Another review of Behe’s book, The Edge of Evolution, has been published, this time in Nature and by Ken Miller. This one focuses on Behe’s central claim, that he has identified a probabilistic limit to what evolution can do that means no differences above roughly the genus level (and in many cases, the species level) can be generated by natural mechanisms. This is his CCC metric, or the probability of evolving something equivalent to the “chloroquine complexity cluster”, which he claims is the odds of evolving two specific amino acid changes in a protein. It’s a number he pegs at 1 in 1020, right at the edge of what a large population of protists can do, but beyond the reach of what a smaller population of slowly reproducing metazoans, like hominids, could hope to accomplish even with geological time limits. It’s the same problem I addressed in my earlier criticism, although Miller manages to slap it down with much greater brevity.
Behe cites the malaria literature to note that two amino-acid changes in the digestive-vacuole membrane protein PfCRT (at positions 76 and 220) of Plasmodium are required to confer chloroquine resistance. From a report that spontaneous resistance to the drug can be found in roughly 1 parasite in 1020, he asserts that these are the odds of both mutations arising in a single organism, and uses them to make this sweeping assertion:
“On average, for humans to achieve a mutation like this by chance, we would need to wait a hundred million times ten million years. Since that is many times the age of the universe, it’s reasonable to conclude the following: No mutation that is of the same complexity as chloroquine resistance in malaria arose by Darwinian evolution in the line leading to humans in the past ten million years.”
Behe, incredibly, thinks he has determined the odds of a mutation “of the same complexity” occurring in the human line. He hasn’t. What he has actually done is to determine the odds of these two exact mutations occurring simultaneously at precisely the same position in exactly the same gene in a single individual. He then leads his unsuspecting readers to believe that this spurious calculation is a hard and fast statistical barrier to the accumulation of enough variation to drive darwinian evolution.
It’s a painfully basic error — Behe is counting on his readership being unaware of basic principles in probability and on having no knowledge of the actual, relevant research on this problem. It’s a safe bet for him, from what I’ve seen of the fans of ID. Unfortunately, when real scientists take a look at what he’s saying, they can see everywhere that he went wrong.
Behe obtains his probabilities by considering each mutation as an independent event, ruling out any role for cumulative selection, and requiring evolution to achieve an exact, predetermined result. Not only are each of these conditions unrealistic, but they do not apply even in the case of his chosen example. First, he overlooks the existence of chloroquine-resistant strains of malaria lacking one of the mutations he claims to be essential (at position 220). This matters, because it shows that there are several mutational routes to effective drug resistance. Second, and more importantly, Behe waves away evidence suggesting that chloroquine resistance may be the result of sequential, not simultaneous, mutations (Science 298, 74–75; 2002), boosted by the so-called ARMD (accelerated resistance to multiple drugs) phenotype, which is itself drug induced.
A mistake of this magnitude anywhere in a book on science is bad enough, but Behe has built his entire thesis on this error. Telling his readers that the production of so much as a single new protein-to-protein binding site is “beyond the edge of evolution”, he proclaims darwinian evolution to be a hopeless failure. Apparently he has not followed recent studies exploring the evolution of hormone-receptor complexes by sequential mutations (Science 312, 97–101; 2006), the ‘evolvability’ of new functions in existing proteins —; studies on serum paraxonase (PON1) traced the evolution of several new catalytic functions (Nature Genet. 37, 73–76; 2005) —; or the modular evolution of cellular signalling circuitry (Annu. Rev. Biochem. 75, 655–680; 2006). Instead, he tells his readers that there is just one explanation that “encompasses the cellular foundation of life as a whole”. That explanation, of course, is intelligent design.
This is a trend for Behe. Both of his popular books that have fed the Intelligent Design movement have relied on gross ignorance and misrepresentation at their core. One has to cringe a little bit to see it: Behe really seems to believe that he has had a deep insight into a real problem with evolution, and it’s really nothing but a deep mistake on his part…and he keeps digging his hole deeper.
Miller KR (2007) Falling over the edge. Nature 447:1055-1056.
and it’s really nothing but a deep mistake on his part
And there’s nothing quite like the fawning of Behe’s base to convince him that he is correct.
Ha! I was there first:
At any rate, off I go to add Miller’s review to the list.
Dang it, I’ve added Miller to the list, but the article is behind a subscription wall!
Yeah, one of the great problems with Behe’s books are that the errors are so obvious — you read them, and the first thing you think is “wait a minute…hasn’t that probability problem been brought up by creationists time and time again?” If he had one critical reviewer who pointed to these glaring problems, he might not have so thoroughly embarrassed himself (and the book probably wouldn’t have been published). The way this drivel gets to market, though, is that he only has ID sycophants examine it.
