Evolution Impossible (9 page)

In cancer research, malignancies are characterized by mutations, and in cancer cells the mutation rate is much greater than in normal cells. In fact, most organisms have genes whose role is to preserve the genetic information against mutations and repair damaged DNA so that mutations are minimized. Where DNA repair genes are down regulated by some factor, the risk of cancer and other diseases is increased.
²⁷

So what we actually observe in organisms are mechanisms to minimize mutations. These are mechanisms that minimize diversity outside of that which has been already coded for in the DNA. When mutations do occur, they often lead to disease or death of the organism. So where Darwin assumed that mutations would be nature’s way to maximize diversity for survival, which would in turn constitute the platform for evolution, we observe that, in fact, the very opposite is true. And as Spetner points out, “On theoretical grounds random mutations cannot form the basis of evolution.”
²⁸

Another aspect to consider in regard to mutations is the “bottleneck effect.” In relatively small populations, for example, 100 or so individuals, mutations accumulate as a result of in-breeding and form a bottleneck of damaged DNA that eventually leads to the extinction of the population. A new, fitter species does not evolve; instead the population dies out unless fresh genetic information is introduced via breeding with another population of the same species to release the bottleneck. Reducing the accumulation of mutations is thus a key factor in saving endangered species from extinction.
²⁹

The statistical improbability of evolution becomes more obvious when we consider the enormous amount of detailed genetic information encoded in the unique DNA of each species that is foundational to the millions of different types of plants and animals inhabiting the earth.

An Australian government-commissioned report published in 2009 noted that there were 1,899,567 different species reported in the published scientific literature.
³⁰

This list included the following:

5,487 different species of mammals

9,990 different species of birds

8,734 different species of reptiles

6,515 different species of amphibians

31,153 different species of fish

47,000 different species of crustacean (that is, crabs, lobsters, etc.)

100,000 or thereabouts of different species of insects

102,248 different species of arachnida (that is, spiders, scorpions, ticks, and mites, etc.)

85,000 or thereabouts of different species of mollusca (that is, snails, shellfish, squid, and octopus, etc.)

310,129 or thereabouts of different species of plants including 12,272 algae species

98,998 different species of fungi

7,643 different species of bacteria

Additionally, there are 1,086,670 other known types of organisms.

This breathtaking diversity of life comes about as a result of each organism containing quite different genetic information. According to the theory of evolution, all this new information to produce all the different types of eyes, arms, legs, and wings, the different types of feathers and skin, the different types of leaves and flowers, the different types of reproductive systems has to arise by chance. And this information is so complex that it is taking teams of scientists years to try to figure out how it works — which genes do what and so on. In fact, the diversity of the genetic information is such that the genomes (DNA) of two different strains of a singular species of
E. coli
bacteria were found to be different by 72,304 pairs of information encoding nucleotide bases.
³¹
If there is this much difference between two strains of the same species of bacteria that are single-celled organisms containing a lesser amount of genetic information than other higher organisms, it is almost impossible for the human mind to comprehend the magnitude of the different genetic information on this planet at this time.

It has been estimated, based on the diversity of species in the fossil record, that somewhere between 98 and 99 percent of all the species that have ever existed are now extinct.
³²
In other words, the genes that have made up the unique and different DNA of 100 to 200 million different species of life have somehow been created in the past. According to the proponents of evolution, most of these life forms have evolved over the past 600 million years.
³³
That means that new species would have evolved on average every three to five years. Given the millions of species that now exist in the world, the potential to observe new genetic information being created over the past 50 years of scientific observation should be quite high. But not a single example of some new intermediate arm or leg system or some intermediate new superior eye, or some new intermediate “anything” with totally new genetic information evolving, has been reported in the literature.

While about 18,000 new species are being described in the scientific literature each year, they are fully formed, already-existing species that are being discovered — mainly in remote wild regions of our planet.
³⁴
They are not evidence of new genetic information evolving. On the other hand, scientists are observing the continuous loss of genetic information as more and more species become extinct.

The eminent biologist E.O. Wilson has estimated that the earth is currently losing about 0.25 percent of its remaining species each year.
³⁵

This extinction trend, as well as data being collected by the International Union for the Conservation of Nature and Natural Resources (IUCN),
³⁶
together with the evidence of mass extinctions in the past recorded in the fossil species of the world,
point to the continuous loss of genetic information over time. This loss of genetic diversity has been highlighted recently by Professor Alan Cooper, director of the Australian Centre for Ancient DNA (ACAD), who has stated: “In contrast [to the proposal that the loss of genetic diversity at the end of the last Ice Age may not have been as extensive as previously thought], ancient DNA studies have revealed that the loss of genetic diversity in many surviving species appears to have been extremely severe.”
³⁷
In other words, what we see in the real world is the massive loss of preexisting genetic information.

In this chapter I have attempted to give an overview of the evidence that is currently available to us in regard to evolution. It is evidence we can check here and now. The following has been shown from this study:

• No confirmed examples of type 3 evolution have been observed and reported in the scientific literature.
  
• Biologists are still trying to figure out a mechanism that could explain type 3 evolution. There is currently no known and proven mechanism. In other words, scientists still have no explanation for how the massive amount of genetic information that we observe around us came into existence.
  
