So the Discovery Institute’s most recent addition has chosen to reply to my post about
tautologies. (Once again, I’m not linking to him; I will not willingly be a source of hits for the DI website when they’re promoting dangerous ingorance like this.) Typically, he manages to totally miss the point:
Darwinist blogger and computer scientist MarkCC (why don’t they use their real names?) called me a lot of names a couple of days ago. The most profane was that I am a ‘bastion of s***headed ignorance.’ Profanity seems to be a particular problem with the computer-math Darwinists. A dysfunctional clad, perhaps. They’re dysfunctional because, as Aristotle wrote, effective rhetoric has three characteristics: logos, ethos, and pathos. Effective rhetoric appeals to the best in reason, ethics, and emotion. When I’m called unprintable names merely for expressing my skepticism about the relevance of Darwin’s theory to the practice of medicine, I’ve already won the ‘ethos’ and ‘pathos’ skirmishes. I can concentrate on the logos.
Yes, Dr. Egnor. Let’s make sure that we focus on issues of style rather than substance. Because we both know that you have nothing to say in response to the substance of my criticism of your pigheaded ignorance.
First – I do go by my real name. As anyone who takes the most cursory glance at my
blog can see, my name is “Mark Chu-Carroll”, but since that’s a bit long, I tend to use the
abbrevation of my email address: MarkCC. Not that what name I go by has anything to do
with the points I made, but since Egnor feels that the fact that I abbreviate my name is an issue
worth commenting on, I thought it was worth pointing out what an idiotic comment it is –
particularly since it’s quite clear that it’s part of a tactic: distract the reader, by focusing on
irrelevant issues like style, in order to obscure the fact that he has nothing to say about the actual issues that were included in the post he’s allegedly responding to.
Second – I don’t consider myself a “darwinist blogger”. I consider myself a math blogger with basic literacy in science. And anyone who’s actually literate in science recognizes the reality of the process of evolution. Calling someone a darwinist is part of the ongoing campaign by the DI and their cohorts to paint anyone who recognizes scientific fact as part of some kind of fanatical pseudo-religious movement of Darwin worship.
And third – another style versus substance issue. Yes, I used profanity in my criticism of Dr. Egnor. When I watch someone who I care deeply about suffering, and someone like Dr. Egnor dismisses the cause of his suffering with a pigheadedly ignorant casual handwave, I get rather pissed off. Dr. Egnor isn’t personally responsible for my father’s illness. But people like Dr. Egnor, with their practice of casually dismissing the ongoing process that produced the bacteria that nearly killed my father, are, to a great deal, responsible for the way that
these highly resistant bacteria have developed and proliferated over the last several years.
Mark took umbrage at my podcast comment that Darwinism wasn’t indispensable to understanding antibiotic resistance in bacteria. His father seems to have had a very hard time with a resistant strain of bacteria, and he blames me and my view of Darwinism, sort of. I’ve treated thousands of people with serious infections, and I’ve dealt, in a very first-hand way, with the difficulties of bacterial resistance to antibiotics. I’m sorry about his dad’s illness. But Mark hasn’t shown any real insight into medicine or into what doctors actually need to understand in order to deal with serious infections.
Actually, Dr. Egnore is the one who isn’t showing much real insight into the science of the biology that underlies his medical practice. He wants to wave his hands around, shout “tautology, tautology” as if it actually said anything about the actual science, and pretend that the
cause of antibiotic resistance is no big deal, nothing to worry about.
And that brings us to the point that Egnor continues to either ignore or handwave his way past. 20 years ago, there were virtually no widespread strains of staphylococcus that were resistant to multiple antibiotics. 10 years ago, multiply resistant strains were becoming common – but staph infections that were resistant to methicillin and vancomycin were quite rare. Today, methicillin resistant staph is common – infection with methicillin-resistant staph is one of the most common complications from major surgery in American hospitals. How did that happen? The answer is: evolution.
Dr. Egnor wants to ignore that, by dismissing the undeniable fact of the process of change in common bacteria as a tautology: “Bacteria that don’t get killed by antibiotics don’t get killed by antibiotics”. Yes, that is a tautology. But as I pointed out in my previous post, any legitimate scientific theory can be stated as a tautology. And in this case, that tautology is the most remarkably clear statement of exactly what’s happening to common bacteria. We overuse antibiotics; the bacteria that don’t get killed by the antibiotics don’t get killed by antibiotics, and so they’re the ones that reproduce and spread. Repeat that process for a couple of decades, and you get bacterial straints like the staph strain that infected my father – a bacteria that’s resistant to all penicillin family antibiotics, to 1st, 2nd, and 3rd generation cephalosporins, to methicillin, and to vancomycin.
Dr. Egnor also wants to ignore the fact that the staph strain that infected my father is
dramatically different than the staph strains of 20 years ago. It’s got a different
cell-wall structure; it uses different enzymes for a variety of its reproductive functions.
Through his denial of the reality of evolution, Dr. Egnore further ignores the simple fact that
by careless prescription that doesn’t consider evolutionary effects, he’s helping to produce
the truly terrifying superbug: at the moment, there are two distinct mechanisms that produce dramatic multiple antibiotic resistance: glycopeptide resistance, and β-lactam resistant. At the moment, we haven’t seen single straigns of bacteria with both glycopeptide and β-lactam resistance modes. But we know the genetics – and there is nothing incompatible between the glycopeptide resistance mutation and the β-lactam resistance mutation. A staph strain with both of those would, effectively, be entirely resistant to pretty much every antibiotic
we know of. Good doctors are incredibly careful about how they use antibiotics – to make sure that they do not do anything that’s likely to help produce this terrifying new potential strain.
Do Doctors need to be aware of evolution? Does awareness of evolution have anything to do with how Doctors should respond to infections? As an answer, let me tell you a bit about what my children’s pediatrician has told us:
- As a pediatrician, she does not routinely prescribe antibiotics. For a basically healthy child, no matter what the infection, she won’t prescribe antibiotics for at least 4 days, to give the child’s immune system a chance to defeat the infection on its own.
- She does not prescribe antibiotics for any illness until there is
hard proof that it’s caused by bacteria. - When she prescribes antibiotics, she does it in a very strict way. The first prescription
for a child without drug allergies is always penicillin. - After the first time that they prescribe antibiotics, the practice
keeps careful track of exactly what has been prescribed to which child when; they follow
a strict rotation process with antibiotics to try to not repeatedly prescribe the same
antibiotic to a child within a six-month period.
Why such a strict process? Because bacteria are evolving resistance to antibiotics. By following a strict process like this, they minimize the quantity of antibiotics that they prescribe, and they try to prevent a chronically ill child from becoming a walking incubator of resistant bacteria. (And yes, when talking about this, she does specifically say that bacteria are evolving resistance.)
So – yes, I do blame Dr. Egnor’s way of thinking for my father’s illness. By ignoring the fact of evolution within bacteria, his mode of thinking about these problems provides
the common excuses and practices that have led to the modern crisis in antibiotic resistance.
And in response to this, Egnor basically continues to wave his hands around, denying
reality, taking refuge behind semantic games.
Mark, your dad’s illness didn’t happen because his doctor didn’t know enough about random mutation and natural selection. Our battle against bacterial resistance to antibiotics depends on the study of the intricate molecular strategies bacteria use to fight antibiotics, and our development of new antibiotics is a process of designing drugs to counter the bacterial strategies. We use molecular biology, microbiology, and pharmacology. We understand that bacteria aren’t killed by antibiotics that they’re resistant to. We understand tautologies. Darwin isn’t a big help here.
No, my father’s illness didn’t happen because his doctor didn’t know enough about
evolution. His surgeon is actually quite aware of the process by which resistant bacteria are evolving, and takes as many reasonable steps as he can to both combat resistant bacteria in his patients, and to avoid contributing to the evolution of more resistant bacteria. But his illness is the result of the actions of many doctors – doctors like Dr. Egnore who ignore reality, and don’t practice medicine with an awareness of how their actions contribute
to the evolution of the other species that surround us. It’s people like Dr. Egnor who hand out antibiotics like candy, because after all, bacteria don’t evolve, and so their prescription practices can’t possibly contribute to a process that doesn’t happen. It’s people like Dr. Egnore
who’s attitudes allow the use of third generation cephalosporins – which are restricted for use in humans – to be used in cattle feed. Because after all, evolution doesn’t happen, so what harm can it possible do to have volumes of these antibiotics floating in the
manure pools that are used to produce the fertilizer that used to grow the vegetables we eat?
No, Dr. Egnor. You do not understand tautologies. You do not understand
science. And you are a disgrace to your profession, and a danger to your patients.
Not to mention that you’re an asshole.
Egnor seems to be happy making up his own personal theory how antibiotic resistance magically appears, rather than using the vast body of scientific evidence — and medical evidence.
I suppose he teaches that each prysician should come up with his own theories about illnesses and cures. Like, say, Evil Spirits.
MarkCC said: “No, Dr. Egnor. You do not understand tautologies. You do not understand science. And you are a disgrace to your profession, and a danger to your patients.”
To give credit where it’s due, he seems to be a fine neurosurgeon from the couple of reports I’ve read regarding surgical cases of his.
Regarding his antibiotics prescribing practices, since I don’t know what they are, I can’t say whether he’s a danger to his (and others’) patients in that regard. I would imagine there are antibiotics prescribing protocols at the facilities where he works that he most likely follows.
Regarding the evolution of bacterial resistance to antibiotics, my working theory would be the old reliable “Never attribute to conspiracy what can adequately be explained by stupidity.” That is, I’d guess that over-prescription of particular antibiotics can be explained less well by some anti-evolution movement among physicians, than by office staff accustomed to filling out prescription pads for the same drugs pushed by the same companies’ pharmaceutical salesmen and time-pressed doctors scrawling signatures on those prescriptions with their attention focused elsewhere.
“Not to mention that you’re an asshole.”
I’d have to agree there. There certainly seems to be a political-religious agenda behind the particular instances (Terri Schiavo, evolution) where this doctor who apparently knows full well what constitutes proper medical and scientific evidence (he’s published papers in professional journals in his field) chooses to ignore science and logic in favor of rhetorical nonsense.
Well done Mark. Topical, direct, and on point.
Dr. Egnor is an asshole. He knows full well he is wrong. I guess he is trying to get some money from the ID people. If he was ever my doctor I would fire him. He did say one thing I agree with….”Darwin isn’t a big help here.”, that is because Darwin is no longer alive. On the otherhand both gentics and understanding evolution is very helpfull in combating and understanding bacteria evolution. 🙂
Your kids do seem to have a reasonably aware pediatrician. Good for her.
I don’t understand how it is that you can explain, in a few paragraphs, a phenomenon that I had never heard of before, and have it make perfect sense to me and convince me that this is a major problem, and yet there are people out there who have the biological background to really understand the details and yet simply refuse to believe it.