And why does a great university like Lehigh keep him on the biology faculty?
Re anon
Lehigh University keeps Behe on their biochemistry faculty because he has tenure. He achieved tenure before he turned into a whackjob, unlike Prof. Gonzalez at Iowa State Un. In order to revoke tenure, a professor must be guilty of gross misconduct (e.g. Ward Churchill at Un. of Colordo). Thus far, Behe has been careful not to give the powers that be at Lehigh a plausible excuse.
In order to revoke tenure, a professor must be guilty of gross misconduct (e.g. Ward Churchill at Un. of Colordo).
Quite frankly, I wouldn’t say that Churchill’s misconduct is worse than Behe’s.
There’s a reason tenure is sought so highly…. it’s incredibly difficult for colleges to get rid of tenured professors.
That generally means, that for some, they can simply loaf and live off past successes…
For some, it means having the opportunity to indulge in ‘edgy’ research
For others, it means being able to be a stupid fucking wanker on a regular basis
It’s the price we pay for the effort to achieve tenure (where much of the good research happens)
Perhaps Behe should learn about sexual reproduction and its shuffling of genes (hint to Behe–there is an evolutionary, non-design reason why something as complex as sexual reproduction exists). He seems genuinely unaware of the role that sexual reproduction plays in evolution (well, obviously in sexually reproducing organisms like Plasmodium sp.), and how it might actually be that neutral, or slightly helpful or harmful, alleles might come together via sex to produce a highly favorable (or deleterious) effect.
I mean, how stupid does he think we are? Alternatively, how stupid ought we to suppose Behe is?
Glen D
http://tinyurl.com/35s39o
Dawkins reviews this weekend in the N.Y.Times.
Just got the preview:
I had expected to be as irritated by Michael Behe’s second book as by his first. I had not expected to feel sorry for him. The first — “Darwin’s Black Box” (1996), which purported to make the scientific case for “intelligent design” — was enlivened by a spark of conviction, however misguided. The second is the book of a man who has given up. Trapped along a false path of his own rather unintelligent design, Behe has left himself no escape. Poster boy of creationists everywhere, he has cut himself adrift from the world of real science. [continues]
Glen @ 9
Apparently Behe is now officially *very stupid*.
If Ken Miller says so, it must be true.
Why wouldn’t Demski with a Ph.d. in Mathematics catch a basic error such as this?
Because there’s nothing wrong with the math itself. It’s the assumptions upon which the math is based which are way off.
He achieved tenure before he turned into a whackjob, unlike Prof. Gonzalez at Iowa State Un.
I think Behe probably just came out as a whackjob after tenure. I suspect he was a whackjob well before.
Why wouldn’t Demski with a Ph.d. in Mathematics catch a basic error such as this?
Maybe he just doesn’t care or he knows that the intended audience for the book is not scientists and mathematicians so he’s not too concerned about such errors.
I have a sad story to relate, that this new Behe post has reminded me of.
I recently took a stroll through my local Barnes & Noble. It’s an infrequent trip for me, but frequent enough that I noticed the changes in the book store since I was last there.
There is no longer a dedicated row for Science. Science was relegated to two shelves near the Information Technology section. The GLBT, women’s studies, etc. section had been collapsed to one section as well. These changes allowed for the store to add a third aisle of religion books. A full 18 bookshelves full of religious books to science’s two.
To make matters worse, Behe’s book was on the science shelf, along with many other ID books. No matter that ID is not science.
I walked out of the bookstore empty handed and mourning for our future.
The Barnes & Noble at Astor Place in NYC doesn’t seem to have a science section. If there is one I could’nt find it.
The hardest lies to detect are the ones you tell to yourself. Behe came up with his “answer” and has been trying to find the question that fits it. But when your whole research involves nothing but thought experiments, that’s what you get.
Besides, he developed the wrong answer right from the start. We all know the answer is 42.
The problem with 42, for IDiots, et al, is that to understand it they need to find some more digits….
(Base 13 is a beyatch)
That to my mind was the central and glaring fallacy of Behe’s lame argument. Sex is supposed to exist to shuffle genes around, getting rid of deleterious ones and allowing the spread of adaptive genes and combinations.
Malaria as it turns out has sexual recombination stages. This would allow drug resistance mutations from the whole extended gene pool to end up in the same organism.
