Intelligent Design, Science Literacy and the Case of Antibiotics

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Science literacy is increasingly seen as important for people to be effective participants in a society where the pace of scientific discovery and translation to products and processes is increased. Effective engagement with GM crops, stem cell therapies, burgeoning healthcare costs and global warming require a reasonable degree of science literacy.

The need for science literacy is emphasised by a recent post at Uncommon Descent by commentator Gil Dodgen, who makes this remarkable statement:

In the meantime, medical doctors should prescribe multiple antibiotics for all infections, since this will decrease the likelihood that infectious agents can develop resistance through stochastic processes. Had the nature of the limits of Darwinian processes been understood at the outset, the medical community would not have replaced one antibiotic with another in a serial fashion, but would have prescribed them in parallel.

As I’ve said before in a different context, to paraphrase Mr. Babbage[1], I cannot apprehend the confusion of mind that would result in the above statement. One would have to be ignorant of 60 years of biomedical research and medical practice to say that. Both Humble Monkey and The Sandwalk have already commented on this post, and it’s got a big helping of Respectful Insolence, but I want to discuss this from a pharmacological perspective.

Combination therapies to combat resistance have been in use since the 1940’s to prevent the rapid emergence of streptomycin resistance during therapy for tuberculosis (streptomycin and p-aminosalicylic acid was the drug combination, Kucers, 1997)). The understanding of the need for antibiotic combinations was firmly grounded in evolutionary biology then as now (see also Allan et al 1985, Millatovic et al, 1987).

A brief look at Goodman and Gilman’s Manual of Pharmacology and Therapeutics shows combination therapy indicated to reduce the development of resistance (page 712); it’s also in the Medicines Australia Handbook. G&G is hardly an obscure publication and is one of the mainstays of medical education, so it is hard to be unaware of combination therapy. Combination therapies for TB and leprosy are standard practice. In the world of viruses, triple therapy for HIV, is the standard, and has resulted in significant long term survival and improved quality of life. With protozoa, dual therapies for malaria are recommended by the WHO. This is not an exhaustive list of micro-organisms where combination drugs are given to slow the rise of resistance, merely the better known ones. While Mr. Dodgen is not expected to have a medical therapy reference handy, even a brief search on the internet would acquaint him with the long history of the use of combination antibiotic therapies in medicine.

Now, while we may with justification roll our eyes at Mr. Dodgen’s ignorance, he does ask an interesting question. Given that we know (and have known for some time, based on our understanding of evolution), that combination therapies slow the appearance of resistance, why are not all anti-microbial therapies combination therapies? The reasons are manyfold, and not related to the medical research communities firm understanding of the rise of resistance (a recent Medical Journal of Australia article carrying the plaintive title “Why do we not yet have combination chemotherapy for chronic hepatitis B?” gives some good insights into this question)

One of the reasons is simple; to have a combination therapy, one must have multiple drugs to combine. In the case of HIV, before we could have triple therapy, we need to develop several drugs to deliver. In the early days of HIV, there was only one drug AZT, which bound to the enzyme reverse transcriptase. It was only after several years of intense research that we were able to provide several different drugs to combine.

Another problem is that the targets for these drugs must be different; a drug variant that binds to the same site on a target protein will be affected by the same or similar mutations that produced resistance in the first place. But in drug development, variants of a successful structure are easiest to make, so these will be first to be made. It took a while, but drugs were developed that could inhibit reverse transcriptase through other binding sites (the non-nucleoside analogs) and finally drugs were developed that could inhibit HIV protease, the viral enzyme required for processing viral proteins into their functional forms. Now triple therapy, a combination of two reverse transcriptase inhibitors (both AZT-like and non-nucleoside) and a HIV protease inhibitor, is standard. But it took a while to get there.

The principle applies to combination antibacterials. We have a wider range of cellular targets to hit in bacteria, compared to viruses (which hijack our own cellular machinery, making them difficult to target), but that range of targets is not immense. Many of the antibiotics we have are variants on the same basic structure, and while these have very important therapeutic properties, they are not good candidates for combination therapies. As I mentioned above, it is generally easier in drug development to modify an existing drug to have improved properties then to come up with a completely new drug that acts at a different target (but not always, drug design can have all sorts of surprises in store). Despite what people may think, it takes quite a bit of work to make a new drug, and drugs that may have wonderful properties in the test tube fail utterly in humans (one classic was at the turn of the century when a promising new group of antibiotics failed because they were insoluble in water). As well, given the costs of drug development, there is little incentive for drug companies to develop new antibiotics acting at unique targets. In The Pipeline has some interesting ruminations on drug development that may help you keep all this in perspective.