Not to mention that Dr. Egnor’s explanation of how the problem should be dealt with seems to be nothing more than pigheadedness. Yes, I can see that studying “the intricate molecular strategies bacteria use to fight antibiotics” and using this knowledge to create new antibiotics is a good idea, but why ignore a medical practice that might help, and certainly won’t hurt? Are there any potential dangers to rotating antibiotics, or any reason not to do it other than some additional paperwork?
Egnor Dissembled thusly:
Darwinist blogger and computer scientist MarkCC…
If ever Egnor’s intellectual dishonesty were to be laid bare, this is it. He apparently understand mathematics and mathematicians even less than he understands evolution. Mathematicians could give a flying fuck about Darwin per se. All they care about is the math, just ask Noam Chomsky. He was surprised when presenting his ideas to a group of mathematicians, how little they were interested in his lack of credentials, and how much interest they had in his math. If the math didn’t back evolution, the mathematicians like MarkCC would be against it, it is as simple as that.
Egnor and his ilk know their political agenda can’t handle the formidable implications of such things as divergent fields like mathematics and biology independently verifying each other on the subject of evolution. So they have to invent the “Darwinist Comspiracy” to try to explain it away. The problem is that the idea of a conspiracy between the science bloggers evaporates instantly the moment one examines their frequent and sometimes heated disagreements on a whole host of issues. Notice how little you see of that on creationist/intelligent design sites.
A blind man could see this with a cane. The only conspiracy among scientists is to deal with the evidence. The conspiracy among Egnor and the rest of the creationists/Iders is to pretend there is a conspiracy any time the evidence goes against them.
I have a modest proposal.
Instead of calling ID advocates, ID advocates, we should call them “Johnsonites” in honor of Philip Johnson.
It’s my opinion that calling advocates of the theory of evolution, “Darwinists” is an attempt to reduce a working scientific theory to a cult of personality.
We should return the favor.
It seems as if you good doctor is ignorant of a vast amount of literature. Here are a few examples (cross-posted to Mike’s blog) – the list is pretty much endless:
Woodford, N. and Ellington, M.J. (2007) The emergence of antibiotic resistance by mutation. Clinical Microbiology and Infection, 13, 5-18.
The emergence of mutations in nucleic acids is one of the major factors underlying evolution, providing the working material for natural selection. Most bacteria are haploid for the vast majority of their genes and, coupled with typically short generation times, this allows mutations to emerge and accumulate rapidly, and to effect significant phenotypic changes in what is perceived to be real-time. Not least among these phenotypic changes are those associated with antibiotic resistance. Mechanisms of horizontal gene spread among bacterial strains or species are often considered to be the main mediators of antibiotic resistance. However, mutational resistance has been invaluable in studies of bacterial genetics, and also has primary clinical importance in certain bacterial species, such as Mycobacterium tuberculosis and Helicobacter pylori, or when considering resistance to particular antibiotics, especially to synthetic agents such as fluoroquinolones and oxazolidinones. In addition, mutation is essential for the continued evolution of acquired resistance genes and has, e.g., given rise to over 100 variants of the TEM family of beta-lactamases. Hypermutator strains of bacteria, which have mutations in genes affecting DNA repair and replication fidelity, have elevated mutation rates. Mutational resistance emerges de novo more readily in these hypermutable strains, and they also provide a suitable host background for the evolution of acquired resistance genes in vitro. In the clinical setting, hypermutator strains of Pseudomonas aeruginosa have been isolated from the lungs of cystic fibrosis patients, but a more general role for hypermutators in the emergence of clinically relevant antibiotic resistance in a wider variety of bacterial pathogens has not yet been proven.
Roumagnac, P. et al. (2006) Evolutionary history of Salmonella typhi. Science, 314, 1301-1304
For microbial pathogens, phylogeographic differentiation seems to be relatively common. However, the neutral population structure of Salmonella enterica serovar Typhi reflects the continued existence of ubiquitous haplotypes over millennia. In contrast, clinical use of fluoroquinolones has yielded at least 15 independent gyrA mutations within a decade and stimulated clonal expansion of haplotype H58 in Asia and Africa. Yet, antibiotic-sensitive strains and haplotypes other than H58 still persist despite selection for antibiotic resistance. Neutral evolution in Typhi appears to reflect the asymptomatic carrier state, and adaptive evolution depends on the rapid transmission of phenotypic changes through acute infections.
Nilsson, A.I. et al. (2006) Reducing the fitness cost of antibiotic resistance by amplification of initiator tRNA genes. PNAS, 103, 6976-6981.
Deformylase inhibitors belong to a novel antibiotic class that targets peptide deformylase, a bacterial enzyme that removes the formyl group from N-terminal methionine in nascent polypeptides. Using the bacterium Salmonella enterica, we isolated mutants with resistance toward the peptide deformylase inhibitor actinonin. Resistance mutations were identified in two genes that are required for the formylation of methionyl (Met) initiator tRNA (tRNAi)(fMet): the fmt gene encoding the enzyme methionyl-tRNA formyltransferase and the folD gene encoding the bifunctional enzyme methylenetetrahydrofolate-dehydrogenase and -cyclohydrolase. In the absence of antibiotic, these resistance mutations conferred a fitness cost that was manifested as a reduced growth rate in laboratory medium and in mice. By serially passaging the low-fitness mutants in growth medium without antibiotic, the fitness costs could be partly ameliorated either by intragenic mutations in the fmt/folD genes or by extragenic compensatory mutations. Of the extragenically compensated fmt mutants, approximately one-third carried amplifications of the identical, tandemly repeated metZ and metW genes, encoding tRNAi. The increase in metZW gene copy number varied from 5- to 40-fold and was accompanied by a similar increase in tRNAi levels. The rise in tRNAi level compensated for the lack of methionyl-tRNA formyltransferase activity and allowed translation initiation to proceed with nonformylated methionyl tRNAi. Amplified units varied in size from 1.9 to 94 kbp. Suppression of deleterious mutations by gene amplification may be involved in the evolution of new gene functions.
Courvalin, P. (2005) Antimicrobial drug resistance: “Prediction is very difficult, especially about the future”. Emerging Infectious Disease, 11, 1503-1506.
Evolution of bacteria towards resistance to antimicrobial drugs, including multidrug resistance, is unavoidable because it represents a particular aspect of the general evolution of bacteria that is unstoppable. Therefore, the only means of dealing with this situation is to delay the emergence and subsequent dissemination of resistant bacteria or resistance genes. Resistance to antimicrobial drugs in bacteria can result from mutations in housekeeping structural or regulatory genes. Alternatively, resistance can result from the horizontal acquisition of foreign genetic information. The 2 phenomena are not mutually exclusive and can be associated in the emergence and more efficient spread of resistance. This review discusses the predictable future of the relationship between antimicrobial drugs and bacteria.
Denamur, E. et al. (2005) Intermediate mutation frequencies favor evolution of multidrug resistance in Escherichia coli. Genetics, 171, 825-827.
In studying the interplay between mutation frequencies and antibiotic resistance among Escherichia coli natural isolates, we observed that modest modifications of mutation frequency may significantly influence the evolution of antibiotic resistance. The strains having intermediate mutation frequencies have significantly more antibiotic resistances than strains having low and high mutation frequencies.
I don’t think so. I think he’s so blinded by his religious beliefs that he honestly, genuinely believes that evolution has nothing to do with antibiotic resistance. Of course, as Mike the Mad Biologist pointed out, he actually describes the evolution of bacterial resistance fairly well; he simply labels it as “not evolution.”
Heh. I wonder what he’ll say about me if he ever deigns to address my challenge. Of course, I’d be happy to e-mail him my “real” name if he e-mails me to request it. Or he could just ask DaveScot.
May I suggest that against religionists one has to use arguments which they can understand?
Against stupidity the gods themselves contend in vain.
Friedrich von Schiller
German dramatist & poet (1759 – 1805)
A note on acceptance of evolution and overprescription of antibiotics:
I live in the Czech Republic, where acceptance of evolution is at something like 85%, reckon more like 99% of those with postsecondary degrees. So you would reckon that physicians would think about diseases in evolutionary terms and be careful about antibiotic prescription? WRONG. Every time I get bloody anything it seems, I get a script for Augmentin. I have one unopened pack in the fridge, a couple years past expiry, and I’ve never bothered to fill the others, because I’ve never had a culture taken and even the doc giving the prescription admitted that what I had was viral, but said I should take the meds anyway ‘just in case.’ And this is very common practice here–the only advantage I see is in a placebo effect, because most Czechs I know firmly believe their dreadful cold or bronchitis or ‘angina’ (I’m still trying to figure out what that is, since it has nothing to do with the heart) gets better once they start antibiotics.
Concerns over bacteria developing resistance are just not part of the medical paradigm here, at least for GPs, though the younger docs might be more savvy, as I think the med school curriculum here has recently got out of the 50s.
Oh, Orac would also love the amount of herbal meds my GP recommends…
Then there was my chronic otitis externa, which I finally went to an ENT for. Even though she took a culture and no pathogens were found, just ordinary skin bacteria, she still put me on antibiotic drops. For months. All this time I’d noticed–pardon if this is TMI–black residue in my ear, looking for all the world like shower mold, but I thought, heck, if there was such a thing as fungal otitis externa, my ENT would know about it, wouldn’t she?
After 6 months of this, I finally Googled around for it and found an NHS site that said that most chronic otitis externa is fungal and that antibiotics are contraindicated. I still haven’t got rid of the condition completely but I keep it well under control with supermarket 8% vinegar diluted 3:1, as per a pharmacist friend’s advice (you cannot get acetic acid ear drops in this country).
MarkCC,
Well stated and clear explanation of the evolutionary effects of selection induced by antibiotic use. Your pediatrician shows appropriate acumen in this area.
Another example from an area that I am more familiar with by experience is the rotation of pesticide use in raising foods. If one uses the same pesticide over and over again all you will accomplish is the creation of insects that will eventually eat your pesticide for breakfast and your crop for lunch. If you rotate the use of different pesticides you can mitigate the evolutionary effects of pesticide induced selection and probably raise your crop with fewer pesticide applications at lower concentrations. These effects have been known in agriculture for about a hundred years.
Where has the good doctor been? The practical applications of an understanding of evolutionary theory are everywhere.
Jim51
The inherent stupidity and implied ignorance of Mr. Egnor’s last quote is truly mind-boggling. I think, by his own logic, Egnor could be succesfully sued for malpractice by a savvy and shrewd attorney if one of his patients developed a resistant infection.
I guess multidrug resistant tuberculosis has always been around, too. What a complete tool.