For someone to write a book on evolution and adaptation and not mention sexual recombination, what it is, what it is good for, and how ancient it is (back to the dawn of time) is outrageous. But really, Behe isn’t writing a science book, he is writing a propaganda tract for the True Liars of the Pack of Lies cults.
Behe responds to critics. He is rather contemptuous of the reviews so far:
http://www.amazon.com/gp/pdp/profile/A3DGRQ0IO7KYQ2/ref=cm_blog_dp_pdp/105-1176708-6988463
If I had a hammer….(cue folk guitar)
*shrug* Probably the same reason why Behe with a PhD in biochemistry didnt/doesnt catch basic biochemistry errors.
CalGeorge– Dawkins should know better than to feel sorry for these leeches. On a humorous note, from Dawkins description, it appears Behe has become trapped at a local fitness maxima. I suppose that can happen when youre a one dimensional character.
Blake– You missed one of mine :P ‘Behe vs HIV’
I don’t know anything about population genetics but in reading Behe’s text he discusses the probability of such mutations in a parasite. Then he immediately says this is impossible in humans. Is Behe applying statistical inference from a blood parasite population to a human?
I’m not sure whether everyone reads Orzel over here, but the other day he linked to a Zork-style text adventure game that seems relevant here:
Really, I’m quoting this for the phrase “dread B’ehe” and the joy that comes from kicking him.
re: Ericb
Yes, the Astor place B&N does not have a science section. Pretty large computer section though. But, I think it is made up for by the science section at the Union Sq. B&N and the college textbook B&N on 5th and 18th. You should definitely give both those places a look.
Does anyone really know what is up with Behe? Has he simply mortgaged his reputation to such an extent that he is just trying to grab some money out of the ID movement? or acclaim?
With the assumption Behe is not a complete idiot, he is purposeful in his work. He is not ignorant. Assuming he has some real core religious belief’s, it is sad that he would toss those values out the window for money or acclaim (from ID’ists).
This has become a very sad affair.
But isn’t that exactly the problem, PZ? If Behe bothered with fact-checking, his publication record would be bupkis. It’s like a retired journalist friend of mine says, repeating a favorite adage of reporters: A careful investigation can often ruin a great story.
Unsurprisingly, I don’t think you are fairly characterising Behe’s arguments – that’s certainly not what I understood from the book. But it must be cool when you have authority simply by voicing an opinion against something, regardless of how sound that opinion is.
Error of fact: he didn’t overlook the existence of other chloroquine resistant strains (p.62 – “Although some other mutations in some other proteins are thought to contribute to chloroquine resistance, none are nearly as effective as that in PfCRT”).
Error of fact: He didn’t disregard the fact that several different mutational routes are possible to the same end. He suggested, however, that whilst the number of possible DNA sequences increases exponentially with length, the number of possible solutions increases arithmetically, and therefore even a hundred “solutions” to an evolutionary “problem” isn’t really going to help if they are hidden amongst 10^40 “candidates”. (You might like to argue that the frequency of “solutions” is much higher. I think this could be modelled. If chloroquine resistance was easy to achieve, for example, wouldn’t we expect to find a range of different malaria populations, with different solutions? In fact, as I understand it [you are welcome to correct me here] the same “solution” is shared across the whole parasite population.
Error of fact: He didn’t disregard sequential mutations (p.101 – “More rarely, several mutations can sequentially add to each other to improve an organism’s chances of survival. An example is the breaking of the regulatory controls of fetal hemoglobin to help alleviate sickle cell disease.”) And the implication was that this was more likely than simultaneous (cont. “Very, very rarely, several amino acid mutations appear simultaneously to confer a beneficial effect, such as in chloroquine resistance with mutant PfCRT.”) What he was arguing was that this was not going to do the job of generating new structures, and the control mechanisms that they require.
In a sense, this is beside the point. I have yet to see any attempt to determine a limit of what evolution could achieve from the anti-ID side. So who’s doing the science here? Those people that are trying to tease out the implications of how evolution might work? Or those people who just sit there picking holes and sneering? Perhaps you could give your reasons why AFGP’s have appeared in notothenioid fish and yet malaria parasites require a warm climate – Behe has given his.
Ummm, he mentions them, and then ignores them. If there are other mutations that can confer resistance, even if less effective than the two-amino acid change, then selection can get a grip. If there are alternative routes, then his calculation is irrelevant. And his calculation, by the way, was basically plucked out of his ass; the 1 in 10^^20 number is poorly sourced and not credible.
Oh, and “because the designer made it so” is not a reason.
Shouldn’t that be ExileFromARN???
