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Can we all agree on specified complexity?

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Amid the fog of recent controversies, I can discern a hopeful sign: the key figures in the ongoing debate over specified complexity on Uncommon Descent are actually converging in their opinions. Allow me to explain why.

Winston Ewert’s helpful clarifications on CSI

In a recent post, ID proponent Winston Ewert agreed that Elizabeth Liddle had a valid point in her criticisms of the design inference, but then went on to say that she had misunderstood what the design inference was intended to do (emphases mine):

She has objected that specified complexity and the design inference do not give a method for calculating probabilities. She is correct, but the design inference was never intended to do that. It is not about how we calculate probabilities, but about the consequences of those probabilities. Liddle is complaining that the design inference isn’t something that it was never intended to be.

He also added:

…[T]he design inference is a conditional. It argues that we can infer design from the improbability of Darwinian mechanisms. If offers no argument that Darwinian mechanisms are in fact improbable. When proving a conditional, we are not concerned with whether or not the antecedent is true. We are interested in whether the consequent follows from the antecedent.

In another post, Winston Ewert summarized his thoughts on specified complexity:

The notion of specified complexity exists for one purpose: to give force to probability arguments. If we look at Behe’s irreducible complexity, Axe’s work on proteins, or practically any work by any intelligent design proponent, the work seeks to demonstrate that the Darwinian account of evolution is vastly improbable. Dembski’s work on specified complexity and design inference works to show why that improbability gives us reason to reject Darwinian evolution and accept design.

Winston Ewert concluded that “the only way to establish that the bacterial flagellum exhibits CSI is to first show that it was improbable.”

To which I would respond: hear, hear! I completely agree.

What about Ewert’s claim that “CSI and Specified complexity do not help in any way to establish that the evolution of the bacterial flagellum is improbable”? He is correct, if by “CSI and Specified complexity,” he simply means the concepts denoted by those terms. If, however, we are talking about the computed probability of the evolution of the bacterial flagellum emerging via unguided processes, then of course this number can be used to support a design inference: if the probability in question is low enough, then the inference to an Intelligent Designer becomes a rational one. Ewert obviously agrees with me on this point, for he writes that “Dembski’s work on specified complexity and design inference works to show why that improbability gives us reason to reject Darwinian evolution and accept design.”

In a recent post, I wrote that “we can decide whether an object has an astronomically low probability of having been produced by unintelligent causes by determining whether it has CSI (that is, a numerical value of specified complexity (SC) that exceeds a certain threshold).” Immediately afterwards, I added that in order to calculate the specified complexity of an object, we first require “the probability of producing the object in question via ‘Darwinian and other material mechanisms.'” I then added that “we compute that probability.” The word “compute” makes it quite clear that without that probability, we will be unable to infer that a given object was in fact designed. I concluded: “To summarize: to establish that something has CSI, we need to show that it exhibits specificity, and that it has an astronomically low probability of having been producedby unguided evolution or any other unintelligent process” (italics added).

Imagine my surprise, then, when I discovered that some readers had been interpreting my claim that “we can decide whether an object has an astronomically low probability of having been produced by unintelligent causes by determining whether it has CSI (that is, a numerical value of specified complexity (SC) that exceeds a certain threshold)” as if I were arguing for a design inference on the basis of some pre-specified numerical value for CSI! Nothing could be further from the truth. To be quite clear: I maintain that the inference that biological organisms (or structures, such as proteins) were designed is a retrospective one. We are justified in making this inference only after we have computed, on the basis of the best information available to us, that the emergence of these organisms (or structures) via unguided processes – in which I include both random changes and the non-random winnowing effect of natural selection – falls below a certain critical threshold of 1 in 2^500 (or roughly, 1 in 10^150). There. I cannot be clearer than that.

So I was heartened to read on a recent post by Barry Arrington that Keith S had recently endorsed a form of design inference, when he wrote:

To use the coin-flipping example, every sequence of 500 fair coin flips is astronomically improbable, because there are 2^500 possible sequences and all have equally low probability. But obviously we don’t exclaim “Design!” after every 500 coin flips. The missing ingredient is the specification of the target T.

Suppose I specify that T is a sequence of 250 consecutive heads followed by 250 consecutive tails. If I then sit down and proceed to flip that exact sequence, you can be virtually certain that something fishy is going on. In other words, you can reject the chance hypothesis H that the coin is fair and that I am flipping it fairly.

That certainly sounds like a design inference to me.

In a follow-up comment on Barry Arrington’s post, Keith S went on to point out:

…[I]n that example, I am not calculating CSI and then using it to determine that something fishy is going on. Rather, I have to determine that something fishy is going on first (that is, that P(T|H) is extremely low under the chance hypothesis) in order to attribute CSI to it.

To which I would respond: you’re quite right, Keith S. That’s what I’ve been saying and what Winston Ewert has been saying. It seems we all agree. We do have to calculate the probability of a system emerging via random and/or non-random unguided processes, before we impute a high level of CSI to the system and conclude that it was designed.

CSI vs. irreducible complexity: what’s the difference?

In a subsequent comment, Keith S wrote:

I think it’s instructive to compare irreducible complexity to CSI in this respect.

To argue that something is designed because it exhibits CSI is circular, because you have to know that it is designed before you can attribute CSI to it.

To argue that something is designed because it is irreducibly complex is not circular, because you can determine that it is IC (according to Behe’s definition) without first determining that it is designed.

The problem with the argument from IC is not that it’s circular — it’s that IC is not a barrier to evolution.

For the record: the following article by Casey Luskin over at Evolution News and Views sets forth Professor Mike Behe’s views on exaptation, which are that while it cannot be absolutely ruled out, its occurrence is extremely improbable, even for modestly complex biologically features. Professor Behe admits, however, that he cannot rigorously quantify his assertions, which are based on his professional experience as a biochemist. Fair enough.

The big difference between CSI and irreducible complexity, then, is not that the former is circular while the latter is not, but that CSI is quantifiable (for those systems where we can actually calculate the probability of their having emerged via unguided random and/or non-random processes) whereas irreducible complexity is not. That is what makes CSI so useful, when arguing for design.

Does Dr. Dembski contradict himself? I think not

Keith S claims to have uncovered a contradiction between the following statement by leading Intelligent Design advocate Dr. Willaim Dembski:

Michael Behe’s notion of irreducible complexity is purported to be a case of actual specified complexity and to be exhibited in real biochemical systems (cf. his book Darwin’s Black Box). If such systems are, as Behe claims, highly improbable and thus genuinely complex with respect to the Darwinian mechanism of mutation and natural selection and if they are specified in virtue of their highly specific function (Behe looks to such systems as the bacterial flagellum), then a door is reopened for design in science that has been closed for well over a century. Does nature exhibit actual specified complexity? The jury is still out.

and this statement of his:

It is CSI that Michael Behe has uncovered with his irreducbly complex biochemical machines. It is CSI that for cosmologists underlies the fine-tuning of the universe and that the various anthropic principles attempt to understand.

I don’t see any contradiction at all here. In the first quote, Dr. Dembski is cautiously pointing out that the inference that the bacterial flagellum was designed hinges on probability calculations, which we do not know for certain to be correct. In the second quote, he is expressing his belief, based on his reading of the evidence currently available, that these calculations are in fact correct, and that Nature does in fact exhibit design.

Dembski and the Law of Conservation of Information

Keith S professes to be deeply puzzled by Dr. Dembski’s Law of Conservation of Information (LCI), which he finds “murky.” He is especially mystified by the statement that neither chance nor law can increase information.

