Nothing against fossils, but when it comes to tracing the story of human evolution they’re taking a back seat lately to everything from DNA to lice, and even the DNA of lice. A few years ago scientists compared the DNA of body lice (which are misnamed: they live in clothing, not the human body) to that of head lice, from which they evolved, and concluded that the younger lineage split off from the older no more than 114,000 years ago, as I described in a cover story last year. Since body lice probably arose when a new habitat did, and since that habitat was clothing, that’s when our ancestors first needed a haberdasher. The Y chromosome has been an even greater source of clues to human evolution, showing among other things that the most recent common ancestor of all men alive today lived 89,000 years ago in Africa, and that the first modern humans walked out of Africa about 66,000 years ago and became the ancestors of everyone outside that natal continent.
Fred Williams
April 2000*
(Featured in Creation Digest, Autumn 2002)
[An abridged and updated version is available here (April 2003)]
Abstract
Evidence continues to mount contradicting the evolutionist's claim that man and ape share a common ancestry. Over the last 20 years, studies have shown that the human mutation rate is inexplicably too high1,2. A recent study published in Nature has solidified this3. These rates are simply too high for man to have evolved from anything, and if true would show that man must in fact be regressing (a position very consistent with a recent creation of man). Most evolutionists ignore this problem, and those who do attempt to address it leave us with just-so stories void of any supporting evidence.
Exposing the cards
Let's first consider the recent Eyre-Walker & Keightley article in Nature magazine3. By comparing human and chimp differences in protein-coding DNA, they arrived at a deleterious (harmful) mutation rate for humans of U=1.6 per individual per generation. They acknowledge that this seems too high, but quickly invoke something called "synergistic epistasis" as a just-so explanation (I'll address this later).
What is not adequately conveyed to the reader is just how bad this problem is for evolution. It is related to the renowned geneticist J.B.S. Haldane's reproductive cost problem that Walter Remine so eloquently elucidated in "The Biotic Message"4. 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 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 species5). 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^-U6. Therefore, making the substitution,
B = 2e^U. For U=1.6, B = 9.9 births per female!
What pray tell does this mean? What are the authors failing to make crystal clear? It says that females need to produce over 10 offspring just to keep genetic deterioration near equilibrium! A rate less than 10 means certain genetic deterioration over time, because even the evolutionist's magic wand of natural selection cannot help (in fact Eyre-Walker & Keightley had already factored in natural selection when they arrived at a rate of 1.6)
Now consider that extremely favorable assumptions for evolution were used in the Eyre-Walker & Keightley article. If more realistic assumptions are used the problem gets much worse. First, they estimate that insertions/deletions and some functional non-genic sequences would each independently add 10% to the rate. Second, and more importantly, they assume a functional genome size of only 2.25% (60K genes). When they assume a more widely accepted 3% functional genome (80K genes), they cite U = 3.1, which they admit is "remarkably high" (even this may be a favorable assumption, considering Maynard Smith estimates the genic area to be between 9 - 27%7).
Widely recognized geneticist James Crow in an article in the same Nature issue agrees that the deleterious rate is more likely twice the rate cited by Eyre-Walker and Keightley8. So if we use Crow's revised rate of U=3, we get:
B = 2e^3 = 40 births before we get one offspring that escapes a new defect!
The evolutionist's just-so explanation
So are we to believe that upward evolution can overcome what is obviously an insurmountable reproductive barrier? Let's check the evolutionist's explanation and see if it holds water. Crow acknowledges that given these mutation rates and a conventional elimination of mutations, a species with limited reproductive capacity will face "inevitable extinction."8 He then adds: "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.
This brings us back to Eyre-Walker & Keightley'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. Thus, harmful mutations are eliminated "in bunches". Here again we have pure speculation with no real, tangible evidence to support it.
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 40 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.
Crow concludes by stating that the high mutation rate helps explain the advantage of sex to evolution. Sure, sex will certainly slow the propagation of harmful mutations (a conservation property completely consistent with a creationist viewpoint). But Crow is forgetting the other side of the coin, that sex will also slow the propagation of beneficial mutations! Recombination has long been considered a paradox among evolutionists9, since it greatly hinders the spread of those crucial "beneficial" mutations needed to make a man out of a monkey. Right out of the gate the mutation must overcome the 50% recombination barrier. Sex is especially a problem in small populations due to the affect of genetic drift (punctuationists claim that the spawning ground of large-scale evolution occurs in small populations). Regardless, sex certainly doesn't solve, let alone address the reproductive cost problem discussed above.