Once you have new drugs, all is not plain sailing. All drugs have some degree of toxicity, adding drugs together can increase the risk of toxicity, for example the combination of beta-lactam antibiotics and aminoglycosides produce renal toxicity which outweighs the benefits of reduced resistance development. As with this case, not all antibiotics are suitable for combination because of their toxicity. As well, and this may seem surprising to you, some antibiotics interfere with each other to produce less of an effect. For example, bacteriostatic antibiotics (those that slow the growth of bacteria, rather than kill them) interfere with bactericidal antibiotics; this limits our choice of drugs even more.

As you can see, setting up antibiotic combinations is not straight forward. To quote from the above Cochrane review:

The disadvantages of combination therapy may include additional costs, enhanced drug toxicity, the possible induction of resistance caused by the broader antibiotic spectrum (Manian 1996; Weinstein 1985), and possible antagonism between specific drug combinations (Moellering 1986).

So, despite GilDodgen’s claims, we do have combination antibiotic therapies. The failure to develop universal combination therapies for all bacterial infections is not due to blinkered Darwinism, but due to the limitations of the drugs that we humans develop. Limitations that are entirely understandable given the fallible information we have about organisms and their interaction with chemicals, and the finite supply of resources that we have available to develop drugs.

This brings me back to science literacy. I just have to turn 45 degrees to my left to pick up Goodman and Gilman (most physicians will have it or something like it in similar reach). This sort of resource is not available to most people, and I would be surprised if GilDodgen has Goodman and Gilman or Martindales within easy reach. But he probably has read reports in newspapers or seen items on TV about antibiotic resistance. It would be easy then to simply assume that medical science is just rolling out the same old sausage line drugs with little regard to actually thinking about resistance. However, a science literate prson would assume that newspaper reports are limited, and go looking for more in depth information. Google is the modern encyclopaedia, and typing in “combination therapy” antibiotic retrieves a number of hits. The very first discusses combination therapy to reduce the rise of resistance. Then there are others such as this one and the Cochrane review , which clearly shows that combination therapy is used, and it’s limitations. Even typing “combination therapy” antibiotic into Wikipedia will retrieve this reference , which clearly shows the use of combination therapy.

Clearly, scientific literacy is not just having a passing understanding of the facts of science, but also the ability to use the methods and resources of Science. Sadly, the denizens of Uncommon Descent do not have scientific literacy.

Now let’s look at some more of GilDodgen’s claims:

Here’s a prediction and a potential medical application from ID theory: Design a chemical or protein which would require a triple CCC to defeat its toxic effects on a bacterium, and it will exhaust the probabilistic resources of blind-watchmaker mechanisms to counteract the toxic effects.

A “CCC” is a chloroquine resistance cluster, which is not a cluster at all and requires considerably less than a population of 1020 organisms to evolve it (see Nick Matzke’s review of this for more detail). Designing such a drug would be difficult, even with the protein structures we have, designing de novo a drug that requires multiple mutations to displace it is a non-trivial task. Even here, evolutionary biology is required, in order to find which enzymes are critical targets, and which have mutated the least since remote common ancestors, making their structures highly intractable to mutation.

Such a success could and will only come from engineering and reverse-engineering efforts, not from Darwinian theory.

Sadly for GilDodgen and Uncommon descent, no. It will require a large input from evolution and evolutionary theory to design such drugs. We will need evolutionary theory to locate suitable targets first. Then drugs will be developed either from screening natural products, where evolution has crafted many antimicrobial compounds vai paths we aren’t clever enough to understand yet, or developed using drug synthesis approaches that mimic natural selection . Some complete de novo design is done, building drugs from first principles, but this has not been more successful than evolutionary based approaches.

In summary, we do have combinatorial antibiotic therapies, where they are possible and appropriate. New antibiotic therapies with reduced risk of development of resistance will come from the drug discovery process, but only by utilizing our understanding of and the principles of evolutionary biology. The commentators at Uncommon Descent could use some pointers in science literacy.

References

Allan JD,Moellering RC.Management of infections caused by gramnegative bacilli: the role of antimicrobial combinations. Reviews of Infectious Diseases 1985;7 Suppl 4:559–71.

