More Stupid Tautology Arguments from Dr. Egnor

So over at the DI whiners blog, Egnor is, once again, trying to pretend that he’s actually making a case for why evolution is irrelevant to antibiotic resistance. It’s really getting silly; he repeats the same nonsense over and over again, desparately doing the rhetorical version of sticking his fingers in his ears and shouting “La La La! I can’t hear you!”:

The Darwinist assertion that random variation and natural selection (chance and necessity) account for all biological complexity has nothing to do with the mundane observation that it’s unwise to unnecessarily expose populations of bacteria to antibiotics. The observation that an antibiotic will kill the bacteria that are killed by it, and the antibiotic will not kill the bacteria that are not killed by it, is a tautology. If you expose a population of bacteria to antibiotics, the unkilled ones will, over time, outnumber the killed ones. The unkilled ones will be the ones that are resistant to the antibiotics. Think about it. That’s Darwinism’s seminal contribution to our understanding of bacterial resistance to antibiotics.

How many times do we need to go through this? A tautology does not explain anything; and it does not invalidate the explanation from which it was derived.

Egnor wants to keep claiming that all that’s happening with antibiotic resistance is that “bacteria that don’t get killed by antibiotics don’t get killed by antibiotics”. The problem for him is that that’s not the entire story.

The major question is: why are antibiotic resistant bacteria suddenly such a problem? Why can we observe clone-lines of non-resistant bacteria acquiring antibiotic resistance? Why for the first 40 or 50 years of antibiotic use was
there virtually no significant population of antibiotic resistant bacteria outside of hospitals? Why was there virtually no wild bacteria resistant to multiple antibiotics?
Why are we suddenly observing the existence of bacteria with different proteins
in their cell walls than we’ve ever seen before? Where did they come from?

Egnor can’t explain any of that. And yet, those are real, observed facts that require explanation. Those are real phenomena that will kill large numbers of people unless we understand them and alter our behavior accordingly.

Egnor is arguing for, in essence, ignoring the process, and trying to cope with it without taking advantage of the insights that can be acquired by understanding what is going on. Following the course of actions that are suggested by
Egnor’s argument will lead to people dying.

Dr. Egnor, with his willful ignorance, would rather watch patients die than admit that there’s something going on that conflicts with his religion. He will not under any circumstances admit to the evolutionary processes producing the new killer strains of resistant bacteria; and because of that, he’ll never adopt the necessary practices by which we can reduce the threat of antibiotic resistance. Because to do so would be to admit the
validity of evolution; and he won’t do that. He’ll just keep arguing that evolution had nothing to do with it; that the deaths of patients caused by resistant infections are unfortunate but unavoidable. All in the name of denying reality.

20 thoughts on “More Stupid Tautology Arguments from Dr. Egnor

  1. Ex-drone

    So if Egnor believes that bacteria cannot mutate, then he must also believe that bacteria variations are finite, since they were all apparently “designed” at a single point in time. Does that mean we will eventually find an antibiotic or antibiotic cocktail that will be capable of killing all bacteria strains, or did “the Designer” create some time bomb bacteria strain that will prove impervious to all our attempts. If he’s going to go down the design road, the least he could do is give us a hypothesis.

  2. Joshua

    The hypothesis is clear.
    God hates us and wants us all to die, or else he wouldn’t be designing resistant bacteria!
    Egnor’s “tautology” argument is such a complete crock. Ok, let’s grant that we don’t need evolution to tell us that resistant bacteria will survive and multiply and outnumber non-resistant bacteria. Which is ludicrous, because that process is exactly what natural selection is, so it’s basically evolutionary by default. But, Hell, let’s suspend logic and reason just to grant him this part of his argument, since he loves it oh so very much.
    So how do resistant bacteria appear? Where do they come from? As Ex-drone says, the only conclusion possible if you exclude “random” mutation is that all the resistant strains must already exist somewhere.
    This has huge implications for how we treat resistant bacteria! Now we’re looking at an epidemiological problem. We should be able to isolate patients suffering from resistant strains and sequester them. If we can kill every single bacterium in every single patient with a resistant strain, the problem of antibacterial resistance goes away forever! Hooray! Oh, wait. I guess that’s actually not so easy. It must be my Darwinist brain making me think eugenic thoughts, because it seems to me that the only way to really succeed here is to either permanently remove all the resistance carriers from the rest of the population or else just slaughter them wholesale.
    But, hey, we’d conquer the problem of resistant bacteria forever and ever and ever, so it’s a small price to pay, yeah?
    On the other hand, if Dr. Egnor is wrong (Which clearly he could never, ever be! He’s a brain surgeon, don’t you know? But let’s assume for the sake of argument.), then even if we did find and murder and incinerate every single carrier of resistant bacteria in the entire world, we’d have accomplished nothing at all, because resistance would just mutate again and we’d be stuck where we started. Oh, well. I guess us bloodthirsty Darwinists will have to close up the ovens.
    But, wait! If we can determine the most likely evolutionary pathways for the development of resistance from a non-resistant strain (which has been done at least once, though I can’t remember which SciBlogger posted about it), we can develop therapies that target those intermediate stages and make it harder for resistance to evolve. So we can solve the problem of antibiotic resistance without killing anybody or locking them in concentration camps.
    Oh, man, I hate this plan. It’s totally against my nature as a Darwinian fascist who loves eugenics and murder and kicking puppies, but what’s a guy to do?