The idiot makes his rounds, blathering stupidly about all that he doesn’t understand. Paul was trying to explain how “Behe” didn’t quote-mine Coyne on Jason Rosenhouse’s blog, all over a quote-mine that Behe has already blamed on the publishers (rightly or wrongly I wouldn’t know–it’s hard to see why Behe would have brought Coyne’s writings up for any honest reason, but who knows for sure?). Oh yeah, it was mentioned in the thread, but this IDiot can’t read.
Then you’re profoundly stupid, as well as ignorant. Darwin himself brought up these issues. True, he didn’t put fake numbers to them, ignore sexual reproduction, and pre-suppose that regulatory problems would prevent evolution from happening, but why would anybody who was honest?
Indeed, limits to evolution are some of the primary evidences in favor of evolution (you know, evolution, not a ridiculously long and pointless process of creation). Why, dipshit, do organisms reveal functions that are constrained by evolutionary processes such as limits in the numbers of beneficial mutations? Answer that for once, you amazingly IDist-type brain, and quit avoiding everything that tells against your mindless parroting of the mindless?
We discuss limits, we just don’t pretend that we can put numbers to them in most cases, especially not anything as complex and ancient as the bacterial flagellum. Only pseudo-scientists do that.
Why it’s those who follow the lead of the evidence, not those who try to deny the convergent evidence. What makes you think that using false numbers to try to deny what by all appearances happened actually did occur? More importantly, where is the evidence for design, you lying hound?
Yes, the scientists are doing the science, dog-head.
You’re right, you and Behe have plenty to answer for when you do no science but just sit on the sidelines and sneer at those who do.
IOW, how can you be so stupid as not to see the criticisms you level at others only hit you?
Glen D
http://tinyurl.com/35s39o
Why, was he on ARN using the name “Paul”?
I wouldn’t know about that, since I gave up on the endless cycle of enforced polite treatment of disreputable liars on ARN years ago.
One ought to rip into dishonest thugs like Paul, as we can do here.
Glen D
http://tinyurl.com/35s39o
No, he used Exile From Groggs, the name of his website (see link in his name).
Ah yes, I’ve seen stuff from that trained ape some place or other, maybe even on ARN.
Glen D
http://tinyurl.com/35s39o
Guys, quick question: Isn’t Miller backing away from _single,_ sequential, changes in his review? Isn’t the backbone of darwinism _single,_ advantageous changes?
Paul:
I don’t know if you have read PZ’s post, but most of the facts are from Ken Miller’s review of Behe’s book. And if you don’t think much of biologist PZ Myers professional expertize for some unsupported reason, Ken Miller is a renown biologist.
For example, Ken Miller has written books on biology including a textbook and he was a biology science expert witness in the Dover trial. He was rewarded with the American Society for Cell Biology 2006 Public Service Award along with Barbara Forrest:
As noted, he overlooked them in his calculation, which is what matters for the result he claims.
You are playing high and loose with your definition of “fact”.
Paul:
I don’t know if you have read PZ’s post, but most of the facts are from Ken Miller’s review of Behe’s book. And if you don’t think much of biologist PZ Myers professional expertize for some unsupported reason, Ken Miller is a renown biologist.
For example, Ken Miller has written books on biology including a textbook and he was a biology science expert witness in the Dover trial. He was rewarded with the American Society for Cell Biology 2006 Public Service Award along with Barbara Forrest:
As noted, he overlooked them in his calculation, which is what matters for the result he claims.
You are playing high and loose with your definition of “fact”.
Paul:
“… resistance to chloroquine has appeared fewer than ten times in the whole world in the past half century” (Behe, from Edge of Evolution.)
And, more importantly, malaria is one of the greatest evolutionary forces on humans in recent history. Different versions of sickle cell anemia has developed 4 (!) times in humans since it confers resistance ( see http://en.wikipedia.org/wiki/Sickle_cell_anemia and especially the maps).
Paul:
“… resistance to chloroquine has appeared fewer than ten times in the whole world in the past half century” (Behe, from Edge of Evolution.)
And, more importantly, malaria is one of the greatest evolutionary forces on humans in recent history. Different versions of sickle cell anemia has developed 4 (!) times in humans since it confers resistance ( see http://en.wikipedia.org/wiki/Sickle_cell_anemia and especially the maps).
Paul:
[Continuing pga linkfest vs spamfilter…]
If malaria evolution is so important for Behe, how come he disregard the human component in the system? Is it because the changes are so drastic, perhaps?
( http://en.wikipedia.org/wiki/Malaria )
Other established new traits securely or tentatively associated with malaria resistance are the set of thalassemias, non-expression of Duffy antigens, and changes in G6PD, HLA, and IL4 molecules.