One thing that Egnore seems to be avoiding is that, while a simple statement of evolutionary theory may be tautological, there are also the quantitative and descriptive aspects of it. It not only says that “bacteria that aren’t killed aren’t killed”, it says that, “If X% of bacteria aren’t killed when you prescribe Y, then in N generations, you can expect 99% of bacterial to be resistant to Y” (like you say, the worst math is no math); and that “the mechanism behind the development of resistandce is a mutation in gene A, which will produce effects B C and D”
Jud:
I don’t mean to suggest that there’s anything like a deliberate conspiracy to misprescribe antibiotics in a way that leads towards the evolution of resistance. What I’m trying to say is that the willful ignorance and stupidity of people like Egnor causes foolish behavior: if you don’t believe that bacteria are evolving, you’re likely (out of nothing more than pure laziness) to not be as careful about how you prescribe antibiotics. If you look at my description of what my kids’ pediatrician does, it’s a lot of work to prescribe antibiotics properly. If you don’t believe in the danger, you’re not going to do the work. And if you look at prescription records and patterns, you’ll find that the majority of practicing physicians still are not doing it.
bad Jim:
Yes, our pediatrician is wonderful. We’re crazy about her 🙂 But it’s no surprise really; she’s a member of the teaching faculty at Mount Sinai in NYC. We found her by recommendation from my internist, who is also a Mt. Sinai faculty member.
We’ve learned, the hard way, that there is a huge difference in average quality between random doctors in private practice in the suburbs, and faculty members at teaching hospitals. (Not that there aren’t great doctors in private practice – just that the average private practice doctor isn’t nearly as good as the average teaching faculty doctor.) A few years back, before my kids were born, I had surgery for severe gastric reflux. About a year after the surgery, I developed a bunch of weird and extremely painful symptoms. I spent two years dealing with suburban doctors, going through every horrible test you can imagine, making no progress on figuring out what was wrong or what to do about it. I finally agreed to see the doctor who is now my internist, out of desparation. One visit, and she knew exactly what was wrong; got on the phone to get me an immediate appointment with a gastroenterologist whose research focused on exactly my problem; and one visit with him, and the problem was solved. Two years of suburban doctors => no progress; 2 *days* of faculty doctors => solution.
For those who think anti-biotic resistance is evidence for evolution, please read the following:
Is Bacterial Resistance to Antibiotics an Appropriate Example of Evolutionary Change?– In a word- No.
And please check out the credentials of the author.
Also ID is NOT anti-evolution. If anything ID could be considered anti-the blind watchmaker having sole dominion over the evolutionary process. As Dr Behe stated:
In line with Jim51’s comment, I read a disturbing story recently. Apparently weeds have not been able to adapt to the herbicide Roundup. Unfortunately, Roundup also kills some desired plants. Now some people have found bacteria with a resistance to Roundup and are attempting to transfer the resistant gene to “good” plants. Am I wrong in thinking that this is just asking for trouble?
JoeG: we can’t read that, because you didn’t give the link.
Bob
There is no link embedded in the text, so I presume you are the author. Whatever credentials you may have, you are not willing to cite on your blog, which simply says that you “fix things”. Come back when you have something credible to offer.
Mark, this post is one of my all-time favorites (up there with Cosmic Variance’s “Dark Matter Exists” post).
JoeG:
The link you point at is an exercise in deceptive nonsense. It actually admits to evolution as the cause of bacterial antibiotic resistance – but then redefines evolution so as to exclude what’s happening to bacteria. It’s pure semantic word-play to avoid the inescapable truth.
MarkCC: I don’t want to talk past each other here, because I agree with everything you’ve said. I just want to bring out a slightly different point related to Antiquated Tory’s comment above.
That is, I agree with the following: “If you look at my description of what my kids’ pediatrician does, it’s a lot of work to prescribe antibiotics properly. If you don’t believe in the danger, you’re not going to do the work.”
And I also agree with this: “And if you look at prescription records and patterns, you’ll find that the majority of practicing physicians still are not doing it.”
But I’m not inclined to think that the majority of what we see in prescription patterns is caused by doctors not believing there’s a danger. (Of course, my thinking could readily be changed by data.) Rather, I think that although most doctors realize the danger (including Dr. Egnor, though he is, as usual on subjects to do with evolution, quite deliberately not “getting it”), a minority are both willing and able to do the level of office organization necessary to take the precautions your pediatrician does.
Additionally, I agree that doctors who decry evolutionary theory, beyond blinding themselves to the supporting scientific and medical data, are working against lifesaving medical progress in areas such as the acceptance of prescribing patterns that will minimize bacterial evolution of antibiotic resistance.
Who does Egnor think he is, Philip Johnson? Evolution is science, not law–the scientific case is not made by effective rhetoric, but but effectively attributing causations to observations, by constructing theories (scientific, not legal) and hypotheses, and putting them to the test. In his arguments, Egnor has not provided any substantiated explanations for increased resistance or for anything else that has been well explained by evolution.
Denying evolution is as dangerous and as profoundly stupid as denying the germ theory of disease. Is disease a more complex concept than Pasteur realized? Of course. But that’s no excuse not to wash your hands, maintain sterile technique, and avoid dissecting corpses immediately before aiding in childbirth.
In a sane and rational world, Dr. Egnor would be locked away for the protection of society.
Clem,
Your comment…
“Now some people have found bacteria with a resistance to Roundup and are attempting to transfer the resistant gene to “good” plants. Am I wrong in thinking that this is just asking for trouble?”
The short answer to your question is *I am unsure, but concerned.* It seems that horizontal gene transfers have been quite common in the history of life. At least one prominent biologist (Margulis) is convinced that symbiogenesis is a primary source of evolutionary innovation. It seems well accepted that there have been bacterial and viral genetic insertions into the human genome as well. So I am concerned that as we create genetically modified organisms we may create things with a life of their own with potentially unforeseen consequences.
I am out of my depth here, so I too would welcome comments and references from others that may help me learn more.
JIm51
http://www.trueorigin.org/bacteria01.asp
This is NOT deceptive nonsense to those who understand what is being debated. “Evolution” has several meanings.
Even in the strictest YEC model of biological evolution variation is allowed. IOW bacteria “evolving” into bacteria is OK. Linneaus was searching for the “Created Kind” when he gave us binomial nomenclature. He put the “Kind” at the level of “Genus”- meaning speciation is OK in the YEC model of “variation within the ‘Kind'”.
“Evolution” is NOT the question. Nor is it being debated. What is being debated is whether or not “the blind watchmaker” has SOLE dominion over the evolutionary process.
IOW did populations “evolve” solely by culled genetic accidents – or were they designed to evolve?
And what Dr Egnor is saying is that it is unnecessary to think that chimps and humans shared a common ancestor because such a premise is not demonstratable in a lab nor in the wild and effective cures need to be demonstratable in both.
So I take it “the inescapable truth” is you don’t know what is being debated, you don’t care to know and that when presented with “the inescapable truth” you sit there and deny it.
Thank you.
Dominion? I don’t think you’ve quite grasped the concept, JoeG.
The whole point is that culling genetic variation is sufficient to explain the diversity we see – and there’s no evidence whatsoever for a magic sky man with dominion who done it.
See The History of Creationist Thought
What a load of crap, Joe. If ID is so compatible with standard evolutionary theory, why does nearly every IDist rant conclude with “therefore, evolution is wrong and a Designer did it”? Why do IDists spend all their time attacking “Darwinist” straw men rather than proving the utility of their design inference? For Designer’s sake, how do you explain the wedge document?
And, for the record, ID is the watchmaker argument. Why do you think a lot of the ScienceBloggers (PZ, at least) have started referring to “Paleyists”. Paley’s watchmaker argument is exactly the same as the ID argument: This Feature (e.g., watch in the sand, the eye, etc.) is not simple! Therefore, it was Designed.
People who agree with Shelly Batts that religion is OKAY, this is for you, so you can better understand why religion must be stamped out…
Deuteronomy 22: 28 If a man is caught in the act of raping a young woman who is not engaged, he must pay fifty pieces of silver to her father. 29 Then he must marry the young woman because he violated her, and he will never be allowed to divorce her
Deuteronomy 7:1 When the Lord your God brings you into the land you are entering to possess and drives out before you many nations … then you must destroy them totally. 2 Make no treaty with them, and show them no mercy.
Leviticus 21: 9 And the daughter of any priest, if she profane herself by playing the whore, she profaneth her father; she shall be burnt with fire.
Shelly, I would like to buy into this Bible stuff like you do, but it seems too violent for modern society. Here is how a moderate Christian defends abortion…
“The Book of Exodus clearly indicates that the fetus does not have the same legal status as a person (Chapter 21:22-23). That verse indicates that if a man pushes a pregnant woman and she then miscarries, he is required only to pay a fine. If the fetus were considered a full person, he would be punished more severely as though he had taken a life.”
That is the kind of stuff that Christians like Shelley are fine letting others believe. Here is another example…
“By our deepest convictions about Christian standards and teaching, the war in Iraq was not just a well-intended mistake or only mismanaged. THIS WAR, FROM A CHRISTIAN POINT OF VIEW, IS MORALLY WRONG – AND WAS FROM THE VERY START. It cannot be justified with either the teachings of Jesus Christ OR the criteria of St. Augustine’s just war. It simply doesn’t pass either test and did not from its beginning. This war is not just an offense against the young Americans who have made the ultimate sacrifice or to the Iraqis who have paid such a horrible price. This war is not only an offense to the poor at home and around the world who have paid the price of misdirected resources and priorities. This war is also an offense against God.”
Seems like that Christian has actually arrived at the right destination (one of the few who has), AMAZING! I guess the only problem remaining here is the compass (RELIGION), which can be unreliable and is easily misinterpreted.
http://www.beliefnet.com/blogs/godspolitics/
Leviticus 20: 27 A man also or woman that hath a familiar spirit, or that is a wizard, shall surely be put to death: they shall stone them with stones; their blood shall be upon them.
Cheers to PZ Myers and Richard Dawkins and Sam Harris (and myself), who can see the danger in sadistic “fairy tales”.
JoeG said: Also ID is NOT anti-evolution
Then why are all their arguments variants of “here is a weakness in evolution”?
This is NOT deceptive nonsense to those who understand what is being debated.
It is on Trueorigin, isn’t it? The whole site is deceptive nonsense.
Even in the strictest YEC model of biological evolution variation is allowed.
Your religiousity is leaking through again. Science doesn’t “allow” or “not allow” things, that’s what gods do.
IOW did populations “evolve” solely by culled genetic accidents – or were they designed to evolve?
To demonstrate that this is anything more than a semantic ploy, and is actual science, please give a hypothetical experimental result that would imply that latter, but not the former.
I wonder what Egnor thinks about domestic animal breeding. For example the various strains of dogs are obviously bred to a purpose. How much of a leap is it between this and bacteria ‘breeding’ to with the ends of defeating antibiotics?
It’s my experience generally that surgeons are as ignorant of infection as they are of bedside manner. Sterile fields are pretty much as far as they go: they rip the shit out of people’s bodies, and then leave it to OTHER doctors to figure out the little issue of whether the patient will die of post-surgical infection or not.
Clem & Jim51 –
The situation with Roundup is even worse. Resistance was introduced over 10 years ago in several crops, including oilseed rape (canola). It has already escaped (certainly in Canada: I’m not sure about elsewhere): Oilseed rape is a weed in many places, and hte gene is likely to find itself in other brassicas as well (e.g. cabbage).
