` Today, the internet.
` Tomorrow....

` Drinks for everybody! (Stay away from the red, fizzy stuff, though: It ain't wine.)
I hope you enjoy your visit. If my experiments fail, you won't be leaving.
I suppose if youre looking to maintain simplistic explanations then applying Ockham's Razor is the way to go. The problem with applying it, seems to me to automatically bias one from considering a more complex solution. Ockham's Razor is about playing probabilities based on "available" evidence. Which is basically what science needs to adhere to so it doesnt play a game of speculation. Just because applying the Razor with todays available evidence points to not needing an intelligent source, it should not block our mind from possibilities thus biasing further research.` If you are talking about further research of Intelligent Design, it does not: If there is evidence for such a thing, Ockham’s Razor will tell you; ‘Oh, evidently, Darwinian evolution cannot explain this bit, and so it would be very important for biologists to test for it and, if confirmed, use that as an assumption in their experiments to see if they make more sense’ and so on. Only then could an alternate theory of evolution or even something called a ‘Theory of Intelligent Design’ be developed.
As a follower of science i recognise human limitations on researching an intelligent source and therefore i tend to just state "we just dont know"...as opposed to the more rigid " its too complex a solution and theres no need to even consider it".` Despite your own personal impression, the scientific opinion actually is that we don’t know if there’s an intelligent creator – there is simply no evidence (so far) to support that it exists. That’s the thing with being a skeptic – you suspend judgement until there is hard evidence.
Lets say we humans finally get around to really advanced stage in artificial intelligence field and begin making robots that design and make other robots. A few million years from now a scientist comes upon one of these robots traveling through space. Hes going to study this robot and see its amazing capabilities at regeneration. Hes going to study this advanced robot and see its evolved state of being biologically driven creatures like ourselves, instead of the nuts , bolts and electricly driven machine we began with. Hes then going to apply Ockham's Razor principle and conclude this robot creature had no intelligent source before it? Only problem is he would be wrong.` Of course. However, the robots are already evolving on their own. So, that part needs no intervention. There is no evidence that robots – at least anything we would recognize as robots – could arise on their own. You might speculate that futuristic robots with cellular structures might hypothetically evolve on planets that are full of whatever materials they’re made of.
We have to be careful to guard against thinking science offers us certainties when in fact it can only offer us probabilities. We have to be careful in discounting ideas that surpass current scientific capabilities. The wonders of science should humble us to possibilities, not bias us with rigid dogma.` Which is why the object of science is to avoid dogma: It is carefully constructed to catch anything that has greater explanatory power than what may be currently accepted. That is why scientific ideas are tentative and provisionary – any theory that is consistently found to have superior explanatory power compared to a prevailing theory will inevitably replace it.
You say you dont want to teach kids to "not break the rules" and steer clear of "complete contradictions". Maybe if Albert Einstein had been "taught" a little more he would have just been known as a pretty good patent clerk.` You would most certainly not have said that about Einstein if you had understood what ‘rules’ and ‘contradictions’ I was referring to.
Speaking of skeptics -- I'm skeptical of YOU, Spoony. I think it takes a vastly bigger leap of faith NOT to believe in a creator and to declare the whole universe a giant cosmic accident than it does to believe in intelligent design.` Since you say you’re so skeptical of what I have to say, then why not try to refute it using skepticism? Seriously, can you please tell me how it takes a leap of faith to not have faith? According to your own apparent definition, there can’t be a way to not have faith in anything!
NOT having a religion does in fact create its own system of religious thinking. When you say “there are no absolutes”, logically, that single belief in and of itself becomes your absolute!` A seeming paradox I suppose, largely due to the way language is constructed. Just as paradoxical, I suppose, as the fact that everything in the world constantly changes, except for the fact that everything constantly changes.
If you admit that there ARE in fact absolutes of some kind– natural laws if you will, your belief in those rules becomes eerily similar to embracing a religion, because your belief does in fact govern your behavior and the way that you live your life!` What do you mean? Are you talking about the laws of nature? In all practicality, natural laws (such as the Laws of Motion) are valid, and as far as anyone can tell, they have not changed much over time.
