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ScienceDaily: “Slowing Evolution to Stop Drug Resistance” Pathogenic resistance to antibiotics is a textbook example of “direct evidence for evolution”—literally. What does recent work on the topic suggest?
You’ll have to excuse us if you’ve heard this before. For years, evolutionists have pointed to antibiotic resistance as proof of evolution in action. The argument often amounts to this (in simplified form): the fact that certain organisms grow resistant to certain antibiotics is evidence for the evolutionary idea that all animals must have descended from a single ancestor. Collapsing the argument does make it seem a bit silly, but that’s our point.
Natural selection, mutations, and even DNA swapping all contribute to the survival of microbes and also allow them to adapt to our best antibiotics.
We certainly don’t want to belittle the very real threat of dangerous organisms becoming immune to the best drugs we now have (though the vast majority of microbes are actually important to life). But we cringe when media reports continue to dredge up the word evolution for something that is certainly not that. Add this to the personified nature of a supposedly non-intelligent process (e.g., evolution creates, progresses, etc.), and you have a news story.
In this case, Jonas Warringer and other researchers at the Department of Cell and Molecular Biology at the University of Gothenburg hope to find ways to slow the progress of drug resistance in fungi. Fungal cells are particularly problematic because they
are similar to human cells, which means that it is difficult to develop effective drugs that can destroy them without also damaging human cells, i.e. without causing side effects.
To combat the growing resistance, the team takes baker’s yeast and exposes it to a number of drugs to see how the fungus develops resistance. By knocking out one of the 6,000 genes that the yeast has, they are also able to study the impact that each gene has on the organism becoming immune. Over time, they hope to develop drugs that can inhibit fungal resistance.
This, however, is not how the researchers or the news story framed the study. For them, it’s all about using the word evolution as many times as possible to buttress their point (12 times to be exact—not including the title):
“Evolution progresses more slowly in some strains when a specific component is destroyed. These strains are like gold dust to us, because they tell us that these particular components are critical to the speed of evolution,” says Jonas Warringer.
But, as always, this depends on what is meant by evolution. Obviously, the fungi change over time to adapt to environmental stimuli (i.e., the drugs). Some strains don’t survive; some strains do and reproduce. Knocking out genes inhibits the ability of the yeast to adapt as quickly or at all. What this study cannot produce is evidence that the yeast will ever be anything but yeast—and that’s the real core of Darwin’s postulate.
Natural selection, mutations, and even DNA swapping all contribute to the survival of microbes and also allow them, in our fallen world, to adapt to our best antibiotics. As this study shows, we may be able to slow down how fast that happens. But it’s important to remember that all of those observable processes are not evolution in the molecules-to-man sense. Rather, they show us how amazingly designed microbes are.
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