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(Part two of a two part series continued from previous issue.)
    Other experiments with bacteria where beneficial mutations are claimed also involve a loss of specificity.  In a 2006 experiment by Lucinda Notley-McRobba and Thomas Ferenci at the University of Sydney in New South Wales on “Experimental Analysis of Molecular Events During Mutational Periodic Selections in Bacterial Evolution,” Escherichia coli continuous cultures were “analyzed for changes at two loci where mutations provide strong transport advantages to fitness under steady-state glucose limitation,” in order “to understand the processes involved in mutational successions.”1  They reported that "The...mutations of advantage in glucose-limited populations were both loss-of-function changes."2  Loss of functions may be temporarily advantageous, as in the loss of wings on a windy island, but in natural conditions the change is ultimately deleterious.  Furthermore, it has been observed that as mutations accumulate over time, the fitness of the bacteria tends to decline.3
In-Depth Mutation and Evolution Part Two

increment of change has to be great enough to confer some advantage and it has to be in enough of the population to survive, otherwise the mutation is generally removed from the population over time.  While Dawkins insists that a change could be as small as you like (meaning that it could be changed from its predecessor in a very small way), he is wrong here.  There is a minimum size of mutation.  The minimum sized mutation is a point mutation.  But even these small mutations can have profound effects on an organism.  Furthermore, Dawkins considers only the subject of vision.  But a biologically complex organ like the eye also has to have support systems.  There must be light sensitive nerve endings, complex “software” that has the ability to translate what is seen into mental data, muscles to move the eye, etc.  What is meant by a 5% eye is not a fully formed eye that only has 5% vision, but a partially developed structure that has only a few, indefinitely formed elements present in our eyes.  The question takes on new meaning when we consider that “each of the anatomical steps and structures that Darwin thought were so simple actually involves staggeringly complicated biochemical processes that cannot be papered over with rhetoric.”11

     The bio-chemical processes involved in sight are very complicated.  The following summary is based on a description given by Michael Behe in Darwin’s Black Box.  When a photon of light strikes the retina, it transforms the 11-cis retinal molecule into the trans-retinal molecule.  This forces the protein rhodopsin to physically change it’s shape, which changes the way it behaves.  It now clings to another protein called transducin, which attracts a molecule called GTP and this all binds to a protein called phosphodiesterase which all makes a molecule called cGMP.  An ion channel regulates the number of sodium ions in the cell, and a separate protein pumps them out again.  When the phosphodiesterase cuts the cGMP molecule, the ion channel closes and reduces the concentration of positive sodium ions.  An imbalance of charge results sending a current down the optic nerve which is then translated by the brain.  A similarly complex process brings the cells of the eye back to 11-cis-retinal.

     Darwin did not know all of the biochemical functions necessary to make the eye work but with what little he did know he confessed that “to suppose that the eye...could have been formed by natural selection, seems, I freely confess, absurd in the highest possible degree.”12  Yet he nevertheless insisted that the “perfect and complex eye” could be formed through “numerous gradations.”  Steven J. Gould “avoided” what he termed the “excellent question” of what good is a five percent eye by arguing that it was used for something other than vision.13  But Dawkins insists that it must have been used at least in part for vision.  Dawkins further laments that the eye is “poorly designed” because the photo cells point away from the light.  “Intermediates could see even less well than their imperfect ancestors, and it is no consolation that they are building better eyesight for their remote descendants.”14

     Considered biochemically and morphologically, the eye is a very complex organ.  Evolutionists have suggested steps which could illustrate how the eye formed gradually over a relatively short period of time.  Some have suggested as low as 350 thousand years.  But these eye forms all exist today in various living organisms.  Even Darwin knew about these and used them as models for the stages in which he envisioned the eye to have evolved.  Some have suggested that the eye has evolved as many as forty different times.  But scientists have been experimenting on fruit flies for over a hundred years now and have relatively good knowledge of which genes control eye expression.  They can change the color of the eye.  They can remove the eye, or maybe place it in another location, make it bigger or smaller, but they have not demonstrated the steps the eye would have taken in an evolutionary progression from a light sensitive eye spot to a full fruit fly eye.