High rate supports recent creation of man
If the deleterious mutation rate is indeed as high as 3 per individual, not only would it thwart the evolutionary scenario of chimp/man common ancestry, it would clearly argue for a recent creation of man. To illustrate this, let's start with a simple model where we will assume heterozygosity10 throughout the generations (this essentially means no inbreeding), using the rate of 3 harmful mutations per individual. Each generation, offspring will inherit on average 3 harmful mutations from the parents (half of 3 from the mother, half of 3 from the father), plus 3 new mutations during the reproduction process. The number of mutations in each offspring after x generations is U * x, where U is the mutation rate. Using the standard population genetics assumption of 25 years per generation, there are 240 generations in 6000 years. So, 3 * 240 = 720 mutations per individual after 6000 years. This isn't too severe considering the size of the active genome, where we have an estimated 80,000 genes, averaging about 1500 base pairs per gene. So 720 mutations spread over the genome amounts to about one mutation per 111 genes11. However, if we use the evolutionist's estimated time since the split between ape and man of 6 million years, we get 720,000 bad mutations, or about 9 mutations per gene!12 We would more resemble a snail than a human! (it should probably come as no surprise that some evolutionists actually posit that apes de-evolved from humans!13)
Note that more than 50% of these mutations will be recessive, and therefore not expressed. However, as we introduce inbreeding and homozygous fixation of genes into this model, the numbers will obviously get worse. Fixed dominant genes won't have to contend with a good copy on the other chromosome, and recessive genes will have a chance to express themselves (one in four if both parents have the defect). If we take all this into consideration, the evolutionary timescale numbers get exponentially worse compared to a trivial decline in the recent creation numbers.
Mitochondrial-DNA rates offer some collaboration. Consider this article from the journal Science:
"Mitochondrial DNA appears to mutate much faster than expected, prompting new DNA forensics procedures and raising troubling questions about the dating of evolutionary events. ...Regardless of the cause, evolutionists are most concerned about the effect of a faster mutation rate. For example, researchers have calculated that "mitochondrial Eve"--the woman whose mtDNA was ancestral to that in all living people--lived 100,000 to 200,000 years ago in Africa. Using the new clock, she would be a mere 6000 years old."14
The evolutionary squeeze
The evolutionists are in a squeeze, and it's devastating. We have seen from the analysis above that it is implausible for evolution to occur at such a high deleterious mutation rate. But what if you lower the rate? Well, then all kinds of new problems pop up for the evolutionist! A slower rate means a smaller portion dedicated for those rare "beneficial" mutations, so there will be fewer substitutions of new traits over time. Consider that population geneticists typically estimate that only 1 in 50 beneficial mutations have a chance to even reach fixation15. This problem is aggravated by the fact that a cost must be incurred to spread any new trait through the population (those without the trait must eventually die off). The famous geneticist J.B.S. Haldane showed that under favorable assumptions only one new, beneficial substitution could be completely substituted in a population every 300 generations. So in 10 million years, twice the time since the alleged chimp/human split from a common ancestor, only 1667 beneficial substitutions could occur.16 That's only a 0.001% difference between human and chimp genomes. The entire number of substitution differences between man & chimp, ranging from harmful to neutral to beneficial, is estimated to be between 1-3%, or 30-90 million substitutions. Surely 1667 is not enough to make a man out of a hairy, armpit-scratchin, dung throwin' ancestor! Evolutionists need to add about another 1000 trillion years to their cake mix just to get an ape with manners!
Some evolutionists try to "fix" this problem by lowering the amount of functional genome. But as this is lowered, they remove space for new genes that are absolutely essential for their theory. Evolutionists who are aware of the information problem try to solve it by claiming that beneficial random mutations to duplicated genes, under the guidance of natural selection, is what gets upward evolution rolling. But a smaller functional genome obviously means less chance for a duplicated gene to be mutated (all this assuming increased information by random mutation can even occur, which information theory says it can't). Some evolutionists dispute this small of a functional genome. As mentioned earlier, Maynard Smith estimates it to be between 9-27%7. If further evidence expands the functional genome toward 10%, then the mutation rate/reproductive cost problem gets much worse, requiring evolutionists to "fruitfully multiply", and now, if they want a self-fulfilling theory!
