I am always aghast that in the 21st century people still make the claim that mutations are unguided. This is a hold-over idea from before the discovery of DNA, simply because some mutations were found to occur independently of selection.
However, modern evidence has showed that mutations are actually in large part due to mechanisms geared for adaptive purposes, just like the rest of biology. And, just like hearts have heart attacks, mutation systems can break down, too, and lead to disease. Just like bacteria, we discovered mutations first by noting the ones that were causing disease, but with every closer look we see that these are the exception rather than the rule.
To point to a simple example (and one that is even often used as definitive evidence of the efficacy of random mutations!) let’s look at the somatic hypermutation process in the immune system. When a new bacteria invades the body and causes an infection, the body must generate a new gene. So what does it do? It takes a close-fitting antibody gene and mutates it. Now, first of all, you should notice that the mutations only happen in the correct gene – the antibody gene. That’s 1,200 base pairs out of 3,000,000,000. But that’s not all – it also focuses mutations on the part of the gene that attaches to the antigen, not the part that signals the cell (because otherwise it wouldn’t signal the cell correctly). So, that’s roughly 600 base pairs out of 3,000,000,000. The mutation system is highly selective of the sites that it mutates, skipping over the cell signaling systems and focusing on the part that is specific to the antigen.
So, therefore, in this scenario (which is one of the best-studied), teleology (goal-directedness) accounts for 99.99998% of the specificity of the mutation, and randomness / unguidedness / happenstance accounts for 0.00002% of it. Yet somehow the myth persists that we have good evidence that mutations are random.
For more information on this issue, you might be interested in a UD series I did on the modern synthesis and the video below:
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P.S. I originally tried to post this comment on Moran’s blog itself, but was having technical difficulties. So, if it winds up in his moderation queue three or four times under different accounts, I’m sorry, I was just trying to get it posted.
The Elie Wiesel Foundation for Humanity- Nobel Laureates Iinitiative
September 9, 2005
johnnyb,
mutations at cause of disease, they are guided?
sergio
You’re saying that mutation rates vary. Well, yes. We know that. But you’ve shown no evidence that the actual mutations are guided, e.g. that when an organism “needs” a A mutating to a G, it makes this mutation happen.
BTW, the immune system isn’t a good choice for discussing mutation, as it’s only somatic. Better to chose an example where the DNA gets passed on to the next generation. There are some nice examples, but I’ll let you do the work and find them.
A Gene posted:
“You’re saying that mutation rates vary. Well, yes. We know that. But you’ve shown no evidence that the actual mutations are guided, e.g. that when an organism “needs” a A mutating to a G, it makes this mutation happen.”
JohnnyB is easily ghasted.
It would be very surprising if an organism that is a host to a range of pathogens did not develop an autonomous means of dealing with them within is single generation (organisms without this kind of immunological response are unlikely to survive).
But where is the teleology? Is JohnnyB arguing that the human immunological system “knows” in advance what biochemical side-step the next infective bacterium is going to present?
If that is what he means, then he needs to explain the two-way street. To effectively infect a human cell, the bacterium needs to develop the means of side-stepping the host’s existing immunological defences. If it does so, is it imbued with a teleological purpose? If so, what is it and where can we find it?
“You’re saying that mutation rates vary.”
No, I’m saying that mutations are targeted. Did you read the above? The mutational mechanisms *focus* the mutations on the correct 600 base pairs out of 3,000,000,000.
“that when an organism “needs” a A mutating to a G, it makes this mutation happen”
That’s *exactly* what happens. As I said, in this particular case, 99.99998% of the targeting is based on the organism’s need, and 0.00002% of the targeting is haphazard. If one is unable to look at the 99.99998% of the data, and only chooses to look at the 0.00002% of the data that confirms their thesis, I call that willful blindness.
“the immune system isn’t a good choice for discussing mutation, as it’s only somatic.”
There are two reasons this is a good choice. First, this is precisely the mutation system that evolutionists use to demonstrate the efficacy of “random mutations”. Therefore, it is a great example in that regard. Second, there is some evidence that even though they are somatic, these changes can get back into the gametes. Blanden and Steele have suggested that somatic mutations can be reverse transcribed back into the germ line. The evidence for this is pretty small at the moment, but not negligible.
There are other systems which are similar, but for which it is not as easy to see the targeting, such as the SOS system of bacteria, as well as systems which only respond to a much smaller range of issues, such as E. Coli’s responses to the presence of beta glucoside sugars. Thus, it is not a unique situation, but the somatic hypermutation process is uniquely easy to explain to a lay audience.
“If it does so, is it [the bacterial infection process] imbued with a teleological purpose? If so, what is it and where can we find it?”
Certainly – at the very least for the bacteria. We might at some point find an *ultimate* purpose (which we’ll discuss below), but for the moment, I’m just concentrating on the teleology for the organism itself. I think that’s pretty clear – the teleology (purpose) for the host immune evasion process in bacteria is to infect the host.
