Bill Dembski and the case of the unsupported assertion

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While ID ‘scientists’ vociferously object to being labeled creationists, they share one notable feature with the creation scientists of the 80s: their frequent use of discredited sources. In a 1983 PBS special, Duane Gish of the Institute for Creation Research (ICR), a YEC institution, claimed that certain human proteins were more similar to bullfrog proteins than chimpanzee homologues, a claim that would be nearly inexplicable if our current understanding of evolution was correct. However, despite countless public and private requests spanning the last 20 years, Gish has never provided a source for that claim, nor retracted it (see here for more). A few years ago, Bill Dembski claimed that there was evidence of a biochemical system for which any slight modification would not only destroy the system’s current function, but any possible function of that system whatsoever. He concluded that such a system could not have evolved through ‘Darwinian’ evolution, because of the supposed lack of functional intermediates between the current system and any hypothetical precursor. However, as I document in this post, not only is Dembski’s claim unsupported by his lone source, Dembski admits this, and yet he continues to assert that claim, even strengthening it in recent writings. One of those writings was even published in the IDists’ “peer-reviewed” journal PCID, despite the editors’ knowledge that this claim was unsupported. The intention of this blog entry is to add yet another example to the list of shoddy scholarship inherent in IDist writings.

The intelligent design argument basically consists of two parts. The first is the claim that evolution cannot explain the origin of certain features of life. The second is that “intelligence” can, and therefore serves as a better explanation for the origin of those features. In his 1996 book Darwin’s Black Box, Michael Behe made the first half of the argument regarding irreducibly complex (IC) biochemical systems, which are supposedly so complex that they defy evolutionary explanation. Because Behe felt there were no “detailed, testable models” to explain the origin of IC systems, no such explanations were possible. While detailed, testable models for the origin of IC systems already existed prior to DBB, and even more have emerged since its publication, IDists reject those explanations as not being detailed or testable enough for their satisfaction (see the Talkdesign article ID demystified for a more thorough analysis). Even if we took this argument at face value, it still suffers from a major oversight. Just because there’s no known natural mechanism for the origin of IC systems now, doesn’t necessarily mean there won’t be any in the future. In other words, absence of evidence is not evidence of absence. Commonly referred to as the appeal to ignorance, this fallacy is extremely important to the intelligent design argument because there is no evidentiary support for intelligent design (like, say, evidence of a designer). However, it is very easy for even a beginning biology grad student to propose a hypothetical model for the origin of an IC system. What IDists needed to keep this argument from being fallacious was a way to not only eliminate known natural mechanisms, but also unknown ones as well. In describing his October 2002 article, “The Logical Underpinnings of ID”, Bill Dembski made such a claim:

I also note that there can be cases where all material mechanisms (known and unknown) can be precluded decisively.

The relevant section is on page 20, where he writes:

But there is now mounting evidence of biological systems for which any slight modification does not merely destroy the system’s existing function, but also destroys the possibility of any function of the system whatsoever (Axe, 2000). For such systems, neither direct nor indirect Darwinian pathways could account for them. In that case we would be dealing with an in-principle argument showing not merely that no known material mechanism is capable of accounting for the system but also that any unknown material mechanism is incapable of accounting for it as well.

Wow, that’s a pretty bold claim. This assertion, if true, might be considered pretty damning evidence against evolution. However, Dembski offers only a single citation to back this claim, a 2000 Journal of Molecular Biology paper by Douglas Axe entitled, “Extreme Functional Sensitivity to Conservative Amino Acid Changes on Enzyme Exteriors”. Does this article really support Dembski’s claim? Not even close.

