Monkey-Man Hypothesis Thwarted by Mutation Rates

Fred Williams, RMCF VP
April 2003


Evolutionists often argue that DNA similarity between chimps and man is powerful evidence that they share a common ancestor. Recent estimates put the difference at 1.24%[1]. Creationists respond by arguing that DNA similarity would be expected due to common design, and also note that 1.24% still represents a difference of roughly 39 million fixed base pairs between the two[2]. These are valid points that sufficiently expose the weak logic of the evolutionist claim.

However, there are other serious problems with the evolutionist claim that have gone mostly unnoticed. In recent years, study after study have yielded human mutation rates that are inexplicably too high [3,4,5,6]. These rates are determined by doing direct comparison of simian DNA to human DNA. Estimates are then made for the deleterious (harmful) mutation rate for both the human clade and simian clade since their assumed split from a common ancestor 5 to 6 million years ago.

Exposing the cards

Let's first consider a recent study in the science journal Nature [4]. By comparing human and chimp differences in protein-coding DNA, the authors arrived at a deleterious (harmful) mutation rate for humans of U=1.6 per individual per generation. They acknowledged that this seemed too high, but quickly invoke something called "synergistic epistasis" as a just-so explanation (I'll address this later). The authors also acknowledged that favorable assumptions were used in their study. For example, they did not account for the impact of insertions/deletions, and mutations to non-genic sequences such as introns. When they accounted for the impact of these and other assumptions [7], they arrived at a mutation rate of U = 3.1, which they admitted was "remarkably high". Widely recognized geneticist James Crow in the same Nature issue concurred that the deleterious rate was more likely U=3.

Since the Nature study, a recent study published in the journal Genetics revealed that the rate was even more of an underestimate:

"The genomic deleterious mutation rate in humans was previously estimated to be at least 1.6 on the basis of an estimate that 38% of amino acid mutations are deleterious. The genomic deleterious mutation rate is likely much larger given our estimate that 80% of amino acid mutations are deleterious and given that it does not include deleterious mutations in noncoding regions, which may be quite common. [emphasis mine]." [6]

Using a straight extrapolation yields a mutation rate of U=3.4. What exactly does this mean, and why is this a serious problem for evolution? It is related to the renowned geneticist J.B.S. Haldane's reproductive cost problem that Walter Remine eloquently illuminated in "The Biotic Message"[8]. What we will determine is how many offspring are needed to produce one that does not receive a new harmful mutation during the reproduction process. This is important since evolution requires "beneficial" mutations to build up and outpace harmful mutations such that new features and organs can arise (I say "beneficial" loosely, since there are no known examples where a mutation added information to the genome, though there are some that under certain circumstances can provide a temporary or superficial advantage to a species[9]). If over time harmful mutations outpace "beneficial" ones to fixation, evolution from molecules-to-man surely cannot occur. This would be like expecting to get rich despite consistently spending more money than you make.

So, to determine the reproductive impact, let p = probability an individual's genome does not receive a new defect this generation. A female is required to produce two offspring, one to replace herself and her mate. So, she needs to produce at least 2/p to pay this cost and maintain the population. Let B represent the birth threshold:

B = 2/p

The probability p of an offspring escaping error-free is given by e^-U[10].

Therefore, making the substitution,

B = 2e^U. For U=3.4, B = 60 births per female!

What pray tell does this mean? What are the evolutionist authors of these studies failing to make crystal clear? It says that females need to produce over 60 offspring just to keep genetic deterioration near equilibrium! If they produce a rate less than 60, it means certain genetic deterioration over time. Even the evolutionist's magic wand of natural selection cannot help (each study already accounts for the effect of natural selection).

Another study in the journal Genetics, which came out 5 months after my internet version of this article, arrived at a mutation rate of U=3. The authors candidly confirmed the problem:

"For U = 3, the average fitness is reduced to 0.05, or put differently, each female would need to produce 40 offspring for 2 to survive and maintain the population at constant size." [11] [emphasis mine]

These authors went on to endorse the “solution” offered by the Nature study authors, speculating that “synergistic epistasis” and “truncation selection” might mitigate the problem, but admitted it seemed “unrealistic”. I will now address these just-so stories.