  3. Josiah Carlson

    This evening while picking up my wife, I caught a portion of an interview with Francis Collins that made me feel like there may be hope for certain people (though only those who are willing to at least acknowledge that taking the bible literally can lead to inconsistency). In this interview, and in his book, Francis talks about how he “found god” in the human genome, and how as an evangelical, he has no issues combining his faith with his science.

  4. Andrew

    I’m in the same boat. I’m an Evangelical Christian and have little problem reconciling what I know of Science (which is, admittedly, far less than a lot of contributors to this blog) with what I believe to be true from reading the Bible.
    Take Evolution as the current example. I have no problem agreeing with everything Mark has said about evolution and bacterial resistance, and find it hard to fathom that supposedly intelligent people can’t follow the argument.
    I don’t see anything in this usage of evolution that is contrary to scripture. I believe that God created the Universe and everything in it, but I have no problem with the idea that the result of the early stages of this creation process looks to us like something we call “The Big Bang”. Likewise, I have no problem with the idea of God creating life with the capability of evolving, and even using/guiding that capability to create the diversity of species we see today. The fact that we can identify a process that explains our observations does not necessarily preclude a Devine hand behind the process.
    The problem I think most people get into is that they see the Bible and Science trying to do the same thing. The Bible is all about God’s relationship to His creation, and His plan to restore the relationship between Himself and Mankind that existed in Eden (before the incident with the Apple). As such Genesis 1 & 2 are talking about WHY God created what He did and how he viewed that creation (“It was very good”). Genesis is NOT about HOW God created things, and as such, processes like “The Big Bang” and evolution are not precluded.
    On the other side of the argument Science is about explaining HOW things happen. “Big Bang” theory attempts to explain and describe WHAT took place in the first short period of the universe’s existence and HOW it happened, but it doesn’t attempt to explain WHY it happened. Likewise, the Theory of Evolution has a lot to say about HOW one species can develop from another, but has nothing to say about WHY life came into existence in the first place, other than that obvious conclusion that it was possible for it to do so.
    Bottom line is, the Bible says God created the Universe, and Science says that matter accelerated rapidly out of a singularity to form the galaxies, stars and planets, and, eventually, everything else (please excuse any over-simplification). Is it such a stretch to reconcile these two views of the same event?
    Likewise, the Bible says that God created the fish of the sea, the birds of the air, and the beasts of the field. Science says that one species evolved to the next, etc, etc. Again, not a big stretch, I think.
    What are your thoughts in this area, Mark? I know it’s a personal question, feel free not to answer if you so prefer. Id also be interested in hearing the view of PZ over at Pharyngula, but I’ve a fair idea what it may be.

  5. CatMat

    Evolution in ten steps, a case study (antibiotic resistant bacteria):
    1) Features like antibiotic resistance are part of the phenotype but related to the genotype
    2) Mutations do occur and they change the genotype [ of the descendants of a single cell organism, other cases are not relevant here ]
    3) Mutations do not have an effect on an already dead organism
    4) Distribution of genotypes in a population at a given time is dependent on the genotypes of the descendants of the members of the population at a prior time
    5) Presence of antibiotics in an environment favors those organisms that have a resistance to those antibiotics
    6) This selective bias changes the distribution of genotypes in a population over time to increase the portion of genotypes producing resistant phenotypes
    7) Change in the distribution of genotypes changes the likelihood of a mutation occurring in a resistant genotype versus a non-resistant one
    8) Combined, this means that genotype distribution of a population is changed by mutations and natural selection, where the natural selection applies to phenotypes and limits the range of genotypes that are targets to mutation
    9) Even though mutation is essentially random, when applied to a pre-selected population the net result is continued adaptive selection
    10) Continued adaptive selection is commonly associated with evolution
    What, exactly, would be the problematic part here?