Summary of Axe 2000 In the article, Axe reports the results of a series of mutagenesis experiments, focusing primarily on the TEM-1 gene, a bacterial beta-lactamase that confers resistance to the antibiotics penicillin and ampicillin. Axe made conservative amino acid substitutions to residues on the exterior of this protein. Conservative substitutions are ones that exchange an amino acid for another with the same basic shape and charge (e.g. leucine to isoleucine, arginine to lysine). Additionally, because those residues are outside of the active site, they are not considered to have an effect on the activity of a protein. Therefore, evolutionary theory would predict that those residues could switch to other similar amino acids via neutral evolution. Axe tested this prediction by making an increasing number of conservative substitutions to see how many the protein could tolerate while still retaining function. He made four groups of substitutions (blaM, blaY, blaG, and blaB), with 10 substitutions in each group. Here are the results, in his own words:

The single-group substitutions in blaM, blaY, and blaG affect function only mildly, yet these substitutions result in >99% inactivation when combined.

Only the combination of all four groups resulted in the complete inactivation of the protein’s activity. Based on these experiments, Axe concluded that the exterior residues of a protein are more sensitive to conservative substitutions than previously thought.

Let’s compare this to Dembski’s interpretation:

any slight modification does not merely destroy the system’s existing function, but also destroys the possibility of any function of the system whatsoever.

On at least four levels Dembski’s conclusion regarding the Axe paper is completely and utterly wrong.

1. Any slight modification destroys the function of the system. (note that I’m paraphrasing Dembski)

All of the single-group substitutions retained their beta-lactamase activity. Only when they were combined into triple and quadruple group mutations was activity abolished. So clearly there were modifications that did not destroy the function of the system.

2. Any slight modification destroys the function of the system.

As previously mentioned, at least 30 substitutions were required to reduce activity greater than 99%, and 40 mutations to completely abolish it. This amounts to about 20% of the exterior residues, or 10% of the total protein. This can hardly be considered “slight”, by any definition of the word. One substitution would be considered slight, not 30 to 40. This is not just a semantic quibble, as the changes that occur during the course of gradual, �Darwinian’ evolution occur one substitution at a time (except in cases of recombination and exon shuffling).

3. Any slight modification does not merely destroy the system’s existing function, but also destroys the possibility of any function of the system whatsoever.

I don’t know how Dembski can claim that the mutations destroyed other functions of the system, since Axe never tested for other functions. This is basically an appeal to ignorance. However, as it turns out, another group analyzed mutations in the active site of the exact same gene (TEM-1) and found that certain “slight modifications” drastically reduced the original function of the system (penicillin and ampicillin resistance), but increased a separate, distinct function (cephalosporin resistance). In their words:

When purified, mutant enzymes had increased activity against cephalosporin antibiotics but lost both thermodynamic stability and kinetic activity against their ancestral targets, penicillins.

(It should be noted that these researchers studied mutations within the active site, whereas Axe made mutations on the exterior of the protein.) So contrary to Dembski’s claim, mutations that result in the loss of the original function do not necessarily cause the loss of any possible function. This is significant because a major contention of Dembski’s is that protein sequences that contain a function are completely isolated from one another, such that random mutation cannot create one functional protein from another without passing through a non-functional state. However, recent research has shown that oftentimes mutations can increase the activity of a new function of a protein without seriously hindering the protein’s original function, a concept known as promiscuity. Steve Reuland has blogged this topic here.

4. Any slight modification does not merely destroy the system’s existing function, but also destroys the possibility of any function of the system whatsoever.

This point is a little confusing, but if you read Dembski’s claim as a whole, you can infer what I think Dembski is really trying to get at. There are some mutations that can completely destroy a protein’s function. Nonsense mutations, whereby a codon is mutated into a stop codon, creating a truncated protein, is one example. However, many truncated proteins still retain some function. Frameshift mutations, where a nucleotide is either inserted or deleted from the gene, altering its reading frame, more often than not leads to a nonfunctional protein (for example, trying shifting your hand one key to the right and typing a sentence). However, I think what Dembski is trying to claim is a third possibility, that certain single amino acid substitutions can drastically affect the stability of the protein. If, at a key residue, a charged amino acid is substituted for a nonpolar one, or vice versa, this could lead to the inability of the protein to fold properly and rendering it useless. In this case, you could say the mutation destroyed all possibility of function. However, this is a rare event (I can’t think of an example), and certainly not demonstrated in the Axe paper. For Dembski’s claim to be accurate, he would need to find a protein for which all mutations catastrophically disrupt the stability of the protein. Axe never found a single catastrophic mutation in TEM-1, but plenty of non-catastrophic ones.

