Agreed.

I see your time-out call. Maybe in the meantime, the blog masters will deem it worth the while to post that new thread . . .

Now, too, you comment on some points I will take up a bit:

1] You can believe in the fine-tuning concept of the cosmos yet remain so skeptical about darwinian evolution in principle.

First, while I am simply discussing here within the ambit of the generally accepted timescales and cosmology of the past [I will pick up later], I am pointing to the gap in the empirical evidence as respecting the macro-level claims of NDT. I am aware that at micro-evolutionary levels, NDT-style evolution can and does happen. But Galapagos island finch beaks that get a little longer in a drought, then change back, or “species” that are now hybridising and interbreeding, or the like do not cross the key threshold McDonald noted and Meyer picked up.

Further to this, from the Cambrian life revolution forward, there is a characteristic pattern of sudden appearance and stasis then abrupt disappearance (on a temporal interpretation . . .) in the now “almost unmanageably rich” fossil record. All of this is linked to the information generation problem I and others have highlighted, including the mosquito case above.

Until I see clear evidence of ability to cross that core body plan innovation threshold, I will remain skeptical on the common descent through RM + NS etc thesis.

By sharpest contrast, the picture of the origin and development of the physical cosmos, is in my observation not presented dogmatically, but is both provisional and well-anchored on supportive empirical data. (The contrast in tone between, say, my favourite general survey Astronomy text and the tone I have seen in many a discussion on these matters I have found telling!) The Hertzsprung-Russell diagram, the stellar distance scale [the subject of my very first ever scientific presentation and public speech . . .], the observed red shift and Hubble Constant are all anchored pretty directly to observation.

2] Is it not possible that the cosmos was arranged in such a way that evolution would happen as it has?. That is, it would happen in a way that was *indistinguishable* from neodarwinism.

I observe the underlying inference/assertion, that NDT is the actual observed mechanism of origin or is indistinguishable from it. Methinks there is a major evidentiary gap to be bridged before one can assert such, as noted.

In short, the current state of evidence is at macro-level, quite plainly “distinguishable” from NDT’s predictions and explanations.

3] sometimes I wonder if you ID guys don’t simply suffer from a lack of imagination

This is of course a classic gambit. But in fact, the design inference is precisely based on an explanatory filter that reckons with chance, necessity and agency then proceeds to ask how may we credibly and empirically distinguish the three. [Reverse engineering the design is a further stage, and is indeed one being embarked upon. But in the key cases of OOL and macro-evolution, as well as cosmology, the prior issue – given the institutional prevalence of evolutionary materialism as both a guiding philosophy and a paradigm for science -- is whether design is a reasonable and indeed better explanation of the observed data.]

This has been outlined above, and is in the always linked, but we may briefly summarise:

a] It is generally accepted that chance, natural regularities and agency are all known as the three major root causal forces at work in the world.

b] For instance, if a heavy object falls, that is the NR, gravity. If it is a die, the face that is uppermost is effectively a product of chance. If it is tossed as a part of a game, that is agency.

c] When an empirically observed event is: contingent, complex beyond the credible probabilistic reach of chance in its context, and functionally specified, the resulting FSCI/CSI is a well-known, frequently observed marker of intelligent agency. [Think of coming across 500 pennies, all heads uppermost. Which is the better/likelier explanation, a lucky toss or someone who arranged the pennies?]

d] Indeed, in every case where we directly observe an event’s cause in action, if it meets the above filter’s criteria, it is produced by agents. That is, we see here an empirical basis for inferring on a best explanation basis, to agency, even when we do not see the cause in action directly. And – certain well-known cases notwithstanding – this inference is routinely made in science and general life.

So, the matter is not failure of imagination.

Let’s see whether we continue here or elsewhere

GEM of TKI

I see you also linked the same paper on bacterial resistance and its implications.

I would like to pick up one of your points to G_A rather briefly:

All your words, all your concepts, all your arguments, don’t apply in any way to the specific case of mutation of the mosquito, for the reasons already discussed, but apply perfectly to an intelligent designer, Nature . . .