In one sense this isn’t so bad: Monsanto make Roundup, and also the resistant crops. So the more resistant the weeds become, the less Roundup they get to sell.
Bob
If it comes from MarkP it must be deceptive nonsense. Pharyngula is deceptive nonsense. Also I am NOT a christian and don’t have any “religiousity”. Your ignoarnce is very telling. Read the article and check out the credentials of the author. Or wallow in your ignorance.
Start by reading “Not By Chance”…
The DI has explained “The Wedge Document” and it appears that only anti-ID zealots don’t understand it:
http://www.discovery.org/scripts/viewDB/filesDB-download.php?id=349
IDists do NOT conclude “that evolution is wrong therefore a designer did it”.
IDists take the data and weigh it against the options. That is what science should do. And one option is that we owe our existence to an intentional design. The anti-ID materialistic option is sheer dumb luck- including the laws that govern this physical realm. Either that or the metaphysical “the universe is ‘just is'” (the way it is).
BTW “culling genetic variations” do NOT explain the physiological and anatomical differences observed between chimps and humans. Only wishful speculation does that.
This is a rather minor point, but I would encourage you to reconsider this policy. Anyone finding their post through you already has access to the antidote, and I consider it a point of pride that the ‘forces of good’ in this battle have the integrity to cite their sources. It’s so sciency.
Sure it does. Mutation, selection, and drift — that’s all you need.
And why should I check out anyone’s credentials? The ad hominem argument is a logical fallacy.
Incorrect. Chance is only part of evolution – and ‘luck’ has nothing to do with chance in any formal sense. Chance produces variation, and selection winnows down the variation to the viable strategies. Sometimes chance can also affect the population gene pool directly, such as through genetic drift, but this has no tendency to produce adaptations of the kind you’re so concerned about.
The genetic differences between chimps and humans are very small, as your behavior suggests. It would be quite easy for relatively modest evolutionary changes to lead to both from an earlier form.
What’s up? Can’t I post links?
Think about it. Once something can reproduce, mutate, and inherit, evolution is inescapable: due to mutation, there will be variation in the population, and the environment (in this case the antibiotics) will cause some part of this variation to have fewer surviving offspring than the rest (in this case by killing it). No design necessary. You are simply making an unnecessary assumption, and you know what scientists do with unnecessary assumptions, don’t you.
Now the link in plain text:
http://en.wikipedia.org/wiki/Parsimony
That’s what scientists do with unnecessary assumptions.
David Marjanović:
Putting more than one link into a post will throw your post into the moderation queue. MarkCC is pretty good about getting legitimate posts out of the queue and into the threads where they belong, but given that he’s not a superintelligent AI (like Orac), there may be a small delay.
You can sign in with a TypeKey identity and use more links (although I’ve had a TypeKey-authenticated message still get stuck in moderation at least once). The problem is that, at least for me, the comment shows up as “Anonymous”.
Given some of the crap being posted on
Tara Smiths’ blog by the HIV/AIDS deniers, which sounds much like the evolution deniers like Egnor, I wonder what his opinion is about HIV/AIDS. Since many of the clowns over at the Discovery Institute are also HIV/AIDS deniers (e.g. Johnson, Wells), it would be interesting to ascertain Dr. Egnors’ views on the subject.
So Creationists agree that variation is okay, and that changes in frequency of variations over time is okay? And they don’t deny that mutations occur?
So how much change is “allowed” before the Intelligent Designer says “Stop!–any further change would be considered evolution, and that is forbidden!” Certainly, details of the concept of species for bacteria can be argued, but I don’t see any meaning to the idea that bacteria constitute only one “kind” in any sort of species (or genus) sense. Indeed, the notion of “kinds” is merely a means to help Creationists deny that evolution has occurred.
JoeG is also mistaken in his claim that ID is not anti-evolution. If that were true, then the ID Creationists would not be pursuing the “teach the gaps and weaknesses in evolution” strategy of trying to bring pseudoscientific nonesuch into public schools. They would instead be presenting scientific theory; that the Disco Institute now claims they do not wish for ID to be taught is evidence that there is no science there.
Dr. Egnor would most certainly have learned evolutionary theory during his training. My training in the biological sciences overlapped much of the pre-med program and virtually every biology-related course involved coursework on evolution to some extent or another. Egnor’s selective memory may not be a good practice when it comes to ignoring the role of evolution but certainly one he is capable of exercising. Perhaps this is why hospitals have taken the proactive step of protecting their legal asses from such ignorance by establishing a myriad of controls (such as rotating drug therapies). Egnor’s selective egnorance is, in part, counteracted by the procedures and policies the hospitals employ.
Joe:
That may be the argument that you are interested in making. But it is clearly not the argument that Egnor is making, or that I’m discussing here.
Egnor states, in absolutely unambiguous terms, that “Darwinism” and “random mutation and natural selection” are complete irrelevant to antibiotic resistance.
That is clearly not an argument about whether there’s an intelligent agent involved in the process of evolution – it’s an absolute denial that evolution plays any role in, or has any relevance to, antibiotic resistance.
No. That it not what Egnor says. That might be what you want him to say – but it’s not what he said. He has said, repeatedly, that evolution plays no role in antibiotic resistance.
An excellent summary of your own position. You’re completely ignoring the actual debate that’s taking place – that is, whether an evolutionary process plays any role in the development of antibiotic resistance in bacteria – and instead debating whether or not there is an intelligent agent somehow involved in the evolutionary process.
Until Egnor admits that the development of antibiotic resistance in bacteria is an evolutionary process, any debate about what form that evolutionary process takes is irrelevant.
JoeG galloped thusly:
If it comes from MarkP it must be deceptive nonsense. Pharyngula is deceptive nonsense.
None of those sources have a long track record of posting deceptions and distortions. Those creationist sites do, which is why I don’t bother reading them.
The DI has explained “The Wedge Document” and it appears that only anti-ID zealots don’t understand it
Dover dude, Dover. This has all been settled in the fairest arena our system has. Your side had their chance to defend themselves, and those that didn’t bravely run away got shredded. You guys got caught with your pants down replacing “creationism” with “intelligent design”, and we aren’t going to forget it.
IDists do NOT conclude “that evolution is wrong therefore a designer did it”.
They most certainly do, since that is the only argument they have. Again, this has already been exposed, repeating the same refuted nonsense over and over again isn’t going to persuade anyone. But I’m sure you impressed Duane Gish, because that was quite a gallop of unsupportable assertions.
Joe:
So, you’re supposedly not a Christian, but you swallow the nonsense from “trueorigins” without question; and you blindly dismiss anything from MarkP or PZ Myer, again without question; and you accuse MarkP and PZ of being deceptive without bothering to provide any support for your claims of their deceptiveness; and you defend Egnor’s claims without even bothering to see what they actually are.
And you expect to be taken seriously?
Mustafa:
I appreciate your point about linking to Egnor’s rants – and that’s why I provide enough information in the article to make it easy to find his stuff if you really want to. But I won’t provide direct links – direct links are effectively subsidizing the DI. I think that the information I provide is enough to be considered a citation of the source; but it doesn’t provide an easy hit-boost to the DI pages.
Anyone else notice that Egnore misspelled ‘clade’?
One last point in response to JoeD:
As I’ve said before: one of the really beautiful things about real math and science is that credential are irrelevant. Math and science stand on their own, on the quality of their evidence/proof.
A mathematical proof could be written by Grigori Perelman, or it could be written by a second-grader. It doesn’t matter: a mathematical proof is either valid, or it isn’t. If it’s invalid, then it doesn’t matter if someone as qualified and credentialled as Grigori Perelman wrote it – if it’s got an error in it, anyone who pointed out that error would “outweigh” Perelman.
A scientific theory is based on the quality of its reasoning, and how well the theories predictions match observations of the real world. Again, it doesn’t matter whether the theory is proposed by someone like Richard Feynman, or some 16 year old from East Podunk. The theory stands on the quality of its evidence and its predictions, not on the credentials of its author. If the 16-year old from East Podunk can do a better job of explaining the evidence than Richard Feynman, then even Feynman himself would have agreed that his theory should be discarded in favor of the better theory.
In the case of evolution, the evidence is absolutely overwhelming. From fossil matches, to genetic sequences, to biochemistry and biochemical processes in living things, to developmental processes, to observed events – everything supports evolution from a common ancestor.
Try sitting down something and actually reading through some of the evidence for various clade trees. You can derive distinct heirarchical relations based on multiple different chemical markers, developmental similarities and differences, fossil evidence, and genetic similarities and differences – and then when you compare the resulting heirarchies, they’ll be virtually identical. Multiple sources of evidence, interpreted via distinct processes will result in the same hierarchical ancestry relationships.
That’s absolutely astonishing. It’s incredibly compelling evidence, and no other theory that’s been presented so far by anyone can explain that evidence, or predict that incredible perfect hierarchy at all, much less as well as the the theory of evolution.
And please check out the credentials of the author.
Check out JoeG’s credentials – he is a ‘scientist’ because he has a Bachelors of SCIENCE…. in electronics engineering…
And liniing to creationist propaganda websire ‘Trueorigins’? Fantastic!
And don’t bother reading creationist Spetner’s silly book – he thinks all proteins are enzymes, and has admitted that beneficial mutations occur. He’s just trying to prop up his truly bizarre creationist position (such as all birds coming from 365 original kinds of bird and all mammals from 365 ‘kinds’….)
Developing new antibiotics takes TIME, and that seems to be what Egnore doesn’t grasp. Sure, we’ll always find new ones, but they don’t appear or get approved over night.
By realizing that Evolution drives genetics, and being careful about when to proscribe antibiotics, we can limit the rapidity at which bacteria become immune. Take a drug out of rotation for awhile, and it is possible for it to become effective again.
But willy-nilly proscribing new drugs just because biochemists are hard at work developing new anti-biotics is dumb. It takes years. And with some of the new Staph strains out there majorly resistant to whole classes of antibiotics, it may only be a short period of time before a new superbug appears that is resistant to all existing antibiotics, and the possible new drugs to fight it are years away…
Now, I do think we should look into Phage treatments as well. When viruses co-evolve with the bacteria they predattate, immunity doesn’t happen. The Russians have had some success, and I’d like to see more research in this field.
slpage:
Emphasis added to phrase which nearly induced a spit take.
Wow.
I trust he’s keeping track of his patients; anyone placed a bet on how fast he pushes antibiotic resistance in his own patients, compared to the doctors who are being careful out of awareness of selection pressure?
I’d bet there’s a clear difference in a decade (not much, it’s a wild ass guess on no data).
But gad, who but a nonbelieving MD could be such a powerful force for selection of resistant bacteria, eh? Irony.
Daniel:
It’s actually even a bit worse than you say.