Each of these errors by themselves is enough to derail Dembski’s conclusion. Furthermore, each of the four points is absolutely necessary for Dembski to make the conclusion “not merely that no known material mechanism is capable of accounting for the system but also that any unknown material mechanism is incapable of accounting for it as well”. Taken together, these errors demonstrate that either Dembski really doesn’t understand the evidence, or that he is willfully misinterpreting it. While Dembski is not a biologist, and frequently makes claims regarding biology that display a fundamental lack of understanding of the field (see this thread for an example), I’m more inclined toward the latter. In fairness to Axe, his research wasn’t even about Darwinian evolution or the origin of new protein functions. Rather, he focused on the amount of “drift” a protein’s exterior can endure while still retaining function, which is an issue of neutral evolution. In fact, Axe, when asked directly whether his work supports Dembski’s conclusions, remained neutral on the topic, despite the fact that his research was supported in part by funding from the DI, and he was a senior fellow of the DI. Here are his own words, as said in Forrest and Gross’ Creationism’s Trojan Horse [1]:

These three statements summarize my position:

  • I remain open-minded with respect to the possibility that a sound argument can be made for intelligent design in biology.
  • I have not attempted to make such an argument in any publications.
  • Since I understand that Bill Dembski has referred to my work in making such an argument, I shall remain open to the possibility that my published findings may support such an inference until I have had a chance to see his argument.

See Trojan Horse if you want to read more about Axe’s association with the DI.

Calling Dembski’s bluff When Dembski first announced his “Logical Underpinnings of ID” article on the ISCID forum in November 2002, ID critics immediately pounced on him for making such an unsupported claim. After repeatedly hounding him, Dembski finally conceded:

I met with Douglas Axe at the recent RAPID conference and I’ve had a preview of where his research is going for some time (at least since the summer of 2000), so in reading his JMB paper, I’m anticipating where’s he’s going. I agree that the JMB paper does not resolve the issues we are debating. That’s why I put it in terms of “preliminary indications.”

(boldface added for emphasis)

So essentially Dembski agreed that his claim was unsupported by the Axe paper. Is it ethical to make an assertion using a reference that you know does not support it? Ironically, one ISCID forum participant, “charlie_d” commented,

Hopefully, this very basic mistake will now cease to find its way into ID literature.

Unfortunately, he was very much mistaken.

Nearly a year later, in September 2003, Dembski again mentions the Axe paper, this time in an FAQ entitled, “Three Frequently Asked Questions About Intelligent Design”, as an example of research supporting intelligent design in the peer-reviewed literature.

This work shows that certain enzymes are extremely sensitive to perturbation. Perturbation in this case does not simply diminish existing function or alter function, but removes all possibility of function. This implies that neo-Darwinian theory has no purchase on these systems.

Not only does Dembski not soften his interpretation of the paper, he no longer bothers to qualify it as a “preliminary indication”. He did remove the “any slight modification” phrase, replacing it with the more nebulous “perturbation”. However, I don’t think readers will assume that perturbation means “30 to 40 amino acid substitutions”, especially considering that “neo-Darwinian theory” does not propose that proteins evolve 30 to 40 mutations at a time.

In January 2004, Dembski submitted another article for publication on ISCID’s online journal PCID. This article, titled “Irreducible Complexity Revisted”, purported to clarify the IC argument with greater scientific detail. Notice this passage, from page 34.

