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P.falciparum – No Black Swan Observed

The tired old “ID is not scientific” has reared its ugly head again in another thread. This is simply not true.

Karl Popper famously stated that a hypothesis is scientific if it can be falsified. He used swans as an example. He stated a hypothesis:

All swans are white.

Popper said that it can never be proven that all swans are white because there is always the possibility that a black swan exists somewhere but has not yet been observed. He stated that the hypothesis is still scientific because it can be falsified – the observation of a single black swan will falsify it.

The biological ID hypothesis can be stated as:

All complex biological systems are generated by intelligent agents.

We already know, or may reasonably presume, that complex biological systems can be generated by intelligent agents. There’s a whole discipline called “Genetic Engineering” devoted to it. What we don’t know is whether any non-intelligent means can generate complex biological systems. A single observation of a complex biological system generated by a non-intelligent cause will falsify the biological ID hypothesis.

P.falciparum replicating billions of trillions of times in the past few decades represents the largest search to date for a “black swan”. This is orders of magnitude more replications than took place in the evolution of reptiles to mammals wherein there are many exceedingly complex biological systems that separate them. If P.falciparum had been seen generating any complex biological systems such as those that distinguish mammals from reptiles then it would have falsified the ID hypothesis. None were observed. This doesn’t prove ID but it certainly lends strong support to it. All perfectly scientific.

P.S. I understand that an actual black swan has been observed and Popper’s hypothetical example was indeed falsified. That is exactly how science is supposed to work. Now it’s up to the time & chance worshippers to falsify the ID hypothesis. Good luck.

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84 Responses to P.falciparum – No Black Swan Observed

  1. DaveScot,
    If ancient bacterium spores are apparently being revived (Lazarus like), from such places as amber and/or salt crystals, and IDists can further this line of evidence by successfully tracing a particular (or even many different) bacteria through many points of time (many data points) through many millions of years, would not this give IDist another very hard piece of evidence that, while not directly observed as in malaria, would be in convergence with Behe’s observations?

    I was reading yesterday where one scientist commented, that while working with amber fossils, he has revived and sequenced hundreds of ancient bacteria…with relative ease.

  2. Dave, I think you’ve got a book in you. I can see it starting to develop like one of those old Polaroid pictures…

  3. DaveScot,
    You accused me on another thread of avoiding the question about p. falciparum. I’m not a biologist, and I’m in a very different time zone from you, so you’ll have to bear with me a little.

    There is ample evidence that the genetic variability of p. falciparum plays a large role in its transmission success, and tends to stymie efforts to control disease in humans. Recent work has shown that the lack of DNA variation in coding sequences is far from the whole story. In particular, introns have been shown to be deficient in single-nucleotide polymorphisms, and that extends to synonymous sites in coding regions. Together, the data point to the recent origin of p.falciparum. Precursor forms are in fact different on these measures.

    Don’t take my word for it. Here are two (of many) sources:

    Neafsey DE, Hartl DL and Berriman M (2005). Evolution of noncoding and silent coding sites in the Plasmodium falciparum and Plasmodium reichenowi genomes. Mol Bio Evol 22(7): 1621-1626.

    Volkman et al (2001). Recent origin of Plasmodium falciparum from a single progenitor. Science 20 July, vol 293, no 5529, 482-484.

    Time and chance worshippers? Well, that sure advances our understanding of the issues. Read up, people. It’s hard work, but it’s more effective than gratuitous name-calling.

  4. MacT

    P.falciparum is a eukaryote with both asexual and sexual reproduction. No doubt there is variability in its genome that is expressed or repressed in recombination during sexual reproduction. The fact of the matter remains that it is essentially the same organism after billions of trillions replications in past few decades aside from a few trivial (but medically important) nucleotide changes in its genome that serve to defeat a few human produced anti-malarial drugs. The changes moreover actually make the organism less fit in the absence of the drugs. Compare this to all the large scale changes in both genotype and phenotype that made mammals out of reptiles.

    Just so stories of P.falciparum evolving from another plasmodium are conjecture and while it is probably true, just as it’s probably true the mammals descended from reptiles, it does not change by one iota the observation of P.falciparum replicating billions of trillions of times over the past few decades and essentially not evolving at all to say nothing of evolution on the scale of reptiles to mammals.

  5. MacT,
    Forgive me for jumping in on your discussion with Dave Scot, but I wanted to point out that you site evidence that comes from a entrenched preconceived philosophical bias that says, of course, evolution has occurred, just look at these genetic similarities!!!

    ,,,whereas DaveScot, as well as all other ID proponents, start out with the philosophical bias that intelligence may very well be required to generate fantastically Complex molecular structures we are finding in biology….Thus we put evolution to the test and see what it can actually accomplish as far as generating complexity!

    What happened when evolution was put to a real world test…NOTHING OF SIGNIFICANCE THAT WOULD VERIFY EVOLUTION!

    You cite resistance as proof of evolution, yet it is clearly explained in Dr. Behe’s book that all resistance was wrought in malaria by degrading a preexisting function in the malaria…On top of that once the is removed from the malaria population the “mutated” malaria is quickly out competed by the original malaria…

    You said reading is hard work (I would say it depends on if you enjoy it or not?),,,But if you could do a little more hard work and actually read Dr. Behe’s book before criticizing it on this site, then I think it would save us a lot of trouble correcting your mistakes on exactly what the ID theory is.

    I can tell that you are sincere and hope I do not offend you,,but I can guarantee you that all the hard “observed” evidence falls in IDs favor,,,Indeed if you do a little investigation you will be pleasantly surprised.

  6. MacT

    Carried over from a previous thread you, incredibly enough, want to quibble about the definition of “intelligent agent”.

    Here’s how I define it for this context:

    Intelligent agentAny entity which can form an abstract model of a potential arrangement of matter and which can then manipulate matter to actualize the arrangement.

    For instance a monkey qualifies when it sees a banana out of reach and a box that can be repositioned so that the banana can be reached. The monkey forms an abstract model of him first repositioning the box under the banana then stepping onto the box to reach the banana. After forming the abstract model he manipulates the box and himself to realize the model.

    Of course that’s a far shot from Genetic Engineering but that is essentially how engineering is accomplished – abstract models of potential arrangements of matter/energy are made and then the plans are actualized.

    This seems like a simple enough definition for any moderately intelligent person to construct. You seem to be moderately intelligent so it appears you are just being argumentative.

  7. Black swans were discovered in the 1700′s in Australia and the use of the black swan in philosophy of science has been as an example to show the shortcomings of induction.

    Popper used the example of the black swan to show induction cannot mean certainty.

  8. Let us assume there was a recent origin of P.falciparum. How does this hypothetical scenario provide positive evidence for Darwinism in itself? What Darwinian process or mechanism was involved?

  9. Hi,
    isn’t this discussion dependant on having knowledge of what P. falciparum used to be long ago, to know whether it has changed substantially – we don’t have any reeaaly old samples. The Plasmodium genome sequencing project has just started – they’ll be comparing strains from different sides of the planet which should be informative on this issue.

    But we could get an idea about the proto-falciparum IF we assume P. falciparum shares common descent with the other 4 human Plasmodium species and the 200 others found in birds, monkeys and reptiles.

    From recollection P. falciparum has at least one extra gene family (of 50 genes), not present in the other species which infect humans. The var gene products bind a range of human proteins, modulate T cell function, cloak the organism from the immune system and prevent splenic passage.

    Interestingly there are also a range of human genetic counter-adaptations (common in African/Asian populations) combating the products of var genes.

  10. DavesScot,

    “Intelligent agent – Any entity which can form an abstract model of a potential arrangement of matter and which can then manipulate matter to actualize the arrangement.”

    Ok, good. That is a good description of an intelligent agent that can shift a box over to better reach a banana. We have clear, independent observations of such creatures doing exactly that. Your definition allows us to develop an elaborated theory of monkeys as intelligent agents, and to generate hypotheses that can be tested to explore more fully the extent (and limitations) of monkey intelligence.

    Further, we can confidently extend the concept of intelligent agency to other examples that demonstrate similar qualities to monkeys that we can define (opposable thumbs, crossmodal regions of cortex capable of supporting symbolic representation, etc). Piaget’s daughter, Jacqueline, showed very similar abilities of abstract representational thinking, translated to motor action, when she solved the problem of retrieving a box outside her playpen that had to be turned in exactly the right way in order to pass through the vertical bars of the playpen.

    But notice that while both of these examples meet the definition of intelligent agent, any hypothesis we might formulate to further investigate their nature must take into account the definitional premises of the agents in question. It would be silly to suppose that either the monkey or Jacqueline, despite their status as intelligent agents, would be capable of designing a simple machine. For that, we would have to posit additional competence, and state a priori what that competence entails (e.g., knowledge of engineering principles, handy with metalworking tools, etc).

    So: What are the definitional premises of an intelligent agent that is capable of designing a complex biological system?

    It seems to me that by avoiding a definition that includes necessary competence, your account is leaning toward assuming omnipotence. I’m not sure that’s what you actually have in mind, but once in, it is a difficult corner to get out of.