In summary I can’t find a single fact you have correct. Shouldn’t that be important for you since you are interested in “fairly characterising [sic]” things?
Paul:
[Continuing pga linkfest vs spamfilter…]
If malaria evolution is so important for Behe, how come he disregard the human component in the system? Is it because the changes are so drastic, perhaps?
( http://en.wikipedia.org/wiki/Malaria )
Other established new traits securely or tentatively associated with malaria resistance are the set of thalassemias, non-expression of Duffy antigens, and changes in G6PD, HLA, and IL4 molecules.
In summary I can’t find a single fact you have correct. Shouldn’t that be important for you since you are interested in “fairly characterising [sic]” things?
Why wouldn’t Demski with a Ph.d. in Mathematics catch a basic error such as this?
Dembski sucks at biology…he may not understand that the mutations Behe speaks of need not occur simultaneously in the real world. Meanwhile, Behe sucks at math. They’re like the two flailing arms of a lobotomy patient.
Real scientists obviously, not pseudoscience cranks.
Chloroquine resistance evolved and quite recently. This drug is a modern and at one time, highly effective anti-malarial.
Real scientists identified this problem and have determined the many molecular mechanisms. This by the way, is not done by posting crap on the internet or writing nonsense books. People in labs spend a lot of time figuring stuff like this out. They even have a work around for it, artemisin type drugs and combos. This workaround, by real MDs and scientists, saves millions of lives here and there.
Behe is just playing to his audience of morons with bafflegab and hand waving. This isn’t real science, it is a perversion called lying pseudoscience. He doesn’t care.
BTW, the limits of evolution are known. All life that exists and all that existed fall within the capabilities of evolution. Pretty neat, really.
Behe also forgot about sexual recombination. A mechanism that evolved billions of years ago to shuffle genes around in an extended gene pool. Incredibly sloppy to ignore one of the main mechanisms that makes metazoan life possible and evolution happen.
Paul,
If you really want answers to your questions, I highly recommend starting with Sean Carroll’s latest book ‘The Making of the Fittest.’
http://www.amazon.com/Making-Fittest-Ultimate-Forensic-Evolution/dp/0393061639
Carroll addresses almost everything Behe is said to have overlooked or ignored in his book. ANd he does so with waaay cool examples. I haven’t read Behe’s book (and I am not going to), so I can’t comment on how accurate the criticisms are, but they sound like the same old arguments that have been refuted over and over.
It’s funny. Paul will comment here but he won’t dare post a link on his blog to PZ’s post.
Coward.
I don’t understand what you mean, Paleyist.
Miller is the one who mentions that there’s evidence that chloroquine resistance is the result of two sequential mutations instead of two simultaneous mutations.
Evolution = descent with modification by mutation, selection, and drift. Mutation constantly produces variation, and selection narrows the variation down.
I don’t understand what you mean, Paleyist.
Miller is the one who mentions that there’s evidence that chloroquine resistance is the result of two sequential mutations instead of two simultaneous mutations.
Evolution = descent with modification by mutation, selection, and drift. Mutation constantly produces variation, and selection narrows the variation down.
Darwin was concerned with phenotype, not genotype, which he knew nothing about, it not having been discovered yet.
From his point of view, the two mutations that spawn chloroquine resistance ARE a single change: from no resistance, to resistance.
#42 and #43:
I understand the mutations were/could be sequential — but where would the advantage be? How would the first change persist without an advantage?
It doesn’t have to grant an advantage to persist – it just can’t create a sufficiently large disadvantage.
Drug resistance is not all or nothing. In general, there are many mutations that confer low level resistance to a given drug. If you look at how chloroquine is used, readily available by poor people with negligible education, the chances are that many are underdosing, misdosing, and stopping too soon. A guarantee of selecting parasites resistant to low doses of chloroquine.
Stepwise selection and sexual recombination does the rest. There is nothing magic about this. Resistance to antibiotics, insecticides, herbicides, antivirals, anticancer drugs, and anti anything is routinely seen sooner or later. Just like Darwin predicted.
shit, I sometimes comment here as paul, not Paul. Please don’t confuse me with the dumbass.
paul FCD
It is not necessary for a mutation to have an advantage to persist. In fact, most mutations that do persist probably do not confer an advantage. The important thing is that they do not confer a disadvantage. Google ‘neutral theory’ for more information.
I just did, and this looks like a good place to start:
http://www.blackwellpublishing.com/ridley/tutorials/Molecular_evolution_and_neutral_theory1.asp
All life that exists and all that existed fall within the capabilities of evolution.