Moreover, recent work on the extreme functional sensitivity of proteins provides strong evidence that certain classes of proteins are in principle unevolvable by gradual means (and thus a fortiori by the Darwinian mechanism) because small perturbations of these proteins destroy all conceivable biological function (and not merely existing biological function).31

Yes, reference 31 is Axe 2000. Rather than tone the comment down, Dembski apparently decided to bump his claim up a notch or two. Now “preliminary indications” has evolved into “strong evidence”, and “perturbations” into “small perturbations”. Again Dembski implies that 30 amino acid substitutions is “gradual”. So even though Dembski himself admitted over a year ago that this claim was unsupported by Axe 2000, he felt no obligation to leave it out of future writings. Why correct when you can just reassert?

Articles submitted for publication on PCID often have threads created for them on the ISCID chat forum, to allow readers the opportunity to comment on the article. I was so disgusted by this article (sadly, his repeated unsupported assertion wasn’t even its biggest problem, see Mark Perakh’s PT post for more), I challenged the PCID editors (Micah Sparacio and John Bracht) to correct it in that ISCID thread.

there is at least one instance here where an erroneous interpretation, by dembski, of an article he cited that was corrected by ID critics on this very forum, was repeated again in this article. …

i think micah and john need to do some serious soul-searching and decide if this is the kind of material they want ISCID to be known for. i realize that ISCID doesn’t reject many articles, especially those submitted by their big-wigs, but if the editors of PCID want to continue to call their journal “peer-reviewed”, then they need to take responsibility for the material they present.

They certainly saw my challenge, because Micah offered this in response:

as a note, an article published in the Archive is not necessarily published in PCID. Dembski’s article, featured in this thread, has not yet been chosen for an issue of PCID.

According to their review standards, articles are first placed in the archive as a draft, where they are then subject to review by one or more of the ISCID fellows. Only after they are reviewed are they eligible for publication in PCID. Also of note is this requirement: “articles need to meet basic scholarly standards”. Sure enough, the article was published in the next issue of PCID. Was the statement citing the Axe paper removed? Nope.

Moreover, recent work on the extreme functional sensitivity of proteins provides strong evidence that certain classes of proteins are in principle unevolvable by gradual means (and thus a fortiori by the Darwinian mechanism) because small perturbations of these proteins destroy all conceivable biological function (and not merely existing biological function).31

So clearly, correctly supporting statements central to the primary focus of the article is not considered a “basic scholarly standard” for PCID.

Accountability On another thread, created solely to discuss Axe’s paper, in which PCID editor John Bracht participated in, “charlie_d” asked John this question:

what do you think about instituting internal peer-review panels?

While John did not reply, another ISCID heavyweight, Paul Nelson, said this:

I think it’s a good idea. Something more informal than Charlie’s suggestion – in the way of critical peer review – is already going on (e.g., at the recent RAPID meeting), but as the ID research community matures, it’s going to need robust internal quality controls.

So here we have an example of the robust internal quality controls displayed by the ISCID fellows. Ironically, I also made this statement when “IC Revisited” was first made public:

i think it’s safe to assume that in the coming months, this article will be added to the pile of references ID proponents cite when their ideas are questioned by school boards or the press. the next time someone brings up a specific critique of IC, some DI rep like dembski will dismiss their critique as having been answered in this article. we’ve seen it before, we’ll see it again. the purpose of all of this is to give the appearance of a controversy.

And in that same issue of PCID:

Irreducible Complexity Reduced

Dembski shows [in “Irreducible Complexity Revisited”] that this common refrain [that “Behe’s arguments have somehow been refuted”] is inaccurate at best, and that the intervening period since the publication of Darwin’s Black Box has only underscored the acute lack of any meaningful explanation for the existence of irreducibly complex systems on the basis of Darwinian principles.