You are here bringing up the Case III in my always linked, cosmological design. [The onward linked philosophical issues faced by evolutionary materialist worldviews are important but of course not scientific questions.]

The key link is that a fine-tuned cosmos that with minor shifts becomes non-life sustaining, often radically so, exhibits a complex balance that is of a type often set by designers. In this context, should we discover that there is in fact a law of nature that forces or makes highly probable the emergence of life on suitable planets etc, then that is in fact suspicious, given the cosmological finetuning issues in the linked. (BTW, this is also why the project to find a grand theory of everything is actually a design research project, though of course by and large an inadvertent one. Imagine the discovery of a super-law of physics that implies that the sort of fine-tuned cosmos we observe is forced. What does that suggest? And, the often met with alternative, an infinite array of subcosmi with randomly distributed laws or parameters, is of course a resort to ad hoc, ex post facto philosophy not science, and opens the door to the credibility of a Design based worldview alternative.]

Similarly, observe that bacterial resistance to say Cipro, the subject of Fig 1 in the linked paper, is by detuning the folding of the enzyme in question. Fine-tuning in short is linked to sparseness in the local configuration space. [Observe how Wright in the 1932 paper adverted to cosmological instances to help interpret the sparseness issue,t hen failed to follow through on the implications, i.e. Exhaustion of probabilistic resources. I gather in Monod's Chance and Necessity, 1970 or so, the same gap emerges. Methinks this is a systematic gap in the evolutionary materialist research programme, from hydrogen to humans.]

We know that intelligent agents routinely create functionally specific, complex [sometimes, irreducibly complex] information rich systems, that exhibit finely-tuned behaviours, and may have defences for the fine-tuning through error detection and correction, sometimes leading to intelligently programmed graceful degradation.

So, we see here a very familiar pattern . . .

GEM of TKI

5] Further to this, the mutation in view is at root an information-loss incident, not an information-creation event. That is, a previously functioning molecule has been damaged and this in this case frustrates the mechanism by which the insecticide poisoned the cell processes. That is, a sufficiently strong random disruption of the chain of digital information has caused an arbitrary shift in the decoding process, due to the way the code interprets in this case protein coding. [And, BTW, there is evidently a fair amount of redundancy in the code itself including steps that make for graceful degradation by shifting to similar monomers.]

6] Let us note: the change here in view is microevolutionary; it does not rise to the body-plan change level, and the new population is till a population of disease-carrying mosquitoes, just resistant to a formerly successful insecticide — and by the report, less functional as fliers. [This is quite similar to the case with antibiotic immunity through misshapen enzymes etc and reported HIV immunity through a genetic breakdown in the port used by the virus to gain entry, etc. Cf discussions here (esp fig 1 and table 1), here [observe on the failure to recognise the full implications of the high degree of sparseness indicated in this classic paper, starting with abiogenesis], and p. 11 ff. on CCR5 here (also cf the paper as a whole).]

7] The information creation side is, in the end, a challenge to empirically justify a claimed process by which through a cluster of random point mutations, we materially gain novel and coherent biofunctionality in the used code space of the cell, especially at the body plan level. Notice the McDonald threshold for information-creating macro-evolution: novelty in body plans which creates a novel, coherent somatic system. This, has never been actually observed and credibly passes the threshold of exhausting the available probabilistic resources.

8] Further to this, we see beyond this case of modifying an already existing cell, the same challenge at the point of creation of life through proposed abiogenesis mechanisms. For, observed minimally complex life forms have ~ 300 – 500 K or more monomers in their DNA strands, three orders of magnitude of string elements up in information-carrying capacity from the level specified by Dembski as exhausting the PR of the observed cosmos.

9] The information carrying capacity of course increased exponentially with chain length: 4^N; where 4^250 ~ 10^150. 4^300k ~ 9.94*10^180,617. I conclude for good reason that the islands of functionality are effectively impossibly sparse in such a space, relative to random processes that just so happen to chance upon the coherent codes and implementing machinery for the relevant systems we see in the cell. But, we routinely see intelligent agents creating functional digital configurations that are comparably sparse in say text-string space.]

