A Practical Medical Application of ID Theory (or, Darwinism as a Science-Stopper)

_{Gil Dodgen

December 9, 2007

Darwinism, Science}

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In a previous UD thread, a dude named Poachy (where do these guys get these screen names?), with much sarcasm about a comment I made, proposed:

We need to start voting with our feet and eschew all but the medical advances that come from application of the ID paradigm.

Here’s a prediction and a potential medical application from ID theory: Design a chemical or protein which would require a triple CCC to defeat its toxic effects on a bacterium, and it will exhaust the probabilistic resources of blind-watchmaker mechanisms to counteract the toxic effects.

Such a success could and will only come from engineering and reverse-engineering efforts, not from Darwinian theory.

In the meantime, medical doctors should prescribe multiple antibiotics for all infections, since this will decrease the likelihood that infectious agents can develop resistance through stochastic processes. Had the nature of the limits of Darwinian processes been understood at the outset, the medical community would not have replaced one antibiotic with another in a serial fashion, but would have prescribed them in parallel.

This represents yet another catastrophic failure of Darwinian presumption, which is based on hopelessly out-of-date 19th century scientific naïveté.

Comments

Corey busted me on not looking up a study: "When you say “and I would be willing to bet that severe flaws could be found in their study when thoroughly hashed out” it seems malicious to me. Rather than assuming flaws, you could actually check I’m sure. If there aren’t flaws, then wouldn’t you feel silly saying what you did?" So Corey I looked into it and found: http://www.sciencedaily.com/releases/2007/09/070904151351.htm Of special note: "While I don't think we can conclude that the mice we created with the ultraconserved elements deleted are normal, we can confidently conclude that the presence of the ultraconserved elements are not required for the viability of the organism." Edward Rubin, Director of the Joint Genome Institute. Note this sentence Corey; "While I don't think we can conclude that the mice we created with the ultraconserved elements deleted are normal.. Thus Corey even the scientists who conducted the study conceded that he could not conclude that they were "normal". Thus for the purpose of trying to establish a solid evidence to base the radical front-loading scenario on, the evidence, according to the scientists very own words, is clearly not substantial enough.bornagain77_{December 11, 2007
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Thanks ari-freedom, That was very interesting. Actually, I think this "nonrandom variation" evidence of Dr. Spetner's, that you pointed out, fits in very well with the ID/Genetic Entropy mo^del. Whereas environmental cues contradict the neo-Darwinism dogma (and is actually ignored by them according to Spetner), Environmental cues acting on already present information in the "parent" species genome readily explains the "rapid" burst of radiative adaptation following the novel "parent" species abrupt appearance that we consistently see in the fossil record. i.e. Evolution has no solid answers for this enigma whereas we do. In fact I have seen several papers pointing out the insufficiency of natural selection to produce rapid changes in and of itself (Sanford; Genetic Entropy: natural selection "noise"). Thus "nonrandom variation" fills a gap in the ID/Genetic Entropy mo^del by supplying the proper mechanism for the rapid sub-speciation witnessed. But for a starting position I will hold that all "nonrandom variation" will also conform to the overriding principle of genetic entropy since this position is more in harmony with the Law of Conservation of Information and the Second Law of Thermodynamics, as well with the evidence in the fossil record, than the non-random front-loaded mod^el is. I just keep thinking about the enormous amount of time on earth that "unused" genetic information had to survive without any damage in "primitive organisms" and the whole thing just doesn't "feel" right to me at all. As well the fossil record shows a very consistent pattern. "As Niles Eldredge and Stephen Jay Gould pointed out almost three decades ago, the general pattern for the evolution of diversity (as shown by the fossil record) follows precisely this pattern: a burst of rapid diversity following a major ecological change, and then a gradual decline in diversity over relatively long periods of time." Allan MacNeill PhD Another trouble the with radical front-loading mo^del, is that all adaptive radiations of sub-species can be persuasively argued to lose genetic information, for there is a detectable loss in variability from parent species, as with this cichlid study; African cichlid fish: a system in adaptive radiation research http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1635482 of special note: Interestingly, ecological opportunity (the availability of an unoccupied adaptive zone), though explaining rates of diversification in radiating lineages, is alone not sufficient to predict whether a radiation occurs. The available data suggest that the propensity to undergo adaptive radiation in lakes evolved sequentially along one branch in the phylogenetic tree of African cichlids, but is completely absent in other lineages. Instead of attributing the propensity for intralacustrine speciation to morphological or behavioural innovations, it is tempting to speculate that the propensity is explained by