What is an ID proponent's basis of comparison? (edited)

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OK, that whole article is ridiculous but that table simply doesn't support your claim.

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In what way is a mutation which changes gyrase in such a way as to reduce its affinity to Fluoroquinolones a loss of information for the gyrase?

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Because it's a loss of specificity.

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The author is simply demented. He wants us to think that Gyrase has evolved to bind Fluoroquinolones? Does he even understand what these antibiotics are? These are synthetic chemicals which have been developed specifically to inhibit bacterial growth or kill bacteria. It is like thinking that my car has a cigar lighter plug point because it was designed so I could plug my iPod car charger into it. He is getting cause and effect mixed up. So since gyrases clearly didn't evolve to function as Fluoroquinolone binding molecules how on Earth can it be considered a loss of function when their affinity is reduced?

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Wrong! It's the antibiotics that have been designed to bind to the gyrase. When the gyrase looses it's afinity, it looses information.

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There are numerous valid cases where resistance is the result of a genuine information loss such as null mutations removing an entire gene. But the whole argument is undermined by this idiotic attempt to describe every form of resistance as a loss of information/function when you are defining function as being 'binds to antibiotic'.

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Than show me a case where there is an increase in information.

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I think this is all bound up with the approach that whatever the starting state was of an organism, protein or gene sequence when it was first studied is somehow enshrined for IDist/creationists as being the ideal state so any change from that state must necessitate a loss of function/information.

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Again wrong. The organism can fluctuate. But only in the already existing informational range. The genome itslef is constantly deteriorating.

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Will you at least concede that to consider binding affinity for an antibiotic to be an evolved function of the bacteria is nonsensical?

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Of course, since I never said that it was. Where you came up with it I have no idea.

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So the evolutionary process set up by the researcher would evolve ordinary oscillators just like those the researcher probably could have thought of himself? No novelty would come out of this process?

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No novelty. Computers could develop something that scientists have by themselves overlooked. But even that novelty was together with the whole sequence space programmed into the computer.

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None of this addresses my point. The Design Inference is purely negative. Actual designe detection uses positive evidence, too, to construct an inference to the best explanation. Therefore the Design Inference fails to fully capture the way in which we identify design.

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Explain, how exactly is it purely negative.

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1) He ruled out evolutionary explanations on the grounds that Behe asserted that IC systems couldn't evolve. Unfortunately Behe (correctly) admitted in Darwin's Black Box that IC systems could evolve by what he called "indirect" routes. Behe dismisses this option only on the grounds that he considers it too improbable - however he has not provided any solid grounds for this, and even if he did the probability could still be greater than Dembski's probability bound.

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Actually no. He ruled out evolution because of the NFL theorem.

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2) Dembski failed to provide an adequate specification. This is a very important point because the probability calculation that must be done is the probability that the specification is met. Without a valid specification that can be used in the calculation the necessary calculation cannot be done.

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All the specifications are there. The number of genes, and the numbers of proteins used to make a flagellum.

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3) Dembski calculated the wrong probability (and apparently botched the calculation, too - by 65 orders of magnitude). Of course he couldn't calculate the right probability because he wrongly ruled out evolution a priori and failed to provide an adequate specification.
Instead he produces a probability based on randomly assembling an individual flagellum from protein sub-units - without taking into accunt the actual mechanisms by which a flagellum grows.

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Well like I said before. He ruled out the evolution because of the NFL theorem. So the only thing you are left with is blind chance.

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You are incorrect here. A specification must be - in Dembski's term "separable" from the event. That is it must be one that can be DESCRIBED without appealing to specific featues of the event. Perhaps it is better understood as a specification that might reasonably be proposed without detailed knowledge of the event.

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However it is absolutely legitimate - according to Dembski - to use knowledge of the event in proposing the specification (e.g. the specification Dembski uses in the Caputo case is based on the knowledge that the results favoured the Democrats, and the degree to which the results favoured them).