Because of my father’s recent illness, I’ve been doing a lot of reading about bacteria and antibiotics. One of the things that I didn’t realize before was just how few fundamentally different antibiotics there are. There are a relatively small number of basic mechanisms by which antibiotics work. Most of the time, new antibiotics are members of an existing family – that is, they work by essentially the same mechanism as earlier antibiotics in the family.
For example, one of the most common kinds of antibiotic is called a β-lactam antibiotic. β-lactam’s include the entire penicillin family, all four generations of the cephalosporins, and all of the carbapenems. β-lactam’s work by interfering with the bacteria’s ability to generate cell walls when they divide – in particular, one of the types of components of many bacterial cell walls is called a penicillin-binding protein – because it’s what the penicillin latches onto and deactivates; and without the PBPs, the bacteria can’t produce cell-walls.
The different drugs do have differences, which are important. But one of the things that’s been happening recently is that the resistance mechanisms have been getting more versatile, so that they’re resistant to entire families. For example, the main strength of the carbapenems has traditionally been that they’re relatively immune to β-lactamase, which is an enzyme produced by many resistant bacteria to neutralize penicillin-family β-lactams. But recently, many bacteria have developed different approaches to β-lactam resistance – they’re using radically different proteins to form their cell walls, so that they don’t use PBPs at all. PBP-less bacteria are immune to not only current β-lactam antibiotics, but to all possible future β-lactam antibiotics.
Antibiotics based on fundamentally different modes of action are extremely rare. There are only about a dozen fundamental families of antibiotics; and even they aren’t entirely distinct – the cepaholosporins, penicillins, and carbanapems are all β-lactam antibiotics.
So even with the new antibiotics that are coming down the pike, my reading (which is, admittedly, the reading of someone who’s not particularly qualified in the area) is that there’s currently one type of antibiotic with a new mode of action currently under development.
(And yes, I agree that phage therapy is interesting. But there are some questions about the honesty of the reporting of preliminary results, as well as questions about what effect resistance to phage drugs would have on bacterial ecology.)
Yes Splage I was just rushing to post before I did a search to see if someone else pointed it out. The gall of an IDiot dropping the term clade but then denying what it alludes to is staggering.
And please check out the credentials of the author.
Ah yes — he’s editor-in-chief of the “peer reviewed journal” in which his article was published — “Creation Research Society Quarterly”. Naturally, any objective observer like Joe would take what this author says as gospel and ignore what is said by the thousands of biologists who disagree with him.
This is NOT deceptive nonsense to those who understand what is being debated. “Evolution” has several meanings…
Joe doesn’t understand the paper he cited, which argues that
This is utter nonsense that shows a lack of basic understanding of the concept of “fitness”, which is defined entirely in terms of reproductive success in a given environment, not in terms of the possession of this or that physiological characteristic.
The anti-ID materialistic option is sheer dumb luck
No, the materialistic option is natural selection. If you weren’t dumber thatn dirt, realpc … er, I mean Joe G. … you could grasp what those words mean.
Since Egnor (and JoeG) believes in frontloaded resistance mechanisms, it would be interesting to see him explain that.
clem, Jim51:
I’m not familiar with Roundup or the safety concerns, but as it happens Larry Moran just blogged about it in his weekly series of biochemistry, explaining Monsanto’s work. Assuming that this is what you describe, the first process was patented 1994.
Monsanto transfered the resistance gene to crops by a rather intricate work of genetic engineering, involving taking it from one species of bacteria, putting it in a plasmid and letting another bacteria transfer the gene into the target. ( http://sandwalk.blogspot.com/2007/03/roundup-ready-transgenic-plants.html ; to not hold up this comment, I will post the accompanying links in a separate comment.)
Note that herbicide resistance wasn’t the only resistance gene, aside from all the regulatory ones. Monsanto also use two antibiotic resistance genes (a spectinomycin/streptomycin resistance gene and a modified gentamycin resistance gene) as selectable markers. They are used to select the shoots that are successfully treated by killing off the others with the antibiotics.
Now, this is risky for the reason we discuss here, namely resistance evolution (through possible lateral transfer) – they could have used luminance markers, but it would probably cost more with manual selection. It is also wasteful in principle to spread something from the manufacturing process outside the plant. I suppose Monsanto in principle could use Roundup to select the resistant seedlings. I’m not sure why they do not do this.
One commenter noted:
“It’s claimed that antibiotic resistance marker genes might end up in bacteria and thus contribute to the problem of antibiotic resistance. Frankly, this hypothetical scenario seems unlikely as a major problem, especially when compared to the current massive over use of antibiotics in medicine and agriculture – which really is promoting the evolution of antibiotic resistance in a big way.
Nonetheless, plant biotechnologists are well aware of the public concern and have been quietly developing alternatives.
According to my plant scientist friends, there are several different approaches being looked at. One is to simply insert a plant intron into the antibiotic resistance gene. That way, even if it did ‘escape’ and found itself in a bacterial chromosome (and also next to a convenient bacterial promoter), the gene still wouldn’t work.
Another possibility is to move from a selection to a screening-based system. eg the GUS (beta glucuronidase) gene encodes an enzyme whose activity can be detected with a suitable dye.
A third approach is to remove the selection gene altogether before commercial release. To do this, there have been attempts to develop something similar to the Cre/Lox system. ie the antibiotic selectable marker gene is flanked by special DNA sequences recognised by an enzyme that cuts the marker out. The gene for this excision enzyme is inserted into the plant genome together with the selectable marker, but it’s expression is controlled by a pollen/seed-specific promoter. That way, the antibiotic selection marker is removed from the pollen and seed.
Of course, each of these methods will have to undergo their own safety trials etc, so I don’t know how close they are to commercial reality. In any case, even if these alternatives were widely adopted, I have a feeling that anti-GM activists will simply come up with some other reason why they’re still a bad idea…”
For the discussion about the safety of Roundup itself, wait for the links in my next comment or browse Moran’s blog through the above link.
Now, this is a discussion Egnor would never make. 🙂
The remaining Roundup links:
http://sandwalk.blogspot.com/2007/03/mondays-molecule-17.html , http://sandwalk.blogspot.com/2007/03/how-roundup-works.html , http://sandwalk.blogspot.com/2007/03/nobel-laureate-paul-berg.html , http://sandwalk.blogspot.com/2007/03/jim-watson-comments-on-gm-crops-and.html , http://sandwalk.blogspot.com/2007/03/molecular-basis-of-roundup-resistance.html , http://sandwalk.blogspot.com/2007/03/glyphosate-resistant-weeds.html , http://sandwalk.blogspot.com/2007/03/roundup-is-safe.html .
tm:
Yeah, I did try checking up on the author of that paper, just or kicks. It’s pretty hard to imagine just why Joe thinks that his credentials are so impressive.
Assuming I’ve found the right guy, he’s got a PhD in veterinary anatomy, and he’s a professor in the veterinary college of the university of Florida. He’s the editor in chief of the so-called peer reviewed journal that published his paper (and as far as I can tell, has zero experience as an editor or review board member of any other journal), and he’s got a very mediocre publication list for a tenured professor.
Not a bad background – looking at his bio and vita, I certainly would not conclude that he’s a bozo. But it’s also not a particularly impressive background. I’m really not sure why Joe thought that his credentials were so amazingly impressive.
Just for comparison’s sake… As a researcher, from what I can tell, I’m at roughly the same level of seniority as Dr. Anderson; I might be a bit more senior, but not by much. I consider myself to be an adequate researcher – not an outstanding one by any means. If you go by publications (which is the only real information on Anderson’s website), I look as impressive as Professor Anderson – we each have around 20 peer reviewed publications. I do not consider my publication record to be particularly impressive. It’s about average.
To compare him to an impressive person of our seniority level, one extraordinary researcher that I know has 48 peer reviewed publications listed in CiteSeer; past program chair of at least three major conferences, editorial board board member of the three top journals their field, has served on more than 50 different conference program commitees since graduating, and been invited to serve on on the program committee of five major conferences so far in 2007. That is someone with an impressive set of credentials.
People like me and Anderson are just mediocre in comparison.
Joe G posted “IDists do NOT conclude “that evolution is wrong therefore a designer did it”. ” I guess he was correct, the correct interpretation is IDists conclude that “we don’t understand what happened, therefore God did it.” I hope to never be so close minded that I won’t allow that I simply don’t understand something.
Yes, yes, but no one has explained the bacterial evolution of tautologizing. A crucial question remains to be answered as far as how bacteria gained the power of manipulating tautologies for their own benefit.
hate to nitpick- pardon my own ignorance and limited knowledge of biology (although i did study Darwin extensively in college), but isn’t bacterial resistance to antibiotics an example of adaption, not evolution per se? the strains that posses resistance are the same bacteria, with adapted traits. humans are different species than chimps- NOT chimps with adaptations. please correct me if i’m wrong.
voidoid:
You’re falling for a distinction that’s used by creationists to try to mislead people. Adaptation is evolution. Creationists often try to pretend that there are two diferent phenomena, which they either describe as adaptation vs evolution, or micro-evolution vs macro-evolution.
In the real world, there’s no difference. A change in species (i.e., macro-evolution according to creationists) is nothing more than the sum of a large number of small adaptations (i.e., micro-evolution).
Not to mention that our species categorization of bacteria is a bit of a disaster zone; bacteria just don’t classify into strict species as much as we’d like. A recent strain of staph that doesn’t use PBPs to form its cell walls is an extremely different bacteria from the old-fashioned non-resistant staph. It’s a magnitude of difference plenty large enough to call the resistant strain a “new species” of staph.
The thing people rarely seem to get is that what causes speciation, in the sense of introducing reproductive incompatibility, IS just change on the same scale and of the same sort as things like larger beaks, smaller legs, longer snouts. All of those things are specified by genes too. Reproductive incompatibilities crop up because the genomes get different enough from each other simply so that something goes wrong in the process of getting sperm to egg and then developing an embryo. There’s no great awesome mystery to it, and no one degree of change or barrier in all cases. In abalone, for instance, new species can form as easily as one or two mutations in the coat of the sperm cell, with hardly any change at all elsewhere in the animal between species. In dogs, on the other hand, we have extremely diverse morphology while maintaining reproductive compatibility (in large part because a lot of the diversity of the morphology of dogs is based on a complex system of differing genetic repeats rather than entirely nnew embrological mechanisms)
Assuming I’ve found the right guy, he’s got a PhD in veterinary anatomy
According to http://www.creationresearch.org/board.html, he’s got a Ph.D. in microbiology from Kansas State University, and I’ve found no reason not to believe that. According to evowiki, he’s “a research microbiologist with the USDA/ARS-NSRIC”. He also seems to be, or have been, a professor in the department of Farm Animal Health and Resource Management at the College of Veterinary Medicine, Raleigh, NC, focusing on “bacterial & viral foodborne pathogens, molecular detection, epidemiology, microbial food safety, pre-harvest epidemiology in dairy animals”.
humans are different species than chimps- NOT chimps with adaptations
Humans and chimps are both X with adaptations, where X is any common ancester of humans and chimps.
er, ancestor.