Is this really the quality of scholarship we can expect from PCID? I hope that either Dembski or the PCID editors offer a correction, or at least a defense of Dembski’s continued use of this unsupported assertion. If nothing else, he should at least stop using it, since he himself admits that the source does not support his claim. While I doubt any of this will happen, at least we have a documented example of the poor scholarship that IDists display in their works.

Footnotes: 1. Forrest and Gross, Creationism’s Trojan Horse 2003, pages 40-42

(edited 2/16 to add a trackback to Mark Perakh’s post on IC revisted)

22 Comments

Good post Matt.

Moreover, recent work on the extreme functional sensitivity of proteins provides strong evidence that certain classes of proteins are in principle unevolvable by gradual means (and thus a fortiori by the Darwinian mechanism) because small perturbations of these proteins destroy all conceivable biological function (and not merely existing biological function).

I don’t know much about proteins (I’ve done a very little bit of the usual mutagenesis, sequencing, DH5alphas, purification) but that claim is highly suspect on its face, and would have to be backed up with some very serious research to even be considered. Since the cited paper shows no such thing, it can be safely dismissed. For Dembski to continue to make the claim after this has been pointed out.…I wonder sometimes, which creationists are dishonest, and which ones are just clueless. I think this post resolves that question, with regard to Dembski.

Can fiskings be epic? Apparently so…

small perturbations of these proteins destroy all conceivable biological function

I just wonder how Big Bill sleeps at night. Sane people who want to be taken seriously in their efforts to work a scientific revolution should not make such strange assertions. I’d guess that a typical undergrad biology major could sniff out the facially bogus nature of this claim in a couple seconds.

The only way I can see for Dembksi to convince anyone that he was sincere when he made the statement is if argues that when he said “conceivable” he meant “conceivable by Bill Demsbki” and not “conceivable by any creative critically thinking human being.” Or I guess he could just admit that he didn’t know what the word “conceivable” meant but it sounded impressive.

The insistence of the “ID theory” peddlers (implied or otherwise) that each biological “feature” (including proteins) has a limited, knowable and absolutely defined function or set of functions is a popular part of the script. I’ve probably seen Charlie Wagner beat that horse a dozen times. If only that were the only gaping hole in the miserable “theory”! But no, after you drive your truck through that hole, you’ve still got those mysterious alien beings who allegedly designed all this stuff. And beyond that, you’ve got male nipples and Ebola. Oy.

The self-inflicted curse of ID in this regard is trying to prove a negative (‘there is no way to …’), as they have nothing positive to show. Besides being patently inconsistent with existing data in many cases it showcases the hypocrisy of people who pretend to know the right answer in advance and now only have to eliminate all the wrong ones. Then they wonder why they just can’t do this and have to resort to rhetorical tricks to keep pretending.

But there is now mounting evidence of biological systems for which any slight modification does not merely destroy the system?s existing function, but also destroys the possibility of any function of the system whatsoever (Axe, 2000). For such systems, neither direct nor indirect Darwinian pathways could account for them.

Even if the first sentence were true, the second sentence wouldn’t follow – as with IC, the arrow of time runs in the wrong direction. It doesn’t matter whether a mousetrap fails if any part is removed or a biological system fails if modified; these don’t go to the question of whether systems could have evolved so as to result in a system in the current state.

ts’s point is important, I think, There is a gaping asymmetry between Behe’s original operational definition of “irreducible complexity” (knockout) and construction-by-evolution. I think about that now and again, and mean to write something on it one of these days but never seem to get around to it.