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But you always use the knowledge of the event together with your background knowledge. And thais background knowledge in this case is that the 40 out of 41 cases teh Democrats were first on the ballot. And that this coresponds to an independently givven pattern of Democrats having more chance at winning elections, and that Caputo himself was a democrat.

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it means no such thing. It means the search is better than a random search for these types of problems.

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No one is arguing that the search is in any way optimal.

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Everyone is. For an algorithm to perform better than blind search you have to optimize it. The NFL says so.

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I gave the multiply program the same information any human would have. The program is producing the same information that a person multiplying two numbers together would produce. The program could even be modified to model a person carrying out multiplication by hand using pencil and paper. If a person multiplying two numbers together is producing new information, then so is a computer.

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But your program is using the already programmed in instructions from the computer. Like , etc. Did those references appear from thin air, or were they designed prior to your use of them. And could you program anything without them? Obviously not.

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Concerning GA's, of course the algorithm is "programmed in." GA's model evolution, so of course an algorithm that models evolution is "programmed in." The random mutations of evolution are modeled by random changes to design parameters. Natural selection is modeled by an assessing algorithm. Reproduction is modeled by randomly "mating" design alternatives and randomly combining their design parameters.

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Ah, but here comes the problem. Evolution has no knowledge of the search target. Therefore it's as useful as blind chance.

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Are you saying that before a design team even gathers that the solutions are already there, that they just have to find them? This is a much more sweeping argument than you were making before. In effect you're saying that neither computers nor people produce new information. Apparently for you the solutions are already out there just floating around somewhere waiting to be discovered.

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No, people do make new information by calculations. The computers just process them faster than we do.

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I think you're confusing the potential to produce a design with the design itself when you say the solutions already exist, and that the designers task is just a matter of finding them. The multiply program I provided as an example has the potential to solve many multiplication problems, but that doesn't mean the answers already exist. When you run the program and enter two numbers, you get a result you didn't know before. New information has been created for you.

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No, it hasen't it has only been processed by the algorithm you produced. All the relevant information to produce it was already in there. The whole search space was in there from the start. You just optimized an algorithm to find it faster than blind chance.

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"... no operation performed by a computer can create new information."

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Look, no operation by a computer can create new information. It's a well known fact.

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The Evolutionary Informatics Lab - EvoInfo.org

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The initial parameters are part of the model. Just as evolving bacteria in a laboratory experiment have initial conditions, so must any computer model of evolution. The evolutionary model must have access to the same information (or at least a reasonable approximation , or analogous information in the case of GA's) as the real world. The principles of modeling the real world are the same regardless of whether one is modelling the weather or evolution.

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But in the real world, evolution has no information about the search problem.

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I'd love to see this calculation. Could you please provide it?

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It's in the book. But I did manage to find an online version.

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It'se from pages 289 - 302.

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Dembski - No Free Lunch

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I think that if you look up Dembski at Wikipedia you'll find that what I said was true. He really is a professor at Southwestern Baptist Theological Seminary in Fort Worth, Texas, and he really does teach courses there in its Department of Philosophy of Religion. And gee, Wikipedia says the exact same thing!

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The point remains that you didn't mention his other education degrees. Like these:

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He returned to school at the University of Illinois at Chicago (UIC), where he studied psychology (in which he received a B.A. in 1981) and statistics (receiving an M.S. in 1983). He was awarded an S.M. in mathematics in 1985, and a Ph.D., also in mathematics, in 1988, both from the University of Chicago, after which he held a postdoctoral fellowship in mathematics from the National Science Foundation from 1988 until 1991, and another in the history and philosophy of science at Northwestern University from 19921993. He was awarded an M.A. in philosophy in 1993, and a Ph.D. in the same subject in 1996, both from UIC, and an M.Div from Princeton Theological Seminary, also in 1996.

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If you think there's relevant research from the Biologic Institute then please just enter it into the discussion.

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I'm just saying there is ID based reasearch. You made it look like there isn't.

