “Natural Selection”, because “Natural Selection” in the Darwinian sense is not observed to be what really happens in nature when illuminated by modern science.

  34. You may already be aware of this study Sal but if not here it is:

    The Strength of Phenotypic Selection in Natural Populations

    This review demonstrates that our information about the
    strength of phenotypic selection in natural populations has
    increased dramatically in the past 2 decades, but many important issues about selection remain unresolved.

    http://www.oeb.harvard.edu/fac.....1AmNat.pdf

  35. Strike at the core, strike at the heart of Darwinism and the utter destruction it wreaked on science as well as culture and the arts.

    Darwin’s metanarrative stirred up religious fervor for one reason only: it implied progress. We bought into his materialism because he succeeded in convincing us that nature itself was making things better.

    Muller’s research shows that this is nonsense. No ameliorative power of any kind is obervable in nature at the molecular level. Nature has no intrinsic capacity to produce anything of value.

    The Modern age with all of its horrors was based on the notion that men could dispense with God and make their own happiness. Now that the myth of progress has been exposed, it becomes possible to break the stranglehold of Darwinism on the human spirit and being a new dialogue.

  36. Off Topic video:

    Answering the New Atheism: Part 2

    Author’s Scott Hahn and Benjamin Wiker collaborate to debunk Dawkins’ theories and show how inconsistent and illogical his conclusions truly are.

    http://www.godtube.com/view_vi.....f641031562

  37. 37

    BA77 (#5)

    You point to the genetic diversity of one group of modern day humans (Africans) and compare that to the lesser genetic diversity of other groups that diverged from them. You also compare modern day wolves to modern day dogs to the same end. But it seems obvious that if a very small group migrates away from a larger group, that the new group will obviously have less genetic diversity than the larger group it came from.

    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.

    You could also point to genetic diversity in New York City and compare that to the relative lack of it in Salt Lake City and use that to indicate genetic entropy because the Mormon sect migrated from the east. But as Jerry has pointed out that has nothing to do with the accumulation of harmful mutations somehow decimating a population over time, which is what genetic entropy is supposed to be.

    Now that I think of it though, a small isolated population does tend have an accumulation of harmful genetics leading to decimation. But the remedy to that is always the introduction of new genetic variability from an outside source leading to new hybrids which then predominate.

    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… more than 70 percent of early and middle Cambrian species exhibited variation, while only 13 percent of later trilobite species did so

    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)

    Of special note for the Mexican hairless dog (chihuahas)…The gene that determines hairlessness is dominant but lethal when homozygous…Thus clearly the “mutation” that causes hairlessness is not a gain in information.

    (BTW, No one thinks that the morphologic variability in dogs as compared to wolves has anything to do with mutations that have occurred since their divergence.).

    So in the case of the wolf there was all this latent variability preserved presumably for eons, even though it wasn’t favored by survival. Then when humans start dog-breeding, they were immediately able to retrieve all this variability.

    Shouldn’t we assume the same would happen if humans had started breeding trilobytes.

    But to return to the accumulation of harmful mutations in a small in-breeding population. Maybe this principle could be extrapolated to a macro scale and imply that unless new genetic material comes onto the planet (from an “outside source”) that worldwide gradual extinction is inevitable. So the Cambrian explosion was the source of genetic variability that has been dwindling ever since (presumably). But Darwinists etc. would assume the Cambrian explosion itself was a natural event. So shouldn’t ID be trying to prove that the Cambrian explosion could not be a natural event.

    Its already been observed in this thread that the wholescale decimation implied by the theory of generic entropy has not been observed. Thus the premise of the Kondrashov article from the OP, “Why have we not died 100 times over”

    Just to repeat my own comments regarding this paper when scordova brought it up in the “Gambler’s Ruin” thread:

    So, if I’m reading the abstract (which is all that’s available) correctly, it is known fact that neutral mutations are accumulating in a typical species to such a great extent that a lot of harmful configurations of this introduced genetic material has occurred, and yet it is also known that somehow these suboptimal configurations are being dealt with (by some unknown mechanism?). So if they’re being dealt with – its not by miraculous intervention presumably.

  38. For the readers’ benefit, to illustrate the questions at hand, I point to an extreme example where x-ray radiation is at play (a topic for which Muller won the Nobel Prize):

    Consider a population of 10 individuals each with a genome of 4-giga base pairs. They are subjected to intense x-ray bombardment such that each individual on average will get 1,000,000 bad mutations and 1 good mutation. Can any amount of Darwinian selection clear out the genome of such a population if 1,000,000 bad mutations and 1 good mutation are added to each individual on average in each generation? Even if each indivdual bore 100 kids on average and we killed off 99% of the offspring, we would not be able to keep pace against genetic entropy…

    The relationship of the number of offspring needed to the mutation rate “u” is exponential.

    For u = 0.1 we need 2.4 kids per couple just to meet the selective costs.

    For u = 3 we need 40 kids per couple!

    Published estimates of u are higher than 3, maybe 100. I don’t know, but it’s worth looking into.

    For discussion of “u”, see: Nachman’s U-Paradox.

  39. Junkyard wrote:

    Its already been observed in this thread that the wholescale decimation implied by the theory of generic entropy has not been observed.

    Junk,

    Wholescale decimation is not necessarily implied by theory of gentic entropy. You’re making misrepresentations.

    You can have large populations of damaged individuals like populations wingless beetles, blind cave fish, or the other species I listed.

    Furthermore, the decimation may yet happen. You’re making assumptions about how recent the healthiest individuals appeared on the planet. For the sake of argument, even though I’m a creationist, we could argue ET’s or a general front loaded event happened recently, but the decimation may yet come.

    Also, it may be hard to observe something if one is not carefully looking for it.

    I pointed out, some Darwinists are already arguing for “the survival of the sickest” because they are hard pressed to explain the persistence of genetic illness in light of Darwin’s theory.

  40. 40

    scordova (#39)

    “Wholescale decimation is not necessarily implied by theory of gentic entropy. You’re making misrepresentations.

    You can have large populations of damaged individuals like populations wingless beetles, blind cave fish, or the other species I listed.

    Furthermore, the decimation may yet happen”

    Actually, it seems like genetic entropy as a valid principle at least in certain identified contexts would already be quite obvious to everyone, for example, aristocratic dynasties of Europe or Egypt, or in the Appalachians, or Utah, or what have you. (I presume that’s the same concept.) So does anyone actually deny this. So the question is, the extent of entropy, and the frequency and source of new genetic info entering into the system. Did new info just happen once eons ago, with no new natural sources since then?

    Concerning cave fish – had one of those once – revolting fish that swims around constantly moving it jaws hoping to swim into something to eat; it ate all the fins off of a siamese fighting fish.

  41. 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.

    As far as I’m aware, the X chromosome can recombine. The Y chromosome can’t, which is probably why it’s so small and scrappy – it has suffered from genetic entropy. In some species, the Y chromosome (or its equivalent) is simply missing. Of course, this should raise questions about why the other chromosomes haven’t degraded.

    According to wiki, mitochondria can undergo recombination, but this is rare. It’s worth pointing out that, because each cell contains several mitochondria, the population size is larger, so mutational meltdown will be slower than in the Y chromosome.

  42. 42
    JunkyardTornado

    Was thinking about hybridization as a source of new information. Anything different than what was already in a population, if it is introduced into that population, will result in new vigor and new novel hybrids with characteristics not previously seen in either variant. That is the source of new information in the genome that we typically see, and it could not have less to do with design, rather its just, “let’s throw something really really different into the mix.” Invaribly the result is always good. This really doesn’t have the rigor of some of the arguments in this thread, admittedly.

    There’s not just a continual degradation we see in nature. Species are rejunventated, novel characterisitcs are expressed, by new diffent genetic info being randomly introduced into a population, or new traits being brought out as a result of a new physical environment. If a Cave Fish loses its eyes because it doesn’t need them, then some other trait is developing, wich was not expressed in previous populations.

    Do we have any indication that eyes in general are disappearing from the planet? Or Wings? Or infrared vision. Humans may no longer have infrared vision, but its not going anyhwhere, and furthermore we got something better in exchange.

  43. bornagain77,

    Your answers indicate you do not understand anything I have said and you continue to try to destroy things I have not said. I suggest you read carefully what I say and respond to that as opposed to what you want to destroy.

    Let me make it clear for you. The current evolutionary synthesis predicts a narrowing of the gene pool of a population over time. This is exactly what you see in your trilobite example and your other examples. It has nothing to do with genetic entropy. This narrowing of the gene pool is due to isolation and environmental pressures selecting for a subset of the genome which leads to a lost of variety in the gene pool.

    The Darwinist counters this trend of a narrowing gene pool which is predicted by the evolutionary synthesis by saying that there will be new variation created by mutation events which will expand the gene pool. While there is plenty of information for mutation events, Sanford asserts a high rate, there is no evidence of this ever producing anything meaningful and Behe’s Edge of Evolution provides empirical support as to why.

    Sanford’s ideas lead to an immensely more varied gene pool but the variety is dysfunctional and according to Sanford will lead to extinction but not necessarily to less variety in the species. So it is elements of the Darwinian paradigm that point to the narrowing gene pools and not Sanford. I am surprised that no one else has not pointed this out to you. The term entropy represents the chaos Sanford says is happening to all the genomes and not some narrowing of them.

    The basic argument between ID and those who support naturalistic evolution for everything hangs primarily on the creation of new variation in the gene pool and not on the processes of micro evolution which are widely accepted by ID and which predict narrower gene pools over time. Not everything the Darwinists say is nonsense. Micro evolution which they frequently point to is well established.

  44. Junkyardtornado,

    Hybridization is just another name for gene flow which is a basic part of the evolutionary synthesis. Essentially it is an increase in the gene pool by combining two isolated populations of the same species.

  45. As far as I’m aware, the X chromosome can recombine. The Y chromosome can’t, which is probably why it’s so small and scrappy – it has suffered from genetic entropy. In some species, the Y chromosome (or its equivalent) is simply missing. Of course, this should raise questions about why the other chromosomes haven’t degraded.

    According to wiki, mitochondria can undergo recombination, but this is rare. It’s worth pointing out that, because each cell contains several mitochondria, the population size is larger, so mutational meltdown will be slower than in the Y chromosome.

    Thank you, Bob.

    It would appear that mitochondiral DNA and Y-chromosomes in humans would be subject to Muller’s ratchet. In that sense, Muller’s ratchet can be applied to sexually reproducing species.

    Is that a reasonable statement?

    Thanks again.

    Of course, this should raise questions about why the other chromosomes haven’t degraded.

    Agreed. I maintain the possibilty that a recent creation of certain life forms is the reason. It is possible the universe is old, but certain life-forms (in their current state) are recent. It is also possible a front-loaded event happened to create these life forms. I have my opinions….

    I could of course be wrong, but your question still appears to be a legitimate question.

  46. More on Muller’s Ratchet (for linkage blocks in sexually reproducing species):

    The most obvious and extreme form of slection interference is when there is tight physical linkage between beneficial and deleterious mutations. This results in an irreconcilable problem which has been termed Muller’s Ratchet.

    Genetic Entropy
    page 81

    and

    Essentially all of the genome exists in large linkage blocks (Tishkoff and Verrelli, 2003), so this problem applies to virtually every single “building block” of the genome

    With respect to linkage blocks, does this mean when re-combination happens between the DNA of mom and dad, the mixing does not happen at the gene level, but large blocks of genes and other DNA?

    If so, Sanford highlights the difficulty of Muller’s Ratchet on linkage blocks in sexually reproducing creatures:

    Within any given physical linkage unit, there should be, on average, thousands of deleterious mutations accumulated before the first beneficial mutation would even arise…

    Every single beneficial mutation would be inseparably tied to a large number of deleterious mutations.

    Let us supppose we have a linkage block with 20,000 deleterious mutations, and then there appears 1 beneficial one in the linkage block. Sure sleection might happen in favor of the beneficial, but it doesn’t appear that there is much route for the 20,000 deleterious mutation to be purged once this linkage block has been fixed into the population.

  47. 47

    Junkyard,

    it seems obvious that if a very small group migrates away from a larger group, that the new group will obviously have less genetic diversity than the larger group it came from.

    You would think so

    yet this study begs to differ:

    Single male and female sheep maintain genetic diversity.

    A mouflon (considered the parent species of sheep) 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/re.....103157.htm

    So Junkyard according to what you wrote, evolutionary theory did not predict this yet ID/Genetic Entropy does for ID/GE predicts that a parent species will maintain greater CSI diversity over sub-species strains.

    The thing that causes loss of genetic diversity is a culling of preexisting CSI.

    Your Salt Lake City and New York City comparison I believe is an attempt at obfuscation since you clearly know we are talking about the genetic diversity of specific races.

    But to your main point which I think you are sincere about;

    But as Jerry has pointed out that has nothing to do with the accumulation of harmful mutations somehow decimating a population over time, which is what genetic entropy is supposed to be.

    Well Junkyard, evolution (sometimes when its convenient (LOL)) makes the grand claim that all species arose from a universal common ancestor and in contrast Genetic Entropy makes the grand claim that the variability of a parent species will decline over time. This primary claim of Genetic Entropy is exactly what we have in the trilobite studies as well as in the overall pattern of the fossil record.

    “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)

    As well Genetic Entropy will hold that a parent species and all its sub-species will gradually become extinct after this Gradual loss of diversity. Extinction is held to be due to accumulated deleterious mutations resulting in “mutational meltdown. Again this is exactly what the trilobite study tells us. As well the overall fossil record points to this since 90% of extinctions in the fossil are caused by some unknown natural mechanism that is not attributable to natural disasters. Genetic Entropy fits the unknown mechanism very well.
    So we have Genetic Entropy verified in all its primary premises in the fossil record and Evolution is not verified in any of its primary premises in the fossil record.

    To genetics:

    So I go to genetics and find that a loss of gentic diversity occurs with sub-speciation events (I was actually pleasantly surprised to find this out) Yet, You claim I am somehow cheating with the evidence to say that sub-species have less genetic diversity than a parent species,

    Why do you say this? Is not evoultion making the grand clam that random mutations, which are suppose to be what is actually generating more genetic diversity and variability to account for the profusion of life we see around us, are what is in fact driving speciation events? Should not I naturally expect to see more genetic Diversity for sub-speciation, events, at least sometimes if Darwinism is true? Does or Does not Evolution have the grand power of creating new species of life with new more diverse genetic information that you and other evolutionists claim it does? Why must all sub-speciation events I can find be accompanied by a loss of genetic diversity if evolution is true? For you to hold that evolution can create life and then say that all sub-speciation events, that we can currently measure with science, will come at a loss of Genetic diversity is in fact two different claims. You can’t have it both ways, as with bacteria, you must present complexity that is above the level of the parent species to prove evolution true?

  48. 48

    The most obvious evidence we have for Genetic Entropy, and against evolution, is found in the rampant problem of inbreeding. Inbreeding is a major and serious problem facing ALL major domesticated plants that man raises for food, and ALL major animals that man raises for food and companionship. Indeed inbreeding is even a problem for humans themselves. As well, Inbreeding can be found to be a major problem in many “wild” populations such as the cheetah and the panda.