A little further research suggests that there are two Kevin L. Andersons, one (this one) with a Ph.D. in microbiology from KSU, and the other one with a Ph.D. in veterinary medicine from NCSU
Rather important point missing from this discussion of antibioitic resistance evolution in pathogenic (and non-pathogenic) microbes: agricultural practices on this issue are far worse than what goes on in any medical clinic:
Agricultural use of antibiotics and the evolution and transfer of antibiotic-resistant bacteria”
G G Khachatourians 1998
Microbial Resistance to antibiotics is on the rise, in part because of inappropriate use of antibiotics in human medicine but also because of practices in the agricultural industry. Intensive animal production involves giving livestock animals large quantities of antibiotics to promote growth and prevent infection. These uses promote the selection of antibiotic resistance in bacterial populations. The resistant bacteria from agricultural environments may be transmitted to humans, in whom they cause disease that cannot be treated by conventional antibiotics. The author reviews trends in antibiotic use in animal husbandry and agriculture in general. The development of resistance is described, along with the genetic mechanisms that create resistance and facilitate its spread among bacterial species. Particular aspects of resistance in bacterial species common to both the human population and the agrifood industry are emphasized. Control measures that might reverse the current trends are highlighted.”
For example: Monsanto’s bovine growth hormone, when used for dairy milk production, causes the udders to swell and leads to a high incidence of bacterial infection, so rBGH requires antibiotic treatment (as well as normal pasteurization). Ugh. You can imagine how easily this leads to antibiotic resistance.
This is related to outbreaks of antibiotic-resistant E. Coli 0157:H7 in apple juice, where it was traced back to manure contact.
We can also discuss the worst case scenarios: government agencies engineering antibiotic resistance into biological weapons – the Soviets did it, and there are reports that the idiots at Battelle Memorial Institute went and replicated that work. Needless to say, this is sheer insanity of the very worst kind. Whose bright idea was that?
Incidentally, promiscuous plasmid transfer between bacteria is documented in nature via nifty experiments involving chromosomal repressor genes and flourescent gene-expressing plasmids. This is a very different mechanism from single-mutation events; both play roles. The good Doctor is a lunatic; that’s all there is to it.
When you realize that the leading causes of death a century ago were bacterial infections, and that antibiotics and hygiene are the only defenses, and idiots like the Doctor are spouting this nonsense…not good.
RE JoeG: I guess your argument is that the ID only placed some of the fossil bones in the ground to test the faith of the true believers, not ALL of the fossil bones?
I find this little tidbit astonishing:
“…our development of new antibiotics is a process of designing drugs to counter the bacterial strategies.”
What does he mean by bacterial strategies if not evolution? How do bacteria develop new strategies against antibiotics without evolving? Maybe he thinks they have cognitive function? They perceive our attempts to assassinate them and change tactics just to spite us. Thems be some smarty-pants bacteria.
truth machine said: “Humans and chimps are both X with adaptations, where X is any common ancestor of humans and chimps.”
Yep, excellent – and where “adaptations” are those random mutations selected for (via natural selection, sexual selection, genetic drift, etc.) through the generations since the common ancestor.
Also, re plunge and speciation: The “can’t reproduce with each other” criterion for speciation is somewhat of a shorthand that doesn’t always completely describe where to draw the “species line,” e.g., where reproduction is asexual. This is yet another reason why any distinction between “adaptation” and “speciation,” or between “micro-evolution” and “macro-evolution” is just silly. The genetic mutation process has no way of knowing when an accumulation of changes will by academic consensus be considered speciation.
It’s just one species concept out of at least 25. In many cases there is no “academic consensus”.
Which, of course, has led some to argue that species don’t really exist outside of our heads, just like genera, families, orders, classes, phyla, kingdoms, domains, and cre_ti_nist “kinds” don’t.
While radical, this point is not without merit…
Egnor and his kind explicitly blame “Darwinism” for such atrocities as eugenics and the Holocaust, without a trace of evidence or a credible cause-and-effect link. Then one of them acts all shocked (SHOCKED) when Mark blames ignorance of evolution for a particular instance of inappropriate medical treatment leading to his father’s worsening health condition. Just another example of crybaby creationist hypocricy.
I also notice that “Dr.” Egnor refers to Mark’s “dad,” as if he thinks — or wants his intended audience to think — he’s talking down to a child. Let me guess — Egnor didn’t study tact or bedside manner either, because neurosurgeons don’t need to learn such concepts.
Physician, heal thyself. (Now, you knew that was coming, right?)
What does he mean by bacterial strategies if not evolution?
That occurred to me, too – read on:
How do bacteria develop new strategies against antibiotics without evolving? Maybe he thinks they have cognitive function? They perceive our attempts to assassinate them and change tactics just to spite us. Thems be some smarty-pants bacteria.
But you see, it’s not the smarty-pants bacteria, it’s the smarty-pants designer behind the bacteria. Get it? They’re just retro-fitting their little theology onto biology, whatever discovery biologists make; and the idea that this is a strategy in itself, a form of theological exaptation (which they deny), never even occurs to them! 😉
I mean, if they’re going to impose theology onto biology in this manner, why not just become a theistic evolutionist and quit believing in a designer who’s always plodding along a step or two behind the science? Mark manages to reconcile his beliefs and science; maybe Egnor is just jealous.
So god (designer) is sadistic? God designs bacteria and places organisms that have antibiotic chemicals around. Causes countless generations of humans (especially the poor) to suffer and die from infection (think plague) until finally these chemicals and their properties are discovered. Then, once all this comes together and therapies are developed, the designer changes the game to make the bacteria resistant. Wow, now there is a god that inspires you want to kneel down and sing praises, a true beacon of good.
“Also, re plunge and speciation: The “can’t reproduce with each other” criterion for speciation is somewhat of a shorthand that doesn’t always completely describe where to draw the “species line,” e.g.,”
Yes, I know, and this has already been mentioned, and that’s why i specified what I was talking about in my post (“in the case of reproductive incompatibility).
“The genetic mutation process has no way of knowing when an accumulation of changes will by academic consensus be considered speciation.”
Indeed, which was, basically, my point. The changes that happen to cause incompatibilities are not substantively different than those which don’t: there is no magical line anywhere in a genome, or one set of special genes that defines species boundary. The biological species concept is by far the most common and the one best understood by laypeople, so its the one worth discussing here, and the point is that even there, where species boundaries might seem most distinct, there is no way to look at the genes and tell that they won’t produce a viable offspring. It’s the same process of development that has to play out as with anything else.
Or, to be nitpicky, possibly the result of other evolutionary mechanisms such as genetic drift or the proposed concept of group selection.
An good explanation of the history and different meanings behind the macroevolution concept is given in http://www.talkorigins.org/faqs/macroevolution.html . It ends:
“Macroevolution is at least evolution at or above the level of speciation, but it remains an open debate among scientists whether or not it is solely the end product of microevolutionary processes or there is some other set of processes that causes higher level trends and patterns. It is this writer’s opinion that macroevolutionary processes are just the vector sum of microevolutionary processes in conjunction with large scale changes in geology and the environment, but this is only one of several opinions held by specialists.
The misuse of the terms by creationists is all their own work. It is not due to the ways scientists have used them. Basically when creationists use “macroevolution” they mean “evolution which we object to on theological grounds”, and by “microevolution” they mean “evolution we either cannot deny, or which is acceptable on theological grounds”.”
But perhaps selection can be more important than population models lead some to believe:
“A mouflon population, bred over dozens of generations from a single male and female pair transplanted to Haute Island from a Parisian zoo, has maintained the genetic diversity of its founding parents. This finding challenges the widely accepted theory of genetic drift, which states the genetic diversity of an inbred population will decrease over time.
“What is amazing is that models of genetic drift predict the genetic diversity of these animals should have been lost over time, but we’ve found that it has been maintained,” said Dr. David Coltman, an evolutionary geneticist at the University of Alberta.
[…]
He argues that the extreme conditions on the craggy, windswept island have prevented genetic drift due to the premium advantage the more genetically diverse mouflon on the island hold over their less genetically diverse cousins.
“This herd certainly challenges our understanding of genetic drift,” he said. “And I think it shows us the power of natural selection.”” ( http://www.eurekalert.org/pub_releases/2007-03/uoa-rsp030807.php )
The same Wilkins who wrote the above piece goes through the different species concepts David mentioned in several posts on his blog here at scienceblogs.
As I understand it, the difficulties in mapping the descriptive concept of species into a single general choice of what Wilkins names different “conceptions” makes the biologist instead choose and declare a functional concept(ion) that matches the task at hand, whether it is description or modeling.
A biological species concept (based on reproductive isolation) may suit describing mammals. (But not perfectly since different horses and cats can often interbreed when given opportunity.) Some form of phylogenetic species concept suits describing fossils well. (Based on characters; since it is difficult to observe fossils breed. 🙂
And not much seem to match single cell organisms well, which presumably explains some of the difficulties with describing the bushy root and domains of the Tree of life.
Um, yes, of course – this is the more basic reason why species concepts are difficult. There is no magical barrier here either, as for other characteristics.
MarkCC wrote:
No, these are two different people. The University of Florida guy is Kevin J. Anderson, while the editor in chief of the Creation Research Science Quarterly (and author of the execrable article cited by JoeG) is Kevin L. According to this biography the latter’s current position is director of the Van Andel Creation Research Center in Chino Valley Arizona.
David:
Thanks for the correction. I’ll go back and modify the earlier comment to make it clear that I was wrong.
Which is akin to how glyphosate resistance developed:
“The C4 strain of Agrobacterium sp. proved to be just the thing. This is a species of bacteria that was found growing in the waste-fed column at a factory that made glyphosate. The EPSP synthase enzyme from this bacterium (C4 EPSP synthase) was almost completely insensitive to glyphosate.”
Nature is an exciting experiment, which we are fortunate to be able to observe.
I’m guessing that this is different from the Kevin J. Anderson (born 27 March 1962) who is a prolific and best-selling American science fiction author. Right?
It is interesting to assume that I’m wrong. In “Invitation to a Beheading” Nabokov gave a straight-faced description of the process of psychoanalyzing the author of two books that are presumed to have been written by distinct authors, on the alternative presumption that one or both names was a pseudonym, and the works WERE by the same author.
For instance, Steven Hawking and Stephen King being the same horror-physicist…
MarkP wrote: “mathematicians like MarkCC”
When did MarkCC become a “mathematician”? Does he have an advanced degrees in mathematics? Has he written any papers indexed by MathSciNet?
Nat:
I’ve never claimed to be a mathematician – as I constantly say, I’m a computer scientist and a math geek. My advanced degrees are all in computer science. Some of my publications are probably indexed in mathscinet, but since this is my week between jobs, I don’t have subscriber access to check.
But I’ve always found credential fights to be silly. As I’ve said, repeatedly, one of the great things about math is that credentials are irrelevant. When you write a proof, if it’s right, it doesn’t matter whether you’re Grigori Perelman or a third grader.