But, to what I think your question was – I also think that the reason we have trouble seeing an ultimate purpose in this is because we are using loaded terms based on outdated ideas of the role of bacteria in the body. “Evasion” and “infection” imply that the bacteria are necessarily doing something bad. However, many human diseases are the result of bacteria having *difficulty* re-infecting the host. Lactose intolerance and even celiac disease have both been linked with the lack of certain strains of bacteria. Celiac is pretty terrible, and I imagine most celiacs would *love* to be “infected” by bifidobacterium if it relieved their issues.
A Gene-
What, besides our ignorance, demonstrates that all genetic changes are unguided, random, happenstance events?
It is reasonable to propose a Theory that observed changes in living things do not START with a predefined goal. For example: all bears really do NOT want to become whales, but their internal workings are making small changes every day that are gradually turning them into whales, which is why there are so many whales and so very few bears in the 21st century…
This Theory can of course be flawed. But proposing the Theory, researching facts to support it, and debating the implications of the facts are all normal parts of the game. As is admitting that the Theory does not fit the facts.
The minor observation that an individual specimen reacts to disease or changes in its environment to survive is not what is generally meant by “guided development”.
The Theory that there is an External source guiding the overall development of Life in all its variety would explain why individual specimens do not seem to have blueprints embedded in them for changing themselves into something radically different (mice into bats, etc.).
mahuna –
I’m a bit unclear as to the point you are making. Can you elaborate a little further?
Are we saying the same thing? The mutation rate in increased in that region.
Oh, perhaps not. I’m saying that the mutation rate is increased, so there’s a higher chance that the A will mutate, but it could mutate into a T, C or C. Bu you seem to be saying that it will mutate into a G, not a T or C.
JohnnyB said:
““Evasion” and “infection” imply that the bacteria are necessarily doing something bad.”
You may think so, but I certainly don’t.
Infection and immune responses are survival strategies that, if absent, would likely prevent either the pathogen or the target from surviving to pass on their genes. Note of course that the specific immune response derived from an infection event is not heritable. Unless you are making a case for the ideas of M Lamarck.
As A Gene pointed out above, several alternative mutational outcomes are possible at any genetic locus, but only one represents a successful immune response. The human immune system has evolved a capability to rapidly shuffle through random mutations in highly variable parts of its antibody genes. Given this ability, we should not be surprised that it eventually hits on the specific mutation that represents success (hint: if it didn’t have this ability, it would probably be dead). No teleology required.
I must say I like the idea of a teleological bacterium. I thought you were making a joke, but now I see you are serious. Your version of teleology appears to boil down to saying “a particular outcome happened, therefore it must have been intended”. That kind of post-hoc reasoning can be used to justify pretty much any result, which is a polite way of saying it explains nothing.
Whether the Darwinists are being purposely disingenuous to the point that JohnnyB is making I do not know, but if not, it is hard to see how someone could be so blind as to miss the clear point JohnnyB has made.
This clearly is not a truly random mutational process as is required in the theoretical foundation of neo-Darwinism, for a truly random mutational process would have a equal chance of changing any nucleotide in the genome.,,, In fact a few years ago on BioLogos some Darwinists had mistakenly claimed the immune system as proof of ‘evolution in action’. Here are some responses to that mistaken claim:
In fact, neo-Darwinists tried to use the immune system as evidence for evolution in the Dover trial:
In this following podcast, Casey Luskin interviews microbiologist and immunologist Donald Ewert about his previous work as associate editor for the journal Development and Comparitive Immunology, where he realized that the papers published were comparative studies that had nothing to do with evolution at all.
Of related note: Immunity bacteria are shown to be species specific (Regardless of the surprising result, Darwinists still insist evolution did it.)
In fact the deception that neo-Darwinists have tried to pull off with the immune system is very similar to the deception they have tried to pull off with evolutionary algorithms. Here is a very informative interview with Dr. Marks on that whole line of reasoning:
And let’s not forget the waves that Dr. Shapiro is making in this area of ‘random mutations’:
A few comments from the ‘non-Darwinian’ evolutionist, James A. Shapiro PhD. Genetics, on ‘random mutation’:
A Gene –
Modulating the mutation rate is usually meant to imply simply a global increase or decrease in mutagenesis. My point was that this is highly targeted, not just a global increase or decrease in rate.
“so there’s a higher chance that the A will mutate, but it could mutate into a T, C or C. ”
I’m not disagreeing with this at all. This is just the 0.00002% of the targeting that is randomized, as opposed to the 99.99998% that is targeted. Perhaps I need to bump that up to 0.00008% randomized, but I don’t think that affects the discussion much.
“Note of course that the specific immune response derived from an infection event is not heritable. Unless you are making a case for the ideas of M Lamarck.”
There is some evidence for this. Again, Blanden, Steele, and others have done work on this – not conclusive, but certainly interesting. But that is totally beside the point.
“As A Gene pointed out above, several alternative mutational outcomes are possible at any genetic locus, but only one represents a successful immune response.”
True. No argument there.