    What are the adverse effects of Inbreeding; Here is a list from: http://cc.ysu.edu/~helorime/inbred.html

    Inbreeding and it’s General Effects

    Inbreeding depression encompasses a wide variety of physical and health defects. Any given inbred animal generally has several, but not all, of these defects. These defects include:

    Elevated incidence of recessive genetic diseases

    Reduced fertility both in litter size and in sperm viability

    Increased congenital defects such as cryptorchidism, heart defects, cleft palates.

    Fluctuating assymetry (such as crooked faces, or uneven eye placement and size).

    Lower birthweight

    Higher neonatal mortality

    Slower growth rate

    Smaller adult size, and

    Loss of immune system function.

    Evolution tries to get around this problem of inbreeding by saying that large populations will almost never suffer from the problem of inbreeding because the genetic diversity of the larger populations of the species as a whole will prevent the recessive deleterious genetic mutations from ever being expressed. The mutation, evolutionists say, will drift away or it will “magically disappear all together by evolutionary slight of hands” or if it is expressed it will quickly be removed by natural selection).. Yet in order for a recessive deleterious mutation to actually be removed from a population it must in fact become dominant in an individual organism (or remutated to its non-deleterious state), for the organism to be “naturally selected” against and removed from the population. Well what is the recessive mutation doing the whole time while it is waiting to be expressed in an organism so as to be removed from the population? Well obviously, it is spreading throughout the entire population is what it is doing! Natural selection is absolutely powerless to remove the deleterious mutations before it becomes dominant and is expressed. And bear in mind that the vast majority of mutations are in fact now proven to be “slightly” detrimental and recessive in their expression. Thus what we really have is a ticking time bomb for all species on earth since they were created. Indeed, the fossil record shows a fairly constant extinction rate of 3-5million years that is not due to natural catastrophe and most likely is due to “Genetic Meltdown” brought by the “mutational load” brought about by all these deleterious mutations accumulating in genomes. What inbreeding does is in fact allow the recessive mutations, which would not normally be expressed for many generations, to be expressed very quickly. This is because when siblings mate, the defective mutations, that were in one parent and are not “softened” with another genome that does not have the mutation, and they are expressed much more quickly than they normally would be.

    “Human life expectancy presently has an average of about 70 years, and a maximum near 120. However, 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 (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 genetically as a species. The reduced life expectancy of inbred children reflects the overall aging of the genome, and reveals the hidden reservoir of genetic damage (recessive mutation) that has been accumulating. If all this genetic damage were exposed suddenly (if we were all made perfectly inbred and homozygous)- it would be perfectly lethal-we all would be de^ad, our species would instantly become extinct.” (Dr. J.C. Sanford PhD.; Genetic Entropy, page 147)

    So, I maintain inbreeding is in fact showing us exactly what evolution does in the long term. That is, inbreeding is showing the overwhelming destructive power of “evolution” in a very short time! You see, when a population is inbred it allows the recessive deleterious mutations to become dominant for the offspring. deleterious mutations find there match to become dominant Indeed, Inbreeding is a forecaster of what is in store for the population in the future once the “deleterious mutational load” builds up because the deleterious mutations are never, ever, dealt with and WILL CERTAINLY find its match in the genome, sometime, to make it a dominant defect instead of a recessive defect that is below the power of natural selection to remove from the genome.

  49. 49
    JunkyardTornado

    ba77:
    “JT: it seems obvious that if a very small group migrates away from a larger group, that the new group will obviously have less genetic diversity than the larger group it came from.

    ba77: You would think so

    yet this study begs to differ:

    Single male and female sheep maintain genetic diversity.

    A mouflon (considered the parent species of sheep) 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.

    —————

    I said that a smaller group leaving a larger one had less genetic diversity than the entire larger group it came from. I did not say that a group of descendents from a single breeding pair would have less diversity than the single breeding pair they came from.

    The article says that genetic drift is generally held to decrease genetic diversity over time, but that in this case the harshness and variability of the environment kept the species “on their toes”. However genetic drift has been observed repeatedly. This one incident hasn’t invalidated it.

    But anyway, a much smaller subgroup would be less diverse than a larger group they migrated from because they were a smaller group, not because of genetic drift.

    So Junkyard according to what you wrote, evolutionary theory did not predict this yet ID/Genetic Entropy does for ID/GE predicts that a parent species will maintain greater CSI diversity over sub-species strains.

    I’m confused. How did ID/GE predict these results if they predict a lessing of diversity due to genetic entropy and here we have a maintaining of genetic diversity. Maybe entropy is not even relevant here, but how does it predict a maintaining of diversity. (And once again, I personally was talking about something different.)

    The thing that causes loss of genetic diversity is a culling of preexisting CSI.

    Is not CSI a near synonym for genetic diversity. So a loss of of genetic diversity is caused by a culling of genetic diversity. I assume you mean this culling is always due to entropy. So genetic drift or natural selection never cause it?

    Your Salt Lake City and New York City comparison I believe is an attempt at obfuscation since you clearly know we are talking about the genetic diversity of specific races.

    It wasn’t such an attempt. You have a smaller group migrating aways a much larger one. I intended it as directly comparable to the Africa example.

    This primary claim of Genetic Entropy is exactly what we have in the trilobite studies as well as in the overall pattern of the fossil record.

    I sincerely don’t think that’s the case. Not that I don’t accept that genetic entropy is a meaningful concept if applied correctly. I accept the possibility that overall, there may have been a gradual decrease in inherent genetic potential since the Cambrian Explosion due to general decay. After all, we know that organisms die. Maybe the entire worldwide organism is gradually dying. But I think the reduction in trilobyte diversity would have to do with competitive factors and matching to the environment. And possibly also genetic drift. But as I said, in the case of wolves we know there was a huge amount of diversity there even though not expressed but that could still be retrieved, and could probably be the same with trilobytes (just repeating my previous post now).

    But even something that is dying overall could be growing in another sense. Gene flow and the like have generated new varieties that were not visibly present at the Cambrian Explosion. Also organisms would not have displayed certain inherent potentials they had until migrating to an environment where those traits were needed. So you would have to look at the unfolding history of life. Its not as if you are born (or rather conceived) and then immmediately start growing old with everything down hill from there.

    Should not I naturally expect to see more genetic Diversity for sub-speciation, events, at least sometimes if Darwinism is true?

    It seems there would have to be, unless the Cambrian explosion were just all of life in its grand potential just materializing instantaneously, and simulatentously appearing across the planet in mature forms and at peak population levels.

    w/ apologies if I’ve missed some of your points.

  50. 50

    Junkyard,
    Maybe I should make it clear what I am arguing for. I am arguing for the Theistic ID/GE mo^del which will hold that a single male and female parent species (kind) is created by God with all inbuilt ability for variation of kind built in and that once God has created the species (kind) and He does not “tinker” with it anymore after he created it. Letting nature take its course with Genetic Entropy, so to say.
    So we have a overall mo^del to make predictions with. What predictions can we make with this mo^del? Well we can infer quite a lot actually. We can infer rapid environmentally driven adaptations that will all come at a cost of the original information in the genome of the parent species i.e. loss of Genetic Diversity with sub-speciation events. We can predict that sub-species will have less ability to sub-speciate than the original parent species did. We can predict that any naturally occurring mutations to the parent species genome will be detrimental to the overall complexity of the genome even though the “loss of information” may be beneficial for adaptations. We can predict that the longer God does not touch His creation and the longer “nature” alters the genome the more likely the species will lose variability (adaptive flexibility) and the more likely it is the species (kind) will go extinct.

    I probably left a few predictions out but this should be basic outline of the Theistic ID/GE mo^del.

    Well what does the fossil record overwhelmingly say?

    “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)

    The key mystery that the mouflon (parent) sheep surprised evolutionists with is no surprise to this .
    As well junkyard, you seem to be stuck on a Cambrian mo^del for some sort of possible introduction of information from an “outside source”. Yet I point out that this position is not sufficient to explain the fossil record as well as all other overriding evidences.

  51. The Modern age with all of its horrors was based on the notion that men could dispense with God and make their own happiness.

    It has been all down hill since the “Enlightenment” when men decided all they needed was “reason”. I suppose it is wishful thinking to want to go back to before those days.

  52. BA77

    I have Spetner’s “Not By Chance” too. Didn’t care for it near as much as Genetic Entropy. Sanford’s book and hypothesis is very important IMO. You can plug any baseline mutation rate into it instead of accepting the one Sanford worked with. Using the commonly given 1 copy error per 10^9 base pairs for eukaryotes catastrophic genetic entropy happens at about the rate it’s seen to happen in the fossil record. The $64,000 question is still why are ANY large genomed eukaryotes still alive and how did they get here in the first place.

  53. Rates of mutation are crudely esitmated right now, partly because of the extreme expense of gene sequencing…

    The first cut at sequencing the human genome cost $3,000,000,000

    Solexa technology hopes to allow complete sequencing of an individual at the cost of $3,000

    For humans, estimates for baseline mutation rates involve assuming that humans and chimps diverged x number of million years ago, and the number of nucleotide differences gives an approximation of mutation rates for humans. Bryan Sykes refers to it in his book, Seven Daughters of Eve….

    Sykes placed mito-chondrial Eve at 140,000 years ago. See this review at Salon:Seven Daughters of Eve. But Sykes mutation rates assume the Darwinain story for Human evolution. It is not unreasonable, imho, but it still is not the most accurate measurement, in principle.

    This form of “measuring” mutation rates is critically dependent on evolutionary assumptions (and honesty and accuracy by Darwinian paleontologists). A more direct method would involve taking the DNA of large numbers of parents and their children or grand children.

    A professor at LomaLinda Medical school, Dr. Sean Pitman, MD and colleague of our very own Dr. Paul Giem, MD cited a study HERE where this method [comparing parents and children] was applied. The mutation rates returned were higher than the ones Sykes used by a factor of 20.

    This was done on mitochondiral-DNA, not nuclear DNA, and thus it was cheaper and feasible. However with Solexa technology we might be able to do this with nuclear DNA. A fair statement at this time would be, “let’s make more measurements.”

    In any case, the study Pitman cited appeared in the prestigious scientific journal Nature.

    “The rate and pattern of sequence substitutions in the mitochondrial DNA (mtDNA) control region (CR) is of central importance to studies of human evolution and to forensic identity testing. Here, we report a direct measurement of the intergenerational substitution rate in the human CR. We compared DNA sequences of two CR hypervariable segments from close maternal relatives, from 134 independent mtDNA lineages spanning 327 generational events. Ten subsitutions were observed, resulting in an empirical rate of 1/33 generations, or 2.5/site/Myr. This is roughly twenty-fold higher than estimates derived from phylogenetic analyses. This disparity cannot be accounted for simply by substitutions at mutational hot spots, suggesting additional factors that produce the discrepancy between very near-term and long-term apparent rates of sequence divergence. The data also indicate that extremely rapid segregation of CR sequence variants between generations is common in humans, with a very small mtDNA bottleneck. These results have implications for forensic applications and studies of human evolution.

    The observed substitution rate reported here is very high compared to rates inferred from evolutionary studies. A wide range of CR substitution rates have been derived from phylogenetic studies, spanning roughly 0.025-0.26/site/Myr, including confidence intervals. A study yielding one of the faster estimates gave the substitution rate of the CR hypervariable regions as 0.118 +- 0.031/site/Myr. Assuming a generation time of 20 years, this corresponds to ~1/600 generations and an age for the mtDNA MRCA of 133,000 y.a. Thus, our observation of the substitution rate, 2.5/site/Myr, is roughly 20-fold higher than would be predicted from phylogenetic analyses. Using our empirical rate to calibrate the mtDNA molecular clock would result in an age of the mtDNA MRCA of only ~6,500 y.a., clearly incompatible with the known age of modern humans. Even acknowledging that the MRCA of mtDNA may be younger than the MRCA of modern humans, it remains implausible to explain the known geographic distribution of mtDNA sequence variation by human migration that occurred only in the last ~6,500 years.

    Thomas Parsons,
    A high observed substitution rate in the human mitochondrial DNA control region, Nature Genetics vol. 15, April 1997, pp. 363-367

    The Distinguished professor Michael Lynch in Nature 2004

    Alternative approaches in mammals, relying on phylogenetic comparisons of pseudogene loci and fourfold degenerate codon positions, suffer from uncertainties in the actual number of generations separating the compared species and the inability to exclude biases associated with natural selection. Here we provide a direct and unbiased estimate of the nuclear mutation rate and its molecular spectrum with a set of C. elegans mutation-accumulation lines that reveal a mutation rate about tenfold higher than previous indirect estimates and an excess of insertions over deletions.

    Direct measurements appear not to be exactly in line with molecular clocks, but that’s ok, since we know molecular clocks are busted.

    I see that lab measured rates are 10 to 20 faster than what the paleontologists are speculating from various sources. Anyone with data, feel free to weigh in.

    I think Solexa technology will settle the issue. We’ll just have to wait and see in the mean time…

  54. 54

    Jerry I reiterate this for you:

    I go to genetics and find that a loss of gentic diversity occurs with sub-speciation events (I was actually pleasantly surprised to find this out) Yet, You claim I am somehow cheating with the evidence to say that sub-species have less genetic diversity than a parent species, and to claim this as an overall proof that stays within the primary principle of Genetic Entropy,

    Why do you say this? Is not evolution making the grand claim that random mutations are generating genetic diversity and variability to account for the vast profusion of life we see around us? are not new mutations suppose to be the primary driving force for what is in fact driving speciation events? Should not I naturally expect to see more genetic Diversity for sub-speciation events, at least sometimes if not all the time, if Darwinism is actually true? Does or Does not Evolution actually have the grand power of creating new species of life with new, more diverse, genetic information that you and other evolutionists claim it does? Why must all sub-speciation events that I can find evidence for be accompanied by a loss of genetic diversity if evolution is so obviously true? For you to hold that evolution can create life and then in the next breath say that evolution says all sub-speciation events, that we can currently measure with science, are predicted to come at a loss of Genetic diversity is in fact two diametrically different claims for evolution. You can’t have it both ways, as with bacteria, you must present complexity that is above the level of the parent species to prove evolution true, this has never been done for any speciation event I can find? You tell me that I don’t understand these things, yet if your level of understanding blinds you to these clear and obvious facts , I don’t want to know any of your knowledge for it has blinded you to the truth.

  55. bornagain77,

    You have a difficult time with reading comprehension. You are making up things that I have never said. I suggest you read what I say carefully before making disparaging and sarcastic remarks and creating things in your mind which I did not say and do not hold.

    There is no one here who defends the ID position more than I do so you have to control your imagination and read carefully. Maybe you will learn something.

  56. It would appear that mitochondiral DNA and Y-chromosomes in humans would be subject to Muller’s ratchet. In that sense, Muller’s ratchet can be applied to sexually reproducing species.

    Is that a reasonable statement?

    For small parts of the genome, yes probably. I don’t want to say definitely, because I haven’t followed the mitochondrial evolution literature, so there may be evidence for recombination.

    Of course, this should raise questions about why the other chromosomes haven’t degraded.