In addition to his repetition of the misrepresentation of Axe’s paper on the graded loss of activity of TEM-1 in response to mutations, in that same paper in PCID (Irreducible Complexity Revisited) Dembski added two new operational criteria to be met when deciding whether a given structure is IC, making three operational tests that must be passed:

To determine whether a system is irreducibly complex therefore employs two approaches: (1) An empirical analysis of the system that by removing parts (individually and in groups) and then [1a] by rearranging and adapting remaining parts determines whether the basic function can be recovered among those remaining parts. (2) A conceptual analysis of the system, and specifically of those parts whose removal renders the basic function unrecoverable, to demonstrate that no system with (substantially) fewer parts exhibits the basic function. Indispensable parts identified in step (1) and then confirmed in step (2) to admit no simplification belong to the irreducible core of an irreducibly complex system. (p. 5; “[1a]” added by RBH to identify one of the added criteria)

So according to Dembski there are now three tests for ICness, all of which must be passed:

1. Behe’s original knockout operation; 2. a demonstration “… that no system with (substantially) fewer parts exhibits the basic function” (p. 5); and 3. conceptually analyze the system such that “… by rearranging and adapting remaining parts determine … whether the basic function can be recovered among those remaining parts.”

I critiqued Dembski’s additions on ARN here and here in a thread titled “The Death of Irreducible Complexity”, and Mark Perakh extended those criticisms on PT.

Dembski responded briefly to my critique, basically saying “not so!” and by redefining the “function” of a system:

But basic function, as I define it, also includes the way in which the function is performed.

… a flagellum is still IC because

Thus, it is no simplification of the bacterial flagellum to substitute a paddle, say, that doesn’t spin, that propels the bacterium through its watery environment, and that is simpler. Any simplification of the bacterial flagellum would have to be a bidirectional motor-driven propeller.

but a three-legged stool is not IC because

Suppose the stool’s basic function is to provide a seat by means of a raised platform. In that case each of the legs is indispensable for achieving this basic function (remove any leg and the basic function can’t be recovered among the remaining parts). Nevertheless, because it’s possible for a much simpler system to exhibit this basic function (for example, a solid block), the three-legged stool is not irreducibly complex.

I suggested in my ARN critique that by Dembski’s new criteria, Behe’s iconic example of the mousetrap is no longer irreducibly complex. I wonder if he still carries it around in his briefcase.

RBH

This is the type of stuff that needs to get out to every school board in the country.

This is the type of stuff that needs to get out to every school board in the country.

If, at a key residue, a charged amino acid is substituted for a nonpolar one, or vice versa, this could lead to the inability of the protein to fold properly and rendering it useless. In this case, you could say the mutation destroyed all possibility of function. However, this is a rare event (I can’t think of an example), and certainly not demonstrated in the Axe paper.

Does the Cystic Fibrosis gene count? My recollection is that a single mutation prevents the protein from being properly inserted into the cell membrane. Since membrane proteins can’t fold properly if they aren’t in a membrane, this renders the protein functionless.

Just a point of curiosity - I’m not arguing that Dembski is correct.

Since membrane proteins can’t fold properly if they aren’t in a membrane, this renders the protein functionless.

No, it renders the protein incapable of performing one function that humans have identified which requires the “proper” insertion of the protein into the membrane. Note that “proper” merely means “the insertion that humans have observed when they look at the protein”.

Is the protein “useless” unless it’s properly inserted in the membrane?

It’s very difficult to show that a particular protein is “useless” to a cell. Why? Well, for starters, you’d need to culture the cell under a wide range of feasible conditions and show that under those conditions the protein – or any part of that protein – is incapable of performing any useful functions.

TS wrote:

Even if the first sentence were true, the second sentence wouldn’t follow — as with IC, the arrow of time runs in the wrong direction. It doesn’t matter whether a mousetrap fails if any part is removed or a biological system fails if modified; these don’t go to the question of whether systems could have evolved so as to result in a system in the current state.

This is reminiscent of an aviation phenomenon called, rather ghoulishly, ‘coffin corner’. This happens at high altitude, where the thinness of the air means the aircraft has to fly faster at a higher angle of attack to generate enough lift to stay up, but the faster airflow that this causes over the top of the wing risks something called a Mach buffet which also causes catastrophic loss of lift. So it’s possible to fly into a region where going either faster or slower will cause a stall: it’s even possible to reach the point where the two zones cross over and you’re no longer flying no matter what you do. Infamously, the U2 spy plane could do this in a turn, where one wingtip hit a stall and the other went through Mach buffet. The moral of this story is - don’t go near.