10] So, while indeed, the issue of random changes and metrics on information carrying capacity are just a first step, they are an important step as they tell us the size and credible sparseness of the configuration spaces we are working with. In that context, the required increment in biofunctionality coupled to the coding and processing systems and the probabilistic issues as the number of points mounts towards 250+, by direct implication raise the issue of exhausting the probabilistic resources of the situation.

BOTTOM-LINE: A single-point mutation that actually seems to have damaging consequences and works by information loss, seems to be nowhere near the relevant threshold for explaining macro-evolutionary change. [It aptly explains one mechanism for micro-evolution, but micro evolution is uncontroversial across live options and is not the material issue at stake.]

In short, interesting, but not yet the level of explanation required.

Thanks for a good try

GEM of TKI

Seems the blog is having fun with a Japanese cartoon series and with the Templeton story. Anyway, back on issue.

You will note I described information-carrying capacity, as that is the real point of the I = -log2p expression. In this case, a single-point mutation in a 4-state digital system, carries up to 2 bits. My 250-point issue has to do with the associated fact that that gives us a capacity of up to 500 bits, i.e. a configuration state space of ~10^150, linked to the Dembski type bound for a unique specified state. [This extends of course to islands and archipelagos of functionality, too.]

Let’s take up on your point in # 190 that:

perhaps a wayward gamma ray passed in the vicinity . . . the break was repaired, but repaired incorrectly, as happens from time to time. The repair system is not perfect by any stretch of the imagination. So you have your new amino acid. As it happens, it confers resistance to this insecticide. This all happens in the context of a gene duplication, which are also often the result of repair mishaps . . . . How much new information does it contain that has been generated by evolution? I don’t have the foggiest idea. But it’s more than you think it is, at least if you think that biological information is something above and beyond shannon information . . . A process is born, one involving several components . . . . The material substrate change is modest, but the “interpretation” of the substrate change by nature may or not be more dramatic.

Remarking:

1] Of course, I pick the physics-linked case, as that ties into the implications of radiation damage (part of one of the must-do physics major courses I did way back when; recall how the hairs on the back of my neck stood up at appropriate points, too . . . esp. the Hiroshima “expt”). The usual mechanism is ionisation of the most common molecule in the body, H2O, leading to free radicals, thence disruption of DNA and resulting damage. Cell death etc. if bad enough, cancer etc. as a serious possibility, if not that bad. Really minor damage is repairable.

2] You advert to and imply existing and functional repair mechanisms, which are of course error-detecting and correcting systems based on redundancies in the stored information. [The simplest case of such a system, and the first example I studied, was the 3M voting code: repeat the code twice so there are three copies. [M, M, M] Take a vote, bitwise, and majority wins. Obviously, it corrects a single error, but misses a double on the bit point, which would reverse the vote. (For DNA, if there is such a code that would require voting across four possible point states: G/C/A/T [and the match in the neighboring linked complementary strand . . .]; of course, the actual mechanisms are subtler than a brute force voting mechanism.) But observe: error correction mechanisms can be saturated, leading to possibilities for failure in environments that overly stress the system. Mosquitoes subjected to insecticide assault sounds like a stressed situation.]

3] Underlying issue and implication: we see a code-based information system, with a control language and by implication algorithmic error correction processes. So, let us not strain out gnats while swallowing camels: in all cases of error-correcting information processing systems based on codes where we directly know the causal story, they are the produce of intelligent agents. Indeed, this is true of all such cases of functionally specified complex information [FSCI or in Dembski's term, CSI] .

4] That immediately means that relative to what we know – as opposed to speculate – we have a candidate best explanation for such systems that we need a very good reason and evidence to reject.

Pausing . . . .