Darwinian theory admittedly accounts for a number of modern changes. Mutant bacteria thrive when they become increasingly resistant to antibiotics. Scientists have clearly demonstrated that the median beak size of Galapagos finches has changed in response to changing weather patterns. Similarly, the ratio of light to dark-colored moths in England shifted when pollution made lighter-colored moths more clearly visible to predators. These are certainly clear examples of natural selection in the works.` Earth to Dawn: There is no proof of atomic theory, either! Does that mean you reject the concept of atoms? Besides, there is much more evidence for modern evolutionary theory than atomic theory!
However, these specific examples demonstrate only one or a few mutations, and the resulting mutant organism is not all that different from its ancestor. In contrast, to account for the very existence all of life, an endless series of mutations would have to have produced vastly different types of creatures from a common source. I’ve seen no clear proof of that, or even reasonably compelling evidence.
Also, Darwin's theory hits a brick wall when it comes to explaining the development of cellular systems.` This merely reflects such a suppression, some of which you will see demonstrated shortly.
There are a good number of cells that are irreducibly complicated in their design – in other words, they need several components in place before they can function AT ALL, even minimally.` That would make sense only if we were machines. Which we aren’t. And I know you're not assuming that we are.
For the more simple minded – an everyday life example of irreducible complexity is a common mousetrap, built with several components – base, hammer, spring, etc. It is impossible to kill a mouse with just the base of the trap -- all the components have to be in place before it is capable of catching any mice.` This is not a valid analogy, as a mousetrap does not develop, nor does it reproduce, nor does it have eccentrically over-complicated and redundant mechanisms that could potentially be changed with the mutation of offspring.
...Which part could be missing and still allow you to catch a mouse? If the wooden base were gone, there would be no platform for attaching the other components.` What about the floor? The components would still work if they were attached to the floor! Though, what did he have to say to that?
That’s an interesting reply, but you've just substituted another wooden base for the one you were given. The trap still can't function without a base.` Of course, he’s missing the point – a mousetrap can function whether or not it is reliant on its ‘natural environment’ for a base. Not noticing this alternative is somewhat like saying a pig would overheat and die in the summer because it has no sweat glands. In fact, pigs are reliant on their natural environment for sunblock and cooling-off by seeking out mud and water. (Hippos, however, do have such protective secretions, and are therefore probably superior in this manner.)
Just one example of what I understand to be an irreducibly complex cellular system is the flagellum of some bacteria -- the flagellum requires a number of cellular components before it works -- a stator, rotor, and motor. Furthermore, I’ve also read reports that have shown that around 40 various kinds of proteins are found in a working flagellum. I’ve never seen a sufficient explanation for the evolution of a flagellum based upon Darwinian theory.` Of course you haven’t; you’ve been getting your information from people like Michael Behe, who – for one thing – admitted in court that he hasn’t read much about the subject.
‘For nearly than a century and a half, one of the classic ways to argue against evolution has been to point to an exceptionally complex and intricate structure and then to challenge an evolutionist to "evolve this!"` Which you are quite familiar with, evidently: Like a complex machine, Behe contends that any hypothetical intermediate stages of a complex system would not be functional, and so could not be selected for. Therefore, it is impossible to come up with a realistic explanation!
` As [Behe] realizes, however, the mere existence of structures and pathways that have not yet been given step-by-step Darwinian explanation does not make much of a case against evolution. Critics of evolution have laid down such challenges before, only to seem them backfire when new scientific work provided exactly the evidence they had demanded.
` Behe himself once made a similar claim when he challenged evolutionists to produce transitional fossils linking the first fossil whales with their supposed land-based ancestors (Behe 1994: 61). Ironically, not one, not two, but three transitional species between whales and land-dwelling Eocene mammals had been discovered by the end of 1994 when his challenge was published (Gould 1994: 8-15).
` Given that the business of science is to provide and test explanations, the fact that there are a few things that have, as yet, no published evolutionary explanations is not much of an argument against Darwin.
` Rather, it means that the field is still active, vital, and filled with scientific challenges. Behe realizes this, and therefore his principal claim for design is quite different. He observes, quite correctly, that science has not explained the evolution of the bacterial flagellum, but then he goes one step further. No such explanation is even possible, according to Behe. Why? Because the flagellum has a characteristic that Behe calls "irreducible complexity."’
