Is antibiotic resistance really due to increase in information?
22 October 2001; reposted and updated 11 November 2006
This feedback, from Mikko Ilmari N. of Finland, criticises the responses to the PBS series on ostensibly scientific grounds. He accuses CMI of bias, falsehood, and misinformation, but fails to back up his points.
The only issue he does attempt to back up is a claim of information increase that caused increased resistance to antibiotics. But this once again fails to understand the key relationship between information and specified complexity. Once again, supposed evidence for evolution turns out to be better explained by the Creation/Fall model. His letter is printed with point-by-point responses by Dr Jonathan Sarfati (the author of the PBS responses) interspersed as per normal email fashion. MIN’s letter includes quotes from the PBS rebuttal, which are double-indented. Ellipses (…) at the end of one of the paragraphs signal that a mid-sentence comment follows, not an omission.
Just noticed that your ministries have, by assistance of Australian creationist Jonathan Sarfati, responded to the PBS-TV series Evolution.
The Australian creationist Jonathan Sarfati was not just offering assistance; it was part of his (my) job, since I’m part of Creation Ministries International.
The responses have got multiple omissions and scientific errors, …
Really? Let’s see if that claim stands up to scrutiny.
…as well as clues that such flaws are abundant because of [CMI’s] extreme-fundamentalist Biblical-Christianity bias.
Presumably you would regard the atheist leaders of evolutionary theory as the epitome of objectivity? Just how objective is Richard Lewontin’s a priori commitment demonstrated in this quote? Or Scott Todd’s rejection of an intelligent designer as a scientific hypothesis, even if all the evidence supports it, as shown by this quote? One must wonder how many of them share Aldous Huxley’s motivation as expounded in this quote.
(In a later letter, in response to our request for confirmation, he said:
No special problems. I just noticed that [CMI] has provided misinformation in its PBS-“rebuttals”, and I suspect that reason for doing so is [CMI’s] fundamentalist-Christian bias, strictly requiring separately created species, young earth and many other features with which, [CMI’s] personnel sure is also familiar with.
As covered above, CMI staff are not the only ones with biases. It’s just a convenient excuse to avoid having to actually refute the scientific evidence for a young Earth. Note also, as shown in Q&A: Speciation, we do not believe that every one of today’s species was separately created. Rather we predict rapid speciation within a created kind, not requiring any new genetic information but instead recombinations of already existing information and information-losing mutations.
It is, however a mystery to me, how does backing up young-earth-creationist-beliefs with data of very questionable nature and outright falsehoods, advance the sake of Christianity?
It is, actually, a mystery to me, how:
- So many anti-creationists ask leading questions, i.e. self-serving questions that presuppose something that has yet to be proved.
- Many anti-creationists assert that creationists tell lies, that creation has been proven false, or there’s so much evidence for evolution, but cannot actually document any of these.
- Known anti-Christians profess concern for Christianity. One of the most glaring recent examples is the atheist-founded-and-operated, pretentiously-named, evolution-pushing organization, the ‘National Center for Science Education’, producing a study guide for the PBS Evolution series—for churches. Of course the real reason is to white-ant the church from within, using compromising churchians much the same way as Lenin cultivated ‘useful idiots’ in the West.
- Atheists suddenly profess concern for honesty, treating it as an objective moral absolute. But they proclaim that we are basically rearranged pond-scum, with no Designer and hence no moral Lawgiver involved, so no basis for absolute morality (see this exchange between Lanier and Dawkins). Rather, a consistent evolutionist must believe that morality evolved because it conferred survival advantage on one of our alleged ape-like ancestors.)
I’ll take Sarfati’s writings of poison newts as an example: (from [this page], actually)Up to this point, still OK.
Poison newtThe program moves to Oregon, where there were mysterious deaths of campers, with newts found in their sleeping bags. It turns out that these Rough-skinned Newts (Taricha granulosa) secrete a deadly toxin from their skin glands, so powerful that even a pinhead can kill an adult human. They are the deadliest salamanders on Earth. So scientists investigated why this newt should have such a deadly toxin.