I’d like to explain LCI to Keith S in a single sentence. As I see it, its central insight is very simple: that when all factors are taken into consideration, the probability of an event’s occurrence does not change over the course of time, until it actually occurs. In other words, if the emergence of life in our universe was a fantastically improbable event at the time of the Big Bang, then it was also a fantastically improbable event 3.8 billion years ago, immediately prior to its emergence on Earth. And if it turns out that the emergence of life on Earth 3.8 billions of years ago was a highly probable event, then we should say that the subsequent emergence of life in our universe was highly probable at the time of the Big Bang, too. Chance doesn’t change probabilities over the course of time; neither does law. Chance and law simply provide opportunities for the probabilities to be played out.

Someone might argue that we can think of events in human history which seemed highly improbable at time t, but which would have seemed much more probable at a later time t + 1. (Hitler’s rise to power in Germany would have seemed very unlikely in January 1923, but very likely in January 1933.) But this objection misses the point. Leaving aside the point that humans are free agents, a defender of LCI could reply that when all factors are taken into consideration, events that might seem improbable at an earlier time can in fact be demonstrated to have a high probability of occurring subsequently.

Making inferences based on what you currently know: what’s the problem with that?

Certain critics of Intelligent Design are apt to fault ID proponents for making design inferences based on what scientists currently know. But I see no problem with that, as long as ID proponents declare that they would be prepared to cheerfully revise their opinions, should new evidence come to light which overturns currently accepted beliefs.

I have long argued that Dr. Douglas Axe’s paper, The Case Against a Darwinian Origin of Protein Folds, whose argument I summarized in my recent post, Barriers to macroevolution: what the proteins say, demonstrates beyond reasonable doubt that unguided mechanisms could not have given rise to protein folds that we find in living creatures’ body proteins, in the space of just four billion years. I have also pointed out that Dr. Eugene Koonin’s peer-reviewed article, The Cosmological Model of Eternal Inflation and the Transition from Chance to Biological Evolution in the History of Life (Biology Direct 2 (2007): 15, doi:10.1186/1745-6150-2-15) makes a very strong case that the probability of a living thing capable of undergoing Darwinian evolution – or what Dr. Koonin refers to as a coupled translation-replication system – emerging in our observable universe during the course of its history is astronomically low: 1 in 10^1,018 is Dr. Koonin’s estimate, using a “toy model” that makes deliberately optimistic assumptions. Finally, I have argued that Dr. Robin Collins’ essay, The Teleological Argument rules out the infinite multiverse hypothesis which Dr. Koonin proposes in order to explain the unlikely emergence of life in our universe: as Dr. Koonin argues, a multiverse would need to be specially fine-tuned in order to produce even one universe like our own. If Dr. Axe’s and Dr. Koonin’s estimates are correct, and if we cannot fall back on the hypothesis of a multiverse in order to shorten the odds against life emerging, then the only rational inference that we can make, based on what we currently know, is that the first living thing was designed, and that the protein folds we find in living creatures were also designed.

Now, Keith S might object that these estimates could be wrong – and indeed, they could. For that matter, the currently accepted age of the universe (13.798 billion years) could be totally wrong too, but I don’t lose any sleep over that fact. In everyday life, we make decisions based on what we currently know. If Keith S wants to argue that one can reasonably doubt the inference that living things were designed, then he needs to explain why the estimates I’ve cited above could be mistaken – and by a very large margin, at that.

Recently, Keith S has mentioned a new book by Dr. Andreas Wagner, titled, The Arrival of the Fittest: Solving Evolution’s Greatest Puzzle. I haven’t read the book yet, but let me say this: if the book makes a scientifically plausible case, using quantitative estimates, that life in all its diversity could have emerged on Earth over the space of just 3.8 billion years, then I will cheerfully change my mind and admit I was wrong in maintaining that it had to have been designed. As John Maynard Keynes famously remarked, “When the facts change, I change my mind. What do you do, sir?”

For that matter, I try to keep an open mind about the recent discovery of soft tissue in dinosaur bones (see here and here). Personally, I think it’s a very odd finding, which is hard to square with the scientifically accepted view that these bones are millions of years old, but at the present time, I think the preponderance of geological and astronomical arguments in favor of an old Earth is so strong that this anomaly, taken alone, would be insufficient to overthrow my belief in an old cosmos. Still, I could be wrong. Science does not offer absolute certitude, and it has never claimed to.

Conclusion

To sum up: statements about the CSI of a system are retrospective, and should be made only after we have independently calculated the probability of a system emerging via unguided (random or non-random) processes, based on what we currently know. After these calculations have been performed, one may legitimately infer that the system was designed – even while admitting that should subsequent evidence come to light that would force a drastic revision of the probability calculations, one would have to revise one’s views on whether that system was designed.

Are we all on the same page now?