The evolutionist's just-so explanation

Dr. Crow in his letter to Nature acknowledged that given the high mutation rates and a conventional elimination of mutations, a species with limited reproductive capacity would face "inevitable extinction."[12] He then added: "A way out is for mutations to be eliminated in bunches". This is sometimes called truncation selection, a completely speculative process that you will have a very difficult time finding in any college text book on genetics or biology. One possible reason you won't find this in the text books is because there is absolutely no evidence to support that it occurs in nature.[13]

This brings us back to the Nature and Genetics author’s invocation of "synergistic epistasis", which is really a co-star in the "truncation selection" story (the terms are virtually synonymous). This process basically says that each new harmful mutation interacts with prior harmful mutations such that fitness is decreased more than it would have if the new mutation were acting by itself. This allows organisms to push below a fitness threshold where they can more readily be recognized by selection and eliminated from the population (truncation selection). Thus, harmful mutations are eliminated "in bunches". Here again we have pure speculation with no real, tangible evidence to support it. [14]

For the sake of argument, even if synergistic epistasis/truncation selection occurs to sufficiently mitigate the deterioration problem, you still need beneficial mutation fixation to outpace harmful mutation fixation in the eventual survivors. This is unfathomable considering that 60 conceptions are needed just to get an offspring without one of these incremental deteriorating steps. You simply cannot evolve new organs and features when negative hits are outpacing positive ones with such force.


The high mutation rates these studies are yielding were determined by comparing simian to human DNA, under the assumption of shared ancestry. Since the rate is clearly too high, there are only two realistic explanations:

1)       there is a mistake in their data or analysis (very doubtful, especially due to the number of independent studies yielding similar results), or

2)       the base assumption that man and chimp share a common ancestor is flawed (most likely).

The problem of high mutation rates and its cost on reproduction goes away if comparison between simian and man DNA is not used to determine the mutation rate. Remove the flawed assumption that simian and man share a common ancestor, and the problem is solved!

[Note: This article is an updated and abridged version of my original article that can be found at I gave Dr. James Crow an opportunity to respond to the article, and to my surprise he replied "Yours is a serious letter and it deserves a serious answer". He acknowledged it was a "serious problem" for the theory, but not "fatal" (for the record, he made it clear he still believes evolution has overwhelming evidence from other sources, but apparently not from his field of expertise!)]   

1.        Gene data underline primate linkBBC News Wednesday, 16 May, 2001

2.        The human genome contains 3.165 billion base pairs. A difference of 1.24% amounts to 39.2 million base pairs.

3.        A. S. Kondrashov, Contamination of the genomes by very slightly deleterious mutations. Why have we not died 100 times over? J Theor Biol 1995 Aug 21;175(4):583-94. Abstract

4.        Eyre-Walker & Keightley, High genomic deleterious mutation rates in hominids, Nature 397, 344 - 347 (1999)
4.  J. Crow, The high spontaneous mutation rate: is it a health risk? Proc Natl Acad Sci U S A 1997 Aug 5; 94 (16):8380-6.

5.        J. Crow, The high spontaneous mutation rate: is it a health risk? Proc Natl Acad Sci U S A 1997 Aug 5; 94 (16):8380-6.

6.        "Positive and Negative Selection on the Human Genome" (Justin C. Fay,* Gerald J. Wyckoff* ,1 and Chung-I Wu*. Genetics 158, 1227-1234. 2001.).

7.        The Eyre-Walker & Keightley estimate was also based on a gene count of 60K. More recent data indicates the gene count may be closer to 40K. This would slightly reduce their estimate, but not enough to make a serious impact.

8.        W. Remine, The Biotic Message, St. Paul Science, 1993, p. 228-229

9.        L. Spetner, Not by Chance, The Judaica Press, 1998, p. 138 (particularly all of Chapter 5)

10.     This equation is a derivation of the Poisson Distribution where the probability of no events is calculated.

11.     Michael W. Nachmana and Susan L. Crowella, Estimate of the Mutation Rate per Nucleotide in Humans Genetics, Vol. 156, 297-304, September 2000

12.     J. Crow, The odds of losing at genetic roulette, Nature 397, p 293 - 294. (1999)

13.     “Although there is some theoretical support for synergistic epistasis (Szathmary 1993; Peck and Waxman 2000), there is little experimental support for this type of gene interaction (Willis 1993; Elena and Lenski 1997).” - Agrawal and Chasnov 2001. Also, “Current evidence is equivocal as to whether the required levels of epistasis exist.” - Siller 2001

14.    The concepts of "synergistic epistasis" and "truncation selection" would never be brought up if it were not for the high mutation rate problem. These stories were invented to attempt to lessen a clearly serious problem for the modern evolutionary theory. Moreover, even if such forces were at work in nature, they would at best only serve to keep the genetic load in check (that is, slow or bring deterioration to a standstill). What's lost in all this wild speculation by the evolutionists regarding a high deleterious mutation rate is the fate of beneficial mutations, the mechanism that is supposed to bring about new organs and improved functions over time. In the long run you must have more beneficial mutations accumulating than harmful ones for molecules-to-man evolution to be true. The above analysis shows just how implausible this is. You can't save pennies and spend dollars and expect to get rich. But regardless of the rate of mutation, what we've learned from information science is that information can only originate from an information Giver. Random mutations occur, and without new information being fed into an organism by an information Giver, these random changes will certainly cause the organism to slowly deteriorate over time. Other studies showing high mutation rates that do not rely on man/chimp ancestry confirm that deterioration may indeed be occurring.