     I would argue that most mutations are by far either neutral or harmful.  The rare occasion when a mutation confers some selective advantage, it has generally been seen to be a case of a loss of information or temporary advantage.  It has never been seen to increase genetic information in a way that supports the idea we have evolved from simple, single celled organisms to the complex creatures we are today.  Furthermore, there has never been an observed, documented case where mutations have changed an organism’s essential nature.  No fruit fly has changed into something that is not a fruit fly, even after over one hundred years of directed experimentation in controlled laboratory conditions, where mutations have been induced over and over again.  No bacteria have changed into non-bacteria.  The fitness in the bacteria in it’s environment can be improved, often through reducing information in it’s genome, but this cannot serve as an example of the kind of change needed to support evolutionary theory.  Mutations, it would therefore seem, fail to supply the kind of change needed for macro-evolution to occur.  Therefore, mutations seem to prove harmful to the evolutionary hypothesis.


ENDNOTES


1.  Notley-McRobba, Lucinda and Thomas Ferenci, Experimental Analysis of Molecular Events During Mutational Periodic Selections in Bacterial Evolution, Genetics, Vol. 156, 1493-1501, December 2000, p. 1493.

2.   Ibid., p. 1499.

3.   Fox, Charles W., and Jason B. Wolf, editors, Evolutionary Genetics, Concepts and Case Studies, Oxford University Press, 2006, p. 41.

4.   Gartner, T. K., and E. Orias, Effects of Mutations to Streptomycin Resistance on the Rate of Translation of Mutant Genetic Information, Journal of Bacteriology, Mar., 1966, Vol. 91, No. 3, p. 1026.

5.   Boni, Maciej F., and Marcus W. Feldman,  Evolution of Antibiotic Resistance by Human and Bacterial Niche Construction, International Journal of Organic Evolution, Volume 59, Issue 3 (March 2005), p. 477.

6.   Spetner, Lee, Not By Chance, Shattering the Modern Theory of Evolution, The Judaica Press, 1998, p. 141.

7.   Boni, p. 477.

8.   Bourguet, Denis, Thomas Guillemaud, Christine Chevillon, Michel Raymond,  Fitness Costs of Insecticide Resistance in Natural Breeding Sites of the Mosquito Culex Pipiens, Evolution, Volume 58 Issue 1, Pages 128 - 135.

9.   Spetner, pp.  13, 132.

10. Dawkins, Richard, The Blind Watchmaker, Why The Evidence of Evolution Reveals a Universe Without Design, W.W. Norton & Company, NY: 1987, p. 77.

11. Behe, Michael J., Darwin’s Black Box, The Biochemical challenge to Evolution, The Free Press, NY: 1996, p. 22.

12. Darwin, Charles, The Origin of the Species, ed. by E. O. Wilson, in From So Simple A Beginning, W. W. Norton Co., NY: 2006, p. 569.

