I thought I’d check back on this. You’ve missed my points completely and are reduced to repeating yourself. The only way you can continue your assertion of “uniform probability distributions are not valid for biology” is to ignore specific cases where they are and then refer back to cases where they are not. Humorously, you then say that I haven’t addressed your points yet I did not attempt to address them in the first place and took pains to explain why: they are valid within their limited scope as I’ve already said multiple times! If you don’t get it at this point I don’t know what else to say. Others are understanding my meaning. Although, it’s obvious you haven’t read No Free Lunch or other explanations of calculating CSI (or FCSI) since Dembski did exactly what you demanded in #255 and again in #270. You also made a gross error by referring to the entire genome instead of the specified sequence. So at this point I’m forced to conclude that you do not comprehend what you’re attempting to criticize.

Now my copy of No Free Lunch is somewhere in storage. Dembski spent pages going over the flagellum, but the result was 10^-1170 or around 3800+ informational bits (no calculator on hand so that # may be way off). As I said in 267 “the Explanatory Filter can take multiple types of inputs (which also makes it susceptible to GIGO and thus falsification). Two are (a) the encoded digital object and (b) hypothetical indirect pathways that lead to said objects.” Now if MET mechanisms can indeed traverse an indirect pathway to the flagellum then Dembski’s calculations amount to Garbage In.

So, essentially what you’re demanding of Dembski is that he accept what is in question as already verified: to assume that an indirect pathway for every object exists when doing calculations. That premise would make Dembski’s position untenable. But since no one can even come up with a potential indirect pathway then how can we calculate otherwise?

BTW, based upon the flagellum research of the time Dembski ran his calculations based upon the assumed IC core of 30 proteins out of the total 42. It’s possible that less are required for the IC core, but even if halved that would not substantially change the outcome since it’d still be well over 500 informational bits. This is also why Dembski and Behe’s positions are inter-dependent. As Behe acknowledged long ago IC as an indicator for intelligent agency is only sustainable if all potential indirect pathways are infeasible, which is where Dembski’s work comes in. And Behe is trying to research the limits of MET mechanisms, which would validate Dembski’s assumption. But like you I prefer Behe’s line of inquiry since it’s based on things more tangible and easier to comprehend.

On a side note, here’s one foresighted mechanism. And the specific ID-compatible hypotheses I was referring to were variants of front-loading and other hypotheses about foresighted mechanisms (viral, epigenetics, etc.). I cannot help it if you are ignorant about the full breadth of ID thought but please do not attempt to argue with me on this basis alone.

Questions of species don’t change the fact that three single point mutations caused gross changes in the body plan of teosinte AND a new tissue in the covering of the kernels. Do micro evolution three times and presto, you’ve got macro evolution.

“…no one here said teosinte came from corn when it was obvious that it is the reverse.”

I misinterpreted your statement in [269]: “The example of teosinte to corn is an example of devolution since the gene pool of teosinte probably contains the gene pool of corn except for a mutation or two.” But, since this is now the topic of discussion, it would be begging the question to discuss it.

These are interesting examples. And should be brought up at the appropriate time in the new Durston thread. If you do not, then I will. It could mean that I have misinterpreted what Durston has said, always a possibility, or there could be some other explanation. Read Durston’s comments at

http://www.uncommondescent.com.....ent-303307

Thank you for the information.

Maybe this will come out in Kirk Durston’s new thread when it appears but just what are the implications if the distribution is not uniform. Is it a big deal or is it closer to a nit that someone throws out to divert the discussion away from the obvious by posing a pseudo objection?

Excellent question. This should get the conversation back on topic.

If the probability distribution of solutions generated by MET mechanisms is not uniform then the NFL theorems and Dr. Dembski’s two new papers are not applicable, as written, to biological systems.

In fact, MET predicts and observations confirm that the solutions generated by MET mechanisms do not form a uniform distribution, very far from it in fact. Further, the search space itself is not uniform — there are clusters of viability.

Given that, Dr. Dembski’s papers cannot be said to be “pro ID” without further work to tie his results specifically to real world biological systems.

The uniform probability distribution is also important in the calculation of CSI, but the discussion above has already explained that.

JJ

“A more interesting question seems to be can any change or any distribution of changes ever lead to a protein reaching one of these other isolated protein islands of foldable proteins?”

This has been investigated and there are cases where very few changes are necessary to connect two different islands of foldable proteins. One reported artificial example for a small protein (56 amino acids) showed that only seven mutations where necessary to reach a different stable! fold and a new functionality (Proc. Natl. Acad. Sci. USA, Vol. 104, No. 29 pages 11963-11968, Orban, Bryan & coworkers).
An even more extrem example is the so called Arc-repressor protein where two mutations are necessary to change the fold and a single muation results in a protein existing in an equilibrium between two different folds. (Sauer & coworkers, Nature structural biology 2000, Vol. 7, page 1129-1132)
For folds of RNA there is one example where an RNA can adopt two totally different folds associated with two totally different functions.
Thus, the islands of possible protein folds are not necessarily isolated. Furthermore, one should not forget that not all functional proteins must be folded to function but many fold only upon interaction with a ligand. This means that even partially unfolded proteins might not be non-functional.
The cited papers should be open access since they are more then a year old.