Comments
Keith S, You write: "Natural processes are incapable of producing CSI by the very definition of CSI." This, I have to say, is rubbish. As any ID proponent will tell you, natural processes are capable of producing up to 500 bits of CSI. What they cannot do is produce more. The reason is that owing to the finite size and duration of the observable universe, such a structure (or system) would not be expected to occur even once. You also write that "anything that RM+NS can produce never exhibited CSI to begin with. By definition." This, once again, is incorrect. Anything with a concise specification that RM+NS produced can have CSI, but no more than 500 bits. Finally, you write: "How will you determine the "number of bits of information" for something like the flagellum?” As I've written elsewhere, while I'm willing to grant that this might be impractical for a flagellum, or even for a simple cell, there's no good reason why biochemists couldn't calculate the odds of a single molecule emerging – namely, for a 100-amino-acid protein. I must say I expected you to do better than this. I had hoped that my irenically worded post would elicit a rapprochement of sorts from you and from other commenters at TSZ. I see I was mistaken. I also note that while I have made some concessions in debating with you, you have not budged at all in your position. That is indeed regrettable. What would it take to convince you that proteins were designed? You can always appeal to "some unknown mechanism" that might be lying out there. But by so doing, you make your anti-design stance unfalsifiable.vjtorley
November 18, 2014
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Dr. Moose, You ask, "Question, if it could be demonstrated that natural processes are capable of producing CSI, would it change the definition of CSI?" I have already addressed this in a comment on Barry Arrington's latest post, so I'll reproduce what I said there. In response to your question: "does CSI cease to exist if it can be demonstrated that RM+NS is capable of making it?", my answer is: not necessarily. But you would have to show that the initial conditions and/or laws in the universe where RM+NS produces this CSI were themselves very unlikely. In other words, RM+NS can generate astronomically improbable outcomes only in a highly rigged cosmos. That would then shift the argument up one level, from biological Intelligent Design to cosmological Intelligent Design (in other words, the fine-tuning argument, as applied to not only the universe’s laws and fundamental constants but also its initial conditions). You also write that by placing "not achievable by any natural means" in the definition of CSI you make it impossible for the NDEs to accept the definition. There’s nothing in the definition of CSI that says “not achievable by any natural means." As I see it, CSI is just a measure of the probability of unguided natural mechanisms producing the pattern or structure in question. If the CSI is above 500 bits, then we infer design. There's nothing question-begging about the definition here; a Darwinist might well agree to use it. What a Darwinist is most likely to disagree with is the calculated value for the CSI of a system which ID proponents claim is designed. A Darwinist will want to argue that in fact it falls below 500 bits. Hope that helps.vjtorley
November 18, 2014
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Silver Asiatic, Thank you for your post. You write:
We can observe information and we see it in a high-degree active in the bacterial flagellum (information communicated and organized through a variety of parts exhibiting a complex function). Probability studies are secondary.
You have a valid point. However, insofar as CSI refers to something quantifiable (as it is supposed to do), then I can see no way to quantify it except by calculating the probability of its originating via unguided processes. If you’re going to make a non-quantitative design argument, then you can still validly argue as follows: (1) We see living things exhibiting informational properties (e.g. digital codes, programming languages). (2) The only cause known to be capable of generating those properties is an intelligent agent. (3) Therefore it is rational to infer (by abductive logic) that these informational properties of living things were designed by an intelligent agent. That's perfectly fine, but it's not a quantitative argument. If you want a quantitative argument that you can attach numbers to, then the way I see it, you need to calculate probabilities. I hope that helps. Thanks again.vjtorley
November 18, 2014
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Adapa, 102:
All ID has ever offered is “This looks designed to me”. That’s not much of a scientific explanation. In fact it’s no explanation at all.
A textbook example of continuing to repeat a strawman caricature in the presence of a corrective, cf. 83 above. Consider what that tells us about motives, approach to issues, and attitude to duties of care to truth, accuracy and fairness. KFkairosfocus
November 18, 2014
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PPPS: Notice, the significant role of reuse of a library of principles transferred across cases and disciplines, i.e. a library. This finds echoes in object oriented programming etc, and probably not by accident. All of this should sound quite familiar from the world of life also.kairosfocus
November 18, 2014
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PPS: Survey article: http://www.mazur.net/triz/kairosfocus
November 18, 2014
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MD, 88:
we have a very well documented macro-step by macro-step log of the intelligent development of human designs. It is called the USPTO. The patents show, with high resolution, the process of a working intelligent design system.
Not only so, but there is an active theory of inventive problem solving rooted in study of patents and inference of underlying principles. That theory, TRIZ, addresses technological evolution by progressive inventions. Here's Wiki's intro:
TRIZ (/?tri?z/; Russian: ?????? ??????? ???????????????? ?????, teoriya resheniya izobretatelskikh zadatch) is "a problem-solving, analysis and forecasting tool derived from the study of patterns of invention in the global patent literature".[1] It was developed by the Soviet inventor and science fiction author Genrich Altshuller and his colleagues, beginning in 1946. In English the name is typically rendered as "the theory of inventive problem solving",[2][3] and occasionally goes by the English acronym TIPS. Following Altshuller's insight, the theory developed on a foundation of extensive research covering hundreds of thousands of inventions across many different fields to produce a theory which defines generalisable patterns in the nature of inventive solutions and the distinguishing characteristics of the problems that these inventions have overcome. An important part of the theory has been devoted to revealing patterns of evolution and one of the objectives which has been pursued by leading practitioners of TRIZ has been the development of an algorithmic approach to the invention of new systems, and the refinement of existing ones. The theory includes a practical methodology, tool sets, a knowledge base, and model-based technology for generating new ideas and solutions for problem solving. It is intended for application in problem formulation, system analysis, failure analysis, and patterns of system evolution. There are three primary findings of this research. The first is that problems and solutions are repeated across industries and sciences, the second that patterns of technical evolution are also repeated across industries and sciences, and the third and final primary finding is that the innovations used scientific effects outside the field in which they were developed. In the application of TRIZ all these findings are applied to create and to improve products, services, and systems.[4]
Forty-odd main principles, pivoting on constraints and common challenges to be moved from usual compromise tradeoffs to win win cases, where possible. KF PS: With gene modification an existing practice (and controversy on playing God), it seems gene twiddling is not merely theory but fact.kairosfocus
November 18, 2014
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Moose Dr It is reasonable to seek step-by-step evidence from a step-by-step process like NDE. To ask the same from a jump-by-jump process like ID is, well, ludicrous. Wait, didn't you just tell me ID is no different from NDE except with ID the Designer comes by every so often to "twiddle" a gene or two? If that's so why can't we ask for some specifics on the work of the Intelligent Gene Twiddler? :)Adapa
November 18, 2014
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Moose Dr. (I'll play Devil's advocate here. - A) On number of designers — One. Definitely one (caveat, it could be a group working in concert.) Why couldn't if be two Designers working at cross purposes who both swiped a third Designer's DNA intellectual property? After all we do see lots of predator/prey relationships with one species trying to kill and eat every member of another. Why would one Designer try to kill off his own creation? A time line — Unlike other IDers, I am quite convinced that the Intelligent agent twiddles with data frequently, at many points in time How do you tell external "twiddles" from naturally occurring genetic variations that cause morphological change? Especially over the last 500 million years? The mutation miracle must then have floated up into dominance through the process of natural selection (possibly with the designer “protecting” the creatures containing the desired mutation). What about the possibility of neutral drift? Drift can fix mutations in relatively few generations in small populations. The only differences between my position and that of NDE is that I allow for, and believe is necessity, multiple simultaneous mutations, and for these simultaneous mutations to have intention. How do you determine the "intention" of mutations? Does that help? Certainly fun to think about, thanks!Adapa
November 18, 2014
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Orange trees cannot even in principle produce ripe oranges. Any definition of "ripe" is circular. Therefore orange trees cannot even in principle produce ripe oranges.Mung
