Behe’s Elephant

_{Granville Sewell

April 7, 2013

Intelligent Design}

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In Darwin’s Black Box, Michael Behe writes:

Imagine a room in which a body lies crushed, flat as a pancake. A dozen detectives crawl around, examining the floor with magnifying glasses for any clue to the identity of the perpetrator. In the middle of the room, next to the body, stands a large, gray elephant. The detectives carefully avoid bumping into the pachyderm’s legs as they crawl, and never even glance at it. Over time the detectives get frustrated with their lack of progress but resolutely press on, looking even more closely at the floor. You see, textbooks say detectives must “get their man,” so they never even consider elephants.

There is an elephant in the roomful of scientists who are trying to explain the development of life. The elephant is labeled “intelligent design.” To a person who does not feel obliged to restrict his search to unintelligent causes, the straightforward conclusion is that many biochemical systems were designed.

For me, the evidence for design in biology has always seemed so overwhelming, so obvious, that the real question is how so many smart scientists are unable to see the elephant in the room. In Chapter 9 of In the Beginning and Other Essays on Intelligent Design I asked how so many intellectuals could have “lost their minds”:

I think I can explain. 1) When one becomes a scientist, one learns that science can now explain so many previously inexplicable phenomena that one comes to believe that nothing can escape the explanatory power of our science. 2) When one becomes a biologist, or a paleontologist, one discovers many things about the origin of species, such as the long periods involved and the evidence for common descent, that give the impression of natural causes. 3) When one studies history, one may become overwhelmed by the misery and confusion of the human condition, and wonder, why is it so hard to see evidence of the hand of God in human history?

But noticably absent from any list of reasons why intellectuals reject ID is any direct scientific evidence that natural selection of random mutations or any other unintelligent process can actually do intelligent things, like design plants or animals.

So I see three reasons why the elephant in the room, which is so obvious to the unindoctrinated, is ignored by most of our intellectuals, and here is how I would counter each:

Is it possible that this crime could have been committed by an elephant, when all the other crimes the detectives have investigated were committed by humans? Is it possible that we can explain all other phenomena in Nature without invoking design, but we cannot explain the origin and evolution of life without it? Score one point for the other side here, but…of course it is possible, why not? I explained why evolution is so different from other scientific questions that it requires such a different type of explanation, in this video.
Kenneth Miller asked ID advocates to explain why the history of life gives the appearance of evolution, if species were really designed. I answered this with another question in this Evolution News and Views article: “Why does the history of technology give the appearance of evolution, when we know it was the result of intelligent design?” Again, score one point for the other side, but this argument is also not definitive, I gave one possible answer, others are possible.
The presence of evil and misery in our world is an unscientific, but powerful, argument against design. It is unscientific because there is a very simple reply: no one ever claimed that the scientific evidence shows that our designer is good, only intelligent. But it is powerful because neither we nor our critics like this answer. I devoted a chapter in my otherwise scientific book to this objection to design, because it is so powerful, even if it is unscientific. Sometimes my answers there seem convincing, other times they seem naive, even to me. Score 2 points for the other side here, but again their arguments are not definitive.

Despite the above reasons to go after the usual suspects, which seem so powerful to many intellectuals, the evidence implicating the elephant is so overwhelming, so obvious, that the final score is still 1000000 to 4 for the elephant, the way I calculate it.

Comments

Moreover, besides the 'context dependency' as to how proteins are constructed from amino acids, it is now found that proteins are also dependent on the specific context of the particular cellular environment that they may be in. Thus, the sheer brick wall that neo-Darwinian processes face in finding ANY novel functional protein in the first place, (Axe; Sauer), to perform any specific single task in a cell, is only exponentially exasperated by the fact that many proteins are multifunctional and, 'serendipitously', perform several different 'context dependent' tasks within the cell:
Human Genes: Alternative Splicing (For Proteins) Far More Common Than Thought: Excerpt: two different forms of the same protein, known as isoforms, can have different, even completely opposite functions. For example, one protein may activate cell death pathways while its close relative promotes cell survival. http://www.sciencedaily.com/releases/2008/11/081102134623.htm Genes Code For Many Layers of Information - They May Have Just Discovered Another - Cornelius Hunter - January 21, 2013 Excerpt: “protein multifunctionality is more the rule than the exception.” In fact, “Perhaps all proteins perform many different functions by employing as many different mechanisms." Explaining how a protein can perform multiple roles - Cell Biology - December 18, 2009 Excerpt: It’s been known for more than a decade that some cell proteins can carry out multiple functions. For example, it was discovered in 1999 that the protein TyrRS (explained shortly) participated not only in the building of enzymes, but also could function to stimulate the growth of blood vessels. Discovering that the same protein could perform very different roles opened one of the great new chapters in molecular biology. http://scitechstory.com/2009/12/18/explaining-how-a-protein-can-perform-multiple-roles/