“The human immune system has evolved a capability to rapidly shuffle through random mutations in highly variable parts of its antibody genes.”
Actually, to say that it “has evolved” is merely begging the question, and, without a mechanism attached, is pretty much devoid of content. If you look at the genes for this, they are actually formatted, with formatting codes demarcating the beginning and ending of fragments. So, this formatting code would have had to evolve at multiple locations simultaneously at the exact same time that the RAG genes needed to process these evolved. In other words, for this to work, there would have to be hundreds of coordinated evolutionary events!
“Given this ability, we should not be surprised that it eventually hits on the specific mutation that represents success”
Yes, that’s basically the definition of having a guided mechanism.
“(hint: if it didn’t have this ability, it would probably be dead). No teleology required.”
Where did you remove the teleology? You simply described the teleology, and then said it wasn’t required. Describing something doesn’t make it stop existing. You certainly haven’t showed how natural selection could have done this.
“Your version of teleology appears to boil down to saying “a particular outcome happened, therefore it must have been intended”. ”
Quite the opposite. I am using Aristotle’s method of inferring teleology. If the functioning of a part of an organism has a regularly associated benefit to the organism, this is indicative of teleology. So, for the case of bacteria, we see that of all the places where mutations might occur, they happen much more often in locations that help it invade new hosts and adapt to new energy sources than in the housekeeping genes. This is the essence of teleological mutations.
sergio –
For a more in-depth discussion of the relationship between teleology and mutations, you might take look at this paper I wrote a few years ago. It separates out mutations into design-consistent mutations and design-inconsistent mutations, and discusses ways of determining the difference between the two.
JohnnyB- Have you read “Not By Chance” by Dr Lee Spetner?
JohhnyB posted:
“I am using Aristotle’s method of inferring teleology. If the functioning of a part of an organism has a regularly associated benefit to the organism, this is indicative of teleology.”
How and why is it indicative of intention?
““I am using Aristotle’s method of inferring teleology…”
Biologists have done quite a lot of work in the last 2300 years, you might want to catch up…
wd400 posted:
“Biologists have done quite a lot of work in the last 2300 years, you might want to catch up…”
So have baraminologists. To no useful purpose.
A little background on the entire concept of ‘randomness’ is worthwhile to consider. When Darwinists use the word ‘random’ in conjunction with Darwinian evolution they mean that the change was,,,
Yet this metaphysical Darwinian claim of completely unguided ‘random’ processes might rightly strike the Theist as ‘begging the question’ since the Theists believes that even these seemingly random events in the universe are ordained by God:
And indeed when one looks for the ultimate source of randomness in the universe, the Theist is found to be correct in his presupposition that even the supposedly random events of the universe are ordained of God. To prove this point, usually when someone builds a random number generator for use in computers, one looks to the maximum source of entropy so as to generate the maximum amount of randomness in his Random Number Generator:
Yet entropy is found to be, by far, the most finely tuned of initial conditions of the beginning of the universe:
This number is gargantuan. If this number were written out in its entirety, 1 with 10^123 zeros to the right, it could not be written on a piece of paper the size of the entire visible universe, even if a number were written down on each sub-atomic particle in the entire universe, since the universe only has 10^80 sub-atomic particles in it. Moreover, if the atheist tries to postulate randomness as the cause for such ‘ordered randomness’ at the beginning of the universe, he winds up in epistemological failure:
Here is the last power-point slide of the preceding video:
In fact, this ‘lack of a guarantee’ that randomness brings to the epistemological enterprise in science, of trusting our perceptions and reasoning in science to be trustworthy in the first place, even extends into evolutionary naturalism itself;
related notes:
Moreover, The atheist Ludwig Boltzmann’s story on his work on entropy is very interesting to note and is picked up here at the 29:00 minute mark of this following video
Yet what is interesting is that Ludwig Boltzmann, being a materialist/atheist, and him thinking that the ‘random probability’ he had worked out for entropy was the be all end all for his work with entropy (since random chance was his creator in his view of reality) failed to search out the universal constant for entropy. Which is something that the Christian Theist, Max Planck, notes the peculiar omission of here:
Thus the Christian Theist is right to ask the atheist, as does the following author:
etc.. etc.. etc..
As well, it is interesting to note where the maximum source of entropic randomness in the universe is centralized:
further notes:
Verse and music:
wd400:
And they STILL haven’t found any evidence that supports evolutionism.
How much longer are we going to have to wait before they realize evolutionism is a worthless heuristic?
corrected link:
Creed – Six Feet – music
http://www.youtube.com/watch?v=qnkuBUAwfe0
I probably shouldn’t ask this but…
Joe, what is evolutionism? Do you just meant evolutionary biology?
Evolutionism is the premise that all of life’s diversity owes it collective common ancestry to some unknown populations of prokaryotic-like organisms via accumulations of genetic accidents.
“How and why is it indicative of intention?”
