Antibiotic Resistance and Creationism

Antibiotic resistanceIn the most recent(ly discovered by me) article by Brian Thomas, Antibiotic Resistance in Bacteria Shows Adaptive Design, we have the creationist explanation for why Antibiotic resistance is not, apparently, evidence (if not confirmation) for evolution. The article, coincidentally, is very similar to the most recent DpSU I wrote about, which was about the evolution (or ‘adaptation’ to Mr Thomas) of yeast. While this is not a DpSU, if you placed this among 9 articles that were you couldn’t pick it out.

Mr Thomas begins:

Bacterial survival in antibiotics has been taken as proof of evolution in action. But in-depth studies of the specific mechanisms for antibiotic resistance in bacteria show that no evolutionary processes are involved. One recent study even mentioned the possibility that bacteria are able to fine-tune the shapes of their own biochemicals in order to circumvent the harmful effects of antibiotics.

This is a big claim. No evolutionary processes? So the image to the right is incorrect, and there is no selection stage? Interesting…

Antibiotics are tiny chemicals that can kill bacteria, and their use can wipe out almost all the individuals of a bacterial population. But a few bacteria sometimes survive and grow in the presence of the antibiotic, although at a slower pace.

A reasonable introduction to the concept. Creationists are always keen to point out the disadvantages of bacterial resistance. As a general rule, the differences in bacteria that give one resistance where the other does not would not be advantageous – and are likely to be slightly disadvantageous – if they did not have to deal with the drug that they are resistant too. If it was advantageous, they would already be doing it.

How do bacteria acquire antibiotic resistance? Often, a small number were already resistant before the antibiotic was applied. There is no innovation in such cases, but merely a shift in which strain of bacteria dominates the habitat. That’s not evolution.

…It’s natural selection. As wikipedia says:

Natural selection is the nonrandom process by which biologic traits become more or less common in a population as a function of differential reproduction of their bearers. It is a key mechanism of evolution.

Remember what BT said at the start? “[N]o evolutionary processes are involved [in antibiotic resistance]”. This statement, then, is falsified already. Evolution does not end with the creation and modification of new traits. Indeed, that is only the beginning.

Sometimes the DNA of bacteria changes, and this can alter their protein shapes. Though these subtle alterations almost always decrease the protein’s job efficiency, they can ward off antibiotics that would ordinarily disrupt certain proteins.

Only sometimes? You’d better qualify that at some point…

At times DNA changes are random, in which case they are called mutations. But DNA changes are often non-random, which means that they may have been designed to change. Neither scenario helps evolution, which must explain how whole genes and their encoded proteins came into existence in the first place, not how already existing proteins lose efficiency.

The only way that a change in DNA is not a mutation is when a whole section of DNA is moved in some way. Randomness is not part of the definition, really. And what makes them non-random? There are two possibilities as to what he’s getting at. One is that he is claiming that good changes (the equivalent of rolling a six) are, for some reason, ‘non-random’. Alternatively, it could be that he is referring to how, while they may appear random, every mutation has a cause, whether it be ionising radiation or shoddy replication. Or it could be something else entirely…

In the recent study, investigators determined the mechanisms behind methicillin resistance in a strain of common skin bacteria.1 The antibiotic methicillin kills by attaching to a certain site on bacterial ribosomes, jamming their activity. Ribosomes are molecular machines required to build proteins, and are partly made of nucleic acids that require special changes before they can work properly.

So there is a study at the heart of this. That would help. As you can tell, it’s a pretty technical study…

For example, a “methyl group”—in essence, a methane molecule—must be chemically bonded at a specific site. In the wild strain of these bacteria, a protein named RlmN adds a methyl group to carbon number two of the 2503rd ribosomal nucleic acid. Thus, RlmN helps assemble the ribosome, which in turn assembles other proteins, including RlmN.

But in the resistant strain, a very similar protein named Cfr adds the methyl group to carbon number eight instead. This tiny shift keeps methicillin from “clogging” the ribosome and ultimately destroying the bacterium. The resistant bacteria have Cfr and they can therefore continue to survive, although their less-efficient ribosomes manufacture proteins more slowly.

Some further explanation, the purpose of which seems to be to set the situation up as being impossible to happen ‘randomly’.

In the researchers’ scenario, RlmN supposedly evolved into Cfr. But the actual changes from RlmN to Cfr involved a loss of information!2 RlmN had some flexible regions that ensured that the methyl group was added to carbon number two. Cfr no longer has these regions. That’s no help to big-picture evolution, which must account for the origin of all the critical spatial and “electrostatic surface potential” distributions in these proteins—without any intelligent source.1

Citation 2 in this article is to a similar, but not identical DpSU from not long before I started this blog, on the same study. The line there reads:

In the researchers’ scenario, RlmN was supposed to have “evolved” into Cfr. But the actual changes from RlmN to Cfr involved losses of information!