    Agreed. I maintain the possibilty that a recent creation of certain life forms is the reason. It is possible the universe is old, but certain life-forms (in their current state) are recent.

    But then what about the Y chromosome? Was that created before the rest of man?

    I’ve got this image of God putting it aside in his workshop for later, and when He gets round to using it, it’s all manky, but He decides to stuff it in anyway.

  57. 57

    Jerry stated:

    “You don’t seem to understand how micro evolution works and what are the basic tenets of it and where are the weak points of the Darwinian paradigm in total. It is not on the genetic side which is where your examples are from. Genetics predicts all the things you are bringing up. The weakness of the Darwinian paradigm has always been on the creation of new meaningful variation which is why the trilobites gene pool became narrower and narrower. That is what the Edge of Evolution is all about.”


    This is what I addressed in post 54
    And exactly How did I misunderstand this?

  58. 58

    Jerry, As for mistaking you for an evolutionists I am sorry. As you can see, I have a hard time maintaining respect for them. Yet, as in the above passage, when I see you defend a evolutionary position that needs no defending, especially when it falls within the primary principle of Genetic Entropy, If it catches my attention, I will point it out to you.

  59. Sal,

    Personally I believe that further designed mechanisms would be required to maintain data integrity over geological time periods. Of course, one could argue that sexual recombination IS that designed mechanism. But I’m of the same opinion as you, that further evidence beyond current estimates need to be gathered before genetic entropy can be accepted.

  60. 60

    Patrick you said;

    “But I’m of the same opinion as you, that further evidence and not just estimates needs to be gathered before genetic entropy can be accepted.”

    As with the 1st and 2nd law (Conservation of Energy and Entropy) flowing hand in hand to establish thermodynamics, I firmly believe that Conservation of Information and Genetic Entropy will flow hand in hand as primary principles guiding biological research. Though, anomalies may come up with Genetic Entropy, as they have come up with Entropy itself, that have to be dealt with, Genetic Entropy as a primary principle for biology will indeed hold as an overriding guide and structure by which to make biological predictions with.

    As a sidelight, I’ve been mulling over the principle of Conservation of Information, in looking at Zeilinger’s work with quantum teleportation. And somewhat apart from the CSI developed by Dr. Dembski, I find this principle of Conservation of Information to run much, much deeper. Indeed it runs into the fabric of reality itself. Dr. Zeilinger’s work with quantum teleportation actually establishes that “information” is do^min^ate of energy/matter! Yet this is very, very peculiar thing, for as James Joule, the father of the first Law of thermodynamics, wrote:

    “It is manifestly absurd to suppose that the powers with which God has endowed matter can be destroyed any more than they can be created by man’s agency.” i.e. Energy can be neither create nor destroyed.

    Yet information is shown to actually “tell energy what to do” by Zeilinger! Thus it is strongly suggested, by the empirics, to actually be primary and preceding to energy. And if energy can be created nor destroyed by man’s agency who are we to think that “information” should be “less than” energy in this attribute.
    Thus is it not reasonable to think that “information”, which is do^min^ate of energy, can be created or destroyed also. IMO this peculiarity found in quantum teleportation necessitates the inference to the “infinite mind of God” to stay consistent with logic and the first law.

  61. Correction”
    And if energy can not be created nor destroyed by man’s agency, who are we to think that “information” should be any “less than” than energy in this attribute.
    Thus is it not reasonable to think that “information”, which is do^min^ate of energy, can NOT be created or destroyed also. IMO this peculiarity found in quantum teleportation necessitates the inference to the “infinite mind of God” to stay consistent with logic and the first law.

  62. bornagain77,

    you said

    “This is what I addressed in post 54
    And exactly How did I misunderstand this?”

    I think you should read some of the comments you made about what I said. My position at all times has been that micro evolution explains all your examples. Micro evolutionary processes make a great design mechanism to handle a world of varying environments and contingencies. It is fitting of a truly great designer.

    To me, Sanford’s ideas will lead to nothing but chaos and since we do not see chaos, but a fairly well ordered distribution of life, one has to look elsewhere for the explanation. I can see no way that genetic entropy leads to the magnificent variety of life we see on this planet. It predicts a continual down hill struggle where selection can never get purchase. To me it is not fitting of a great designer.

    Micro evolution can explain most of the life we see but not all and I see no role yet for genetic entropy that makes sense. This is not to say mutations do not happen or that many are not deleterious but the complete collapse Sanford is predicting seems like looney tunes.

    As genomes are investigated the proof will be in the pudding. Either the genome is largely preserved or it is a rusted out car as Sanford says. It cannot be both.

    And please do not distort what I say. Micro evolution is not macro evolution. ID disputes macro evolution not micro evolution. So the micro evolution part of the Darwinian paradigm is accepted by most of those who support ID.

    You are welcome to think genetic entropy will lead to what has happened on the planet in terms of life’s transitions and extinctions but I do not see it. So I will argue against it till I see better information.

  63. Jerry ,
    Do you believe micro-evolutionary events above the level of virus ever add information (CSI)? If you do, we disagree, if you don’t, then we agree.

  64. That is to save for re-mutations back to original states of CSI.

  65. bornagain77,

    I do not believe that micro evolution has ever added much functional information to the genome. I never said it did. It can refine a genome and lead to a more efficient variant for a new environment based on what is already in the gene pool. It also explains the varying sizes of genomes but this is probably not related to functionality. I happen to believe there is some junk DNA, just how much is debatable, but it is the most obvious answer for the varying sizes of genomes.

    Occasionally micro evolution can add some small things such as a new variant of an allele. I believe there is evidence for a few small changes of trivial consequence but which could affect survival such as color and length of fur or skin color or maybe the processing of some substance through an enzyme change or the anti freeze example of the antarctic fish. I am open to other examples but the Darwinists provide precious few.

    And I believe micro evolution best explains all your examples. It too leads to extinction for most species but for very different reasons. And if the environment does not change much such as for sea creatures there is no reason to expect much extinction as long as the gene pool is big enough.

    There is no naturalistic explanation that makes sense for the appearance of diverse new classes and orders in the world. But after the gene pool is available, micro evolution can explain the families, genera and species just fine.

  66. 66

    Kinda cool off topic video:

    Another very good argument against evolution

    http://www.godtube.com/view_vi.....deed13799b

  67. 67

    Jerry;
    micro-evolution, as you seem to be using it, will fall somewhat as a mechanism within the overall principle of Genetic Entropy.

    Let me try to be clear of how I am using the term Genetic Entropy since it is broader than how Sanford uses it;

    I am arguing for the Theistic ID(CSI)/GE mo^del which will hold that a single male and female parent species (kind) is created by God, for animals, with all inbuilt ability for variation of kind built in and that once God has created the species (kind) He does not “tinker” with it anymore after He created it. Thus, letting nature take its course with Genetic Entropy, so to say.
    So we have a overall scientific mo^del to make predictions and check results with (not a mechanism but a mind you). What predictions can we make with this mo^del? Well we can infer quite a lot actually. We can infer that the original genome of the parent species is optimal. We can infer adaptations of sub-species will all come at a cost of the original (CSI) information in the genome of the parent species i.e. we can infer loss of meaningful Genetic Diversity with sub-speciation events. We can predict that sub-species will have less of a ability to sub-speciate (to radiate) than the original parent species did. We can predict that any naturally occurring mutations to the parent species genome will be detrimental to the overall complexity of the genome even though the “loss of information” may be beneficial for adaptations. We can predict that the longer God does not touch His creation, and the longer “nature” permanently alters the genome, the more likely it is the species will lose morphological variability and adaptive flexibility, followed by the more likely it is the species (kind) will go extinct.

    I probably left a few very important predictions out but this should be basic outline of the Theistic ID/GE mo^del.

    So this is the basic that I start out with, then I look in detail to different studies such as the trilobite study and I find a consistent, tree like, pattern of radiation away from parent species (kind). I look to present day cichlid studies and again I find that the “ancient lineages” have a greater propensity to radiate, plus I find greater meaningful genetic and morphological diversity (photo-receptors in particular) for the “ancient lineages” of cichlids.
    As well I look at the oldest mtDNA evidence for humans (40 to 50k ya) and I find loss of genetic information. Present day study on humans produce same loss patterns. Dogs same, Sheep same, Pigs same etc. etc.
    I look to the overall fossil record and find a burst of radiation from distinct parent (kinds) species with gradual decline in diversity and variability over long periods of time.
    For me this consistent pattern establishes the mo^del as solid and testable.

    and as I told patrick:

    As with the 1st and 2nd law (Conservation of Energy and Entropy) flowing hand in hand to establish thermodynamics, I firmly believe that Conservation of Information and Genetic Entropy will flow hand in hand as primary principles guiding biological research. Though, anomalies may come up with Genetic Entropy, as they have come up with Entropy itself, that have to be dealt with, Genetic Entropy as a primary principle for biology will indeed hold as an overriding principle, guide and structure by which to make biological predictions with.

    As a sidelight, I’ve been mulling over the principle of Conservation of Information, in looking at Zeilinger’s work with quantum teleportation. And somewhat apart from the CSI developed by Dr. Dembski, I find this principle of Conservation of Information to run much, much deeper. Indeed it runs into the fabric of reality itself. Dr. Zeilinger’s work with quantum teleportation actually establishes that “information” is do^min^ate of energy/matter! Yet this is very, very peculiar thing, for as James Joule, the father of the first Law of thermodynamics, wrote:

    “It is manifestly absurd to suppose that the powers with which God has endowed matter can be destroyed any more than they can be created by man’s agency.” i.e. Energy can be neither create nor destroyed.

    And if energy can not be created nor destroyed by man’s agency, who are we to think that “information”,which has the power to tell energy what to do, should be any “less than” than energy in this attribute.
    Thus is it perfectly reasonable to think that “information”, which is in fact do^min^ate of energy, can neither be created nor destroyed also i.e. It is not reasonable to presume that “information” does not exist since it is primary over energy which can not be destroyed. IMO this peculiarity found in quantum teleportation necessitates, warrants, the inference to the “infinite mind of God” to stay consistent with logic and the first law, indeed to stay consistent with what we know for reality as a whole.

  68. bornagain77,

    Rather than comment on each item in your basic model, I will give you off the top of my head some reactions.

    The term “entropy” is one that describes chaos or orderliness. I am not sure it fits your scenario. While mutations are happening and affecting organisms what you are portraying is a very orderly process even if some of the paths are leading to dead ends. This is a very different concept from what Sanford describes which is an inexorable decline to dysfunction. So I would use another term to describe your model.

    The hypothesis that there were two parents in the deep past with all the genomic information is a form of front loading. However, there are some contradictions in such an approach which is why I was never enamored with a front loading approach. Despite what the Darwinists proclaim there is long twisted path that evolution has followed that leads from simple creatures to more complexity as the eons roll on. James Valentine, the dean of paleontologists, talks about the cell types that were present at the Cambrian Explosion and estimates there were about 40 types and that today most mammals have more than 200 cell types. And along with these cell types there is greater complexity in the organisms especially in the nervous systems and mental capabilities.

    So all this complexity must have been hidden in the original two parents or else it was created along the way. This is why I have a lot of problems with front loading. Why all this hidden capability not subject to selection but being preserved for the right ecological event and then all of a sudden it is gone.

    To me the only two alternatives that make sense are a naturalistic process that builds the complexity over time and intervention by some intelligence. I would accept the first if I thought there was any evidence for it. A naturalistic process does not some how disappear but like the rest of the laws of nature continues to lurk at every moment. But no such process is visible even with today’s advances in science to find such a process. And all the forensic evidence points against it.

    So I am left with the improbable explanation that there has been multiple intelligent interventions into our world. Such a process is ridiculed and mocked by anti ID people as the “poof” theory or “fairy tale” theory. It is also criticized as bad theology as it hypothesizes a lesser God than the omnipotent creator of Judeo Christian theology. ID proposes the God who can’t shoot straight as opposed to One who has planned it out from the very beginning and then let it all unfold, Your model is an unfolding model but it has its problems for me like the other front loaded models.

    Joseph, who comments here every so often, used the term “designed to evolve” and I like that but how many times was there a design event is the real question.

  69. Jerry,
    Your treatment of the “basic mo^del” and the lack of respect you have to the depth to which it ties into the other first principles of science, lacks something to be desired, to put it very mildly.
    Entropy as a principle in thermodynamics, not only reflects present “deterioration from optimal” but if fact suggested an original optimal state long before the “Big Bang” was discovered. In fact the most stunning number to come out of the anthropic principle was deduced by Penrose , when he found, what could be termed to be, the initial entropy of the universe to be Ordered to 10^10^123.
    No Indeed jerry, Genetic Entropy fits the bill very well for the principle that empirical science is alluding to.
    As for any more disagreements with you, I respectfully agree to disagree with you and debate this matter with you no more. further.

  70. Does anyone have anything information on whether Sanford’s characterization of inherited linkage blocks is correct? If so this would be yet another torpedo into Darwin’s sinking ship….

    Seriously, guys, Darwin relied on the ability of the good traits and bad traits to be decoupled, but inheritance of linkage blocks would annihilate his theory.

    Please refer to my comment here for background.

    The question is simple, are linkage blocks inherited like genes? If so, this is really bad for Darwinism…..

    I’d appreciate any input on this topic. Many thanks!

  71. 71

    Scordova,
    Sorry buddy, I not quite sure exactly what Sanford is talking about there, but as far as dealing a crushing blow to Darwinism, that was done when ENCODE found preliminary evidence for a 100% severely poly-functional code, thus eliminating the “junk DNA” required for Darwinism to work on paper.

    i.e.

    The human genome, according to Bill Gates the founder of Microsoft, far, far surpasses in complexity any computer program ever written by man. The data compression (multiple meanings) of some stretches of human DNA is estimated to be up to 12 codes thick (Trifonov, 1989)! No line of computer code ever written by man approaches that level of data compression (poly-functional complexity). Further evidence for the inherent complexity of the DNA is found in a another study. In June 2007, a international team of scientists, named ENCODE, published a study that indicates the genome contains very little unused sequences and, in fact, is a complex, interwoven network. This “complex interwoven network” throughout the entire DNA code makes the human genome severely poly-constrained to random mutations (Sanford; Genetic Entropy, 2005; page 141). This means the DNA code is now much more severely limited in its chance of ever having a hypothetical beneficial mutation since almost the entire DNA code is now proven to be intimately connected to many other parts of the DNA code. Thus even though a random mutation to DNA may be able to change one part of an organism for the better, it is now proven much more likely to harm many other parts of the organism that depend on that one particular part being as it originally was. Since evolution was forced, by the established proof of Mendelian genetics, to no longer view the whole organism as to what natural selection works upon, but to view the whole organism as a multiple independent collection of genes that can be selected or discarded as natural selection sees fit, this “complex interwoven network” finding is absolutely crushing, for the population genetics scenario of evolution (modern neo-Darwinian synthesis) developed by Haldane, Fisher and Wright (page 52 and 53: Genetic Entropy: Sanford 2005)!

    http://www.genome.gov/25521554

    BETHESDA, Md., Wed., June 13, 2007 -” An international research consortium today published a set of papers that promise to reshape our understanding of how the human genome functions. The findings challenge the traditional view of our genetic blueprint as a tidy collection of independent genes, pointing instead to a complex network in which genes, along with regulatory elements and other types of DNA sequences that do not code for proteins, interact in overlapping ways not yet fully understood.”

    http://www.boston.com/news/glo.....ed/?page=1

    “The science of life is undergoing changes so jolting that even its top researchers are feeling something akin to shell-shock. Just four years after scientists finished mapping the human genome – the full sequence of 3 billion DNA “letters” folded within every cell – they find themselves confronted by a biological jungle deeper, denser, and more difficult to penetrate than anyone imagined.”