GEM of TKI

thank you for your answer, which is rich of very interesting insights, and allows a lot of pro ID discussion! The only thing it cannot do, alas, is helping Myers’ position. Let’s discuss why.

First of all, you are elaborating a lot of points which, I think, Myers and those who think like him are completely unaware of. I think that Myers’answer was just what it seemed: the infamous attempt to pass a single aminoacid substitution as the miraculous acquisition of CSI, hoping that nobody would check the biological nature of that mutation (or, perhaps, unaware himself of it). The choice is always the same: lie or ignorance? Fascinating options, both.

But let’s leave Myers alone, and discuss what is much more interesting, that is your points. They are very thoughtful but, again, I cannot agree on the conclusions.

First of all, I would like to complete the “negative” part of my post and point to the only part of your argumentation which is, in my opinion, frankly wrong, in a technical sense. You say:

“But we know when a new feature or process has been generated. And evolution conferring a resistance to a pesticide is a positive instance of some kind of increase of *something.* ”

I don’t agree. In this specific case, which is anyway representative of most, if not all, the “evidence” of darwinists, including antibiotic resistance, no positive instance has been created. We are only witnessing a cellulare “disease” which, by mere chance, happens to make a particular “threat” ineffective for the owner of the disease. The only thing which increases in the mutated mosquito is entropy, or if you want Shannon information, or anyway disorder. Indeed, a protein which was in a way designed to have a specific function (ACE1) loses a small quantity of its designed structure and function beacuse of a random event. That’s all.
Let’s see in more detail the example of antibiotic resistance, which is equivalent but which gives us an interestint further element. For all the details, please read this very good article:

Is Bacterial Resistance to Antibiotics an Appropriate Example of Evolutionary Change? http://www.trueorigin.org/bacteria01.asp

The facts are as follows: in bacteria we have two different mechanisms by which antibiotic resistance is conferred:

a) Mutation of some structure of the bacterium, which was the target of some antibiotic action. This case is the perfect equivalent of the mosquito case.

b) HGT of some enzyme which can inactivate the antibiotic (eg penicillinase). In this case, we have no evidence that penicillinase is generated by random evolution, no more than any other complex enzyme. Penicillinase is a protein with function and CSI, but we find it in the scenario “ready to be used”. The bacterium acquiring penicillinase by HGT is really acquiring “something”, CSI inseed, but that something is only transferred, not created. So, Dembski’s concepts are absolutely confirmed.

But let’s go back to the a) scenario. In that case, the acquisition of resistance is not, in any way, a new “function”. I’ll give a metaphoric example whose only purpose is to clarify the logic here:
If in a population of animals some of them have a genetic mendelian disease, due to a single mutation which inactivates a function, let’s say a coagulation disease, and some bizarre scientist decides that he is interested only in the diseased animals, and not in the normal ones, and he goes on killing the normal animals and keeping the diseased ones, is that a demonstration that the disease is “a positive instance of some kind of increase of *something.* “? Only if you define that “something as disease, loss of function, loss of meaningful information. But positive?
I state it again, in my opinion the only thing which increases is entropy. And CSI, however you want to define it, is certainly decreased.

Now, to the “positive” part of my post. I think you introduce a concept which is of the greatest importance, and which is the cause of great confusion in darwinist thought. It is a confusion which is inherent in the concept of “selection”, and which often expresses itself in the use of so called “pseudo-teleological language” by darwinists. It can be summed up this way: many darwinists are IDers without knowing it (not Dawkins, beware. He is one of the pure).
One of the manifestations of that aspect is the frequent use of inverted commas. Your arguments are a very good example of a honest and creative attempt to express explicitly this bias, and so they are a very good field for discussion. You say:

“It’s the context **in your mind** that matters. The interpretation. And here the weird thing is that the interpreter is nature itself. ”

and:

“What patterns are in the mind of nature that determines what it sees and how it interprets the splotches?”

and:

“That is the “mind,” if you will, of nature. It is the landscape of possibilities it can “imagine” as being viable.”