Kucers A. Evolution of antituberculous therapy. In: Kucers A, Crowe S, Grayson M, Hoy J, editors. The use of antibiotics. 5th ed. Oxford: Butterworth-Heinemann, 1997: 1194.

Milatovic D, Braveny I. Development of resistance during antibiotic therapy. European Journal of Clinical Microbiology 1987;6(3):234– 44.

[1] Charles Babbage was a computer pioneer who had to deal with staggering incomprehension.

On two occasions I have been asked, – “Pray, Mr. Babbage, if you put into the machine wrong figures, will the right answers come out?” In one case a member of the Upper, and in the other a member of the Lower, House put this question. I am not able rightly to apprehend the kind of confusion of ideas that could provoke such a question.

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It's been a while since I've visited the cesspool that is Uncommon Descent, a.k.a. Bill Dembski's home for wandering sycophants, toadies, and lackeys. There's a good reason for this; I just get tired of the sheer stupidity that routinely assaults... Read More

38 Comments

Gil wrote:

“Had the nature of the limits of Darwinian processes been understood at the outset, the medical community would not have replaced one antibiotic with another in a serial fashion, but would have prescribed them in parallel.”

The implication seems to be that “Darwinian processes” have limitations, therefore, evolution ain’t so great and we should be able to easily defeat it since it is after all the enemy. Of course that would only be true if evolution actually happens!

I don’t know why creationists take such delight in the fact that random mutation and natural selection have limitations. Of course they do. It’s only an all-knowing, all-seeing, ever-present God who has no limitations and can plan for the future. So admitting that these limitations exist in nature is evidence for evolution, not for the hand of God.

Ian, as usual, excellent article. This is yet another example of how intelligent design creationism (and William Dembski’s blog/home for the misguided and uninformed) not only fosters ignorance it promotes it.

Chris!

Excellent article. Comments will likely be sparse, due to the actual scientific content.

I think you are being kind to ascribe this particular ID nonsense to “ignorance”. My take is that it is an example of the “Orwellian” school of propaganda. Attack the obvious truth by brazenly claiming the exact opposite.

It is not the ignorance of the writer, but the presumed ignorance and bias of the target audience, which is relevant.

But he probably has read reports in newspapers or seen items on TV about antibiotic resistance.

Maybe. But sadly, many people watching tv or reading newspapers and magazines are seeing articles and ads for coffee enemas, homeopathic remedies, and other quackery.

Excellent post Ian. There are two excellent commentaries in the latest issue of Nature Methods on protein engineering and how that field uses Evolutionary methods to further research. They would both tie in nicely with the point you are making on understanding rational drug design from an evolutionary perspective.

OK, maybe I’m hopelessly naive here, but will GilDodgen be exposed to this post? Is there any way his errors will be brought to his attention. I have this mental image of IDers hiding out in their cliques studiously avoiding confrontation with actual evidence. Is that how it works?

OK, maybe I’m hopelessly naive here, but will GilDodgen be exposed to this post? Is there any way his errors will be brought to his attention. I have this mental image of IDers hiding out in their cliques studiously avoiding confrontation with actual evidence. Is that how it works?

Reading UcD and the comments show the lack of much scientific reasoning involved with Intelligent Design. The ignorance of its followers is staggering, but it does serve its purpose as it seems self evident to most casual observers. This level of ignorance actually helps strengthen the case against ID and for that we should be thankful that sites like UcD exist.

If I understand their CCC logic, to cure Malaria once and for all, you develop a malaria cure, call it the IDquinone, then find out exactly what gene – and what precise mutation(s) – will enable the parasite to overcome the drug, then you beef up the drug so it would require 3, 4 or more mutations to defeat it.

Unless, of couse, The Designer intervenes and Creates the gene malaria needs to overcome IDquinone and make mankind sick.

Uh, phamacology is not advanced enough to come up with dozens of safe anti-malarial drugs to order, and the current state of scientific research gives no clue which genes, which mutations will allow the bacteria or the parasite to overcome said drug.

So either Plasmodium has better researchers than we do, or it is backed by a Designer that care more for it than for us. Go figure.

David Stanton Wrote:

I don’t know why creationists take such delight in the fact that random mutation and natural selection have limitations. Of course they do. It’s only an all-knowing, all-seeing, ever-present God who has no limitations and can plan for the future. So admitting that these limitations exist in nature is evidence for evolution, not for the hand of God.