  11. DaveScot said:
    “The changes moreover actually make the organism less fit in the absence of the drugs. ”

    On a side note, in the case of organisms in certain ecological niches, less fitness is not necessarily an evolutionary disadvantage. A less vigorous parasite is less likely to kill its host, and therefore more likely to reproduce.

  12. Dave Scot -

    I agree with your definition of Intelligent Agent: “Any entity which can form an abstract model of a potential arrangement of matter and which can then manipulate matter to actualize the arrangement.” It’s a good one. In the light of your “monkey reaching a banana by moving a box” example, however, it appears to make the difference between monkeys and men merely one of degree and not kind. It would be helpful to me if you would elaborate a bit on that side of the issue. Thanks.

  13. If evolution is a science, and any hypothesis (speculation) on evolution is science, shouldn’t then the critique of the limits of evolution also be considered science?

  14. Ahoy, Dave!
    I commend you for having put forth a fundamental ID hypothesis. A problem with the potential falsification of your hypothesis, however, is that some (many?) in the pro-ID camp advocate an actively interventionist creator whose tinkering could be manifest anytime, anywhere. So, an observable, confirmable evolutionary innovation can always be ascribed to the Big Tinkerer and need not falsify the ID hypothesis.

    Michael

  15. If biological life on Earth is designed by material beings from elsewhere, those material beings would presumably be “complex biological systems,” right? Well, then they need a designer that is ultimately not a complex biological system.

    We are limited to what we can observe. Right now we can observe living organisms on this planet, so we ask “how did they (we) get here?”

    What are the options?

    No need for regress games. Take things one step at a time, figure it out and then move on.

  16. Together, the data point to the recent origin of p.falciparum. Precursor forms are in fact different on these measures.

    This assume Darwinism and positive upward evolution via Darwinian mechanisms. How do we know the “precursor forms” are even precursors? Why couldn’t they be separate lines that suffered genetic entropy and lost functionality? Perhaps P.falciparum simply suffered less deleterious mutations.

  17. “This assume Darwinism and positive upward evolution via Darwinian mechanisms. How do we know the “precursor forms” are even precursors? Why couldn’t they be separate lines that suffered genetic entropy and lost functionality? Perhaps P.falciparum simply suffered less deleterious mutations.”

    We don’t know anything with 100% certainty. That’s not how science works.

    It might have been caused by an unembodied intelligence. There’s simply no way to exclude that possibility, since we cannot know how or why such an intelligence would act. Leaving that aside, there is evidence that p. Falciparum DID change, and in a sense you are correct in suggesting the changes were less deleterious. I posted a couple of references to the publications that detail these changes.

  18. First, I think DaveScot’s example black swan example makes a lot of sense, and I second the idea of DaveScot writing a book, because unlike some people, he writes very clearly about complex subjects.

    Borne – I have to take issue with your post about mammels not descending from reptiles and fishes. I am sure that DaveScot has written about this many times before, and front loading is clearly an ID topic.

    I also think that you are discounting the Designers’s abilities to a great extent, and whether or not you call the creator God or the Designer, it doesn’t matter.

    Let there be light, and there was light! If He wants to say Let reptiles turn into Mammelss, reptiles are going to turn into mammels.

  19. Getawitness,

    My point is the designer of living organisms on Earth need not be the same designer who designed the universe. It very well could be but it is not any requirement

    Also, with all due respect to Wm Dembski, we do not know if a designer, who was at least at one time beyond this universe, is unembodied or not.

    BTW- thanks for reading my blog!

  20. Pantrog,

    I’ve read your post and can’t really make heads or tails out of the point you are trying to make,,,Are you saying we will find proof of evolution if we look harder and allow more broader assumptions for common decent?,,,If this is what you are saying you are totally missing the whole point.

    This is/was the best chance for evolution to strut its almighty stuff,,,and what did we see evolution accomplish?

    Well here are Dr. Behe’s own words:

    Perhaps even more remarkable than the rarity of malaria resistance to chloroquine — and even more of an indication of the weakness of Darwinian forces — is the puny final result. Truly in this instance the Darwinian elephant labored mightily and brought forth a gnat. After a hundred billion billion chances, we end up with a few measly point mutations in pfcrt. These results from malaria are our best evidence by far of what Darwinian processes can accomplish when given a huge number of chances and strong selective pressure. Behold the result.

    The TREE reviewer goes on to complain about my noting that no protein-protein binding sites evolved in malaria in an astronomical number of opportunities: “He apparently thinks that evolutionary theory says anything should evolve a new binding site in response to any arbitrary situation.” (1) The reviewer’s complaint begs a large question, however: when does evolutionary theory say that a protein-protein binding site should evolve? What non-arbitrary situation would cause that? In fact, evolutionary theory says nothing about specifics of what should or shouldn’t evolve. Therefore, we need to get our ideas about what should or shouldn’t evolve not from evolutionary theory, but from evolutionary data. And what we see in our best set of data from malaria is that no such protein sites evolved by Darwinian means in an astronomical number of opportunities. Furthermore, mutations in only one protein, pfcrt, were really able to do much in the face of chloroquine, showing that the number of proteins that it may be helpful to evolve in any given situation might be extremely small: one, maybe none. Ditto for pyrimethamine resistance.

    If only one protein could evolve to help malaria avoid chloroquine poisoning, why should we think that a cell will luckily have a dozen or score of proteins that happen to be able to evolve to make a molecular machine?

    http://www.amazon.com/gp/blog/.....2SQARF948L

  21. “Gradualism sucks” – Borne

    Hahahaha. Although Borne sounds a bit exasperated, I can understand his frustration. There’s so much faith in swallowing naturalistic evolution. I can’t imagine thousands of ancient fish washing up on land and choking to death until a lung develops. I take the same issue with the development of wings. Dawkin’s speculation on the subject is pretty ludicrous.

    On another note, I think we need to wary about our word choice when, given the Darwinian hypothesis of common ancestry, we say “mammals came from reptiles.” Maybe “modern mammals descended from ancient reptiles”? Just a suggestion…

  22. Falsificationism doesn’t work. In practice, a theory can always be rescued from an anomalous observation.

    The question ‘Is ID science or non science?’ is philosophically obtuse and useful really only for propaganda or for the madness that is the American approach to separation of church and state. (For a nation to claim to be the ‘land of the free’ while their state dictates curriculum to their children is absurd; they can’t take your guns but they can take your kids.)

  23. bornagain77

    Hi, you seem to imply that the Darwinian elephant only produced “a few measly point mutations in pfcrt”, but their existance doesn’t exclude bigger changes having occurred in the species. The mapping experiments to pinpoint chloroquine resistance did not survey the falcipaurm genome to catalogue all changes, just the changes responsible for one phenotype.

    My point is that to detect a “black swan” (e.g. a new gene) we would need to know what genes a P. falciparum strain had in the past, and compare the complement it presently has.

    Given that the reference sequence has only just been published – we can’t tell if any new genes have turned up since, say 1990. We need two or more measurements spaced out in time. That could take a while, so in the interim two obvious alternatives exist:

    1) Sequence different strains separated by geography (hence time).

    2) Sequence different Plasmodium species separated by speciation (hence lots of time).

    Obviously (2) requires an assumption about common descent among Plasmodium species (which maybe unpopular locally) – but if accepted yields clear evidence of dozens (actually hundreds) of new genes in comparison with vivax, malariae, ovale, etc.

    (1) is less contentious, and is also being undertaken as we type. Early results indicate there are indeed differences in gene complement between strains.

  24. Popper made a great contribution to philosophy of science but it was hardly the final word. Falsifiability is a useful concept but can’t absolutely demarcate science from non-science. At the fuzzy edges (which is obviously where all the arguments happen and where we most need a demarcation criterion) it’s far from clear what’s falsifiable and what isn’t (can a claim about the past, for instance, ever be falsifiable?)

    http://www.galilean-library.org/

    This is a great website for all things PoS related.

  25. Pantrog,
    Here is the global genome study of P.falciparum.

    Volkman,S.K., et al. 2007. A genome-wide map of diversity in Plasmodium falciparum. Nat. Genet. 39:113-119.

    http://www.ncbi.nlm.nih.gov/si.....xed=google

    Of special note:
    We performed extensive sequencing of 16 geographically diverse parasites and identified 46,937 SNPs, demonstrating rich diversity among P. falciparum parasites (pi = 1.16 x 10(-3))

    P.falciparum’s genome is about 23 million nucleotides long.

    Thus genetic diversity from all geographic areas studied is approximately: .2% for P.falciparum

    If you were looking for one or some of the groups to be radically different, I’m not impressed with the differences in the least.

    As well the principle of genetic entropy (conservation of information married with the second law) states that all “sub” speciation events (acting by totally material processes) will come at a cost of information. Thus any supposed subspecies of P.falciparum will be found to have less genetic diversity than the parent species. I haven’t studied P.falciparum in detail, but here is the evidence collected for higher organisms.

    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 an ancient 40,000 year old (human) 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.