I am stopping this conversation. Some others can waste their time with you. You do not know what ID is about and seem only to impose your own ill conceived perceptions. So you can have the last word till you start dealing with reality and what people say.

For example, I know all the problems with the definition of species you bring up and they have been discussed here before and I have read about the problem in pro-Darwinian and anti ID books as well as with pro ID books and discussions and so it is a non issue. Wolves and dogs theoretically parted millions of years ago but still remain the same species by biological textbooks. My example of the Chihuahua and the wolf was meant to point out the absurdity of your example.

I just pointed out that it is hard to use an example of one variant of a species morphing into another variant of the same species as proof of Darwinian macroevolution. Especially when it looks like the mechanism is probably artificial selection and not natural selection. And if it was by natural selection, ID accepts that example with open arms. So what point are you making by first choosing it and then defending it. And you defend it badly because no one here said teosinte came from corn when it was obvious that it is the reverse. It seems the indigenous people of the Americas started the process several thousand years ago probably first by accident and then maybe they got smart. So what is your point. Your discussion seems pointless. Don’t bring up trivial examples that ID is wholly in sync with and expect us to take you seriously. Nothing you said so far has any merit except maybe in your own mind. Adios.

Under evolution, there’s just no hard and fast division between two populations that are evolving apart short of reproductive incompatability, even though one is very much needed. For instance, how do you call it when two plants have 99.9999+% identical genomes, but one is a clump of grass and one is corn? Or one is a chihuahua and one is a wolf? You can say they’re both the same species, but if you plant teosinte instead of corn, your family is going to starve and if a chihuahua goes for your throat it’s very annoying, but if a wolf goes for your throat, you’re dead. I guess one way to know if ID or evolution is right is to ask how easy it is to separate species and so far the data points entirely towards evolution.

I’m afraid teosinte is NOT mutated corn. We have archeological specimens of teosinte plants and pollen going back a long, long ways, but corn doesn’t even start to appear until about 9,000 years ago and it’s a very crude, teosinte-like version of corn. Incidently, all of the early differences are due to natural selection. Humans changed the teosinte environment in a big way when they started eating it and planting it. Once people started saving their best plants for seed and eating the lesser plants, it put natural selection on steroids and the plan transformed from teosinte, a barely edible grass, into corn, a highly desireable and nutritious plant to humans, in a few thousand years.

“When we refer to no natural examples of FCSI ever being formed by nature we do not include life since life is the topic under discussion.” My mind just boggles at this. When we refer to no natural examples of FCSI ever being formed by nature, we do not include life, although life is a part of nature, since life is the topic under discussion.” Since the question is, “Does life produce FCSI?” you seem to have constructed an impregnable position. A veritable Maginot line of logic.

“… the changes we have seen are all trivial in terms of genomic change and no complex new functional capabilities have ever been demonstrated.”
It’s certainly true that the changes we see in teosinte to corn are “trivial in terms of genomic change”. There are about 2 billion DNA base-pairs in the corn genome and if we have three point mutations, that’s only 3/2,000,000,000ths of the corn genome. And yet just those three changes make the plant taller and narrower and concentrate the ears near the stalk, the ears get larger and the coating on the kernels gets softer. “Trivial” changes in the genome can obviously make very significant changes in the phenotype and it’s the phenotype that feeds you or rips your throat out.

As for “no complex new functional capabilities have ever been demonstrated”, I’d say that just those three mutations produce functional changes that are complex enough to turn a barely edible weed into something that can start to feed the entire New World.

How many base-pairs do you think mutated to turn teosinte into corn? I’m betting it’s way under a thousand, which, as you say, is “trivial in terms of genomic change”.

I’m glad you brought up bat sonar. I read something about that a few years ago. This is from memory and I don’t have a citation handy, but since it’s the topic under discussion I don’t see why I have to provide one. Don’t want to beg the question, after all. For starters, you and I can already do a crude form of echolocation. If you shout, “Hello!” and hear a fainter “Hello!” a few seconds later, you know you’re some distance from a large reflecting object, such as a cliff. If you say, “Hi!” and hear an almost immediate series of echos, you’re in a gymnasium or concert hall sized room. If you say, “Hi!” and instantly get a load of echos in return, you’re in a small room. If you hear a lot of high frequencies in the echo, the surfaces are hard, if not they’re soft. You can tell direction pretty well too, by using the already existing ability of your ears and brain to tell what direction a sound is coming from. Blind people get very good at this, by the way.