It is indicative of begin *purposeful*. I don’t mean to claim that the organism itself has intentionality (though it is possible – many microbiologists have been moving in this direction). Think about a machine – its actions are purposeful but not intentional – the machine is merely constructed to bring about its end, but doesn’t know anything about it. In life, since organisms are reproducing, their actions can be viewed as purposeful if they contribute towards their own ends. It is in that specific way that mutational mechanisms were thought of as purposeless by the modern synthesis – they didn’t contribute towards function as an intrinsic part of their operation, but the ones that happened to not cause the organism to die collected to produce design-looking things.
So what modern method of inferring teleology would you like me to use? First of all, the notion that ongoing research immediately invalidates anything written before the 1850s is simply ludicrous. Good ideas last – if you have a problem with them, you should cite the problem, not the age of the idea. But in any case, this is precisely the notion of teleological that Ernst Mayr uses, for instance. He claims that evolution is a non-teleological process precisely because mutations are not oriented in a way that contribute to the adaptation of the organism. He is wrong on mutations, but his use of criteria of teleology is precisely the same one used by Aristotle.
But if you want a more modern way of inferring teleology, you can use Active Information, which compares the efficacy of a search process to the likely efficacy of that same search if it did not have intentionality. An overview of the concept is here, and the theoretical reasoning why a more teleological search process cannot be created by a non-teleological one is here.
Now, if only we had a good way of applying this to biology. Oh wait. We do. It turns out that the hypothesis that mutations are random with respect to function in the somatic hypermutation system is wrong by at least 10 orders of magnitude (22.7 bits). It’s actually more like 66 bits (30 orders of magnitude) because the average number of mutations required for creating a match is 3 (going from memory), and the orders of magnitude are additive for every mutation.
So, (a) yes, Aristotle’s definition is still in use, and (b) it has been made more rigorous by others, and (c) with the more rigorous definition, we can see just how ludicrous is the idea that the mutational process is haphazard.
Joe –
No, I haven’t read “Not by Chance”, but I’ve read a lot of Spetner’s online stuff. It’s on my reading list.
Please do yourself a favor by taking it off the list, putting it in your hands and (start) reading it.
Just sayin’…
Johnnyb,
This is ridiculous. Evolutionary biology tells us how we can get apparent purpose as an a postori result of selection, without the requirement for goal-seeking by an organism or a designer. Just going from apparent purpose to design is begging the questions
The somatic mutation system is not directed. That’s like saying the krebs cycle is teleological because it knows it’s going to get sugars at some stage.
wd400 –
“Evolutionary biology tells us how we can get apparent purpose as an a postori result of selection”
No it doesn’t. It presents a speculation on this, but the evidence is lacking. There is evidence of *change*, but not evidence of purpose coming as a result of selection. In nearly every case where we have beneficial mutations, what we find are specific mechanisms which generate them. Thus, the idea that these are the a posteriori result of selection is falsified, because as we can see in this particular example, it is the mechanism doing 99.99992% of the work, and mutation/selection doing 0.00008% of the work. It’s important, but it’s a relatively minor part of the process.
“Just going from apparent purpose to design is begging the questions”
No, it isn’t. It might, perhaps, not be sufficient for proof, but apparent purpose is in fact direct evidence for design. Begging the question would be that we had no evidence for design, so we just assumed it. But apparent design *is* evidence for design. Darwinism was *thought* to be a defeater for this argument, but as modern mutation experiments show, it fails miserably in that regard, by many orders of magnitude.
Can you present either (a) direct evidence that haphazard changes coupled with natural selection can produce something? Or (b) can you at least present a model to validate your claim?
I’ve pointed out experiment and mathematical reasons why fully mechanized processes do not work. Additionally, there are computational reasons as well. In other words, design is required in the causal chain.
If you would like to propose evidence for your idea, I encourage you to do so!
“That’s like saying the krebs cycle is teleological because it knows it’s going to get sugars at some stage”
Again, you are confusing teleology with consciousness. See again my comment about machines. Just to point out, Ernst Mayr would have viewed the Krebs cycle as teleological. He just mistakenly thought that evolution had the power to produce teleological mechanisms from non-teleological ones, which the No Free Lunch theorem and Active Information show mathematically to be a non-starter.
1. Look up what begging the question means.
2. The somatic mutations you are talking about are not directed.
3. You really don’t get the maths if you NFL has anything to say on evolution (although, you’re with Dembski on that one).
OT: JohnnyB, you may appreciate this video:
Evolution Impossible! – video
http://www.youtube.com/watch?v=uIae8PPg-fE
wd400:
That is the evidence-free propaganda, anyway.
JohnnyB posted this:
“It is indicative of begin *purposeful*. I don’t mean to claim that the organism itself has intentionality (though it is possible – many microbiologists have been moving in this direction).”
Let us leave aside the question of who these microbiologists are, and what are their published research papers. JohnnyB then posted this:
“But if you want a more modern way of inferring teleology, you can use Active Information, which compares the efficacy of a search process to the likely efficacy of that same search if it did not have intentionality.”