If you believed Michael Behe's assertion that biochemical machines were irreducibly complex, you might never bother to check.... Musser and Chan did check, and found that two of the six proteins in the proton pump were quite similar to a bacteria enzyme known as the cytochrome bo3 complex. Could this mean that part of the proton pump evolved from a working cytochrome bo3 complex? Certainly.` So, there are actual, known small, working mechanical assemblies that can be combined into larger assemblies, which can be, in turn, combined into yet larger ones? Behe, on the other hand, completely ignores the possibility of such existing structures and insists that the whole thing would have to be assembled from individual units all at once.
` ...[There are] modern organisms that have full, working versions of the cytochrome bo3 complex. Can we make the same argument for the rest of the pump? Well, it turns out that each of the pump's major parts is closely related to working protein complexes found in microorganisms. Evolution assembles complex biochemical machines, as Musser and Chan proposed, from smaller working assemblies that are adapted to fit novel functions. The multiple parts of complex biochemical machines are themselves assembled from smaller, working machines developed by natural selection, as shown in Figure 2
If it is correct, then we should be unable to find examples of functional cilia anywhere in nature that lack the cilium's basic parts. Unfortunately for the argument, that is not the case. Nature presents many examples of fully-functional cilia that are missing key parts. One of the most compelling is the eel sperm flagellum (Figure 3), which lacks at least three important parts normally found in the cilium: the central doublet, central spokes, and the dynein outer arm (Wooley 1997).....` In other words, by looking at the real world, Behe’s statement that such elements of cilia are nonfunctional on their own is demonstrably false.
` The key element of the claim was that: ".. any precursor to an irreducibly complex system that is missing a part is by definition nonfunctional." But the individual parts of the cilium, including tubulin, the motor protein dynein, and the contractile protein actin are fully-functional elsewhere in the cell. What this means, of course, is that a selectable function exists for each of the major parts of the cilium, and therefore that the argument is wrong.
To begin with, there is more than one type of "bacterial flagellum." Flagella found in the archaebacteria are clearly not irreducibly complex. Recent research has shown that the flagellar proteins of these organisms are closely related to a group of cell surface proteins known as the Class IV pilins (Jarrel et al 1996) Since these proteins have a well-defined function that is not related to motility, the archael flagella fail the test of irreducible complexity.` In addition, it should be obvious now that ID proponents generally do not acknowledge the idea that a biological component could evolve for one purpose and later be used for another. In other words, they assume that, just because something performs some function, it would have had to evolve for that purpose alone.
` Clearly, when he speaks of the bacterial flagellum, Behe refers to flagella found in the eubacteria. Representations of eubacterial flagella appear in Darwin's Black Box (Behe 1996a: 71) and have been used by Dr. Behe in a number of public presentations. Surely these structures must fit the test of irreducible complexity? Ironically, they don't.
` In 1998 the flagella of eubacteria were discovered to be closely related to a non-motile cell membrane complex known as the Type III secretory apparatus (Heuck 1998) These complexes play a deadly role in the cytotoxic (cell-killing) activities of bacteria such as Yersinia pestis, the bacterium that causes bubonic plague. When these bacteria infect an organism, bacteria cells bind to host cells, and then pump toxins directly through the secretory apparatus into the host cytoplasm. Efforts to understand the deadly effects of these bacteria on their hosts led to molecular studies of the proteins in the Type III apparatus, and it quickly became apparent that at least 10 of them are homologous to proteins which form part of the base of the bacterial flagellum (Heuck 1998: 410).
` This means that a portion of the whip-like bacterial flagellum functions as the "syringe" that makes up the Type III secretory apparatus. In other words, a subset of the proteins of the flagellum is fully-functional in a completely different context – not motility, but the deadly delivery of toxins to a host cell. This observation falsifies the central claim of the biochemical argument from design – namely, that a subset of the parts of an irreducibly complex structure must be, "by definition nonfunctional." Here are 10 proteins from the flagellum which are missing not just one part but more than 40, and yet they are fully-functional in the Type III apparatus.
