Table of Contents

Refuting Evolution 2, revised and expanded edition, 2011



Unit 1

Chapter 1

Argument: Creationism is religion, not science

Chapter 2

Argument: Evolution is compatible with Christian religion

Chapter 3

Argument: Evolution is true science, not ‘just a theory’

Unit 2

Chapter 4

Argument: Natural selection leads to speciation

Chapter 5

Argument: Some mutations are beneficial

Chapter 6

Argument: Common design points to common ancestry

Chapter 7

Argument: ‘Bad design’ is evidence of leftovers from evolution

Chapter 8

Argument: The fossil record supports evolution

Unit 3

Chapter 9

Argument: Probability of evolution

Chapter 10

Argument: ‘Irreducible complexity’

Chapter 11

Argument: Evolution of sex

Chapter 12

Argument: Evolution of mankind

Appendix 1

Common arguments for evolution that have been rejected

Appendix 2

Common arguments for creation that should not be used

Refuting Evolution 2—Chapter 5

A sequel to Refuting Evolution that refutes the latest arguments to support evolution (as presented by PBS and Scientific American).

by with Michael Matthews

Argument: Some mutations are beneficial

Evolutionists say, ‘Mutations and other biological mechanisms have been observed to produce new features in organisms.’

First published in Refuting Evolution 2, Chapter 5

When they begin to talk about mutations, evolutionists tacitly acknowledge that natural selection, by itself, cannot explain the rise of new genetic information. Somehow they have to explain the introduction of completely new genetic instructions for feathers and other wonders that never existed in ‘simpler’ life forms. So they place their faith in mutations.

In the process of defending mutations as a mechanism for creating new genetic code, they attack a straw-man version of the creationist model, and they have no answer for the creationists’ real scientific objections. Scientific American states this common straw-man position and their answer to it.

10. Mutations are essential to evolution theory, but mutations can only eliminate traits. They cannot produce new features.

On the contrary, biology has catalogued many traits produced by point mutations (changes at precise positions in an organism’s DNA)—bacterial resistance to antibiotics, for example. [SA 82]

This is a serious misstatement of the creationist argument. The issue is not new traits, but new genetic information. In no known case is antibiotic resistance the result of new information. There are several ways that an information loss can confer resistance, as already discussed. We have also pointed out in various ways how new traits, even helpful, adaptive traits, can arise through loss of genetic information (which is to be expected from mutations).

Mutations that arise in the homeobox (Hox) family of development-regulating genes in animals can also have complex effects. Hox genes direct where legs, wings, antennae, and body segments should grow. In fruit flies, for instance, the mutation called Antennapedia causes legs to sprout where antennae should grow. [SA 82]

Once again, there is no new information! Rather, a mutation in the hox gene (see next section) results in already-existing information being switched on in the wrong place.1 The hox gene merely moved legs to the wrong place; it did not produce any of the information that actually constructs the legs, which in ants and bees include a wondrously complex mechanical and hydraulic mechanism that enables these insects to stick to surfaces.2

These abnormal limbs are not functional, but their existence demonstrates that genetic mistakes can produce complex structures, which natural selection can then test for possible uses. [SA 82]

Amazing—natural selection can ‘test for possible uses’ of ‘non-functional’ (i.e., useless!) limbs in the wrong place. Such deformities would be active hindrances to survival.

Gene switches: means of evolution?

William Bateson (1861–1926), who added the word ‘genetics’ to our vocabulary in 1909, found that embryos sometimes grew body parts in the wrong place. From this he theorized that there are underlying controls of certain body parts, and other controls governing where they go.

Ed Lewis investigated and won a Nobel Prize in 1995 for discovering a small set of genes that affect different body parts (Hox or Homeobox). They act like ‘architects of the body.’ Mutations in these can cause ‘dramatic’ changes. Many experiments have been performed on fruit flies (Drosophila), where poisons and radiation induced mutations.