November 18, 2014
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keiths:
After two years, do you still not understand what P(T|H) stands for in Dembski’s equation?
Yet another non sequitur. Let's try again. 1.) CSI was devised as a measure. 2.) CSI was not devised as a measure. keiths:
I can back up my claims.
Or not. keiths:
I can back up my claims.
Mung:
Please do so. Or was my argument too difficult for you to follow? keiths: CSI was never intended to be construed as a measure. That claim is inherent in your position against CSI. That natural processes cannot “produce” CSI is just so much nonsense. It’s like claiming that orange trees cannot produce ripe oranges.
Mung
November 18, 2014
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Moose Dr, Ok, Now the designer also is responsible for entire universe. Moose Dr, Why don't you just come out and say you are making a case for God as the designer and that it is couched in scientific language ?Me_Think
November 18, 2014
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centrestream (104) "Why not?" Let me help you out a bit. Consider that you find two people in a remote wilderness surrounded by high mountains. One tells you that he hiked to get there. The other tells you that he hired a plane and flew. It is reasonable enough to ask the person who hiked to show you some footprints, but unreasonable to ask the person that flew. (Maybe you would ask the person that flew or an invoice from the plane charter company.) Or consider that you met two snails. One said that he snailed his way there, the other said that he caught a ride on the back of a horse. It may be reasonable to ask to see portions of continuous track from the snailing snail, but from the riding snail, the only evidence you would expect are periodic footprints -- not a continuous track. The bottom line is that each proposed method of transport (from no life to humanity in this case) should leave different kinds of evidence. It is reasonable to seek step-by-step evidence from a step-by-step process like NDE. To ask the same from a jump-by-jump process like ID is, well, ludicrous.Moose Dr
November 18, 2014
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Me_think, "From time to time by unknown mechanism he inspects billions of species and billions of processes and jets around ..." Think about this, think. This "designer" is presumed to be the same "designer" that engineered the big bang.Moose Dr
November 18, 2014
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Summary of Moose Dr @ 105 One Designer creates entire life process. From time to time by unknown mechanism he inspects billions of species and billions of processes and jets around fixing whatever needs to be fixed. thanks for the ID explanation Dr.Me_Think
November 18, 2014
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Adapa, "We’d just like to see some detail, ANY detail. Like a timeline. Or a manufacturing mechanism. Or the number of Designer(s). Or the powers / limitations of the Designer. ANY detail." Though I have published some of this detail on this site, I would say that you have a point. Part of the schtick is that ID is a big tent. It includes young earthers and common descenters (of which I am one.) I have personally sought, and to some extent found, answers to some of your questions. On number of designers -- One. Definitely one (caveat, it could be a group working in concert.) It is clear that we have one life system. Even if you hold to a common design model, there is still one design style. As a software developer I have worked within the legal system to demonstrate ownership of software. Software, even on the compiled level, shows the style of the author. If there are multiple authors, that clearly shows up. DNA clearly has the style of a single author (or no author). If you hold to UCD, then you must recognize that the first life form must have come into existence. The fact that a single life form came into existence would indicate that it has a single designer (or none). The big bang, interestingly, is a single, singularity event. If it was caused by any, it was caused by one (or, of course a group acting in concert.) A time line -- Unlike other IDers, I am quite convinced that the Intelligent agent twiddles with data frequently, at many points in time. I have considered this in light of the HAR1F rna gene. This thing took on 18 mutations somewhere between human and the last common ancestor. This thing should be a grand puzzle to NDEs, as it does not appear possible to have evolved the change by individual point mutations. The only way to have evolved the thing is with multiple truly simultaneous mutations, or a big cut and paste that included a bunch of identical nucleotides. It would appear to me most likely that this mutation happened at a single point in time -- a miracle event. Let me put more body on this. For UCD to be true, each such "miracle mutation" must not cross the classic species barrier. Rather the organism (primate in this case) that received the lucky mutation must have been able to mate with its pre-mutated peers. The mutation miracle must then have floated up into dominance through the process of natural selection (possibly with the designer "protecting" the creatures containing the desired mutation). Another UCD possibility exists -- that the mutation is given simultaneously to a male and a female -- instantly creating a new species. This, however, presents evidential problems. The strongest case that I have seen for UCD (at least a common ancestor between human and chimp) is the fact that there are numerous disease producing point mutations that are shared by humans and chimps. For this to be so, there must have been a community that migrated to become human, rather than an individual human pair coming to be -- even if by the injection of DNA modification. More generally on a timeline -- I think that the science being done produces the timeline of individual mutational events, just as it does with NDE. The only differences between my position and that of NDE is that I allow for, and believe is necessity, multiple simultaneous mutations, and for these simultaneous mutations to have intention. I am sure that many IDers would disagree with me on the above. I am sure that many IDers could give their own "meat" on the bones of their personal ID compatible sub-theory. However, none of the above can possibly become part of the big tent of ID simply because of its big tent nature. Does that help?Moose Dr
November 18, 2014
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Moose Dr.: "It is therefore expected that ID cannot produce a mutation by mutation account of the creative activity." Why not? If you expect it from the opposing theory, why shouldn't it be expected from the ID hypothesis?centrestream
November 18, 2014
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Moose Dr. When I was in highschool (some decades ago) there was a lot of buzz about zapping fruit flies with radiation. It produced a lot of really strange, albeit all dysfunctional, bugs. However, it didn’t produce anything that was more suited for any particular environment, as far as I can tell. (facepalm) That's not how evolution works, by zapping a bottle full of Drosophila with harmful doses of radiation. C'mon, you know better than that. Experiments with bacteria have produced living organism simulations that involve more organisms and more generations than all of the mammals that have ever lived. So? Bacteria aren't multicellular animals. With multicellular animals we haven't come withing a parsec of the time and population sizes evolution has had to work with. Even with that we have clearly identified the genetic mechanism for variation and have ample evidence the effects of such variations can be cumulative.Adapa
November 18, 2014
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Moose Dr The ID process is a process of complex synthesis by the intelligent agent. It is therefore expected that ID cannot produce a mutation by mutation account of the creative activity No one has asked ID for a mutation by mutation account. We'd just like to see some detail, ANY detail. Like a timeline. Or a manufacturing mechanism. Or the number of Designer(s). Or the powers / limitations of the Designer. ANY detail. All ID has ever offered is "This looks designed to me". That's not much of a scientific explanation. In fact it's no explanation at all.Adapa
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Mung, After two years, do you still not understand what P(T|H) stands for in Dembski's equation? I atill remember when you thought P(T|H) was a fraction with T in the numerator and H in the denominator. That was funny.keith s
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Moose Dr. DAVID BERLINSKI; In "A Scientific Scandal," I observed that Dan-E. Nilsson and Susanne Pelger's paper, "A Pessimistic Estimate of the Time Required for an Eye to Evolve," was a critic's smorgasbord. There are so many things wrong with it that even the finickiest of eaters could leave the table well-satisfied and ready for a round of Alka-Seltzer. But, in itself, there is nothing here that suggests a scandal. Dan-E. Nilsson is a distinguished scientist. Witness his discovery that the mysid shrimp, ptro-mysis pauciponisa an organism whose eyes are at once simple and compound (D. Nilsson, R.F. Modlin, "A Mysid Shrimp Carrying a Pair of Binoculars," Journal of Experimental Biology, Vol. 189, pp. 213-236, 1994), or his precise work on the optical system of the butterfly (D. Nilsson, M.F. Land, J. Howard, "Optics of the Butterfly Eye," Journal of Comparative Physiology, A 162, 341-366, 1988). Together with Susanne Pelger, he has simply written a silly paper. It happens. And in the literature of evolutionary biology, it happens very often. No, the scientific scandal lies elsewhere. Nilsson and Pelger's paper has gained currency in both the popular and the scientific press because it has been misrepresented as a computer simulation, most notably by Richard Dawkins. Word spread from Dawkins's mouth to any number of eagerly cupped but woefully gullible ears. Subsequent references to Nilsson and Pelger's work have ignored what they actually wrote in favor of that missing computer simulation, in a nice example of a virtual