Well, that’s the lower bound… I don’t think all that much of the DNA space has actualy been explored by evolution yet, which has a lot to do with the constraints of starting at a single point.
That’s one of the things that “turned” Denton, BTW.
One more question:
Do any of you guys get the feeling that we should all quit arguing over anything touching the genome, life, etc…..
….at least until this RNA thing is fleshed out a bit?
Do any of you guys get the feeling that we should all quit arguing over anything touching the genome, life, etc…..
….at least until this RNA thing is fleshed out a bit?
-wnelson
No.
Just because we don’t know everything is no reason to let stuff that contradicts what we do know go unchallenged.
What Graculus said.
Besides, just try to get scientists to stop arguing. It’s what we do.
I mean, how would we flesh out ‘the RNA thing’ a bit without forwarding hypotheses to test, proposing experiments to do, and presenting our interpretations of the results? At each stage of the process there are plenty of opportunities for argument from experts in the area. And that is how it must be for science to progress.
I think many lay people have this idea of science as genteel process done by genteel people in sterile, brightly lit labs, while assisted by a cadre of eminently capably, yet stunningly attractively assistants (ok, maybe that last part is just me). And once we have done all of the experiments correctly and have all the answers, the other scientists agree with us and let us write our results in the Big Book of Science.
The truth is that science is usually about one step more (but sometimes less) genteel than rugby, with people trying to poke holes in your ideas (and ego) from start to finish. Again, that is how it has to be.
Malaria resistance even to chloroquine is a lot more complicated than Behe states. There have apparently been many independent evolutions of this resistance. Some include the K76T A220S haplotype. Some don’t. He is wrong on the basic science. To make matters worse, malaria has evolved resistance to the other drugs used as well. Some of these are triple mutants. His example, malaria, seems to be able to evolve double and triple mutant resistances to drugs without even breathing hard. And this proves…..GODDIDIT. And evolution is falsified. Behe has slid beyond the realm of pseudoscience quackery into the realm of outright lying. It is a christian creo thing.
I expect in years to come he will just start thinking less and lying more until he becomes a Demski, Meyers, Hovind, or Ham. For anyone who still thinks Gonzalez got a raw deal at ISU. No way. They were looking at a Behe or Duesburg in the making and what university needs a crackpot filling in a tenured position and contributing to a return to the dark ages.
Antimicrob Agents Chemother. 2003 Nov;47(11):3500-5. Links
pfcrt Allelic types with two novel amino acid mutations in chloroquine-resistant Plasmodium falciparum isolates from the Philippines.Chen N, Kyle DE, Pasay C, Fowler EV, Baker J, Peters JM, Cheng Q.
Department of Drug Resistance and Diagnostics, Australian Army Malaria Institute, Enoggera, Qld, Australia.
Mutations in the pfcrt and pfmdr1 genes have been associated with chloroquine resistance in Plasmodium falciparum. Ten and five mutations, respectively, have been identified in these genes from chloroquine-resistant parasites worldwide. Mutation patterns in pfcrt revealed that chloroquine resistance evolved independently in southeast Asia, South America, and Papua New Guinea. However, the evolution of chloroquine resistance in the rest of the Pacific region is unclear. In this study, we examined sequence polymorphisms in these genes in isolates from Morong, Philippines, and compared them to known chloroquine resistance sequences. Two novel mutations, A144T and L160Y, were identified outside of the 10 known mutations in pfcrt in Morong isolates. These novel mutations were identified only in parasites with K76T and N326D but without the common A220S mutation found in most chloroquine-resistant isolates. This represents a unique chloroquine resistance allelic type (K76T/A144T/L160Y/N326D) not previously found elsewhere in the world. One Morong isolate also had an additional C72S mutation, whereas only one isolate possessed an allelic type typical of chloroquine resistance in Asia. Parasites with the novel pfcrt allelic types were resistant to chloroquine in vitro and were unresponsive to verapamil (0.9 microM) chemosensitization, similar to chloroquine-resistant parasites from South America and Papua New Guinea. These results suggest that chloroquine resistance evolved independently in the Philippines and represents a second chloroquine resistance founder event in the South Pacific.
#52-
How do you propose to “flesh out the RNA thing” (whatever it is) without evolutionary biology?