Well which is it? Defined as you do it, “purposefulness” is simply an attribute of a system that is apparently “fit to its purpose”, which is precisely what evolutionary biology predicts about systems selected by their environment (system components that reduce an organism’s purposefulness will be selected out, those that increase it will be selected in).
But then (18 minutes later) you claim to be able to identify “intentionality”, which seems to imply that you think that the agent involved (the actual biological organism) is able to predict (pre-dict before the event) the appropriate system response to a future challenge.
It is probably just me, but I am confused about what you are actually claiming.
wd400 claims:
and yet:
Thus wd400 you have highly sophisticated machinery of the cell making tightly regulated changes to the DNA, moreover no significant information is created. Thus there are two problems with your claim that the SHM are random (not directed). 1. SHM ARE directed! and 2. Even if they were truly random and undirected mutations in the Darwinian sense (i.e. randomly caused by replication error, radiation, entropic decay, etc.. instead of imposed by the sophisticated machinery of the cell) you still have not demonstrated that what you claim are purely Darwinian processes can generate any non-trivial functional information above that which is already present in the system.
Notes:
Moreover wd400, even if you could explain the origination of a single novel functional protein domain by Darwinian processes, you still have not even scratched the surface of ‘body-plan information’:
This video may be of ‘random’ interest to some:
BA, that quote doesn’t say the mutations are directed… because they aren’t.
timothya –
My side note about intentionality was just that – a side note. It is *irrelevant* to this discussion whether or not organisms have intentionality. My definition of purpose was exactly what I had said before – that it was fit to a function.
You are conflating several things – first of all, the purposefulness of the organism and the purposefulness of the evolutionary process. My point was that, contra the modern synthesis, the evolutionary mechanism itself is purposeful. As Larry Moran points out for us, the modern synthesis excludes purpose from the evolutionary process itself.
The conjecture of many evolutionists is that natural selection allows evolution to create purposeful structures without having a purpose itself. However, the key link that is used to defend this conjecture – that the mutation process is haphazard – is simply incorrect. There are stochastic pieces to it, and some mutations do come in that are haphazard, but mostly it operates purposefully just like the rest of the organism.
In addition to the experimental evidence that has been pointing against the conjecture that the evolutionary mechanism is haphazard, no evolutionary biologist that I am aware of has proposed a model that would make even the idea that natural selection could produce purposeful mechanisms plausible.
Prior to natural selection, purposeful mechanism was indicative of design. The only reason why anyone doubted this line of reasoning was because it was thought that Darwin produced a mechanism which could mimic purpose without design. However, now that we see that he hasn’t, then there is no evidence left against the original intuition. Note that it is still true that purposeful mechanisms may have evolved, but, given the nature of the evolutionary process, it is likely that if they evolved, they evolved according to their programmed directions.
JohhnyB posted this:
“You are conflating several things – first of all, the purposefulness of the organism and the purposefulness of the evolutionary process. My point was that, contra the modern synthesis, the evolutionary mechanism itself is purposeful. As Larry Moran points out for us, the modern synthesis excludes purpose from the evolutionary process itself.”
I certainly do not conflate the two concepts. Evolution, if true, will select mechanisms that are “purposeful” precisely because those mechanisms improve the fitness of the organism in relation to the environmental challenges it faces. If you want to assign that “purpose” to a pre-existing “intention” then it is up to you to provide the evidence.
And then posted this:
“Prior to natural selection, purposeful mechanism was indicative of design.”
Presumably you mean that people believed this. So what? People in history have believed many things that are now evidently unture. To whit: the authors of the Christian Old Testament.
wd400,that article does say the SHM are ‘tightly regulated’ which permits the mutations to ‘achieve a defined objective’ and ‘Chance is bounded by the limits of the system in which it operates’. Thus despite you assertion that the article does not say that the mutations are directed, the article is very clear that the mutations are ‘tightly regulated’ ‘to ‘achieve a defined objective’. Clearly you are defending a a-priori philosophical commitment to materialism rather than letting the evidence speak for itself. Why???
timothya –
“Evolution, if true, will select mechanisms that are “purposeful” precisely because those mechanisms improve the fitness of the organism in relation to the environmental challenges it faces.”
You say it will “select” them, but that assumes they are being generated. How do you know that evolution will generate them? This is precisely my point. For evolution to work, it must generate complex adaptations. Simply saying it will “select” them is silly – of course it will select them. But will it generate them? My contention, and what the evidence indicates, is that to the extent that it generates them, it is generated by predominantly purposeful mechanisms of mutations, not predominantly haphazard ones.
“Presumably you mean that people believed this. So what? People in history have believed many things that are now evidently unture.”
But you missed my point. The reasons for thinking it untrue are no longer valid. Until you can re-establish their validity, common, uniform experience tells us that purposeful mechanisms are generally indicative of design.
Hello Timothya,
Evolution requires the existence of heritable recorded information, as well as the existence of a mechanism to transfer that information. Recorded information is properly disambiguated as form (i.e. the form of a thing) instantiated in a material medium. As such, it demonstrates material requirements. Our confidence in the existence and validity of these material requirements is supported by both their logical necessity, as well as their direct observation during the transfer.