  72. 72
    JunkyardTornado

    ba77: “In June 2007, a international team of scientists, named ENCODE, published a study that indicates the genome contains very little unused sequences and, in fact, is a complex, interwoven network. This “complex interwoven network” throughout the entire DNA code makes the human genome severely poly-constrained to random mutations (Sanford; Genetic Entropy, 2005; page 141). This means the DNA code is now much more severely limited in its chance of ever having a hypothetical beneficial mutation since almost the entire DNA code is now proven to be intimately connected to many other parts of the DNA code.
    .
    .
    .
    http://www.genome.gov/25521554

    It seems a casual reader of the above might assume that the ENCODE project had concluded that the genome is polyconstrained to beneficial mutations and also that they concluded something about Genetic Entropy. But the article which I think you’ve posted maybe a hundred times does not mention the words “mutation” “mutate” or “genetic entropy”. Maybe the ENCODE project had something more specific to say elsewhere about the possibility of beneficial mutations, but not in the article you repeatedly post. In fact, it has the following to say, which I have pointed out before:

    According to ENCODE researchers, this lack of evolutionary constraint may indicate that many species’ genomes contain a pool of functional elements, including RNA transcripts, that provide no specific benefits in terms of survival or reproduction. As this pool turns over during evolutionary time, researchers speculate it may serve as a “warehouse for natural selection” by acting as a source of functional elements unique to each species and of elements that perform the similar functions among species despite having sequences that appear dissimilar

  73. Well Junkyard don’t read it if you read it before DUH,

    Since the authors are evolutionists in the first place and evolution can’t possibly be false in their eyes,(All Hail, to king Darwin) I think their interpretation may be a little skewed and that they will try to find any way possible to say that their nak^ed emperor has clothes on. But hey let’s look at the evidence as it really is: na^ked.
    Darwinism would have died a very natural death at the hands of Mendelian genetics, when the whole organism was taken away from Darwinists for selection purposes, if it had not been for the work of Haldane, Fisher and Wright who formulated the modern neo-Darwinian synthesis. Through obscure mathematics, that most no one really understood, they were able to meld Mendelian genetics with Darwinism. Mendelian genetics had established that specific traits in organisms are passed down through discrete elements of each parent called genes (This fact took away the element of variability that Darwinism needed to be viable as a theory) Yet by “mathematically” showing that individual genes could possibly vary and be selected for or against, they thus saved Darwinism from death. Yet now with ENCODE, Darwinism has to deal with a couple of brand new and bigger problems. One fact is that the Genes are now proved not to be such individual elements which may selected or discarded as NS sees fit, but that they are in fact interconnected in vastly complex interlocking ways with other genes and elements that make them severely poly-constrained to any random mutations (Sanford: Genetic Entropy). Thus, discrete individual genes are taken away from Darwinists as a element for selection, yet Mendelian Genetics still holds solidly in its explanatory power for science. The second thing that is crushing to Darwinists from ENCODE, is that Darwinists required huge sections of the Genome to be considered “Junk DNA” so as to have room do their magical math in and make Darwinism work on paper. But alas for the faithful of the church of Darwin, the large sections of “Junk DNA” that they magically made appear on paper has now disappeared in the empirical evidence of ENCODE.

    If you would rather not believe this simple truth I’ve illustrated I’m sure you can find someone over at PT to obfuscate the crap out of you and make this simple fact disappear and make you believe everything is fine in Darwinland so you can sleep well at night. But as for me, I will tell you the truth, the emperor is as na^ked as a jay-bird and has been ever since he has slipped out of Darwin’s crafty mind..

  74. Does anyone have anything information on whether Sanford’s characterization of inherited linkage blocks is correct? If so this would be yet another torpedo into Darwin’s sinking ship….

    I guess it won’t surprise you to learn that I think he’s wrong.

    The studies he cites give evidence that there are haplotype blocks. This is not surprising – it’s the sort of thing one would expect to see with drift etc. But Sanford goes further, and assumes (with no evidence whatsoever) that these blocks are permanent. We would expect the linkage disequilibrium within these blocks to break down over time. For Sanford’s ideas to work, he would have to show that mutation accumulation would work more quickly than the decline in LD.

  75. 75

    Bob you stated:

    But Sanford goes further, and assumes (with no evidence whatsoever) that these blocks are permanent.

    LOL, A Darwinists saying “with no evidence whatsoever” LOL. Bob it is too early in the morning to make me laugh so hard.

    Well Bob what evidence do we have that the genome is inherently stable and resistant to change:

    Though it is impossible to reconstruct the DNA of the earliest bacteria fossils, that scientists find in the fossil record, and compare them to their descendants of today, there are many ancient bacterium fossils recovered from salt crystals and amber crystals that have been compared to their living descendants of today. Some bacterium fossils, in salt crystals, dating back as far as 250 million years have had their DNA recovered, sequenced and compared to their offspring of today (Vreeland RH, 2000 Nature). To the disbelieving shock of many scientists, both ancient and modern bacteria were found to have the almost exact DNA sequence.

    “Almost without exception, bacteria isolated from ancient material have proven to closely resemble modern bacteria at both morphological and molecular levels.” Heather Maughan*, C. William Birky Jr., Wayne L. Nicholson, William D. Rosenzweig§ and Russell H. Vreeland ; (The Paradox of the “Ancient” Bacterium Which Contains “Modern” Protein-Coding Genes)

    http://mbe.oxfordjournals.org/...../19/9/1637

    Revival and identification of bacterial spores in 25- to 40-million-year-old Dominican amber; (R. Cano)

    Dr. Cano and his former graduate student Dr. Monica K. Borucki found slight but significant differences between the DNA of the ancient 25-40 million year old amber-sealed Bacillus sphaericus, and that of its modern counterpart (sub-species), thus ruling out that it is a modern “contaminant”, yet, at the same time, severely confounding Darwinists since the change is not nearly as great as the Darwinists “genetic drift” (Junk DNA) theory would require on paper.

    But can the slight difference that is found in the ancient amber sealed bacteria to the modern bacteria at least prove that some complexity has been gained by Darwinian Processes in those millions of years?

    Commenting on my inquiry for such a “fitness” test Dr. Cano stated:

    “We performed such a test, a long time ago, using a panel of substrates (the old gram positive biolog panel) on B. sphaericus. From the results we surmised that the putative “ancient” B. sphaericus isolate was capable of utilizing a broader scope of substrates. Additionally, we looked at the fatty acid profile and here, again, the profiles were similar but more diverse in the amber isolate.”
    RJ Cano and MK Borucki

    Thus the ancient parent species of bacteria apparently had a greater level of complexity since it had more of a ability to utilize substrates, though, I must add that Dr. Cano said he is “undecided” as to whether it is definite proof for loss of complexity.

    That seems like pretty solid evidence to me Bob. What does evolution have Bob”? Suggestive similarities of sequences and obfuscating “just so” stories of how hypothetical beneficial mutations produces these changes? Admit it Bob evolutionists have no evidence whatsoever for there fanciful conjectures!

  76. BA77 – I see you went for scorn, and then changed the subject. Does that mean you have no better reply to what I wrote?

  77. 77

    The subject IS stability of the genome!
    If I seem scornful to you so be it, Yet I assure it is actually “non-personal” contempt for your poverty of actual evidence that can withstand scrutiny and thus the lack of reasoned judgment for the matter at hand.

  78. I was replying to Sal’s question about Sanford’s statements about haplotype blocks. Sanford only discusses this in humans. So evidence from bacilli hardly seems relevant.

  79. 79

    Bob I think you know I don’t have to point this out,

    If the genome of bacteria, (which we supposedly came from) is overwhelmingly stable, and even deteriorates, over millions of years, it is indeed revelent and of interest to establishing whether human genomes may also have this type of flexibility required by darwinian conjectures. Variability is a primary foundation of evolution is it not? It appears to me that you are just ignoring the foundational evidence I presented since it is inconvenient for you in this matter. But if you want, we can always go into genetic disorder studies of humans and see if you got any hope there for the “beneficial” flexibility of the human genome that you are required to demonstrate to be considered plausible.


    “Professional evolutionary biologists are hard-pressed to cite even one clear-cut example of evolution through a beneficial mutation to DNA that would violate the principle of genetic entropy. Although evolutionists try to claim the lactase persistence mutation as a lonely example of a beneficial mutation in humans, lactase persistence is actually a loss of a instruction in the genome to turn the lactase enzyme off, so the mutation clearly does not violate genetic entropy. Yet at the same time, the evidence for the detrimental nature of mutations in humans is clearly overwhelming, for doctors have already cited over 3500 mutational genetic disorders (Dr. Gary Parker).

    “Mutations” by Dr. Gary Parker

    http://www.answersingenesis.or.....ations.asp

  80. 80

    How about this study Bob:

    Ancient DNA and the origin of modern humans

    http://www.pubmedcentral.nih.g.....rtid=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

    HMM Bob, stable record for humans presence and the only thing of note to report in changes to the genome is a loss of a mtDNA sequence. (Suggest Genetic Entropy and overall Stability to me)

    And in this analysis of the preceding study

    http://www.godandscience.org/e.....ional.html

    excerpt:

    Overall, the lack of “evolution” for humans over the last 40,000 years stands in sharp contrast to the large differences seen between modern humans and Neanderthals over the same period of time.

  81. Sorry, BA, but how can stability in bacteria be relevant to the extent of linkage disequilibrium (LD) in humans? Their population sizes are much larger (which means LD is slower to build up), and they have little to none recombination (which is one thing that reduces LD).

  82. Mitochondrial DNA doesn’t have recombination every generation either.

  83. I guess it won’t surprise you to learn that I think he’s wrong.

    The studies he cites give evidence that there are haplotype blocks. This is not surprising – it’s the sort of thing one would expect to see with drift etc. But Sanford goes further, and assumes (with no evidence whatsoever) that these blocks are permanent. We would expect the linkage disequilibrium within these blocks to break down over time. For Sanford’s ideas to work, he would have to show that mutation accumulation would work more quickly than the decline in LD.

    Much appreciated Bob for your thoughts. I put the question out because I had reservations about this portion of Sandford’s thesis….

    Once upon a time, I mistakenly presumed that individual nucleotides from paired chormosomes (from mom and dad) re-combined by something approximating the concept of two long rows of nucleotides (one row for one chromosome, one from the other chromosome), and one-by-one a nucleotide was crossed-over from one row to the other. But I was mistaken….

    Then I began to think, we get some genes from one chromosome and then some genes from the other chromosome, where the recombination is more at the gene level than individual nucleotides…

    Now it seems it may be the case that not only are whole genes recombined but sets of genes and regulatory elements in the form of linkage blocks.

    I kept seeing the term “Linkage Disequilibrium” in Kimura’s writings and it’s only in the course of our discussion I’m appreciating what it represented. I generally skipped reading Kimura’s papers on the topic…

    Bob wrote:

    We would expect the linkage disequilibrium within these blocks to break down over time.

    I get the impression from a mechanistic standpoint, we are still learning about linkage blocks. But is there evidences these blocks are hardwired to be recognized as whole units in the genome?

    For example, we view a chromosome as a whole unit, but its individual parts can re-combine. No question there. However, are linkage blocks whole units which tend to resist re-combination of it’s parts?

    Also, are Haplotypes and Haplogroups strongly related to the concept of linkage blocks?

    The term haplotype is a contraction of the term “haploid genotype.” In genetics, a haplotype (Greek haploos = single) is a combination of alleles at multiple loci that are transmitted together on the same chromosome. Haplotype may refer to as few as two loci or to an entire chromosome depending on the number of recombination events that have occurred between a given set of loci.

    In a second meaning, haplotype is a set of single nucleotide polymorphisms (SNPs) on a single chromatid that are statistically associated. It is thought that these associations, and the identification of a few alleles of a haplotype block, can unambiguously identify all other polymorphic sites in its region. Such information is very valuable for investigating the genetics behind common diseases, and is collected by the International HapMap Project.[1][2]

    Many genetic testing companies use the term “haplotype” to refer to an individual collection of STR allele mutations within a genetic segment, while using the term “haplogroup” to refer to the SNP/UEP mutations which represents the clade to which a collection of potential haplotypes belong.[3]

  84. But is there evidences these blocks are hardwired to be recognized as whole units in the genome?

    No there isn’t. They are purely a human invention – the papers Sanford refers to just observe that there are these blocks in the genome where there is very high LD, but there is no evidence that the blocks are the result of any real biological phenomena. It’s just chance that means there has been little or no recombination in them.

  85. 85

    Bob, so evolution is shown not to happen for bacteria for 250 million years, yet we can infer that evolution happens for humans? Please explain your logic Bob! As well, I believe that ancient Human DNA of this nucleotide variety does not yet exist for analysis but may become available soon. So Bob When and if the ancient Human nucleotide DNA does become available, Do you care to make any predictions for what will be found?

  86. Bob,

    Thank you again. However, just as a matter of mechanisms, it is clear human biology is able to recognize information units (like chromosomes and genes), it’s a little hard to believe there aren’t mechanisms that mark the beginning and end of blocks. We can’t just willy-nilly slap half a linkage block into the middle of another and expect this won’t result in disaster at some point….

    There are genetic changes that can affect more than one gene. One such genetic chage is known as recombination, in which two chromosomes, or parts of chromosomes exchange pieces…

    Recombination is not a simple process. We do not yet understand how the breaking of the chromosomes and the swapping of the pieces is done as precisely as it is. We do know, though, that it is controlled by special enzymes that break the pieces, and rejoin the free ends

    not only is it under enzymatic control, it also needs certain special structures in the cell to make it work…
    bio physicist, Lee Spetner
    Not By Chance
    pag 39-40

    We can’t just willy nilly take software modules and cut them in random places and rejoin them in random places. The code blocks and rejoinings need to make sense.

    Thus, analogously speeaking, I have to hold out judgement that linkage blocks can just be broken apart that easily. If we don’t know how chromsomal segments are identified for recombination, isn’t it pre-mature to suggest that linkage blocks aren’t real entitities? Especially in light of high linkage disequilibrium. In fact it appears the HapMap project is couting on the persistence of physical linkage disequilibrium. They use the word Haplotype, but is this not tied to the concept of linkage blocks?

    For example see : Haplotype and linkage block structure in human genome

    For each highly conserved linkage block region, a phylogenetic network can be obtained, and then the phylogeny of different genes can be compared.