Moreover, protein-protein interactions and domain-domain interactions for proteins are tentatively found to be very different in different species
A Top-Down Approach to Infer and Compare Domain-Domain Interactions across Eight Model Organisms Excerpt: Knowledge of specific domain-domain interactions (DDIs) is essential to understand the functional significance of protein interaction networks. Despite the availability of an enormous amount of data on protein-protein interactions (PPIs), very little is known about specific DDIs occurring in them.,,, Our results show that only 23% of these DDIs are conserved in at least two species and only 3.8% in at least 4 species, indicating a rather low conservation across species.,,, http://www.plosone.org/article/info:doi/10.1371/journal.pone.0005096
Yet, as with functional proteins, protein-protein interactions (domain-domain interactions) between proteins are very hard to achieve by neo-Darwinian processes of mutation and selection:
"The immediate, most important implication is that complexes with more than two different binding sites-ones that require three or more proteins-are beyond the edge of evolution, past what is biologically reasonable to expect Darwinian evolution to have accomplished in all of life in all of the billion-year history of the world. The reasoning is straightforward. The odds of getting two independent things right are the multiple of the odds of getting each right by itself. So, other things being equal, the likelihood of developing two binding sites in a protein complex would be the square of the probability for getting one: a double CCC, 10^20 times 10^20, which is 10^40. There have likely been fewer than 10^40 cells in the world in the last 4 billion years, so the odds are against a single event of this variety in the history of life. It is biologically unreasonable." - Michael Behe - The Edge of Evolution - page 146 A review of The Edge of Evolution: The Search for the Limits of Darwinism The numbers of Plasmodium and HIV in the last 50 years greatly exceeds the total number of mammals since their supposed evolutionary origin (several hundred million years ago), yet little has been achieved by evolution. This suggests that mammals could have "invented" little in their time frame. Behe: ‘Our experience with HIV gives good reason to think that Darwinism doesn’t do much—even with billions of years and all the cells in that world at its disposal’ (p. 155). Michael Behe, The Edge of Evolution, pg. 162 Swine Flu, Viruses, and the Edge of Evolution "Indeed, the work on malaria and AIDS demonstrates that after all possible unintelligent processes in the cell--both ones we've discovered so far and ones we haven't--at best extremely limited benefit, since no such process was able to do much of anything. It's critical to notice that no artificial limitations were placed on the kinds of mutations or processes the microorganisms could undergo in nature. Nothing--neither point mutation, deletion, insertion, gene duplication, transposition, genome duplication, self-organization nor any other process yet undiscovered--was of much use." http://www.evolutionnews.org/2009/05/swine_flu_viruses_and_the_edge.html
Supplemental notes as 'top down' control of proteins:
Watching a protein as it functions - March 15, 2013 Excerpt: When it comes to understanding how proteins perform their amazing cellular feats, it is often the case that the more one knows the less one realizes they know. For decades, biochemists and biophysicists have worked to reveal the relationship between protein structural complexity and function, only to discover more complexity.,,, A signaling protein usually responds to a messenger or trigger, such as heat or light, by changing its shape, which initiates a regulatory response in the cell. Signaling proteins are all-important to the proper functioning of biological systems, http://phys.org/news/2013-03-protein-functions.html An Electric Face: A Rendering Worth a Thousand Falsifications - September 2011 Excerpt: The video suggests that bioelectric signals presage the morphological development of the face. It also, in an instant, gives a peak at the phenomenal processes at work in biology. As the lead researcher said, “It’s a jaw dropper.” http://darwins-god.blogspot.com/2011/09/electric-face-rendering-worth-thousand.html The (Electric) Face of a Frog - video http://www.youtube.com/watch?v=ndFe5CaDTlI Stephen Meyer - Functional Proteins And Information For Body Plans - video http://www.metacafe.com/watch/4050681
Quote and music:
"Too often, we envision the cell as a "factory" containing a fixed complement of "machinery" operating according to "instructions" (or "software" or "blueprints") contained in the genome and spitting out the "gene products" (proteins) that sustain life. Many things are wrong with this picture, but one of the problems that needs to be discussed more openly is the fact that in this "factory," many if not most of the "machines" are themselves constantly turning over -- being assembled when and where they are needed, and disassembled afterwards. The mitotic spindle...is one of the best-known examples, but there are many others. Funny sort of "factory" that, with the "machinery" itself popping in and out of existence as needed!,,," - James Barham Eric Church - Like Jesus Does (Acoustic) http://www.youtube.com/watch?v=wuG1rLPjVkk
bornagain77_{April 8, 2013
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A few notes as to 'beneficial' mutations. It is now found that proteins are 'context dependent', in that the 'whole' of the protein structure takes precedence over how the parts of the amino acids are used thus further severely constraining the 'evolvability' of proteins.