These physical requirements include two arrangements of matter; one acting as a representation of form in order to evoke an effect within a system (where the arrangement is necessarily arbitrary to the effect it evokes), and the second arrangement which serves as a transfer protocol (to materially establish the otherwise non-existent relationship between the representation and the effect). These two arrangements of matter form an (empirically and logically validated) irreducibly complex core which is fundamentally required in order to transfer recorded information (i.e. one is entirely useless without the other). These physical requirements also include the dynamic relationship between the two material arrangements just mentioned; that is, neither of them becomes the effect (i.e. the necessarily arbitrary relationship between the representation its material effect is preserved within the transfer by the protocol). Finally, the requirements include the production of unambiguous function in order to be identified (i.e. an arrangement of matter that does not produce a functional effect cannot be validated as ‘containing information’). People can say that such an irreducibly complex system (one that produces every single instance of biofunction observed on Earth) “does not have a purpose”, but then again, people can say anything. They do what profits them.
Regarding your comment, the long and short of it is this: This system is not the product of evolution because evolution itself requires the system in order to exist. To say that evolution produced this system is to say that a thing that does not yet exist can cause something to happen – which is obviously false.
The post is talking about the location of the mutations – they’re focused to particular places. They aren’t directed in the sense that the changes being made are the ones that are needed, which is what is meant by directed mutation in this thread.
wd400 –
“The post is talking about the location of the mutations – they’re focused to particular places. They aren’t directed in the sense that the changes being made are the ones that are needed, which is what is meant by directed mutation in this thread.”
You have missed the point – in the adaptive immune system, the place where the mutations are focused *is* the place where it is needed. They are not only focused on the correct gene, but the correct *half* of the correct gene. In other words, if the mutations were focused merely somewhere else in the same gene, the necessary evolution would not happen.
Now, if you are simply saying that the mutations are 99.99992% directed rather than 100% directed, then I agree totally. I just have to really wonder about an idea that disregards the 99.99992% and makes grandiose statements about the 0.00008% as if they were the main focus.
No, I get your point, I just think it’s, and this is really something, probably the stupidest argument I’ve ever heard for ID.
BTW, re “the necessary evolution would not happen”, you do know that somatic mutations can’t contribute to evolution… yes?
johnnyb,
So HIV is designed is it? It has a purposeful mechanism, wikipedia descirbes it as follows:
Complex stuff, no? Too complex to have evolved?
And it’s mutational strategy is to evade the human immune system and so far it’s done a fantastic job. So that strategy is obviously designed, as you show in this thread!
johnnyb
Um, perhaps at one point they were and that organisms failed, leaving the fitter with the current configuration to survive.
Otherwise you get into the argument “well, why did the designer make things to infect you in the first place?”, as it seems a bit silly to give you an immune system that can’t cope with 100% of what’s thrown at it (or people would never die of infections or AIDS) and to keep inventing new things (directed mutations in HIVS) to throw at it.
Not sure I like the sound of your “designer” so much TBH.
JohnnyB posted:
“You have missed the point – in the adaptive immune system, the place where the mutations are focused *is* the place where it is needed.”
I have to say that I think this idea is braindead. It should be obvious that if a genome has an ability to hyper-mutate, then that ability will be expressed somewhere in the genome.
The “where” is irrelevant to explaining why and how it arose. As a minimum, you have to explain why the capability to hyper-mutate inside somatic cells, and thereby generate non-heritable immune responses, is evidence of design. Or more to the point, to demonstrate why this capability cannot arise via natural evolutionary pathways. You haven’t done so, armwaving about Aristotelean “inferences” notwithstanding.
mphillips –
“So HIV is designed is it? It has a purposeful mechanism, wikipedia descirbes it as follows:”
I think it is, or at least the descendent of something designed (corrupted design is not problematic to ID, for instance).
“And it’s mutational strategy is to evade the human immune system and so far it’s done a fantastic job. So that strategy is obviously designed, as you show in this thread!”
Exactly – glad you are catching on.
Your more serious point is here:
But there are 3,000,000,000 base pairs, leaving 3,000,000,000 places to target. Perhaps you could get as small as 5,000,000 (since the target area is 600 base pairs wide – it would at least have to overlap the target region somewhat). In addition, it has to be timed right. In other words, mutating that region at the wrong time leads to failure as well. Finally, it is a conglomeration of multiple genes and introns and even DNA secondary structures that all contribute to this targeting. So, you would need all of these pieces simultaneously. Without them all simultaneously, the whole mechanism would be selected against. This is the problem of incipient structures which was first pointed out by Mivart.
Here you are getting beyond the bounds of current ID theory. ID can detect the design present in Stonehenge, but can’t tell you why it was built. In addition, it can’t tell you how many designers there are (perhaps HIV and other organisms had different designers?)
