Does Antibiotic Resistance Prove Evolution?
Antibiotic resistance is a real and immanent health threat for the US and around the world. The US Centers for Disease Control and Prevention estimates that at least 2 million people acquire an antibiotic-resistant bacterial infection, killing 23,000 people annually (https://www.cdc.gov/drugresistance/about.html accessed 8 October 2018). My grandmother died from such an infection several years ago, so the topic of antibiotic resistance is very practical in my life. But what do you say to evolutionists that frequently cite antibiotic resistance as proof of evolution happening? The truth is that antibiotic resistance does not support evolution for several reasons.
How do bacteria become resistant to antibiotics?
The first matter we need to address is how do antibiotics cause antibiotic resistances. It is commonly known that people are supposed to take antibiotics for a regular infection as prescribed from the doctor. When people take those antibiotics, they are supposed to take them fully, not miss a dose, and for the full duration of the prescription. The bacteria you have during that infection are constantly being bombarded with medicine that is not usually killing the bacteria (i.e., bactericidal), but preventing them from growing (i.e., bacteriostatic). So the bacteria during the infection are facing the antibiotic in a regular fashion so long as you are taking it regularly. While taking the antibiotic regularly, the bacteria are unable to grow and they are killed off by your immune system. But when you use the antibiotic intermittently, the bacteria get a chance to become resistant to the antibiotics.
Bacteria have a series of mechanisms whereby they become resistant to the very antibiotics you are using for the infection. In almost every instance, the mechanism of action for the antibiotic is often related to the mechanism of resistance. For instance, penicillin works by targeting the bacterial cell wall and the mechanism of resistance to penicillin involves incorporation of an alternate subunit to the bacterial cell wall. There is no exception to this rule for how antibiotic resistances emerge (with one exception). To understand the various mechanisms of resistance, then, one has to study the mechanism of action for the various antibiotics. The five basic mechanisms of action to antibiotics are: inhibit cell wall synthesis, inhibit protein synthesis, inhibit DNA or RNA synthesis, injury to the plasma membrane, or inhibition of metabolite synthesis (Tortora et al. 2018). Equally, the four basic mechanisms of resistance to antibiotics are: blocking entry, inactivating enzymes, altering the target molecule, or efflux of the antibiotic (Tortora et al. 2018). The mechanisms of resistance are each documented to occur via mutation in the chromosome of the bacteria.
But is it evolution?
Next, we need to address what is meant by the term evolution. Simply put, evolution means change. But when scientists use the word evolution they mean the goo-to-you version of evolution. Evolution is supposed to happen because of evidences like bacteria evolving resistance to antibiotics. However, there is a problem with the term evolution in the previous sentence that needs clarification. When most people talk about the evolution of bacteria becoming antibiotic resistant, they mean to use the word microevolution. Microevolution is the small changes that occur to living things that are observable. Bacteria becoming resistant to antibiotics are a great example of microevolution happening today. But people often cite the microevolution of bacteria to antibiotics as proof of macroevolution. Macroevolution is supposed to be the accumulation of mutations over deep time like millions of years. By definition, macroevolution is not observable because no one can do an experiment for millions of years. That being said, there is no documented proof of microevolutionary changes leading to macroevolution. The reason for this absence of proof is that accumulation of mutations is insufficient to explain how monkeys and man shared common ancestry.
How fast do bacteria become resistant?
The central question of whether antibiotic resistances prove evolution comes down to a matter of mutation rates for bacteria versus humans. Regularly in my classes, I show how easy it is to select for streptomycin-resistant E. coli. The way we do this is to grow an overnight culture of E. coli and place it onto petri dishes containing streptomycin in it. Spontaneously, there are mutations that occur during the first overnight which are selected for the following overnight by growing in the presence of the streptomycin. The rate for streptomycin resistance is 0.00004 mutations per 100,000 cells. So antibiotic resistance is something that can happen overnight and at a rate that is easy to calculate. This rate of 0.00004 is supposed to be the rapid rate that evolutionists want for evolution to be true. But the problem with this number is that it is actually low compared to the mutation rates for human disorders such as retinoblastoma (1.2-2.3), achondroplasia (4.2-14.3), or Huntington’s chorea (0.5) (Dobzhansky 1970). The mutation rates for human disorders are roughly 10,000 times faster than for antibiotic resistance of bacteria. The conclusion must be that either bacteria are microevolving too slowly or that humans are microevolving too fast. This observation of known mutation rates means that humans and bacteria must have existed for the same length of time and that we cannot have existed for too long. We cannot have existed for millions of years with this fast of a mutation rate because we would overmutate into extinction.
Conclusion
Antibiotic resistance cannot be used for proof of evolution. Antibiotic resistances are actually great proof of creation. Antibiotic resistances are actually just great examples of microevolution, which does not lead to macroevolution. Known mutation rates are too slow for bacteria to be evolving into antibiotic resistant bacteria. If we apply the same logic that bacteria are evolving fast, then humans must be evolving even faster. And if humans are evolving faster than bacteria, then humans cannot have existed for millions of years. The entire idea of using antibiotic resistance as proof of evolution is just hogwash. All the available data for antibiotic resistances demonstrate how intricately designed bacteria are to show the glory of God.
