Design Detection Reported on CBS’s 60 Minutes
| November 30, 2008 | Posted by Barry Arrington under Intelligent Design |
This evening the CBS News show 60 Minutes reported on an impressive example of design detection in the on-line poker world.
Online gambling has grown in a few short years to a 16 billion dollar a year industry, and a big part of that growth has come from internet poker. Recently several professional gamblers at one of the larger internet poker sites, Ultimatebet.com, noticed that some of their opponents were playing extremely poorly, yet winning consistently. They suspected cheating.
One of the professionals obtained tracking data on one of the suspected cheaters, and after running the numbers determined that the suspect’s winning hand percentage was 13 standard deviations away from the mean percentage. This is equivalent to winning a 1,000,000 to 1 lottery six times in a row. The professionals took their findings to the licensing authority. Denyse, you’ll get a kick out of this. Most internet poker sites are licensed by a sovereign Indian nation near Montréal, Canada, the Mohawk Kahnawake tribe. The tribe hired a professional gaming expert to investigate, and sure enough there was cheating. One of Ultimatebet’s employees had gotten an administrative password, which gave him the ability to play poker at the site while looking at the other players hands! In all, the employee stole more than $20,000,000. Read the whole story here.
How does this relate to ID? The investigation was pure scientific design detection. Here is how the investigator employeed the scientific method to reach his conclusion.
Step 1: Decide on a question one would like to explore. In this case, the investigator suspected cheating, but it was just a gut feeling. The poker players among us know that in any given hand the worst player in the world can beat the best player in the world by pure dumb luck. I have personally seen a player win a hand in which the probability that he was going to win was only 1%. But blind luck like this succeeds only in the short run. In the long run, the better player will always come out ahead. Here, the investigator saw data that seemingly contradicted that maxim. A player (let’s call him Joe) who was playing very poorly, constantly taking foolish risks, was nevertheless winning not only in the short run, but also in the long run.
Step 2: Form a hypothesis. This was easy enough. The investigator hypothesized that the Joe was cheating.
Step 3: Test the hypothesis. The investigator gathered data about Joe’s history and performed a statistical analysis to test his hypothesis. He determined that Joe was winning at a rate that was 15 standard deviations above the mean. In the story the investigator is quoted saying, “Now, this sort of stuff just doesn’t happen in the real world.” In other words, the investigator cannot rule out random chance in an absolute sense, but as a practical matter, he is certain that Joe is cheating.
Step 4: Form a conclusion. The data indicate that Joe is cheating.
Acting on his scientific findings, the investigator reported Joe to the licensing authority, which performed its own investigation and found that Joe had in fact been cheating by using the administrative password to look at the other players’ hands while he was playing.
How is design detection in this instance different from the design detection employed by ID proponents? As far as I can tell, not at all.
128 Responses to Design Detection Reported on CBS’s 60 Minutes
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Khan,
The glossary of Douglas Futuyama’s Evolutionary biology text book, third edition says
Macro evolution – a vague term for the evolution of great phenotypic changes, usually great enough to allocate the changed lineage to distinct genus or higher taxon.
So maybe we have to agree on being more precise when using this term. I have a long discussion of the issues involved here which I will post for you so that we can discuss things on an even basis and not talk past each other because we are using different definitions.
Essentially when I am using the term macro evolution, I am using it in a sense of the formation of new complicated capabilities and in a technical sense the formation of a new genus or even a family may not qualify as this. So I will try to find my classification scheme for evolutionary biology in order to emphasize where the dividing lines lie.
ribczynski:
I really don’t know how to qualify the ever increasing superficiality of your posts, which is matched only by your obstinacy in not addressing the answers we give you.
I gave you detailed confutations of all your points in #103 in my post #104. What have you done? Nothing. You just go on accumulating superficial nonsense about issues that you seem not to understand.