(A Reply To PZ Myers) Estimating the Probability of Functional Biological Proteins? Kirk Durston , Ph.D. Biophysics – 2012 Excerpt (Page 4): The Probabilities Get Worse This measure of functional information (for the RecA protein) is good as a first pass estimate, but the situation is actually far worse for an evolutionary search. In the method described above and as noted in our paper, each site in an amino acid protein sequence is assumed to be independent of all other sites in the sequence. In reality, we know that this is not the case. There are numerous sites in the sequence that are mutually interdependent with other sites somewhere else in the sequence. A more recent paper shows how these interdependencies can be located within multiple sequence alignments.[6] These interdependencies greatly reduce the number of possible functional protein sequences by many orders of magnitude which, in turn, reduce the probabilities by many orders of magnitude as well. In other words, the numbers we obtained for RecA above are exceedingly generous; the actual situation is far worse for an evolutionary search. http://powertochange.com/wp-content/uploads/2012/11/Devious-Distortions-Durston-or-Myers_.pdf Proteins with cruise control provide new perspective: Excerpt: “A mathematical analysis of the experiments showed that the proteins themselves acted to correct any imbalance imposed on them through artificial mutations and restored the chain to working order.” http://www.princeton.edu/main/news/archive/S22/60/95O56/ Why Proteins Aren't Easily Recombined, Part 2 - Ann Gauger May 17, 2012 Excerpt: In other words, even if only 10% of non-matching residues were changed, the resulting hybrid enzyme no longer functioned. Why? Because the substitution of different amino acids into the existing protein structure destabilized the fold, even though those same amino acids worked well in another context. Thus, each protein's amino acid sequence works as a whole to help generate a proper stable fold, in a context-dependent fashion. http://www.evolutionnews.org/2012/05/why_proteins_ar_1059771.html "Why Proteins Aren't Easily Recombined, Part 2" - Ann Gauger - May 2012 Excerpt: "So we have context-dependent effects on protein function at the level of primary sequence, secondary structure, and tertiary (domain-level) structure. This does not bode well for successful, random recombination of bits of sequence into functional, stable protein folds, or even for domain-level recombinations where significant interaction is required." http://www.biologicinstitute.org/post/23170843182/why-proteins-arent-easily-recombined-part-2 Stability effects of mutations and protein evolvability. October 2009 Excerpt: The accepted paradigm that proteins can tolerate nearly any amino acid substitution has been replaced by the view that the deleterious effects of mutations, and especially their tendency to undermine the thermodynamic and kinetic stability of protein, is a major constraint on protein evolvability,, http://www.ncbi.nlm.nih.gov/pubmed/19765975
As well, the 'beneficial mutations' that are found to 'naturally' occur in protein sequences are found to be 'designed errors':
Cells Defend Themselves from Viruses, Bacteria With Armor of Protein Errors - Nov. 2009 Excerpt: These "regulated errors" comprise a novel non-genetic mechanism by which cells can rapidly make important proteins more resistant to attack when stressed, http://www.sciencedaily.com/releases/2009/11/091125134701.htm
Moreover the Genetic Code is also 'designed' to resist the harmful effects of mutations:
DNA - The Genetic Code - Optimal Error Minimization & Parallel Codes - Dr. Fazale Rana - video http://www.metacafe.com/watch/4491422 Deciphering Design in the Genetic Code - Fazale Rana Excerpt: Sixty-four codons make up the genetic code. Because the genetic code only needs to encode 20 amino acids, some of the codons are redundant. That is, different codons code for the same amino acid. In fact, up to six different codons specify some amino acids. Others are specified by only one codon.,,, Genetic code rules incorporate a design that allows the cell to avoid the harmful effects of substitution mutations. For example, six codons encode the amino acid leucine (Leu). If at a particular amino acid position in a polypeptide, Leu is encoded by 5? (pronounced five prime, a marker indicating the beginning of the codon). CUU, substitution mutations in the 3? position from U to C, A, or G produce three new codons, 5? CUC, 5? CUA, and 5? CUG, all of which code for Leu. The net effect produces no change in the amino acid sequence of the polypeptide. For this scenario, the cell successfully avoids the negative effects of a substitution mutation. Likewise, a change of C in the 5? position to a U generates a new codon, 5?UUU, that specifies phenylalanine, an amino acid with similar physical and chemical properties to Leu. A change of C to an A or to a G produces codons that code for isoleucine and valine, respectively. These two amino acids also possess chemical and physical properties similar to leucine. Qualitatively, the genetic code appears constructed to minimize errors that result from substitution mutations.,,, The genetic code’s error-minimization properties are actually more dramatic than these results indicate. When researchers calculated the error-minimization capacity of one million randomly generated genetic codes, they discovered that the error-minimization values formed a distribution where the naturally occurring genetic code’s capacity occurred outside the distribution.18 Researchers estimate the existence of 10^18 possible genetic codes possessing the same type and degree of redundancy as the universal genetic code. All of these codes fall within the error-minimization distribution. This finding means that of 10^18 possible genetic codes, few, if any, have an error-minimization capacity that approaches the code found universally in nature. http://www.reasons.org/biology/biochemical-design/fyi-id-dna-deciphering-design-genetic-code
Though the DNA code is found to be optimal from a error minimization standpoint, it is also now found that the fidelity of the genetic code, as to how a specific amino acid is spelled in the sequence, is far greater than had at first been thought:
