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Index to Creationist Claims,  edited by Mark Isaak,    Copyright © 2008
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Claim CB101:

Most mutations are harmful, so the overall effect of mutations is harmful.


Morris, Henry M. 1985. Scientific Creationism. Green Forest, AR: Master Books, pp. 55-57.
Watchtower Bible and Tract Society. 1985. Life--How Did It Get Here? Brooklyn, NY, pg. 100.


  1. Most mutations are neutral. Nachman and Crowell estimate around 3 deleterious mutations out of 175 per generation in humans (2000). Of those that have significant effect, most are harmful, but the fraction which are beneficial is higher than usually though. An experiment with E. coli found that about 1 in 150 newly arising mutations and 1 in 10 functional mutations are beneficial (Perfeito et al. 2007).

    The harmful mutations do not survive long, and the beneficial mutations survive much longer, so when you consider only surviving mutations, most are beneficial.

  2. Beneficial mutations are commonly observed. They are common enough to be problems in the cases of antibiotic resistance in disease-causing organisms and pesticide resistance in agricultural pests (e.g., Newcomb et al. 1997; these are not merely selection of pre-existing variation.) They can be repeatedly observed in laboratory populations (Wichman et al. 1999). Other examples include the following:
  3. Whether a mutation is beneficial or not depends on environment. A mutation that helps the organism in one circumstance could harm it in another. When the environment changes, variations that once were counteradaptive suddenly become favored. Since environments are constantly changing, variation helps populations survive, even if some of those variations do not do as well as others. When beneficial mutations occur in a changed environment, they generally sweep through the population rapidly (Elena et al. 1996).

  4. High mutation rates are advantageous in some environments. Hypermutable strains of Pseudomonas aeruginosa are found more commonly in the lungs of cystic fibrosis patients, where antibiotics and other stresses increase selection pressure and variability, than in patients without cystic fibrosis (Oliver et al. 2000).

  5. Note that the existence of any beneficial mutations is a falsification of the young-earth creationism model (Morris 1985, 13).


Williams, Robert. n.d. Examples of beneficial mutations and natural selection.
Williams, Robert. n.d. Examples of beneficial mutations in humans.


  1. Boyden, Ann M., Junhao Mao, Joseph Belsky, Lyle Mitzner, Anita Farhi, Mary A. Mitnick, Dianqing Wu, Karl Insogna, and Richard P. Lifton. 2002. High bone density due to a mutation in LDL-receptor-related protein 5. New England Journal of Medicine 346: 1513-1521, May 16, 2002.
  2. Dean, M. et al. 1996. Genetic restriction of HIV-1 infection and progression to AIDS by a deletion allele of the CKR5 structural gene. Science 273: 1856-1862.
  3. Elena, S. F., V. S. Cooper and R. E. Lenski. 1996. Punctuated evolution caused by selection of rare beneficial mutations. Science 272: 1802-1804.
  4. FAO/IAEA. 1977. Manual on Mutation Breeding, 2nd ed. Vienna: International Atomic Energy Agency.
  5. Long, Patricia. 1994. A town with a golden gene. Health 8(1) (Jan/Feb.): 60-66.
  6. Moffat, Anne S. 2000. Transposons help sculpt a dynamic genome. Science 289: 1455-1457.
  7. Morris, Henry M. 1985. Scientific Creationism. Green Forest, AR: Master Books.
  8. Nachman, M. W. and S. L. Crowell. 2000. Estimate of the mutation rate per nucleotide in humans. Genetics 156(1): 297-304.
  9. Newcomb, R. D. et al. 1997. A single amino acid substitution converts a carboxylesterase to an organophosporus hydrolase and confers insecticide resistance on a blowfly. Proceedings of the National Academy of Science USA 94: 7464-7468.
  10. Oliver, Antonio et al. 2000. High frequency of hypermutable Pseudomonas aeruginosa in cystic fibrosis lung infection. Science 288: 1251-1253. See also: Rainey, P. B. and R. Moxon, 2000. When being hyper keeps you fit. Science 288: 1186-1187. See also: LeClerc, J. E. and T. A. Cebula, 2000. Pseudomonas survival strategies in cystic fibrosis (letter), 2000. Science 289: 391-392.
  11. Perfeito, Lilia, Lisete Fernandes, Catarina Mota and Isabel Gordo. 2007. Adaptive mutations in bacteria: High rate and small effects. Science 317: 813-815.
  12. Prijambada, I. D., S. Negoro, T. Yomo and I. Urabe. 1995. Emergence of nylon oligomer degradation enzymes in Pseudomonas aeruginosa PAO through experimental evolution. Applied and Environmental Microbiology 61(5): 2020-2022.
  13. Sullivan, Amy D., Janis Wigginton and Denise Kirschner. 2001. The coreceptor mutation CCR5-delta-32 influences the dynamics of HIV epidemics and is selected for by HIV. Proceedings of the National Academy of Science USA 98: 10214-10219.
  14. Weisgraber K. H., S. C. Rall Jr., T. P. Bersot, R. W. Mahley, G. Franceschini, and C. R. Sirtori. 1983. Apolipoprotein A-I Milano. Detection of normal A-I in affected subjects and evidence for a cysteine for arginine substitution in the variant A-I. Journal of Biological Chemistry 258: 2508-2513.
  15. Wichman, H. A. et al. 1999. Different trajectories of parallel evolution during viral adaptation. Science 285: 422-424.
  16. Wright, M. C. and G. F. Joyce. 1997. Continuous in vitro evolution of catalytic function. Science 276: 614-617. See also: Ellington, A. D., M. P. Robertson and J. Bull, 1997. Ribozymes in wonderland. Science 276: 546-547.

Further Reading:

Harter, Richard. 1999. Are mutations harmful?

Peck, J. R. and A. Eyre-Walker. 1997. The muddle about mutations. Nature 387: 135-136.
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created 2001-2-17, modified 2008-6-20