form of virtual reality finally displacing the real thing altogether. This misrepresentation of scientific work is a species of fraud, no different in kind from plagiarism in journalism or the fabrication of data in experimental physics. It is the indifference to this fraud that I denounced as scandalous. Recognizing so many fond familiar faces among my critics—Paul Gross, Jason Rosenhouse, Matt Young, and Mark Perakh have replied to previous essays of mine in Commentary—I hoped that self-interest, if nothing else, might have prompted a moment of critical self-reflection. No very delicate moral sense is involved in determining that fraud is fraud. If Richard Dawkins is one of their own, all the more reason to apply to him the moral standards that Messrs. Gross, Rosenhouse, Young, and Perakh are accustomed to applying to their intellectual enemies. Reading their letters, I realize that they had no intention of saying boo. What could I have been thinking? Dan-E. Nilsson is persuaded that I wrote my essay because I am moved to reject "uncomfortable scientific results." He is mistaken. The length of time required to form an eye is a matter of perfect indifference to me; had he and Susanne Pelger been able to demonstrate that the eye was in fact formed over the course of a long weekend in the Hamptons, I would have warmly congratulated them. As I have many times remarked, I have no creationist agenda whatsoever and, beyond respecting the injunction to have a good time all the time, no religious principles, either. Evolution long, evolution short—it is all the same to me. I criticized their work not because its conclusions are unwelcome but because they are absurd. The vertebrate eye, Nilsson and Pelger claim, emerged from a patch of light-sensitive cells. Climbing up evolution's greasy pole, or adaptive peak, those cells got to where they were going by invagination, aperture constriction, and lens formation. In explaining the evolution of the eye in terms of such global geometrical processes, Nilsson and Pelger rather resemble an art historian prepared to explain the emergence of the Mona Lisa in terms of preparing the wood, mixing the paint, and filling in the details. The conclusion—that Leonardo completed his masterpiece in more than a minute and less than a lifetime—while based squarely on the facts, seems rather less than a contribution to understanding. It is hardly surprising, then, that while theoretical optics serves qualitatively to justify the overall connection Nilsson and Pelger draw between morphology and visual acuity, nothing in their paper and nothing in their references justifies the quantitative relationships they employ to reach their quantitative conclusion. To be sure, Mr. Nilsson denies that this is so. "Contrary to Mr. Berlinski's claim," he writes, "we calculate the spatial resolution (visual acuity) for all parts of our eye-evolution sequence, and the results are displayed in figure 1 of our paper. The underlying theory is explained in the main text, including the important equation 1 and a reference to Warrant & McIntyre (1993), where this theory is derived." In fact, no underlying theory whatsoever is explained in Nilsson and Pelger's main text, or in the legend to figure 1; and while they do assert that calculations were made, they do not say where they were made or how they were carried out. The burden of Mr. Nilsson's denials is conveyed entirely by equation 1 and by his references. Let us start with equation 1, and with figure 1b that this equation is said to control. It is in figure 1b that aperture constriction takes over from invagination in getting an imaginary eye to see better. The graph juxtaposes aperture size against detectable spatial resolution. Having dimpled itself in figure 1a, Nilsson and Pelger's blob is now busy puckering its topmost surface to form a pinhole in figure 1b.* In a general way, the curve they present is unremarkable. No one doubts that spatial resolution is improved in an eye when its aperture is constricted. But why is it improved in just the way that Nilsson and Pelger's graph indicates? Equation 1 is of scant help in this regard, despite Nilsson's insistence that it is important. Drawing a connection among visual acuity, focal length, light intensity, and noise, the equation specifies the local maximum of a curve, the place where it stops rising. In other words, it specifies a point; and it does nothing more. "We can now use this relationship," Nilsson and Pelger nevertheless declare, "to plot resolution against aperture diameter." They can do nothing of the sort, at least not in my calculus class. Knowing that a man has reached the summit of Mt. Everest, we still know nothing about the route he has taken to get there. What is needed if Nilsson and Pelger are to justify their graph is the equation from which equation 1 has been derived by differentiation. It is not there, just where I said it would not be. Similarly with Nilsson and Pelger's references, which do nothing to support their argument. Quite the contrary. Three papers are at issue: (1) A.W. Snyder, S. Laughlin, and D. Stavenga, "Information Capacity of the Eyes" (Vision Research, vol. 17, 1163-1175, 1977); (2) A.W. Snyder, "Physics of Vision in Compound Eyes" (in Vision in Invertebrates, Handbook of Sensory Physiology, edited by H. Autrum, vol. VII/6A, pp. 225-313, 1979); and (3) E. J. Warrant & P.D. McIntyre, "Arthropod Eye Design and the Physical Limits to Spatial Resolving Power" (Progress in Neurobiology, vol. 40, pp. 413-461, 1993). Of these papers, the first is recapitulated (and corrected) in the second, and the second is summarized in the third. In what follows, references to Snyder are always to the Snyder of his second paper. As their titles might suggest, both 'Physics of Vision in Compound Eyes" and "Arthropod Eye Design and the Physical Limits to Spatial Resolving Power" deal with compound invertebrate eyes. Nilsson and Pelger's work is devoted to the evolution of the camera eye characteristic of fish and cephalopods. Theoretical considerations that apply to bugs do not necessarily apply to fish or octopuses, the more so since their eyes are structurally different, as are their evolutionary histories. Writing about the compound eye, Nilsson himself has remarked that "it is only a small exaggeration to say that evolution seems to be fighting a desperate battle to improve a basically disastrous design" (Dan-E. Nilsson, "Optics and Evolution of the Compound Eye," in Facets of Vision, edited by D.G. Stavenga & R.C. Hardie, p. 3075, 1989). Whatever the desperate battle going on among the arthropods, there is no battle at all taking place among the vertebrates or the cephalopods. Nilsson and Pelger's eye moves from triumph to triumph with serene and remarkable celerity. If the papers by Snyder and Warrant & McIntyre say nothing about fish or octopuses, neither do they say anything about evolution. No mention there of Darwin's theory, no discussion of morphology, not a word about invagination, aperture constriction, or lens formation, and nothing about the time required to form an eye, whether simple, compound, or camera-like. The purpose of these three papers is otherwise. No less than any other system of communication, the eye represents a balance struck between signal and noise. There is the object out there in the real world—whether a point source like a star, or an extended source like a grating of light and dark lines—and there is its image trembling on the tips of the retina's budded nerve cells. Slippage arises between what the object is and how it is seen. Noise occurs in the visual system as the result of the random nature of photon emission, and it also occurs as the result of inherent imperfections in the eye's optical system. The theoretical optician abbreviates these limitations in one mathematical instrument. Imagine one of Nilsson and Pelger's plucky light-sensitive cells, and then extend two flanking lines from the cell up past the constricted aperture and out into space, so that the cell and those two flanking lines form a cone with a flat top. In the center of the cone, where a cherry would sit atop the ice cream, there is a light source. The cherry moves to the sides of the cone in angular steps; the cell dutifully responds. The correlation between moving cherry and twitching cell constitutes the optician's "angular-sensitivity function." Equation B15 (p. 238) in Snyder's "Physics of Vision in Compound Eyes" defines the signal-to-noise ratio of a hypothetical eye in terms of noise, modulation contrast (the difference in intensity between black and white stripes in a grating), and the modulation-transfer function, which is simply a mathematical transformation of the eye's angular-sensitivity function (its Fourier transform). Lumbering in Snyder's footsteps, Warrant & McIntyre split his equation into two of their own (equations 10 and 11 in Warrant & McIntyre, p. 430), the one describing the signal, the other the noise in a hypothetical visual system. They observe what is in any case obvious: whatever the parameters affecting visual acuity, signal and noise will always reach a point where the first is drowned out by the second and the system fails, a point evident enough to anyone trying to see in the dark. These equations lead by primogeniture to Nilsson and Pelger's equation 1, which, as it happens, does not appear anywhere in their sources in the form in which they express it. But neither Snyder's original equation nor Warrant & McIntyre's bright bursting clones in any way suggest that the tipping point between signal and noise is unique. The ratio of signal to noise in an optical system depends on a host of factors, including head size and eye movement, most of which Nilsson and Pelger ignore. Nor, for that matter, do these equations taken in isolation justify any particular quantitative conclusions. Until the angular-sensitivity function is specified, whether theoretically or experimentally, its role is ceremonial. Such specification is no easy business. Determining the shape of the angular-sensitivity function is a little like trying to guess an astronaut's weight in space. Scales are not likely to be of use. In an early paper dealing with this subject and devoted experimentally to flies, K.G. Götz noted that the angular-sensitivity function in Drosophila seemed to follow what is known mathematically as