  6. John H

    What makes Egnor’s campaign particularly quixotic is that, as I understand it, many creationists and IDers claim to accept natural selection mechanisms within existing “kinds” (“microevolution”) while rejecting it as the basis for origin and diversity of life today (“macroevolution”). Indeed, the Answers in Genesis crowd positively insist on very rapid speciation following the Noahic Flood.
    So antibiotic resistance would not be seen by those creationists as violating the creationist account of life and its origins. Which makes it even more difficult to see why Egnor is continuing with this line of argument. Either (a) he’s even more ignorant than other creationists and ID proponents, or (b) this shows that, while creationists may have been forced to accept natural selection in some circumstances, in their heart of hearts they really can’t bring themselves to accept it.

  7. G. Shelley

    It’s not easy to see his point with

    If you expose a population of bacteria to antibiotics, the unkilled ones will, over time, outnumber the killed ones. The unkilled ones will be the ones that are resistant to the antibiotics.

    He doesn’t seem to be arguing that it isn’t true, or that it isn’t important (though I could be mistaken on that). He seems to just be playing semantics (and doing so poorly) and thinking he can prove “Darwinism” has no relavence by doing so

  8. Jud

    Egnor says “it’s unwise to unnecessarily expose populations of bacteria to antibiotics,” so in spite of whatever magic juju he thinks accounts for the development of resistance, it appears he’s willing to take steps to minimize the likelihood of its occurrence. Also, as I’ve mentioned in a comment on a previous post, my guess is that the facility/ies where Dr. Egnor practices have protocols about that sort of thing that he no doubt follows.
    So he’s not saying the phenomenon of bacteria developing resistance to antibiotics doesn’t occur, and he doesn’t even appear to disagree that overuse of antibiotics is causative. He just doesn’t ever, under any circumstances, want to call the process “evolution,” or admit it can take place without God/the Designer’s involvement. So it’s just more definitional sleight-of-mind and the usual insistence that we need a magic wand to make it all happen, not a denial that it *does* happen.

  9. Bongob

    Lurking Pedant detects defenceless minor typo, ears go back, begins to stalk there an “unless” missing from the sixth paragraph?
    I’m an innumerate layman who can usually only point and hoot at these debates like a Gary Larson caveman, but I’m having really severe difficulties following this one. I still don’t understand Egnor’s position or argument, and I’m not sure it is an argument. Am I being unfair, or is there more to Egnor’s position than tautology and repetition?

  10. _Arthur

    It is pretty bizare than many Creationists strenuously deny that natural selection happen, for example there is a whole chapter in Ann Coulter book to deny that natural selection ever happened in the case of the peppered moth,
    and then, for bacterial antibiotic resistance, they just concede the point, say the phenomena is utterly trivial, and that it is absolutely not “natural selection” in the Darwinist sense, it is “Adaptation” in the Egnorant way.

  11. Mark C. Chu-Carroll

    I think there’s more to it than that. Egnor is willing to admit that using antibiotics makes resistant strains more prevalent. But I think he’s arguing that no new strains of bacteria are evolving. That is – I think that he believe that antibiotic resistance is strictly a process of selecting individuals possessing the trait of antibiotic resistance from a basic static population – that all antibiotic resistant bacterial types already exist, and that all we’re doing is isolating them.
    But the reality is that we are seeing changes – *new* types. That’s why in the lab we can start a clone line from a single non-resistant bacteria, and by repeated exposure to antibiotics, we can create a multiply-resistant strain.
    Egnor doesn’t believe that. And that’s what makes the fact that he’s a practicing doctor so scary: fighting antibiotic resistance doesn’t just mean being stingy with antibiotics – it means following a strict protocol about how to select antibiotics, what doses to use, what isolation procedures to use, what tests to perform before prescribing, etc.