By the ID logic, if the plane can’t fly slower than it is flying then it couldn’t have flown there in the first place. I imagine the same is true of take-offs…

It is clearly possible for a system to move into a condition where it can no longer step back to a previous condition by reversing the previous change, even when this was a simple and seemingly linear process and when the two conditions are only marginally different. You must have more evidence to back up a bald statement to the contrary.

Rupert

I think this thread should be given a “sticky” and cut-and-pasted to the ID apologists (and trolls, and worse) as a blanket response when they assert that ID is valid and scientific.

Andrew, since it’s the case that a proposition can be true in spite of a faulty argument for it, I suugest something slightly different: this thread should be given a “sticky” and cut-and-pasted to the ID apologists (and trolls, and worse) as a blanket response when they assert that Bill Dembski tells the truth, or that ID carries out ‘peer review’.

by GWW: It’s very difficult to show that a particular protein is “useless” to a cell. Why? Well, for starters, you’d need to culture the cell under a wide range of feasible conditions and show that under those conditions the protein — or any part of that protein — is incapable of performing any useful functions.

I would imagine that a protein that can’t even fold would be insoluble and crash out of solution. For a protein like that, you could say all “possibility” of function was destoyed. I wouldn’t really know how to detect that, though. Is there a way to measure the half-life of a protein? Maybe a western blot would do the trick.

Alternatively, one could make a fusion of two proteins, like GFP and luciferase, and test for function following mutagenesis. If a single amino acid substitution eliminated the function of both, you might infer that the protein was unstable.

Honestly, can anyone here think of an example of a protein where one amino acid substitution renders it totally unstable and unfoldable? I can’t think of any, but there must be some out there.

also note: I added a link to Mark Perakh’s post on Dembski’s “IC Revisted”

Harry Frankfurt’s essay On Bullshit has been on my mind lately—I just happened to read it recently, and then it turns out that it’s being issued by Princeton University Press as a book, which I’ve seen mentioned on a few different blogs.

I’m probably not the first to point this out, but Frankfurt’s essay seems quite relevant to the activities of people like Dembski. It can help to answer the question of whether Dembski is incompetent or dishonest, for example. The answer is that he’s neither, exactly. He’s a bullshitter.

According to Frankfurt, the difference between a liar and a bullshitter is that the liar has at least some regard for the truth (“A person who lies is thereby responding to the truth, and he is to that extent respectful of it”), while the bullshitter just doesn’t care whether his statements are true or false as long as they advance his agenda.

Frankfurt goes on:

For this reason, telling lies does not tend to unfit a person for telling the truth in the same way that bullshitting tends to. Through excessive indulgence in the latter activity, which involves making assertions without paying attention to anything except what it suits one to say, a person’s normal habit of attending to the ways things are may become attenuated or lost. Someone who lies and someone who tells the truth are playing on opposite sides, so to speak, in the same game. Each responds to the facts as he understands them, although the response of the one is guided by the authority of the truth, while the response of the other defies that authority and refuses to meet its demands. The bullshitter ignores these demands altogether. He does not reject the authority of the truth, as the liar does, and oppose himself to it. He pays no attention to it at all. By virtue of this, bullshit is a greater enemy of the truth than lies are.

Sound familiar?

Honestly, can anyone here think of an example of a protein where one amino acid substitution renders it totally unstable and unfoldable? I can’t think of any, but there must be some out there.

Well, I suppose you could have a mutation to a stop codon right before you got to a transmembrane region, which might destroy the present function of the protein. But nothing of that sort would do what Dembski needs. If you could show that for a certain protein, any substitution at any position would destroy its current function, that still wouldn’t prove that it’s unevolvable, or that it lacks any possible function.