Now here is an excellent opportunity for the ID community to do some research and demonstrate the capabilities of their “intelligent designer”. Using themselves as guinea pigs, they could infect themselves with HIV or some other nasty virus and then pray to their designer for an exquisitely designed cure. All they have to do is design a protocol, submit it to a respected journal, get favorable peer review and accolades, and finally clinical trials on their followers and FDA approval for the procedure. Piece o’ cake.

The only problem with your suggestion, Mike, is that the ID community is far too frightened of the idea of submitting their findings to peer review.

Perhaps pointing out that aside from the extreme technical difficulty with this proposed research maybe just maybe someone should point out that evolutionary reasoning leads to the same proposal. Except that being staff by compotent people they realize that drug design isn’t anywhere close to that precise. If only we knew every interaction… it just might work out.

This was a wonderful piece, Ian. When I read UD, I get angry and muddled; it’s hard for me to come up with a cogent response. You put into lovely, clear words the ideas that skewer the cdesign proponentsists through their vitals. Thank you!

I found this passage particularly telling:

Sadly for GilDodgen and Uncommon descent, no. It will require a large input from evolution and evolutionary theory to design such drugs. We will need evolutionary theory to locate suitable targets first. Then drugs will be developed either from screening natural products, where evolution has crafted many antimicrobial compounds vai paths we aren’t clever enough to understand yet, or developed using drug synthesis approaches that mimic natural selection.

How on earth does GilDodgen imagine one would go about designing a drug? Does he think it’s pretty much like whittling a peg to fit into a hole with a prescribed shape? Or maybe like piloting a guided missile?

We see farther by standing on the shoulders of giants, but GilDodgen makes me wonder what happens when you pretend that the giants do not exist at all, and the fact that you can see farther is entirely due to your remarkably keen eyesight.

Given as how Behe suggests that the Designer “designed” malaria to kill people, I’m not sure if ID proponents would even want to develop a cure for diseases, anyhow, as, that would be thwarting the will of the Designer, after all.

Observer: I think that the answer to your question is no because of willful blindness. That pretty much sums up the whole ID crowd in general and the denizens of UD in particular. These people apparently live in their own alternate reality.

ive always said the the anti-science nonsense of ID and creation science is going to kill people if we allow it

Combination drugs are used to treat malaria. One older combination of two drugs is not very effective because of resistance.

The resistance mutations are known. It took malaria 5 mutations, 3 in one gene and 2 in another to evolve resistance to this combination. Five.

Malaria can evolve resistance to drugs requiring 5 mutations without even breathing hard. Whatever the limits to evolution, they are way beyond anything the IDists can imagine.

Gil Dodgen has no idea what he is talking about. Worse, he doesn’t care. Anyone could look this info or similar up on the internet with a few mouse clicks.

Abstract on quintuple mutant Plasmodium is below. Speaks for itself.

Acta Trop. 2003 Mar;85(3):363-73. 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.

The failure to develop universal combination therapies for all bacterial infections is not due to blinkered Darwinism, but due to the limitations of the drugs that we humans develop.

It’s also due to the amazing variability of evolution by natural selection. But we don’t expect poor Gil to think that hard.

Well aside from the solution we already know about for drug resistance in malaria, biological systems seem to have this amazing knack for producing new solutions when the need arises. Biggest problem I always had in molecular biology was the darn bacteria evolving in ways other than what I wanted. Nothing like a selection experiment and picking colony after colony and not having it be what you want at all.

In comment 137674

Dan Gaston Wrote:

There are two excellent commentaries in the latest issue of Nature Methods on protein engineering and how that field uses Evolutionary methods to further research. They would both tie in nicely with the point you are making on understanding rational drug design from an evolutionary perspective.

You presumably mean Nature Methods December 2007, Volume 4 No 12, Protein engineers turned evolutionists pp991 – 994 Sergio G Peisajovich & Dan S Tawfik doi:10.1038/nmeth1207-991 and Dissecting protein structure and function using directed evolution pp995 – 997 Courtney M Yuen & David R Liu doi:10.1038/nmeth1207-995 (may require subscription). There was also an interesting editorial on Intellligent design. While these are excellent articles on protein evolution, I was thinking of the uses of genetic algorithms and selection to develop small molecule drugs. Examples include this article on genetic algorithms in Modern Drug Discovery, this article on combinatorial chemistry in Nature Methods (free access), and this nice review article again on genetic algorithms in drug discovery.