    It would appear that at least for “highly conserved” linkage blocks, there is some hard-wiring for its identification as some sort of integrated information unit. Non-recombining linkage blocks do not appear to be purely an artifact of our imagination.

  87. I have a question for those who understand the hapmap project.

    Couldn’t Sanford’s ideas be evaluated by the data in this data base? If Sanford is predicting a constant deterioration of the genome by mutations, shouldn’t we be able to recognize such a pattern? I realize it is a limited subset of the entire genome but every subset should show signs of genetic entropy if in fact it is operating.

    This data base seems to be a fascinating resource but it seems like we will need a primer on just what is in it and how it can be used or what to expect from it.

    I too am interested in what is known about recombination at the gamete level and whether it may be affected by epigenetic markers or other elements so the recombinations are never random. It would seem a random recombination has a potential for causing havoc in the zygote. I am certainly not knowledgeable about this so if these questions sound naive, it is due to ignorance.

  88. …it’s a little hard to believe there aren’t mechanisms that mark the beginning and end of blocks.

    But there is no evidence that the blocks are “real”. They were just areas where there was little or no observed recombination, but that doesn’t mean that no recombination is possible in the blocks. The data sets used only cover a small proportion of human diversity (IIRC the only African data was the Yoruba data), and the blocks may well be split up in other populations.

    We can’t just willy-nilly slap half a linkage block into the middle of another and expect this won’t result in disaster at some point….

    That would be a translocation, and yes it often will lead to disaster.

    But in recombination, the block is being slapped into the middle of the same block – it replaces an almost identical sequence. This happens without any problems – it’s the basis of gene mapping in eukaryotes. Indeed it’s difficult to stop without killing the organism.

  89. jerry – I think the big problem with using the hapmap data to assess Sanford’s ideas is that we would have to have measures of fitness as well. And we would have to have them in a common environment.

    Random recombination causing havoc may not be too big a problem, as long as the havoc is caused early enough, so that the embryo dies very early on in development.

  90. Bob O’H

    I know this is asking an awful lot of a person like you but I think it would be a good idea if you read the book before talking about what’s in it.

  91. 91

    Bob,
    I know mtDNA does not apply to the random evolutionary scenario you are trying to apply here, but as to the integrity of mtDNA as a measure for stability and the warranted inference to the Genetic Entropy we may find in the genome of of modern humans, when compared to ancient Human mtDNA, I found this following site very interesting:

    Ancient DNA (A compilation of DNA haplotypes extracted from ancient human remains)

    http://www.isogg.org/ancientdna.htm#Demasduit

    It is somewhat surprising to me that they are able to gather enough detail, to surmise exactly which race of humans belong to which mtDNA group thus tracing, with accuracy, the timing and geographic origination of each group.

    In fact they were able to debunk the recent “Jesus Tomb” with mtDNA analysis;

    mtDNA Sequences From “The Lost Tomb of Jesus”

    mtDNA extracted from human remains contained in two ossuaries recovered from the Talpiot tomb in Jerusalem; one ossuary labeled “Jesus” and the other labeled “Mariamene e Mara” provided conclusive evidence that the two individuals did not share a common maternal line ancestor.

    Name Haplo Haplotype

    Jesus ? 270G, 278T

    Mariamene
    e Mara ? 290G

    Thus my question Bob, is if mtDNA is successfully being used to trace actual ancestral lineages, why is it not also sufficient evidence to establish the overall pattern of Genetic Entropy we may find in ancient DNA? i.e. why should we infer a complete disconnect in the pattern of loss of complexity from ancient mtDNA since it is in fact such a reliable marker of human ancestry?

  92. Bob O’H,

    Sanford uses the metaphor of a rusted out car to describe genetic entropy and each rusted out car has to be unique in its ping marks of rust and different from its neighbor because the ping marks are mostly the result of random processes. And according to Sanford we are well on our way to being completely rusted out. If the hapmap data showed an order to the data as opposed to a system wide large scale discrepancy of each genome from each other then this would tend to falsify Sanford’s thesis.

    After reading Sanford, I get the impression that each genome will become a pop marked replica of the original genome hundreds of generations in the past but that each deterioration should be unique. Such a pattern of disarray should be discernible whether it is fit or not fit because of the random lack of similarity with other genomes.

    I am not sure how much fitness would affect it because the parent organism was there and theoretically fit because it reproduced and according to Sanford on its way to being rusted out. Such a pattern should show up as one compares genomes. But I am the amateur in this and have no experience with comparing genomes so have no ideas what the problems would be or what to look for or how much differences there are from one genome to the next of the same species.

    Essentially I am just trying to follow the logic of Sanford’s thesis to some logical hypotheses and then look to see whether any real data either supports or falsifies his ideas. The hapmap looks like a convenient set of real data that should be relevant.

    Separate subject – the possible recombination in forming the gamete in humans has 23 opportunities for recombination. How many possible recombinations per chromosome is possible? Is there always recombination for each chromosome or is it random? I am just curious as to what is known?

  93. 93

    Something tells me that, though investigating this subject, we will find that there is indeed an impressive amount of “information” juggling going on in the humans genome, that will be impossible for Darwinism to reconcile to the overall stability of the Genome yet at the same time it will beyond our ability to completely trace to totally natural mechanisms.

    Just a hunch that that is what will be found.

    Psalm 139:13
    For you created my inmost being; you knit me together in my mother’s womb.

  94. Um, Dave, if you mean the Sanford book, I have read it. Would you like to be more specific in your criticism? He does mis-represent quite a bit of the literature, so it might be that you’re relying on his representations to criticise me.

    BA77 –

    Thus my question Bob, is if mtDNA is successfully being used to trace actual ancestral lineages, why is it not also sufficient evidence to establish the overall pattern of Genetic Entropy we may find in ancient DNA?

    Mainly because it doesn’t recombine. So mitochondria don’t get all the advantages of sex. Poor things.

    jerry – if we could perfectly sequence the complete genomes from several parents and offspring, we would be able to see what mutations had occurred. But we’re some way off this, particularly as genotyping errors will look like mutations. But then we would need to look at the fitness, which is going to be difficult. And then we would have to look at how these mutations are selected over several generations.

    a lot of the ideas about the genome being imperfect are well accepted. But a lot of the lethal mutants are rare and recessive, so we barely see them. If I was going to investigate Sanford’s ideas, I wouldn’t use humans, I would use something with a smaller generation time, and preferably something for which we have DNA from several generations. We have that for a few species, but the genotyping technology isn’t good enough yet (too slow and too expensive), so I think we would have to keep on collecting DNA. Which some groups are doing anyway, because it’s interesting for other reasons.

    To answer your other question – many recombination events are possible per chromosome (IIRC, the average is 1. I can’t remember where I saw that, so you don’t have to believe me). Recombination is always (or almost always) between homologous sites, i.e. the same place on the two copies of a chromosome. Sometimes it does go wrong, which can have unfortunate consequences if a vital gene is removed. If its duplicated, it might not have an adverse effect, and indeed might be the start of the evolution of a gene with a new function.

    Recombination is random: there could be more than one recombination event on chromosome. However, the rate of recombination does vary across a chromosome, so some parts tend to have more recombination events than others.

  95. Bob O’H

    re: “Random recombination causing havoc may not be too big a problem, as long as the havoc is caused early enough, so that the embryo dies very early on in development.”

    I wondered why you were talking about genetic problems so severe as to cause the unlucky embryo to abort in the context of Sanford’s book about genetic entropy. Anyone that read and understands what he wrote knows that genetic entropy is all about the accumulation of nearly neutral mutations that are invisible to natural selection. If you read the book then I apologize for insinuating you did not. It must instead be a failure to understand what you read.

  96. Bob O’H
    you stated:

    Mainly because it doesn’t recombine. So mitochondria don’t get all the advantages of sex. Poor things.

    Bob you have not established your case for your disconnect in logic, since sequential DNA is supposedly foundational to diploid DNA in the evolutionary scenario. I have established that Genetic Entropy is currently detectable at the base level of DNA organization for ancient bacteria and for ancient human mtDNA and you have not provided any reason why this pattern cannot be extrapolated to diploid DNA other than to say “sex” is not involved.

  97. Bob O’H,

    So just to clarify. If the recombination takes place in the middle of a gene it most often means that the new gene is viable but potentially different from either the mothers or fathers gene. It is just the combination of the parent’s gene, the first part coming from one parent and the second part coming from the other.

    I can imagine all sorts of things going wrong but also this is possibly the creation of a new allele that has never existed before. Is this an accurate observation? Sorry to be a pest, but this is interesting.

  98. Regarding the Y-chromosome, is there re-combination there? It would seem, that notwithstanding the issues of linkage blocks in other chomosomes, the Y-chromosome appears to stand out in terms of linkage block preservation. It would appear genetic entropy and Muller’s ratchet must surely be present in Y-chromoses.

    Bob OH:

    As far as I’m aware, the X chromosome can recombine. The Y chromosome can’t, which is probably why it’s so small and scrappy – it has suffered from genetic entropy. In some species, the Y chromosome (or its equivalent) is simply missing.

    As an aside, there are an intersting questions about the Cohen Haplotype and Y-chromosomal Aaron. See: Y-chromosomal Aaron.

    Is this evidence of the persistence of linkage blocks in Y-chromosomes?

    Does it seem reasonable that linkage blocks exist and persist in Y-chromosomes?

  99. With respect to my ideas about front-loading, I believe that a large number of critical mutations in the human lineage were non-random and happened in a punctuated sort of way over a few generations, and then stablized.

    I believe variety of various racial and other features arrived suddenly, after which there was relative stability and lack of major innovation thereafter. Front-loading (in the creationist sense, not in the more general sense like Mike Gene and others) for humans happened over limited time spans. That is my speculation, and I could of course be very wrong…I have been wrong in the past.

    That said, let us suppose we have persistence of linkage blocks after the front loaded event. That would make the detectability of things like the Cohen Haplotype feasible.

    But I should point out, a front loading over a short period of time would create a hierarchical structure in patriarchal lines.

    One patriarchal hierarchy that could be confirmed by studying Y-chromosomal linkage blocks and haplotypes would be the one outlined in The Table of Nations.

    We know that the top part of the hierarchy is today beyond dispute. We call the top part “Y-chromosomal Adam”. Creationists believe “Y-chromosomal Adam” to be Noah. But let us suppose how the hierarchy plus limited front loading might by confirmed.

    “Y-Chromosomal Adam” should have 3 major lineages. Each of those 3 lineages has its own hierarchical charactersitcs, and those can be confirmed….

    We will see. In the mean time, I would like to hear data about the persistence of linkage blocks in the Y-Chromosome.

  100. Dave – nearly neutral mutations would not “cause havoc”. Causing havoc is what jerry was asking about, and that’s what I was responding to.

    BA77 – for a start the Muller’s ratchet argument doesn’t work with recombining DNA, and secondly the recent evolution of sex theory suggests a difference. And if you want empirical evidence, compare the deterioration of the y-chromosome with the autosomes.

    jerry – No need to apologise, you’re asking decent questions! You’re exactly right (even down to the “things could go horribly wrong. A deletion or insertion of a single base would usually nicely destroy the function of the gene).

    Sal –

    Is this evidence of the persistence of linkage blocks in Y-chromosomes?

    Yes. The lack of any evidence for recombination.

  101. With respect to recombination in animals, there are at least two ways to look at geneome evolution:

    1. A front-loaded “explosion of diversity” followed by a stable period where few new alleles are introduced into the populations

    2. a constant steady stream of new alleles into the population…..

    The creationist front-loaded hypotheses are represented by Spetner’s NREH, or Ashcraft’s homologous recombination.

    Aschraft supposes a spurt of homologous recombination. See: Evolution God’s Greatest Creation.

    I’m not saying anyone is right, merely pointing out we might be able to falsify certain ideas with more sequences and data mining. The data appear to support a front-loaded “explosion of diversity” followed by a stable period.

    It would be a good area of investigation if the genomic data actually falsify a gradualist introduction of new alleles, versus a more punctuated evolution. Punctuated evolution would favor front loading.

  102. 102

    scordova, as far as the divergence of races in humans we have fairly good overall evidence that this is the result of Genetic Entropy (culling of preexisting information) and not the result of information being added.

    see subtractive color mixing

    http://en.wikipedia.org/wiki/Subtractive_color

    as well as what can tentatively be called the loss of “front loaded” genetic diversity.

    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.”

  103. scordova, as far as the divergence of races in humans we have fairly good overall evidence that this is the result of Genetic Entropy (culling of preexisting information) and not the result of information being added.

    I’m reluctant at this time to presume genetic entropy is the cause of all evolutionary events. Personally, and this is a speculation, the correct model of evolution, imho:

    1. Special Creation
    2. Front Loaded Events
    3. Genetic Entropy

    For example, creationists think that Dogs, Foxes, Jackals, Wolves, etc. descended from a common ancestor. Are these varieties the result of genetic entropy or front loading. I’d argue they are the result of front loading. Genetic entropy is not the appropriate model for how these varieties came about. That’s my opinion at this time, I could of course be wrong.

    I just don’t see that the emergence of Dogs, Foxes, Wolves, and Jackals is the result of a disasterous set of genomic mistakes….

    What will be important is whether the genomes suggest punctuated explosion of alleles which was not repeated ever since. This would confirm front-loading of alleles….

    The more general Front-Loaded evolution which some subscribe to (like Mike Gene, DaveScot, possibly Mike Behe…) involves the front loading of major body plans or big divisions of biology. My focus is on a more recent front loaded event of alleles, not majro body plans….

    I would be interested in how we can test the hypothesis of allele front loadiing followed by genetic entropy after the alleles de-repressed (to use John Davison’s terminology) into the populations…I think the Y-chromosomal data in humans and comparable studies in animals will accord with allele front-loading followed by gradual increase in genetic entropy.

  104. 104

    Well scordova,
    again the way I am using Genetic Entropy is consistent with Theism in that

    a.
    Special creation of a optimal genome for a undetermined parent species (Kind) (This satisfies Conservation of Information requirement)

    b.
    A fairly rapid unfolding of “front-loaded” diversity and variability that would stay within the overriding principle of Genetic Entropy by decreasing “meaningful” genetic diversity (information) of parent species genome. i.e. (any decrease from a less than optimal genome, from any method, is still within the overriding principle of Genetic Entropy)

    c.
    a long slow decline in within species, and within kind, variability and diversity. (This also stays within the overriding principle of Genetic Entropy, but the main mechanism for this is the actual decay of the genome from deterioration of its integrity.

    So do our mo^dels mesh now scordova?

  105. 105

    I forgot the last part of Genetic Entropy,

    d. eventual extinction of all species of the kind from “genetic meltdown”.

  106. jerry asked: “It would seem a random recombination has a potential for causing havoc in the zygote.”

    bob answers: “Random recombination causing havoc may not be too big a problem, as long as the havoc is caused early enough, so that the embryo dies very early on in development.”

    The question and answer are irrelevant to Sanford’s genetic entropy hypothesis. Don’t confuse people. Sanford’s “genetic entropy” is the accumulation of nearly neutral mutations which are by definition individually invisible to natural selection. As these accumulate the reproductive population becomes weaker and weaker until something happens (a new predator, climate change, etcetera) that the weakened species can no longer survive and booya -they become quickly extinct, disappearing from the fossil record in an eyeblink of geologic time.

