From Soapberry Bugs to SuperBugs: Nature’s slippery slide down.

In the second video of Session 1 I documented immense confusion in attempts to try to identify a natural process which can be observed to increase the information and/or functional content in biological organisms.  And given the confident (but mistaken) claims of its detection and operation it is obvious that naturalists (in the sense of those who believe natural processes can explain life through an evolutionary process) expect it to be observable, i.e. the implicit prediction is that this process should be detected.  I surveyed the stickleback fish case study – written about in many university textbooks and popular books on evolution – and showed from what they themselves say this was simply a loss process – a slide down, not a gain up.  Then we saw that though birds can lose wings, and mutations can cause Apert’s Syndrome, these are not examples of gain-of-function processes – even though they are touted as such in the textbooks.  Natural selection, though observed, is also not a gain-of-function process.  They all decrease the information – that is – these processes of nature slide genomes downwards, not push them upwards to more functionality.

In our previous post we saw the cell function at the microscopic level, a point-of-view that convinced long-time atheist Antony Flew to change his mind for Intelligent Design.  But what rebuttals are given in university texts?  Let’s take a look at a prominent one: The Evolution of the Soapberry Bug.

The Soapberry Bug: A Case Study in Evolution

It took me some time (and a lot of reading) to arrive at this conclusion.  And if this is a new thought for you I am sure that likewise this will require more consideration.  But I am not just maliciously picking on some ‘mistaken’ examples in a sea of correct ones.  The examples I covered in the video are endemic across the literature.  But how can this be?  Analyzing another case study, taken from Evolutionary Analysis by Scott Freeman and JC Herron, can help us better understand how it occurs.

Soapberry bugs: Before & After

Soapberry bugs: Before & After the New Host Plant

In this study, soapberry bugs in Florida had traditionally fed on the Balloon vine fruit as shown in this figure taken from the text.

But in 1926 a new host plant for this bug was introduced and almost immediately biologists noticed a change in the beak length.  Our text concludes that:

the soapberry bug population evolved …the characteristics of soapberry bugs … have changed substantially (pg 41)

So again, an example of observed evolution is claimed.  A graph of beak lengths over time is presented from the text to support this conclusion.  I added the green vertical 1926 line which is the point at which beak lengths changed.  So what can we conclude?  As you can see, before 1926 soapberry beak lengths ranged from 9 to 5.5 millimeters – a 3.5 mm range.  After 1926, when this new tree was introduced the beak size range was reduced from 7.5 to 5.5 millmeters – a 2 mm range.  The title for the graph (which I circled) states this as ‘evolutionary change in soapberry bugs’.  But was anything new gained or developed?  Were even new beak lengths, not previously seen, observed?  No! Not at all!  All that happened was that after the new tree was introduced, beak sizes from 7.5 to 9 millimeters disappeared.  Information was lost!  A certain allele that produced long beaks was selected against in the new environment and was now gone.  Change –Yes!  Natural Selection – Yes!  Evolution – definitely not!  Their own data refutes it!

Evolution: Not just any Kind of Change

But how can this case study, which simply documents a loss (of longer beak lengths), be touted as an example of evolution?  It is simple.  The authors have equated ‘evolution’ with ‘change’.  But that is erroneous at best and misleading at worst.  Evolutionary naturalism as the establishment’s answer to Design is a claim to account for the origin and development of all life, and is supposed to be a process that over long time produces new information, genes and structures that were not previously there.  That is not just any kind of change, but a certain kind of change – one that increases genetic information and function.  To reason like these authors is like saying that increasing company profits is simply a change in the balance sheet, and thus if one can show any balance sheet change – such as a corporate loss  – this would demonstrate increased profits since a change has occurred in the balance sheet??!!   This is such a basic logical error – called the fallacy of equivocation – whereby the definition of a key term is subtly modified during the reasoning process (in this case ‘evolution’ is modified from ‘change with new function and information’ to ‘any change’) that I found it breathtaking to see it not just once, but again and again in so many university textbooks and books promoting naturalism and evolution.

Bacterial Resistance to Antibiotics: A Case of Evolution?

And this is also true of the cases of Superbugs, perhaps the strongest cases in the public mind of observed evolution.  We have all heard of bacteria that have become resistant to antibiotics, having thus ‘evolved’, and now threatening humans with an epidemic.  What is happening in these situations?  Are new enzymes, processes, or organelles that were not previously there being developed by these bacteria?  That is what I had originally thought.  If so that would be an example of an innovative evolutionary process.