As a tangent, I happended to be reading today a paper which “fleshes out a biology thing”; it idenifies a gene which tells us why small dogs are small and big dogs are big:
http://www.sciencemag.org/cgi/content/full/316/5821/112#REF11
the technique they use is based on a statistical model which relies on evolutionary biology. In (very distilled) essence, they rely on markers near genes which change breed characterisics (e.g. black coat or small stature) to have less variability than other markers, which one expects to be more random. The expectation that other markers will be more random comes from a model of evolutionary biology.
If evolutionary biology were a crock of the proverbial, then this technique just would not work, as the dog genome would conform to whatever statistical model the Deity put there and used to create dog breeds, not the statistical model that evolutionary biology has.
See also:
http://www.genome.org/cgi/content/abstract/15/12/1809?ijkey=1c294e64209214238bc54b55933af103a03daa99&keytype2=tf_ipsecsha
If you think my hunchbacked dwarf assistant Igor, is attractive…..you need to get out more. LOL
Graculus said:
————
No.
Just because we don’t know everything is no reason to let stuff that contradicts what we do know go unchallenged.
————
Yes, but this could mean a total upending of how we understand life, etc. We’d all end up arguing for our same points, but for much different reasons.
Seems a little screwy.
Yes, but this could mean a total upending of how we understand life, etc. We’d all end up arguing for our same points, but for much different reasons.
Seems a little screwy.
– wnelson
If someone had a real, honest-to-whatever empirical reason for arguing a particular point, rather than just making stuff up (See: Deepak Chopra) then it’s part of the process of getting from ignorance to understanding.
But when people ignore the evidence, misrepresent the evidence, and just plain invent “evidence”, we (and I mean everyone) get to call them on it.
Science doesn’t claim to have The Answer, it claims to have a way of getting close to answers.
Call me stupid but is Behe really saying that his god made a special effort to intervene and make malaria no longer resistant to our medications so it could kill more people?
i won’t call you stupid, but i think you meant “make malalria more resistant” or something like that. it’s not stupid to ask a very, very important question of the creationist jackassery. not by a mile.
No, he says that the entire malaria parasite genome was intelligently designed to kill people, and random evolution can only make small adjustments to make it even more efficient at killing people. He is not saying that the drug resistance was designed, but he might as well since the whole thing makes no sense anyway.
Which RNA thing exactly? Textbooks today contain lots more knowledge about RNA than they did 10 years ago, and I know people working on RNA but not discovering any big surprises so far. Which great mystery are you talking about? ~:-| In other words, I don’t know how much you know, or perhaps rather how much you don’t know.
Which RNA thing exactly? Textbooks today contain lots more knowledge about RNA than they did 10 years ago, and I know people working on RNA but not discovering any big surprises so far. Which great mystery are you talking about? ~:-| In other words, I don’t know how much you know, or perhaps rather how much you don’t know.
A quick review of the literature reveals that malaria evolves resistance to drugs routinely. In the case below, resistance to a drug combo is associated with mutations in 5 genes. One is a triple mutant in dhfr combined with a double mutant in dhps. Behe is claiming that double mutants in the chloroquine resistance gene is the edge of evolution. Here we have a simple case of a triple and a double mutation in the same organism.
His assumptions are faulty, his science is faulty, and his conclusions are false. This is your basic Demski-Meyers class fraud. Fraud and lies are the signatures of christian creo thinking, an internal contradiction that insults both the religion and science.
Malaria can accumulate multiple mutations to become resistant to many drugs without breathing hard. Science/medicine can explain these without breathing hard, standard evolution aided by sexual recombination. It’s too bad for the patients. Malaria is like TB, there are strains resistant to most drugs and strains resistant to all drugs are on the horizon. One of these days we may well be hearing about Extremely drug resistant malaria (XDR-M) and some lawyer will pick up a case somewhere and introduce it to the US, :>(.
Acta Trop. 2003 Mar;85(3):363-73. Links
High prevalence of quintuple mutant dhps/dhfr genes in Plasmodium falciparum infections seven years after introduction of sulfadoxine and pyrimethamine as first line treatment in Malawi.Bwijo B, Kaneko A, Takechi M, Zungu IL, Moriyama Y, Lum JK, Tsukahara T, Mita T, Takahashi N, Bergqvist Y, Björkman A, Kobayakawa T.
Department of International Affairs and Tropical Medicine, Tokyo Women’s Medical University, 8-1 Kawada-Cho, Shinjuku-Ku, Tokyo 162 8666, Japan.
