Evolutionists frequently point to the development of antibiotic resistance by bacteria as a demonstration of evolutionary change. However, molecular analysis of the genetic events that lead to antibiotic resistance do not support this common assumption. Many bacteria become resistant by acquiring genes from plasmids or transposons via horizontal gene transfer. Horizontal transfer, though, does not account for the origin of resistance genes, only their spread among bacteria.
Mutations, on the other hand, can potentially account for the origin of antibiotic resistance within the bacterial world, but involve mutational processes that are contrary to the predictions of evolution. Instead, such mutations consistently reduce or eliminate the function of transport proteins or porins, protein binding afﬁnities, enzyme activities, the proton motive force, or regulatory control systems. While such mutations can be regarded as “beneﬁcial,” in that they increase the survival rate of bacteria in the presence of the antibiotic, they involve mutational processes that do not provide a genetic mechanism for common “descent with modification.” Also, some “relative ﬁtness” cost is often associated with such mutations, although reversion mutations may eventually recover most, if not all, of this cost for some bacteria. A true biological cost does occur, however, in the loss of pre-existing cellular systems or functions. Such loss of cellular activity cannot legitimately be offered as a genetic means of demonstrating evolution.
Because of their rapid rate of replication, ease of laboratory analysis, and the wide diversity of laboratory-generated mutants that can be obtained, bacteria have been described as an excellent model for studying the processes of evolution (Mortlock, 1984). Acquiring resistance to a specific antibiotic provides a clear benefit to the bacterium when exposed to that antibiotic. Thus, the acquisition of antibiotic resistance is commonly cited as an example of “evolutionary change,” and has become a popular example of so-called “evolution in a Petri dish.” Miller (1999) refers to the development of antibiotic resistance as an example of evolution’s “creative force.” Barlow and Hall (2002) refer to it as “the unique opportunity to observe evolutionary processes over the course of a few decades instead of the several millennia that are generally required for these processes to occur.” (p. 314)
Evolution is often described simply as ‘change’ or ‘change in gene frequency over time’ (Dillon, 1978; John-son, 2000; Patterson, 1978), and evolutionists have almost universally maintained that any change in genotype (or even phenotype) is an “evolutionary change.” As such, any biological change of an organism, including antibiotic resistance, would fit within this definition. However, mere biological change also fits within a creation model, and thus this “vanilla” definition does not readily distinguish itself from creation. This definition also does not specify the type of change (such as deleterious versus beneficial), thus it fails to offer any predictive value to the theory.
What is more, any change that appears to provide a so-called “beneficial” adaptation is commonly seen as a driving force of evolution. Indeed, some mutations, such as antibiotic resistance, can be beneficial since they may provide the organism an increased ability to survive under very specific environmental conditions. Thus, evolutionists typically conclude that genetic examples of “evolutionary change” are abundant and that creationists are forced to deny this readily observed evidence….
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