Natural Selection on Pre-Existing Traits: Not Evolution

But if we examine the literature we find this is not the case.  Consider the following:

‘most cases’ antibiotic resistance results from selection of an existing genetic trait, especially those traits that are highly variable, such as the natural defences that all organisms possess[1]

In other words in most cases, there were bacteria prior to the introduction of the antibiotic that already had the resistance.  The other bacteria were selected away by the antibiotic and we are left with the resistant bacteria.  For example, there was a 1988 University of Alberta study of bacteria on the bodies of Arctic explorers frozen in 1845.  Investigators discovered that some of the bacterial strains were resistant to antibiotics. The study, which evaluated six strains of Clostridium on three men who had been buried in permafrost, found the bacteria were particularly resistance to clindamycin and cefoxitin, both antibiotics that were developed over a century after the men died.[2]

Conjugation: Not a Gain of New Information

Bacteria can also physically transfer DNA from one organism to another – a process called conjugation.  In 1990 “a strain that was resistant to cadmium, penicillin, kanamycin, neomycin, streptomycin, tetracycline, and trimethoprim. … could resist, to varying degrees, some thirtyone different drugs. … The most common mode of passage was conjugation: one bacterium simply stretched out its cytoplasm and passed plasmids to its partner.”[3] This is similar to how we transfer information from one computer to another by using a USB stick.  But transferring information from one organism to another (or one computer to another) is not a process that is making or developing new information.  It is simply copying existing information.

Mutation in Streptomycin: Degradation not Evolution

Certain antibiotic resistances do occur from mutation.  But again these mutations do not develop new enzymes, processes or organelles.  They in fact damage existing enzymes and degrade the function of the bacteria.

Perhaps the best known example of this is resistance to the antibiotic streptomycin.  The figure on the left shows how this works.  Mycin antibiotics attack bacteria by having the right ‘fit’ to attach to a specific receptor site on the bacteria’s ribosomes, and thereby interfering with their protein-manufacturing process.  As a result, the proteins that the bacteria produce are non-functional – and they die.  Mammalian ribosomes do not contain the specific site where myosin drugs can attach, and for this reason the drug does not interfere with their ribosomes. Therefore, mycin drugs adversely affect bacterial growth without harming the host (us).

With resistant bacteria, mutations cause the bacteria to become resistant to streptomycin if the ribosome site where the streptomycin attaches is damaged by the mutation. As a result, the streptomycin no longer can bind, and therefore does not interfere as well with the ribosome function.  This is shown in the next figure.

Streptomycin with mutant resistant bacteria

Streptomycin with mutant resistant bacteria

Streptomycin-resistant bacteria actually are weaker in the wild for several reasons. The major reason is the ribosome’s specific shape is degraded in bacteria that become resistant to streptomycin, and as a result the ribosomes’ ability to translate certain RNA transcripts into protein is less effective.  Thus the mutations that confer resistance decrease the fitness of bacteria in environments without antibiotics. As a result they do not reproduce as quickly as non-resistant bacteria.  Evidence discovered so far indicates that these mutations render bacteria less fit in the wild because the mutant strain is less able to compete with the wild type.

No Observed Gain-of-Function

The mutations causing resistance to mycin is a case similar to birds on remote islands losing wings – it may be an advantage since there are no predators on those islands – but it is not an example of gain-of-function.  In the specific antibiotic environment, having a misshapen ribosome prevents the antibiotic from readily attaching and there is thus resistance.  But the ribosome does not function as well as non-mutant ribosomes and thus these bacteria are selected out (eliminated) in the wild.

Bacteria: No Evolution Observed

French biologist Pierre Grasse remarked on the irony of using bacteria as a showcase to try to observe evolution.  He stated:

Bacteria, the study of which has formed a great part of the foundation of genetics and molecular biology, are the organisms which, because of their huge numbers, produce the most mutants . . . bacteria, despite their great production of intra-specific varieties, exhibit a great fidelity to their species. The bacillus Echerichia coli, whose mutants have been studied very carefully, is the best example. The reader will agree that it is surprising, to say the least, to want to prove evolution and to discover its mechanisms and then to choose as a material for this study a being which practically stabilized a billion years ago.[4]

Resistance to Insecticide: No Evolution

These same processes also explain insect resistance to DDT and other insecticides.  Evolutionary biologist Francisco Ayala reports that:

Insect resistance to a pesticide was first reported in 1947 for the housefly (Musca domestica) with respect to DDT. Since then the resistance to pesticides has been reported in at least 225 species of insects and other arthropods. The genetic variants required for resistance to the most diverse kinds of pesticides were apparently present in every one of the populations exposed to these man-made compounds.[5]

Fruit Fly Mutations: No Observed Evolution

The fruit fly is another small insect from which investigators have tried to ‘observe’ evolution. Rifkin writes about this