The problem is that they are always harmful. PBS 2 showed an extra pair of wings on a fly, but failed to mention that they were a hindrance to flying because there are no accompanying muscles. Both these flies would be eliminated by natural selection.

Walter Gehring of the University of Basel (Switzerland) replaced a gene needed for eye development in a fruit fly with the corresponding gene from a mouse. The fly still developed normal fly eyes, i.e., compound eyes rather than lens/camera. This gene in both insects and mammals is called eyeless because absence of this gene means no eyes will form.

However, there is obviously more to the differences between different animals. Eyeless is a switch—it turns on the genetic information needed for eyes. But evolution requires some way of generating the new information that’s to be switched on. The information needed to build a compound eye is vastly different from that needed to build a lens/camera type of eye. By analogy, the same switch on an electric outlet/power socket can turn on a light or a laptop, but this hardly proves that a light evolved into a laptop!

All the same, the program says that eyeless is one of a small number of common genes used in the embryonic development of many animals. The program illustrated this with diagrams. Supposedly, all evolution needed to do was reshuffle packets of information into different combinations.

But as shown, known mutations in these genes cause monstrosities, and different switches are very distinct from what is switched on or off. Also, the embryo develops into its basic body plan before these genes start switching—obviously they can’t be the cause of the plan before they are activated! But the common genes make perfect sense given the existence of a single Creator.

Increased amounts of DNA don’t mean increased function

Biologists have discovered a whole range of mechanisms that can cause radical changes in the amount of DNA possessed by an organism. Gene duplication, polyploidy, insertions, etc., do not help explain evolution, however. They represent an increase in amount of DNA, but not an increase in the amount of functional genetic information—these mechanisms create nothing new. Macroevolution needs new genes (for making feathers on reptiles, for example), yet Scientific American completely misses this simple distinction:

Moreover, molecular biology has discovered mechanisms for genetic change that go beyond point mutations, and these expand the ways in which new traits can appear. Functional modules within genes can be spliced together in novel ways. Whole genes can be accidentally duplicated in an organism’s DNA, and the duplicates are free to mutate into genes for new, complex features. [SA 82]

In plants, but not in animals (possibly with rare exceptions), the doubling of all the chromosomes may result in an individual which can no longer interbreed with the parent type—this is called polyploidy. Although this may technically be called a new species, because of the reproductive isolation, no new information has been produced, just repetitious doubling of existing information. If a malfunction in a printing press caused a book to be printed with every page doubled, it would not be more informative than the proper book. (Brave students of evolutionary professors might like to ask whether they would get extra marks for handing in two copies of the same assignment.)

Duplication of a single chromosome is normally harmful, as in Down’s syndrome. Insertions are a very efficient way of completely destroying the functionality of existing genes. Biophysicist Dr Lee Spetner in his book Not By Chance analyzes examples of mutational changes that evolutionists have claimed to have been increases in information, and shows that they are actually examples of loss of specificity, which means they involved loss of information (which is to be expected from information theory).

The evolutionist’s ‘gene duplication idea’ is that an existing gene may be doubled, and one copy does its normal work while the other copy is redundant and non-expressed. Therefore, it is free to mutate free of selection pressure (to get rid of it). However, such ‘neutral’ mutations are powerless to produce new genuine information. Dawkins and others point out that natural selection is the only possible naturalistic explanation for the immense design in nature (not a good one, as Spetner and others have shown). Dawkins and others propose that random changes produce a new function, then this redundant gene becomes expressed somehow and is fine-tuned under the natural selective process.

This ‘idea’ is just a lot of hand-waving. It relies on a chance copying event, genes somehow being switched off, randomly mutating to something approximating a new function, then being switched on again so natural selection can tune it.