` In other words, various components of the flagellum are known to have a selective purpose, just as skin has an important purpose even when it is not utilizing the limbs of certain squirrels or marsupials as a gliding surface.Proteins that make up the flagellum itself are closely related to a variety of cell surface proteins, including the pilins found in a variety of bacteria. A portion of the flagellum functions as an ion channel, and ion channels are found in all bacterial cell membranes. Part of the flagellar base is functional in protein secretion, and once again, all bacteria possess membrane-bound protein secretory systems.
` Finally, the heart of the flagellum is an ion-driven rotary motor, a remarkable piece of protein machinery that converts ion movement into rotary movement that makes flagellar movement possible. Surely this part of the flagellum must be unique? Not at all. All bacteria possess a membrane protein complex known as the ATP synthase which uses ion movements to produce ATP. How does the synthase work? It uses the energy of ion movements to produce rotary motion. In short, at least four key elements of the eubacterial flagellum have other selectable functions in the cell that are unrelated to motility.
What this means, in scientific terms, is that the hypothesis of irreducible complexity is falsified. The Darwinian explanation of complex systems, however, is supported by the same facts.` Indeed, ‘the scientific community [does] not greedily embrace its startling claims’, as Behe has suggested they should, because this argument (as well as others of his) are demonstrably false. There is undeniable proof of the existence of things he claims don’t exist, the absence of which are what his entire ‘irreducibility’ is based on.
The intracellular transport systems in plant and animal cells are also extremely complicated. Cellular components including proteins and enzymes have to be transported between various cellular compartments. Some components are packaged into molecular “trucks”, and each truck has its own unique “key” that can only fit the “lock” of its cellular destination. Other types of proteins act like loading docks -- opening and dumping the contents into the compartment once the transport system has reached its destination. Of course, I’m simplifying this and am speaking in lay terms. It reality, it is all much more complex than this.` Yes, I am not ignorant of these facts. Are you suggesting that this is too complicated to have evolved, just because you cannot imagine this happening? A few IDists have written on such subjects, suggesting that it cannot. For example, Lee Spetner has written all about how ligands and receptors could not possibly evolve because, he says, evolution cannot produce new information. It sounds like you are familiar with his work.
It is interesting that in a book supposedly about information theory, the classic formulation of information theory of Shannon and Weaver (2) does not get mentioned.` Yes, quite interesting! It turns out that most people who are attempting to discredit evolution also ignore this most important tool.
In this review I will consider if Spetner's metrics can be validly applied to biology, and how Spetner actually applies them to real world examples. Although his arguments are superficially plausible, a closer look with some knowledge of biochemistry shows significant flaws. I will first briefly describe Spetner's metric of information, I will then show that 1) Spetner's metrics depend on a binding mechanism that does not occur in nature, 2) that Spetner's metrics require that substances bind to enzymes in an all or nothing fashion, whereas real substrates do not bind in this way. Furthermore, I will show that Spetner himself is inconsistent in his application of his metrics. In his Xylitol example he does not actually use the measure he develops, and in the streptomycin example he swaps to a different metric, when his original metric would show increased information. Finally, I will show that his "directed evolution" model is based on a misunderstanding of one form of random mutation.` So, first of all, Spetner’s binding mechanism that he says must be designed does not actually exist.
...[I]t might seem intuitively obvious that a more specific lock accepting only one key has more information a less specific lock which accepts many keys. This is actually incorrect, but rather than go into this here see this paper on cryptography and master keys.... For the moment we will accept this though.` And, of course, he goes on to explain in what way biology does work, if you would be so interested to learn.
` Analogously we might expect an enzyme is more specific because it has more binding points than an enzyme that is less specific (and there is also the unstated assumption that single substrate enzymes are more important than multi substrate enzymes. They are not).
For example we might imagine an active site that uses 4 binding points has more information than one with two binding points.... Unfortunately, biology doesn't work that way.
...in the real world the binding of a ligand to a protein is not an all or nothing affair, substrates have varying degrees of "stickyness", which is not addressed by Spetner's metric. Even a very specific enzyme will bind one ligand very tightly, a few not so tightly, and a great number very weakly. One cannot simply say that only very strongly bound ligands will be considered, as very weak ligands may be of great physiological importance, if they are present in a high enough concentration.... This has a theoretical and a practical implication....` Which Musgrave then explains, if you should be so curious.