The fruit fly has long been the favorite object of mutation experiments because of its fast gestation period (twelve days). X-rays have been used to increase the mutation rate in the fruit fly 15,000 percent. All in all, scientists have been able to “catalyze the fruit fly evolutionary process such that what has been seen to occur in Drosophila (fruit fly) is the equivalent of many millions of years of normal mutations and evolution.” Even with this tremendous speed-up of mutations, scientists have never been able to come up with anything other than another fruit fly.[6]

The ability to observe this alleged process has eluded scientists since Darwin so eloquently argued for it.  However, instead of coming clean about this, textbooks and news articles confuse us in a slippery way by equivocating evolution with ‘change’.  And this is always presented as a scientific (ie observed) answer to Design.  But Soapberry bugs to SuperBugs simply attest, along with all other observed changes, that Nature is simply on a slide downwards.  To-date there is no observed alternative to Design.

[1] Palumbi, S.R., Evolution—humans as the world’s greatest evolutionary force, Science 293:1786–1790, 2001; p. 1787

[2] McGuire, R., Eerie: human arctic fossils yield resistant bacteria, Medical Tribune, 29 December, 1988, pp. 1, 23

[3] Garrett, L., The Coming Plague: Newly Emerging Diseases in a World Out of Balance, Farrar, Straus, and Giroux, New York, 1994. P 413

[4] Pierre P. Grasse, Evolution of Living Organisms. New York, Academic Press, 1977 p.87

[5] Francisco Ayala. “The Mechanisms of Evolution” Scientific American  Vol 239 September 1978.  p 63

[6] Jeremy Rifkin,  Algeny 1983  p.1983

5 thoughts on “From Soapberry Bugs to SuperBugs: Nature’s slippery slide down.

  1. I will concede, though, that you may have a case with your “accumulation of deleterious mutations” argument. I don’t have an (or “know the,” as a stalwart evolutionist should say) answer to that yet. It may be that mutations are not as commonly deleterious as has previously been thought, but rather are more usually neutral.

  2. I’ve noticed that this “loss of information” argument seems to be a mainstay of anti-evolution, but I don’t buy it.

    What is even meant when creationists say, “information”? Do you mean genetic material? Do you mean genetic variation? Both of these have been observed to increase (search Lenski, 1991, Long-term experimental evolution in Escherichia coli. I. Adaptation and divergence during 2,000 generations and Alves, 2001, Evolution in action through hybridisation and polyploidy in an Iberian freshwater fish: a genetic review).

    Vagueness aside, if the decrease in soapberry bug beak length is a “loss of information,” then an increase in soapberry bug beak length should be a “gain of information.” And since soapberry bug beak length does increase when the only available food is the balloon vine, now you have an example of “gain of information” according to your own definition of “information.”

    Also, you say that the claim, that the results of those experiments are examples of evolution, commits the fallacy of equivocation. That can only be true if we define evolution the way you do, namely as “change with new function and information.” Again, the vagueness of your usage of “information” interferes with our ability to communicate, but even besides that, what if I said that evolution IS just “change”? Then it’s you committing the logical fallacy, though this time it’s the straw man. My point is, we disagree on the very definition of the term “evolution,” which renders your point (that evolution is not observed here) moot.

    • Thanks for your comments Justin. You mention Lenski. I had been planning on putting up a post on Lenski sometime in the future so I will not address him specifically just now. But your comments on information do warrant some discussion. ‘Information’ is not an Intelligent Design or Creation concept. It is a reality (and concept) that everyone accepts. For example, in the 2nd video in Session 1, you will note that Richard Dawkins (certainly no ID or creationist) in the interview states: ’the great mystery of life is to explain where the complexity of life came from … another way of talking about complexity is to say information. Information is a kind of measure of complexity … and they [animals] look like they are beautifully designed machines…’ To take another evolution textbook which I did not quote in either my post or in the videos of Session 1 talks about information in the following way:

      ‘Almost all organisms use DNA to encode their genetic information, which is transcribed into RNA and then translated by a single universal genetic code into protein sequence.’ (Evolution. 2007 by Nicholas H Barton et. al p.66)

      If you read the Wikipedia article on ‘information’ you will come across the following

      “Information is any type of pattern that influences the formation or transformation of other patterns. In this sense, there is no need for a conscious mind to perceive, much less appreciate, the pattern. Consider, for example, DNA. The sequence of nucleotides is a pattern that influences the formation and development of an organism without any need for a conscious mind.”

      For further information on ‘information’ (no pun intended) I recommend ‘In the Beginning was Information’ by Dr. Werner Gitt (Director of the German Institute of Physics and Technology).