Indeed I “will”! You are perfectly describing the point of view of a designer. You are describing Nature as the designer. All your words, all your concepts, all your arguments, don’t apply in any way to the specific case of mutation of the mosquito, for the reasons already discussed, but apply perfectly to an intelligent designer, Nature, who can:

a) Determine non random mutations

and/or

b) Select random mutations which are potentially useful according to a predetermined plan or design.

That’s what Nature does, if we want to call the designer Nature. I don’t know how he/she does it, but he/she does.
The fact is: according to a strict naturalist view, and that’s a beautiful paradox, Nature does not even exist. Or at least, it exists not as an entity, but as the sum of what exists and of the laws at work. In other words, you could well subsitute the world “reality” for nature, in a naturalistic sense. A naturalistic reality is not only blind, it is by definition not conscious, it is only the outcome of rigid deterministic laws. So, unless you define new laws which I am not aware of, nature has no purpose, it selects nothing, it implements nothing.
You call it “landscape”, implying again that in some subsets of reality we can find some appearance of meaning. Landscape is a human word. It is the way a conscious being sees a piece of reality and gives meaning to it. It is the way the conscious mind reconstructs apparently meaningless bits of information, sometimes inferring, if the poetic mood is working, a designer or an artist behind them. A landscape exixts only in a mind. Nature exists only in a mind.
Ouside of a mind, only deterministics laws (not many laws, only three or four, depending how you count them) exist, at least according to present science. So, if you infer special behaviours in nature, which are characteristic of minds, or of a mind possessing Nature, you should show how such behaviours can arise from the strict application of the known laws. That’s exactly what darwinism can’t do, and what it gives for granted. Because to analyze that assumption means to delve deeply in the nature of information, of thought, of order, it means considering and applying serious sciences like mathematics and statistics, and why not, physics. Better stay off from that, and leave it to Dembski and the like of him, calling them fraud, or bad science, or anything else one can device.

A last note. You say:

“There is that gene–the one that’s been altered–but it will also have a support system of transcription factors, etc, that regulate its expression. They are all oriented now within the context of a new process, which is to provide insect resistance.”

That’s exactly the point. That’s what the concept of “irreducible complexity” is all about. The interesting fact is that your argument does not apply to the mosquito case, for the reasons already discussed: in that case, the new “diseased” gene is completely alone, there is no new “support system of transcription factors, etc, that regulate its expression”, because the regulations remain the same as before the mutation, there is nothing “oriented”, there is no “process”, there is nothing trying to “provide insect resistance”. The only “selecting” thing here is the insecticide, whose only fault is of not being able to “predict” the gene’s “disease” (but a new, well designed model certainly could…).
But your words apply perfectly to the case of a designer: it is perfectly true that any variation in a gene, any true variation which implements a new function, is perfectly meaningless unless it is managed by a coordinated system of regulation, at the transcritpion level and at many other levels. That’s why, for me, any new biological function is irreducibly complex, because the designer has to implement the effector (usually the final protein), but also, and especially, the procedure, that is the code necessary to correctly use the effector. And the procedure is usually more complex than the effector itself. May be much more complex. The procedure implies information processing, boolean checkpoints, measures, quantitative evaluations, decisions, coordination with all the other procedures, interfaces, and so on. Irreducible complexity, in its purest form.

Enough for now.

How much new information does it contain that has been generated by evolution? I don’t have the foggiest idea. But it’s more than you think it is, at least if you think that biological information is something above and beyond shannon information (You have to think that, by the way, otherwise Egnor’s question/challenge is nonsensical). Because the information differential between mosquitoVersion1 and mosquitoVersion2 is more than just an amino acid change. It now *does* something different. A process is born, one involving several components. There is that gene–the one that’s been altered–but it will also have a support system of transcription factors, etc, that regulate its expression. They are all oriented now within the context of a new process, which is to provide insect resistance. To accurately assess the information attained by that single amino acid change, we’ll have to weigh in the added information value of the specification of “mechanism of insecticide resistance” and however that breaks down into primitive components. We haven’t really been told how to do that exactly.

