Can Darwin Help Your Doctor?
Are you sick? Should you rely on Darwinism or Science?
by Jerry Bergman, PhD
Under the headline “Darwin can help your doctor,” a press release from the University of Groningen claimed that “Evolution and ecology inspire clinical research in infections and antimicrobial resistance”. The editors explain: “Taking an evolutionary view can inspire new ideas in clinical microbiology. For example, evolutionary studies can reveal why some antimicrobial dosing regimens are better than others in preventing the development of drug resistance.”
As I read the review, it soon became apparent that the word evolution was tacked onto the report for no good reason except to give obeisance to Darwinism. The approach described in the report had nothing to do with Darwinism but was rather an example of the classic empirical experimental approach. This approach requires scientists to evaluate the proposed “antimicrobial dosing regimens” on patients and then study the outcome. For example, a sample of affected patients would be randomized into 5 treatment groups of 20 patients each, then the outcome of each group is compared. If statistical differences are found at the alpha 0.05 level or better (such as alpha 0.01) to insure the difference between the two is very unlikely due to chance, this lends evidence to the conclusion that the protocol found most effective is actually, as a whole, more effective. The report then added:
Looking at microbial communities, rather than just the pathogenic micro-organisms, can also lead to new insights. That is why clinicians, bioinformaticians analysing pathogens and evolutionary biologists should all work together. These are the conclusions of a diverse group of scientists led by University of Groningen microbiologist Marjon de Vos, in a short review published by The Lancet Infectious Diseases on 30 April.
Again, this is an example of an obvious truism. Of course, “clinicians, bioinformaticians analysing pathogens and evolutionary biologists should all work together.” I have to wonder what evolutionary biologists could possibly contribute. Microbiologist
De Vos studies urinary tract infections. She realized that a lot could be gained by collaborating with different specialists … For example, … bacteria involved communicate with each other and can form a stable ecosystem, which affects their susceptibility to antibiotics.’ This realization led to an interdisciplinary workshop in 2017, which in turn resulted in the review paper now published in The Lancet Infectious Diseases.
Still no answer as what this research has to do with evolution. So I read on.
The article then discussed cystic fibrosis
The review mentioned bioinformatics, which is an analysis of “the vast amount of genetic data collected on infectious diseases.” This also has nothing to do with evolution unless one is searching for long-term, millions of years, evolutionary trends. In this case, the bioinformatics technique is a fishing expedition looking for trends in gene expression patterns that may relate to the medical condition of concern. The doctors explain that cyclic antibiotic treatments in cystic fibrosis patients are used to treat chronic lung infections which are common in this condition. To minimize the development of drug resistance, treatment alternates with two different drugs. If the pathogens become resistant to one drug, ideally, the other will be effective. Obviously, this approach could result in multi-drug resistance.
This is the claim I was expecting, which has nothing to do with evolution. I will cover the most common claim, that is antibiotic resistance due to mutations which create bacteria incorrectly termed “superbugs.”
How do bacteria develop resistance to antibiotics?
Although bacteria can become resistant due to mutations, all these mutations studied so far are either loss mutations, or damage-to-gene-expression mutations that damage the system that speeds up the removal of, or the inactivation of, antibiotics. None of these effects are the result of new cellular innovations, but are caused merely by damaging something in the bacteria.
One type of mutation can alter the shape of the antibiotic binding site. The antibiotic works by fitting into the antibiotic binding site and, like a lock and key, if the keyhole is damaged, the key will no longer fit into the lock. Likewise, if the antibiotic binding site is distorted as a result of damage caused by mutations, the antibiotic will no longer fit into the antibiotic binding site, protecting the bacteria from the antibiotic.
A side effect is the mutation can degrade or destroy the function for which the bacteria binding site was designed. For example, a neutral mutation in one amino acid that prevents the required antibody-enzyme interaction alters the binding site on the 4-quinolone antibiotic which disables the DNA gyrase enzyme in bacteria. The gyrase enzyme is an essential bacterial enzyme that catalyzes the ATP-dependent negative super-coiling of double-stranded closed-circular DNA. It reduces the twisting strain occurring while double-stranded DNA is being unwound by elongating RNA-polymerase.
The classic example of mutations in the antibiotic mechanism which causes the bacteria to become immune to the antibiotic is ribosome point mutations that renders streptomycin and other mycin antibiotics ineffective. Mycin antibiotics function by attaching to specific receptor sites on the bacteria’s ribosomes which are required to produce protein to keep the bacteria alive. The result is this antibiotic action interferes with the bacteria protein-manufacturing process. The proteins the bacteria produce are, as a result of the mutation, either non-functional, or are not even produced. The result is the bacteria cannot grow and divide, or propagate.
Bacterial mutations cause the bacteria to become streptomycin-resistant if the ribosome site, where the streptomycin attaches, is altered by mutations. As a result, the streptomycin no longer can bind on the host ribosome, and therefore it no longer can interfere with the ribosomal function of producing protein. Mutation-caused changes that enable the bacteria to become mycin-resistant can occur in several different locations on the ribosome.
Mammalian ribosomes do not contain the specific site where myosin drugs attach, and for this reason the drug does not interfere with mammal ribosome function. Consequently, mycin drugs adversely affect bacterial growth without harming the host. Because fundamental differences exist between prokaryotic (bacterial) and eukaryotic ribosomes, these variations often are exploited in order to produce antibiotics to kill bacteria without harming the host. Actually, many antibiotics used are produced by fungi or other bacteria to protect them from enemy bacteria. Humans obtain them to protect them from the same pathogenic bacteria.
