Antibiotic Resistance, Darwin’s Theory, and My Discussion with Mr. Dunford

Darwinist Mike Dunford is incensed with the manner in which I quoted him in one of my recent posts. I pointed out, using Mr. Dunford’s own words, that the assertion that an understanding of natural selection was essential to laboratory research on bacterial resistance to antibiotics was inconsistent with the Darwinist assertion that the biological evidence for natural selection disproves the theory of intelligent design. It’s a fairly obvious point, when you think about it carefully, and it was refreshing that Mr. Dunford made the point in such a clear (if inadvertent) way. The observation is worth reviewing.
First, two definitions:


Natural selection is selection in nature, presumably arising without intelligent agency. An example of natural selection would be the differential reproduction of organisms in nature, without the evident guidance of an intelligent agent.
Artificial selection is selection caused by intelligent agency. An example of artificial selection would be the intentional breeding of bacteria by a scientist in a research lab.
The distinction between natural selection and artificial selection is at least matter of definition, and perhaps there are empirical differences as well.
What is the relationship between natural selection and artificial selection? There are two possibilities:
1) Natural selection is substantially different from artificial selection. If true, then breeding of bacteria in a research lab in order to study antibiotic resistance doesn’t depend substantially on the theory of natural selection.
2) Natural selection is substantially the same as artificial selection. If true, then breeding of bacteria in a research lab in order to study antibiotic resistance does depend substantially on the theory of natural selection. However, if natural selection is substantially the same as artificial selection, then biological change in nature (natural selection) is in some ways the same as biological change caused by intelligent agency (artificial selection). That’s an assertion that some of the evidence in evolutionary biology is consistent with intelligent design.
What did Mr. Dunford think of my observation about his argument? Mr. Dunford:

…when a dog pisses on a fire hydrant, it’s not committing an act of vandalism. It’s just being a dog. It’s possible to use that analogy to excuse a creationist who takes a quote wildly out of context, I suppose, but I don’t think it’s really appropriate. Creationists might indulge in quote mining with the same casual disregard for public decency as a male dog telling his neighbors that he’s still around, but, unlike dogs, the creationists are presumably capable of self-control…

Comentators on Mr. Dunford’s blog didn’t like my observation either. ‘GvlGeologist’, FCD, wrote:

Mike [Dunford], what are the chances that you could email Egnor directly and ask for an apology for the deliberate twisting of your posting, and CC it to other members of his department, especially the chair of neurosurgery?

Commentator ‘Paul Burnett’ suggested:

Write Egnor a simple one-page request for an apology, detailing his transgressions. Cc: everybody: The chair of neurosurgery, all the neurosurgeons, all the surgeons and anesthesiologists and other specialists, the nurses and office staff, the PR office, the accounting office, the local newspapers and TV stations, the DA and the Chamber of Commerce and the Better Business Bureau…wallpaper his world. Google his name to find his office(s) address(es), then Google the building(s) address(es) and sent a copy to everybody in his building(s). Find out every association he’s a member of and send it to all the officers, past and present. Send it to the FBI, intimating he’s Client Number 8 (naah, maybe that’s too low.)

Commentator ‘T. Bruce McNeely’, a Darwinist pathologist/microbiologist, wrote

…if Dr. Egnor were practising at my hospital, I would be lobbying for suspension of his antimicrobial prescribing privileges.

The vituperation is remarkable. Simply expressing disagreement with Darwinian orthodoxy evokes ad hominem attacks and threats to one’s reputation and livelihood. Yet there’s no reason to be so vindictive. I merely quoted Mr. Dunford’ own arguments, in a way that makes his logical structure clear. Mr. Dunford seems to have understood my point, and has followed with a much more thoughtful post about the role of Darwin’s theory in antibiotic research. I agree with much of it.
Yet there is an important point that Mr. Dunford raises on which I disagree. He writes:

“Darwin’s theory” is …: if a heritable trait makes it more likely that those who possess it will successfully reproduce, the trait will spread through the population. That process drives the spread of antibiotic resistance. That may not be something that Egnor objects to, but it’s still part and parcel of “Darwin’s theory”.

I agree with Mr. Dunford that differential reproductive success drives the spread of antibiotic resistance through the population of bacteria. That is obviously important, and lends itself to study (for example by mathematical modeling) that can be very important to medical research.
However, the observation that organisms have different degrees of reproductive success is not Darwin’s theory. Darwin’s theory is this:
All natural biological complexity arose by the mechanism of non-teleological heritable variation (random mutations) and non-teleological differential reproductive success (natural selection).
The essence of Darwinism– from Darwin’s orgininal theory to the modern synthesis and all of its variants– is that biological evolution is non-teleological. The inference to teleology in biology is the core of the debate about intelligent design and Darwinism. Differenential reproductive success is only a part of Darwin’s theory, and it is not the part of Darwin’s theory that is at issue in the ID-Darwinism debate. If Darwin had merely asserted that differential reproductive success played a role in population dynamics of organisms, his theory, while obviously true, would not have caused controversy. In fact, Darwin’s invocation of the role of differential reproductive success in population biology was rudimentary; population biology depends heavily on mathematics, and Darwin knew no mathematics. It was for later evolutionary biologists and mathematicians– Vito Volterra, A.J. Lotka, J.B.S. Haldane, Sewall Wright, R.A.Fisher and many others– to develop a meaningful mathematical theory of differential reproduction and population biology. What made (and makes) Darwin’s theory so important was his assertion that the mechanism of non-teleological heritable variation and non-teleological differential reproductive success accounts for all natural biological complexity. It was Darwin’s denial of teleology in biology that made his theory revolutionary and controversial. His observation that organisms have different reproductive success was only a part– a rudimentary and non-controversial part– of his theory.
Supporters of Darwin’s theory (that there is no teleology in biology) invoke his non-controversial observation about differential reproductive success because it is one part of his theory that is demonstrably (and logically) true. It is a way of circumventing the real issue on which that truth of Darwin’s theory stands or falls. What is at issue in the ID-Darwinism debate is the issue of teleology; is there any evidence that purpose– design– played a role in evolutionary history? The issue of teleology in evolution is the central question in our debate, and bacterial resistance to antibiotics has no direct bearing on that issue.
The phenomenon of bacterial resistance to antibiotics is tangential the ID-Darwinism debate, and Darwin’s theory of the non-teleological origin of biological structure and function plays no scientific role in medical research. If intelligent design theory were true– if there were evidence for teleology in some aspects of biology– medical research would continue, unhindered.

Michael Egnor

Senior Fellow, Center for Natural & Artificial Intelligence
Michael R. Egnor, MD, is a Professor of Neurosurgery and Pediatrics at State University of New York, Stony Brook, has served as the Director of Pediatric Neurosurgery, and award-winning brain surgeon. He was named one of New York’s best doctors by the New York Magazine in 2005. He received his medical education at Columbia University College of Physicians and Surgeons and completed his residency at Jackson Memorial Hospital. His research on hydrocephalus has been published in journals including Journal of Neurosurgery, Pediatrics, and Cerebrospinal Fluid Research. He is on the Scientific Advisory Board of the Hydrocephalus Association in the United States and has lectured extensively throughout the United States and Europe.

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