    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 (breeds of) 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 dogs than for 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!

    This overall pattern of evidence (morphology and genetic diversity) conforms strongly to the evidence supporting the principle of Genetic Entropy found for humans.

    Maize molecular diversity is roughly 2- to 5-fold higher than that of other domesticated grass crops (1). Tenaillon et al. (2) reported that in 25 maize individuals, one nucleotide every 28 base pairs is polymorphic, and overall nucleotide diversity is almost 1.3%. That study, the largest examination of random maize loci, found almost no evidence of selection in 21 genes along chromosome 1. Maize’s closest wild relative, Z. mays ssp. parviglumis (a teosinte), often has levels of nucleotide diversity that surpass 2% (3–6). The tremendous diversity of maize and teosinte has been the raw genetic material for the radical transformation of maize into the world’s highest yielding grain crop.
    http://www.pubmedcentral.nih.g.....tid=130568

    Thus even maize exhibited a loss in diversity from its parent crop.

    These studies of sheep are interesting:

    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 s 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

    Genetic Diversity in Algerian Sheep Breeds, Using Microsatellite Markers
    http://www.springerlink.com/co.....5547xr75m/

    Heredity – Diversity and evolution of the Mhc-DRB1 gene in the two …
    Low levels of genetic variation were detected in both subspecies, ….. Is the decline of desert bighorn sheep from infectious disease the result of low MHC …
    http://www.nature.com/hdy/jour.....1016a.html

    Thus the parent species of sheep (mouflon) exhibited had no problems with inbreeding as the sub-species with much larger populations are having…

    I don’t think I have to remind you that this fits in well with what the Theistic prediction for ID would say!

  26. Michael

    A problem with the potential falsification of your hypothesis, however, is that some (many?) in the pro-ID camp advocate an actively interventionist creator whose tinkering could be manifest anytime, anywhere.

    Those who propose that aren’t proposing a scientific hypothesis unless they include an observable mechanism. It has the same problem as the modern synthesis – i.e. chance can, in principle, account for any physically possible pattern. A hypothesis that explains everything explains nothing. Someone asked me in another thread to propose a mechanism for a constantly tinkering designer and I offered a retrovirus as an observable means a tinkering designer could employ to introduce novel genetic complexity that would appear as saltation and match up with the fossil record.

    So, an observable, confirmable evolutionary innovation can always be ascribed to the Big Tinkerer and need not falsify the ID hypothesis.

    Clearly ID is not monolithic. I concede that my hypothesis only applies to a designer who is no longer active in the process. The strength of it is that it is perfectly scientific and a live alternative if it is not falsified in the manner proposed. It seems the only objection to accepting it as a valid hypothesis would be fear that it will never actually be falsified by observation. That doesn’t reflect much confidence in evolution by time & chance and makes it appear that the time & chance “theory” is more a matter of faith than one of reason.

  27. Borne

    You were at one time a single cell that transformed in a matter of weeks into very large number of specialized cells organized into a plethora of tissue types, organ types, and complex body plan. Clearly huge phenotypic transformations are possible since we see it happen in ontogenesis.

    I suggest that reptiles turned into mammals in the same manner that ontogenesis turns a single cell into a mammal – it was a predetermined process. The phenotypic complexity of a mammal was there all along in the genome of one or more species of reptiles waiting to be expressed upon some signal event. Phylogenesis mirrors ontogenesis. Both are predetermined self-terminating processes where little if anything is left up to chance and the environment at most provides cues for advancing to the next level of diversification.

  28. BA77

    Excellent quote from Behe in comment 24. I wish I could write that well.

  29. Correction: The Dutch explorer Willem de Vlamingh recorded sighting a Black Swan on January 10, 1697 (in the 17th century) when he sailed into, and named, the Swan River on the western coast of New Holland. See: The Bird Emblem of Western Australia,

    Black Swans

    About Black Swans

  30. Pantrog:

    Just two comments:

    1) Although you are right that a strict sequence comparison between actual parasite and the parasite as it was at the moment of the introduction of chloroquine is not possible, because the sequencing of the genome has only been completed now, still there is probably no evidence that any significant phenotypic difference has been observed to emerge in the parasite during those years.

    2) But that is really not the point. The point is that, after the introduction of chloroquine, the main selective pressure in the so called “fitness landscape” has become the drug. So, we have a model where a very strong environmental challenge has emerged, which is exactly what is supposed to be a very strong motivation to evolution in a darwinian scenario. So, the point is not if the parasite in those years has started to evolve some occult difference, but rather why it has not evolved any complex and non trivial adaptation to chloroquine, in the presence of such a strong selective force, and with so many reproductive cycles available. Why not a “cloroquinase”, or some equivalent mechanism, for instance? Why not a complex new pathway, let’s say 3 or 4 proteins in cascade whose purpose could be to metabolize the drug, or to couple it to some molecule to make it ineffective. Why not new cellular functions which may allow the parasite’s survival in the presence of choroquine? Why not a deeply renovated parasite, much more dangerous and resistant than its ancestor?

    There are many possible ways to adapt, exactly as darwinian theory postulates, in the presence of a very strong environmental selective pressure. According to the theory, that’s why new species arise, new body plans are formed, new brains and functions arise, and often in less reproductive cycles than the parasite has experienced in the few years fron the introduction of the drug.

    So, Behe’s argument stays perfectly valid: why can’t we see any creative evolution in the parasite, when all the necessary ingredients are there? Why only few trivial single point mutations?

    The answer is simple: because that’s all random variation can accomplish, in absence of a design implementation.

  31. bornagain77,

    Yes, Volkman et al. 2007 “A genome-wide map of diversity in Plasmodium falciparum.” is an interesting paper. They find 46,937 SNPs – in the regions they sequenced, which was not the full 23 million bp. Could you tell us what the correct denominator is? – I also note they sequence 16 haploid genomes, this will find fixed differences between isolated populations – but not will not catalogue all polymorphic varaints.

    It would be interesting to report how many insertions, deletions, copy-number variants, inversions, were also found between strains?
    I note from a previous paper authored by Volkman “A Systematic Map of Genetic Variation in Plasmodium falciparum” Kidgell et al 2000. They report over a dozen strain-specific whole gene duplications at that time.

    I take your point that all falciparum sub-species could have a common mega-progenitor with a super-set of genes, from which strains are just genetic sub-sets. However the progenitor genome would be rather bulky, many of the strain-specific duplication events seem to relate to drug resistance and all the substrains seem perfectly capable of doing their job of infecting humans rather effectively – even after trillions of replication events.

    Does ID expect Plasmodiae to decay to the point when they are no longer capable of being pathogenic? And are you saying the principle of ‘genetic entropy’ prohibits gene duplication?

    Regarding the additional citations, I would refer you to the standard population genetic explanation (that would be accepted by every author you cited) which is that “heterozygosity is proportional to effective population size”. Strains/species will lose variation when their population size is small. However population genetic theory predicts new diversity is generated again when population size increases.

  32. Sorry, thats “A Systematic Map of Genetic Variation in Plasmodium falciparum” Kidgell et al., _2006_

    Its available free from PLoS Pathogens:

    http://www.ncbi.nlm.nih.gov/si.....s=16789840

  33. sorry … and I also forgot:

    pi

    In population genetics stands for nucleotide diversity.

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

    It tells you exactly the average number of variant sites per nucleotide between 2 sequences. i.e. 0.116% difference – between any 2 parasites (just in SNP-type varaition alone).

  34. In regards to the comments of a “Tinkerer” periodically messing with His creation. I firmly believe this is not a “pie in the sky” dream of interventionists, such as I, but is a thoroughly discernible hypothesis. This will be accomplished through tracing the points of the origination of complex specified information (CSI)into life forms. In fact tracing points of origination for CSI is a natural outcome of this very line of study for ID on this very site, since this site ultimately seeks to falsify evolution through its inability to generate CSI in real world situations of molecular biology!
    Think about it,,,We finally (I believe we have already) reach a point where natural processes are overwhelmingly confirmed to be incapable of generating CSI for molecular machinery and for genomes…What is the next logical avenue of investigation? Well obviously, It is tracing the CSI to find out exactly when was the CSI inserted into life forms! That will be the primary line of study for ID!!!
    Then if the timing of insertion can be established to overwhelming satisfaction then the next step will be to ascertain, as best we can, exactly what was the method on which the CSI inserted.

    This will be the primary scientific course that ID takes in fulfilling its scientific duty to relentlessly pursue a more complete understanding of the truth!

  35. bornagain77:

    I completely agree with you. I am, indeed, an interventionist, as you are, ad I have never believed in front-loading, least of all in theistic evolution. So, you are perfectly right, if, as we believe, design has been implemented in biological beings during time, it is fundamental to understand when that happened, with what modalities (continuous, discontinuous), and if possible how.

    The “how” question is not out of context, even if one believes in a “spiritual” designer, because any agent, however transcendent, has to “interact” with observable reality at some level, if he/she/it has to effect a change in it. So, the problem of “how” always applies, if we assume a design intervention, and will always be scientifically approachable, and observable, from the point of view of its phenomenic effects.