They theorized that a predator was driving this ‘evolution’, and they found that the Common Garter Snake (Thamnophis sirtalis) was the newt’s only predator. Most snakes will be killed, but the Common Garter Snake just loses muscle control for a few hours, which could of course have serious consequences.Here the Evolution-program makes a good point how scientific research of evolution can be done, with satisfying results, indeed.
And as I pointed out, the assumption of goo-to-you evolution was unnecessary and in fact is irrelevant—this is perfectly well explained by the Creation/Fall model. Note that the creationist Edward Blyth talked about natural selection 25 years before Darwin wrote Origin.
But the newts were also driving the ‘evolution’ of the snakes-they also had various degrees of resistance to the newt toxin. Are their conclusions correct? Yes, they are probably correct that the predators and prey are driving each other’s changes, and that they are the result of mutations and natural selection. Although this might surprise the ill-informed anti-creationist, this shouldn’t be so surprising to anyone who understands the Biblical Creation/Fall model.Why the involvement of mutations and natural selection should surprise so-called “ill-informed anti-creationists”?
Because they present a caricature of creationism that pretends that we believe in fixity of species.
And what on earth has any so-called ‘Biblical Creation/Fall-model’ to do with this phenomenon?
Obviously, as explained, because the Fall entails deterioration, and this includes copying errors in the genes (mutations). How does Darwinism in its original sense predict them? Darwin believed in pangenes, and had no idea about Mendelian genetics, which was also discovered by a creationist!
So is this proof of particles-to-people evolution? Not at all. There is no proof that the changes increase genetic information. In fact, the reverse seems to be true.[CMI’s] text slips into obvious falsehoods. The main point of the Evolution-program here is that (a) other species form large part of the environment of one species, …
Since when did we deny this? The problem is, this has nothing to do with particles-to-people evolution. So where is the ‘obvious falsehood’?
… (b) mutations, recombinations and natural selection is the clue how the species absorbs information from it’s environment thru generations following each other.
This is gobbledygook. There is no information from the environment to absorb! One wonders what meaning you assign to the term information. I have a fair idea where you picked up this nonsense, and the source of this misinformation is refuted in detail by the article The Problem of Information for the Theory of Evolution <www.trueorigin.org/dawkinfo.asp>.
(As a side point, it is very important to notice that this increase of information in a species does not conflict the Second Law of Thermodynamics, as life on planet Earth is energetically open system.)
As a Ph.D. physical chemist, needing no instruction in thermodynamics, I’m always amused by anticreationists, mainly biologists and geologists, who think they know something about this topic, when they obviously don’t. As I point out in The Second Law of Thermodynamics Answers to Critics, an open system is necessary but not sufficient for an increase in information content.
Since the PBS episode provides no explanation of the poison’s activity, it’s fair to propose a possible scenario (it would be hypocritical to object, since evolutionists often produce far more hypothetical ‘just-so’ stories): suppose the poison normally reacts with a particular neurotransmitter to produce something that halts all nerve impulses, resulting in death. But if the snake had a mutation reducing production of this the neurotransmitter, so the poison has fewer targets to act upon. Another possibility is a mutation altering its precise structure so that its shape no longer matches the protein. Either way, the poison would be less effective. But either reduced production of the neurotransmitter or a less precise shape, slow nerve impulses, meaning that muscle movement is slower.Rather than producing these “just-so” stories and trying to dig an excuse to do so from “evolutionists”, …
This was perfectly legitimate given the available information. It is far more legitimate than the evolutionary just-so stories that you evidently tolerate, because my explanation of an information-losing mutation is based on the observed fact that the more resistant snakes suffer from a disability.
… could [CMI] PLEASE make a note that protein structures can be examined to see if these more-effective poisons actually show loss of information or less-complicated structures than less-effective poisons.
Indeed they can be, and in every case they have shown a reduced specificity, which may be beneficial. So please provide actual evidence—patronising assertions are unimpressive.
Indeed, I have come across the similar kind of (creationist) claim than yours about antibiotic resistence earlier. Finnish creationist Dr. Pekka Reinikainen claimed that bacteria with better antibiotic resistence always show having less information or simpler structure.
I haven’t heard of Dr Reinikainen, but from the limited amount of information you provide, he seems to know what he’s talking about.
