Featured In

This Issue

Many examples of mutations that produce phenotypic changes are ‘loss mutations’ in which the mutation causes the loss of a structure. Loss mutations that result in a non-functional protein or structure can be beneficial if the functional protein loss or malformation somehow benefits the organism (or, far more often, humans—as in the case of the loss of seeds in a fruit, producing a convenient seedless fruit).

One of the first and most common examples of the latter was an alleged new breed—Huxley called it a race, others labeled it a species—that resulted when Massachusetts farmer Seth Wright noticed in 1791 that he had a very short-legged sheep in his flock.1,2 The story is usually claimed that, realizing the advantages of this trait to sheepherders, Wright bred a ‘flock’ of the short-legged ‘species’ of sheep, all of whom were unable to jump over ordinary stone walls or fences.3,4

Called the Ancon or Otter ‘breed,’ it was believed to reduce the need for tall fences, as well as reducing the number of lost sheep.1 In addition, the short legs limited the sheep’s ability to run so that, as a result, they were less active, more gentle, and gained weight far more readily then other sheep breeds.5

Charles Darwin and Ancon sheep

Charles Darwin was evidently the first person to use the Ancon breed as evidence for evolution. He discussed them at least three times in his published books. In the Origin of Species, first published in 1859, Darwin speculated that some animal variations ‘have probably arisen suddenly,’ or by one step ‘in one generation.’ One example that Darwin used was ‘the turnspit dog.’ He then added that such ‘one step’ rapid evolution also is known ‘to have been the case with the Ancon sheep.’6 In another work, Darwin claimed that in a

‘… few instances new breeds have suddenly originated; thus, in 1791, a ram-lamb was born in Massachusetts, having short crooked legs and a long back, like a turnspit-dog. From this one lamb the otter or ancon semi-monstrous breed was raised; as these sheep could not leap over the fences, it was thought that they would be valuable … . The sheep are remarkable from transmitting their character so truly that Colonel Humphreys never heard of “but one questionable case” of an ancon ram and ewe not producing ancon offspring. When they are crossed with other breeds the offspring, with rare exceptions, instead of being intermediate in character, perfectly resemble either parent; even one of the twins has resembled one parent and the second the other. Lastly, “the ancons have been observed to keep together, separating themselves from the rest of the flock when put into enclosures with other sheep”.’7

Is the Ancon mutation beneficial?

Other evolutionists such as Kenneth Miller have also touted Ancon sheep as an example of evolutionary jumps. But this is deceptive because the condition actually is ‘pathological,’ known as achondroplasia (where cartilage fails to develop, from Greek a-, not; chondros, cartilage; plassein, to mould or form—a form of dwarfism) or a related pathology,8 and

‘… would bring about the extinction of these creatures in a natural environment, rather than an advance through natural selection. The suggestion, by Miller, that the four-winged fly and the Ancon sheep present evolutionary advances was simply a deceptive ploy.’9

Actually, the mutation has proved lethal in a protected environment as well. Gish concludes that Ancon sheep are deformed animals, specifically, the

‘… product of a pathological condition, called achondroplasia. In his presentation, Miller pointed out that these sheep have been bred by sheep breeders because they are short-legged and thus cannot jump fences—an advantage for those who raise sheep. What he did not say was that their condition is caused by a mutation which results in the failure of the cartilage between the joints to develop. There is thus little or no cartilage between the joints of their legs, causing them to be short. This abnormal condition would, of course, result in their rapid extinction in a natural environment and could never be considered an evolutionary advance.’9

The Ancon mutation, in harmony with our general experience with mutations, was harmful to the sheep for many reasons. Achondroplasia is a type of genetic dwarfism characterized by slow limb growth relative to the rest of the skeleton.10

Many other abnormalities aside from short legs have been discovered as a result of Ancon sheep postmortems. These included looser leg joint articulations, abnormal spines and skulls, flabby subscapular muscles, and crooked bent inward forelegs that caused the legs to appear like elbows while the sheep were walking.11,12 This prominent trait is the reason for the term Ancon (ancon is the Latin transliteration of the Greek word for elbow, αγκων). The Ancon legs resemble the clubfeet condition, and, in fact, as adults were clumsy cripples that could neither run nor jump like other sheep.13

Conclusion

A major problem for Darwinists is that the Ancon mutation (a Mendelian recessive), as is true with most other mutations, is a loss mutation. This type of mutation does not result in an information gain, as Darwinism requires, but an information loss (often of a complete structure or protein). A chief difficulty in arguing for macroevolution by mutations is the fact that most expressed mutations are either lethal or semi-lethal. Either they kill the organism outright, or they prove harmful, so that in the ordinary course of life they are eliminated. This includes both mutations in which the fertility rate is reduced as well as mutations that result in the loss of certain structures.

And as shown, even the rare ‘beneficial’ mutation, as some might consider the Ancon to be, are the result of information loss. Therefore they are going in the opposite direction from what goo-to-you evolution requires.14

Help keep these daily articles coming. Support AiG.

Footnotes

  1. Schwartz, K. and Vogel, J., Unraveling the yarn of the Ancon sheep, Bioscience 44:764–768, 1994. Back (1) Back (2)
  2. Dodge, R.A. Elements of Biology, Allyn and Bacon, Inc., Boston, 1959. Back
  3. Curtis, H. and Barnes, N.C., Biology, Fifth Edition, Worth Publishers, Inc., 1989. Back
  4. Dodge, Ref. 2, p. 598. Back
  5. Dwight, T., Travels in New England and New York, Volume III, Harvard University Press, Cambridge, pp. 89–90, 1969. Edited by Barbara Miller Solomon, with the assistance of Patricia M. King. Back
  6. Darwin, C., The Origin of Species by Means of Natural Selection or the Preservation of Favored Races in the Struggle for Life, Sixth Edition, D. Appleton, New York, p. 34, 1897. Back
  7. Darwin, C., The Variation of Animals and Plants Under Domestication, D. Appleton, New York, p. 104, 1896. Back
  8. Maroteaux, P. and Lamy, M., Achondroplasia in man and animals, Clinical Orthopaedics and Related Research 33:91–103, 1964. Back
  9. Gish, D.T., Creation Scientists Answer Their Critics, Institute for Creation Research, El Cajon, p. 93, 1993. Back (1) Back (2)
  10. Chang, T.K., Morphological study of the skeleton of Ancon sheep, Growth 13:269–297, 1949. Back
  11. Schwartz and Vogel, Ref. 1, p. 764. Back
  12. Maroteaux and Lamy, Ref. 8, p. 101. Back
  13. Dwight, Ref. 5, p. 89. Back
  14. Wieland, C., The evolution train’s a-comin’, Creation 24(2):16–19. Back