  12. Flex

    Bongob wrote, “Am I being unfair, or is there more to Egnor’s position than tautology and repetition?”
    My first reponse to this question was ‘no’. Which wasn’t enough reason to post. But on consideration, as to why the answer is ‘no’, I think there is an avenue to explore.
    Let’s look at the structure of some of the arguments, from the rationalists and the irrational theists (excluding the rational theists who manage to handle the ‘non-overlaping magistra’.)
    Rationalist: Evolution is the overarching theory of biology; encompassing most aspects of living beings and how they interact with both living and a non-living aspects of their environment. It provides a framework to explain speciation, mutation, variation, species development as well as individual development, and even variation on a cellular level.
    Irrational Theist: We already have a concept which does all that. We call it ‘God’.
    Argument #1.
    Rationalist to Irrational Theist: How does saying, ‘God did it’ account for our being able to account for all the steps of a given evolutionary event, and replicate them, in laboratory conditions?
    Irrational Theist response: That particular example is simply nit-picking and doesn’t diminish the value of the entire theory of ‘God did it’. Further, by definition God is everywhere, including your laboratory, so your example is not a good one.
    Argument #2.
    Irrational Theist: How does your theory of evolution explain the great influence religion has had on history and society, including ethical and moral behaviors and the apparently non-adaptive behavior of martyrs?
    Rationalist: Evolutionary theory has some proposed answers to those problems, but we don’t claim to know everything. Using this particular example as evidence that the theory is innacurate is nit-picking and doesn’t diminish the value of the evolutionary theory.
    These arguments are the same form. Both sides claim an overarching theory, and both sides feel that ‘minor’ counter-examples do not detract from the importance of the theory. Both sides have developed responses to the counter-examples, ranging from denial to suggested mechanisms.
    This does not mean that the accuracy of the viewpoints are equal. Simply that the arguments often take the same form.
    The value of evolutionary theory is that it is a predictive theory. Evolutionary theory not only tells us how antibiotic resistance bacteria develop, it even gives us fairly accurate predications of how fast and what forms it will take. These predictions are only going to improve as our knowledge improves.
    The predictive value of the ‘God-did-it’ overarching theory of biology is absolutly zero.
    So Egnor’s position, faced with the clear evidence that antibiotic resistance bacteria have developed, is one of, of course it developed, we saw it happen! It makes perfect sense that if your tool used to kill bacteria didn’t kill all the bacteria, the ones that survived would become more common. Thus his tautology is born.
    From the evolutionary perspective however, we can determine the selection rate, the mutation rate, and the reproduction rate of bacteria treated with antibiotics and predict how often these antibiotic resistant strains will occur, where they will be found, and how many we will find. (And we get upset at every television commercial advertising antibacterial soaps for general home use.)
    So the reason Egnor is repetitiously arguing that the development of antibiotic resistant bactria is a tautology is interesting. A tautologic argument is an invalid form of argument if there is no additional evidence to support any of the statements contained in the tautology.
    As many Sciencebloggers have pointed out, there is plenty of evidence available, and a theory which ties it all together, for the tautology being discussed. But until Egnor accepts the connections between the tautology and the rest of evolutionary theory, he can claim that the tuatological portion of the argument is invalid.
    There is a sequence in Hofstadter’s ‘Godel, Escher, Bach’ which discusses this logical problem rather neatly in the discussion of infinite regression.

  13. tristero

    Marc C C-C beat me to it. As a lay person, it sounds to me that all Egnor’s saying is that both resistant and non-resistant bacteria have always existed, that the antibiotics have killed off the non-resistant and therefore all that’s left are the resistant. About which he concludes, “That’s what Darwin’s theory amounts to here. Big Deal.”
    But, and please correct me if I’m wrong, Egnor has a problem, namely demonstrating that resistant bacteria, as a semi-robust species or variety, are as old as non-resistant – Mark alludes to experiments which suggest this is not necessarily the case. But even if Egnor could make a case regarding the pre-existence of resisant bacteria, he would still, if he wants to dispute nat/sel in general, have to explain why there are no fossils of human beings concurrent with T. Rex. or any other dinosaur.
    And so on. As a layperson, it’s not merely the single example that seems so compelling in favor of nat-sel. It’s the overwhelming *number* of examples, the lack of counter-examples, and the enormous amount of related, converging evidence – correlations with geology, for example – that point to the efficacy of natural selection.

  14. Jud

    MarkCC said: “That is – I think that he believe that antibiotic resistance is strictly a process of selecting individuals possessing the trait of antibiotic resistance from a basic static population – that all antibiotic resistant bacterial types already exist, and that all we’re doing is isolating them.”
    That would indeed be the logical inference from what Dr. Egnor is saying.
    But then how can he deal with the “reality…that we are seeing changes – *new* types,” as you say? My guess is that the well-worn nonsense of “front loading” will be trotted out: that like some never-ending sequence of Matryoshka dolls, resistance to any antibiotic that will ever be formulated has been Designed into the genomes of all these bacteria, and is expressed when antibiotics are used. (Funny how only some bacteria can express this inbuilt resistance, while others die, apparently needlessly.(?!))