Synonymous Codons: Another Gene Expression Regulation Mechanism - September 2010 Excerpt: There are 64 possible triplet codons in the DNA code, but only 20 amino acids they produce. As one can see, some amino acids can be coded by up to six “synonyms” of triplet codons: e.g., the codes AGA, AGG, CGA, CGC, CGG, and CGU will all yield arginine when translated by the ribosome. If the same amino acid results, what difference could the synonymous codons make? The researchers found that alternate spellings might affect the timing of translation in the ribosome tunnel, and slight delays could influence how the polypeptide begins its folding. This, in turn, might affect what chemical tags get put onto the polypeptide in the post-translational process. In the case of actin, the protein that forms transport highways for muscle and other things, the researchers found that synonymous codons produced very different functional roles for the “isoform” proteins that resulted in non-muscle cells,,, In their conclusion, they repeated, “Whatever the exact mechanism, the discovery of Zhang et al. that synonymous codon changes can so profoundly change the role of a protein adds a new level of complexity to how we interpret the genetic code.”,,, http://www.creationsafaris.com/crev201009.htm#20100919a
Throw on top of all that the multiple mechanisms of DNA repair and perhaps now even Darwinists can start to see the insurmountable problem that this presents to neo-Darwinian evolution:
The Darwinism contradiction of repair systems Excerpt: The bottom line is that repair mechanisms are incompatible with Darwinism in principle. Since sophisticated repair mechanisms do exist in the cell after all, then the thing to discard in the dilemma to avoid the contradiction necessarily is the Darwinist dogma. Repair mechanisms in DNA include: A proofreading system that catches almost all errors A mismatch repair system to back up the proofreading system Photoreactivation (light repair) Removal of methyl or ethyl groups by O6 – methylguanine methyltransferase Base excision repair Nucleotide excision repair Double-strand DNA break repair Recombination repair Error-prone bypass
etc...bornagain77_{April 8, 2013
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I have a follow-up question about mutations - nucleotide substitutions in DNA. Isn't it true that even a beneficial mutation isn't beneficial at all without corresponding epigenetic mechanisms in place? The transcription of the new code has to be regulated. This involves all sorts of mechanisms that have to be finely tuned. Let's assume that we are talking about a new potentially beneficial protein. It is only beneficial for the cell in the right amount in context with different stages in the cell's life.
'The essence of cellular life is regulation: The cell controls how much and what kinds of chemicals it makes; when it loses control, it dies’, Michael Behe, Darwin’s black box, p.191.
So just a beneficial DNA mutation is not enough. There has to be a synchronized change in epigenetic factors as well, otherwise the cell loses control and dies.Box_{April 8, 2013
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"such would need to search through far more than 22 combinations to find a specific amino, correct?"
Sorry Eric, I suppose this is overstated.Chance Ratcliff_{April 8, 2013
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Eric @26, yes indeed, but considering a mutation that effects a single base, such would need to search through far more than 22 combinations to find a specific amino, correct? Depending on the target amino, the target space could be anywhere from two, to six codons out of sixty-four possible words I believe. Regardless, I ended up answering my own question while trying to clarify, becoming aware of the flaw in my reasoning. It was a silly mistake. The probability of a specific point mutation, given one occurs in uniform distribution at the codon level is, I believe, between 2/64 (phenylalanine for instance) and 6/64 (leucine) multiplied by one over the size of the genome in codons. My initial mental collapse wrt post #17 is noted and appreciated. :PChance Ratcliff_{April 7, 2013
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Also, there aren't really 64 codon-produced words, due to redundancy. 20 + start and stop (if we assume there is truly no difference in the amino acids built under redundancy -- probably true, although we haven't really gotten into the construction details yet or examined all the quantum features in biology). But let's keep it simple and say 22, rather than 64.Eric Anderson_{April 7, 2013
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Joe @19, you are correct sir, my #21 was ill-conceived, and the result of a mental block! ;)Chance Ratcliff_{April 7, 2013
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Eric @23, thanks for engaging my question. It doesn't appear as straightforward as I imagined when I wrote it down. Let me try and simplify. For a 3 million base pair genome, where a codon is comprised of 3 base pairs, there are 1 million codons. Each codon can be one of sixty-four words. That gives a sequence space of 64^1,000,000 at the codon level, correct? Or am I missing something? However I just discovered the error in my reasoning while typing this response. A single mutation doesn't imply a single sequence, so the probability is indeed 1/64,000,000 in my hypothetical, not 64^-1,000,000 for an entire sequence. Joe was correct at #19, it's not too difficult for a single substitution to be conferred multiple times in a genome of that size in a population of prokaryotes. Thanks to both of you. :)Chance Ratcliff_{April 7, 2013
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Chance @17:
Suppose a selective advantage could be introduced by a single substitution mutation conferring antibiotic resistance by modification to a protein binding site. Should we expect that the same replication error could be discovered twice? With a genome that size [3M bp], there are one-million codons with 64 possibilities each, for a grand total of 64^1,000,000 possible variations. How is it that the same random mutation could occur twice at the same codon? What am I missing? By my assumption of the sequence space, even for a much-smaller genome, we shouldn’t expect to see a single point mutation occur by random twice in the entire age of the universe.