Another example of a mutation-caused resistance is, in Mycobacterium tuberculosis bacteria, an enzyme in the bacteria that changes the antibiotic called isoniazid into its active form that kills the bacteria. If a mutation damages the enzyme that converts the antibiotic into its active form, the antibiotic remains in its inactive and harmless conformation. As a result, this mutation confers antibiotic resistance to the mutant bacteria. The mutation that damages the enzyme which prevents the antibiotic from killing the bacteria also cripples the bacteria, an effect called the fitness cost.
When bacteria become resistant to antibiotics as a result of mutations, all the mutations studied so far are either loss mutations, or gene-expression mutations that result in speeding up the systems that removes or inactivates antibiotics. None are the result of new cellular innovations but are caused merely by altering the regulation control.
all the mutations studied so far are either loss mutations, or gene-expression mutations
Evolution by retreat
In short, this brief discussion illustrates the fact that all known examples of antibiotic resistance are due to inbuilt systems designed to achieve symbiosis, or damage to some system in the host or pathogen that prevents it from properly defending itself. In short, so-called super bacteria are actually damaged bacteria that have an advantage in an environment loaded with antibiotics, such as in a hospital.
Conversely, mutations that add new systems, such as a new regulatory system, energy-generating system, or transport system, have never been documented. Mutations increasing certain enzyme affinity may be beneficial, but often occur rapidly, indicating that design is involved. For example, mutations effecting hemoglobin-oxygen affinity help the host to acclimatize to a high altitude, but the same mutation can also cause polycythemia. This response is not evolution, but rather designed adaptation.
Mutations that alter a protein which results in antibiotic resistance are also likely to weaken the organism. Mutations that both confer resistance, and allow the bacteria to survive, do not improve the bacteria fitness in its normal environment. The bacteria actually render them less able to survive in an antibiotic-free environment. Thus, when the bacteria becomes resistant to a drug, it is likely to become less fit in other ways. This is called the cost of resistance, or the fitness cost. Often the cost is very high and the mutation renders the resistant stain poorly able to survive in a non-antibiotic environment.
The last claim covered in the The Lancet Infectious Diseases article was resistance plasmids. Resistance plasmids are small circular DNA that confers resistance to bacteria that can easily be exchanged between bacteria. The Lancet review admits “we still don’t know how changes in genes lead to the different characteristics of these pathogens. We need experiments by evolutionary biologists in order to understand the link between the genotype, the DNA sequence and the phenotype – for instance, the level of resistance.”
The 11-page Lancet article contained the word evolution 103 times and, after analyzing each example, the same problem was found as I have documented in this paper. Of interest is the article’s list of examples of the successes of microbial evolutionary medicine, including the exploitation of the alleged bacterial evolutionary molecular clock to trace transmission events over time in hospitals and continents in spite of the fact that the molecular clock has been a dismal failure, at least for long periods of time.
 “Darwin can help your doctor.” Science Daily. 30 April 2019. https://www.sciencedaily.com/releases/2019/04/190430103424.htm.
 “Darwin can help your doctor.” Science Daily. 30 April 2019. https://www.sciencedaily.com/releases/2019/04/190430103424.htm.
 Davies, A. P., et al., 2000. “Comparison of Fitness of Two Isolates of Mycobacterium tuberculosis, One of which had developed Multi-Drug Resistance during the Course of Treatment.” Journal of Infection, 41(2):184-187, Sept.; Davies, J. and M. Nomura, 1972. “The Genetics of Bacterial Ribosomes.” Annual Review of Genetics, 6:203-234.
 Didier, E. S., D. C. Bertucci, and L. Leblanc, 1999. “Inhibition of Microsporidia Growth in vitro.” Abstracts of the General Meeting American Society Microbiology, 99:11
 Wieland, Carl, 1994. “Antibiotic Resistance in Bacteria.” Cen Tech J., 8(1):5-6, p. 5.
 Wieland, 1994, p. 6.
Spetner, Lee, 1997. Not by Chance. Brooklyn, NY: The Judaica Press, p. 144.
Lenski, Richard E., 2002. “Cost of Resistance” in Encyclopedia of Evolution. Volume 2, pp. 1008-1010. New York, NY: Oxford University Press. Mark Pagel (editor), p. 1009.
Baquero, Fernando, 2002. “Antibiotic Resistance: Origins, Mechanisms, and Extent of Resistance” in Encyclopedia of Evolution. Volume 1, pp. 50-54. New York, NY: Oxford University Press. Mark Pagel (editor). p. 51.
 “Darwin can help your doctor.” Science Daily, 30 April 2019. https://www.sciencedaily.com/releases/2019/04/190430103424.htm.
 Andersen, Sandra B., 2019. Evolutionary medicine: from theory to clinical practice. The Lancet Infectious Diseases, online 30 April 2019. https://www.thelancet.com/action/showPdf?pii=S1473-3099%2819%2930045-3.
 Jeffrey Tomkins and Jerry Bergman, 2015. “Evolutionary Molecular Genetic Clocks–A Perpetual Exercise in Futility and Failure.” Journal of Creation, 29(2):26-35.
Dr. Jerry Bergman has taught biology, genetics, chemistry, biochemistry, anthropology, geology, and microbiology at several colleges and universities including for over 40 years at Bowling Green State University, Medical College of Ohio where he was a research associate in experimental pathology, and The University of Toledo. He is a graduate of the Medical College of Ohio, Wayne State University in Detroit, the University of Toledo, and Bowling Green State University. He has over 1,300 publications in 12 languages and 40 books and monographs. His books and textbooks that include chapters that he authored, are in over 1,500 college libraries in 27 countries. So far over 80,000 copies of the 40 books and monographs that he has authored or co-authored are in print. For more articles by Dr Bergman, see his Author Profile.