    The same applies to any interaction between consciousness and matter, which is not a rare event (it happens continuously in us). If consciousness interacts with matter (and it certainly does), whatever consciousness is, and however transcendent its origin may be, the interaction will be observable at least from the side of phenomena, and up to a level which has still to be defined. I do believe that the consciousness-matter interaction and the designer-designed interaction, are really strongly related subjects.

    All these questions are beyond the primary purpose of ID (inferring the existence of design), but they are certainly very important theoretical problems, and possible fields of research, once the design is admitted. So, again, ID is all but a science stopper: it is an opener of new perspectives, of new questions, of new research scenarios.

  36. jerry

    Induction is a must for science especially when that which cannot be proven is actually true.

    Consider the physical constants such as speed of light and the four forces. We measure them in detail when and where we can then from that detailed knowledge we form the general principles that these forces are the same as our measured values at all times and in all places. These are perfect examples of Popper’s black swan falsification premise. Obviously we cannot measure the physical constants in all places at all times but until there is an observation which doesn’t match the theory we hold them to be true. Science and engineering would be in a fine mess if the physical constants were actually variables.

  37. Dave,

    Don’t take my comment that I do not believe in the utility of induction. We would get nowhere in science let alone life without it. I am just pointing out what Popper claimed and how the black swan is the poster child for problems with induction. There is a recently published book titled

    “The Black Swan: The Impact of the Highly Improbable”

    An example of where induction failed is with Einstein’s theories of time, motion etc. and until his ideas appeared there were no examples of where Newton’s laws did not apply.

  38. Pantrog,

    First off, I don’t think populations genetics is in any way viable as a hypothesis any more, if it ever even was in the first place!

    http://www.genome.gov/25521554

    of special interest:

    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.

    and:

    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.

    This proof of a complex interwoven network makes the genome polyfunctional. If the genome is polyfunctional then it is now proven to be polyconstrained to any random mutations. (Sanford; Genetic Entropy 2005 page 141).

    Page 52 of same
    “Haldane..intended.. as had Fisher..and Wright..to dispel the belief that Mendelism had killed Darwinism…Fisher, Haldane and Wright then quantitatively synthesized Mendelian heredity and natural selection into the science of population genetics.” The Origin of Theoretical Population Genetics. Provine, 1971.

    “Indeed, Darwinism would have died very naturally at this point in time, except for this major intellectual invention”.

    There is one serious problem with the re-definition of the problem in this way. That problem is that the new picture (generated by population genetics) is categorically false. Populations are not even remotely like pools of genes, and selection is never, ever for individual nucleotides (selection is always a take or leave proposition for the whole organism). To justify this radical new picture of life, the theorists (Haldane Fisher and Wright) had to axiomatically assume a number of things- which were in fact all known to be clearly false. For example, they had to assume that all genetic units could be sorted independently – so each nucleotide would be inherited independently – as if there were no linkage blocks (totally false) (note; Encode severely amplified this particular problem since Sanford wrote these words!) Likewise they had to assume no epistasis – as if there were no interactions between nucleotides (totally false). They also typically assumed essentially infinite population sizes (obviously false). and they generally assumed the ability to select for unlimited number of traits simultaneously (which we will show to be false). So from the very beginning of population genetic theory many unrealistic and unreasonable assumptions needed to be made, to make the mo^del appear even feasible.
    On On this very false foundation was built the theoretical pillars of modern population genetics. The theorists’ mo^dels did not match biological reality, but these men had an incredible aura of intellectual authority, their arguments were very abstract, and they used highly mathematical formulations which could effectively cow most biologists. Furthermore most biologists were also committed Darwinists, and so were philosophically in agreement with the population geneticists….

    There you have it Pantog,,,,a very imaginative mathematical framework that in reality fails real world testing at every crucial point….Most people ignore the fact that it has no “conclusive” proof since evolution is already thought to be true prior to investigation…

    You also mentioned duplication as a source for falsifying Genetic Entropy…Yet if I repeat this sentence,,,Yet if I repeat this sentence… Yet if I repeat this sentence…Yet if I repeat this sentence,,,Have I really increased effective information of what I wrote or have I really just wasted your time and energy with needless repetitions…Thus this same type of waste is becoming increasingly apparent in duplications in molecular biology. (down syndrome for one clear example out of many)..

    Must run right now but willaddress the other questions from you and jack Krebs later..)

  39. Jack Krebs:

    Can you outline a method for determining the moment of the insertion of the CSI? If such a method could be both measurable and reproducible by independent investigators, then it would establish the possibility of a scientific determination between what is designed and what is not. This seems to me, and has for many years, a project the ID research community should be engaged in.

    I’ll address each of your three sentences separately.

    First, to determine the actual moment of insertion of CSI is a tremendously ambitious undertaking, and even a next to impossible one unless means are found to extract genomic information from extinct species. The recent discovery in the sea cucumber (anenome?) of a gene for the formation of digits on limb structures is evidence that CSI was “front-loaded”. But, by way of analogy with human construction methods, if in a particular geographic area, Texas, e.g., you looked at the ‘materials list’ for the various type houses constructed within that area, I imagine the ‘materials list’ would be quite similar—though the actual ‘look’ of the houses would be different. That’s where the architectural plans come in; they are decisive in determining the final ‘look’ (phenotype) of the houses. Thus, I suspect that the actual ‘plans’ for one major class of animals is likely to be found in what, today, is called ‘non-coding’ DNA (formerly, “junk-DNA”; as well, there is growing evidence that ALL of DNA is expressed/coded). So, until such time as advances have been made wherein both extinct and extanct ‘non-coding’ DNA can be analyzed and understood, I don’t know that we’re in a position to determine what entered the genome when.

    Second, determining “what is designed and what is not” seems to be a question we can get at without recourse to the above undertaking(s). Information theory itself suggests to us that the information contained in the genome had to have come about by an ‘intelligent agent’. In this sense, ALL of the genome is ‘designed’.

    But perhaps you’re after the distinction between, e.g., species and sub-species; IOW, the kind of ‘randomness’ that allows for adaptation, and how this ‘randomness’ interplays with genomic information. While there certainly seems to be such an ‘interplay’, whether or not this ‘interplay’ was intended to occur from the start becomes a different question in terms of design.

    Thirdly, regarding “a project the ID research community should be engaged in”, my reply would be: How can an ID research community exist when any disavowal of Darwinism within the scientific community is met with derision, hostility, and career endangerment? Just as Darwin thought that the ‘young’ would buy onto his theory, the only hope now (and it appears to be a growing hope) is that the ‘young’ biologists/scientists of today are much more open to criticism of Darwinain theory, and the day may even come when in certain universities departments will be set up to do “ID type” of research. But we’ll have to wait twenty years for that.

  40. Getawitness – Thank you for your support.

    Bornagain77 – I am rather surprised by your vituperative comments, as I addressed my comment to Bourne. I am sure that Denyse O’Leary, Michael Behe me and millions of Catholics are all wondering where your hatred of Catholicism came from, and we will pray for you to recant your hatred at least by your deathbed.

    We need to come together to help back ID and overthrow the neo-Darwinists as you say, and not let century old arguments derail our support of ID.

  41. Does ID expect Plasmodiae to decay to the point when they are no longer capable of being pathogenic? And are you saying the principle of ‘genetic entropy’ prohibits gene duplication?

    1. Sanford’s Genetic Entropy and ID are separate subjects, although there has been an increasing interest in Genetic Entropy amongst ID proponents on this site. Many agree with Sanford about genetic entropy in general but disagree with the estimated rate at which it accrues.
    2. 1st question: No. The short version is that fast replicators avoid this problem.

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

    Although it’s possible that some minor functionality can be lost that does not prevent strains from surviving. Kind of like if a human were born without the smallest toe (there is a limit to this analogy since six fingered people is not the introduction of CSI).
    3. 2nd question: No.

  42. Jack Krebs,
    Although somewhat difficult, I do believe a relatively easy avenue exist to establish the timing of insertion of CSI.

    First and foremost, it will come through thoroughly ruling out gross changes in genomes (i.e. ruling out the monkey to man theory on the genetic/genome level) I myself believe that gross changes are already ruled out because of the virtual 100% detrimental effect of any type of random mutations to genomes (Gerrish Lenski; Sanford; Spetner).

    Yet to persuade someone of Dave Scot’s philosophy, who believes in a radical front loading scenario, it will be necessary to first establish a virtual 100% functionality of the entire genome in order to rule out any “codes in waiting” theory (note ENCODE is working on this 100% functionality fact). But besides 100% functionality, even more is needed to rule out the radical front loading scenario. To thoroughly rule out the radical front loading scenario, it would be necessary to find moderate to severe polyfunctionality across the entire genome studied and to thus establish that genomes are indeed severely polyconstrained to any type of insertion of any type of information from the outside in any way, shape, or form. That fact plus the law of conservation of information clearly iterated by Dembski & Gitt, which states it is impossible for material processes to generate CSI, thus impossible for an existent genome to increase its own CSI, would effectively, if not completely, rule out the genome generating CSI by itself, or CSI being inserted from the outside into a proven severely polyfunctional system.