Now if you’re a small flying mammal hunting insects in dim light, what kind of changes can help you find more insects via echo-location? Well, for starters you can shout, “Hi!” louder. This will detect insects farther away. You can make your shouts shorter, too, which makes your distance measurements more accurate. Or, like some bats, you can “chirp” where you send out a loud cry that sweeps from a low to high frequency. That helps you sort out the mass of echos that come back to you. If you hear low and high sounds, you’ll know that the low pitched sounds are coming from a greater distance away because they were uttered first.

Better ears will help too. If the shape of your outer ears changes, they can make sounds coming from different directions have phase relationships that increase your ability to tell direction. Your face can change too, to make those phase relationships clearer. (That’s why bats tend to have faces like gargoyles – it helps them determine directions.) If you develop a really, really loud chirp or yelp, you can have a problem with your voice damaging your hearing. (I’ve heard some bats have such loud calls that they can stun insects with them.) Contracting muscles in the middle ear while you shout can clamp the auditory bones, protecting them from damage. I’m sure there are many more ways to improve echo location.

Now can you tell us which, if any, of these changes are impossible to produce? And remember before answering that all of them and more exist in contemporary bats and other echo-locators.

A more interesting question seems to be can any change or any distribution of changes ever lead to a protein reaching one of these other isolated protein islands of foldable proteins?

JayM 261

First

You only succeed in continuing the “non-uniform argument” by changing the metric to things that seem nonsensical. You might as well have said, “I ignore what you just said, I ignore the pointed questions, and I prefer to focus on aspects of the discussion that are already acknowledged as being valid.”

Frankly, I could leverage the same charge against you, with far more supporting evidence. You have responded with great verbosity, yet have not even begun to address a single one of my arguments. Allow me to demonstrate:

Now back to the main disagreement. Which is that uniform probability distributions do not apply to biology at ALL in regards to MET. In fact, I would expect non-uniformity to be more complete in its breadth if some ID-compatible hypotheses are true.

Why? What specific hypotheses do you mean?

But to be fair we’re assuming MET and Darwinism as a starting point in evaluating its claims.

My understanding as well is that they are equally likely, but MET mechanisms do not create genomes from scratch so the assumption of a uniform probability distribution across the entire genome is invalid.

I’m struggling to even comprehend your objection. Non-foresighted variation is produced by copying errors. How does the mere act of replication cause these copying errors at any particular point(s) in the genome to become unequally probable/non-uniform?

MET mechanisms do not assert that every location in a genome is likely to change, as would be required by a uniform probability distribution. In fact, MET mechanisms are very conservative. Genomes change very, very little from generation to generation. Further, only those changes that are viable are preserved and only those that are viable and result in surviving offspring are propagated. This is far from a uniform distribution in genome space.

Depending on the form of variation, and the error correction (human versus bacterium) they’re certainly unequal in size or scope, but that does not change this observation.

What observation? The fact is that MET mechanisms result in child populations differing very, very little from their parent populations in terms of allele frequency. There is not a uniform distribution of potential changes.

And at this point natural selection (the localized search you’re so focused on) is irrelevant since it’s after the fact and may not even be a component at all in calculations.

I have no idea what point you’re trying to make here. Natural selection operates on the non-uniform distribution of changes, probabilistically preserving those with greater fitness. This mechanism is completely at odds with the assumption of a uniform probability distribution of solutions.

Now if we have foresighted variation that seems to be outside of the bounds of MET (and said existence was predicted by ID proponents). Although some insist that the non-foresighted mechanisms of MET somehow produce the foresighted mechanisms we’ve observed.

What foresighted mechanisms have been observed? I have seen nothing in the ID or peer-reviewed mainstream literature to suggest that foresight has been rigorously documented.

This is why Dr. Dembski’s papers, however interesting, do not appear to be directly supportive of ID theory.

And the ID theory of Dembski and Marks conflicts with micro-evolution how?

Not at all. In fact, the papers do not describe any “ID theory” at all and do not tie their assumptions and conclusions to any real or hypothesized biological mechanisms.

Again, I’d rather Dembski and Marks make the connection to biology specific but my assumption is that their focus is narrow and they’re largely constraining their argument to specific cases relevant to (a) macro-evolution via the unguided processes of MET and (b) OOL.

However, they do not do this. Their arguments do not address the claims of MET at all, as far as I can see. That’s why these two papers cannot be said to support ID as they stand.

This would still not be a uniform probability distribution, because the probabilities of small changes given MET mechanisms is much greater than that of large changes.

You’re changing the metric again.

No, I am not. A uniform probability distribution requires that all changes be equally likely so that subsequent populations are exploring the whole genome space. That is not the claim of MET and is not what is observed in real biological systems.