And the line between Math and many related fields can be so thin that it’s essentially arbitary. This year’s Turing award winner doesn’t have any degrees in CS. Are you going to say that she’s not a computer scientist?
Greg Chaitin has published some extremely practical work in computer science – using graph coloring algorithms for register allocation in optimizing compilers. Is he somehow less qualified to write a computer science paper for being a mathematician?
One member of my thesis committee in grad school was John Case. John is a pioneer in a very strange field called recursive learning machine theory. Is he a computer scientist or a mathematician? Which field would you claim his students have credientials to discuss?
The comment that MarkP made was about thought processes – and my way of thinking is pretty much exactly what MarkP described. If the math didn’t support evolution, I would be the first to publicly denounce it and do my best to demonstrate the errors. But the math is sound. And it doesn’t matter whether I say that as a mathematician or a computer scientist.
Mark wrote: “Some of my publications are probably indexed in mathscinet”
No, they’re not.
“But I’ve always found credential fights to be silly.”
You seemed to be engaging in some fairly extensive credential checking above.
“As I’ve said, repeatedly, one of the great things about math is that credentials are irrelevant. When you write a proof, if it’s right, it doesn’t matter whether you’re Grigori Perelman or a third grader.”
What percentage of your attacks on bad math involves you providing an actual mathematical proof that the “a**holes” are wrong? More than zero?
Nat:
I looked up the credentials on Anderson just because I was curious, because the commenter who originally brought him up made a big deal about his credentials. And if you bother to look back at the comment thread, you can even see that in action. My first response was to content of the linked article; my second was about how irrelevant credentials are; and it wasn’t until a day later that I got around to trying to check the allegedly “impressive” credentials of the author.
And as for your last comment: I do my best to clearly point out the mathematical errors in the things I critique. I try to keep the blog entertaining to read, so I don’t structure my posts -especially the “bad math” posts – as methodical proofs. But the content is there: I don’t just point my finger and call names – in my posts, I try to identify specific errors.
If you disagree, feel free to point it out. If you just want to float around and make essentially content-free obnoxious comments, you’re free to do that too, but it doesn’t accomplish much except to make you look obnoxious.
“Our battle against bacterial resistance to antibiotics depends on the study of the intricate molecular strategies bacteria use to fight antibiotics, and our development of new antibiotics is a process of designing drugs to counter the bacterial strategies.”
Good grief.
For most scientists and medical professionals, language like that above is a metaphor; they don’t seriously believe bacteria are developing strategies, because they know the bacteria are simply under an evolutionary pressure causing them to change. This creates the appearance of tactical maneuvering.
But Egnor rejects evolution, even microevolution it seems. So what the heck does he think causes the bacteria to develop these strategies? Does he seriously think the bacteria are sentient, and deliberately out to very cunningly defeat our antibiotics? Or does he think God is responsible for the change? (As a devout Christian, I find that notion even scarier, quite honestly — the idea of a God who likes to sic superbugs on us.) What a whacko….
MarkP wrote: “mathematicians like MarkCC”
My bad, I don’t often meet nonmathematicians that know more math than I do. Ironically, however, my mistake makes the point Nat doesn’t care for – it’s the math we care about, not the credentials.
Can anyone in the reading audience with access please let us all know whether this article in the journal Microbial Drug Resistance (note last co-author) mentions anything about the evolution of vancomycin-resistant bacteria?
Huh. Didn’t realize “mathematician” meant that much. I thought it was just a version of “math geek” that’s less likely to be used as an insult.
Just wanted to say great post, Mark, and good discussion all around. Your efforts here are much appreciated. 🙂
And thanks for not having those video ads that are slowing down some of the other Science Blogs…very annoyingly so.
‘Hope your dad is doing OK, too.
Couple of points to add to what is an excellent article and scintillating discussion (apart from the usual suspects…)
Re speciation, I’ve often wondered what anti-evolutionists would make of a ring species. They admit ‘micro-evolution’, eg the small changes that occur between neighbouring populations, but not ‘macro-evolution’, or that micro leads to speciation. How then do they explain away the herring gull: it can interbreed contiguously around the globe, but ends up back in Britain as a separate bird entirely, the lesser black-backed gull. The 2 populations look different, were long thought to *be* different, live side by side, occupying different niches, and do not interbreed (although theoretically I believe they _could_).
And re genetic engineering: as I understand it there could be 2 approaches.
You can engineer a plant species to be resistant to a pest, then grow it and watch it thrive against the pest’s reduced attacks. All well & good, & I would probably support that idea.
Or you can engineer a plant to be resistant to a herbicide, grow it, drench the new plant and everything else around with 10 times the normal strength of that herbicide, and watch everything except the new plant die. I believe that that is Monsanto’s strategy, & I find it very scary.
For Nat Whilk:
MarkCC is a practitioner of the formal sciences that is : mathematics, formal or mathematical logic and computer science. The overlaps between the three disciplines are so large that to call a computer scientists a mathematician is maybe semantically incorrect but is substantially of no real importance.
Alan Bird,
Your comment…
“You can engineer a plant species to be resistant to a pest, then grow it and watch it thrive against the pest’s reduced attacks. All well & good, & I would probably support that idea.”
This scenario is what I was alluding to in a comment well above. I am concerned about the problems this could create. This genetically modified plant could become an artificial invasive species. Think Zebra Mussels in the Great Lakes, or Purple Loostrife in the wetlands of the northeast. Whenever a genome enters an ecology that has heretofore not seen that genome the normal biological checks and balances that would limit its biological reproductive potential may not exist. It can then begin to crowd out other species. Once these other species are crowded out there can be ripple effects.
So the GMO crop now resistant to its insect or bacterial control crowds out plants A and B. Insects C and D that used to eat plants A and B now become scarce. Bird E that used to eat insects C and D now cannot feed its young very well, and so on and so on…
Invasive species are already causing more than sufficient ecological perturbations.
GMO has nothing to do with it. Conventional breeding methods are also used to develop plants with improved pest resistance, which pose the same risks.
I think they’re both strategies used by Monsanto, among others. Bt plants have improved pest resistance. Glyphosate-resistant plants are resistant to the herbicide glyphosate. I believe Monsanto produces both kinds.
I don’t find herbicide resistance particular scary. It’s designed to be immune to the herbicide, and it is. It would make a rather lame horror movie.
It’s designed to be immune to the herbicide, and it is. It would make a rather lame horror movie.
Oops, that was me.
El Christador,
You are correct that artificial selection can also create resistance and this does represent an altered genome. This has been going on for a long time in agriculture but it works rather more slowly than cutting edge GM techniques. Whether this slower pace buys us much I am unsure. I tend to think that it may. But I don’t think it is really true that genetic modification techniques have “nothing to do with it.” If the genetic modifications, however they are accomplished, are heritable, then it could have something to do with “it.” If by “it” we mean creating ecological perturbations.
On Alan Bird’s point I don’t think he was envisioning something like “The Corn Plants That Ate Chicago.” He can correct me if I misinterpreted. I think his concern was regarding dumping large quantities of herbicides into the environment.
A good many doctors don’t get it about MRSAs. Egnor refers to bacteria as if the individual bacteria encounters the antibiotic and immediately starts planning strategies to survive. Maybe I misunderstand Egnor but it seems he is making the same mistake as Lamarck.
At any rate, I still remember a physician whose patient had been on years-long antibiotic therapy for otitis media and when the patient presented with an MRSA after a week in the hospital, he went ballistic at medical staff, outraged that indigent or nursing home patients had been admitted to “his” floor and infected his patient.
No amount of explaining could make him understand that the MRSA was generated by bugs that his patient generated and the reason that IV antibiotics were not working was because of the years of gratutious antibiotic dosing that killed off the susceptible bugs and left the resistant ones to breed future generations.
I have to wonder if Egnor considers MRSA as G1 or G2 or G3 or whatever in terms of generation or if he thinks MRSA is simply a G1 bug that has figured out a way to survive the antibiotics?
entlord:
I agree with you. My son had chronic ear infections when he was a baby, and after it didn’t clear up after a couple of rounds of antibiotics, we were sent to an ENT who put in
ear tubes. A lot of people, on hearing that we were
having tubes put in his ears threw fits at us – how could we do that to him? What kind of terribly parents were we to allow surgery (even minor surgery) on a one year old? Why wouldn’t our doctor just give us more antibiotics?! Even some doctors that we knew were upset about getting ear tubes instead of just prescribing more antibiotics.
People just don’t have a clue about this stuff. Keeping a kid on antibiotics for two years until they grow up enough to have proper drainage in their ears is dangerous. It’s not harmless to keep a kid on antibiotics for that long. And there’s no reason to.
The ear-tubes solved his problem literally overnight. One day, we had a grouchy unhappy kid who kept tugging at his ears; the next day, once the anaesthetic wore off, we had a happy, bouncy, hyperactive little monster. And he never had another ear infection. He’s going to turn four in two weeks; I think that since his first birthday, he’s taken antibiotics once, when his big sister brought home strep. (And I have to add – putting in ear tubes has become an amazingly trivial procedure. From the time they took him in to give him anaesthesia until the time the procedure was done and they brought us to him in the recovery room was under 10 minutes. The device that the surgeon uses looks almost like a sort of gun, and the process of inserting ear tubes basically comes down to sighting through the insertion device to pick the location where the tube will go, and pulling a trigger. The tube-inserter makes the incision, inserts the tube, and suctions out the fluid built up behind the eardrum.))
The only thing keeping him on antibiotics for another year would have accomplished is to increase his risk of a deadly infection by turning him into a walking incubator for resistant bacteria.
It is really a very poor article. Essentially the author’s argument boils down to the following logical fallacy: Natural selection is proposed as a mechanism for the evolution of new functions, so anything that does not create a new function is not evolution by natural selection.
The errors begin in the abstract:
The error here is that the author is presuming that if something does not account for the origin of a gene, then it isn’t evolution. But the theory of evolution does not depend upon the source of the heritable variation (indeed, Darwin didn’t even know what it was)–it could be genetic mutation, or it could be horizontal gene transfer, it is still evolution. No, acquiring a gene by horizontal gene transfer doesn’t explain the original origin of the gene, but there is nothing in evolutionary theory that demands that each organism create its genes de novo.
Now this is just stupid. A loss of function mutation is still a modification that can be inherited, and thus constitutes “descent with modification.” And the author’s suggestion that it is somehow “contrary to the predictions of natural selection” reveals a profound ignorance of the theory. In fact, it is exactly what the theory predicts. There are almost always more ways in which an existing function can be lost than ways of creating a new function, so loss of function mutations will be more frequent. Therefore, the theory predicts that if fitness can be improved by a loss of function mutation, then that is most likely the path which natural selection will take, at least initially.