I will comment on your posts #115 and 117 just in case some reader may think that you have some points, although it should be obvious to anybody that you have none. But I have not much hope that you will answer. I just go briefly about the errors in your post:
#115
“An obvious first question: Why do IDers believe that microevolutionary changes cannot accumulate over time to yield macroevolution?”
Because macroevolution is not the sum of microevolutonary changes.
“Some have argued that mutations are always deleterious. ”
That’s nonsense. Most mutations are probably neutral, as most darwinists well know. Many are indeed deleterious. Rare ones can be useful in very specific contexts.
“Well, the first thing to point out is that any genetic sequence can be converted to any other by an appropriate series of mutations.”
That’s trivial. There was no necessity to point it out.
“If sequence B is an improved version of sequence A, it is mathematically impossible for all of the mutations along the way from A to B to be deleterious. At least some must be beneficial.”
It depends on what you mean with “improved”. If we are discussing an existing protein with an existing active site with an existing function, and we are just discussing the possibility that the existing function “improves”, in the sense that the affinity of the active site for the substrate increases, that’s a very simple scenario where single mutations can be useful, deleterious or neutral according to the effect they have on the active site’s affinity. That’s a scenario where theoretically some darwinian mechanism could take place, because the target (B) is only one or a few aminoacid distant from the existing protein (A), and function could increase one step at a time. I say in theory, because in practice we don’t know well defined examples of such a mechanism. And in any case that would still be microevolution.
But if your A and B are two different proteins with different functions, and say different folding, then what you say has no meaning. Single mutation steps can only be neutral or deleterious to the existing function, or wxceptionally improve it (which is not our target). But they cannot give the new function until a very different sequence has been achieved, with a different folding and a different active site. Until then, no new function arises and NS can in no way intervene to “guide” mutations toward the new sequence.
That means that if the distance between the old sequence and the new sequence is big enough (let’s say 50 aminoacids), the new sequence will never be reached by RV because there is simply too low a probability that that happens (I am pruposely staying at a level which is still very distant from the UPB: let’s state it clearly, the UPB is excessive as a limit, I am no more available to make gifts to darwinists).
“What about a less sweeping claim: that in an actual series of mutations connecting one sequence to a fitter sequence, there must be at least one deleterious mutation that stops natural selection in its tracks?”
That’s not the problem. he problem is not that “there must be at least one deleterious mutation that stops natural selection”. There is no need for deleterious mutations. As I said in the previous point, it’s the sheer improbability to reach a new function by RV (a “new” function, which is “different” from the existing function) which makes macroevolution impossible. It’s not the occurrence of deleterious mutations. Indeed, if the new function has to arise, it’s obvious that the old function must be gradually lost. That’s why darwinist imagine that the “evolution” takes usually place on duplicated genes. That would allow the conservation of the old function. But that cuts completely out NS, even negative NS, until the new function arises.
Your remaining points in #115 are still based on that false concept of necessary negative mutations, so I will not deal with them.
#117:
“The claim that mutations cannot produce information can be easily disproven. Suppose that a mutation causes a sequence to lose information. We then apply the inverse mutation to restore the original sequence. We’ve regained all the information we lost via the first mutation. Therefore the second mutation has increased the information content of the sequence.”
That’s simply silly. The second mutation has simply “restored” the information which was already present. Only one “bit” (in the sense of nucleotide) of that information had been lost: the rest was still there. The second mutation is just restoring the lost bit.
“More generally, we can create a series of mutations to link any sequence A to a sequence B containing more information. Therefore, at least some of the mutations must cause an increase in information.”
The first sentence is trivial. We certainly can. The second sentence is false. If what we have to achieve is a new function, no mutation will be useful until the new function arises. But perhaps you mean that a single correct mutation, in other words one of the “50″ which are needed for the new function, is causing an increase in information. That’s true only for a designer who knows what the target sequence is. But it’s not true for NS, which doesn’t.