I'm not sure I'm following your math. Are you talking about nucleotide substitutions in DNA or amino acid substitutions in proteins? I'll focus on nucleotide substitutions just for sake of simplicity. The mutation rate of an organism like c elegans is around 2.1 x 10^-8 mutations per base per generation. (Incidentally, the human mutation rate is pretty similar. It depends primarily on the age of the father at the time of conception and varying for other factors, but it is a decent working number.) If we use a similar mutation rate in your hypothetical organism with 3M bases, the odds of getting a mutation each generation is 0.063 (taking a single DNA strand and ignoring for a moment the complementary DNA strand). Therefore, after 16 generations you will get one mutation. Put another way, if you had 16 individuals in the population, the population would experience one mutation every generation. Now we also have to factor in your generation time. C elegans has a generation time of about 4 days. Let's call it 3.65 days, just to make the math easy. So every year, we go through approximately 100 generations. Thus, following a single individual's line, we would have about 6.3 mutations/year. Obviously if we are looking at the entire population, the number of mutations in the population would go up commensurately. Anyway, I'll stop there for now as I'm not sure whether your real question relates to: (A) the odds of (i) a particular pre-specified mutation occurring, or (ii) any mutation occurring, multiplied by (B) the odds of the mutation occurring again (i) in a single lineal descent line, or (ii) in the entire population.Eric Anderson_{April 7, 2013
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Eric @20,
"I understand your point, but I would argue that in such a situation at least some information has been preprogrammed into the system in order for it to narrow the search space and come up with a workable solution. If it is not something that occurs purely by the force of chemistry and physics, and is not directly guided, then something still has to provide the organism with the ability to narrow the search space to something that can be realistically achieved."
Absolutely, but I'm suggesting that the changes observed in podarcis sicula may not have been some sort of targeted search, but a preprogrammed environmental response that could have been dependent on a preexisting mechanism for such a display of plasticity. I'm not sure we know what causes that sort of rapid morphological change. Is this distinction making sense? Features of the immune system look like targeted searches, but certain displays of phenotypic plasticity might be a little more concrete with regard to cause and effect, I suppose.Chance Ratcliff_{April 7, 2013
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Joe @19, yes 3 million sounds reasonable at first blush, because if a mutation is likely to occur at some codon, then the probability is 1/1,000,000 or 10^-6. Then multiply by 1/64 for the probability of selecting the right codon. That's only 1/64,000,000 probability. This sounds pretty likely for a replication error to be able to find it twice or more. But that doesn't square with the calculation for the sequence space of that hypothetical genome, which by my reasoning would be 64^1,000,000. One of those numbers is wrong, and it must be the first one -- that probability calculation assumes independent events, and doesn't cover the search space.Chance Ratcliff_{April 7, 2013
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Chance @16:
It should also be noted that even if we hypothesize a bottom-up intelligent causal mechanism operating through physical laws to organize matter into biologically relevant configurations, why do we not see such processes in action today?
Good point. The typical response is: it takes too long, so we can't see it in action. Could be. But it might also be that it isn't happening at all. Another one I've heard is that, with respect to OOL at least, because the conditions on earth today are different than on the pre-biotic earth, the newly-formed nascent polymers are quickly eaten up/absorbed/destroyed by all the biotic reactions going on now. Indeed, that was Darwin's thought too in his "warm little pond" musing. Nevertheless, those "explanations" ring rather hollow and it remains an reasonable question why we don't see these newly-formed biological systems emerging at least somewhere on occasion.
This would be explicable by reference to the organism’s existing configurational makeup, with no need of smuggling information from external sources, whether random accumulations or bottom-up intelligent processes.
I understand your point, but I would argue that in such a situation at least some information has been preprogrammed into the system in order for it to narrow the search space and come up with a workable solution. If it is not something that occurs purely by the force of chemistry and physics, and is not directly guided, then something still has to provide the organism with the ability to narrow the search space to something that can be realistically achieved.Eric Anderson_{April 7, 2013
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It's just stumbling change. If it happens to be beneficial then so be it. 3 million base pairs- that's a small sample space. So given a large population, I would say it is very likely. It's the lottery- high odds but many players.Joe_{April 7, 2013
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ID makes no judgments about the designer--for all we know, among the "billions and billions" of planets in the universe, there are likely to be some clever aliens who seeded the Earth. If that were indeed true, many of the arguments used by Darwinists would sound silly: If superior aliens brought life to Earth . . . 1. Why are their designs imperfect? After all, I know a perfect design when I see one! 2. Why is there so much suffering and misery? Not that I cause any myself. 3. It invalidates Science. Why must you invoke the "Aliens of the Gaps?" By extrapolation, we can easily predict that ALL questions will have terrestrial explanations. We don't need aliens to explain anything even if they were the designers.Querius_{April 7, 2013