Note that the amino [acids] are in different positions in the different receptors... partly because the AT2 receptor has a longer C-terminus, and also due to an insertion into the sequence between N and K and between K and H in the AT2 receptor. [There are illustrations here to help people from getting lost.] Thus the concept of "precise sequence" is not exactly applicable to receptor binding. The amino acids are [brought] close (but not into a linear sequence, more like a ring) by the three dimensional folding of the proteins, and this three dimensional folding is [brought] about by very different sequences.` Again, what Spetner says might make intuitive sense, but it does not match up to the real world. Indeed, modeling proteins after words is not a very accurate way to describe them:
` This is problematic for Spetner's claims, as the sequence DNKH depends on a number of factors that are NOT dependent on that sequence, thus the "true" information content is not reflected by the binding sequence alone. Again note that the three dimensional folding is not rigid, and flips between a number of different states (Protein chains are somewhat flexible, more like a ball of semi-cooked spaghetti than the rigid shapes they are sometimes drawn as, thus enzymes and receptors are "floppy" locks and ligands are "floppy" keys: this is relevant to Spetner's claims, more later)
Broadly analogous to ghtshi-lightship "binding". F actually binds to both K and H. This is mostly electrostatic interactions rather than the physical "bumps and hollows" Spetner uses in his (incorrect) analogy for streptomycin binding. The basic amino acid R binds electrostatically to the acidic amino acid D, Y and N form hydrogen bonds and F forms a pi bond with H, and a hydrogen bond with Y. (In SarAsp, the acidic D interacts with the acidic D, but dipole charge distribution means that they bind rather than repel. Chemistry and common sense do NOT go well together. (5,6))` After this, he then goes on to address the fact that the length of the binding string is not actually related to the number of ligands.
` But as we look at SarIle and SarAsp, we can see Spetner's model of binding is going badly wrong....
So, what happens when we shorten the binding string DNKH. According to Spetner's model, you should increase the number of ligands bound. We can mutate the amino acid H to A (alanine), Q (glutamine) or R (arginine). The Q mutation keeps charge and size, but loses the pi bonding, the R mutation keeps the charge, the A mutation loses charge and size, thus mutations from H to R and A are like truncating the binding string to DNK. In the AT1 receptor, the binding doesn't change with any of these mutations. When we mutate H to Q or R in the AT2 receptor, all binding is lost (7,8). Either way, Spetner's model is dead wrong about what happens when the "string length" of a ligand binding string is shortened (and this again invalidates his measure).` What is going on here is that Spetner has insisted that the substrate number corresponds to the amount of information in the proteins. Musgrave is explaining that nature does not function in this way.
` Even worse, what happens when you mutate N in DNKH (Asparagine at position 111 in the AT1 receptor and position 126 in the AT2 receptor)? If you mutate N to G (glycine) a very short neutral amino acid, unlike the longer charged asparagine, there is no contact with the ligand and the G, so the binding sitestring becomes DKH. Despite this truncation, you still bind AII, AIII, etc., but AIV has become "stickier"(something which Spetner doesn't actually address in his metric). As I mentioned before, the AT receptors flop between several conformational shapes. The N->G mutation restricts the receptor to fewer conformational shapes, making it MORE specific....
` Thus binding is a critical function of 3D shape, not covered by Spetner's metric, and a single mutation can increase specificity (as according to Spetner's criteria, a protein that has one conformational shape has more specificity than one with multiple conformational shapes).
He does consider a biochemical measure called specificity, but this is not Spetner's specificity measure.... Critically, two substrates can have the same binding specificity, but different catalytic efficacy which confounds the information analysis.` He goes on and on and on about everything in this experiment, from Spetner’s irrelevant measuring practices to filling in information that was completely glossed over – in light of which Spetner’s arguments make no sense.
...If you exclude a lock and key binding allosteric modulator of enzyme action like streptomycin from consideration, then you are ignoring biology.` Indeed; Spetner seems unusually fond of doing that....