genomic properties that reflect a history of repeated episodes of lacustrine radiation: the propensity to radiate was significantly higher in lineages whose precursors emerged from more ancient adaptive radiations than in other lineages. Thus as you can see, the evolutionists are mystified that the radiations are not happening for the "sub-species" of cichlids but are always radiating from the "more ancient" parent lineage. This fact is totally contrary to what we would expect to find if the variation found in the sub-species were truly wrought by random mutations in the DNA generating novel information for variability! And this result is to be totally expected if the parent species were indeed created with a certain amount of flexibility for adaptation to differing environments already programmed in its genetic code! I will have to look deeper into this, and make sure I have all my bases covered, but I feel Spetner's work will fit in very well with ID/Genetic Entropy mo^del.bornagain77_{December 11, 2007
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Bettawrekonize I am sure that garlic plays a part in a well balanced diet but the key phrase is "well balanced." I do not buy for one minute the idea of a "super" food or herb, just as I don't believe that pharmaceutical drugs will solve all our problems.ari-freedom_{December 11, 2007
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When you say "and I would be willing to bet that severe flaws could be found in their study when thoroughly hashed out" it seems malicious to me. Rather than assuming flaws, you could actually check I'm sure. If there aren't flaws, then wouldn't you feel silly saying what you did? There probably would be some sort of "flaw" but that's kind of how science works, eh? You do an experiment and see what it tells you. Then you realize that isn't the final answer and you go do another experiment and see what that tells you.Corey_{December 11, 2007
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yes you. thanks. I'm thinking about the experiments in chapter 7, page 187-191 Or for example the cichlid/guppy experiment on page 206.ari-freedom_{December 11, 2007
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ari-freedom you ask, I would like to know how you would explain the examples shown in Spetner’s book. Is the question for DaveScot or me? If me, I happen to have Spetner's book, so if you could give me a page number I would be happy to look it up and see how it fits into Sanford's work.bornagain77_{December 11, 2007
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For the environmental cue to have something to work on in the radical front-loading scenario, should not the scenario be required to demonstrate a tangible amount of radically novel and beneficial morphology through these mutational studies? i.e. Should not radically new structures appear at least some time in any one of these extensive studies?
The trick would be to find a species that has not yet self-terminated. Now if that it is not immediately observed the other part of the hypothesis, the conversation method, could found.Patrick_{December 11, 2007
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We know that there are at least several cases of pleiotropy, where one gene codes for more than one trait and polygeny, where one trait is coded by more than one gene. I would like to know how you would explain the examples shown in Spetner's bookari-freedom_{December 11, 2007
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Thanks DaveScot you gave me quite a bit to chew on and clearly pointed out that there is quite a lot I/we have left to learn. I guess you already know what I'm going to point out as to the weakness of your scenario. Extensive mutational studies, of what I would consider more primitive life-forms (bacteria, worms, fruit flies etc..etc..), have never shown even a slight minor beneficial effect to support the tangibility of the front-loading hypothesis. This includes the infamous HOX gene studies. For the environmental cue to have something to work on in the radical front-loading scenario, should not the scenario be required to demonstrate a tangible amount of radically novel and beneficial morphology through these mutational studies? i.e. Should not radically new structures appear at least some time in any one of these extensive studies? To me this (radical front-loading hypothesis) is a nascent hypothesis "still" searching for actual validation when the hypothesis has not yet been physically demonstrated to actually produce the radically novel structures that it is absolutely required to produce in order to be considered compellingly valid scientifically. This is something akin to the evolutionists trying to find that elusive set of "beneficial" mutations that would validate their hypothesis also. To me, the following is your strongest piece of circumstantial evidence: "There is also compelling experimental evidence of highly conserved DNA (between mouse and man, conserved for over 100 my of divergent evolution) where its function could not be identified in the mouse when thousands of conserved sequences were knocked out all at once from the mouse and the GM mice were healthy and indistinguishable from normal mice." As you have already pointed out there is a huge amount that we do not understand as far as genomes are concerned. I could raise several questions like how extensive were the altered mice tested for robustness? How much adaptive radiation was lost to the offspring of the mice? and I would be willing to bet that severe flaws could be found in their study when thoroughly hashed out. As well as the larger genomes are concerned that you pointed out, I could ask, "Is there a certain "encoding" reason why the larger genomes could not be "compressed" as radically as man's genome is ?(remember 12 codes thick in some places). So yes, there is a huge amount for me/us left to learn, and to tell you the truth, I really feel quite na^ked sometimes, as far as my knowledge is concerned, when asking these cutting edge questions at places where man has just barely started to unravel the mystery of life.bornagain77_{December 11, 2007