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I'd like to ask a semi-OT question about random mutations that perhaps somebody would be willing to address or correct me on. How likely is it for a truly random mutation to stumble upon a beneficial change more than once? Let's presume a hypothetical prokaryote with a genome consisting of three-million base pairs. Let's also stipulate that any site along the genome can be mutated by a replication error with equal probability, that any substitution can be made, and that the error rate is such that a mutation occurs about once every replication, given whatever reasonable replication time one sees fit. Suppose a selective advantage could be introduced by a single substitution mutation conferring antibiotic resistance by modification to a protein binding site. Should we expect that the same replication error could be discovered twice? With a genome that size, there are one-million codons with 64 possibilities each, for a grand total of 64^1,000,000 possible variations. How is it that the same random mutation could occur twice at the same codon? What am I missing? By my assumption of the sequence space, even for a much-smaller genome, we shouldn't expect to see a single point mutation occur by random twice in the entire age of the universe.Chance Ratcliff_{April 7, 2013
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Eric @15, thanks much. Nightlight should also reference your post #7, which makes similar points eloquently. It should also be noted that even if we hypothesize a bottom-up intelligent causal mechanism operating through physical laws to organize matter into biologically relevant configurations, why do we not see such processes in action today? Behe's The Edge of Evolution looked at changes in malaria and in the populations which it infects and found that, if memory serves, it took 10^20 generations for malaria to stumble upon chloroquine resistance conferred by two substitutions. He did this giving the benefit of the doubt that evolutionary processes have been in operation the whole time; so whether mutation, selection, drift, gene duplication, horizontal gene transfer, etc., all were free to operate in whatever capacity they could to produce chloroquine resistance. Since the result was empirical, we can substitute any putative hypothetical process we want, and still find that it takes malaria about 10^20 generations to develop the trait. If intelligent processes are guiding everything from the bottom up, they don't appear to be doing much of anything today that isn't already part of a given organism's internal configuration. I think it's likely we'll find that, for such instances of "evolution" such as the podarcis sicula lizards on Pod Mrcaru (see here) the changes most likely resulted from a reconfiguration of existing genetic material via a signalling process triggered by something like dietary changes. This would be explicable by reference to the organism's existing configurational makeup, with no need of smuggling information from external sources, whether random accumulations or bottom-up intelligent processes.Chance Ratcliff_{April 7, 2013
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Chance @14: Good points, particularly your last two. Design of life in the lab will demonstrate that life can be designed. It will also eliminate the oft-made, but absurd, objection to ID that because we don't "know" life can be designed, then we can't infer it. I personally would welcome knowing that life can come about through purely natural processes if it is true. However, such an idea is preposterous the evidence points strongly the other direction.Eric Anderson_{April 7, 2013
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nightlight @13,
#5 Granville Sewell: “Evolution” does not necessarily imply the absence of design, even in common usage. And the similarities between the “evolution” of life and the evolution of technology go even further than that, as pointed out in my link.
That’s a very powerful argument and it’s a pity that it is not often used by the ID side to counter noe-Darwinian claims such as, that microevolution observed in the lab (or even in nature) is result of “random mutation” + NS, especially when that is allegedly “proven” via reverse engineering in the lab of the DNA changes behind the phenotypic adaptations.
A few points. First, ID is not incompatible with common descent or change-over-time evolution. This should be clear to anyone familiar with ID. Second, ID specifically takes issue with the RM+NS mechanism for producing formal novelty of sufficient complexity. However, it does not rule out the potential influence of random mutations in principle, nor should it. Third, ID does *not concede* that any changes which occur, in the lab or outside it, are the necessary result of random mutations.
I think the underlying reason that substantial fraction of ID side routinely concedes RM+NS as sufficient mechanism behind such lab observed microevolution is that they, along with neo-Darwinians, imagine that somehow any actions of intelligent agency must come from heavens, as it were, and since lab observations failed to detect any such heavenly (‘supernatural’) intervention, and have even uncovered molecular basis behind phenotypic effects, then they concede defeat and accept the gratuitous “randomness” claims by the neo-Darwinians which doesn’t follow from any such observations.
ID is about design detection, not supernatural causation.
While one may still temporarily cling on the non-observation of ‘macro-evolution’ or of ‘origin of life’, that’s a very fragile position to hold in case the intelligent agency is acting from inside (like driver controlling the car from inside), rather than coming down to intervene from heavens (supernaturally).
What specifically about ID denies that intelligence might be acting "from the inside"? Who among prominent ID proponent makes any claims about how biological design must be implemented?
It’s only a matter of time before a live organism is synthesized from scratch in the lab, and what then? The origin of life will be conceded, and this faction of ID will have to retreat to its last castle, the fine tuning of the physical constants (which may not last too long either).
This is profoundly mistaken. If life is synthesized in the lab it will demonstrate that life is capable of being intelligently designed. This can hardly undercut ID. If instead you mean that we might discover self-organizational properties of matter under specific conditions, it's a risk worth taking, since all evidence indicates otherwise. In addition, because ID is interested in empirical evidence, it would welcome the actual demonstration of the principle, instead of the uncritical belief that such a self-organizational process must exist.
In other words, such position of expecting heavenly interventions such as violations of laws of physics, is a recipe for defeat.
