John Smith provided this research paper in a Facebook discussion,, requesting an explanation for phenomena routinely referenced as “beneficial mutations.”

John wrote:

“Two arguments I hear frequently are either A) beneficial mutations never occur, or B) beneficial mutations occur, but not frequently enough to produce the variation we see today and is needed for evolutionary change. One experiment shown below found the rate of beneficial mutations in E. Coli to be a whopping 12%.”

Here’s my response:

A. Argument #1: “Beneficial mutations never occur.”

This is not an argument. It is a meaningless and unqualified statement. There are many different kinds of mutations. There are mutations induced by different kinds of radiation, and then there are common genetic mutations that are responsible for most of the variations between different populations of the same species and members in a family. Mutations might not be molecular, but a reference to a visual phenotype that is noticeably different than normal.[1] This is a relative term as it could only have meaning depending upon the context of what kind of mutation is specifically referenced, and what is meant by the term, “beneficial.” Since the word “never” is employed, the hypothetical assertion is begging to be a logical fallacy. The representation is vague and ambiguous, and also unfounded because there is not quote or source cited that might be examined to determine the adequacy of the claim to a specific situation.

B. Argument #2: “Beneficial mutations occur, but not frequently enough to produce the variation we see today and is needed for evolutionary change.”

This statement is clearer. There is still a problem here in defining the term “mutation,” but I assume that it is referring to a gene translation or transcription copying error. It is the position held by ID proponents that mutations are inadequate to cause the variation required to result in the diversity of life. The issue, however, is not that mutations are “beneficial” to an organism, but whether the mutation leads to an increase of information in the genome of a population. The increase of information in the genome of a population necessary for evolution to occur must generate a new biochemical structure, which would lead to greater complexity. ID holds Darwinian mechanisms (i.e., mutations) do not cause such increase of information, and only ID Theory explains the increase in complexity. Therefore, whether copying errors are “beneficial” in some manner lending a cell or organism to be more fit to an environment is irrelevant.

C. “One experiment shown below found the rate of beneficial mutations in E. Coli to be a whopping 12%.”

Based upon the foregoing comments, so what?

There is very little rebuttal by Darwin dissenters written on this 2001 Lenski research paper. Although Lenski’s later research papers will receive high publicity, this particular 2001 paper received very little notoriety. I would attribute most of the silence on this paper because the findings were insignificant and the issue essentially irrelevant based upon my comments above. No Creationist organization or any ID proponents consider this paper significant enough to be worth the effort to respond to its claim of “beneficial mutations.” The kind of mutation that is supposedly “beneficial” in this experiment is so inconsequential that it remains questionable that the mutations heralded in this research as “beneficial” are by any means actually advantageous.

When anti-Darwinists use the term “beneficial mutation,” they are usually not referencing a common copying error mutation. In fact, variations are EXPECTED to be beneficial. For example, in humans, a person with darker skin will benefit by being able to withstand sun exposure than a person with a lighter complexion. These are not the kinds of “mutations” that are referenced when someone argues that “beneficial mutations never occur.” When someone generally asserts, “beneficial mutations never occur,” they are likely noting the common observation that noticeable unprecedented visual changes in phenotype are always negative, and often disastrous. This is just the opposite of the evidence desired, which is to see a biochemical system display a new function or see the introduction of a new biochemical structure that actually benefits the organism. This is what is meant when someone generally states, “beneficial mutations never occur.”

In the instant experiment, Lenski (2001), the organism is not a plant or animal that we would like to see such a beneficial mutation occur. The organism is a bacterium, E. coli. E. coli is unicellular with no nucleus, and is one of the most primitive life forms on Earth. Although Darwinist are quick to claim that bacteria has increased in complexity over billions of years, it is nothing much different than the original bacteria cell was, a single-cell organism lacking a nucleus. Here we have had billions of years of opportunity for evolution to occur, and yet nothing has essentially happened. This is our specimen; this is where it is claimed that beneficial mutations are occurring. If E. coli has such a high 12% propensity to incur beneficial mutations, it is even more disappointing that after billions of years of supposed evolution to be happening with the organism, it has not ceased to be anything other than they way it started out billions of years ago – a unicellular organism with no nucleus. Anyway, let’s proceed with our review of the Lenski 2001 paper.

In 1988 Richard Lenski, an evolutionary biologist at Michigan State University, began culturing 12 identical lines of E. coli. Over 44,000 generations and 23 years later, the experiment continues. The bacteria are grown in medium, which has a small amount of glucose (a primary carbon source for E. coli) and abundant citrate (a carbon source not utilized by E. coli). Every 500 generations, Lenski’s lab takes samples of the bacteria, which in essence produces a “fossil record” of the different lines. Lenski has observed many changes in the E. coli as they adapt to the culture conditions in his lab.

Lenski et al[2] determined that after 10,000 generations in the same cultivation conditions, a population of Escherichia coli contained a diversity of mutant strains. Each of these mutants had an increased adaptation to the cultivation condition, manifesting itself in a 50% greater relative fitness compared to the parental wildtype. Thus, the mutations appeared to be beneficial and were positively selected. In the instant research paper, 12% of the mutations were “beneficial.”