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But if you're going to invent your own lingo you have to tell people what it means. In this case there's no way to know whether your "turned on" corresponds to cleaved or uncleaved.

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The articels ays that they interfer witht he working of LexA and the evolution of resistance stops.

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Edited by Admin, : Shorten long link.

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Edited by Admin, : Change angle brackets to literals, fix errors in quoting.

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You were saying the NFL theorem says that evolution can be no better than random search. Just repeating that claim is no help to me. In order for me to assess your claim you need to provide a general idea of how random search differs from evolution.

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It doesn't. They give you the same results on average.

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Sure it can. In Shannon information the problem of communication can be reduced to reproducing at one point a message from a set of messages at another point. Everything that happens in the universe can be interpreted this way.

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Uh, no. I cited the articelw here it says that it can't. Did you miss it? If his model does not account for semantics than it can't be used to measure biological function.

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This is untrue, but the real question is why you believe that statistical approaches are excluded from the biological realm.

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Oh, but it's very true.

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In Shannon's revolutionary and groundbreaking paper, the work for which had been substantially completed at Bell Labs by the end of 1944, Shannon for the first time introduced the qualitative and quantitative model of communication as a statistical process underlying information theory, opening with the assertion that

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...

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Using a statistical description for data, information theory quantifies the number of bits needed to describe the data, which is the information entropy of the source.

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See, it's only about the statistical aproach.Information theory - WikipediaAnd I never said that statistical aproach is excluded from biological realm. I'm saying that it's not enough to describe an measure biological information. You need more than that.

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I understand that you accept the claims of people like Dembski, Abel and Trevors, but you need to go beyond just repeating their claims. I provided an example of how the amount of information in a population is increased by random mutation. If you think I was incorrect then you have to go beyond just stating I'm wrong. You have to show how I'm wrong. Here's the example again:

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Oh, you mean that D appears. Well, in that case, such a thing has never been observed. Furthermore having more genes does not equal more information.Consider this example."MY HOUSE IS BIG"This statement is made of 4 words. This represents information.Now if I were to double this, I would have:"MY HOUSE IS BIG"
"MY HOUSE IS BIG"By your definition I would have more information. But I do not. I would only have more statistical part of information. But no new meaning. And sice information consists of: statistics, syntax, semantics, pragmatics, and apobetics, you need to increase all 5 to have new information. Not just the statistical part.To get more information you would have to type something like this:"MY HOUSE IS BIG"
"IT HAS A RED ROOF"Now you know something else. And thus you have more information.Gene duplication does not give you that. It has never been observed to create new biological functions. YOu might have more genes, but they do not perform new functions.

Um, that was rather my point. The antibiotics are designed to bind to gyrase. Are you claiming that after the antibiotics were designed the information content of gyrase just magically went up without any change in its genetic sequence because it suddenly had a high affinity binding molecule created for it?If you are talking about a loss of specificity in the gyrase are you claiming that the binding affinity is a result of complex specified information in the gyrase? If so then how are you not claiming that the gyrase had evolved or been designed to bind the antibiotic, rather than the other way round. And unless this is the case how can it possibly be a loss of information for the gyrase when it mutates in such a way as to lose this affinity? Then how can it be considered a loss of information for the gyrase? The only 'functional' element lost to the gyrase is that of binding a molecule which makes it damaging or possibly lethal to the organism, and that was a function that didn't exist until the antibiotic was developed.Are you saying that gyrase was intelligently designed to be susceptible to the antibiotics in the future? That seems a lot of effort for the intelligent designer to go to for only a few decades of antibiotic protection.Simply saying 'it's a loss of specificity' is not a sufficient answer. How is this substantially different? Are you saying 'this is the range of informational variation we know about, anything beyond this is a loss of information'? If not how can we measure this existing range? This can hardly be anything other than pure speculation since we don't know what all the existing genetic variations have been for a whole species ever. So how can you possibly know what the existing 'informational range' is for anything? Than why haven't bacteria simply vanished over the billions of generations of their existence?TTFN,WK

traderdrew responds to me:

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I see a lot of huffing and puffing from you about Behe but no real evidence so far.