Have you read any books by Meyer, Behe, Dembski, Wells, Denton, etc? If so, it's a great opportunity to present specifics, and discuss what ID proponents actually say.Chance Ratcliff_{April 7, 2013
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#5 Granville Sewell: "Evolution" does not necessarily imply the absence of design, even in common usage. And the similarities between the "evolution" of life and the evolution of technology go even further than that, as pointed out in my link. That's a very powerful argument and it's a pity that it is not often used by the ID side to counter noe-Darwinian claims such as, that microevolution observed in the lab (or even in nature) is result of "random mutation" + NS, especially when that is allegedly "proven" via reverse engineering in the lab of the DNA changes behind the phenotypic adaptations. I think the underlying reason that substantial fraction of ID side routinely concedes RM+NS as sufficient mechanism behind such lab observed microevolution is that they, along with neo-Darwinians, imagine that somehow any actions of intelligent agency must come from heavens, as it were, and since lab observations failed to detect any such heavenly ('supernatural') intervention, and have even uncovered molecular basis behind phenotypic effects, then they concede defeat and accept the gratuitous "randomness" claims by the neo-Darwinians which doesn't follow from any such observations. While one may still temporarily cling on the non-observation of 'macro-evolution' or of 'origin of life', that's a very fragile position to hold in case the intelligent agency is acting from inside (like driver controlling the car from inside), rather than coming down to intervene from heavens (supernaturally). It's only a matter of time before a live organism is synthesized from scratch in the lab, and what then? The origin of life will be conceded, and this faction of ID will have to retreat to its last castle, the fine tuning of the physical constants (which may not last too long either). In other words, such position of expecting heavenly interventions such as violations of laws of physics, is a recipe for defeat. Fundamental laws of physics (quantum theory) are statistical, e.g. like statistical laws or regularities of traffic flows, that still leave plenty of room for intelligent control of each car by the driver from inside without any violation of the coarse grained statistical laws of the traffic flows. Hence, there is plenty of room for intelligent action which doesn't require any violation of the statistical laws of fundamental physics. However, if one takes a more coherent (principled) view and assumes that intelligent agency that created universe and life in all its forms is active at all times, from within every particle and up, continuously upholding their very existence and all their behaviors, then one would challenge neo-Darwinian claim of "randomness" as generator of novelties the same way one would challenge it in evolution of technologies. Just because the gigantic hand didn't come down through the ceiling of the lab to tweak the E. Coli DNA in the famous 1988 Cairns' experiments, that doesn't mean that the same intelligence behind life didn't actually figure out very quickly how to design and build an efficient cellular lactase factory via suitable DNA modifications out of the materials given in the experiment (E. Coli on a lactase substratum). The only way to distinguish "random" vs non-random (intelligent) generator of novelty would be to probabilistically model event space, enumerate all possible alternate DNA configurations consistent with the laws of physics & chemistry (under given initial & boundary conditions), compute their probabilities, them compute the odds of given number of bacteria in a given time randomly picking out the correct one which yields that E. Coli lactase factory (as illustrated in this dice calculation example). Since such odds calculations (quantum theory of molecules) are out of question at present for any large molecule such as DNA, one should reject neo-Darwinian attribution of novelty to random mutation, even if they show exact DNA change that occurred. Accepting these claims based on such observations would be like accepting fairness claim in that dice example as soon as someone shows what the obtained dice pattern is (such as getting triple one in 10 or fewer tries). Just seeing 3 dice come out with 3 ones, without anyone reaching down and turning them around by hand, doesn't imply the dice tosses were fair ("random"). Yet, in microevolution observed in the lab, such as evolution of bacterial resistance or new metabolic pathways, neo-Darwinians get away with such "randomness" claims without almost any opposition from the ID side, especially when the exact DNA changes were uncovered. In short, biological evolution (micro and macro) is the best ally of ID (better even than the Behe's irreducible complexity or Dembski's CSI), not the enemy as commonly perceived, since updating and improving existent designs takes lot more intelligence then producing single version one of a product and then running out of creative juices. The evolution of technology analogy illustrates this perfectly -- the smarter the company the quicker and better it will keep up with the market by evolving new designs.nightlight_{April 7, 2013
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About argument #3: “If you think of this world as a place intended simply for our happiness, you find it quite intolerable: think of it as a place of training and correction and it’s not so bad.” CS Lewis, God in the Dock, page 52Box_{April 7, 2013
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Another unfortunate event that has shaped the biased attitudes towards ID of modern thinkers is the confusion of the methods of science with the concept of what reality is. It is in this light that men of faith and science ( Newton, Pascal, Planck ) practiced science and believed in God. A. By the mere fact that scientific experiments insist on reproducibly, the practice of the scientific method must assume methodological naturalism. What should be understood by all, ( and is ignored by fools ), is that point A is a statement about the limitations of science. It has no bearing about what the reality looks like. The questions that science can not answer are simply the question that science can not answer. People who do not see science as a tool of humanity, but instead have made it their god, unfortunately must insist on a reality which is limited to the small portions of reality that can be investigated by science. No wonder they reject the true and living God.JDH_{April 7, 2013
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Eric, I did mean, as you said, that it is powerful in the sense of swaying lots of people. It is primarily an emotional argument, but a very powerful emotional argument.Granville Sewell_{April 7, 2013
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Dr. Sewell: Thanks, as always, for your post. However, I'm having a hard time seeing any "points scored by the other side" in anything you wrote. All the things you listed as objections to design are readily dealt with, manifesting that the objectors' attempts have missed the mark, gone into foul territory, ended wide of the goal, been stopped at the 1-yard line, bounced off the rim . . . To the objective arbiter watching from the sidelines, no points have been scored, only a myriad of errant attempts made. This one in particular, which has been addressed in detail so many times in the past (including by you):
The presence of evil and misery in our world is an unscientific, but powerful, argument against design.