Furthermore, mutations do not occur in just the duplicated gene; they occur throughout the genome. Consequently, all the deleterious mutations in the rest of the genome have to be eliminated by the death of the unfit. Selective mutations in the target duplicate gene are extremely rare—it might represent only 1 part in 30,000 of the genome of an animal. The larger the genome, the bigger the problem, because the larger the genome, the lower the mutation rate that the creature can sustain without error catastrophe; as a result, it takes even longer for any mutation to occur, let alone a desirable one, in the duplicated gene. There just has not been enough time for such a naturalistic process to account for the amount of genetic information that we see in living things.

Dawkins and others have recognized that the ‘information space’ possible within just one gene is so huge that random changes without some guiding force could never come up with a new function. There could never be enough ‘experiments’ (mutating generations of organisms) to find anything useful by such a process. Note that an average gene of 1,000 base pairs represents 41000 possibilities—that is 10602 (compare this with the number of atoms in the universe estimated at ‘only’ 1080). If every atom in the universe represented an ‘experiment’ every millisecond for the supposed 15 billion years of the universe, this could only try a maximum 10100 of the possibilities for the gene. So such a ‘neutral’ process cannot possibly find any sequence with specificity (usefulness), even allowing for the fact that more than just one sequence may be functional to some extent.

So Dawkins and company have the same problem as the advocates of neutral selection theory. Increasing knowledge of the molecular basis of biological functions has exploded the known ‘information space’ so that mutations and natural selection—with or without gene duplication, or any other known natural process—cannot account for the irreducibly complex nature of living systems.

Yet Scientific American has the impertinence to claim:

Comparisons of the DNA from a wide variety of organisms indicate that this [duplication of genes] is how the globin family of blood proteins evolved over millions of years. [SA 82]

This is about the vital red blood pigment hemoglobin that carries the oxygen. It has four polypeptide chains and iron. Evolutionists believe that this evolved from an oxygen-carrying iron-containing protein called myoglobin found in muscles, which has only one polypeptide chain. However, there is no demonstration that gene duplication plus natural selection turned the one-chained myoglobin into the four-chained hemoglobin. Nor is there any adequate explanation of how the hypothetical intermediates would have had selective advantages.

In fact, the proposed evolution of hemoglobin is far more complicated than Scientific American implies, though it requires a little advanced biology to understand. The α- and β-globin chains are encoded on genes on different chromosomes, so they are expressed independently. This expression must be controlled precisely, otherwise various types of anemia called thalassemia result. Also, there is an essential protein called AHSP (alpha hemoglobin stabilizing protein) which, as the name implies, stabilizes the α-chain, and also brings it to the β-chain. Otherwise the α-chain would precipitate and damage the red blood cells.

AHSP is one of many examples of a class of protein called chaperones which govern the folding of other proteins.3 This is yet another problem for chemical evolutionary theories—how did the first proteins fold correctly without chaperones? And since chaperones themselves are complex proteins, how did they fold?4

Identifying information-increasing mutations may be a small part of the whole evolutionary discussion, but it is a critical ‘weak link’ in the logical chain. PBS, Scientific American, and every other pro-evolution propaganda machine have failed to identify any evidence that might strengthen this straw link.

References and notes

  1. See D. Batten, Hox (homeobox) Genes—Evolution’s Saviour?
    D. DeWitt, Hox Hype—Has Macro-evolution Been Proven?.
  2. See J. Sarfati, Startling Stickiness, Creation 24(2):37 (March–May 2002).
  3. A. Kihm et al., An Abundant Erythroid Protein That Stabilizes Free-haemoglobin, Nature 417(6890):758–763 (13 June 2002); comment by L. Luzzatto and R. Notaro, Haemoglobin’s Chaperone, same issue, p. 703–705.
  4. See S.E. Aw, The Origin of Life: A Critique of Current Scientific Models (PDF), Journal of Creation 10(3):300–314, 1996.

Note about citations: Quotations from the Scientific American article by John Rennie will be labeled ‘SA’, followed by the page number. Quotations from, and other mentions of, the PBS-TV series ‘Evolution’, will be labeled ‘PBS’, followed by the episode number, e.g. ‘PBS 6’ refers to Episode 6. Return to article. 

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