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bornagain77 The front loading hypothesis doesn't require that there be any "code in waiting" today. Consider the possibility that creative evolution has come to an end and there's nothing left in the preprogrammed sequence to produce. In other words, the program has self-terminated with rational man as its final product. In the front loading hypothesis phylogeny parallels ontogeny. Both are self-terminating when a final product (an adult form) is produced. That said, only a diminshingly small fraction of the genomes on this planet have been sequenced and only a tiny fraction of what's contained in those that have been sequenced is understood. It's premature, to say the least, that there is no evidence any of that undiscovered country is "code in waiting". The c-value enigma is alive and well. There are organisms ranging from bacteria to frogs to water lillies with grossly large amounts of DNA that is quite obviously not needed to sustain their present form since there are closely and distantly related forms phenotypically as complex or more complex with far less DNA. There is also compelling experimental evidence of highly conserved DNA (between mouse and man, conserved for over 100 my of divergent evolution) where its function could not be identified in the mouse when thousands of conserved sequences were knocked out all at once from the mouse and the GM mice were healthy and indistinguishable from normal mice. Natural selection is the only known conservation mechanism and it is incapable of conserving unexpressed genomic content. The best explanation at this time for the evidently unexpressed but highly conserved mouse DNA is that some mechanism is conserving it for contingency. This is exactly what the front loading hypothesis requires - contingency conservation. I'd call that a good bit of evidence for front loading. Identifying the contigency function (if any) of that conserved DNA would be much more illuminating but at the present time it is beyond our experimental and/or analytic capability to determine what function(s) unexpressed DNA performs. If it doesn't closely resemble DNA with a known function and nothing happens when it is deleted that's essentially a brick wall we can't see past with the current state of the art.DaveScot_{December 11, 2007
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ari-freedom comments; I’m confused. I thought the whole lesson from disproving junk DNA was that we can’t underestimate the levels of complexity in the genome. The genome is turning out to be extremely complex, far more complex than some evolutionists, even now after ENCODE, are willing to admit (The finding, when thoroughly fleshed out, will be absolutely crushing to ANY evolutionary scenario). Yet this extreme complexity in the genome, far from enabling more information to be generated in the genome, from all preliminary evidence and scientific principles we have, is severely poly-constraining to the CSI that is originally put into the "parent" species genome (Sanford; Genetic Entropy). As far as we currently know, there is no known natural law or sequence of events that will ever be able to naturally generate information (CSI) in a genome by purely natural methods (William Dembski, Werner Gitt). So from what we currently know in science, we can expect that there is no "information generating code" in the genome awaiting some hypothetical environmental cue. From this evidence, and several other lines of evidence, we can now build a case for Genetic Entropy. Which states that all favorable radiations/adaptations from the parent species will always occur at a loss of information from the CSI that was originally present in the parent species genome. Can a infinitely powerful Designer, mess with our heads and, gradually insert more complex information on top of the poly-constrained information that is present? Yes He could, but the fossil record, and all the available long term genetic evidence, I've been able to find, which is not much right now, indicates that radical CSI was inserted at the level of parent species or parent order. Thus also conforming to Dr. Behe's tentative "Edge" estimate.bornagain77_{December 11, 2007
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Dog_of_War: Surely you don't see sickle cell as an example of good design? It seems to me rather more indicative of evolution, just like the adaptations in bacteria that are the focus of Gil's post: an adaptation beneficial in limited situations that comes at an expense of function in a wider environment.George DW_{December 10, 2007
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wow, I just read my comment, can you tell I was burnt out from studying for finals?gore_{December 10, 2007
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my thoughts are with you ari-freedom, it alost seems he forgot which side of the opinion he is sharing. Is he saying the scenario is for disproving junk dna as junk has no empirical basis? Wow, I guess I have been reading nothing about lies when it coes to that subjectgore_{December 10, 2007