a Gaussian probability distribution (K.G. Götz, "Die optischen Übertragungseigenschaften der Komplexaugen von Drosophila," Kybernetik, 2, pp. 215-221, 1965). It was an interesting idea, but one that led to very considerable computational difficulties. Looking Götz-ward, and understandably recoiling, Snyder adopted a different strategy. In assessing the weight of an astronaut in space, it is simpler to count the calories he consumes and the exercise he undergoes than to try to measure his weight directly. His weight, although unmeasured, follows inferential-ly. In just the same way, Snyder thought to consider the angular-sensitivity function indirectly by considering the structures that determined its shape. These, he assumed, were the eye's retinal receptive field—area of the retina responding to signals—and its optical "blur spot"— the smeared image represented on the retina corresponding to the sharp object being seen. Let them both, he declared, be identically Gaussian. Why not? Both parameters had simple mathematical natures. The retinal receptive field is given as the ratio of the rhabdom's diameter to its posterior nodal distance, the optical blur as the ratio of the wavelength of stimulating light to the eye's aperture. From this the shape of the angular-sensitivity function followed. The result is known as the Snyder model. "The great beauty of this model," Warrant & McIntyre remark (in words that they have italicized), "is that if one knows some very simple anatomical information about the eye" (i.e., the nature of its optical blur spot and retinal receptive field) "one has the ability to predict . . . the approximate shape of the angular-sensitivity function" (p. 434). In referring to Warrant & McIntyre, Nilsson and Pelger are, in fact, appealing to Snyder, the maestre behind their masters—for, like Snyder, they, too, assume that retinal receptive fields and optical blur spots are identically Gaussian (p. 54). But theory is one thing, and living flesh another. Staking their all on Snyder's model, Nilsson and Pelger must live with its consequences. "Having considered the physical limitations to resolving power," Snyder wrote, "in addition to the absolute sensitivity of eyes, we now apply our concepts to real compound eyes." This is something that Nilsson and Pelger never do. And no wonder. For Snyder then added the rather important caveat that bringing theory to bear on life "requires precise knowledge [of various optical parameters] in the various regions of the eye" (Snyder, p. 276, emphasis in the original). If precise knowledge is needed in applying Snyder's model, precise detail is what is lacking in Nilsson and Pelger's paper. Precise detail? Any detail whatsoever. And for obvious reasons. When tested, Snyder's model turns out to be false across a wide range of arthropods. As Warrant & McIntyre note glumly, "The model, on the whole, works best for those eyes for which it was originally formulated—apposition compound eyes functioning according to geometrical optics—but recent careful and sensitive measurements of angular sensitivity reveal that even in these types of eye, the model often performs poorly." Readers may consult figure 34 (p. 441) of Warrant & McIntyre's paper to see how poorly the Snyder model does. In studies of the locust Locustia, real and predicted angular-sensitivity functions do not even share the same qualitative shape. Responding to my observation that no quantitative argument supports their quantitative conclusions—no argument at all, in fact—Mr. Nilsson has thus (1) offered a mathematically incoherent appeal to his only equation; (2) cited references that make no mention of any morphological or evolutionary process; (3) defended a theory intended to describe the evolution of vertebrate camera eyes by referring to a theory describing the theoretical optics of compound invertebrate eyes; (4) failed to explain why his own work has neglected to specify any relevant biological parameter precisely; and (5) championed his results by means of assumptions that his own sources indicate are false across a wide range of organisms. In acknowledgments to their paper, Nilsson & Pelger thank E. J. Warrant for help with their computations; in the acknowledgments to their paper, Warrant & McIntyre thank Mr. Nilsson for critically reading what they have written. Schnapps all around, I am sure. I turn next to the morphological units that are missing from Nilsson and Pelger's paper. It makes no sense to say of a ruler that it is one long. One what? When the "what" has been specified, a physical unit has been indicated: one inch, say, in the case of length, one pound in the case of weight. If one inch and one pound are units, length and weight are their dimensions. Only an origin in zero remains to be specified to complete the picture. In my essay, I observed that Nilsson and Pelger had not specified their unit of morphological change. Nilsson now asks me to consider again their remarks on p. 56 of their paper. There, he is certain, I will find the missing unit carefully explained. Here is what they write, and it is all that they write: "Our principles have been to use whole-length measurements of straight structures, arc lengths of curved structures, and height and width of voluminous structures." Very well. These are the fundamental units. They are none too clearly explained—try estimating the volume of a donut by looking at its height and width—but I know roughly what Nilsson and Pelger are getting at. What they do not say is how these three separate fundamental units are combined in a single overall derived unit of change. A homely example may make this more vivid. Except for the fact that it cannot see, a Swedish meatball is rather like an eye. And plainly it makes no sense to ask of two Swedish meatballs, one of them twice as greasy but half as wide as the other, which of them is bigger—at least not until units of grease and length have been combined. But this is, in general, no easy task, not even when shape alone is under consideration. "It is important to keep in mind," C.P. Klingenberg and L. J. Leamy write ("Quantitative Genetics of Geometric Shape in the Mouse Mandible," Evolution, 55(11), pp. 2342-2352, 2001), "that shape is a multivariate feature and cannot be easily divided into scalar traits without imposing arbitrary constraints on the results of the analysis." To see how difficult a conceptual problem Nilsson and Pelger have set themselves, readers may follow the trail of Klingenberg & Leamy's references to the badlands of current work on geometric morphometrics. Operating perhaps on the principle that a difficulty disclosed is a difficulty denied, Nilsson and Pelger do mention this very point, citing an example of their own on p. 56 to show just how arbitrary can be the business of calculating combined or derived units. In then justifying their own procedure, which is never explained, they remark: "As we are going to relate our measure of morphological change only to general estimates of phenotypic variation—in visual acuity, "we will be safe as long we avoid unorthodox and strange ways of comparing origin and product." Origin and product? I am sure they meant origin and unit. No matter. The remark speaks for itself. There is next the matter of random variation: the heart of the matter so far as I am concerned. Nilsson and Pelger's paper is not an exercise in theoretical optics. It is intended to serve polemical purposes. Thus, they write: "In this context it is obvious that the eye was never a real threat to Darwin's theory of evolution"(p. 58). By "this context," they mean one in which only "eye geometry" and "optical structures" are up for grabs. But whether in this context or any other, it is as a defense of Darwin's theory that Nilsson and Pelger's theory fails most obviously. Let me review the chief steps in their argument. There is morphological change on the one hand, visual acuity on the other. As their population of light-sensitive cells alters its geometry—by means never specified—visual acuity perks up. In all, they assert, 1,829 steps are involved in tracing a path from their first patch to their final "product." Just how do Nilsson and Pelger's light-sensitive cells move from one step on that path to the next? I am not asking for the details, but for the odds. There are two possibilities. Having reached the first step on the path, the probability that they will reach the second (and so on to the last) is either one or less than one. If one, their theory cannot be Darwinian—there are no random changes. If less than one, it cannot be right—there is no way to cover 1,829 steps in roughly 300,000 generations if each step must be discounted by the probability of its occurrence. Demonstrating the existence of a path between two points in the history of life is in general not hard. What is hard is determining how the path was discovered. (This was the point of the linguistic example I offered in my essay.) If one assumes, as Nilsson and Pelger do, that probabilities need not be taken into account because all transitions occur with a probability of one, there is no problem to be discussed—but nothing of any conceivable interest, either. In responding to this obvious point by generously suggesting that I need to spend more time by the lamp with D.S. Falconer's Principles of Quantitative Genetics, Mr. Nilsson has covered an embarrassment by addressing an irrelevance. Neither population size nor natural selection is at issue. A few minor matters. Falconer's response variable R is a measure, all right: a measure of the extent to which the mean of some quantitative phenotypic character—snout length, crop yield, scab color, or scrotum size (examples from the literature, I am afraid)—rises or falls as the result of natural selection. Just what I said, just as I explained. Although I offered no definitions in my essay, the paraphrases I employed were harmless. Why not say "sensitivity to vision" instead of "visual acuity," just to vary pace and prose? But in one respect, Mr. Nilsson is right: I did not distinguish between selection and intensity of selection. Neither does he. Neither does Falconer's response statistic, which contains only one selectional parameter, and that one measuring the intensity of selection. Neither does anyone else in this context. His paper with Susanne Pelger, Mr. Nilsson writes, has never been