Any mathematics that presumes a uniform probability distribution, as do the NFL theorems, is not applicable to biological systems.

Yes, small changes are more probable.

Thank you. You have admitted that MET mechanisms do not result in the uniform probability distribution required by the two papers under discussion.

But your point is only relevant to the localized search. What exactly about the OCCURRENCE of unguided variation makes small or large changes to any specific location of the genome unequally probable?

We’re not talking about “unguided variation” in general, we’re talking about MET mechanisms in particular. They do not result in uniform probability distributions of genomes within genome space.

Here’s the point related to biology. I forget the informational bits for the flagellum as calculated by Dembski (isn’t that in No Free Lunch…it’s been years since I read it?). But if anyone submits a reasonable hypothesis for an indirect pathway composed of steps which are less than 500 informational bits EACH then Dembski’s design inference for that particular biological object is rendered invalid.

This is “ID of the gaps.” We need to prove that it couldn’t happen, not sit back and challenge scientists to prove it couldn’t. MET mechanisms demonstrably generate complexity by funneling information from the environment to the genomes of subsequent populations. So far, evolutionary biologists haven’t demonstrated something as complex as a flagellum evolving, but they have shown the evolution of some structures and pathways. Until we show real limits to those mechanisms, the idea that many small steps result in a large journey is at least credible.

In addition, the calculation of CSI uses the length of the genome as a factor in determining how “specified” a sequence is. That is not logical given the small changes possible with MET mechanisms.

The calculation of CSI in biology does??

Yes.

Can you be more specific in what you mean (or provide a reference)? Or did you mean the “length[complexity] of the specified sequence”?

Exactly.

Dembski’s specification is very general in its application. Which leads to the problem of subjective specifications. Art is subjective and requires an intelligent agent to identify it (although I suppose it can be argued that realist landscapes can be objectively specified on a comparative basis). But biology contains objective specifications independent of the observer based upon the machine functionality. That’s why people refer to FCSI in regards to biology.

None of this addresses the problem I pointed out, namely that the CSI calculation assumes creation from scratch, which is not the claim of MET.

Further, people refer to FCSI, but no one in the ID camp has yet demonstrated how to calculate it objectively for real world biological organisms or structures.

Viable regions are clearly clustered or you and I wouldn’t be here.

We each differ from both of our parents, and yet we live. That demonstrates that there are multiple connected points in genome space that are viable.

The question, of course, is how large these regions are and how connected.

You make my point for me, which is all I meant by saying “‘can’ be clustered”.

If they are clustered, then MET mechanisms can easily keep subsequent populations in the “sweet spot”, so all the calculations that assume a uniform distribution of solutions in the genome space are not applicable.

If we want to make ID theory truly scientific, we have to address what is known and provide better predictions of what is not known. That means finding where the real “edge of evolution” lies, not attempting to apply invalid assumptions like uniform probability distributions to observed phenomena to which they clearly do not apply.

JJ

Poor choice since both are the same species. Just as a Chihuahuas and a wolves are the same species. You are confusing physical difference with macro evolution of complex new functional capabilities which all take place at the genome level. It is also not clear which differences between teosinte and corn are due to artificial selection and which to natural selection.

The example of teosinte to corn is an example of devolution since the gene pool of teosinte probably contains the gene pool of corn except for a mutation or two. It is unlikely you could get teosinte from corn but it may happen and would be an interesting experiment.

When we refer to no natural examples of FCSI ever being formed by nature we do not include life since life is the topic under discussion. Let me lay out the logic of the argument for you.

Excluding life there is no example of FCSI forming by law or chance. That is nature does not create FCSI. You can not point to life because that is begging the question. Intelligent activity produces FCSI all the time. Now if one set of causes has not shown the capability of producing the outcome while another set of causes does it all the time it seem reasonable to say that the reason for the FCSI could be due to the activity that does it all the time and not to the one that has never done it. Notice I did not say absolutely only that it is reasonable that it originated this way. One cannot do it and another can. So which one would you include as a potential cause. Think how unreasonable it would be to say that the process that has never done it is the only that can be considered as the cause while the process that does it all the time cannot be considered. How does one justify that logic?

Now once FCSI is there and there are mechanisms for changing it, then one has to look at these mechanism and see what power they might have to create new FCSI through this change mechanism. So ID does not deny that these change mechanisms may generate new FCSI. It is just that the changes we have seen are all trivial in terms of genomic change and no complex new functional capabilities have ever been demonstrated. In other words not only does the gene pool have to be significantly increased but this increase along with other elements that were there previously must coordinate a system with new capabilities that did not exist before. Think bat sonar, insect wings, avian oxygen processing system for some starters not a a morphing of teosinte to corn or a wolf to a Chihuahua.