But as a provisional answer, if you are indeed needing one, is that over and over again, most bacteria and viruses that cause disease are either (a) out of place ecologically (in other words, there is an ecological place where they function in a mutualistic situation), or (b) a descendent of an organism that wasn’t disease-causing. In other words, the design is deteriorating.
So why isn’t the immune system 100%? Perhaps the same reason everything isn’t 100% – because the design is deteriorating. This de-evolution is actually a much more empirically sound version of evolution that the Darwinian evolution which is often proposed.
As I said, just like hearts have heart attacks, it doesn’t mean that hearts don’t have functions in the organism.
timothya –
See my response to mphillips above. Also, the “something had to happen, why not this?” argument is simply ignoring a large part of what we see – that what *did* happen correlates very heavily with function. In fact, you state at the outset that you are going to ignore the data:
The “where” is precisely what is both interesting and useful about the system, yet you think that it should be ignored in explanations of how it arose? I guess Darwinism turns ignoring evidence from an accident into a habit.
wd400:
If organisms are not goal seeking why are you posting here?
Going from apparent purpose to no purpose is begging the question.
wd400:
The Krebs cycle is teleological.
You’re probably mistaken about WHY it is teleological. No surprise there.
wd400:
I’m sure you’ll be able to fill us in on the last 2300 years of progress by biologists.
wd400:
Huh?
http://en.wikipedia.org/wiki/N.....timization
wd400 @33:
This has of course been established via empirical methods which you can cite.
Mung,
Mutations being directed are the provenience of ID.
Therefore it would be more relevant were you to show that they are directed, rather then placing the onus on others who are not making that claim. If you are genuinely interested on why it is generally accepted that mutations are random with respect to fitness then there is plenty of reading material out here.
Furthermore, I would ask you how you would test a set of dice to see if they were “fair”?
Is there any test that you can perform on the dice that would unequivocally show that they are not being directed?
In your world, Maus, is there such a thing as a set of provably fair dice?
johnnyb,
Why is it that it has to be corrupted design? Is your method of telling “corrupted design” simply that the organism does something which you don’t like?
Perhaps you could give a few examples of designs that are still as the designer intended them to be and some which are not?
But this is an argument that HIV is designed in it’s current form. Given the difficulty that evolution has (as has been detailed here over the years) making even the simplest of changes I find it hard to understand from an ID perspective how a harmless organism could acquire the complex molecular machinery to become a deadly virus that can evade the immune system and medical technology.
Not a very good design in the first place was it then? And if that’s really the case then can this rate of deterioration be calculated? How?
Why “is it likely”? So you want to have it both ways, even if it can be shown to have evolved then it evolved that way due to programmed directions.
Given that we have the complete DNA sequences of many organisms now perhaps you could make a start on finding those “programmed directions”?
Or you could say why you feel these “programmed directions” even exist all all other then to save your version of ID from irrelevance?
Then demonstrate it empirically! If we look at the fossil record we don’t see a pattern of deterioration. If we look at a bacteria over many generations we don’t see a pattern of deterioration. The only “pattern of deterioration” we see is the one you invent to explain why HIV etc exists. Other then that, it’s invisible.
I quite agree. Please explain the origin of *anything* from an intelligent design perspective without using the phrase “it was designed”.
“Why is it that it has to be corrupted design?”
It doesn’t have to be corrupted design. It is funny that my every side note of options is being interpreted as a dogmatic statement. Whether or not the design is original or corrupted is not part of ID, at least at the present moment.
“Perhaps you could give a few examples of designs that are still as the designer intended them to be and some which are not?”
Again, I could list things that *I* think are corrupted, but that is not part of ID proper. I will refrain from listing them because you have trouble distinguishing between when I am conjecturing and presenting reasoned arguments.
“But this is an argument that HIV is designed in it’s current form”
It’s an argument that the mechanism you mention is designed in it’s current form. Also note that one form of corruption is simply being out-of-place. Of course, I shouldn’t say any of this, because you will think that I’m telling you an established ID position.
“Why “is it likely”? So you want to have it both ways, even if it can be shown to have evolved then it evolved that way due to programmed directions.”
Which two ways do I want to have it?
The reason why it is likely is because
(a) there is no empirical evidence that natural selection acting on random mutations alone can build the sort of structures needed,
(b) there is theoretical reasons to think that it can’t (see here and here),
(c) there is empirical evidence to show that interesting mutations do happen as the result of prior information being present in the genome (see this post, and also this book)
(d) Shannon’s channel capacity theorem, as shown by Yockey, provides a theoretical basis for understanding information transfer over many generations, and why evolution can work if it starts with an information-rich starting point rather than an information-poor starting point.
Therefore, given the empirical these facts, you see that there are two possibilities – either evolution happens in a very limited fashion, evolution happens in a downward fashion primarily (de-evolution), or evolution happens according to pre-existing information.
“Then demonstrate it empirically!”
Oh, goodness. That’s pretty much every experimental and theoretical study on selection. While the beneficial mutation rate is much higher than previously assumed (it was assumed to be lower because the idea of a teleological mutational mechanism never occurred to them), it turns out that selection against slightly deleterious mutations is problematic – it isn’t strong enough to remove them.