  107. Dave,

    My question had nothing to do with Sanford or his ideas. I was just interested in what recombination does and how it works and how it might affect a gamete.

    After reading Sanford and watching the dialogue here, I am not too big a fan of genetic entropy. That could change if someone presented evidence of the deterioration that Sanford predicts. This should come in the near future as Salvador and Bob say, the mapping of genomes gets cheaper and faster.

  108. Oxford Geneticist Bryan Sykes

    Male infertility is on the increase. Under the microscope a high proportion of human sperm from what we would consider a normal human male are already visibly deformed. Sperm counts are falling dramatically though there are other contributory causes as well as Y-chromosome decay. The Y-chromosome has been decaying for a very long time and will continue to do so; and we have to expect a progressive decline in male fertility as these injuries accumulate. One by one Y-chromosomes will disappear and eventually only one remains. when that chromosome finally succumbs, men will become extinct.

    page 293
    Adam’s Curse

    ‘But when?’ I hear you ask. Before I answer that question — before I even attempt an estimate — I must urge you not to confuse what I see as the inevitability of the process with my confidence producing an accurate figure. So here goes. For the purpose of this estimate, I am going to assume that nothing else come into it other than the rate at which we already know Y-chromosomes are deaying at the present time. Let us begin with the figure of 7 per cent for the proportion of infertile men, and take it that 1 per cent of all men are infertile because of a Y-chromosome muation. These mutations must have occurred in the fathers of these men, since by definition their fathers were not infertile. So these mutations are the last straw as far as that particular Y-chromosome is concerned. It cannot be saved except by artificial means. Lots of other, less serious, mutations that decrease, but do not eliminate, male fertility will also have occurred in all men. In wartime, casualty lists always include more wounded than dead, and genes under attack from mutation are no different. For the sake of simplicity, I will also take 1 per cent as the rate at which wounding Y-chromosome mutations occur in male germline cells. When passed on to their sons, these mutations make them not clinically infertile but less fertile than their father. Taking these figures, and in the absence of any other influence, the fertility of the whole population will decline by 0.1 per cent (1 percent of 10 per cent) in each generation owing to Y-chromosome decay alone. What effect does that progressive delcine have in the futhere? I won’t bore you with the formula, but have a look at the graph in figure 6.
    Adam’s Curse

    The graph in figure 6 is a simple exponential decay.

    On this estimate, the fertility caused by Y-chromosome decay drops to 1 per cent of its present level within 5,000 gemerations.

    Hence extinction happens in 100,000 years. The uncomfortable conclusion of genetic entropy is not a happy one if ture. But what are the facts independent of our biases?

    It appears Muller’s ratchet applies to the Y-chromosome. A reasonable question is why are we still alive in light of these considerations?

  109. “A reasonable question is why are we still alive in light of these considerations?”

    A reasonable answer is that there is something wrong with the theory. We are looking at man in a lot of our examples but the 300,000 beetle species seem to be doing fine except where man encroaches.

    What species are deteriorating out of existence due to genetic problems? What are examples or counter examples? So far all I have seen are Sanford’s arguments.

  110. 110

    I gave this earlier of a present day example of the Genetic entropy mo^del being obeyed.

    African cichlid fish: a model system in adaptive radiation research

    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,

    Thus the younger lineages of cichlids are severely constrained in their ability to radiate while the most ancient line retains its ability.
    This fits perfectly with the previously stated model in post 104,

    I point out that it shows both loss of genetic diversity as well as a tangible, undeniable loss of morphological variability that does not have to be deduced such as human skin color does..

  111. 111
    JunkyardTornado

    ba77:
    “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,
    Thus the younger lineages of cichlids are severely constrained in their ability to radiate while the most ancient line retains its ability.”

    The only way genetic entropy would be demonstrated is if the ancient lines were losing abilities as well.

    scordova (#108):

    So in the past 150 years the world population has been increasing geometrically, while the fertility rate has been decreasing 0.1% every twenty years. If a male’s Y chromosone is defective, it takes whatever genes he has out of the gene pool. But it opens a niche for someone else, with no necessary loss in population at all. Don’t know how the 100,000 years figure was derived, but it seems a decrease in fertility could only have an adverse affect indirectly, by increasing the homogeniety of the gene pool (extremely gradually), thus making it susceptible to a catastrophic event. (Or is that what you were saying). It seems ultimately you could have a world of disease-free identical clones.

  112. There are some DNA repair mechanism on the human Y-chromosome. Nevertheless:

    Oxford geneticist Bryan Sykes in the UK Gaurdian: Do we need men

    Of all our chromosomes, it is the only one that is permanently locked into the germ cells of men, where the frenzy of cell division and error-prone DNA copying required to keep up the daily output of 150m sperm creates the ideal conditions for mutation. And it shows. Seven per cent of men are infertile or sub-fertile and in roughly a quarter of cases the problem is traceable to new Y-chromosome mutations, not present in their fathers, which disable one or other of the few remaining genes. This is an astonishigly high figure, and there is no reason to think things will improve in the future – quite the reverse in fact. One by one, Y-chromosomes will disappear, eliminated by the relentless onslaught of irreparable mutation, until only one is left. When that chromosome finally succumbs, men will become extinct.

    But when? I estimate that, at the current rate, male fertility caused by Y-chromosome decay will decline to 1% of its present level within 5,000 generations – roughly 125,000 years. Not exactly the day after tomorrow – but equally, not an unimaginably long time ahead. Unless something changes in the way we breed, women will vanish too and Homo sapiens will disappear in the next 1-200,000 years. But is extinction inevitable?

    Plenty of species a lot older than our own are still going, so how is it that they are not vulnerable to extinction by the same process of Y-chromosome decay? They will all eventually face the same challenge and I suspect that many species have already gone under for this very reason. Some, however, have found a way round their death sentence.

    One strategy is to recruit genes on other chromosomes to take over the job of male development. It is a race against time. Can a species get all the genes it needs off the Y-chromosome, or recreate them elsewhere, before the chromosome finally vanishes? Always the last gene to go will be SRY, the male master switch itself. We know it is capable of smuggling itself onto another chromosome – the evidence lies in the rare cases of males who have no Y-chromosome.

    Lots of species may have tried variations on this theme to avoid extinction, but it seemed that none succeeded until, in 1995, researchers found a mammal that had managed to escape this fate. When they looked at the chromosomes of a small burrowing rodent called the mole vole, Ellobius lutescens, which lives in the foothills of the Caucasus mountains, they discovered that the male voles didn’t have a Y-chromosome. Neither, it transpired, did they have a master SRY gene either. This inconspicuous little rodent has managed to activate a gene relay one or two stages down the line from SRY. And only just in time. The mole vole Y-chromosome has now completely disappeared. The vole is now safe from Y-chromosome-driven extinction, the only mammal species known to have succeeded in getting itself out of danger.

    Regarding the Y-chromosome in other species.

    Also Decoding offers view of humans and hairier cousins

    The 16 X-related genes are present in only single copies. Page and his colleagues thought the chimpanzee genome might show how they were protected. To their surprise, they report in Nature, the protection was not there.

    The chimp Y chromosome has lost the use of five of its 16 X-related genes. The genes are there, but have been inactivated by mutation.

    David Page

    and Rodent Y chromosome TSPY gene is functional in rat and non-functional in mouse

    Recombination is believed to prevent genetic deterioration in sexual populations because it allows conservation of functional genotypes by removing deleterious mutations. Moreover, evidence that non-recombining segments of a genome deteriorate is provided by genetic experiments in Drosophila and yeast. Y chromosomes generally do not recombine along most of their length, and thus Y chromosome genes, despite having been selectively maintained for their function, could be lost from the genome. Here we present definitive evidence that functional Y genes can be lost from the mammalian genome.

  113. 113
    JunkyardTornado

    scordova:

    I may have misunderstood, I don’t know. I believe the ratio of male to female births is 1.06 to 1. Apparently there’s been a drop in that the last few decades, but I don’t suspect that’s “genetic entropy” kicking into high gear. This y chromosome problem will be manifest once we start seeing like 45% males to 55 females in the general population with that ratio continually decreasing, I guess. I’ll just lurk for a while.

  114. 114

    Off topic:

    In mulling over the law of “Conservation of Information”

    I believe the final “Conservation of Information” law may look something like this,

    All information that can exist does exist completely separate of the physical realm in the transcendent realm and cannot be created or destroyed in the physical realm, but can only be “borrowed” and/or imprinted from the transcendent realm.

    The key for me in this deduction, to the law, is “transcendent information’s domin^ation of energy” (telling energy what to be/do) in Zeilinger’s teleportation experiments.

    Since the first law states energy can be neither created nor destroyed, anything having dominion over energy must, of necessity, possess even greater qualities than energy. Therefore information, in the least, cannot be created or destroyed either.

    This inference to the “Conservation of Information” warrants even further reference to the “Mind of God” when the foundation of the created universe, we are living in, is shown not to be a “dead” chaotic foundation of “chance”, but is shown, and now known, to be a exceedingly stable transcendent foundation that exhibits intent, purpose and foresight.

    Thus since we can deduce intent, purpose and foresight in the foundation of the universe, This means the transcendent information is “alive”.

    Now it is fair to say this:

    Since transcendent information can not be created nor destroyed, and since “information” exhibits dominion and purposeful control of the “material realm”, then we may now say that all “information” that can possibly be “known” is already “known” by the “infinite mind of God”.

  115. jerry

    Millions and millions of extinctions in the fossil record and hundreds in recorded history are evidence of genetic entropy. The real question is why do an exceedingly small percentage of germ lines in higher plants and animals avoid extinction for hundreds of millions of years when almost all their peers go belly up in a comparatively short amount of time? My money says that we’ll eventually discover that the answer is anticipated in intelligent designs created by human agency – some form of highly protected core code.

    The beetle example is poorly thought out. The smaller the genome the less susceptable it is to genetic entropy and/or the larger the number of progeny the less susceptable it is to genetic
    entropy. This is because the number of individuals whose genome is a flawless copy of its parents’ genome rises in proportion with both those factors. Nearly neutral mutations don’t accumulate as quickly, if at all, in that case. This explains why P.falciparum is still here and unchanged even after undergoing more replications every year for the last 50 years than all the mammals that ever lived. I calculated that 95% of them are flawless copies of their parents. But they’re such prodigious replicators that the other 5% allows them to quickly adapt if needed (within The Edge of Evolution, of course) to a wide range of environmental insults. It also explains the recent finding of why 250mya bacteria are virtually identical at the genetic level to modern descendents (BA77 has been pointing this out repeatedly recently). Beetles, on average, have much smaller genomes than mammals and reproduce in much larger numbers.

  116. Dave,

    “Millions and millions of extinctions in the fossil record and hundreds in recorded history are evidence of genetic entropy.”

    I don’t think your conclusion follows. Micro evolution could lead to the same phenomena of extinctions. Each sub population is more limited and so is the overall population if the environment changes dramatically. Each culls the gene pool so when a new environmental change happens the species is even more subject to extinction.

    I would have no problem with genetic entropy if it could be showed it is actually happening. This is not some thing in the deep past but hypothesized to fill all life currently on the planet.

    We are within a few years of developing the data bases to investigate genetic entropy. We are also within a few years of investigating the structure of all the species around and verifying or falsifying that nearly all appeared by micro evolutionary processes.

    One thing that could frustrate Sanford’s hypothesis is that most of the genome is useful and not subject to too much mutation and thus preserved. So the nearly neutral mutations are not that neutral at all but in reality harmful. Also if genetic entropy was the cause of all the past extinctions then why did it stop. There is no evidence that any or many of the recent extinctions has to do with genetic deterioration, Thus, as macro evolution has seemed to disappear from the planet so has these mass extinction events. This is not a finding that is consistent with the continual battering of the genome hypothesized by Sanford. We should see a constant parade of extinctions and also some very sick current genomes ready to go belly up.

  117. jerry

    The estimated average tenure of vertebrates in the fossil record is about 10 million years. There are about 50,000 different ones alive today. If you bother to do the math it means we should expect to see one vertebrate species go extinct every 200 years. We’re seeing far more than that in recent history not all of which can be attributed to catastrophic environmental stress (man-made or otherwise). Individual vertebrates, if they don’t get killed by an accident, eventually die of old age. Vertebrate species are no different – if not an accident they just get old and die too.

  118. 118

    scordova,
    That was interesting,
    I get the impression that recombination may allow many “stopgap” measures in order to preserve functionality, but these examples you cited all seem to be done because of “entropic” necessity not evolutionary novelty.

    “This inconspicuous little rodent has managed to activate a gene relay one or two stages down the line from SRY. And only just in time.”

    It is like the function is saying “Hey it is time to jump ship into a “leaky” lifeboat” This is all fine and well with the Genetic Entropy principle, and in fact may explain “why we have not 100 times over”.

  119. Dave,

    We will know in few years a lot more about comparative genome structures. By then there may be a host of new theories about extinctions or lack of and their causes. And a lot more about potential paths species took over time.

    One thing I don’t expect is a naturalistic explanation of macro evolution to appear but expect to see more evidence that there are very small differences between what we call species, genera and families. In other words Darwinian micro evolution will be king but Darwinian macro evolution will still be dead in the water.

    And the real mystery is where did it all come from in the first place.

  120. 120

    Jerry,
    I’ll give this one more try:

    you stated:

    “Darwinian micro evolution will be king”

    All evidence that I have ever seen presented on this blog, and elsewhere, for evolution of even the “micro” variety always turns out to “micro-evolve” at the cost of a “parent” genomes complexity. Even the trumpeted HIV protein/protein binding site, which Darwinists tried to use to defeat “The Edge” with, came at a far greater cost of complexity for the life of the host it infected (people) than it ever gained in its hypothetical march to become a life-form itself. Thus even Darwinists most prime, and pathetic, example of a gain of information actually stayed well within the principle of Genetic Entropy, since it actually destroyed far more complexity than it ever gained. This “Entropic” fact; The fact that there has never been a clearly demonstrated gain in complexity of a sub-species over its parent species is what falsifies Darwinian evolution as far as science is concerned. The fact is that we consistently have the exact opposite of evolution going on even when adaptive advantages are gained by the organism. We have a constant slow methodical march in loss of complexity for life forms, even though a “mutation” may sometimes happen that is “compensatory” in its effect. Even the compensatory mutations of the organisms never achieve the level of complexity equal to the complexity of the parent species, unless, of course, it is just a “remutation” back to its original state.

    This consistent, demonstrated, loss of complexity from all “parent species” studied, ties semi-directly to the 2nd Law of Thermodynamics, Thus ID is now able to make almost a direct reference to a foundational principle of physical science. As well Genetic Entropy makes it crystal clear that life is NEVER evolving but is slowly decaying and dying, and will continue to be on this long slow downhill march as long as God continues not to directly intervene.

  121. It appears Muller’s ratchet applies to the Y-chromosome. A reasonable question is why are we still alive in light of these considerations?

    Because we have an X chromosome?