It is not a powerful argument. It is a naive, philosophically-motivated, and poorly-thought-through argument. It is a terrible argument. I suppose it may be "powerful" in the sense of swaying lots of people, in the sense of appearing convincing to those who have only superficially thought through the issues or who come to the table with deep a priori religious or philosophical biases. But it is not powerful in any rational or logical sense.Eric Anderson_{April 7, 2013
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Joe,
Not if the purpose of the design of the universe was for discovery. Misery, evil and breakdowns all drive us to learn so we can understand and maybe correct some things. The imperfections in our universe give us reason to explore
Your conclusions are pretty similar to mine, in the book chapter (Epilogue) I referred to.Granville Sewell_{April 7, 2013
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nightlight and Joe, regarding the comment Joe quotes @4: I think it is true that in the past many evolutionary critics, including ID supporters, have been willing to concede that (i) there is evidence for microevolutionary changes, (ii) some of these are adequately explained by random mutations, and (iii) possibly many, if not all, of them may be explained by random mutations. This was a reasonable position to take, both because it was largely consistent with the evidence at the time, and because conceding (iii) does not interfere with the real question of ID, which relates to the origin of complex specified information. The fact that (iii) is becoming less clear in many cases, in that we are learning that many previously-thought "random" mutations are actually directed or at least under the higher control of a "mutation" system, certainly should allow opponents of evolutionary theory to take a stronger stance, but it probably can't fundamentally affect the structure of the argument. It is still the case that many microevolutionary events are observed and it is still the case that some of them can occur through random natural processes. Specific disputes could be raised in particular instances, but battling about how many, what percentage and so forth -- while an important nuance and a meaningful discussion in its own right -- does not change the overall engagement. The primary battle to be waged still lies with the macroevolutionary events and the infusion of large amounts of information into the biosphere.Eric Anderson_{April 7, 2013
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Kenneth Miller asked ID advocates to explain why the history of life gives the appearance of evolution, if species were really designed.
Today's species were not really designed. Today's species are the result of many generations of genetic entropy. They are evolved versions of the original designs.
The presence of evil and misery in our world is an unscientific, but powerful, argument against design.
Not if the purpose of the design of the universe was for discovery. Misery, evil and breakdowns all drive us to learn so we can understand and maybe correct some things. The imperfections in our universe give us reason to explore.Joe_{April 7, 2013
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(Nightlight) We even routinely use the term "evolution" to describe the development of aircraft or operating systems, say. Thus I could say I believe mankind "evolved" from lower animals, in the same sense that Windows 8 evolved from Windows 95 (or whatever went before that, can't remember back any further!). "Evolution" does not necessarily imply the absense of design, even in common usage. And the similarities between the "evolution" of life and the evolution of technology go even further than that, as pointed out in the above link.Granville Sewell_{April 7, 2013
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nightlight:
For some reason, both neo-Darwinians and ID supporters go along with such unwarranted leap — if something is observed in the lab (e.g. some case of micro-evolution) and no heavenly/supernatural intervention was observed, then they both leap to the conclusion that novelty was produced by random rearrangements of the DNA (random mutation).
Maybe some ID supporters do. Definitely not all. My positioon is that if living organisms were designed then they were designed to evolve and evolved by design. Then there is "Not By Chance", which came out in 1997. And one of the UD authors- johnnyb I think- that also has posted about non-random evolution. And even James Shapiro's "natural genetic engineering" is against random rearrangements.Joe_{April 7, 2013
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It is surprising that argument #2 is not seen more often from the ID side -- any biological evolutionary phenomenon for which there is analogous phenomenon in cultural or technological evolutions cannot be used as proof of "randomness" as a mechanism of evolutionary innovation since in the latter instances, randomness is at most a trigger for intelligent creative processes of human designers. This argument is especially applicable to microevolution which is largely conceded by ID to be "explained" by "random mutation" (RM) and natural selection (NS), e.g. in antibiotic resistance. Microevolution is quite common phenomenon in evolution of technologies (e.g. service packs, minor tweaks & fixes between the major versions). For example, the 'antibiotic resistance' analogue can be easily observed in software malware, which quickly adapts and becomes resilient to the latest anti-malware measures. With the bottom-up approaches to intelligent agency, such as Planckian networks (intro post), the designer, the blueprints and the product are all inside the product (like driver inside the car). Hence the failure to observe some giant hand coming down fom heavens (i.e. a supernatural phenomenon) to adjust the DNA molecules no more implies the evolutionary novelty was produced by "random mutations", than the similar absence of heavenly intervention/supernatural implies the randomness as a source of novelty in evolution of technologies. For some reason, both neo-Darwinians and ID supporters go along with such unwarranted leap -- if something is observed in the lab (e.g. some case of micro-evolution) and no heavenly/supernatural intervention was observed, then they both leap to the conclusion that novelty was produced by random rearrangements of the DNA (random mutation).nightlight_{April 7, 2013
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G.Sewell, only three books left in stock at Amazon. After my visit it is down to two. The treatment of your Applied Mathematics Letters paper is an outrage!Box_{April 7, 2013
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