“Concerning the argument that while mutations can increase information, they cannot produce CSI: Suppose we’re considering a large but unlikely mutation that would qualify as producing CSI, if it happened. Now construct a series of simple mutations that, if performed in sequence, would have an effect equivalent to that of the larger mutation. None of the simple mutations contains CSI, so IDers cannot rule it out on that basis. But if none of them are ruled out, then the sequence stands, and the sequence as a whole produces CSI. So the IDers’ claim is disproven.”
You have simply not yet understood what CSI is. CSI is a property of a whole piece of information with complexity and function. No single mutation can “contain” CSI. CSI is a property of the functional protein. A sequence of random events cannot produce CSI. A sequence of guided events can.
“But if none of them are ruled out, then the sequence stands, and the sequence as a whole produces CSI.”
No, you again don’t understand. Your sequence is just too unlikely, because it’s one of a huge number of possible sequences. That’s why it does not happen. There is no need to “rule out” anything. It’s the whole unlikely sequence which does not happen.
“What if the IDer claims that in all such cases, the series of mutations cannot happen because at least one of them reduces fitness and acts as a barrier to natural selection?”
You are always making the same mistake.
“Therefore the burden of proof is on the ID supporter to show that it is true for all of the fitness landscapes encountered by terrestrial lifeforms.”
False, as all your other statements. They descend all from the same error of thought. The burden of proof is of the darwinian supporter, who has to show how the probabilistic process that he himself is suggesting has a credible probability.
“As for the final argument that natural selection requires a source of CSI, and that the CSI must come from outside since random mutations cannot produce it: we’ve already seen that mutations can produce CSI, so the argument fails.”
We have seen nothing like that.
“In any case, selection is not random, so the environment itself is a source of CSI for natural selection.”
You really can’t understand what CSI is, can you? You are not just pretending?
Let’s take one protein: myoglobin. The CSI here is linked to the right sequence of 154 aminoacids which can give the function. Are you suggesting that the environment “knows” what that sequence is? That’s the only way the environment could be a “source of CSI” for our protein before natural selection can recognize the emerging function and fix it. Are you saying that? Or what?
Continuing from comment #117.
One final comment about the alleged theoretical limits of natural selection, and then I’ll start addressing comments and objections from ID supporters.
1c. The argument that natural selection cannot produce IC structures.
This has been adequately refuted by a trio of arguments: (a) the cooption argument; (b) the scaffolding argument; and (c) the “optional part becomes indispensable” argument. These are pretty well known, so I won’t rehash them unless someone challenges them or wants to hear them explained.
1d. The “coordinated changes” argument.
IDers (and creationists) sometimes claim that certain features could not have evolved via unguided evolution because they require simultaneous, coordinated changes to multiple systems in the organism, and that this sort of coordination cannot be achieved by a blind evolutionary process. This claim is reminiscent of, but not identical to, the IC argument.
One example they cite is the giraffe’s system for regulating blood pressure in the head. Because of its long neck, a giraffe’s body requires special mechanisms to boost blood pressure to the brain when the animal is upright and to limit it when the animal leans down. The claim is that all three things — the long neck and the two blood pressure regulatory systems — had to appear at the same time, which is beyond the capability of natural selection.
The argument fails because evolutionary biologists do not claim that these systems appeared full-blown, all at once. If they did, then IDers would be right to object.
Instead, biologists think that these systems evolved gradually, via many mutations. So for example, a mutation would occur that made the neck slightly longer. This would create a need for slightly better blood pressure regulation, so that when such a mutation occurred, it would be preserved. Then, with better blood pressure regulation in place, it would become possible for the neck to become slightly longer still, and so on.
When the changes are made incrementally rather than all at once, the need for intelligent coordination is eliminated.
Ribczynski (#123):
You write:
“1c. The argument that natural selection cannot produce IC structures.
“This has been adequately refuted by a trio of arguments: (a) the cooption argument; (b) the scaffolding argument; and (c) the “optional part becomes indispensable” argument. These are pretty well known, so I won’t rehash them unless someone challenges them or wants to hear them explained.”