    If the sex chromosomes started off as homologous, then the X chromosome would carry the same genes. Even as the Y chromosome decayed, the same genes would still be present on the X chromosome.

  122. jerry wrote:

    A reasonable answer is that there is something wrong with the theory. We are looking at man in a lot of our examples but the 300,000 beetle species seem to be doing fine except where man encroaches.

    I’m not so sure.

    There are beetle species that are wingless and even missing testis:

    Absence Asymmetry: The Evolution of Monorchid
    Beetles

    ABSTRACT Asymmetrical monorchy, or the complete absence of one testis coupled with the presence of its
    bilateral counterpart, is reported for 174 species of the carabid beetle tribes Abacetini, Harpalini, and Platynini (Insecta: Coleoptera: Carabidae) based on a survey of over
    820 species from throughout the family. This condition
    was not found in examined individuals of any other carabid
    beetle tribes, or of other adephagan beetle families.

    One monorchid taxon within Platynini exhibits symmetrical
    vasa deferentia at the beginning of the pupal stadium, suggesting that developmental arrest of the underdeveloped vas deferens takes place in pupation. The point
    at which development of the testis is interrupted is unknown.

    Complete absence of one organ of a bilateral pair—absence asymmetry—is rarely found in any animal clade and among insects is otherwise only known for testes in the minute-sized beetles of the family Ptiliidae, ovaries in Scarabaeinae dung beetles, and ovaries of some
    aphids. Based on current phylogenetic hypotheses for
    Carabidae, testis loss has occurred independently at least three times, and up to ?ve origins are possible, given the variation within Abacetini. Clear phylogenetic evidence for multiple independent origins suggests an adaptive or
    functional cause for this asymmetry.
    interaction among the internal organs of these beetles,
    possibly due to selective pressure to maximize the comparatively
    large accessory glands found in these taxa.

    However, as the ordering of these evolutionary events of testis loss and accessory gland size increase is not known, large accessory glands might have secondarily evolved to compensate for a decreased testicular output.

    Asymmetrical loss of a plesiomorphically paired
    organ is rare among bilateral metazoan animals. Among vertebrates, such losses are largely restricted to snakes or snake-like animals, where one
    or the other lung has been reduced during evolution of various lineages (Bellairs, 1970), and to birds, where most taxa are characterized by the loss of one
    ovary (Kinsky, 1971). Monorchy, or the presence of only one testis, is reported for many nonvertebrate

    Notice they have to just attribute even a degenerative loss to natural selection — “survival of the sickest”. To them, it can’t possibly be that selection doesn’t work. But even granting selection selects for genomic deterioration, how can this be an argument against genetic entropy?

    Also SPECIES IN DECLINE

    Large numbers of Britain’s 4,000 beetle species are thought to be declining in abundance and range.

    Even if man is partly the cause, it shows that Darwinian selection doesn’t work to evolve a population out of danger due to environmental stress. It demonstrates Darwin’s false assumption that species will always be given enough time to evolve.

    I think environmental wipeouts are fair arguments in favor of genetic entropy, where environmental wipeouts are an extreme form of genetic entropy.

    Darwin was overly optimistic that the environments wouldn’t be so harsh as to actually destroy more species than it creates….he has zero evidence to support that optimism.

  123. Salvador,

    I use the 300,000 beetle species as an example a lot not because I am enamored with beetles but because it is such a large number and it begs the question of why so many. It is a form of hyperbole to make a point. I probably wouldn’t know a beetle from most other bugs that inhabit the flower beds and trees around where I live.

    So if in fact there are 300,000 beetle species, why are there so many? (I got the 300,000 from Wikipedia; they use 350,000 in their current article) Given our understanding of mutations and genetic problems it is not unusual that a couple of them are having problems. So pointing out the problems with a few is really an admission that most are doing well. This does not in any way support Sanford’s ideas. We would need a lot more than that. Those who support Sanford here are very much like the Darwinists. A lot of rhetoric but few examples. I find it quite similar. Sanford sounds reasonable but so does Darwin till you look at the details.

    Micro evolution predicts that many lines will reach extinction because of the basic processes of selection and drift and environment change. It now includes a whole host of other processes that affect the genomes of gametes and embryos.

    All I am saying is that micro evolution is a more likely explanation of the declines and extinctions we see and also for the thrivings that we also see. If one wants to deny that there is a lot of life thriving in a potpourri of wild environments then they are in big time denial. The pattern of life across the planet fits the micro evolution paradigm. It doesn’t explain everything but it explains a lot. Maybe it won’t be as robust when more about the genomes are understood. And yes it is attributable to Darwin and those who expanded on his theories. Darwin’s problem and his successors is that like many men before them, they became arrogant in their knowledge and thought that their ideas explained everything. Consequently they shoe horned everything into their pet theory and it has failed miserably. But that does not mean that basic selection is not working on what the genetic processes produce in the world including deterioration of some or a lot of genomes. Darwinian macro evolution is a flop but like the life on the planet, Darwinian micro evolution is thriving,

    And before anybody accuses me of not supporting ID, forget it. There is no explanation for the origin of the original gene pools and to me micro evolution is God’s gift to us and a masterful process worthy of a great designer after these gene pools came into existence. But science and life march on and as we learn more from future mappings of genomes we will probably revise just how it works.

  124. jerry:

    just to go back to an old discussion. We probably don’t know the genones of your 300000 species of beetles. But can you explain by a microevolution model the known differences between the two best known worms?

    We know almost everything about C. Elegans, and very very much about its companion species, C. briggsae. The two animals are amongst the simplest multicellular beings, and they are almost indistinguishable. Still, they are two different species.

    Here are some data.

    Genome length:

    C. elegans: 102 Mb
    C. briggsae: 104 Mb

    Protein coding genes:

    C. elegans: 20,621
    C. briggsae: 19,507

    Note: Despite the similarity of the number of genes shared by the two species, C. briggsae has about 800 genes that have not be found in C. elegans, while C. elegans has 1,061 genes that have not been found in C. briggsae (Stein et al., 2003).

    Orthologs:

    The InParanoid database (April 2005 release), using a recent C. elegans gene set, lists 12,858 C. briggsae and C. elegans ortholog pairs.

    Introns:

    There are more introns per gene in C. elegans than in C. briggsae (see Table 1). Comparative analysis, by aligning orthologous protein-coding genes between C. briggsae and C. elegans, revealed 6,579 species-specific introns among the 60,775 introns in the orthologous pairs of protein-coding genes. Roughly two-thirds (4,379) are C. elegans-specific, while one-third (2,200) are C. briggsae-specific, which suggest rates of intron gains or losses of about 0.5 per gene in the 80–110 million years since the split between C. briggsae and C. elegans. This rate is dramatically higher than that of mouse and human, which is 0.01 intron gains or losses per gene in 75 million years

    Gene families:

    Altogether, TRIBE-MCL clustering analysis demonstrated that for gene clusters with five or more C. briggsae and C. elegans genes, there were 202 clusters (corresponding to gene families) with gene number differences of at least 2-fold between C. briggsae and C. elegans (Stein et al., 2003).

    Morphology:

    Morphologically C. briggsae is almost identical to C. elegans. However, as described above, a comparison of the genome sequences between the two species has revealed a significant number of species-specific genes (~2,000 in total; Stein et al., 2003). Hence, an obvious question is: why are these changes not reflected in significant morphological or behavioral differences?

    And so on. All these data are taken from Wikipedia and from the online WormBook. In conclusion, there are certainly many similarities, but also a lot of differences, especially in the genome, between the two species. And we are speaking of two species which are practcally indistinguishable, both morphologically and functionally, and of one of the simplest multicellular organisms. Moreover, there is no simple evolutionary (functional) explanation for those differences, as even the official sources say.

    What do you think we will observe when all your beetles’genomes will be sequenced?

    And, for those who have not noticed, it is useful to remark that those tiny and very “simple” worms have practically the same number of protein coding genes as humans.

  125. 125

    Good post gpuccio:

    somewhat in relation:

    Greatest Mysteries: How Many Species Exist on Earth?

    http://www.livescience.com/str.....ecies.html

    excerpt:

    The National Science Foundation’s “Tree of Life” project estimates that there could be anywhere from 5 million to 100 million species on the planet, but science has only identified about 2 million.

  126. So pointing out the problems with a few is really an admission that most are doing well.

    That’s not correct because the rest might only appear to be doing well because we have such sickly ones. This is like someone trying to tell you you’re well off by listing the excessive misery of others…

    I cited these examples to point out that genetic entropy happens in beetles. Who is to say we won’t find more if we are willing to look.

    I went through the trouble of digging because I didn’t want the readers to walk away with the impression beetles don’t suffer from gentic entropy as well. But consider if such a horrible thing which happened to beetles happened to humans, it would be like missing arms and missing testis…these are powerful examples that natural selection (micro evolution) doesn’t weed out the bad and preserve the good as Darwin erroneously suppposed.

    Why so many beetle populations? If we show that there is not a steady influx of new alleles today as the engine of subspeciations (such as happened in the branching of a common ancestor into dogs,wolves, jackals, foxes), it would imply a front-loaded infusion of alleles that happened over a short time span, or special creation, or both.

    The fittest don’t survive, but rather the sickest (in a manner of speaking, not literally)….
    And if Random selection mechanisms are far more powerful than natural selection, most supposed speciation events in the wild aren’t attributable to Darwinian micro-evolution either! Origin of species via geographic isolation, genetic drift and nearly neutral mutation might be a more valid model (next to front loading and special creation).

    I don’t believe the mutation rates were approximately constant over time, but rather there were times when the mutation rates were explosive — punctuated evolution.

    Nor do I believe that the most important mutations were random, but rather designed. I think there was a major de-repression that happened over a short time span which was not repeated. That is why we will be able to trace the Cohen Haplotype and many other lineages…

    The existence of the well-defined Haplotypes is suggestive of a front loaded infusion of alleles. We might even be able to estimate when this event happened and whether it happened simultaneosly to all species. Why would it happen to all species at once? Perhaps a common environmental stress like a global cataclycsm where extreme chemical and radioactive events (like cosmic radiation).

  127. 127

    Jerry you stated:

    Micro evolution predicts that many lines will reach extinction because of the basic processes of selection and drift and environment change. It now includes a whole host of other processes that affect the genomes of gametes and embryos.

    All I am saying is that micro evolution is a more likely explanation of the declines and extinctions we see and also for the thrivings that we also see. If one wants to deny that there is a lot of life thriving in a potpourri of wild environments then they are in big time denial.

    Jerry micro-evolution, even as you are using it in this “limited” sense is unfalsifiable. You say that it is both the cause of extinction and the cause of the potpourri of life. Yet you have provided no evidence that micro-evolution can generate meaningful information other than to point at the diversity of life and say that it happened.

  128. Following up on Sal’s point about what we’d find (regarding beetles) if we looked:

    Modern Insect Extinctions, the Neglected Majority

  129. gpuccio,

    I am not sure what you are trying to get at. Did these two worms get this way by genetic entropy? Are they the result of massive changes in the genome caused by the accumulation of neutral mutations? Are they both going extinct after 90 million years?

    I am not sure what the point you are making? By pointing to an interesting question, one does not undermine a basic process somewhere else. I am sure if you dig deep enough you will find lots of interesting questions that are not yet solved.

    Are you saying that the two worms could not have evolved through micro evolutionary processes? I did not get that from your post that this was an impossibility. Are you saying they were created that way with all those introns and have essentially remained the way they are now for 90 million years.

    By the way they are not my beetles. I only pick beetles because they represent the largest number of a type of species I could find. As I said, I know very little about them. They are everybody’s beetles and apparently some have some wild capabilities that involve sophisticated biological systems which could not easily evolve through micro evolutionary processes. But for the most part they are very similar but I would expect many of them would have genomes as dissimilar as your two worms despite the similarity. After all, there are after all over 300,000 of them. But so what. It has nothing to do with the point I am making. And if some how their genomes were mapped we might learn a lot as to how species change over time. We could probably see the different path each little variant took.

  130. One thing that I found in the work of Sternberg and Cavenaugh and the rest of the Baraminology study group was that even where the creationists agreed with the evolutionists about particular common ancestors, there seemed to be precisely defined radiations from a common ancestor. The patterns of diversification did not look random! They created a software tool called ANOPA to detect these non-random radiations.

    Johnnyb is more adept at this topic than I. Sternberg and Cavenaugh published the ANOPA work in peer-reviewed literature.

    All this to say, I don’t think Darwinian micro-evolution explains the origin of subspecies, especially the more interesting radiations from a common ancestor.

    Who is to say that mutations (in the front-loaded past) don’t lead to species that are pre-adapted to new environments?

  131. Just to reiterate for the zillionth time. No where did I ever say micro evolution created new information. On some very rare occasions it may create a trivial new capability and if this is information creation so be it. Behe gives the example of the ice fish in the Edge of Evolution. This is new information but it is small and within his edge.

    It will be interesting to see how people distort what I say since few read it closely.

    Salvador,

    you say

    “I cited these examples to point out that genetic entropy happens in beetles. Who is to say we won’t find more if we are willing to look.”

    you have no basis for making the claim that genetic entropy was the cause of the particular problems of the beetles you cited. There is no evidence of this result being caused by massive accumulation of neutral mutations. The result was probably the result of some mutation but this is not necessarily Sanford’s genetic entropy. At best you are speculating like the Darwinists do about macro evolution. And if even this was the case in this particular situation then of what relevance is it unless all the rest of the beetles were also so inflicted. It is interesting why Sanford has to be so defended by many people here.

    Also your citing of random selection is irrelevant because it is a natural process that effects some species events but it does not mean that this is the only thing operating nor is it the main thing operating nor does it mean that after a random selection event that natural selection can not operate. I am not sure what you are trying to get at by invoking it. Are you saying that all speciation events are random. No one will buy into that, It also sounds like an anti ID philosophy to me. We are the result of random processes. I do not buy into that.

    Also what has random selection have to do with Sanford genome deterioration scenario since it is only an occasional thing? I know he mentions it but it seems to be a weakness in his arguments since random events could just as easily go the other way and make it easier for a beneficial mutation to survive. And over time you would expect this to happen millions of times.

  132. Dave,

    Thank you for the link on insect extinctions. Based on the abstract it seems that micro evolutionary processes are the main cause for modern extinction.

  133. 133

    Jerry you state,

    No where did I ever say micro evolution created new information.

    So if no new information is being created, how is Genetic Entropy falsified, since it is semi-directly tied to the second law?

  134. jerry wrote:

    . Based on the abstract it seems that micro evolutionary processes are the main cause for modern extinction.

    If an environmental catastrophe happens and species go extinct as a result, do you classify that as micro evolution?

    I’d classify it as a case of unrecoverable genetic entropy. This is genome “damage” in the extreme.

  135. you have no basis for making the claim that genetic entropy was the cause of the particular problems of the beetles you cited. There is no evidence of this result being caused by massive accumulation of neutral mutations. The result was probably the result of some mutation but this is not necessarily Sanford’s genetic entropy.

    Genetic entropy happens when bad mutations aren’t weeded out and the good mutations aren’t preserved by Darwinian selection.