Conclusion
The high mutation rate from the Eyre-Walker & Keightley study was determined under the assumption of common ancestry between chimps and man. Since the rate is clearly too high, there are only two realistic explanations:
1) there is a mistake in their data or analysis (doubtful), 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!
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.
Finally, a double-edged sword shows that while high rates of mutation cause harmful mutations to overwhelm any beneficial ones, lower rates slow evolution to a crawl. But regardless of the rate of mutation, what we've learned from information theory 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.
Addendum
Dr. James Crow, whom I cited in the article, graciously commented on the article soon after I wrote it. Via personal email 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). He presented "quasi-truncation selection" as a possible "partial solution" to the problem.
Other vindication for my article comes from a paper in the science journal Genetics published 5 months after I wrote this article. They write
"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." [emphasis mine]
They also acknowledge that this number is probably an underestimate!
"This assumes that all mortality is due to selection and so the actual number of offspring required to maintain a constant population size is probably higher." [emphasis mine]
Their ultimate explanation is the same used by Eyre-Walker, Keightley, Crow, et al, truncation selection. Again, there is NO evidence to support that such strict truncation selection occurs in nature, and even if it did would not solve the problem. The Genetics authors admit that truncation selection "seems unrealistic", but submit this view simply because the alternative explanation is unacceptable to them - that men and apes do not share a common ancestor.
3/22/2002 - Yet more support comes from the recent article in Genetics titled '"Positive and Negative Selection on the Human Genome" (Justin C. Fay,* Gerald J. Wyckoff* ,1 and Chung-I Wu*. Genetics 158, 1227-1234. 2001.). This article was unwittingly brought to my attention by evolutionist Dr Scott Page (see our debate on this matter). The authors of the Genetics article write:
"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]."
Using their estimates, the required offspring number rises to at least 60 offspring per breeding couple! (for explanation, see my opening comments in my debate with Dr Page.)
* Article updated 12/09/2001 to improve the explanation of synergistic epistasis, and to add 'Addendum' section.
* Article updated 3/2/2002 to better emphasize in the conclusion the flawed assumption of man/chimp ancestry as the reason for the high mutation rate.
1. 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
2. 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.
3. Eyre-Walker & Keightley, High genomic deleterious mutation rates in hominids, Nature 397, 344 - 347 (1999) Abstract
4. W. Remine, The Biotic Message, St. Paul Science, 1993, p. 228-229
5. L. Spetner, Not by Chance, The Judaica Press, 1998, p. 138 (particularly all of Chapter 5)
6. This equation is a derivation of the Poisson Distribution where the probability of no events is calculated.
7. Maynard Smith, Evolutionary Genetics, Oxford University Press, p. 204
8. J. Crow, The odds of losing at genetic roulette, Nature 397, p 293 - 294. (1999)
9. See Walter Remine's The Biotic Message, page 196-200 for a full list of evolutionist=s comments on the paradox of sex (recombination) to evolution.
10 - Heterozygous means there is another version of the gene (presumably a good copy, for this model) on its peer-chromosome.
11 - mutations per gene = (120 mil base pairs / 720) / 1500. Base pair number is based on 3% typically cited on the internet.
12 - Years since split = 6 mil, generation time = 25 years, mutation rate = 3 per generation, giving (6*10^6 / 25) * 3 = 720,000. Mutations per gene = (120 mil / 720000) / 1500 = .11
13 - D. Gish, Evolution: the Fossils STILL say NO!, 1995, p. 308-310
14 - A. Gibbons, Calibrating the Mitochondrial Clock, Science, Vol 279, No. 5347, Jan 1998, pp. 28 - 29.
15. This assumes a favorable selection advantage of 1%. See Maynard Smith, p. 161-162
16 - For a great discussion of Haldane's Dilemma, see Walter Remine's "The Biotic Message", St. Paul Science, 1993, p. 208-236. Some of this is discussed here.