• On the basis of mathematical calculations, mutations cannot produce the new genetic information for type 3 evolution to occur.
  
• Organisms have mechanisms in place to reduce mutation rates by repairing DNA; also, there are mechanisms in place to prevent mutations that would result from interspecies breeding. In other words, organisms have mechanisms that serve to minimize evolutionary changes.
  
• Even simple single-celled organisms have extremely complex genetic information.
  
• A huge amount of different genetic information has existed in the past, and most of it has been permanently lost.
  
• Scientists continue to observe the permanent loss of existing genetic information.
  

The theory of evolution proposes that in the past there were populations of simple single-celled organisms that evolved into more complex organisms as a result of acquiring complex genetic information from random mutations. This process has never been observed, and on the basis of our current knowledge of biochemistry and probability it is absolutely impossible. That is, new types of organisms cannot evolve by random mutations. Moreover, more organisms have existed in the past than the present, so what we actually observe in the fossil record are extinctions, not evolution. The evidence for this is explored in more detail in the next chapter.

1
Richard Dawkins,
The Greatest Show on Earth: The Evidence for Evolution
(London: Bantam Press, 2009), p. 18.

2
. See, for example, numerous articles on the following websites:
http://www.discovery.org/csc/
;
http://www.icr.org/
;
http://creation.com/
;
http://www.creationresearch.org/
.

3
. Dawkins,
The Greatest Show on Earth,
p. 405.

4
. Ibid., p. 133–139. See also E.P. Solomon, L.R. Berg, and D.W. Martin,
Biology,
7th edition (Belmont, CA: Thomson Brooks/Cole, 2005), p. 349–350.

5
. Solomon, Berg, and Martin,
Biology
, chapters 17–19.

6
. C.J. Dorman, “DNA Topology and the Global Control of Bacterial Gene Expression: Implications for the Regulation of Virulence Gene Expression,”
Microbiology,
vol. 141 (1995): p. 1271–1280. See also G.W. Hatfield and C.J. Benham, “DNA Topology-mediated Control of Global Gene Expression in Escherichia coli,”
Annual Review of Genetics,
vol. 36 (2002): p. 175–203.

7
. Richard Dawkins,
The Genius of Charles Darwin,
part 1, TV documentary shown August 4, 2008, Channel 4, UK.

8
. S. Venkatesan, A. Petrovic, D.L. Van Ryk, et al., “Reduced Cell Surface Expression of CCR5 in CCR5Delta 32 Heterozygotes Is Mediated by Gene Dosage, Rather Than by Receptor Sequestration,”
Journal of Biological Chemistry,
vol. 277, no. 3 (2002): p. 2287–2301.

9
. A. Orr, “Testing Natural Selection,”
Scientific American
(January 2009): p. 30–36.

10
. S.E. Antonarakis, M. Krawezak, and D.N. Cooper, “Disease Causing Mutations in the Human Genome,”
European Journal of Pediatrics,
vol. 159, supplement 3 (2000): p. S173–S178.

11
. L.A. Loeb, J.H. Bielas, and R.A. Beckman, “Cancers Exhibit a Mutator Phenotype: Clinical Implications,”
Cancer Research,
vol. 68, no. 10 (2008): p. 3551–3557.

12
. R. Eri, J.R. Jonsson, D.M. Pandeya, et al., “CCR5-Δ32 Mutation Is Strongly Associated with Primary Sclerosing Cholangitis,”
Genes and Immunity,
vol. 5 (2004): p. 444–450.

13
. Orr, “Testing Natural Selection,” p. 30–36.

14
. K.A. Bettelheim, “Enerohaemorrhagic
Escherichia coli
: A New Problem, an Old Group of Organisms,”
Australian Veterinary Journal
, vol. 73, no. 1 (1996): p. 20–26.

15
. Solomon, Berg, and Martin,
Biology,
p. 130.

16
. Lee M. Spetner,
Not by Chance! Shattering the Modern Theory of Evolution
(New York: Judaica Press, Inc., 1997), p. 107. See also A. McIntosh, “Just Add Energy,” 2007,
http://www.apologetics.org/JUSTADDENERGY/tabid/82/Default.aspx
.

17
. Solomon, Berg, and Martin,
Biology,
p. 377.

18
. Evolution 101, 2009, “The Big Issues,”
http://evolution.berkeley.edu/evosite/evo101/VIIBigissues.shtml
.

19
. Dawkins,
The Greatest Show on Earth,
p. 131.

20
. Z.D. Blount, C.Z. Borland, and R.E. Lenski, “Historical Contingency and the Evolution of a Key Innovation in an Experimental Population of
Escherichia coli,
”
Proceedings of the National Academy of Sciences,
vol. 105, no. 23 (2008): p. 7899–7906.

21
. J. Clune, D. Misevic, C. Ofria, et al., “Natural Selection Fails to Optimise Mutation Rates for Long-Term Adaptation on Rugged Fitness Landscapes,”
PLoS Comput Biology,
vol. 4, no. 9 (2008): e1000187.

22
. Human Genome Project Information,
Functional and Comparative Genomics Fact Sheet,
last modified September 19, 2008. See
http://www.ornl.gov/sci/techresources/Human_Genome/faq/compgen.shtml
, accessed 1/13/2010.