13. Dawkins, p. 81.

14. Dawkins, p. 94.





     Another example offered of as proof of evolution is bacteria that can mutate to become resistant to certain drugs.  We currently face a situation where we are in need of new drugs that can control harmful bacteria.  This is why the doctors urge patients to take all of their medicine until it is gone because strains of bacteria may mutate (or may have already mutated) to survive the antibiotic prescribed.  This new strain becomes stronger and more resilient, requiring even stronger antibiotics. Streptomycin, for instance, and other mycin drugs, bind to a site on the ribosome of the bacteria which keeps it from making proteins that it needs, making in its stead proteins that don’t work, and, hence, cannot grow, divide, or propagate.  Streptomycin given to a patient, then, stops the bacteria from growing.  Because the ribosomes of mammals do not have the site where the mycin drug molecules attach, they are not affected by them.  But bacteria can mutate to become resistant to streptomycin.  But how does this occur?  In this example, the mutation occurs anywhere along the ribosome where the streptomycin attaches, preventing it from stopping the bacterial ribosome from growing and propagating.  It was “the result of a decreased specific activity.”4  However, “the resistant strains are usually less fit than the antibiotic-sensitive wild-type strains in the absence of antibiotic treatment.”5 Again, in this example, the mutation causes something to cease.  Instead of saying that it has gained a resistance to streptomycin, we should say it lost its sensitivity to it.6  Furthermore, “when treatment ceases or is slowed, the population can revert back to sensitivity, though this reversion is usually slow.”7  
     One other mutation that is often offered as an example of a beneficial mutation is sickle cell disease.  Sickle cell disease “is an autosomal recessive disorder that causes anemia, joint pain, a swollen spleen, and frequent and severe infections.”  On its own it causes serious health issues.  In certain parts of Africa, however, many who have sickle cell disease are afforded an advantage of being either completely resistant to malaria or only develop very mild cases of it.  While the carriers of the sickle cell disease may not suffer from its symptoms, of their offspring 25 percent may get sickle cell disease and another 25 percent may get malaria.  This does not seem to be an advantageous mutation.  
     It is necessary to make the point again.  Creationists do not necessarily doubt that selection is a process that works in nature.  Breeders use selection all the time to breed animals and plants that bear certain traits that are desired.  Creationists certainly do not doubt that mutations occur.  We all see the result of these mutations in the diseases that afflict humanity.  Creationists do not doubt that on rare occasions mutations may be selected which may provide for a new, perhaps even beneficial, trait in a given environment.  What Creationists do say, though, is that these mutations are not the kind of thing evolution needs to go from less complexity to more complexity and often the results are deleterious in the long run.   Insects can become resistant to insecticides, but they do this by losing sensitivity to insecticide at the binding site.8  Rats may become resistant to certain poisons, but they do so by losing sensitivity to that poison when the enzyme affected by this becomes less efficient.  Some crops may, through a mutation which degrades a regulatory gene, increase their yield.  Humans occasionally suffer a mutation that removes a regulatory gene and leads to gigantism.  Those who suffer with this mutation are given the temporary advantage of being able to reach higher places where food might be found, etc., but they also suffer weakened muscles, difficulty in breathing and pumping their blood, not to mention that man-made and natural objects are often too small to be used by them efficiently.  But these are all examples of a loss of information, a loss of specificity.  The MIT graduate Lee Spetner observes:
I don’t say it’s impossible for a mutation to add a little information.  It’s just highly improbable on theoretical grounds.  But in all the reading I’ve done in the life-sciences literature, I’ve never found a mutation that added information.  The NDT (Neo-Darwinian Theory–ELP) says not only that such mutations must occur, they must also be probable enough for a long sequence of them to lead to macroevolution.9
This leads us to another question concerning mutations: Since macro-mutations are deleterious, can many very small mutations lead to the kind of information increase needed for evolution to occur?
    Other experiments with bacteria where beneficial mutations are claimed also involve a loss of specificity.  In a 2006 experiment by Lucinda Notley-McRobba and Thomas Ferenci at the University of Sydney in New South Wales on “Experimental Analysis of Molecular Events During Mutational Periodic Selections in Bacterial Evolution,” Escherichia coli continuous cultures were “analyzed for changes at two loci where mutations provide strong transport advantages to fitness under steady-state glucose limitation,” in order “to understand the processes involved in mutational successions.”1  They reported that "The...mutations of advantage in glucose-limited populations were both loss-of-function changes."2  Loss of functions may be temporarily advantageous, as in the loss of wings on a windy island, but in natural conditions the change is ultimately deleterious.  Furthermore, it has been observed that as mutations accumulate over time, the fitness of the bacteria tends to decline.3

     Consider the eye.  Neither Creationists nor evolutionists doubt that the eye is a marvelous piece of delicate machinery.  The question here is could the eye be the product of mutations?  Richard Dawkins, perhaps the leading apostle of evolution in our time, argues in his book The Blind Watchmaker, that the eye could not have come from no eye at all in “a single step.”10 This would be a “miracle” and that is not permissible in his paradigm.  However, he claims that given multiple steps of ever so small, incremental change, it is possible to get from no eye at all to a complex eye such as ours.  He believes a five percent eye is better than a four percent eye and one percent is better than blindness.  He believes that cumulative selection, working on mutations, can bring about the eye.  But the problem with this approach is at least twofold.  First, the change must provide a selective advantage.   The



Copyright Eric L. Padgett  03-30-2012
Christian Apologist