Malawi changed its national policy for malaria treatment in 1993, becoming the first country in Africa to replace chloroquine by sulfadoxine and pyrimethamine combination (SP) as the first-line drug for uncomplicated malaria. Seven years after this change, we investigated the prevalence of dihydropteroate synthase (dhps) and dihydrofolate reductase (dhfr) mutations, known to be associated with decreased sensitivity to SP, in 173 asymptomatic Plasmodium falciparum infections from Salima, Malawi. A high prevalence rate (78%) of parasites with triple Asn-108/Ile-51/Arg-59 dhfr and double Gly-437/Glu-540 dhps mutations was found. This ‘quintuple mutant’ is considered as a molecular marker for clinical failure of SP treatment of P. falciparum malaria. A total of 11 different dhfr and dhps combinations were detected, 3 of which were not previously reported. Nineteen isolates contained the single Glu-540 mutant dhps, while no isolate contained the single Gly-437 mutant dhps, an unexpected finding since Gly-437 are mostly assumed to be one of the first mutations commonly selected under sulfadoxine pressure. Two isolates contained the dhps single or double mutant coupled with dhfr wild-type. The high prevalence rates of the three dhfr mutations in our study were consistent with a previous survey in 1995 in Karonga, Malawi, whereas the prevalences of dhps mutations had increased, most probably as a result of the wide use of SP. A total of 52 P. falciparum isolates were also investigated for pyrimethamine and sulfadoxine/pyrimethamine activity against parasite growth according to WHO in vitro standard protocol. A pyrimethamine resistant profile was found. When pyrimethamine was combined with sulfadoxine, the mean EC(50) value decreased to less than one tenth of the pyrimethamine alone level. This synergistic activity may be explained by sulfadoxine inhibition of dhps despite the double mutations in the dhps genes, which would interact with pyrimethamine acting to block the remaining folate despite dhfr mutations in the low p-aminobenzoic acid and low folic acid medium mixed with blood.
Glen wrote: “Perhaps Behe should learn about sexual reproduction and its shuffling of genes (hint to Behe–there is an evolutionary, non-design reason why something as complex as sexual reproduction exists). He seems genuinely unaware of the role that sexual reproduction plays in evolution (well, obviously in sexually reproducing organisms like Plasmodium sp.)”
Plasmodium is a single-cell organism. Does it really come in male and female halves? That is fascinating.
Thankyou Raven,
Definitely fascinating.
Plasmodium is a genus of protozoa, eukaryotes, and thus is, or was (in this case “is”), sexually reproducing (eukaryotic bdelloid rotifers are getting cranky after 10s of millions of years w/o sex, but, as it is with other asexual eukaryotes, their asexuality is secondarily aquired). Like other protozoa, however, this isn’t a matter of coming in male and female entities or “halves”, at least not initially.
It’s at the gametocyte stage that humans begin to call P. falciparum “male” and “female”, the “microgametocytes” being the former and the “macrogametocytes” being the latter. Then these produce “male” and “female” gametes. It’s convenient to utilize these terms, for it takes into account the differences between gametes and their proximate sources. However, it is not so clear how “male” and “female” in P. falciparum relates to “male” and “female” in animals and plants.
The life-cycle of P. falciparum may be found here:
http://www.wehi.edu.au/MalDB-www/intro.html
Note the interesting, though largely meaningless to malaria sufferers (but not to researchers), fact that we are the “intermediate hosts”, while the mosquito is the primary or definitive host. This is simply because the definitive host is defined as the one in which sexual recombination occurs, which is the Anopheles (at least mostly) mosquito.
Another source on the malaria life-cycle:
http://www.museums.org.za/bio/apicomplexa/plasmodium.htm
It is a somewhat fascinating subject, all right, one that Behe ignored in order to come up with a “point” which cannot stand, in part because he ignored such crucial factors which bring together and “recombine” separate mutations in order to “try out” new modes of resistance.
In fact, parasitism is considered to be one of the main reasons for the evolution (and maintenance) of sexual reproduction. Usually this is considered from the hosts’ perspectives, however it has been recognized (by non-IDists anyway) that the sexual malaria and the sexual sleeping sickness (trypanosomes) parasites both have advantages over asexual organisms like bacteria (with their limited, though highly important, recombination capacity) in adapting to their hosts’ defenses.
Glen D
http://tinyurl.com/35s39o
Thanks to you too Glen, though I learned from Raven’s links what I needed, yours were valuable too.
Cheers
The main thing that Behe ignored in his calculation is that mosquitoes aren’t treated with chloroquine, so that during the life cycle, the fitness landscape reverses, giving the advantage to the wild-type Plasmodium in the mosquito (and any humans not taking chloroquine).
Amazingly, Behe does note the higher fitness of wild-type over mutant in the absence of chloroquine, but fails to consider the implications of this fact in his calculations.