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Huh? I've given you specific examples. Every single example Behe has ever put forward as an example of "irreducible complexity" has been shown to be not only reducible but we have found evolutionary pathways for them. From the blood clot cascade the flagellum. Every single one has been shown to be evolved. In his books, he boasts that nobody has ever studied these things when all it takes is a tiny amount of searching in PubMed to find that he's talking out of his ass. For the blood clot cascade alone, there were literally hundreds of papers on the biochemical evolution of it that he claimed didn't exist when he wrote Darwin's Black Box. Why don't you know this. If you're going to bring Behe up, why don't you know what he's said?I am not here to do your homework for you. If you're going to put forward Behe as someone to pay attention to, then you're going to have to know what it is that he's claiming. I can't make you read his argument. You have to do that for yourself.

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The reason why I was skeptical that your statement of whoever it was who threw down the publications or journals that refute Behe's irreducible complex arguments, is that is a friggin courtroom and I don't know who you are.

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Did you bother to look it up? Are you incapable of doing your own homework? This is hardly some rare, isolated case that only legal buffs would have ever heard of. It made the national news. And I don't want you taking my word for it. I want you to learn about it on your own.

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I really have some studying up to do. So I would rather see some evidence rather than participate in a dragged on useless debate.

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Then go do your homework. We'll still be here when you come back.

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Rrhain

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Thank you for your submission to Science. Your paper was reviewed by a jury of seventh graders so that they could look for balance and to allow them to make up their own minds. We are sorry to say that they found your paper "bogus," specifically describing the section on the laboratory work "boring." We regret that we will be unable to publish your work at this time.

Smooth Operator responds to me:

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No, some live and some die because come confer resistance for an example.

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But if your claim of "no new information" is true, then they all have the same genetic profile. Therefore, they should either all die or all live. With no new "information" to confer resistance, then the entire lawn necessarily behaves as one as they are all descended from a single ancestor.So since the the lawn is not behaving as a single unit, since only some live and some die, the premise that no new "information" has been introduced is proven false.

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But this resistance is aquired by degradation of existing information. Not by an increase.

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Incorrect. Because you can repeat the process by taking the new, resistant bacteria, isolating a single bacterium, and having it reproduce to form a lawn and re-infecting the lawn with T4 phage. By your logic, with no new "information" to confer infectivity, the entire lawn should survive. Instead, we find plaques starting to form.Now, this can't possibly be a case of the bacterium reverting to wild-type. If there were a bacterium that had reverted, it would be infected by T4 and die, but it is surrounded by the immune bacteria who would reproduce and fill in the gap.So it clearly isn't the bacteria that evolved but rather the phage.But by your logic, since all this is "loss of information," how on earth is anything still alive?

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All resistances have been aquired by loss of information.

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Kevin Anderson? Creation Research Society Quarterly? Those are your references? At any rate, your reference doesn't actually support the claim. The antibiotics disrupt cellular activity via a certain pathway. The bacteria acquire mutations that allow them to reproduce without using that pathway. That isn't "loss of information."And for further evidence, the process by which bacteria become resistant to ciproflaxacin (one of the antibiotics in your source) is by actually creating new genes with an altered amino acid sequence such that the ciproflaxacin doesn't bond well to the topoisomerase anymore.Where is this "loss of information" you are crowing about?

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Simple. Because the mutatins deform their receptors to different antibiotics in differnt way.

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But you can keep running the experiment over and over, having the two continually change their genes to maintain the standoff. If this were the result of "loss of information" as you keep claiming, then eventually there wouldn't be anything left in either genome.So since the bacteria and phage are still around and have just as big a genome as they always have, where did the "loss of information" go?

