P.falciparum – No Black Swan Observed

_{November 6, 2007

Intelligent Design}

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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.

Comments

"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.Pantrog_{November 8, 2007
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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.getawitness_{November 8, 2007
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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.DaveScot_{November 7, 2007
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Pantrog you stated, If ID has anything to say on potential therapeutic targets, I’d be excited to hear. In this thread: https://uncommondescent.com/intelligent-design/behe-vs-mothra-no-mrsa/#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/fullpage.html?res=990CEFD61439F93AA25756C0A963958260&sec=&spon=&pagewanted=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.bornagain77_{November 7, 2007
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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.Pantrog_{November 7, 2007
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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.bornagain77_{November 7, 2007
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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.Patrick_{November 7, 2007
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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 ? ...Pantrog_{November 7, 2007
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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)bornagain77_{November 7, 2007
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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.jerry_{November 7, 2007
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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. ;-)Borne_{November 7, 2007
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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.bornagain77_{November 7, 2007
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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. https://uncommondescent.com/intelligent-design/genetic-entropy-and-malarial-parasite-pfalciparum/ 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.Patrick_{November 7, 2007
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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.Glarson24_{November 7, 2007
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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.PaV_{November 7, 2007
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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/globe/health_science/articles/2007/09/24/dna_unraveled/?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..)bornagain77_{November 7, 2007
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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.jerry_{November 7, 2007
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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.DaveScot_{November 7, 2007
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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.gpuccio_{November 7, 2007
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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!bornagain77_{November 7, 2007
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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).Pantrog_{November 7, 2007
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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/sites/entrez?db=pubmed&cmd=retrieve&list_uids=16789840Pantrog_{November 7, 2007
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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.Pantrog_{November 7, 2007
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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.gpuccio_{November 7, 2007
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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 SwansDLH_{November 6, 2007
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BA77 Excellent quote from Behe in comment 24. I wish I could write that well.DaveScot_{November 6, 2007
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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.DaveScot_{November 6, 2007
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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.DaveScot_{November 6, 2007
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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/sites/entrez?db=pubmed&uid=17159979&cmd=showdetailview&indexed=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.gov/articlerender.fcgi?artid=33358 Of special note: Adcock et al. (7) clearly demonstrate the actual extinction of an ancient mtDNA lineage belonging to an anatomically modern human, because this lineage is not found in living Australians. Here is a Paper that has confirmation of dogs and grey wolves staying within principle of Genetic Entropy. http://jhered.oxfordjournals.org/cgi/reprint/90/1/71.pdf of special note: Some sequences found in dogs were identical to those in wolves… The sequence divergence within (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.gov/articlerender.fcgi?artid=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/releases/2007/03/070309103157.htm Genetic Diversity in Algerian Sheep Breeds, Using Microsatellite Markers http://www.springerlink.com/content/h4qp4g35547xr75m/ 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 ... www.nature.com/hdy/journal/v99/n4/full/6801016a.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!bornagain77_{November 6, 2007
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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.BenK_{November 6, 2007
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