    Once the radical front loading scenario is ruled out completely, then tracing CSI will become simply (I use the term loosely) a matter of tracing the loss of genetic diversity (CSI) from original parent species to sub-species…

    I find it interesting in my preliminary look at genetic diversity that genetic diversity of a parent species is always greater than the total genetic diversity found across the entire spectrum of sub-species that emanate from the parent species.

    for one example:

    The sequence divergence within (breeds of) 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 dogs than for wolves)

    Genetic Entropy may somewhat throw a monkey wrench in all this though, because the longer a sub-species is separated from its parent species, the longer genetic degradation will occur and in effect destroy CSI and also in effect skew a pure reading of the diversity across the entire sub-species spectrum.

    facts would have to be established ,,,such as how much Genetic Entropy can a genome withstand before meltdown,,, and how much diversity is required by the CSI of parent species?

    I hope I explained myself clearly in this matter.

  43. Dave Scot:
    “You were at one time a single cell that transformed in a matter of weeks into very large number of specialized cells organized into a plethora of tissue types, organ types, and complex body plan. Clearly huge phenotypic transformations are possible since we see it happen in ontogenesis.”

    So we may as well subscribe to Haekel’s drawings then? At least in principle? Sorry, I’m not buying.

    I’d be willing to bet that Jonathan Wells and probably other specialists of developmental biology would dispute you on that.

    “Both are predetermined self-terminating processes where little if anything is left up to chance and the environment at most provides cues for advancing to the next level of diversification.”

    This sounds exactly like Darwinian NS. Some clue in the environment magically triggers macro-evo. The only difference I see is in the pre-determination.

    Why doesn’t this articles’ P.falciparum get triggered for macro changes? Or are there only certain organisms that correspond to front-loading?

    But what all genomes may share (don’t know but suspect)is the same core or kernel traits and programming. Does that prove front-loaded macro-evo.? I hardly think so.

    It does prove one thing though – a common designer, using the same OS kernel and re-usable code libraries. But that is no evidence, let alone proof, of common descent of mammals from reptiles or pelicans from t-rex.

    Still I suggest you examine what I said again, tell me how (and for heaven’s sake why!) front-loaded, well adapted fish got out of water to walk on land and breathe air? Or why and how well adapted reptiles would need to become mammals or birds?

    IMO, Even using a typical Darwinist just-story it cannot be done.

    Perhaps you could enlighten us. ;-)

  44. Jack Krebs,

    You have presented no empirical evidence, only an argument from authority. Like every other supporter of neo Darwinism before you, you have punted, deflected or essentially admitted there is no evidence.

    Since this thread is about induction, I can expect to ask the same question a million times and expect to get the same answer, namely nothing. Maybe as David Hume said on the millionth and one time I ask the question I will get an answer that proides evidence. But then again maybe not.

    Now if I challenge you on something even more complex than neo Darwinism such as the standard theory of Physics and said it was bogus, I bet within an hour or two I would get dozens of replies that outlined the empirical data behind it even if a lot of it was hard to understand.

    Why is it that a theory accepted by everyone in the science community has no takers? Jack, can you answer that.

    I will answer it for you. It is because there is no empirical data to support it and your answer just confirmed it. If you could provide some, you would be all over it and so would anyone else who supports neo Darwinism.

  45. Pantog you asked:

    Does ID expect Plasmodiae to decay to the point when they are no longer capable of being pathogenic?

    ID by itself only infers that Irreducibly Complex systems, displaying CSI, in the Plasmodiae cannot be generated by totally material processes, and says nothing about the degradation of Plasmodiae, whereas Genetic Entropy (a marriage between conservation of information and the second law) would hold that the Plasmodiae might or might not eventually decay, depending on its ability to keep its originally designed genome intact (presuming radical front-loading is false).

    Right now, as far as microorganisms are concerned, ancient DNA studies have shown that the Genetic Entropy of micro-organisms is exceedingly slow. (Thus their high population sizes are very effective in overcoming negative mutations and stabilizing the genome over long periods of time.)

    Yet microorganism are still bound to genetic entropy for they will never generate CSI of their own accord, nor will they escape the second laws eventual power in dispersing all material objects (every single particle of every single atom) on this world into final equilibrium in this universe. (unless of course something (namely God) comes along to overcome entropy)

  46. bornagain77,

    thanks for the extensive reply, I’d like to mention some additional data from Volkman’s paper – they sequence 2 parasites completely HB3 from Honduras and Dd2 from Indochina, they found 26,845 SNPs (comparing these 2 with the reference sequence called 3D7). Comparsion of just 3D7 and HB3 uncovered 37,039 indels of at least three bases, in addition to the SNPs.

    Highly variant gene families like var, rifin and stevor had nucleotide diversity levels (just SNPs) upto 6% – i.e. comparing two haploid organisms one SNP is found every 17 bases.

    The local feeling maybe to dismiss gene duplication, but comparing strains suggest falciparum sub-types have used this strategy on at least a dozen occasions – to generate novel functions. Drug resistance is a major new function – but as someone has pointed out this is the big topological feature in the organism’s fitness landscape. The other copied genes are involved in folate biosynthesis, surface proteins, cyclophillins and others. How dark-grey do these swans need to get?

    If anyones willing (just maybe) to accept common descent between Plasmodium sub-species (e.g. with rodent malaria) this suggests there are over 600 falciparum-specific genes (Kooij et al., 2005 “A Plasmodium Whole-Genome Synteny Map: Indels and Synteny Breakpoints as Foci for Species-Specific Genes”).

    This all on the background of us not knowing what most plasmodium genes do, and having only sequenced half a dozen falciparum genomes.

    And is anyone else amused by the quirk that – all the model organisms in which prospective conttrolled experiments in ‘genetic enropy’ could be conducted, are conveniently immune from the effects ? …

  47. How dark-grey do these swans need to get?

    How about providing ANY evidence against “all complex biological systems are generated by intelligent agents”? First, we have to swallow the assumptions related to hypothetical scenarios. Secondly, you provide no positive evidence that Darwinian mechanisms are even capable or that they were ever involved in these hypothetical scenarios.

  48. Pantog,

    And is anyone else amused by the quirk that – all the organisms in which prospective controlled experiments in ‘genetic entropy’ could be conducted, are conveniently immune from the effects ?

    This is indeed very interesting Pantog!

    You hit a nail on the head in your observations, I would love to trace the lineage of several different genomes in accordance with Genetic Entropy, and am extremely confident that all sub-speciation events will come at a cost to CSI…in fact that is exactly how one would correctly go about tracing the correct genomic lineage in accordance with the foundational principles of how we know information (CSI) will act in organisms.
    You mention other organisms, if I read you right, that are immune to the effects of malaria. I would be willing to assert that the malaria parasite could very well have had a somewhat essential purpose at one time, and that that purpose could very likely have been corrupted by a mutation of some sort or other i.e. corrupted by some type of genetic entropy.

    Where IDists run into problems right now in doing such things, is that evolutionists are very eager to have any increase in complexity explained by evolution, whereas IDists are always adamant to demand experimental proof that the complexity was generated by totally material processes.
    As Dr. Behe clearly pointed out, when closely looked for, evolution does not happen. Thus, denying evolutionists the very one crucial piece of conclusive proof they, absolutely, need to verify their theory!
    Yet, when we are using genome similarity comparisons, evolutionists are very quick in saying any increase of complexity across species genome, orders genome, and even phyla genome is conclusive proof of evolution, common ancestry, etc…etc… When clearly it is not conclusive evidence but only very suggestive evidence at best!

    Thus the process, of drawing correct genome lineages, seems to be muddled, since evolutionists are constantly trying to prove something that is false on first principles of science, and IDists are open to attack if they veer to far from demanding proof of CSI generation from purely material processes.

    Hopefully this situation can be remedied, I believe that many wonderful may be possible once a correct understanding is gained in biology.

  49. bornagain77

    “Hopefully this situation can be remedied, I believe that many wonderful may be possible once a correct understanding is gained in biology.”

    I totally concur, the primary objective in studying falciparum is to figure out how to speciecide it. If ID has anything to say on potential therapeutic targets, I’d be excited to hear.

    “You mention other organisms, if I read you right, that are immune to the effects of malaria. ”

    I was more meaning immune to the malign influences of “genetic entropy” – the model organims one could study seem to get exemptions. Its a little convenient.

  50. Pantrog you stated,

    If ID has anything to say on potential therapeutic targets, I’d be excited to hear.

    In this thread:

    http://www.uncommondescent.com...../#comments

    we were discussing something along this line, although the discussion did not fully develop as I was hoping it would.

    Of special note;

    I was studying ancient bacteria and stumbled across this:

    Dr. Cano is so confident of his latest findings that he has founded a company, the Ambergene Corporation, in San Carlos, Calif., to develop pharmaceutical products derived from the putative ancient organisms. Ambergene has already applied for patents for at least three of the new antibiotics he believes the bacteria have helped him to produce.