criticized in the peer-reviewed literature. I am certain that this is so. Paul R. Gross takes the occasion of his current letter to assure readers that what he meant in his last letter he did not say and what he said he did not mean. Like golf, Mr. Gross suggested in the 1986 essay from which I uncharitably quoted in the March Commentary, science is rather a clubby affair, and just as a great many men prefer to cover the links sedately in the company of men like themselves—tassels on their shoes, alligators on their polo shirts—so scientists prefer to keep company with their own, men and women who share their tastes, point of view, outlook on life. These are sentiments so candid that I was surprised to find Mr. Gross expressing them. But he is now prepared to disown what he said. The club is just fine, and just look at those splendid greens! The admissions board is to be faulted only when, by accident or inadvertence, it excludes one of its own, a scientist who like L.V. Heilbrunn has published in the literature. Such men are entitled to wear the gold cufflinks with the crossed golf clubs; keeping them out would be irresponsible. But keeping out the others is not only good science but good sense. Ipse dixit. A few other points deserve comment. In offering Nilsson and Pelger the oil of his approval, Mr. Gross affirms that I have misunderstood or misinterpreted critical elements of their paper. In keeping with his longstanding policy of never documenting his discontent, he does not say which elements. As I keep reminding him, this is not sporting. Still, it is inconceivably droll to see Mr. Gross excusing Richard Dawkins's misrepresentation of Nilsson and Pelger's work by appealing to the fact that Dawkins expressed his views in a trade book. Mr. Gross apparently believes that outside the country club, a man can say anything he wants, a policy that he would not dream of applying to critics of Darwin's theory. A few of Mr. Gross's remarks suggest a need for remedial reading. I have never argued that 'evolutionary theory cannot explain the eye." How on earth would I know that? And explain what in particular? Its emergence, its structure, its physiology, its biochemistry? What I contended specifically is that Nilsson and Pelger's paper is just nuts. Conspiracies and cover-ups are, in any case, not in my line, and I never suggested or supposed that evolutionary biologists who failed to criticize Richard Dawkins for misrepresenting Nilsson and Pelger did so as part of a conspiracy. Like droshky horses, they were only doing what comes naturally: turning a blind eye. If the burden of Nilsson and Pelger's paper was to demonstrate the existence of "one possible evolutionary pathway to the geometry of a fish-like eye from a patch of photoresponsive cells," as Mr. Gross writes, they have surely wasted their time. The existence of such a path is hardly in doubt. Every normal human being creates an eye from a patch of photoresponsive cells in nine months. I certainly agree that the "only explanation we have for the structure of the eye . . . is Darwinian evolution." But neither an orchestra nor an explanation becomes good by being the only game in town. On the other hand, I disagree that Darwin's theory is as "solid as any explanation in science." Disagree? I regard the claim as preposterous. Quantum electrodynamics is accurate to thirteen or so decimal places; so, too, general relativity. A leaf trembling in the wrong way would suffice to shatter either theory. What can Darwinian theory offer in comparison? Finally, I would hardly dispute Mr. Gross's claim that "with the discovery of the developmental regulatory genes, we have learned how subtle, how versatile, and yet how simple the mechanism can be for transforming one biological structure to another." If he were to re-read the correspondence (Commentary, September 1996) following the publication of my "The Deniable Darwin" (June 1996), he could not fail to be struck by my reply to his own letter, in which I specifically called attention to work on regulatory genes and eye formation—the very work that he now suggests I am keeping from my readers. Subtle and versatile, those genes? Yes, indeed. Absolutely astonishing? That, too. But hardly a triumph of Darwin's theory. For one thing, no Darwinian theorist had predicted the existence of these genes; for another, no Darwinian theorist has explained their emergence. The facts are simply far more fascinating than anything that poor drab Darwin, endlessly sifting time and chance, could possibly have imagined. Citing those ever useful but eternally anonymous "creationists," Matt Young argues yet again, as he did in our earlier exchange, that Nilsson and Pelger have given the lie to creationist claims. If it was their computer simulation that originally lent ardor to his asseverations, now it is their paper itself. Mr. Young is a man plainly prepared to rely on an endless series of fallback positions. In the end, he may have to argue that his refutation is its own best friend, and that Nilsson and Pelger's paper is itself superfluous. No one doubts that the eye has evolved. Not me, in any event. Fish have eyes; rocks do not. Those eyes came from somewhere—right?—and if coming from somewhere counts as evolution, count me among its champions. No one doubts, furthermore, that the "eye could have evolved in 350,000 generations." As I remarked earlier, the eye could have evolved in a weekend. The issue is whether it could have evolved in 350,000 generations given the constraints of random variation and natural selection. I have absolutely no idea. Neither do Nilsson and Pelger. And neither does Matt Young. Arguing now from the last trench before the bunker, Mr. Young writes that Nilsson and Pelger's paper deals with the development of invertebrate eyes, and triumphantly chides me for overlooking this point. On p. 56 of their paper, Nilsson and Pelger write: "After constriction of the aperture and the gradual formation of a lens, the final product becomes a focused camera-type eye with the geometry typical for aquatic animals (e.g. fish and cephalopods)." Fish are, of course, vertebrates, as anyone who has picked the flesh from a flounder knows. Perhaps I will be forgiven if I refer to this exchange as shooting fish in a barrel. Making the point that the emergence of even the most modest eye will require simultaneous and parallel evolutionary development, Mr. Young asks that I defend my claim that this process could not have taken place by quantitative steps. In the first place, I made no such claim, if only because its truth struck me as obvious. But were I to make such a claim I would observe, as Richard Dawkins does, that to the extent that simultaneous and parallel changes are required to form a complex organ, to that extent does the hypothesis of random variation and natural selection become implausible. It is one thing to find a single needle in a haystack, quite another to find a dozen needles in a dozen haystacks at precisely the same time. Surely the burden of proof in such matters is not mine. I am not obliged to defend such mathematical trivialities as the proposition that as independent events are multiplied in number, their joint probability of occurrence plummets. I have no idea what Mr. Young means when he writes that the number 1.00005 is not a percentage. Every number can be expressed as a percent, and every percent is a pure number. But he gets half credit for spotting a slip: the figure of 1.00005 between parentheses on p. 33 in my text should have been .005. Mr. Nilsson, who also spotted the slip, gets the other half. Me? I blame my editors. Finally, I did not fault the scientific community for failing to criticize Nilsson and Pelger's work. I did the job of criticism myself. I faulted the Darwinian community—Mr. Young included—for failing to denounce scientific fraud, specifically the misrepresentation of Nilsson and Pelger's work by Richard Dawkins. Now I see that Mr. Young feels I have manhandled him in these exchanges. Too bad. Commentary is not some academic mouse hole. Mark Perakh, a sensei of the "noted scientists say" school of self-defense, is right in one respect: the computer simulation missing from Nilsson and Pelger's paper has no bearing on what they actually said and claimed. And right in a second respect: "The real question [is] whether an eye could have developed in a geologically short time via a Darwinian mechanism" (emphasis added). But then, although quite confident that I am wrong in my criticisms, he offers nothing by way of rebuttal. Like so many of these martial-arts types, he is too busy preparing himself to run from the field with honor to bother doing battle. Contrary to what Mr. Perakh asserts, not only can I imagine, I do not doubt, that "distinguished scientists," many with a record of "substantial achievement," can have an opinion different from my own. It happens all the time. I would not dream of accusing ten respected scientists of fraud simply because they passed on the opportunity to have a go at Nilsson and Pelger. The men and women I criticized earned my contempt the hard and dirty way, by saying nothing about scientific misconduct when it was right under their noses. Like Mr. Perakh and Paul R. Gross, Jason Rosenhouse regards Richard Dawkins's misrepresentation of Nilsson and Pelger's work as a "minor error." Some minor, some error. What, may I ask, is the difference between inventing data out of whole cloth and inventing a computer simulation out of whole cloth? Should not evolutionary biologists be held to the same standards as physicists? Or even journalists? What part of the declaration that fraud is fraud does he fail to endorse? These are not semantic issues. If I claimed in print that Mr. Rosenhouse has four eyes, his denials would not turn on what I meant. Two eyes, I am sure he would say, are not there. Two eyes, and one computer simulation. Mr. Rosenhouse believes that Nilsson and Pelger made an important discovery: namely, "that there is a smooth gradient of increasing visual acuity linking a light-sensitive spot to a lens-bearing eye." This is not their discovery, it is a restatement of their chief assumption. "The model sequence is made," they write, "such that every part of it, no matter how small, results in an increase of the spatial information the eye can detect" (p. 53). Note: made, not discovered. To