Subsequent genetic analysis of some of these E. coli mutants found that they possessed insertion sequences, or IS elements. IS elements are a small segment of DNA that can insert into numerous sites of the chromosome. The standard copying errors are frameshift mutations and gene duplication. Of the frameshift type, there are insertions and deletions. In the instant paper we are reviewing, “Contribution of individual random mutations to genotype-by-environment interactions in Escherichia coli,” the mutations are single random insertion mutations.

These IS elements were indigenous to the chromosome, and their activity did not depend on horizontal transfer from neighboring cells. Movement of these elements produced various insertional mutations in the E. coli chromosome.[3] In fact, these types of mutations appear to be the primary function of these IS elements.[4] These insertional mutations either create “knockout mutations”, disrupting gene function or genetic activity at the point of insertion, or they may carry a promoter or other regulatory segments that activate adjacent genes.[5]

One specific IS disruption of gene activity in some of the mutants was the loss of the ribose operon.[6] In other words, while the fitness of the bacteria had increased (as compared to the starting bacteria), it came at a cost. In related E. coli experiments, all the lines lost the ability to catabolize ribose (a sugar).[7] Some lines lost the ability to repair DNA.[8] These bacteria may indeed be more fit in a lab setting, but if put in competition with their wild-type (normal) counterparts in a natural setting, they would not stand a chance.

In the instant Lenski (2001) research involving single random insertion mutations. The researchers noted “mutations that showed evidence of being beneficial did so in maltose” environment but not in glucose.[9] As such, the researchers admit that “they are only conditionally beneficial.”

What is perhaps a greater problem is that the means of measuring fitness in this experiment was the ability for the E. coli to endure changes in temperature. This is an infinitesimally small measure to rely upon to infer that the insertion mutation has caused any variation whatsoever. There is no change in function here. There is no increase of information in the genome. There is merely an announcement that one population that incurred the insertion mutation was able to endure a greater temperature variance than the control population in a maltose environment. This is hardly persuasive evidence to suggest that copying error mutations are “beneficial” based on just the results of this experiment. The researchers admitted several times that their results are contrary to known facts about these kinds of mutations, often repeating the phrase, “extremely rare.”


1. There are several reasons for these kinds of mutations, the most common are switch genes that turn on and off certain functions or structures. Here are a couple examples: (a) Darwin called attention to wingless beetles on the island of Madeira. For a beetle living on a windy island, wings can be a definite disadvantage, because creatures in flight are more likely to be blown into the sea. Mutations producing the loss of flight could be helpful. (b) The sightless cavefish would be similar. Eyes are quite vulnerable to injury, and a creature that lives in pitch dark would benefit from mutations that would replace the eye with scar-like tissue, reducing that vulnerability. In the world of light, having no eyes would be a terrible handicap, but is no disadvantage in a dark cave. While these mutations produce a drastic and beneficial change, it is important to notice that they always involve loss of information and never gain. One never observes the reverse occurring, namely wings or eyes being produced on creatures that never had the information to produce them.

2. Lenski, R. E., J. A. Mongold, P. D. Sniegowski, M. Travisano, F. Vasi, P. J. Gerrish, and T. Schmidt, 1998. Evolution of competitive fitness in experimental populations of E. coli: What makes one genotype a better competitor than another? Antonie van Leeuwenhoek 73:35–47.

3. Schneider, D., E. Duperchy, E. Coursange, R. E. Lenski, and M. Blot, 2000. Long-term experimental evolution in Escherichia coli. IX. Characterization of IS-mediated mutations and rearrangements. Genetics 156:477–488.

4. Anderson, K. L., 2003. The complex world of gastrointestinal bacteria, Ref. 3. Canadian Journal of Animal Science 83:409–427.

5. Schneider, D., and R. E. Lenski, 2004. Dynamics of insertion sequence elements during experimental evolution of bacteria. Research in Microbiology 155:319–327.

6. Cooper, V. S., D. Schneider, M. Blot, and R. E. Lenski, 2001. Mechanisms causing rapid and parallel losses of ribose catabolism in evolving populations of E. coli B. Journal of Bacteriology 183:2834–2841.

7. Vaughn Cooper, et al., “Mechanisms Causing Rapid and Parallel Losses of Ribose Catabolism in Evolving Populations of Escherichia coli B,” Journal of Bacteriology 183 no. 9 (2001): 2834–2841.

8. Paul Sniegowski, et al., “Evolution of High Mutation Rates in Experimental Populations of Escherichia coli,” Nature 387 (1997): 703–705.

9. Susanna K. Remold and Richard E. Lenski, “Contribution of individual random mutations to genotype-by-environment interactions in Escherichia coli” doi: 10.1073/pnas.201140198 PNAS September 25, 2001 vol. 98 no. 20 11388-11393, p. 11393;

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