These guys know there’s no scientific merit to ID. And Inlay’s post shows that there’s dishonesty afoot. So I think it’s much more likely that this stuff is just a pseudoscience smokescreen. The point is to generate tons of pseudoscience, appear to create scientific controversy. It’s all about putting on a show.

Like SteveS said, it’s bullshit. The point is to create lots and lots of bullshit, and fool the rubes in Kansas.

I would imagine that a protein that can’t even fold would be insoluble and crash out of solution.

Sure, although that would require that the protein in question be synthesized in multiple copies per cell, at least.

And don’t forget that there are proteases in cells that chew up proteins.

Interestingly, that reminds me of an amusing theory that was first proposed by … gosh, was it Bruce Alberts? maybe Tom Steitz? Arthur Kornberg? … to explain a mysterious protein whose “function” was difficult to determine. The “function” of such a protein might be merely to “sop up” non-specific proteases so they don’t chew up more important proteins! We used to have a name for this theory but I can’t remember what it was … some metaphor relating to mosquitos, maybe?

Speaking of the evolution of irreducible complexity and the evolution of the definition of “irriducible complexity”, this brings up a question I’ve been meaning to ask some of the more studious chroniclers of ID:

1) While I have seen numerous disparate references to inconsistencies in definition, what is the single most complete compendium of the changing definitions of IC?

2) Does anyone have any additions which have been observed since #1?

It doesn’t matter that they lie, bullshit or anything in between. What matters is that they are published in the NY Times doing it.

The rubes have no idea what “peer review” is and even if they did, they would be able to dismiss it as science’s rigging the rules (well, science is rigging the rules: we’re quite clear that it excludes the supernatural!). What they do know is that there is a controversy. They know that some people – who invoke God – think atheist scientists are wrong. As if it mattered what the evidence was!

Re SteveS’s comment about Harry Franfurt’s new book On Bullshit, it promises to be a fabuluous read and a probable accurate guide to what afflicts Dembski and his fellow IDiots. The publisher’s website observes…

We have no clear understanding of what bullshit is, why there is so much of it, or what functions it serves. And we lack a conscientiously developed appreciation of what it means to us. In other words, as Harry Frankfurt writes, ‘we have no theory.’”

…and that he then proceeds to develop the theory.

Further Frankfurt observes…

”…bullshitters seek to convey a certain impression of themselves without being concerned about whether anything at all is true. They quietly change the rules governing their end of the conversation so that claims about truth and falsity are irrelevant. Frankfurt concludes that although bullshit can take many innocent forms, excessive indulgence in it can eventually undermine the practitioner’s capacity to tell the truth in a way that lying does not. Liars at least acknowledge that it matters what is true. By virtue of this, Frankfurt writes, bullshit is a greater enemy of the truth than lies are.”

As SteveS asked, “Sound familiar?” Frankfurt is a long time professor of philosophy at Princeton, but clearly no stuffed shirt. I have no idea what he’s like in person, but I can imagine he would devastate Demski, Johnson and company in a personal encounter, even if he knows nothing about evolution of ID.

It is perfectly correct to maintain that Intelligent Design is not scientific. It is a necessary given and fundamental to any further discussion of evolution. It cannot be questioned any more than can a Copernican view of the planets. Would anyone be so weak minded as to say that a demonstrable reality need be described as scientific? I certainly hope not. To question Intelligent design is to question evolution. Without the former there could never have been the latter. The next thing you know, someone will be telling us that Newton’s Laws of Motion were produced by Natural Selection. Such fundamentals are not subject to question, only to discovery. Intelligent Design was discovered centuries ago. Only homozygous atheists (Darwinians) continue to ignore it.

John A. Davison

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This page contains a single entry by Matt Inlay published on February 16, 2005 12:06 AM.

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Homo floresiensis on Darwin Day is the next entry in this blog.

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