However, the articles you have drawn my attention to require a blog post of their own, as they blow yet another hole in the assumptions Behe uses in his claims for the “unevolvability” of complex systems. Maybe not this week though. Many thanks for that

In comment 137719

Form&Function Wrote:

How on earth does GilDodgen imagine one would go about designing a drug? Does he think it’s pretty much like whittling a peg to fit into a hole with a prescribed shape? Or maybe like piloting a guided missile?

Well, actually, one method of drug design is just like fitting a peg into a hole of prescribed shape. You need an accurate X-ray crystal structure for your enzyme (this is not always possible) and a good 3D library of compounds known to bind to your enzyme (again not always possible) locate a binding pocket (usually the catalytic pocket of the enzyme – especially if you want inhibitors of enzyme activity), then you use small molecular building blocks to construct a ligand to fit into the binding pocket and bind with high affinity. It is of course not straight forward for many reasons. See this excellent set of lecture notes on the process (warning, 0.8 Mb download). In some limited situations de novo works straight off (and the lecture gives a good example), more often we need to use evolutionary techniques to select small molecule choices to link up and then refine them (again, the lecture gives a good example).

So yes, in certain situations we can do the “peg whittling to fit a hole” thing, but for finding new drugs to hit recently discovered targets, evolutionary techniques will be needed to both select the targets and design the drugs.

Stanton:

The only problem with your suggestion, Mike, is that the ID community is far too frightened of the idea of submitting their findings to peer review.

Got that right. They’re too afraid to let dissenting voices speak on their blog. Only the most tepid responses seem to be allowed. Go into any great detail, and it’s deleted.

In comment 137676

Observer Wrote:

OK, maybe I’m hopelessly naive here, but will GilDodgen be exposed to this post? Is there any way his errors will be brought to his attention.

There is one post alerting people to the article being discussed on Panda’s Thumb (comment 55), but at the moment they are engaged in a rather clueless discussion of Junk DNA and the ENCODE study. No one over there seems to have cracked open a book on medical therapeutics. One person has pointed out tht multiple antibiotics can be used, but they have been largely ignored. I don’t think they are concerned with people pointing out the mistakes in their arguments.

There is one post alerting people to the article being discussed on Panda’s Thumb (comment 55),

They’re too busy playing design theorist at UD to notice. Wouldn’t do much good anyhow, those guys are too crafty to fall for the old fallacy of facts argument.

Mr_Christopher Wrote:

They’re too busy playing design theorist at UD to notice.

Actually, two of the last three posts have been given over to global warming denialism. They seem to be too busy embracing cranks causes to deal with facts.

Well, actually, one method of drug design is just like fitting a peg into a hole of prescribed shape. You need an accurate X-ray crystal structure for your enzyme (this is not always possible) and a good 3D library of compounds known to bind to your enzyme (again not always possible) locate a binding pocket (usually the catalytic pocket of the enzyme – especially if you want inhibitors of enzyme activity), then you use small molecular building blocks to construct a ligand to fit into the binding pocket and bind with high affinity.

Thank you, Ian. Of course you’re right and I should have been more clear. I intended to express my amusement that Gil seems to think that the holes (like the targets of my “guided missile” analogy) are already well-known and described, when in fact they often are not. Deciding which drug targets to choose for the best effect would be a hit-or-miss affair without using evolutionary theory to guide us.

“Deciding which drug targets to choose for the best effect would be a hit-or-miss affair without using evolutionary theory to guide us.”

And, what current drug or genetic research CANNOT do, is to guess which genes in the bacteria or the parasite, *WILL* mutate to counter the new drug, and to count how many point mutations will be needed for that.

Just finding a drug that work, and that has no ill effects, is already quite an achievement.

Gil read this article…And still doesn’t get it. Too funny!

Gil’s response is PT is being mean to him and that proves his claims are right.

Nice. All science so far!

Better yet, Gil claims that the very fact that PT is responding to him means his claims are right!

Reynold Hall:

Stanton:

The only problem with your suggestion, Mike, is that the ID community is far too frightened of the idea of submitting their findings to peer review.

Got that right. They’re too afraid to let dissenting voices speak on their blog. Only the most tepid responses seem to be allowed. Go into any great detail, and it’s deleted.

And yet, ID proponents accuse us of being closeminded.