Oddly enough, human attempts to combat disease generally use the same strategy. The vast majority of drugs do not add a new function–they work by causing a loss of function–impairing the function of some enzyme or other component of the body. The reason is the same: it’s a lot easier to find a way to break something than to improve it. So if a disease can be combatted by “breaking” something–for example, impairing the function of the sodium-potassium ATPase to increase cardiac output (digitalis and other cardiac glycosides), or blocking cyclooxygenase to relieve pain and inflammation (aspirin and other NSAIDS), that’s probably how we’ll do it, at least at first. “Rational drug design” has long been a dream of pharmacology (and the term tells you by contrast what pharmacologists think of the usual methods of drug discovery), but most drug discovery is still driven by clumsy heuristics that are not half so intelligent as natural selection.
Of course, improving with fitness by loss of function is not the best way to do it, because that function was probably there for a reason. It may enhance bacterial fitness when the antibiotic is present, but impair fitness when the antibiotic is absent. As the author acknowledges
In other words, once the initial loss of function occurs, there is then a selective advantage for mutations that recover the abilities that were sacrificed, while retaining antibiotic resistance. This is why antibiotic resistance often tends to become “locked in”–it doesn’t go away even if you stop using the antibiotic, because there is no longer a selective advantage for the bacteria to return to the original form of the protein, even if the antibiotic is no longer around.
So even though the initial evolutionary step is a loss of function, the bacteria frequently end up with a net gain of function, “having their cake and eating it too.” They now have a protein that exhibits its original activity, but now with a valuable (to the bacteria, at least) new feature: antibiotic resistance.
Ah. I see.
The point of making herbicide-resistant plants — or at least, glyphosate resistant — isn’t so you can increase the quantities of herbicides used. It’s so you can decrease the amount of herbicides used by using different ones. The whole idea is to save the farmers’ money, and increasing herbicide use isn’t going to save money. Glyphosate kills everything that’s a plant. That means that instead of having to use, say, ten different herbicides to kill different weeds, if the plants you want are glyphosate resistant, you can do all your weed-killing with just glyphosate applications.
As a bonus, glyphosate is a very environmentally friendly herbicide (except for the particular plants with which it comes into contact, which it kills): it binds to the soil, it’s not very mobile (i.e. it stays where you put it), and it’s non-persistent, breaking down quickly into common, and harmless*, natural materials (specifically, methanol, glycine and phosphate).
*harmless to the environment, that is. Methanol is harmful to people if they drink it, but that’s not the situation here. As a breakdown product of a herbicide it is not an environmental concern.
Ok, sure. I see your point: no change without risk, hence changing nothing is one risk-reducing strategy. My point was just that it’s the increased pesticide resistance that would present the risk about which you’re concerned, not whether it was arrived at by recombinant DNA techniques rather than “conventional” breeding techniques.
El Christador said:
“[Glyphosate breaks down into] harmless*, natural materials (specifically, methanol, glycine and phosphate).
“*harmless to the environment, that is.”
What about eutrophication from phosphate runoff?
Thanks for the great post. As a sidenote of there not being any VRSA/MRSA combination strains, scarily THERE ARE. The good news is that there aren’t any out in the wild that we know of. I do S. aureus research, and one day we were ordering a bunch of strains from NARSA (narsa.net). We were basically going down the line ordering what they had, and an email came back to us later asking if we REALLY REALLY REALLY wanted a particular strain. It was this one:
http://narsa.net/control/member/viewisolatedetails?repositoryId=105&isolateId=281
It’s COL (an older, naturally methicillin resistant strain) with vancomycin resistance moved over into it via phage transduction. We were stunned that that strain was available and quickly canceled it from our order.
Second, and even more scarily, at a conference on undergraduate science down in DC a few years ago, I came across a project done at NYU where the PI (who did TB research) had their undergrad trying to move vancomycin resistance from Enterococcus into S. aureus over and over again to address the question of whether it was possible in the real world. The undergrad’s experiments didn’t work, but it was incredibly ignorant and dangerous of this PI to even try this type of experiment, much less with an undergraduate doing it (nb – I’ve had tremendously talented undergraduates helping me with Staph research).
So regardless of what nature’s going to produce in terms of V/MRSA, researchers may unwittingly produce it first.
Niles
El Christador,
Thanks for your substantive and balanced response. I don’t really know much about herbicides, having never used them myself. So I have learned a little bit here.
Jim51
I’m not sure if this is the right thread. The point is that fitness landscapes are a more general concept than for biological evolution by natural selection. two recent examples from the arXiv:
q-bio.QM/0703044
Title: On the existence of potential landscape in the evolution of complex systems
Authors: P. Ao, C. Kwon, H. Qian
Comments: latex, 18 pages
Subj-class: Quantitative Methods; Molecular Networks
Journal-ref: Complexity 12 (2007) 19-27
A recently developed treatment of stochastic processes leads to the construction of a potential landscape for the dynamical evolution of complex systems. Since the existence of a potential function in generic settings has been frequently questioned in literature,herewe study several related theoretical issues that lie at core of the construction. We showthat the novel treatment,via a transformation,is closely related to the symplectic structure that is central in many branches of theoretical physics. Using this insight, we demonstrate an invariant under the transformation. We further explicitly demonstrate, in one-dimensional case, the contradistinction among the new treatment to those of Ito and Stratonovich, as well as others.Our results strongly suggest that the method from statistical physics can be useful in studying stochastic, complex systems in general.
cond-mat/0703478
Title: Stochastic Models of Evolution in Genetics, Ecology and Linguistics
Authors: R. A. Blythe, A. J. McKane
Comments: 60 pages, 7 figures, for the JSTAT Special Issue relating to the Isaac Newton Institute Programme “The Principles of the Dynamics of Nonequilibrium Systems”, Cambridge, 2006
Subj-class: Statistical Mechanics; Populations and Evolution
We give a overview of stochastic models of evolution that have found applications in genetics, ecology and linguistics for an audience of nonspecialists, especially statistical physicists. In particular, we focus mostly on neutral models in which no intrinsic advantage is ascribed to a particular type of the variable unit, for example a gene, appearing in the theory. In many cases these models are exactly solvable and furthermore go some way to describing observed features of genetic, ecological and linguistic systems.
I’ll second that, likewise being new to the world of herbicides.
Thanks one and all for the fascinating contributions to this discussion. As usual when more and better information comes my way, I’m both illuminated _and_ confused. The situation now seems both clearcut and ambiguous (an uncomfortable feeling; it must be nice to be as ignorantly certain as an IDiot…).
I have to admit to getting some of my original information from a polemical journalist called George Monbiot, who while having his heart in the right place does have a certain agenda to follow. Apart from the biological topics tackled above, he thinks Monsanto are trying to lock farmers in the third world into a financial relationship with Monsanto which is controlled entirely by Monsanto and which is definitely not in the interests of the farmers. Perhaps some of you would like to comment.
Very well written, Mark. I’m sorry I wasn’t in the discussion earlier (two weeks in China makes for a lot of catching up.) What you said here…
…was one of the best responses to the argument from (pseudo-)authority that I’ve yet read.
Antiquated Tory: re: ototic fungal infection: Have you had your thyroid levels checked, and been tested for diabetes? Abnormally low thyroid hormone levels can lead to susceptibility to such infections, as can diabetes I believe.
Elliott:
My son had his ear tubes put it at 13 months; they fell out naturally about 4-5 months later, and he hasn’t had an ear infection since.
In my family, we’re *very* aware of diabetes, because on my mother’s side of the family, there seems to be a strongly inherited tendency towards diabetes: my mother and her only brother; my grandfather and all of his siblings, and *his* father all had very serious diabetes; and my older brother is showing signs of developing it. So I’m justifyiably paranoid.
On ear tubes — my daughter had them put in at 14 months, after 7 weeks of pretty much non-stop ear infections, and that improved things greatly.
They didn’t come out on their own for about a year, which was a bonus in another way: when she was 20 months old and we took a plane trip, she was NOT experiencing extreme discomfort on descent, which her twin brother was. (And I found out the hard way that if you have two children in the row with you, one with ear tubes and one without, you want to have the one without the tubes next to you, because it’s difficult to reach across the one to attempt to comfort the other. I kept that in mind for the return trip….)
The following is a fine counterexample to ID twaddle about genes only being able to microevolve by point mutations from pre-existing genes (although ‘Out Of Nowhere’ can easily be misinterpreted by Creationist loons as “Out of the omnipotent mind of He With a Long White Beard and a Halo and stuff”):
Fruit Fly Gene From ‘Out Of Nowhere’ May Change Ideas About How Genes Are Formed
http://www.sciencedaily.com/releases/2007/07/070723160028.htm
Source: Cornell University
Date: July 25, 2007
Science Daily — Scientists thought that most new genes were formed from existing genes, but Cornell researchers have discovered a gene in some fruit flies that appears to be unrelated to other genes in any known genome.
Fruit fly (Drosophila melanogaster). (Credit: Image courtesy of Cornell University)
The new gene, called hydra, exists in only a small number of species of Drosophila fruit flies, which suggests it was created about 13 million years ago, when these melanogaster subgroup species diverged from a common ancestor.
And early evidence indicates that the new gene is functional (as opposed to being nonfunctional “junk” DNA) and is likely to express a protein involved in late stages of sperm cell development (spermatogenesis). This finding is consistent with work of other scientists who are discovering that many of the most recently formed functional genes in any species also are expressed in male testes and appear related to spermatogenesis.
“This is a de novo — ‘out of nowhere’ — gene,” said Hsiao-Pei Yang, a senior research associate in Cornell’s Department of Molecular Biology and Genetics and senior author of a paper published in the July 6 issue of the online journal PLoS Genetics (Public Library of Science Genetics). “People used to think that new genes were always formed from tinkering with other genes, but with this gene we can find no homologues [genes with a similar structure]. You cannot find any related genes in the fly genome or any species’ genome, and that is what is unique.”
Yang conducted part of this research while at the National Yang-Ming University in Taiwan and part of the work in collaboration with Cornell’s Daniel Barbash, assistant professor of molecular biology and genetics.
The researchers do not yet know how the hydra gene was created, but they speculate that the gene may have developed from a piece of DNA junk called a transposable element (also known as a “jumping gene”), which may have been inserted into the genome by a virus. These transposons are known to copy and insert themselves into DNA sequences. For example, one theory is that when a transposon sits next to a gene and then jumps to a new location, it carries part of the gene sequence it was next to and inserts it in the new location. Often, transposable elements appear to have no function or may be harmful and are eliminated by natural selection, but researchers are beginning to think transposons may be a source for creating new functional genes as well.
The hydra gene is named after the Greek mythological beast that had a hound’s body and nine snake heads, because it has nine duplicated first exons (sections of the gene that contain protein-coding information). Each of these exons may serve as alternative starting positions for the gene to become activated. The researchers found that most of these exons had a sequence for a transposable element sitting right next to it. Duplicated sequences generated by transposons may be part of the mechanism for creating new genes, as the duplications provide more chances for a gene to evolve.
The work was funded by the National Sciences Council in Taiwan.
Note: This story has been adapted from a news release issued by Cornell University.
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