Michael Cremo - Human Devolution - A Vedic Alternative To Darwin's Theory

First, let us consider the report from the researchers who relied on interspecific calibration of the rate of mutation (Vigilant et al. 1991). Their calibration of the mutation rate was made using either 4 million or 6 million years as the time since the human line supposedly diverged from the chimpanzee line. These times of divergence, when used in calculations that take into account statistical uncertainty, give times of coalescence for human mtDNA of 170,000 and 256,000 years respectively (Templeton

1993, p. 58). But Gingerich (1985) estimated that the divergence between humans and chimps took place 9.2 million years ago. A rate of change based on this date, would greatly increase the time to coalescence for modern mtDNA diversity, making it as much as 554,000 years (Templeton

1993, pp. 58–59). Furthermore, Lovejoy and his coworkers (1993) pointed out that Vigilant et al. (1991) made a mathematical error (they used the wrong transition-transversion), which when corrected gives an age for Eve of at least 1.3 million years (Frayer et al. 1993, p. 40).

It is easy to see that this whole “molecular clock” business is extremely unreliable, because it is based on speculative evolutionary assumptions. It is not at all certain that humans and chimps had a common ancestor of the kind proposed by Darwinian evolutionists. And, as we have seen, even if we assume that chimps and humans did have a common ancestor, the time at which they diverged from that common ancestor is not known with certainty, thus leading to widely varying calibrations of mutation rates and widely varying age estimates for the time to coalescence of modern mitochondrial DNA diversity.

Now let’s consider the conclusions of those who relied on intraspecific calculations—i.e. the rate that mutations accumulate in humans, without any reference to a supposed time of divergence between the chimpanzee and human lines. Templeton pointed out that this methodology did not take into account several “sources of error and uncertainty.” For example, in actual fact, mutations don’t accumulate at some steady deterministic rate. The rate of mutation is a stochastic, or probabilistic, process, with a Poisson distribution. The Poisson distribution, named after the French mathematician S. D. Poisson, is used in calculating the probabilities of occurrence of accidental events (such as spelling mistakes in printed books or mutations in DNA). “In this regard,” says Templeton (1993, p. 57), “it is critical to keep in mind that the entire human species represents only one sample of the coalescent process underlying the current array of mtDNA variations. Hence, even if every human mtDNA were completely sequenced, the rate calibration were known with no error, and the molecular clock functioned exactly like an ideal Poisson process, there would still be considerable ambiguity about the time to coalescence. . . . stochasticity therefore sets an inherent limit to the accuracy of age estimates that can never be completely overcome by larger sample sizes, increased genetic resolution, or more precise rate calibration.”

Stoneking and his coauthors of a 1986 study acknowledged the problem of stochasticity but did not, says Templeton, take adequate steps to account for it. Stoneking and his coauthors estimated that the divergence among the mtDNA samples in the human populations they studied amounted to between 2 and 4 percent. How long did it take for this amount of divergence to accumulate? Stoneking and his coauthors calculated it to be about 200,000 years. But Templeton found that if probabilistic effects are properly taken into account, a figure of 290,000 years is obtained. Templeton (1993, p. 58) then pointed out that “the actual calibration points in their paper indicate a fivefold range (1.8% to 9.3%), and the work of others would indicate an even broader range (1.4% to 9.3%).” These broadened rates give times to coalescence ranging from a minimum of 33,000 years to a maximum of 675,000 years.

African Eve theorists, and others, believe that mitochondrial DNA is not subject to natural selection. This is taken to mean that the only factor influencing the differences in the mitochondrial DNA sequences in different populations is the accumulation of random mutations at some fixed rate. If this is true, then the molecular clock would be running at the same speed in different populations. But if natural selection is influencing the differences in the DNA in different populations, that would mess up the clock. For example, if in one population natural selection were eliminating some of the mutations, this would make that population appear younger than it really is. If such things do happen, there would no longer be any firm basis for attaching absolute numbers of years to a particular degree of variation, nor would there be any firm basis for making relative age judgments among different populations. There is some evidence that natural selection is in fact operating in mitochondrial DNA. For example, Templeton (1993, p. 59) points out that there is a difference in the degree of variation in the protein coding and non coding regions of the mitochondrial DNA in certain populations. If the mutation rate were neutral, this should not be the case. The rate of mutation should be the same in both the coding and noncoding parts of the mitochondrial DNA. Other researchers (Frayer et al. 1993, pp. 39–40) reach similar conclusions: “All molecular clocks require evolutionary neutrality, essential for constancy in the rate of change. But continuing work on mtDNA has documented increasing evidence for selective importance in mtDNA. For example, studies by Fos et al. (1990), MacRae and Anderson (1988), Palca (1990), Wallace (1992), and others have conclusively demonstrated that mtDNA is not neutral, but under strong selection. . . . mtDNA is a poor gear to drive a molecular clock.”

Frayer and his coauthors (1993, p. 40) also state: “Since random mtDNA losses result in pruning off the evidence of many past divergences, the trees constructed to link present populations are altered by unknown and unpredictable factors. Each of these unseen divergences is a genetic change that was not counted when the number of mutations was used to determine how long ago Eve lived. Since these changes are influenced by fluctuations in population size and the exact number of uncounted mutations depends on the particular details of the pruning process, unless the complete population history is known, there is no way to calibrate (and continually recalibrate) the ticking of the clock. Given the fact that each population has a separate demographic history (with respect to random loss events), this factor alone invalidates the use of mtDNA variation to ‘clock’ past events (Thorne and Wolpoff 1992).”

That such things happen is confirmed by the discovery of an anatomically modern human fossil from Lake Mungo, Australia, which was 62,000 years old and had mitochondrial DNA greatly different from any known from modern humans (Bower 2001). This shows that lines of mitochondrial DNA have in fact been lost, thus calling into question the accuracy of the mtDNA molecular clock.

There are other factors affecting the mtDNA diversity in today’s human populations, in various regions of the world, that can throw off the accuracy of the mtDNA clock. One such factor is population size expansion. If the population increases in one region more rapidly than in another, this can cause greater diversity in that population. But the diversity is not an indication that this population is necessarily older than (and hence the source of) other populations in other regions. Also, the diversity observed in various populations can point not to population movements from one place to another, but the movement of genes through a population that is already distributed over a wide area. And this does not exhaust the possible causes of mtDNA diversity found in different human populations. Summarizing the problem, Templeton (1993, p. 59) says: “The diversity in a region does not necessarily reflect the age of the regional population but rather could reflect the age since the last favorable mutation arose in the population, the demographic history of population, size expansion, the extent of gene flow with other populations, and so on.” In general, these factors contribute to underestimation of the age of the human species (Templeton 1993, p. 60). Sophisticated statistical methods, such as “nested cladistic analysis,” allow scientists to discriminate to some degree between the various possible models for the generation of mitochondrial DNA diversity in human populations (as between geographical expansion models and gene flow models). Applying nested cladistic analysis to human mitochondrial DNA variation, Templeton found no evidence of a massive migration out of Africa that replaced all other hominid populations. Templeton (1993, p. 65) said, “The failure of the cladistic geographical analysis to detect an out-of-Africa population expansion cannot be attributed to inadequate sample sizes or to low genetic resolution . . . Hence, the geographical associations of mtDNA are statistically significantly incompatible with the out-of-Africa replacement hypothesis.” Templeton concluded (1993, p. 70 ): “(1) the evidence for the geographical location of the mitochondrial common ancestor is ambiguous, (2) the time at which the mitochondrial common ancestor existed is extremely ambiguous but is likely to be considerably more than 200,000 years.”