      But let’s work with these concepts as presented (patterns in the DNA which represent protein sequences) and apply them to the Soapberry bug situation. It is not that the reduction in length per se of the beak is a loss of information. It is the reduction in range of sizes. Some allele (let’s call it ‘A’) was the DNA ‘pattern’ that gave rise to long beaks. Another allele (let’s call it ‘a’) gave rise to short beaks. In the pre-1926 population, since there were both long and short beaks present there were more patterns in existence (both ‘A’ and ‘a’) in the genome. So the set of patterns – the information – was {A,a}. After 1926 ‘A’ was removed (lost) so the genome is now left with only ‘a’ – leading to short beaks. In other words we start with a set of patterns {A,a} and end up with a smaller set of {a}. We end up with less ‘patterns’ than we started with.
      Now evolution is supposed to be a process that over time makes more patterns in the DNA. This has to be the case since over time new functions, systems and processes have emerged (ex. sight, flight, fur, feathers, hearts and lungs were not there in the beginning but – supposedly – arose over time through a certain process.) In other words, when you say you ‘believe in evolution’ you are talking about a story of how long long ago (3.5 billion years) the first life arose. This life had no eyesight, flight etc. But over a long time, through this process the life form changed so that it eventually gained these new functional properties. And these functional properties are stored as information in the DNA. Thus the set of patterns in the DNA would be increasing. What I was saying is with the Soapberry bug is that this observed process of going from a set of DNA patterns of {A,a} to {a} cannot be this gain. The set of patterns is shrinking not growing. They are not observing the process that they think they are by citing this case. They get away with it by equivocating what they are talking about.

      • Them soapberry bug researchers never claimed to see a growth in the set of patterns, only a shift in the distribution. It is also highly unlikely that the set of patterns shrank, which, if that were your hypothesis, would predict the population’s inability to recover longer beaks again (which is not observed, as beak lengths can indeed lengthen).

        It’s important to remember that very few traits are determined by simple Mendelian genetics — for example, height in humans (and probably beak length in soapberry bugs) is influenced by a huge number of genes, each of which contributes a little to the overall phenotype. These are called quantitative traits, and the phenomenon of multiple influences is called polygenism. In other words, it is doubtful that the soapberry bug population’s allele set went from [A,a] to [a]. I see no loss of information. But no, I wouldn’t say there was a gain of information either.

        • Justin, I think we are converging :) I totally accept (and believe) what you say that there is usually more than a one-to-one correspondence between genes and physical traits. I used a set of one Gene {A,a} to keep the concept simple. But having more genes in the set affecting beak lengths (say {A,a,B,b} -> {A,a,B}) does not change the principle that the set of genes is decreasing. And as you say therefore, the Soapberry Bug case is not an example of gain of information.

          I also accept (and believe) that probably this loss was temporary in that there were Soapberry bug populations in (for example) neighbouring Alabama that retained the full set of alleles (whether {A,a} or {A,a,B,b}) so that from the species-wide point-of-view there was no permanent loss. If the environment goes back to the original host plant then the allele(s) that were lost in Florida could then migrate back in. So the net result is simply shifting frequencies in alleles – a back and forth so to speak. But there are instances where if from the overall species point-of-view alleles are lost, then the species loses the ability to adjust and respond to environmental changes. Cheetahs are an example of this. They have few alleles and thus cannot adjust much and they are a threatened species (from what I have read) for this reason.

          But my overall point, with the qualifications you mention, still stands – is that this example only demonstrates a loss (albeit temporary) and therefore cannot be one demonstrating a gain. Now I am not trying to prove by this one example that therefore all observed processes go ‘down’ and that therefore evolution is falsified. I am merely walking us through an example used by a reputable source (university text teaching evolution) to analyze the logic used. And the logic is wrong. That does not necessarily mean the whole theory is wrong for sure. But once I can understand and breakdown the logic here and I then go looking for a proper example elsewhere I am struck by how again and again the same kind of wrong reasoning shows itself. It happens with antibiotic resistance. Last year I was talking to a PhD in biology who insisted that this was an example of gain-of-function – that bacteria were in fact developing novel enzymes, organelles and systems to defeat the antibiotic. But he is flatly wrong. It was because he had never trained his thinking to analyze the logic that he was wrong in his understanding. In the Session 1 videos I also covered the stickleback fish, loss of wings in birds, Aperts Syndrome – these are also wrong examples. Now, this does not prove that all processes universally go down. It just shows that there is lots of misunderstanding out there, and that there could (possibly) still be that missed process that produces new functions (genes, proteins, organs and systems). But it makes this question (which one would think could be easily resolved if evolution was indeed such a universal and observable process) of whether such a process has indeed been observed a real live question. But more of that in a later post.

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