I don’t deny that the above-named processes, taken as complete abstractions, can be seen as methods of generating irreducible complexity. But the devil, as always, is in the details. Who has shown any one of these to be plausible in any particular case of a major new organ or system, with reference to the nitty-gritty genetic and developmental facts?
For example, after years of arguing, the best Ken Miller can do with the bacterial flagellum is to point out the type three secretory system (TTSS) as a possible intermediate, because it contains many of the parts of the flagellum. Well, sure, it’s possible. But if you’re swimming across a lake a hundred miles wide, and will drown if you don’t rest every mile, you need 99 islands along the way. Even on Miller’s account, the path to the bacterial flagellum is missing 98 islands. All the intermediate steps between no-TTSS and TTSS, and all the intermediate steps between TTSS and flagellum, are entirely missing in Miller’s account. What would those steps have been, and would they have given the bacterium selective advantage? How can we reconstruct them, or the environments in which they lived? And that’s not even touching on the genetic questions, such as: exactly what parts of the genome would have had to change to produce the TTSS? And what parts would have to change after the TTSS? Would a large number of co-ordinated changes have been needed for each step? Are such co-ordinated changes likely? The truth is that neither Miller nor anyone else has answers to these questions. The TTSS is an island in the middle of the stream, and there is no known swimming stroke that can get us to it.
Regarding the giraffe’s neck, your argument, to the extent that it is plausible, depends upon the unlikely happenstance of neck-length increases and pumping-mechanism improvements being (a) frequent; and (b) happening in the right order to be able to work together. But if after, say, the third neck length increase, toenail length increases instead of the pumping mechanism, the giraffe is out of luck. And given the millions of possible mutations in the giraffe genome, how likely is it that you are going to get a third lucky blood pressure increase, as opposed to a toe-nail length increase, or an albino skin coloration, or something else? And don’t forget, the time allotted for this lucky ABABAB sequence to turn an okapi into a giraffe is limited by the fossil record. So you need numbers. How often do mutations occur, period? And how often is it likely that mutations of the particular parts of the genome required for neck length and pumping mechanism will occur often enough, and in the right order, for your scenario to work out? Has any evolutionist pinpointed the parts of the giraffe genome which would have to be altered, and the probability of their being so altered over the last few million years, in the way proposed? I know of no such detailed account. So once again, ID asks for quantitative science and the Darwinists offer qualitative storytelling.
In any case, even if we suppose that such an upward-crawling co-ordination of two already existing things, blood pressure and neck length, could occur, this is nothing at all like the much more daunting task of creating a radically new system or organ that never existed before, and this is what Darwinism must explain. It needs to explain flagella, eyes, and cardio-vascular systems. Right now it can explain antibiotic resistance and finch beaks. I.e., right now Darwinian science cannot get beyond microevolution. The rest is speculative extension. If such speculative extension is going to be forced upon ninth-grade students, at least science educators should have the decency to label it as such, and stop presenting it as a scientific truth as well-grounded as the work of Newton and Pasteur.
T.
ribczynski:
Let’s go to the end then.
#123:
IC. You say it has been “adequately refuted” by:
“(a) the cooption argument; (b) the scaffolding argument; and (c) the “optional part becomes indispensable” argument. ”
Indeed, b and c are only theoretical and stupid arguments which try to show that ir is logically possible to evolve an IC structure by steps. Well, we know that. IC is not a purely logical argument. It is an empirical argument. It is logically possible, but empirically impossible, to evolve an IC structure by steps. We know that. Again you, like most darwinists, seem not to understand the difference between logical and empirical, which Behe anyway has well specified in his book.
The cooption argument is silly just the same, but at least Miller et al. have spent some time trying to build up a model for it, and so it deserves some more specific confutation. Indeed, the first time I read about it, I could not believe that any reasonable person could take it seriously. But it seems that many people do, and so…
Cooption: so if you cannot explain the design of a complex system, where the function arises from the cooperation of different parts, you say: but those parts could be there, just like for a miracle: it is enough that each one has evolved for a different function and there it is, how can they not realize that there is a completely new future for them if they just stick together?