An article from a popular science magazine, concerning this antibiotic-resistence showed that Reinikainen had it wrong. Increase of information and new structural complexity has been observed in not just some, but in fact, many cases.
As will be shown, you have failed to demonstrate this in even one case! You would benefit by reading Dr Spetner’s book (Not by chance!) and his more detailed explanations of information in terms of specified complexity (Part 1 <www.trueorigin.org/spetner1.asp> & Part 2 <www.trueorigin.org/spetner2.asp>)—True Origins site, also hyperlinked on Q&A: Information.
The original magazine (which is not at hand now) was a Finnish popular scientific magazine Tiede 2000 i.e. Science 2000. It had some non-technical examples of antibiotic resistance which however showed clearly that in many cases we cannot honestly call the evolution of antibiotic resistance, "a loss of information". Instead, I have put (as an attachment) an article by Petrosino, Cantu and Palzkoll, titled “β-Lactamases: protein evolution in real time”
This was Trends in Microbiology 6(8):323–327, August 1998. Some bacteria produce β-Lactamases to destroy β-Lactam antibiotics, which include penicillin.
You may “judge” it and check if it’s always about “loss of information” as frequently claimed by some creationists. (Or maybe you accept increased information by evolution in this case without any further problems … your original article was about poisonous newts, indeed.)
Right, I read this paper as you requested. But despite its title, it does not support your points, but ours! For example, one mechanism featured in the article was acquisition of genes from other bacteria. I.e. the genes already existed—hopefully it should be obvious that this is irrelevant to the origin of these genes in the first place, which is what goo-to-you evolution is supposed to explain! The other clue is the statement ‘many of the mutations located around the active site pocket result in increased catalytic activity for hydrolysis of extended-spectrum substrates.’ Mutations far from the active site also increase extended spectrum catalysis. This provided an advantage to the bacteria containing these mutations, because they could destroy more types of antibiotics. But here was yet another example of an information loss conferring an advantage.
To understand this properly, it’s necessary to realize enzymes are usually tuned very precisely to only one type of molecule (the substrate), and this fine-tuning is necessary for living cells to function. Mutations reduce specificity and hence would reduce the effectiveness of its primary function, but would enable it to degrade other substrates too. But this loss of specificity means loss of information content. Dr Spetner analyzes this with rigorous mathematics using standard definitions of information. He presents the two extremes:
- An enzyme has activity for only one substrate out of n possible ones and zero for the others—here the information gain is log2n.
- The second is where there is no discrimination between any of the substrates—here the information gain is zero.
Real enzymes are somewhere in between, and Dr Spetner shows how to calculate their information. As explained above, living organisms require enzymes to do a specific job, so their information content is very close to the maximum in case 1. Quite close to the other extreme are ordinary acids or alkalis, which hydrolyse many compounds. These have wonderful extended-spectrum catalytic activity, but are not specific, so have low information content, so would be useless for the precise control required for biological reactions. All observed mutations reduce the specificity and trend towards the second extreme case. The trend described in the β-Lactamases is just the same as that described in ribitol dehydrogenase, the enzyme some bacteria use to metabolize ribitol, a derivative of a type of sugar (left). That is, the mutant acquired the new ability to metabolize xylitol, so it was thought to be an example of new information arising, and that it could trend towards a highly specific xylitol dehydrogenase. But on further inspection, it turned out not only to reduce its ability to perform its original specific function of metabolizing ribitol, but also to increase the ability to synthesize lots of other things, including arabitol. The trend is towards loss of specificity and producing an ordinary broad-spectrum catalyst, i.e. from case 1 to case 2. A graph of wild v. mutant β-Lactamase activity on various antibiotics would be essentially the same as this graph of wild v. mutant ribitol dehydrogenase activity on the different types of sugars.
In conclusion, there is nothing to support any information gain at all. But evolution posits that the information content of the simplest living organisms, the mycoplasma with 580,000 ‘letters’ (482 genes), was increased to, say, the 3 billion letters equivalent in man. If this were so, we should be able to observe plenty of examples of information gain without intelligent input. But we have yet to observe even one, including the example you cited.
And so on …
(Dr) Jonathan Sarfati