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Some simple questions:

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Which has more information: A or AB?
Which has more information: A or B?
Which has more information: A or AA?

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Depends by which definition of information.

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Use any one you want. For those three comparisons, which one has more "information"?

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Rrhain

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Thank you for your submission to Science. Your paper was reviewed by a jury of seventh graders so that they could look for balance and to allow them to make up their own minds. We are sorry to say that they found your paper "bogus," specifically describing the section on the laboratory work "boring." We regret that we will be unable to publish your work at this time.

Or this:"MY HOUSE IS BIG"
"MY MOUSE IS BIG"A doubling followed by a small mutation can easily result in new information. This is how it can and does happen in genomes. It has been observed and documented. Repeatedly negating this fact doesn't make it go away. It makes one look ignorant.

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"Ignorance more frequently begets confidence than does knowledge: it is those who know little, not those who know much, who so positively assert that this or that problem will never be solved by science." - Charles Darwin.

This loss of information we keep hearing about from IDers bears a striking resemblance to the religious belief in "devolution" since "The Fall."It has no basis in science.And they expect us to believe them when they claim that ID is not religion lite.

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Religious belief does not constitute scientific evidence, nor does it convey scientific knowledge.

I think you meant to say that the instructions come from people, right?But a person performing multiplication using pencil and paper is just following the instructions he learned in fifth grade. There's no difference between a person following an algorithm and a computer following an algorithm when it comes to creating new information.The implication of your position is that no new information has been created from performing multiplication since someone first figured out how to do it. That inventor of multiplication created new information, and everyone since has just been following instructions. And even the inventor of multiplication was just taking advantage of information he was taught by others before him and merely economized by showing how people could perform multiplication of many digits just by memorizing the times table for single digits, so he didn't create new information, either.Obviously that's an unworkable definition of new information.Shannon defined the problem of communication as one of replicating at one point a message from a set of messages originating from another point. When a message from the message set is sent from point A to point B then information has been communicated.So it works like this. A person sending you messages from his message set (his personal store of knowledge that he keeps in his brain) is adding to your own personal message set every time he tells you something you didn't already know. For you, everything you didn't already know is new information. You add it to your personal message set, and now this becomes a message that you can send to someone else.So let's say you're chatting online with someone who tells you that 17x26 is 442. This is new information for you. You could have easily have figured it out yourself, but you didn't, so your online friend has now added information to your message set. Your message set has increased in size. For the length of time that you remember that 17x26 is 442, this is a message that you can pass on to others, thereby increasing their personal message sets.But it makes no difference where the message that 17x26 is 442 came from. If you had instead used your calculator you would have still added new information to your message set. In other words, it doesn't matter if the new information came from a person or an object. For all you care the clouds could have formed into the equation "17x26=442" in the sky and it would still represent new information for you.In other words, the creation of new information doesn't mean that the same information hasn't been created before. It would make no sense to say that of two independent inventors who create the same invention with no knowledge of the other's work, that the inventor who completed the invention first created new information and the other did not.So new information is everything you learn that you didn't already know. The source of the information is irrelevant.All that remains is to add to this the fact that information is sent and received by everything everwhere in existence. In other words, the sharing and creation of information is not a special trait of human beings. It is possessed by all matter everywhere. This is half correct. Mutation has no knowledge of any "search target," but selection is the very opposite of random. The best adapted survive and contribute their genes to the next generation, including any mutations they might have. That's why white rabbits evolve in the arctic and not the rain forest. If evolution were truly random then white rabbits could evolve anywhere.So we're back to the same question. You cited the NFL theorem which holds that one algorithm cannot perform better than another algorithm unless it has more information. So you're talking about two different algorithms, one that you call "evolution," and the other that you call "random". How does the "evolution" algorithm differ from the "random" algorithm? So the whole search space is there from the start, and if designers search the search space and find a solution, then that is new information. And if a computer searches the search space and finds a solution, then that's not new information.Your position keeps knocking into contradictions. But you can't just cite Mr. Robertson. You have to understand why Mr. Robertson said this and explain here why I'm wrong. Otherwise I can go off and search the web for quotes of people saying that computers *can* create new information. The purpose of discussion isn't to make arguments from authority, otherwise we'll end up arguing who cited the best authority. The goal is to actually understand what you're debating to the point where you can make the arguments yourself.But since you offered a bare reference with no argument I will do the same. Read this rebuttal from What is thought? by Eric B. Baum, especially the part beginning in the middle of page 429 and that concludes like this: Moving on: You refer me to a Google Books page in Croatian? That doesn't work?If you have an argument to make about CSI based upon Dembski's book No Free Lunch, could you please enter the argument into the discussion in your own words? I didn't mention any of Dembski's degrees. The point is that scientists aren't producing advances based upon CSI, not even Dembski who is working as a professor at a Bible college where he teaches courses in the philosophy of religion. If you think the Biologic Institute is producing evidence of CSI, then I think it would be highly relevant to this discussion if you would tell us about it. You're just stating your original position again.I have no idea why the authors of the article chose to overstate the point. Obviously evolution does not stop. There is no process that can make the copying of genetic material perfect.--Percy