Streptomycin-binding ribosomes turn out garbage proteins because streptomycin messes up the proof-reading centre (which is how streptomycin kills bacteria). The mutant version which doesn't bind streptomycin is actually MORE accurate, i.e. more SPECIFIC, than the wild type. The wild-type proof reading centre makes a few mistakes even in the absence of streptomycin, and the mutant forms make even fewer mistakes than the wild type( roughly 85% fewer; 12).` Does this not sound the least bit intriguing to you? And, as for mutations which supposedly imply a driving force behind them:
This is a clear increase in Spetner's binding specificity:1 - The mutant gene product doesn't bind streptomycin at all (it has one ligand rather than two)Does Spetner acknowledge this? No, Spetner now swaps to the expectation measure and claims (without evidence) that since there must be more S12 sequences that don't bind streptomycin than those that do, information must have decreased (why didn't he do this analysis on the ribulose enzyme?).
2 - It binds the substrate peptidyl tRNA more accurately
3 - It catalyses more accurate peptide synthesis.
However, he is dead wrong....
The apparent existence of "directed" mutations was based on some early work by Barry Hall. However, Spetner did not follow up the more recent research on this work, and misunderstands the origin and significance of "directed" mutations.` Which are henceforth known as “Fred.”
"Fred" occurs only under non-lethal selection in non-dividing cells, and has been suggested to be a neo-Lamarkian mechanism for getting environmental information into the genes. However, "Fred" is no such thing (16,17,18), and is not directed in the sense that Spetner suggests....` Indeed, he goes right ahead and shows a real-world instance of this. If you'd like to actually read this article, it is here for the viewing! And, if you take issue with Musgrave, go complain to him on his blog! (Actually, a much more constructive place to get his attention is The Panda's Thumb. It's fun!)
` ...So the following model shows how "adaptive" mutations occur. Nutritionally deprived non-growing cells are under stress, stress leads to double stranded breaks in the DNA, recombination vis RecBCD primes the DNA synthesis, DNA PolIII finishes the job but makes mistakes, which slip through because starvation has largely turned off mismatch repair. This results in genome wide mutation at a faster rate than normal, and the occasional mutant that can utilize the "selective" substrate (16,17,18).
A wide variety of other examples could be cited, but this isn’t MY blog.` And, so far as I have seen, those are also just as easily refuted.
What is boils down to is that even cells -- the most basic ingredient in life -- are breathtakingly complex.` Biologists are well aware of this breathtaking complexity, as well as the fact that cells are also assembled rather haphazardly, full of closely-related structural ‘copies’ that do different things, other parts that are atrophied into uselessness, and generally full of lots of little extraneous molecular bits which do not inhibit functioning when removed from the system. (In fact, they only seem to get in the way!)
James Shapiro, a professor of biochemistry at the University of Chicago, once wrote, "There are no detailed Darwinian accounts for the evolution of any fundamental biochemical or cellular system, only a variety of wishful speculations." I would have to agree with him.` True, he says this although did you know that he does not find any evidence for Intelligent Design, either? Besides, the fact that he’s a scientist is no reason to take him seriously. That’s what objectivity is needed for!
Scientists have on occasion suggested non-Darwinian theories to account for the origins of the cell, but I don't find any of them the least bit convincing. Instead, I find it most likely that the complex systems were in fact deliberately designed. I’ve seen no evidence of another mechanism aside from deliberate design, including Darwin's theory of evolution, which is capable of producing that kind of complexity.` Non-Darwinian accounts of the cell? I'm not even going to get into that. So far as I see, you are so completely hung up on complexity even though you do not seem to know what it is. High levels of complexity do not necessitate a designer in many cases; an overly-simple example is the fact that a naturally-forming crystal is a much more complex structure than a crystal ball that has been ground and polished by humans; yet, which was constructed with an intent?
If scientists demonstrated that bacteria without a flagellum could systematically evolve such a feature, or evolve any new structure of comparative complexity, my system of thought would be called into question. But so far, this hasn’t happened, and I doubt that it ever will.` And of course, I have directed you to a few articles which do indeed demonstrate both the scientific principles behind flagellum evolution as well as at least one possible way it could have come about: Just because Behe is ignorant of such research does not mean that you have to be.
But, I AM open-minded, and my belief in a creator doesn’t mean that I am unable to consider that this creator might have used mechanisms that I hadn’t considered to do the creating.` Here is one thing I hope you are willing to consider: Intelligent Design proponents don’t care about scientific accuracy as long as they succeed in making Christianity a part of science in the public eye.