Most evolutionary changes are probably similar in kind to this in nature. The material substrate change is modest, but the “interpretation” of the substrate change by nature may or not be more dramatic. It’s like that optical illusion where two faces are staring at each other. Or maybe it’s a single vase, depending on what you saw first. Sometimes you see it one way, sometimes another. You might add a little splotch for an eyespot, though, and suddenly the faces image is impossible to not see. It’s the context **in your mind** that matters. The interpretation. And here the weird thing is that the interpreter is nature itself. Mutations in the organism are (I’m currently trying to flush out this analogy more in the near future, so bear with me) a sort of Rorschach text for nature itself. What patterns are in the mind of nature that determines what it sees and how it interprets the splotches? The patterns consist of the complex fitness landscape that I am always ranting about here. That is the “mind,” if you will, of nature. It is the landscape of possibilities it can “imagine” as being viable. The landscape we don’t understand it well enough to even begin to calculate something like CSI, even if such a thing could be calculated. That is why Egnor’s question can’t be answered in the fashion that he demands.

But we know when a new feature or process has been generated. And evolution conferring a resistance to a pesticide is a positive instance of some kind of increase of *something.* I can’t tell you the magnitude of that something, but I’m confident that you can’t either. So, in light of the fact that formal calculations are impossible to make, and in light of the fact that the timescales involved for things potentially more interesting can’t be observed–and you know if he tried to argue by reconstructing historical data, everyone’d cry foul b/c maybe agency was involved back then or something–I think Myers’ answer is among the best possible among these constraints.

Let’s wait for that onward thread . . . and let’s note where it is here whenever it appears.

You make an interesting note:

the concept itself of body plan in multicellular beings is almost inconceivable if not in terms of design. One of the interesting aspects of the body plan (indeed, plan!), meaning not only the general form of the body, but also the detailed spacial and functional organization of parts at many levels and sublevels, of segments in the body, of organs in the body parts, of subparts in each organ, and so on…, is that nobody can say where it is written . . . . mutations in the homeobox genes certainly can macroscopically derange the normal order of gross body parts, but that does not mean that homeobox genes are the repository of the body plan. [I]t seems obvious that the realization of a complex macroscopic body plan, realized by coordinating the growth, differentiation and spacial placement of billions of individual cells, cannot be realized unless a tremendous work of regulation, control, error management, continuos transcription fine tuning, and so on, is accomplished under the guide of precise information about the final result to be obtained.

This is indeed a major issue, especially in light of the point made by Meyer through citing McDonald:

McDonald notes that genes that are observed to vary within natural populations do not lead to major adaptive changes, while genes that could cause major changes–the very stuff of macroevolution–apparently do not vary. In other words, mutations of the kind that macroevolution doesn’t need (namely, viable genetic mutations in DNA expressed late in development) do occur, but those that it does need (namely, beneficial body plan mutations expressed early in development) apparently don’t occur.6

We are dealing with highly complex, tightly integrated, functional processes that are seriously information-driven, and information-controlled [error detection ands correction . . .]. the architecture of the information system we see in outline before us, the languages used to code the software side, the nanotechnology of the genetic and related functional molecules, the fact that this constitutes a self-replicating automaton, etc etc all point to vast informational complexity and finely balanced coupling [finetuning . . .]

When I work with telecommunication or information-pocessing devices, systems and networks, and see similar coupling, integration and complexity — in some cases they are species within the same genus [two state digital bit strings in RAM or on hard drives, four state digital GCAT strings in DNA, etc.] – save that the life systems are vastly more sophisticated – I cannot consistently infer to design in the one case and dismiss design in the other just because it is not in line with the views and agendas of certain key individuals and institutions. I refuse to swallow a camel whilst straining out gnats.

So, let us see what the onward discussion brings out. And, it is indeed a pleasure to discuss with Great_Ape, as he has been both civil and serious. Kudos to him. (I would indeed like to see his answer . . .)

All the best

GEM of TKI