Over at Uncommon Descent

GilDodgen Wrote:

Just for the entertainment value, I checked out the Panda response to my post…

Did you find it amusing to see that you were wrong, that medical researchers have been using combination antibiotic therapy for over 60’s to combat resistance, that many of our current therapies use combination therapy to combat resistance (and it’s even recommended in standard therapy manuals) and that our main barriers to using wide spread combination therapy is toxic drug interactions, antibiotics that interfere with each others actions and the high cost of developing new drugs.

GilDodgen Wrote:

If my UD posts were as scientifically and logically vacuous as the Pandas claim, no response would be required,…

False claims do need a response, and you made several empirically false claims.

GilDodgen Wrote:

…empirically verifiable science is what I do every day for a living…

Then what stopped you from doing a five minute internet search to verify the claims you made? You should be very familiar with the need to verify claims if you do empirical research, and be be familiar with the details of searching the literature. As I demonstrated, even a simple Google search will show that antibiotic combinations are used to combat resistance. Why didn’t you find this out yourself?

Mr. Dodgen, it is neither vitriol nor ire to point out that your facts are wrong, and that this could be established by a simple internet search. It is not an insult to point out that your prediction was vacuous, and that evolutionary biology had been brought in to combat resistance and design antibiotics long, long ago.

How about dealing with the substantial arguments Mr. Dodgen? Will you concede that we have been using combination therapy here practical and appropriate for over 60 years?

If my UD posts were as scientifically and logically vacuous as the Pandas claim, no response would be required,

Translated from cdesign proponetist rhetoric this means that if you respond it must mean I had a valid point and if you don’t respond it means that you can’t find anything wrong with what I said.

Translated from cdesign proponetist rhetoric this means that if you respond it must mean I had a valid point and if you don’t respond it means that you can’t find anything wrong with what I said.

And don’t forget the ever popular you found a fossil in the gap, so now there are two gaps where there was just one!

Henry

Oh, and btw, cdesign and proponetist aren’t in the spell checker!

The entire quote from GilDodgen:

“Just for the entertainment value, I checked out the Panda response to my post. I seem to have a penchant for arousing their ire and vitriol, and I can explain why.

If my UD posts were as scientifically and logically vacuous as the Pandas claim, no response would be required, but they seem to have a passion for devoting both tomes and insults to refuting my arguments. I am perpetually labeled as being completely ignorant about science (even though empirically verifiable science is what I do every day for a living). Yet, whenever I post an incisive comment about the empirical, observational, mathematical, or computational problems with blind-watchmaker Darwinism, the Pandas go into a feeding frenzy.

I’ve struck a nerve. The personal insults and claims that I know nothing about science are very telling.”

Clearly, you can’t rely on some people to ever be honest or fair. When you click on the “Gildodgen” link, you are taken to here:

http://www.worldchampionshipcheckers.com/

I fail to see the connection between playing checkers and doing science.

wikipedia:

The standard “short” course treatment for tuberculosis (TB), if it is active, is isoniazid, rifampicin, pyrazinamide, and ethambutol for two months, then isoniazid and rifampicin alone for a further four months. The patient is considered cured at six months (although there is still a relapse rate of 2 to 3%). For latent tuberculosis, the standard treatment is six to nine months of isoniazid alone.

There is nothing new about antibiotic combinations. They have been used for decades for tuberculosis, HIV, and malaria and occasionally for MRSA.

They are also no magic wand. A lot of TB is now multidrug resistant TB and there is a new strain that is XDR TB, extremely resistant to all commonly used antibiotics. Mortality of this mutant can be quite high, up to 98%.

wikipedia:

There is currently an epidemic of XDR-TB in South Africa. The outbreak was first reported as a cluster of 53 patients in a rural hospital in KwaZulu-Natal of whom 52 died.

Behe would say MDR TB and XDR TB were designed by god because…well, whatever god does when she is in a bad mood or whatever. Docs know that sooner or later any pathogen will evolve resistance to whatever they are treated with by a well known process called evolution.

Drug combos are tricky and each one must be tested and optimized. Drug-drug interactions are common and can be fatal. Seldane was taken off the market. A great antihistamine and safe. Except when given with a cytochrome p450 inhibitor which inhibits its metabolism. It can then cause fatal heart arrhythmia. It is estimated that at least 50 people died this way in the USA.

Dodgen is just wrong and ignorant. It is a good thing the DI is practicing pseudoscience rather than pseudomedicine.

Antibiotic abuse situation is already very serious, indeed doctors should use composite. Some drug information can search here: 医搜

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