  15. Jonathan Vos Post

    There’s a very abstract sense in which “all possible” species already exist in a superspace of genotypes/phenotypes. To a Spinoza-influenced theologian, once could say that all possible creatures already exist in “the mind of God.”
    But which ones can actually occur on our planet depends on which other ones already exist on our planet, because the fitness of the organism depends on the developmental possibilities (i.e. a mammoth might be able to be gestated by an elephant) and the ecosystem in which the organism will compete.
    If Egnor saw a unicorn, would he say that all the non-unicorns have been hunted to death, and only the unicorns tautologically remain?

  16. Reed A. Cartwright

    I think we are going at this the wrong way.
    Egnor is ignoring the theory of evolution via natural selection. Darwin didn’t just point out the “tautology” of natural selection, but built upon it by pointing out how natural selection can result in evolution. Darwin described how if the variation in a feature of some organisms lead to different reproductive success, and if the feature can be partially or completely inherited by the offspring, then the features that promote reproduction will become more common.

  17. Torbjörn Larsson

    Ok, let’s grant that we don’t need evolution to tell us that resistant bacteria will survive and multiply and outnumber non-resistant bacteria.

    We could do that. It wouldn’t even be an ad hoc, but perhaps a robust theory against the observations he may want to do. Rather like Newton gravity (resistance) against general relativity (evolution).
    But even this analogy which follows from Egnor’s position has two problems.
    First, here the simpler theory follows after the more general. So even if Egnor would be the Isaac Newton of resistance theory, he would have nothing to be proud of.
    Second and more seriously, the more constrained theory isn’t robust against better theories. It is always replaced by the more general theory due to the laters increased predictive power and ability to grow and connect with other theories. Egnor is confusing theory with model here. It is when we model specific examples we may want to use the most constrained, simplest, model we possibly can find.
    Perhaps this is why he haven’t presented an alternative creationist theory like the frontloading theory. Not understanding the hallmark and importance of predictiveness in theories, not understanding the difference between modeling and theory – egnorance of science seems to be the trademark of Egnor.

  18. Jonathan Vos Post

    It’s even worse for ID than Egnor thought, at least for the evolution of antibiotic resistant bacteria.
    Nature News
    Published online: 10 August 2007; | doi:10.1038/news070806-12
    The best is the enemy of the good
    Slightly helpful mutations in E. coli much more plentiful than thought.
    It’s all in:
    Perfeito, L. & Fernandes, L. & Catarina, M. & Gordo, I. Science 317, 813-815 (2007).
    This is blurbed thus:
    Brendan Maher
    E. coli: so many ways to make it better…
    Beneficial mutations in the bacterium Escherichia coli occur 1,000 times more frequently than previously predicted, according to research from a group in Portugal.
    In a study of E. coli populations of various different sizes, Isabel Gordo and her collaborators at the Gulbenkian Science Institute in Oeiras, Portugal, found that thousands of mutations that could lead to modest increases in fitness were going unseen because good mutations were outperformed by better ones. The authors say that the work could explain why bacteria are so quick to develop resistance to antibiotics….

  19. Jonathan Vos Post

    Nature Reviews Genetics 8, 619-631 (August 2007) | doi:10.1038/nrg2158
    Mutation rate variation in multicellular eukaryotes: causes and consequences
    Charles F. Baer1, Michael M. Miyamoto1 & Dee R. Denver2
    A basic knowledge about mutation rates is central to our understanding of a myriad of evolutionary phenomena, including the maintenance of sex and rates of molecular evolution. Although there is substantial evidence that mutation rates vary among taxa, relatively little is known about the factors that underlie this variation at an empirical level, particularly in multicellular eukaryotes. Here we integrate several disparate lines of theoretical and empirical inquiry into a unified framework to guide future studies that are aimed at understanding why and how mutation rates evolve in multicellular species.
    Author affiliations
    1. Department of Zoology, University of Florida, Gainesville, Florida 32611, USA.
    2. Department of Zoology and Center for Genome Research and Biocomputing, Oregon State University, Corvallis, Oregon 97331, USA.


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