    These , Dr. Cano said, could fill therapeutic gaps created by the increasing immunity of certain disease-spreading microbes to antibiotics.

    http://query.nytimes.com/gst/f.....nted=print

    Of course I don’t know all the intricacies but this sounds very promising:

    Ambergene has already applied for patents for at least three of the new antibiotics he believes the bacteria have helped him to produce.

    I have many questions; how are these antibiotics new i.e. are they using different pathways to destroy the bacteria? If so then there is promise for developing effective treatment for infections.

    I believe that Dr. Behe,,describes the process of a supergerm acquiring resistance in this following manner, a rare “unlucky” individual in a population will have a “luckily” resistant germ to a new dr^ug, thus this resistant germ spreads throughout the population… This germ becomes problematic and dr^ug B is discovered and developed at which point the resistant germ will again have a “luckily” resistant germ in a rare “unlucky” individual and thus repeating the cycle…

    Thus it goes to reason that the most effective treatment for problematic germs is to hit them all at once with multiple dr^ug co^ktails at the inception of attacking the problem and thus ensuring that the entire population of germs in the entire population of people is wiped out…completely in one fell swoop!

    Will this help for already resistant strains, No Of course not…And once the multiple resistant strain is present in a existent population of germs,,,even though the existent population of germs easily out compete the mutated germ (in a dr^ug free environment),,I believe that it will be found that a tiny remnant of the multiple resistant strain will persist in the germ population, for a fairly long time, before it is outcompeted into oblivion…(Of course the more weakened by accumulated mutated resistance of the germ is,,the more quickly the germ will reach zero on the decay curve (that is of course, once the germ is forced into competing with the original strain in a dr^ug free environment)) My first reaction is that the decay curve will reach into many, many, years before a virtual zero is attained on the decay curve for the multiple resistant germs.

    Thus clearly, the only effective treatment to totally eradicate a existent resistant germ is to develop multiple new dr^ugs (or maybe even a single dr^ug that requires the germ to make too many “lucky” mutations) and deploy them all at once and deny the germ the stepwise fashion it needs to acquire “super-resistance” we are now seeing in hospital germs..

    So if several questions can be answered yes indeed ID does seem to offer concrete solutions to problems.

  51. I’m going to delete every comment on this thread that mentions religion or is otherwise off topic. Don’t bother posting any more of it unless you like wasting time.

  52. DaveScot,

    I respect your decision. There’s no way to move such comments (to an off-topic threaad) without deleting them, is there? This thread now contains answers to invisible questions.

  53. “Thus clearly, the only effective treatment to totally eradicate a existent resistant germ is to develop multiple new dr^ugs (or maybe even a single dr^ug that requires the germ to make too many “lucky” mutations) and deploy them all at once and deny the germ the stepwise fashion it needs to acquire “super-resistance” we are now seeing in hospital germs..”

    This of course is the current strategy taken with HIV, malaria, TB and others. The problem of ‘lucky’ mutations spreading in the population – is the standard evolutionary theory interpretation of antibiotic resistance.

    I was pondering if the ID insight -that the battle with micro-organisms is not “man vs. undirected natural selection entity”, but “man vs. designed parasite” – had practical implications … e.g. if there is front-loading of anti-therapeutic countermeasures in the parasite (e.g. a degredative enzyme to an as yet unconcieved drug) one could reverse-engineer the genome looking for clues to potential therapies (computer hackers do this with security updates for operating systems).

    Still there are ethical and philosophical issues – if the designer has built in mechanisms to stop therapeutic interventions – should this warn us of from treating disease? what does this tell us about the designer? I mean if a powerful alien had come to earth and designed a highly effective range of killer microbes – we would perhaps have grounds for grievance? It sounds like biological warfare.

  54. The huge population size is a very poor substitute for a sufficient number of generations needed for anything complicated to evolve. Several thousand generations isn’t enough to make any weakly selectable new trait prevalent, let alone a complicated sequence of improvements.

  55. Panrog,

    Dr. Behe addressed this objection here;

    Kenneth R. Miller and the Problem of Evil, Part 3

    http://www.amazon.com/gp/blog/.....20-3159839

    Here is an excerpt;

    Why couldn’t a grieving mother justifiably demand of an infinitely powerful God that He explain why He chose such a sloppy process to make life, instead of a more efficient process that would not produce natural evils such as parasites and tsunamis? One that wouldn’t cause such enormous pain? It seems to me that designing a poor Darwinian process that inevitably spins off natural evils leaves One as vulnerable to being sued for incompetence as directly designing them as finished products.

    My own view (which Miller spectacularly fails to grasp) is that, as a scientist, one is obliged to look at the evidence of nature dispassionately and nonjudgmentally. If the coherence and complexity of the malaria parasite point to its purposeful design by an intelligent agent, then that’s where the data point. As a scientist, one is not allowed to pass judgment on the morality of nature. To reject the weight of evidence because it shows the universe to be something unpalatable is to betray science.

    On the other hand, as a theist one can make an argument that what strikes us as evil in nature is part of a larger whole which is good. In his recent book Francisco Ayala wrote that one could regard tsunamis as the unintended side effect of a good process (plate tectonics) which is necessary to build a habitable world. Well, heck, one can make the same argument for parasites and viruses. It may well be that such seemingly vile creatures actually play positive roles in the economy of biology, of which we are in large part unaware. If that’s the case, then directly designing parasites and viruses is as defensible in terms of the overall goodness of nature as is designing the processes of plate tectonics. The fact that they are dangerous to humans is an unintended side effect of something that is good in itself.

    I hope this helped Pantrog, But this subject digresses from our main discussion;

    I wanted to show you a rather humorous antidote someone “an IDists” had for the supergerms:

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

    Likewise, you contract a hospital infection only in a hospital. The hospitals are spraying disinfectants on every available surface to kill off their so-called supergerms, and, most importantly, dealing with serious clinical infections requiring powerful antibiotics. Maybe they would do better to bring in a few truckloads of dirt off the street every six months, and spread that around and sweep it off!

    Maybe the hospitals would do even better to do research on inoculating superinfection patients, not with more antibiotics, but with a competing infection that would crowd out the supergerms. (I doubt that this would work, but it’s worth exploring, especially when germs that kill by bacteriotoxins are concerned.)

    Now that should definitely be food for thought Pantrog! LOL

  56. Hu

    How do you figure only thousands of generations for falciparum? It infects a billion humans every year, asexually replicates itself into a trillion parasites in a full blown infection, and is carried by God only knows how many mosquitoes (presumably more mosquito hosts than human hosts) where it reproduces sexually. That’s billions of trillions of generations.

  57. I was calling all those countless currently existing falciparum parasites one generation. The previous generation, the immediate ancestors of the current one, lived mostly two days ago, the generation before that four days ago and so on. I presume the concept is clear, even though I may be using the wrong terminology. Anyway, at the rate of one “generation” in two days, you get about 11,000 “generations” in the time chloroquine has been used as an antimalarial, about 60 years. (I thought chloroquine was a more recent invention and didn’t check; hence “several thousand”. I’m sorry.)

    Of course, I’m not denying that each such “generation” consists of a huge number of individual parasites, but that’s less important than time.

  58. And of course although release of a new generation of merozoites is every couple of days – the parasite is effectively clonal and haploid, the time between meotic events (when recombination can take place between strains) is weeks.

    Gametocyte production starts 1 – 2 weeks after infection, then they need ingested by a mosquito – then theres the sequence of ookinete, oocyst and sporozoites formation which may add days to the amount of time before inoculation of the new clone generation.

    Still there’s a big replication potential.

  59. Every single time an individual parasite replicates, be it asexual or sexual, its genome is copied from mother to daughter. Each and every time the genome is copied to a daughter cell there is an opportunity for random mutation to introduce changes. These changes are heritable. Each replication is a new generation. Ergo there have been billions of trillions of generations in the last several decades.

  60. For clarity it would probably be better to use the term ‘replication’. In the malaria literature ‘generation’ is often used to refer to the time between fertilized zygotes (~2 weeks+).

    e.g. “A generation in malaria is the average time taken for it to complete its life cycle”

    The Evolution of Drug-Resistant Malaria: The Role of Drug Elimination Half-Life Ian M. Hastings, William M. Watkins, Nicholas J. White Philosophical Transactions: Biological Sciences, Vol. 357, No. 1420, Reviews and a Special Collection of Papers on Human Migration (Apr. 29, 2002), pp. 505-519

    After all there will be thousands of asexual cell divisions between you and your offspring. By convention these aren’t generations.

    Alternatively you could refer to ‘generations of merozoites’ that would also be clearer.

  61. After all there will be thousands of asexual cell divisions between you and your offspring. By convention these aren’t generations.

    Yes but those are somatic cells and mutations in them are not heritable. Falciparum has no somatic cells. Any genetic change in falciparum, whether it occured during sexual or asexual reproduction, is heritable.