Dobzhansky, T. 1970. Genetics of the Evolutionary Process. Columbia University Press: New York, NY. p.70.
Tortora, G. J., et al. 2018. Microbiology, an Introduction. 13th ed. San Francisco, California: Pearson Co.
How do bacteria become resistant to antibiotics?
The first matter we need to address is how do antibiotics cause antibiotic resistances. It is commonly known that people are supposed to take antibiotics for a regular infection as prescribed from the doctor. When people take those antibiotics, they are supposed to take them fully, not miss a dose, and for the full duration of the prescription. The bacteria you have during that infection are constantly being bombarded with medicine that is not usually killing the bacteria (i.e., bactericidal), but preventing them from growing (i.e., bacteriostatic). So the bacteria during the infection are facing the antibiotic in a regular fashion so long as you are taking it regularly. While taking the antibiotic regularly, the bacteria are unable to grow and they are killed off by your immune system. But when you use the antibiotic intermittently, the bacteria get a chance to become resistant to the antibiotics.
Bacteria have a series of mechanisms whereby they become resistant to the very antibiotics you are using for the infection. In almost every instance, the mechanism of action for the antibiotic is often related to the mechanism of resistance. For instance, penicillin works by targeting the bacterial cell wall and the mechanism of resistance to penicillin involves incorporation of an alternate subunit to the bacterial cell wall. There is no exception to this rule for how antibiotic resistances emerge (with one exception). To understand the various mechanisms of resistance, then, one has to study the mechanism of action for the various antibiotics. The five basic mechanisms of action to antibiotics are: inhibit cell wall synthesis, inhibit protein synthesis, inhibit DNA or RNA synthesis, injury to the plasma membrane, or inhibition of metabolite synthesis (Tortora et al. 2018). Equally, the four basic mechanisms of resistance to antibiotics are: blocking entry, inactivating enzymes, altering the target molecule, or efflux of the antibiotic (Tortora et al. 2018). The mechanisms of resistance are each documented to occur via mutation in the chromosome of the bacteria.
But is it evolution?
Next, we need to address what is meant by the term evolution. Simply put, evolution means change. But when scientists use the word evolution they mean the goo-to-you version of evolution. Evolution is supposed to happen because of evidences like bacteria evolving resistance to antibiotics. However, there is a problem with the term evolution in the previous sentence that needs clarification. When most people talk about the evolution of bacteria becoming antibiotic resistant, they mean to use the word microevolution. Microevolution is the small changes that occur to living things that are observable. Bacteria becoming resistant to antibiotics are a great example of microevolution happening today. But people often cite the microevolution of bacteria to antibiotics as proof of macroevolution. Macroevolution is supposed to be the accumulation of mutations over deep time like millions of years. By definition, macroevolution is not observable because no one can do an experiment for millions of years. That being said, there is no documented proof of microevolutionary changes leading to macroevolution. The reason for this absence of proof is that accumulation of mutations is insufficient to explain how monkeys and man shared common ancestry.
How fast do bacteria become resistant?
The central question of whether antibiotic resistances prove evolution comes down to a matter of mutation rates for bacteria versus humans. Regularly in my classes, I show how easy it is to select for streptomycin-resistant E. coli. The way we do this is to grow an overnight culture of E. coli and place it onto petri dishes containing streptomycin in it. Spontaneously, there are mutations that occur during the first overnight which are selected for the following overnight by growing in the presence of the streptomycin. The rate for streptomycin resistance is 0.00004 mutations per 100,000 cells. So antibiotic resistance is something that can happen overnight and at a rate that is easy to calculate. This rate of 0.00004 is supposed to be the rapid rate that evolutionists want for evolution to be true. But the problem with this number is that it is actually low compared to the mutation rates for human disorders such as retinoblastoma (1.2-2.3), achondroplasia (4.2-14.3), or Huntington’s chorea (0.5) (Dobzhansky 1970). The mutation rates for human disorders are roughly 10,000 times faster than for antibiotic resistance of bacteria. The conclusion must be that either bacteria are microevolving too slowly or that humans are microevolving too fast. This observation of known mutation rates means that humans and bacteria must have existed for the same length of time and that we cannot have existed for too long. We cannot have existed for millions of years with this fast of a mutation rate because we would overmutate into extinction.
Conclusion
Antibiotic resistance cannot be used for proof of evolution. Antibiotic resistances are actually great proof of creation. Antibiotic resistances are actually just great examples of microevolution, which does not lead to macroevolution. Known mutation rates are too slow for bacteria to be evolving into antibiotic resistant bacteria. If we apply the same logic that bacteria are evolving fast, then humans must be evolving even faster. And if humans are evolving faster than bacteria, then humans cannot have existed for millions of years. The entire idea of using antibiotic resistance as proof of evolution is just hogwash. All the available data for antibiotic resistances demonstrate how intricately designed bacteria are to show the glory of God.
Dobzhansky, T. 1970. Genetics of the Evolutionary Process. Columbia University Press: New York, NY. p.70.
Tortora, G. J., et al. 2018. Microbiology, an Introduction. 13th ed. San Francisco, California: Pearson Co.
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