    I never said genetic entropy was SOLEY a massive accumulation of neutral mutations, neither did Sanford. You’re making a strawman argument.

    Massive near-neutral mutations are part of the reasons for genetic entropy, but there are other issues like random selection and the cost of selection that preclude weeding out the bad even if the deleterious mutations are not neutral. Those are also part of Sanford’s theory…

  136. Also what has random selection have to do with Sanford genome deterioration scenario since it is only an occasional thing?

    Random selection is NOT an occasional thing, it is the major mechanism of what really happens in the wild. Darwinian selection is the exception, not the rule.

    See page 90-91 and onward.

    almost all of this “natural selection for the fittest”, will really only be selection for the luckiest — not the genetically superior.

  137. Salvador,

    The interesting thing going on here is the tone of the discussion. As I said people tend to distort what I say to suit their purposes.

    Read the abstract on insects. It mentions a change of environment as the reason for the extinctions. This is one aspect of micro evolution. You then go on to cite catastrophes as a cause for extinction. This is a micro evolution event. The genomes of the species affected by the catastrophe could not handle the new environment. There is no indication that the genomes have deteriorated and this is the reason for their extinction, If the catastrophe caused changes to the genomes through some type of radiation or other contaminant that is not Sanford’s genetic entropy which is caused by the slow accumulation of mutations over time. So catastrophes are not related to genetic entropy. It is interesting why you would bring up such an example.

    If you want to deflect from the basic issue of massive near-neutral mutations by bringing up random selection and the idea of cost of selection and call my focussing on the mutations a straw man argument then so be it, The essential part of Sanford’s ideas are all the mutations that have accumulated slowly over time. So use what rhetoric you wish. It has nothing to do with the basic criticism of Sanford’s ideas which have no real world examples as verification.

    And remember the occasional genome gone awry is not support for Sanford. He is painting a massive deterioration of genomes world wide and that is what one has to find to support Sanford. So when you bring up the occasional problem with a genome because of mutations you are not talking about genetic entropy. No one would care a rat’s rear end about someone’s theory who said an occasional genome went astray because of mutations.

    As I said it interesting why Sanford’s concepts have to be defended so vigorously when there is no evidence to support them and lots of evidence to contradict them. Everyone here has run into a similar blind adherence with the Darwinists.

  138. lots of evidence to contradict them.

    Say what Jerry? Cite some evidence of large scale genomic improvement and evidence that more species are being created rather than going extinct via Darwinian evolution or micro-evoltion in today’s world. Cite some evidence that there are comparable numbers of good mutations to bad ones…..

    So when you bring up the occasional problem with a genome because of mutations you are not talking about genetic entropy.

    You brought up the beetles as being fine, and it became evident you didn’t even look to see if they were fine. They are not all fine, and many species are dead….

    What was in evidence in the cases I cited was the inability of selection weed out that bad, and that supports the thesis of genetic
    entropy by way of micro example. And as far as the large number extinct species, are you saying their genomes are healthy? :-)

    The hypothesis might get further confirmation with more exploration. But to argue that there is NO evidence merely because we’ve not sequenced genomes world-wide is wrong headed. There is at least some evidence, and if you’d open your eyes, you’d see there is more. You can’t see it if you just pull examples out the air without even looking….

    You then go on to cite catastrophes as a cause for extinction. This is a micro evolution event.

    I beg to differ. Darwinian micro-evolution involves competition among individuals such that inherently better traits have the chance to reach fixation. This is known as Phyletic transformation. This competition can not even take place if all the individuals are dead due to a catastrophe. Therefore this could hardly be clasified as micro-evolution, unless one defines it in such a loose way as to be totally meaningless.

    And even when individuals compete, genetically superior genomes are not favored that much more than inferior genomes because of random selection.

    If the catastrophe caused changes to the genomes through some type of radiation or other contaminant that is not Sanford’s genetic entropy which is caused by the slow accumulation of mutations over time

    That’s a strawman, Jerry. Genetic Entropy in sum:

    Mutational entropy appears to be so strong within large genomes that selection cannot reverse it. This makes eventual extinction of such genomes inevitable. I have termed this fundamental problem Genetic Entropy. Genetic Entropy is not a starting axiomatic position — rather it is a logical conclusion derived from careful analysis of how selection really operates.

    Mutational entropy can be induced by radiation. Sanford does not preclude that possibility. See page 25 for a discussion of what happens when radiation is a source of mutational entropy.

    Careful analysis of how Darwinian selection operates shows that Darwinain selection doesn’t work if all the individuals of a population are dead. Duh! Sanford was generous to grant the assmumption that individuals were even alive in the first place so that competition was possible in order to supposedly save the genome.

    To try to prove that Darwinain micro-evolution works by citing only examples where it works is like aguing PZ Myers is swell guy except when he’s not. It’s a meaningless statement. There are more examples of where nature does not folow the Darwinain micro evolutioanry model than those that do. Sanford shows theoretically that even in the cases where micro-evolution might work, it won’t in the long run.

  139. jerry

    micro evolutionary processes are the main cause for modern extinction

    If by “micro-evolutionary processes” you mean random mutation & natural selection then yes, I agree. When the mutations are predominantly slightly deleterious such that they can’t be “seen” and “eliminated” by natural selection then they accumulate in the gene pool in larger and larger number over millions of years making the species progessively less and less fit. Think of it like individuals that get weaker as they grow older – they get more prone to accidents and disease, eyesight gets worse, bones get brittle, joints get arthritic, etcetera. Species age this way too. Glad you finally saw the light about genetic entropy.

  140. Salvador,

    As I said, I find the tone the most interesting thing and that somehow this man’s ideas must be defended at all costs. The main refutation to Sanford is right out your window. The biological world is doing fine. If you think not then you are welcome to your view but you are seeing a different world than I.

    You can push Sanford. Certainly that is your prerogative. I will look for what I consider more relevant explanations but I will continue to raise my objections to his ideas as he gets brought up in the future because I have yet to see anything that supports his thesis. The occasional sick species or even the massive number of extinctions in the past are not support. I am always open to new information but have not seen it on this thread so far. What I see is blind adherence,

  141. The biological world is doing fine.

    What I see is blind adherence,

    Before you keep accusing me and others of blind adherance, here are some relevant data points you can provide:

    Cite some evidence of large scale genomic improvement and evidence that more species are being created rather than going extinct via Darwinian evolution or micro-evoltion in today’s world. Cite some evidence that there are comparable numbers of good mutations to bad ones…..

    Then maybe you’ll be a bit more justified in accusing us of blind adherance.

  142. 142

    Blind adherence Jerry?

    The genetic evidence we do have good record of all points to the same thing, loss of information on sub-speciation and deterioration of species from random mutations.

    In the fossil record, there is even record of entire branches of phyla going extinct since the Cambrian. Yet you look around and say “Hey look at all this profusion of life around us and thus Genetic Entropy must be false!” Yet in the very next breath, and I find this a complete disconnect in logic, you say no new information can arise by micro-evolutionary processes.
    Well you won’t admit to deterioration of genomes and you won’t claim generation of new information in genomes, so what exactly is your mo^del for biology?

  143. Dave,

    Are you saying that most of the genome is junk or are you saying that on the non junk parts that mutations may not make a difference till many accumulate?

    On the first part I believe that there are some junk parts in many species but nearly not as much as once was hypothesized, On these junk parts there should be no limit to the number of mutations that could accumulate since it is just junk. So this will never lead to extinction.

    On the non junk parts who is to say that even one so called neutral mutation might not abort the fetus. I have a hard time understanding how a host of these so called neutral mutations could accumulate before causing havoc and aborting the fetus or preventing the organism from having offspring if the part of the genome is essentially to functioning of the fetus or organism. And this would have to happen to all the members of the population.

    By the way whatever happened to the large section of the genome that was knocked out and the mice continued to do just fine. Was that section full of a large number of near neutral mutations? I thought it was a preserved section. Isn’t the concept of preservation antithetical to Stanford’s ideas? Whatever happened to all the homologous genes in various organisms that are similar such as the various forms of hemoglobin? How could all these survive with genetic entropy causing random changes in each individual genome of a species or as it seems a whole kingdom. I would think this would be enough to shoot down Sanford.

    I will ask you a question about my pet beetles. How did all these species come about? And if there are truly 350,000 of them is it not possible that a few are at the end of the road while the rest of them are fine? If that is the case then isn’t that a refutation of Sanford? And are there other possibilities for this end game for these few unfortunate beetles besides Sanford’s genetic entropy? And are some of these possibilities a continual narrowing of the gene pool due to environmental and selection pressures and maybe even occasional mutations? The last I believe is called Darwinian micro evolution.

    I too think that many species are getting “old” but not because of Sanford’s ideas but mainly because they are losing variety in the gene pool. This is a prediction of Darwinian micro evolution and is one of the problems the Darwinists have is that their own theory predicts doom. Their way out is that mutations will add variety over time. Something which I don’t believe has ever happened.

  144. Salvador,

    you asked

    “Cite some evidence of large scale genomic improvement and evidence that more species are being created rather than going extinct via Darwinian evolution or micro-evolution in today’s world. Cite some evidence that there are comparable numbers of good mutations to bad ones…..”

    All irrelevant questions. I never said there was evidence of large scale genomic improvement. In fact I claim the opposite, there is little if any improvement. Read #131. Do I have to repeat it a zillion and one times? By the way this does not mean there is genomic deterioration nor does it mean that a species can not become more fit over time. I happen to believe that genomes are deteriorating but from micro evolution processes and not genetic entropy. Future genome mappings will either negate this or support this hypothesis.

    I do not know how many species are going extinct today but as Dave has pointed out they are due to micro evolution reasons. I think the number is probably exaggerated to day because of political reasons.

    How many species are being created? I have no idea but how that relates to genetic entropy, I haven’t a clue. Denton’s book “Evolution: A Theory in Crisis” discusses some examples. And by the way I understand the problem of how does one define a species. The answer is there is no good way.

    I have no idea how many good mutations there are but they have little relation to anything I have said. I shall I repeat again that what I say gets distorted. My guess is that beneficial mutations are few and far between. Except for the obligatory ones such as skin or fur color and length, I am at a lost, Maybe you could provide some examples. They have no relevance for much or anything I have said.

    I do not know how any of this relates to blind adherence since it is I who am questioning Sanford, not defending him without evidence.

  145. 145

    I do not know how any of this relates to blind adherence since it is I who am questioning Sanford, not defending him without evidence.

    No Evidence?

    It is entirely in line with the accidental nature of naturally occurring mutations that extensive tests have agreed in showing the vast majority of them to be detrimental to the organisms in its job of surviving and reproducing, just as changes accidentally introduced into any artificial mechanism are predominantly harmful to its useful operation” H.J. Muller (Received a Nobel Prize for his work on mutations to DNA)

    “Mutations, in summary, tend to induce sickness, death, or deficiencies. No evidence in the vast literature of heredity change shows unambiguous evidence that random mutation itself, even with geographical isolation of populations leads to speciation.” (Lynn Margulis – Acquiring Genomes [2003], p. 29).

    “But there is no evidence that DNA mutations can provide the sorts of variation needed for evolution… There is no evidence for beneficial mutations at the level of macroevolution, but there is also no evidence at the level of what is commonly regarded as microevolution.” Jonathan Wells (PhD. Molecular Biology)

    “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.” Dr. Lee Spetner (Ph.D. Physics – MIT)

    “I have seen estimates of the incidence of the ratio of deleterious-to-beneficial mutations which range from one in one thousand up to one in one million. The best estimates seem to be one in one million (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). Therefore, I cannot …accurately represent how rare such beneficial mutations really are.” (Sanford; Genetic Entropy page 24)

    The fate of competing beneficial mutations in an asexual population (Philip J. Gerrish & Richard E. Lenski)

    “Clonal interference is not the only dynamic that inhibits the progression of beneficialmutations to fixation in an asexual population.Asimilar inhibition may be caused by Muller’s ratchet (Muller, 1964; Haigh, 1978), in which deleterious mutations will tend to accumulate in small asexual populations. As shown by Manning and Thompson (1984) and by Peck (1994), the fate of a beneficial mutation is determined as much by the selective disadvantage of any deleterious mutations with which it is linked as by its own selective advantage.”

    http://myxo.css.msu.edu/lenski.....Lenski.pdf

    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/jour.....7270a.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/...../5434/1748

    ” 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.”

  146. jerry:

    I hope you didn’t resent my “your beetles”. It was just friendly irony. I am quite happy with “my worms”, anyway. :-)

    But let’s get serious. In brief:

    I was not making a point about genetic entropy. As you have noticed, I don’t get too much involved on that subject. In general, I believe in the principle of genetic entropy and in the intelligent control in genomes as a measure against it, but I am not too sure about the details.

    I was trying to make a point about the huge differences at genomic level even in apparently almost identical species. That, in my opinion, is a sign of independent design even at the species level. And I am sure that it would be even more clear with “our” beetles.

    Obviously, it is possible that those differences are just a sign of neutral mutations, but do you believe it? More than a thousand different protein coding genes?

    I agree with you that there are a lot of things we don’t understand, and many more we are discovering daily. I was just suggesting that the differences between similar species are just one of those things, and that they are not easily explained by microevolution models.

    Anyway, I will certainly go back to my worms in the future. They are at present the best known model of multicellular organization we have. C. elegans is the only living being of which we know practically each single cell and nervous connection!

  147. gpuccio,

    We can share the worms as well as the beetles so they will be our worms and our beetles. I do not have any problem with the worms looking similar but having substantially different genomes. It could have arisen via micro evolution or some other means a long time ago.

    Suppose the following (and I am no means proposing this as truth or the way it happened so no one say that this is what I believe:)

    Each worm had the same common ancestor, another worm with all the genes of both. Then two separate sub populations broke off and over time lost part of their genome which included the genes in question, They had 90 million years to devolve in such a way. I am not aware that there is any genetic principle that prevents a species from losing part of its genome over time. All the controversy is over whether it can gain any.

    (Now the Darwinist would say that each had the common ancestor but that each sub population separated and then added the genes in question over time through macro evolution processes. Nothing supports that this is possible so I prefer something similar to mine.)

    And if none of these genes affect the morphology of the worms then they could look and act alike today. I have no idea if this is true but we could ask some evolutionary biologist if such a scenario was possible.

    My assessment of what has happened in general is that there is much of a chunk of life that is a mystery as to its origins. However, until micro evolution is ruled out, I am going to defend it for most of our beetles and hypothesize that they are descended from some population of beetles that existed a long time ago and through separation, environmental pressures and selection numerous sub populations developed until we now have 350,000 species.

    My guess this number is way too high and the only difference between many of the species is the voluntary inter breeding, That is they could breed but won’t for a variety of reasons. And because of this they are listed as separate species. I also do not believe anyone could really check this many different beetles out so the actual number is an estimate.

    I believe the evidence supports such a scenario for most individual species but will have to wait for the genomes to be mapped till we see just how varied they all are and see how they could have evolved or a better word is devolved from an original gene pool.

    Now many will not agree with such a scenario but to me it sounds the most reasonable based on what we know today,

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