    I would have thought that clear without belaboring the point but evidently it wasn’t clear to everyone. I guess I should have known since Bob O’Hara, an expert I believe in fungi, claimed that evolution doesn’t occur in individual mycelial colonies and that it could only happen when spores are produced by sexual reproduction. I still don’t think he gets it that each cell in the colony can mutate during asexual reproduction and any clonal cell has the potential for participating in sexual reproduction.

    By all rights falciparum should be an extremely rapid evolver. Each year a billion isolated clonal populations of up to a trillion parasites grow in human hosts. The fittest of these are then sampled by God only knows how many billions of mosquitos and in the mosquito’s gut recombination occurs allowing any of the beneficial mutations in the clonal populations to spread into other cell lines. It’s difficult to imagine a more opportune situation for random mutation and natural selection to do what it is claimed it can do.

  62. “Yes but those are somatic cells and mutations in them are not heritable”

    You’ve forgotten sperm,

    There are perhaps 40 somatic cell generations between human male zygote and sertoli cells – there are then thousands of germline replications – all with the potential for heritable change.

  63. [correction]

    There are perhaps 40 cell divisions between human male zygote and sertoli cells.

    (they’re not somatic if the eventually contribute to the germline – and ‘generation’ is, as we have learnt, ambiguous.)

  64. Pantrog, “and ‘generation’ is, as we have learnt, ambiguous.”

    Not really. From The Oxford Dictionary of Science:

    A group of organisms of approximately the same age within a population. Organisms that are crossed to produce offspring in a genetics study are referred to as the parent generation and their offspring are the first filial generation.

    DaveScot’s point is beyond my understanding, but his language isn’t: he was clearly using “generation” in a non-standard sense.

  65. 66

    DaveScot,”Each replication is a new generation. Ergo there have been billions of trillions of generations in the last several decades.”
    I’m no expert in this area, but it seems to me that using this definition of “generation” that my siblings and I should be considered of different generations?

  66. Please bare with me. I know a bit about the theory of evolution, and I’m trying to find out whether the evidence for ID is stronger. I’m not convinced by your example, as you don’t take into account a factor that potentially has a huge impact. I’ll present an oversimplified mathematical model just to illustrate that one point.

    Suppose we have two populations, one of which consists of 10^21 individuals, the other of 10^6 individuals. After one time unit, all individuals are replaced by their immediate descendants. (A time unit for P. falciparum would be two days, for a proto-mammal maybe a year or two.) Every new individual has 1 chance in 10^6 to carry a new slightly beneficial mutation, which increases its procreation probability by 10^-4. You can imagine every normal individual gets 10,000 lottery tickets and every mutant 10,001 tickets. As many tickets are drawn at random as there are individuals in the population, and each lucky draw corresponds to a descendant. Usually, the effect of k mutations in the same individual is just k times the effect of one mutation, i.e., the individual gets 10,000 + k tickets. However, any combination of 8 mutations has 1 chance in 10^65 of being strongly beneficial and becoming prevalent in a very short time.

    What happens to the large population in 10,000 units of time? In one unit of time, the number of carriers of existing mutations is multiplied roughly by 1.0001, and 10^15 new mutations will occur. Unless some roundoff errors accumulate more than I estimated in my head, somewhat less than 2×10^19 individuals or 2% of the population will carry at least 1 mutation. Assuming the mutations are mixed well by sexual reproduction, the number of individuals with 8 mutations will be about 10^21 / (50^8 x 8!) or about 600. If new combinations of mutations are created at each time unit, the expected number of lucky combinations is certainly less than (600 x 10,000)/10^6 = 6.

    How about the smaller population? On the average, one beneficial mutation occurs in one unit of time. It has 1 chance in 10,000 to become prevalent, so once in 10,000 time units a new beneficial mutation will start the process of spreading to the entire population. In about 150,000 time units, it will spread to the majority. In 400,000 time units, there will be about 25 well-established mutations around, and there are a bit more than 10^6 ways to choose 8 mutations out of 25. So, even assuming that the 17 mutations that weren’t part of the lucky combination are totally out of luck and will never have an effect, it won’t take more than about 2,400,000 time units for the smaller population to achieve more than the larger population did in 10,000 time units.

    I saw it mentioned somewhere that chloroquine resistance seems to be caused by 8 mutations, but I’m afraid I lost the URL. I took your estimate of the population size of P. falciparum and my own calculation of the time involved. I pulled the rest of the numbers out of thin air, trying to be vaguely realistic and tweaking them to get within an order of magnitude from observations.

    If you can show that some factor I left out (there are many) essentially nullifies my argument, I’ll be very eager to learn from my mistake.

  67. Oops, typo: A set of 8 slightly beneficial mutations has 1 chance in 10^6, not 1 in 10^65, of being strongly beneficial. Sorry for forgetting to proofread.

  68. Hu

    Every new individual has 1 chance in 10^6 to carry a new slightly beneficial mutation

    Presuming falciparum has the average eukaryote mutation rate of 1 in 10^9 nucleotides copied then with a genome of 23 million base pairs only 3% of the individuals will have any mutation at all while 97% are perfect copies.

    If the beneficial mutation rate of 1 in 10^6 mutations (Gerrish and Lenski, 1998) is correct then for falciparum the number of individuals with a single beneficial mutation is 3 per 10^8 individuals.

    This seems reliable enough for falciparum since atovaquone resistance, which requires only a single changed nucleotide, arises in approximately 5 of 10^10 individuals. Chloroquine resistance requires 2 simultaneous point mutations for any benefit at all and one or more additional point mutations on top of that for full resistance. The chance of getting a two-nucleotide beneficial mutation in one individual falciparum, based on the observed atovaquone rate, is about 5 in 10^20 individuals. This also seems reliable enough since chloroquine resistance arises about 3 times per year (10^20 replications).

    Extrapolating from this the probability of a set of 8 simultaneous beneficial nucleotide changes would be 5 in 10^80. Clearly that number is far too large to have any reasonable chance of ever happening. Even just 3 simultaneous beneficial nucleotide changes, 5 chances in 10^30 individuals, is essentially out of reach for even such a prolific species of eukaryote as falciparum. The only real chance of ever getting 8 beneficial mutations in one individual falciparum is through a sequence of 8 single-nucleotide beneficial mutations (maybe one dual-nucleotide mutation in the sequence) where each single or dual event is selectable by itself.

    Thus the “edge of evolution” is established by observation that matches what is predicted given numbers of 1 of 10^9 nucleotide copy errors and 1 in 10^6 of those being beneficial. The $64,000 question is how, in light of the observational evidence in falciparum, could reptiles evolve into mammals by random mutation when the number of replications for that transition is orders of magnitude fewer than observed in falciparum and the number of beneficial mutations required in the transition is orders of magnitude greater than what falciparum was able to accomplish. Non sequitur.

  69. Stanton

    The mistake was someone else using “generations” instead of “replications”. Each of you and your siblings can have different heritable mutations. Each of you represents one chance for random mutation to generate descent with modification. So if you have 3 siblings that’s only one generation but 4 chances for random heritable change. I merely pointed out that the definition for generation and replication must be equivalent if you want to swap terms like that.

  70. DaveScot, I thought Hu [55] was using “generations” correctly. But I may have been mistaken; I’m still learning this stuff.

  71. Extrapolating from this the probability of a set of 8 simultaneous beneficial nucleotide changes would be 5 in 10^80. Clearly that number is far too large to have any reasonable chance of ever happening. Even just 3 simultaneous beneficial nucleotide changes, 5 chances in 10^30 individuals, is essentially out of reach for even such a prolific species of eukaryote as falciparum. The only real chance of ever getting 8 beneficial mutations in one individual falciparum is through a sequence of 8 single-nucleotide beneficial mutations (maybe one dual-nucleotide mutation in the sequence) where each single or dual event is selectable by itself.

    Like Hu, I remember reading about speculations that a gradual/stepwise direct pathway existed for developing CQ resistance. The main issue is that such pathways should not be conflated with indirect non-gradualistic pathways that require simultaneous changes (it’s not stepwise). Behe of course is focused on analyzing those types of non-gradual indirect pathways since the majority of objects under debate cannot be broken down into gradual/stepwise direct pathways.