That they give the same results is what you claim the NFL theorem tells us about the two different algorithms, "random" on the one hand and "evolution" on the other. How do these two algorithms differ in their definition? I know how evolution works. How does this "random" algorithm that your contrasting evolution with work? I think you're confusing what a gene does with meaning. Meaning and semantics are a human interpretation. Semantics cannot be quantified, is not part of information theory, and isn't even relevant. This goes back to Shannon's original paper, A Mathematical Theory of Communication: This is as true today as it was then. Yes, I know you believe this, but can you support your position with evidence and arguments? You're most common responses to everyone seem to be variants of either, "No, I'm right," or "No, you're wrong."Population genetics is an extremely statistical science, and this flatly contradicts your position.Almost all medical studies are statistical in nature, and this also flatly contradicts your position.Need I go on providing examples?But my original reason for responding was to point out you were wrong to say that Shannon information "deals only with statistical aspect of information" in your Message 182. Are you talking about the quantification of information? Not statistical. Are you talking about the introduction of noise into communication? Very statistical. In other words, Shannon information has both statistical and non-statistical aspects. Like many things. I thought the Widipedia article made this pretty clear.So statistical approaches are appropriate in the biological realm. Indeed, where wouldn't statistical approaches be appropriate? Statistics is a tool (among many) that one can probably apply to virtually any problem. Mutations not currently present in a population have never been observed? Could you please return to reality? My example was the addition of a single allele to a pre-existing gene, but gene duplication adds even more information. Let's go back to Shannon again, saying what I've already said, but I want to show you that I've been accurately describing information theory: So if we increase the number of alleles in a gene from 3 to 4, the amount of information in the message set rises from 1.585 bits to 2 bit, an increase of .415 bits.You evidently thought I was talking about gene duplication when I was actually talking about a single mutation causing the addition of an allele, but let's talk about gene duplication using your example.First you have this gene: Then there's gene duplication and you have this: We can argue about whether this represents more information or not, but we don't need to. Now the duplicated gene experiences a mutation and we get this: And then another mutation: And another: And so on, every change creating new information. And assuming there was reproduction involved, this new gene now has the alleles "My house is big," "My mouse is big," "My mouse is bit" and "My mouse is lit." That's quite a bit of new information in the population.--PercyEdited by Percy, : Improve formatting.

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Um, that was rather my point. The antibiotics are designed to bind to gyrase. Are you claiming that after the antibiotics were designed the information content of gyrase just magically went up without any change in its genetic sequence because it suddenly had a high affinity binding molecule created for it?

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No, there certainly was a change in the genetic sequence, but it degraded the information.