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I think the difference between computer viruses and these bacteria is that computer viruses were designed maliciously, while if bacteria were designed (and I'm not so sure yet that they were) then I think that the idea would be that the designer was not malicious.Corey_{December 10, 2007
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I'm confused. I thought the whole lesson from disproving junk DNA was that we can't underestimate the levels of complexity in the genome.ari-freedom_{December 10, 2007
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bornagain, could you clarify what you mean when you say "bacteria. . . are apparently designed optimally." Also, I'm not so sure that antibiotic resistance is always as deleterious as some of these posts make it out to be. For example, lets take the chemistry of the ?-lactamase that gives bacteria resistance to penicillins. It isn't a damaged piece of the cellular machinery that stops penicillin from working, but rather it breaks the penicillin molecule down so that it can't function. That is the bacteria doesn't just throw out (or break) the piece of itself that penicillin is attacking. Using this enzyme it actually detoxifies the antibiotic.Corey_{December 10, 2007
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I think that the sickle cell/malaria example is a perfect proof of man's place in the world. That the design of malaria cannot better the design of sickle cell is telling.Dog_of_War_{December 10, 2007
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Joseph, you stated: Bornagain77- again you miss my point. RV/NS is IRRELEVANT if malaria was designed to evolve via Dr Spetner’s “non-random evolutionary hypothesis”. The “non-random evolutionary hypothesis” as you term it, is what I call the "radical front-loading scenario", Many IDists hold/held your position, I believe DaveScot holds your view, though I don't know if he currently does, at the present time, since he has just finished reading Dr. Sanford's book: "Genetic Entropy". The problem with this “non-random evolutionary hypothesis” is that there is absolutely no evidence that there is some "unused code in waiting" waiting to be expressed in a genome from some environmental cue. In fact, the best evidence we currently have indicates that this scenario is not plausible. The evidence I'm referring to is the recent ENCODE findings that point to a virtual 100% poly-fuctional and thus virtual 100% poly-constrained genome for Humans. This finding, if it holds for microorganisms as the preliminary evidence is indicating that it will, will all but rule out the "radical front-loading scenario". i.e. There will be no unused code in the genome to "turn on" and produce novel structures with. This scenario you refer to: “non-random evolutionary hypothesis” had a fairly large amount of plausibility when the genome was thought to be mostly "junk", But not that "junk DNA" has been disproved, this scenario is severely compromised of any empirical basis.bornagain77_{December 10, 2007
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GilDodgen in No. 40 states:
Malaria was designed not to be totally cured? No, malaria was not designed to be capable of evolving to become resistant to anything.
How do we know this, categorically, without knowing the intentions of the designer? Seems a bit, well, presumptuous. "Trust in the LORD with all thine heart; and lean not unto thine own understanding. In all thy ways acknowledge him, and he shall direct thy paths." (Proverbs 3:5,6)JWarner_{December 10, 2007
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Malaria was designed not to be totally cured?-Leo S
As far as we know what malaria was designed for and what it does today are two totally different things. Again it's the effects of random processes on a once very good design. Another point- we don't know whether or not malaria has conquered sickle-cells. For all we know there could be a population of such malaria somewhere that just haven't shown up in sickle-celled humans. Bornagain77- again you miss my point. RV/NS is IRRELEVANT if malaria was designed to evolve via Dr Spetner's "non-random evolutionary hypothesis".Joseph_{December 10, 2007
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I wonder what if malaria had an original benign and symbiotic purpose? New Clues to Malaria's Origin http://bric.postech.ac.kr/science/97now/01_7now/010720c.html of special note: The researchers sequenced 25 introns from eight strains of P. falciparum. They found that just three base pairs differed between the strains. From that, they calculated that modern P. falciparum all trace their ancestry to a single small population that began to flourish between 9500 and 23,000 years ago--about the time when early hunters set up farming communities. That agricultural revolution increased population densities and probably led to more stagnant pools in which mosquitoes can breed--two factors favoring the spread of malaria, Wirth says. The results match that of another study, published in Science last month (ScienceNOW, 25 June). Hmmm, Bet the YEC's could do something with that ,,LOLbornagain77_{December 10, 2007
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Malaria was designed not to be totally cured? No, malaria was not designed to be capable of evolving to become resistant to anything.GilDodgen_{December 10, 2007
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So Dacook, In diagnosing a patient, you are saying it is not always possible to know the exact pathogen your dealing with? For Dr. Behe's method to be effective the specific pathogen would have to be identified and hit with a Dr^ug that surpasses the triple CCC limit for bacteria. This sounds like a major obstacle since the specific pathogen would have to known beforehand.bornagain77_{December 10, 2007