    I’ll just quote myself here (with some mods):

    The interesting thing about the Darwinist commentators on Amazon is that they were so focused on “we must prove Behe to be wrong somehow” that they fail to realize they’re shooting themselves in the foot. If CQ resistance did indeed come about by a gradual/stepwise direct pathway scenario then all that does is make this example of the “all-mighty powers of Darwinian mechanisms” even more trivial than before! After all, a direct stepwise scenario is much more likely to occur than one that requires simultaneous changes or an indirect pathway. Yet even then Darwinian mechanisms have a hard time bring about such a change even with the extremely high number of replications (in comparison to higher animals). (BTW, I would rank in order of difficulty from easiest to hardest: direct gradual, indirect gradual, direct multiple/simultaneous, and then a combination of direct gradual changes combined with indirect multiple/simultaneous)

    Now I have seen excerpts where scientists hypothesize more complicated gradual scenarios…

    Current evidence from transfection studies (71, 187) strongly suggests that the mechanism of P. falciparum resistance to CQ is linked to mutations in the pfcrt gene, especially the substitution of threonine for lysine at position 76. However, other mutations in the pfcrt gene at positions 72 to 78, 97, 220, 271, 326, 356, and 371, as well as mutations in other genes such as pfmdr1, might be involved in the modulation of resistance (173, 223). CQ resistance seems to involve a progressive accumulation of mutations in the pfcrt gene, and the mutation at position 76 seems to be the last in the long process leading to CQ clinical failure (53, 92).

    http://www.sciencemag.org/cgi/.....98/5591/74

    …mutation 4 allows parasites to infect people 6 days after treatment rather than 7 days. The relatively rapid elimination of CQ means that these are rather weak selective forces (6) and that the spread of these first mutations will be slow. Eventually, mutation 8 arises, which allows the parasite to survive therapeutic levels of CQ. Once above this threshold, the selective advantage conferred by this mutation becomes enormous…

    Behe is of course narrowing the focus down to position 76 and 220. But just because other scientists are discussing other scenarios for generating CQ resistance that “must” mean Behe is lying in the minds of many Darwinists. Also, this may be the information Hu was thinking of.

    Otherwise, many of the Amazon commentators do not seem to have bothered to read what Behe had said previously:

    Incidentally, this bears on Coyne’s comment on Miller’s review that “one of the two mutations that Behe claims are ‘required’ for CQR is not actually required (Chen et al. 2003, reference accidentally omitted from Miller’s piece).” If you read that paper you see that, yes, A220S is not found in some resistant strains, as it is in most. (By the way, I was always quite careful in my book to state that A220S had been found in most strains, because I was quite aware of the several exceptions.) However, one also reads that the strains missing A220S have several other, novel mutations, which may be playing a comparable role in them that the mutation at position 220 plays in most other strains. My argument does not depend on exactly which changes are needed in the protein. Rather, the important point is that multiple changes appear to be required for resistance in the wild.

  72. DaveScot:

    Thank you for the data supporting a more precise estimate on the basic mutation rate. The estimates on beneficial mutation rates seem to vary by several orders of magnitude, and my assumption seems to fall within the empirically supported range. (See Perfeito L, Fernandes L, Mota C, Gordo I Adaptive mutations in bacteria: high rate and small effects. Science. 2007 Aug 10;317(5839):813-5.) Anyway, accepting your estimate for the sake of argument, one only needs to multiply the effect of a mutation by three and the size of the smaller population by ten to obtain similar results.

    My point stands: under identical assumptions, time can be vastly more important than population size. The total number of replication events is an inadequate measure.

  73. Hu

    Total number of replications where mutations are heritable is all that counts when probability of any certain mutation occuring is what you’re trying to ascertain.

    If you cast a single die the chance of getting a six is one in six. If you cast a thousand die at once the chance of getting a six is almost 100%. You can cast a single die a thousand times and the chance of getting a six in one of those casts is the same as casting a thousand at once.

  74. DaveScot,

    I don’t know enough to assess the debate between you and Hu. But I have to say, the term “generations” is misused all over the place here, and not just in this thread. Consider the moderation FAQ:

    Behe’s latest work of analyzing what billions of trillions of generations of p.falciparum accomplished in the way of generating novel complexity without benefit of intelligent agency supports the prediction that only intelligent agency is capable of producing complex specified information.

    When I search for “billions of trillions of generations” as a phrase, I get six hits. I think that, for each of those times, you really mean “replications.” Thanks. You probably don’t want to change the comments, ’cause that would erase the history, but you might want to change the “arguments not to use” page.

  75. 76

    DaveScot said,

    Total number of replications where mutations are heritable is all that counts when probability of any certain mutation occuring is what you’re trying to ascertain.

    If you’re looking for the probability of a “certain mutation” occurring, you’re looking for something that’s already happened, which means the probability is 1.

  76. DaveScot,

    Re my comment [75], the moderation FAQ has been corrected.

    Uh, you’re welcome?

  77. I edited the FAQ (Dave wrote the original version but I’ve been editing and adding a lot of content). Personally I think quibbling over the usage of “replications” or “generations” is a waste of time since it’s irrelevant to the main points. But I’d rather make the change than have people get caught up in analyzing minutiae.

  78. Patrick,

    Thanks for editing the FAQ. I’m just trying to help make sure that we use the standard terms when talking science. Not using the standard terms would detract from our credibility.

  79. Good point, although I’d add that you cannot please everyone. For example, some Darwinists are perfectly fine with using the term “Darwinist”. Others object to its usage, since they believe it does not reflect the changes to evolutionary biology. But I haven’t heard a good replacement term to describe the group as a whole. Same thing with “RM+NS”. Personally I was using it to reference all possible Darwinian mechanisms. But I can see how that can be confusing. So I now prefer RV+NS.

  80. DaveScot:

    Total number of replications where mutations are heritable is all that counts when probability of any certain mutation occuring is what you’re trying to ascertain.

    Yes, that’s obvious. (Any realistic difference in mutation rates is clearly dwarfed by the difference in population sizes.) The same applies to any set of simultaneous mutations.

    However, the situation changes if there’s a set of slightly beneficial mutations that together give a substantial advantage. In the huge population of P. falciparum, many mutations certainly keep occurring over and over again, but if there’s a number of them that individually have only a slight beneficial effect in the presence of chloroquine and none otherwise, they haven’t had the time to spread much, so there’s little overlap. A tiny fraction of the total number of replications can suffice to produce a suitable combination if selection has enough time to make the mutations prevalent. I gave a specific theoretical example.

  81. Hu,
    you stated:

    However, the situation changes if there’s a set of slightly beneficial mutations that together give a substantial advantage.

    Please give proof for an unambiguous beneficial mutation.

    I have failed to see any evidence for beneficial mutations.

    The primary thing that is crushing to the evolutionary theory is this fact. Of the random mutations that do occur, and have manifested traits in organisms that can be measured, at least 999,999 out of 1,000,000 (99.9999%) of these mutations to the DNA have been found to produce traits in organisms that are harmful and/or fa^tal to the life-form having the mutation! (Sanford; Genetic Entropy page 38)

    “I have seen estimates of the incidence of 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) Since neutral mutations can be inferred to almost never occur in a genome, then the ratio of deleterious to beneficial mutations seems to be one million to one.” (Sanford; Genetic Entropy, page 38: Note: this statement has been revised to reflect the evolutionary belief of some totally neutral mutations of Gerrish and Lenski)

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

    Even if there were totally neutral mutations, which is highly unlikely given the overwhelming interrelated complexity of the genome, Gerrish and Lenski most likely used a incomplete measure of fitness/information in order to arrive at their one in a million number for beneficial mutations. I maintain that their, one in a million, estimate for beneficial mutations is flawed and that ALL mutations to a genome will be found to be harmful/fatal when using a correct measure of fitness/information. The following articles points out this flaw, in measuring the total fitness/information of a organism, by evolutionary scientists and thus skewing the already crushing, but biased, mutational studies:

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

    http://www.answersingenesis.or.....apter5.asp

    ” 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.”

    In fact, from consistent findings such as these, it is increasingly apparent that Genetic Entropy is the overriding foundational rule for all of biological life with no exceptions at all, and that belief in beneficial mutations is nothing more than wishful speculation that has no foundation in science whatsoever:

    The foundational rule for biology can be stated like this:

    All adaptations away from a parent species for a sub-species, which increase fitness to a particular environment, will always come at a loss of information from the parent species. (Note: At present viruses are excluded from this rule.)

    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 disorders (Dr. Gary Parker).

    “It is entirely in line with the al 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 ally 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)

    “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)

    So Hu, please do give an unambiguous example of a beneficial mutation that has not in reality involved loss of either function or information, before you state beneficial mutations might occur!

  82. Hu, You cited this article for your basis of beneficial mutations of 1 in 10,000:

    Fitness effects of advantageous mutations in evolving Escherichia coli populations

    http://www.pubmedcentral.nih.g.....rtid=14717

    And in this study they do indeed state your 1 in 10,000 number, but also mention the fact that it is often negated by what they term “clonal interference” which in reality refers to the 100% polyfunctionality of the genome.

    In other words your study is flawed in that it says: This is the rate of beneficial mutations (1 in 10,000): Yet at the same time they clearly state that the effect of the beneficial mutations is negated by other “beneficial mutations”.

    Thus we are back to Garrish and Lenski’s 1 in 1,000,000 estimate for beneficial mutations being beneficial. Yet even in Garrish and Lenski’s study, I will maintain that the parent species will always be found to have more information.

    In other words Hu, beneficial mutation studies always come with a flaw of some sort. When you dig deep enough you always find their flaw.

    Since the study you cited was on e-coli, here is a paper that gives some detail to what I am talking about:

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

  83. bornagain77:

    Please give proof for an unambiguous beneficial mutation.

    Please replace mentally “beneficial mutation” with “ambiguous beneficial mutation” in my arguments above.

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