Well, let’s take the only model of supposed cooption which has been suggested up to now (I will not consider Miller’s mouse trap – tie holder): the flagellum would not be irreducibly complex because part of it is similar to TTSS. That’s simply ridiculous. The flagellum is a highly complex and brilliant machine, and the only reason why there is some similarity (but not identity) between some of its proteins and those of the TTSS is that those proteins have a similar function on both machines: they are a special secretory apparatus. In other words, the similarities between TTSS and the flagellum are based on partial functional similarities between the two machines, in other words they are based on design considerations. But the flagellum remains irreducibly complex, even if it uses a sub-machine which can be found in similar, but not identical, way in another machine, with different function. In other words, designers can (and indeed do) use similar solutions for different sub-parts of different machines, when it is appropriate. Let’s make an example in computer programming: you can write a word-processing software and a spreadsheet. They are very different softwares, do different things, have different complexity, different parts, and definitely you cannot derive one from the other. But there are certainly procedures and parts which can be common, especially if they have been written by the same programmer. For instance, you could find the same ordering algoritm in both.
Miller and co. have in no way presented a model of how you could evolve the flagellum (a much more complex machine) from the TTSS, least of all of how both could have evolved from a common precursor. The function of the flagellum is motion. That function cannot be obtained by the TTSS. Where is the model of how the TTSS became the flagellum? Of how all the parts which contribute to the IC of the flagellum came into being? Of how proteins changed? Of which proteins changed? Of how the delicate regulation and assemblage of the flagellum came into being, when no new function (motion) could still be obtained? Miller’s “argument” is like all other darwinist arguments: imagination and magic, with a pinch of myth.
And I am really tired of all this fuss about the flagellum, as though it were the only complex machine in the cell. Are we kidding? The cell is stuffed with complex machines which are IC. The body plans, the morphological features of multicellular organism, are almost always evidently IC. Function, when it is not elementary, is IC. Almost all complex functions are attained by the cooperation of parts, of simpler functions, of interactions and regulations and so on. Sub-functions never explain the higher function, except in Miller’s imagination. Were all those examples of IC machines, billions of IC machines, all assembled by cooption? Are all functions deconstructable as random assemblage of elementary functions?
What an interesting perspective!
Darwinist go on denying the obvious, and the obvious is in this case the truth: there are infinite levels of complexity in biological beings, each of them superimposed to the previous one, and all of them are structured in a wonderful global interaction which we can hardly guess at present. The lowest level is the single protein, the single gene. Darwinists cannot even begin to explain that. For the rest, there is simply no game.
gpuccio
The same argument is used to support evolution, that layers of complexity would be expected as structures are incorporated into new function.
However, what do you mean “infinite levels of complexity”? There cannot be infinite levels, it must have an upper bound, or do you have a particular specific reason for using infinite? Are you hinting that the complexity extends past the purely physical realm?
PhilipBaxter:
“The same argument is used to support evolution”
Why am I not surprised? I have seen darwinists use all possible arguments to support their views. The fact remains that the more complexity we observe, and the more that compexity is structured in efficient and interacting levels, the less it can be explained by unguided models.
Regarding the “infinite”, I think I was just saying that for emphasis. But as you say: “Are you hinting that the complexity extends past the purely physical realm?”, just because you are asking, I think I could well answer yes.
But I was probably referring in my post “only” to the fact that, up to now, every time we deepen our understanding of biological realities, new and deeper levels of mystery seem to emerge. We have no idea if and when that trend will change, and I think we are very, very distant from the “end”, if an end exists.
Or are you expecting the “end of biology”, just as physicists were expecting the “end of physics” at the end of the nineteenth century?
Barry has created a new thread for our macroevolution discussion, so let’s continue over there.