WHY DO YOU BELIEVE IN EVOLUTION?

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	“In short, the notion that molecules of germ cells … are in states of perpetual change is not, in our present understanding of cell biology, tenable. This doesn’t mean that “molecular change” does not occur; only that mechanisms provoking such change in germ cells are likely instantaneous and stochastic and probably often lethal (Maresca and Schwartz 2006) – which will preclude their persistence into future generations.” —Jeffrey H. Schwartz and Bruno Maresca “Do Molecular Clocks Run at All? A Critique of Molecular Systematics” Biology Theory, 2006, Vol. 1, No. 4, Pages 357-371 http://www.mitpressjournals .org/doi/abs/10.1162/biot .2006.1.4.357

Genetic Recombination

As evolutionists slowly back away from citing mutations and natural selection as mechanisms that produce novel and more complex traits, the prominence of genetic recombination is rising. Genetic recombination is now more frequently mentioned, but its feasibility is wrought with the same utter lack of proof as with mutations and natural selection.

Genetic recombination occurs in two types of cells that make up an organism:

• Somatic cells
  http://en.wikipedia.org/wiki/Somatic_cell
  Somatic cell recombination is called mitosis http://www.cellsalive.com/mitosis.htm, which does NOT pass on genetic changes to offspring.
  (Note: The immune system’s somatic cells perform in a seemingly contrary manner, but they do not generate novel or more complex traits.)
• Germ cells
  http://en.wikipedia.org/wiki/Germline
  Germ cell genetic recombination is called meiosis http://www.cellsalive.com/meiosis.htm, which does transfer genetic change to offspring.

During meiosis, male and female chromosomes combine to create an offspring that has a ‘blend’ of the two difference sets of homologous (same DNA structure) alleles. Alleles are coding sequences found in specific locations (loci) of each chromosome and they determine the unique and specialized genotype of an organism.
http://www.genome.gov/glossary.cfm?key=allele

Genetic recombination during the stages of meiosis is a precise mechanism that has safeguards and, if the integrity of the original DNA is not retained, birth defects, disease, or programmed cell death (apoptosis) is guaranteed:

• “At the genomic level, recombination creates diversity by reshuffling genetic information between homologous chromosomes … Alterations in the normal recombination pattern are often associated with errors in chromosome segregation in humans, and these errors are a major cause of spontaneous abortions and congenital birth defects, including mental retardation.”
  (Under section, Meiotic Recombination Does Not Occur at Random Throughout the Genome)
  http://biology.plosjournals.org/perlserv/?request=get-document&doi=
  10.1371/journal.pbio.0050333
  
• “Within the last decade, aberrant meiotic recombination has been confirmed as a molecular risk factor for chromosome nondisjunction in humans. Recombination tethers homologous chromosomes, linking and guiding them through proper segregation at meiosis I. In model organisms, mutations that disturb the recombination pathway increase the frequency of chromosome malsegregation and alterations in both the amount and placement of meiotic recombination are associated with nondisjunction. This association has been established for humans as well.”
  http://content.karger.com/ProdukteDB/produkte.asp?Doi=86896
  
• “No nucleotide sequences are altered at the site of exchange; the cleavage and rejoining event occur so precisely that not a single nucleotide is lost or gained.”
  "Essential Cell Biology” textbook, Second Edition, Section 6:21, 2003 Garland Science (See PDF)
  
• “Meiotic cells possess a surveillance mechanism referred to as the ‘pachytene’ checkpoint or the meiotic recombination checkpoint that monitors these critical meiosis-specific events … In response to defects in recombination that lead to accumulation of unrepaired DSBs and/or other recombination intermediates, the pachytene checkpoint triggers meiotic cell cycle arrest or delay to prevent meiotic chromosome missegregation (Roeder and Bailis, 2000)."
  http://jcs.biologists.org/cgi/content/full/116/2/259
  
• “Apoptosis, or programmed cell death, is a normal component of the development and health of multicellular organisms. Cells die in response to a variety of stimuli and during apoptosis they do so in a controlled, regulated fashion … “
  http://www.sgul.ac.uk/depts/immunology/~dash/apoptosis/
  
• “In females of many species, over half of the germ-cell (oocyte) population dies by apoptosis before birth … Krakauer and Mira have interpreted this death of germ cells as a developmental solution to the accumulation of mutations in mitochondria, proposing that prenatal oocyte apoptosis effectively removes oocytes carrying mutant mitochondria.”
  http://www.nature.com/nature/journal/v403/n6769/full/403500a0.html

Non-homologous genetic recombination during meiosis is cited another possible mechanism to create novel or more complex traits. The premise that dissimilar alleles could successfully combine with each other without the chromosome being damaged, repaired or purged by cell death is pure fantasy, let alone having any proof behind it.

The final genetic recombination process cited by evolutionists to create novel or more complex traits is called ‘site-specific’ recombination. This occurs when intermittent short sequences of mobile genetic elements insert themselves in specific locations (loci) within chromosomes. Evolutionists claim that these mobile genetic elements rearrange sequences enough to cause novel and more complex traits to appear. But, since evolutionists don’t know what the mobile elements really are, how they originated, nor how they supposed get randomly inserted in a seemingly precise manner, site-specific recombination is better thought of as a divine interaction, not one of chance.

	"Other sources of variation, such as sexual reproduction, genetic crossing over, and transposition, primarily produce only rearrangements of existing information and do not create new genetic information. These other mechanisms of change yield phenotypic variations that will produce, at best, only a limited amount of microevolution." —Jerry Bergman, Ph.D. Human Biology, M.S. Biomedical Science, Ph.D. Measurement and Evaluation, Fellow of the American Scientific Association, member of The National Association for the Advancement of Science, in ‘Darwinism and the Deterioration of the Genome,’ Vol. 42, No. 2 of the Creation Research Society Quarterly. http://www.trueorigin.org/mutations01.asp