In this article, there is no source for the statement that information was lost. This is not entirely unexpected. The word ‘information’ in this context is a creation of creationists, who never seems to have a working definition of it. As a result, it can always be claimed as a last resort that any example of evolution is a ‘loss of information’, which then makes it perfectly ok, if ‘information’ has not previously been defined. I am quoting for you every line of this article – as you can see, there was no definition of ‘information’ anywhere.

He does sort-of provide it immediately afterwards, when he talks about how the protein does not have “some flexible regions”. However, this does not necessarily mean that ‘information’ has been lost anywhere. As an example, take the Mandelbrot set (or any other fractal). It might take a certain amount of ‘information’ to tell something how to make it normally. However, say you want to remove from your result a section, in this case every thing to the left of the boundary of the largest and second largest area of black space in this image. To do that, you would need to add more information to your algorithm at some point, even though you have removed stuff from the result. As we are not told what ‘information’ is here, nor what is causing the change to happen (which is very important), we don’t know whether or not something like that has happened. The ‘information’ line therefore is meaningless.

The study authors deduced that, although certain regions had been removed from RlmN to turn it into Cfr, nothing was lost from its crucially structured core. They said that these changes suggested “an extended interaction surface to fine tune control of substrate [ribosome] binding and site selectivity.”1

The mere presence of such tiny machines is clear evidence of the Creator’s handiwork, but even clearer evidence of super-intelligent design are systems that fine-tune the shapes and activities of those tiny machines so that they can adapt to different situations in the cell. Adaptive programming, not evolution, appears to be responsible for the ability of these bacteria to survive in methicillin.

“[T]iny machines”? What are we talking about here exactly? And forget ‘intelligent design’ – it’s super intelligent design!

And where does ‘adaptive programming’ come from. As I mentioned in my last DpSU post, is Brian Thomas an advocate for Lamarckism? It’s possible that there could be a way for organisms to directly modify their own genome in order to do this kind of thing, but if it’s heritable, it’s evolution. Mr Thomas does not say what it is that makes the proteins different – we can only assume that it’s a mutation somewhere, which wouldn’t exactly be beyond evolution’s capabilities – and so we can only speculate. All in all, not a DpSU that answers all the questions.

And that’s all. The next question is whether there’ll be a new article by Mr Thomas on Monday or not…

6 thoughts on “Antibiotic Resistance and Creationism

  1. Pingback: More Fruit Fly Larvae « Eye on the ICR

  2. the bacteria changed over time and as a result of an environmental stressor

    sounds like evolution to me

    no matter how much creationists stamp their feet and threaten to hold their breath

  3. Pingback: The ICR’s Acts and ‘Facts’ – August « Eye on the ICR

  4. Pingback: IEE: Faith and Science « Eye on the ICR

  5. I would like to thank the creationists for admitting that they do believe in the existence of DNA. That is a good first step, and shows that we are getting through.

    However, they seem to think that the encoded information in DNA is static (unchanging), and that if it does change (addition or loss), then it must be God working some sort of magic.

    The reality is that every cell division involves a process in which DNA, or its close cousin RNA used in protein-making, is split apart and copied via chemical transcription—a process during which errors occur. Sometimes these errors result in no real changes. Sometimes one error, or several together, is lethal to the organism (think about human birth defects such as spina bifida, which was lethal before the advent of modern medicine). But, every so often, the error results in some trait that confers an advantage.

    In the case of methicillin-resistance, in the article referenced above, a transcription error has resulted in the loss of a particular gene that made it vulnerable to the antibiotic. Without this vulnerability, a bacterium has a survival advantage.

    The reason that we are able to study evolution in bacteria (and other microorganisms) so effectively is that their life-cycles are measured in mere minutes or hours, whereas in larger organisms they may occur over decades. In hours or days one can observe the effects of tens, hundreds, or even thousands of generations of bacteria, but it takes hundreds of years to see evolutionary changes in human traits.

    Evolutionary advantages involve some trait that confers a reproductive advantage. For example, think about humans who are not very attractive—for example, people who are very short and have huge noses or elephant ears, caused by some gene mutation(s). These people have a terrible time competing for mates, starting early on in school (think: bullying). The fact that certain traits, although they occur in the population, are not the norm, shows that their carriers have not had much reproductive success, and their genes have not survived.

    But think about the trait for tallness, which is generally perceived to be more attractive. We have, indeed, been able to record the change in human height across the centuries, as measured by bed lengths, clothing, etc. This shows that the carriers of genes for tallness have more reproductive success.

    It has been scientifically proven, via DNA testing, that one out of every 100 humans born has a random mutation of a gene in the DNA sequence. This is not in response to any stressor, but just random errors in DNA transcription during gamete production or embryo development. If the same error rate is true in bacteria, then every few minutes we have potential candidates for antibiotic resistance. This would be no cause for alarm—if we weren’t constantly producing new antibiotics and using them in animal feed!


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