repeat, the flaw in Nilsson and Pelger's work to which I attach the greatest importance is that, as a defense of Darwinian theory, it makes no mention of Darwinian principles. Those principles demand that biological change be driven first by random variation and then by natural selection. There are no random variations in Nilsson and Pelger's theory. Whatever else their light-sensitive cells may be doing, they are not throwing down dice or flipping coins to figure out where they are going next. Mr. Rosenhouse's conviction that the randomly occurring changes required by Darwin's theory are nevertheless "plainly implied" throughout Nilsson and Pelger's paper owes nothing to the facts and little to common sense. If changes in their model were really random, their temporal estimates would be apt to change by orders of magnitude, a point I made in my essay and again in my reply to Dan-E. Nilsson above. In my essay I also questioned Nilsson and Pelger's decision to hold selection pressure constant over time. In this, I found myself echoing John Gillespie (The Causes of Molecular Evolution, 1991, p. 294). "[W]e must be concerned," Gillespie writes, "with models of selection in variable environments. How could it be otherwise? Natural selection is a force adapting species to their environments. Environments are in a constant state of flux; selection coefficients must be in a constant state of flux as well." What is good enough for Gillespie is good enough for me. In approving of the value chosen by Nilsson and Pelger for selection pressure, Mr. Rosenhouse writes that it is "ludicrously low for almost any environment." Is it indeed? The figure that Mr. Rosenhouse calls ludicrous, Nilsson and Pelger term pessimistic, and Mr. Gross reasonable. The correct term is arbitrary—as in, it is anyone's guess what the variance among a bunch of fish might have been a couple of million years ago. Studies of variance and heredity typically deal with tiny populations and small periods of time. Studying the collard flycatcher, Ficedula albicollis, Merilla, Kruuk, and Sheldon collected eighteen years of data for 17,171 nestlings in order to reach some quite modest quantitative conclusions (J. Merilla, L.E.B. Kruuk, and B.C. Sheldon, "Natural Selection on the Genetic Component of Variance in Body Condition in a Wild Bird Population," Journal of Evolutionary Biology 14, pp. 918-921, 2001). Nilsson and Pelger's imaginary population ranges over space and time in a way that could not possibly be disciplined by the data. Nick Matzke believes that Nilsson and Pelger provide a mathematical model for the development of the eye. Let us be honest: beyond a few finger-counting exercises, there is no mathematics in their model, and while their references do contain some legitimate mathematics (nothing beyond second-semester calculus, but also nothing to sneeze at), their references, as I have shown in patient detail, do not support their theory. The task of modeling the eye's complicated geometry from light-sensitive cell to fully functioning eye is utterly and completely beyond our powers, as a glance at any textbook dealing with embryology would show. Mr. Matzke devotes the greater part of his otherwise interesting letter to doing battle with various "creationist straw men." It is useful work, I am sure, the more so since the creationists are never named. But whoever they are, I am not among them. Quite the contrary, I am as eager to do right by the snails as he is: why should he think otherwise? It is only when he passes to matters of fact that we part company. Nilsson and Pelger's theory is intended to encompass the evolution of the eye in fish and cephalapods. Fish indisputably have bones, an attractive skull, and for the most part two staring eyes. The cephalochordate Branchiostoma (Amphioxus in a now out-of-date system of nomenclature) is widely taken by paleontologists to be a very plausible ancestral model to the vertebrates. It has certain vertebrate features while lacking others. These others include bones, a skull, a brain, and paired sensory organs: in other words, it has no eyes. Mr. Matzke's very confident assertion that cephalochordates have "primitive eyes" is simply untrue. Now that I have swept away a few straw men of my own, let us see what is left to clean up. In my essay I wrote that Nilsson and Pelger made no attempt to discuss the cost-benefit payoffs associated with an improvement in visual acuity. My aim in discussing the reconstruction of the fish skull was not to argue that eyes came first or that bones did. Paired sensory organs and bones are characteristics of the vertebrates. Plainly they evolved together. Plainly, too, one function of the bony skull in vertebrates is to provide protection for the paired sensory organs located on their heads. The protection racket, as every Mafia boss is aware, does not come cheap; but Nilsson and Pelger, in adding up the benefits of visual acuity, did not ever bother to consider the vigorish. This is such an unobjectionable point that I cannot imagine why Mr. Matzke found it fishy. I very much appreciate the letters from David Safir and Norman Gentieu. http://www.discovery.org/a/1509bornagain77
November 18, 2014
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keiths:
I can back up my claims.
Please do so. Or was my argument too difficult for you to follow? keiths: CSI was never intended to be construed as a measure. That claim is inherent in your position against CSI. That natural processes cannot "produce" CSI is just so much nonsense. It's like claiming that orange trees cannot produce ripe oranges.Mung
November 18, 2014
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Adapa, "One good example is Nilsson and Pelger’s breakout of approx. 2000 steps required in eye evolution." Hmmm, interesting. I just googled it quickly. It appears that what Nilsson & Pelger did was not much different from Dawkins "weasel" program. They did no analysis, as far as I can tell, on the genetic level. They just morphed shapes around in a computer. This is very far from what I would seek as evidence that NDE actually works. When I was in highschool (some decades ago) there was a lot of buzz about zapping fruit flies with radiation. It produced a lot of really strange, albeit all dysfunctional, bugs. However, it didn't produce anything that was more suited for any particular environment, as far as I can tell. Experiments with bacteria have produced living organism simulations that involve more organisms and more generations than all of the mammals that have ever lived. What is the best they have done? Once or twice it looks like they have pulled of a two mutation (where neither alone is beneficial) mutation pair. Ooooh. I'm buyin' into NDE right now -- after all in real world simulations it so clearly works.Moose Dr
November 18, 2014
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Adapa, "Tell me why ID should be allowed to demand such fine granularity from evolutionary theory but can’t provide even the simplest of details itself? Seems pretty hypocritical don’t you agree?" First, I do not know anything about Nilsson and Pelger's work. I'll google it in a few minutes. Second, in "Edge of Evolution" Behe presented published evidence that the granularity that neo-Darwinism requires is the individual mutation event. That's how neo-Darwinism works. ID doesn't work that way at all. The ID process is a process of complex synthesis by the intelligent agent. It is therefore expected that ID cannot produce a mutation by mutation account of the creative activity.Moose Dr
November 18, 2014
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keiths: "defend all my claims I can, or not."Mung
November 18, 2014
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keiths:
Natural processes are incapable of producing CSI by the very definition of CSI.
Mung:
And here I thought CSI was a measure. So keiths, on this view of CSI, is asserting that natural processes cannot be measured, even in principle. odd.
Darth Vader: The logic is not strong with this Mung. Yoda: Janitors the Empire also needs.keith s
November 18, 2014
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Moose Dr Centrestream, you seem unclear on the concept. The neo-Darwinian model is a “step-by-step” model. It is reasonable, therefore, to show a “step-by-step” pathway to significant CSI. This has been attempted before. One good example is Nilsson and Pelger's breakout of approx. 2000 steps required in eye evolution. However as soon as the work came out ID Creationists started yelling it wasn't detailed enough. They demanded a mutation-by-mutation listing. There was some suggestion that ID be renamed "IDID", for "I Demand Infinite Detail!". Tell me why ID should be allowed to demand such fine granularity from evolutionary theory but can't provide even the simplest of details itself? Seems pretty hypocritical don't you agree?Adapa
November 18, 2014
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keiths:
Natural processes are incapable of producing CSI by the very definition of CSI.
And here I thought CSI was a measure. So keiths, on this view of CSI, is asserting that natural processes cannot be measured, even in principle. odd.Mung
November 18, 2014
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Tamara Knight:
We can experimentally determine the probability of “likely” events, but not the probability of “very unlikely” ones.
You really need to read Dembski's latest book.
We can experimentally determine the probability of “likely” events...
How?
We can experimentally determine the probability of “likely” events, but not the probability of “very unlikely” ones.
This is self-contradictory.Mung
November 18, 2014
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OldArmy94 Answer me this: who designed Stonehenge? Human beings, particularly nomadic tribes that inhabited England around 3000 BC to 2400 BC. There is some archaeological evidence they originated in Spain and colonized parts of northwest Europe and Great Britain after migrating northwards. They used standard stone carving tools and techniques known at the time and got their raw materials from a site in Wales some 140 miles away. Who designed the bacteria flagellum? When was it done, what tools were used, where did the raw materials come from?Adapa
November 18, 2014
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