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until the organism was identified. - and after it's identified, only one antibiotic was used, right? It usually takes quite some time to work...I'm not a doctor so you'd know better but I had pneumonia (ended up in the hospital for 4-5 days) and took antibiotics for quite some time but it was only one antibiotic.ari-freedom_{December 10, 2007
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I guess by "always" I meant "ever since before I went into medicine." I entered medical school in 1983. It was (and is) SOP to put a patient with a serious infection on 2 or 3 antibiotics until the organism was identified. I don't know how long before that. For non-serious infections only one antibiotic is still commonly used, with follow-up. Just 15 minutes ago I put a patient on a single antibiotic for a minor-looking skin infection following a mole removal done by someone else. If it doesn't improve in a few days I'll broaden coverage. For minor, common infections it's usually not worth the cost, inconvenience, and possible side effects to start with multiples. But for serious ones (the kind I usually see) it always is.dacook_{December 10, 2007
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Joseph you stated, "It’s a population thing. The goal is for the population to survive not each individual. It makes more sense that way- having multiple individuals trying to resolve an issue in different ways. One is bound to find a solution." That is the whole point of Dr. Behe's book. Dr. Behe looked for what was reasonable (the Edge) for the RV/NS scenario to accomplish in the "ENTIRE" world-wide population of microorganisms. He estimated from several different lines of evidence that a triple CCC mutation is unreasonable for the RV/NS scenario to accomplish in the ENTIRE world-wide population. That limit is the limit that ID stands by currently. That limit is far below what is required of Evolution to produce for living organisms. In other words it is a barrier established by empirical evidence that we have no reason to suspect will ever be violated by natural methods. And unlike evolution this is very falsifiable. Indeed, just clearly demonstrate a violation of the triple CCC limit and Dr. Behe's (ID's) estimate is falsified immediately.bornagain77_{December 10, 2007
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dacook --The ID (Infectious Disease) consultant I use routinely recommends multiple antiobiotics for infections. We have always done this if the organism is unknown. Do you know how long this was SOP?tribune7_{December 10, 2007
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ari-freedom (post 28) first comment: I agree. In fact, some doctors used to prescribe / recommend pro - biotics to supplement anti - biotics so that the anti - biotics will kill the bad bacteria and the pro - biotics would replace the good bacteria. If bacteria were designed for a useful purpose in humans then it stands to reason that the bad bacteria maybe degenerates of the original useful bacteria. Second comment: I read studies that indicate raw garlic kills all kinds of bacteria and is virtually impossible to immune to. It even destroys many viruses. Of course, pharmaceutical corporations have an incentive to skew such information by making bias studies and telling people otherwise. See, when garlic is in its natural form, it doesn't have a certain enzyme (allicin). Allicin kills all living cells, including some of you own. However, when crushed (ie: if an insect bites into it) it produces allicin (by combining two separate enzymes, allilin and alinin ?) and the allicin kills the insect (or wardes it away) and quickly evaporates before being able to kill much of the plant. Garlic was designed to resist resistance.Bettawrekonize_{December 10, 2007
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If bacteria had “built-in responses to environmental cues” ala Dr Spetner’s “non-random evolutionary hypothesis”- ie they were designed- then wouldn’t it be possible for them to develop a triple CCC?
Perhaps, but the evidence is that malaria, for example, was not designed to have this capability, since it has not been able to evolve resistance to sickle cell.-Gil
1- Not every problem has a solution. 2- The random effects that do exist could have crippled its capabilities. Those same or similar random effects that made it a killer. All I am saying is that if we ever did see a triple CCC arise in say one or two generations (some small number) it would support Dr Spetner, not Darwin.
Thus it goes to reasoning, the chance of any one bacteria having all the necessary mutations to combat all the different antibiotics, deployed at the same time, against a specific pathogenic bacteria, is far, far greater than any one bacteria developing just one deleterious mutation for resistance.-bornagain
It's a population thing. The goal is for the population to survive not each individual. It makes more sense that way- having multiple individuals trying to resolve an issue in different ways. One is bound to find a solution.
1) if bacteria were designed then maybe it is not such a good idea to try to kill them in the first place.- ari-freedom
Computer viruses are designed also. And it is definitely a good idea to kill them. Just because things are designed does not make them "good".Joseph_{December 10, 2007
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