Kondrashov, for instance, points out that deleterious mutations which cannot be selected against represent a range of 4 orders of magnitude! In other words, in any reasonable population genetic scenario, you are going to primarily get de-evolution rather than evolution. To get beyond these results, you would have to propose a mutational system more radically teleological than what I’m suggesting. There’s even a software system that allows you to test this at home.
“Please explain the origin of *anything* from an intelligent design perspective without using the phrase “it was designed”.”
Why? Please explain the thermodynamics of *anything* without using terms such as “heat” and “energy”. The point of ID is that agency is a fundamental, not a derived, cause (at least in relation to the other commonly-used fundamental causes).
However, for a mathematical look at what design is (which might be what you are looking for), see this conference presentation.
mphillips-
Mutations being undirected are the provenience of the theory of evolution.
Therefore it would be more relevant were you to show that they are undirected, rather then placing the onus on others who are not making that claim.
LoL! They have to random, period. Mutations can be random wrt fitness and still be directed.
So what do YOU have besides your belligernece towards ID?
Joe,
Of course. And many other things might be true as well. The point is what you can demonstrate.
You should, however, be able to understand this:
http://evolution.berkeley.edu/.....berg.shtml
In 1952, Esther and Joshua Lederberg determined that many of the mutations for antibiotic resistance existed in the population even before the population was exposed to the antibiotic — and that exposure to the antibiotic did not cause those new resistant mutants to appear.
So if mutations were indeed “directed” as you claim Joe then the results would have been different. Or perhaps this is just a special case and the designer knew it was an experiment and did not do what it usually does?
johnnyb,
So why don’t we see bacteria “de-evolving” over the many thousands of generations we are able to observe them over?
Where can I see this “devolution” in action, in near-real time? If it’s as ubiquitous as you claim….
Joe,
The mechanics behind directing every mutation rules out your position as impracticable, if for no other reason. We’d have noticed by now!
Are you really proposing that “the designer” reaches in and directed every single mutation?
That’s laughable. I’d suggest you search google scholar for “spontaneous mutations” but then you’d simply reply “there’s nothing there that proves the mutations are not really directed after all” or perhaps “you can’t use what you are trying to explain to explain the origin of the thing you are talking about”. You seem to use those two alot.
Nice strawman.
Nope, never said nor implied such a thing.
Well it is clear that you cannot demonstrate anything beyiond ignorance and belligerence.
mphillips falsely believes:
Yet the truth is:
In fact, the loss of morphological traits over time, for all organisms found in the fossil record, was/is so consistent that it was made into a ‘scientific law’:
as to ancient bacteria:
In reply to a personal e-mail from myself, Dr. Cano commented on the ‘Fitness Test’ on the ancient bacteria, I had asked him about:
Thus, the most solid evidence available for the most ancient DNA scientists are able to find does not support evolution happening on the molecular level of bacteria. In fact, according to the fitness test of Dr. Cano, the change witnessed in bacteria conforms to the exact opposite, Genetic Entropy; a loss of functional information/complexity, since fewer substrates and fatty acids are utilized by the modern strains. Considering the intricate level of protein machinery it takes to utilize individual molecules within a substrate, we are talking an impressive loss of protein complexity, and thus loss of functional information, from the ancient amber sealed bacteria.
ba77,
Seems to me the opposite. Modern strains have a better or just different diet. Therefore they have evolved.
Considering the intricate level of protein machinery it takes to utilize individual molecules within a substrate, we are talking an impressive loss of protein complexity, and thus loss of functional information, from the ancient amber sealed bacteria.
In that specific example, perhaps. And so?
The point is that every human is “infected” by more then 200 strains of bacteria, adults have between 11,000 (forearm) and 1.5 million (scalp) bacteria per square centimeter of skin.
So if your claim was true, then nobody as told all these bacteria as they seem to be filling their ecological niches quite well indeed.
If we can have many generations of bacteria how many will have to pass before we notice any sign at all of this inevitable deterioration you claim is happening?
mphillips you claim that there is no evidence of deterioration and yet the fitness test conducted by Dr. Cano showed a loss in ‘fitness. But when shown this evidence you state: “Seems to me the opposite”,,, Perhaps you should take a closer look at exactly what ‘the fitness test’ measures so that your ‘seems to’ misconception can be corrected:
As to your quote ,,, ‘filling their ecological niches quite well’,,, nothing like assuming your conclusion into the very question being asked so as to insure you get the answer you want, is there mphillips???
i.e. Immunity bacteria are shown to be species specific (Regardless of the surprising result, Darwinists still insist evolution did it.)
As to calculating varying rates of genetic entropy for different forms of life, which I hold large populations of bacteria to be extremely resistant to, you can use this computer program to get a ballpark figure:
Also of note:
further notes:
mphillips
Hardly. Are you certain you’re using the word provenience correctly?
Living organisms are themselves the source of directed mutations. Catch up on the latest science please.