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If you are talking about a loss of specificity in the gyrase are you claiming that the binding affinity is a result of complex specified information in the gyrase? If so then how are you not claiming that the gyrase had evolved or been designed to bind the antibiotic, rather than the other way round. And unless this is the case how can it possibly be a loss of information for the gyrase when it mutates in such a way as to lose this affinity?

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Becasue the gyrase was designed to do it's job. It was doing it just fine. And if it can not perform it anymore as good, it must have lost information in the process.

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Then how can it be considered a loss of information for the gyrase? The only 'functional' element lost to the gyrase is that of binding a molecule which makes it damaging or possibly lethal to the organism, and that was a function that didn't exist until the antibiotic was developed.

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The function and the shape was always there. It lost it die to mutations.

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Are you saying that gyrase was intelligently designed to be susceptible to the antibiotics in the future? That seems a lot of effort for the intelligent designer to go to for only a few decades of antibiotic protection.

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Simply saying 'it's a loss of specificity' is not a sufficient answer.

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But that's what it is. What am I supposed to say. The gyrase was designed the way it was. Just becasue we find some weakness doesn't mean it wasn't designed.

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How is this substantially different? Are you saying 'this is the range of informational variation we know about, anything beyond this is a loss of information'? If not how can we measure this existing range? This can hardly be anything other than pure speculation since we don't know what all the existing genetic variations have been for a whole species ever. So how can you possibly know what the existing 'informational range' is for anything?

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You are confusing expression with degradation of informaton. Since we know that a physical process can not produce new information, than it is obvious that all changes are either due to gene expression, or degradation of information.

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Than why haven't bacteria simply vanished over the billions of generations of their existence?

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Maybe becasue they are not billions of years old?

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But if your claim of "no new information" is true, then they all have the same genetic profile. Therefore, they should either all die or all live. With no new "information" to confer resistance, then the entire lawn necessarily behaves as one as they are all descended from a single ancestor.

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So since the the lawn is not behaving as a single unit, since only some live and some die, the premise that no new "information" has been introduced is proven false.

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No, that's simply not the case. There are billions of ways a genome can mutate. So there are billions of ways some individual can have a specific genetic profile.

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Incorrect. Because you can repeat the process by taking the new, resistant bacteria, isolating a single bacterium, and having it reproduce to form a lawn and re-infecting the lawn with T4 phage. By your logic, with no new "information" to confer infectivity, the entire lawn should survive. Instead, we find plaques starting to form.

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Now, this can't possibly be a case of the bacterium reverting to wild-type. If there were a bacterium that had reverted, it would be infected by T4 and die, but it is surrounded by the immune bacteria who would reproduce and fill in the gap.

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So it clearly isn't the bacteria that evolved but rather the phage.

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But by your logic, since all this is "loss of information," how on earth is anything still alive?

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Didn't I already respond to this?

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Kevin Anderson? Creation Research Society Quarterly? Those are your references? At any rate, your reference doesn't actually support the claim. The antibiotics disrupt cellular activity via a certain pathway. The bacteria acquire mutations that allow them to reproduce without using that pathway. That isn't "loss of information."

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And for further evidence, the process by which bacteria become resistant to ciproflaxacin (one of the antibiotics in your source) is by actually creating new genes with an altered amino acid sequence such that the ciproflaxacin doesn't bond well to the topoisomerase anymore.

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Where is this "loss of information" you are crowing about?

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Yes, it is a loss of information, since the pathway has become non functional.

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But you can keep running the experiment over and over, having the two continually change their genes to maintain the standoff. If this were the result of "loss of information" as you keep claiming, then eventually there wouldn't be anything left in either genome.

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So since the bacteria and phage are still around and have just as big a genome as they always have, where did the "loss of information" go?

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Yes that's true. The genome is deteriorating. Read Sanford's Genetic Entropy.

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Use any one you want. For those three comparisons, which one has more "information"?

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1.) In Shannons case AB, in Gitt's case AB2.) Both the same in any case.3.) In Shannon's case AA, in Gitt's case both the same.