The Demise Of Mitochondrial Eve

Brad Harrub, Ph.D. and Bert Thompson, Ph.D.

2003 Apologetics Press, Inc.
All Rights Reserved.
Reproduced by Permission from Apologetics Press

n the first day of 1987, a scientific discovery seized the attention of the
popular press. The original scientific article that caused all the commotion
Mitochondrial DNA and Human Evolutionappeared in the January 1, 1987 issue
of Nature, and was authored by Rebecca Cann, Mark Stoneking, and Allan C. Wilson
(see Cann, et al., 1987). These three scientists announced that they had proven that
all modern human beings can trace their ancestry back to a single woman who lived
200,000 years ago in Africa. This one woman was nicknamed Eve (a.k.a.,
mitochondrial Eve)much to the medias delight. An article in the January 26,
1987 issue of Time magazine bore the headline, Everyones Genealogical Mother:
Biologists Speculate that Eve Lived in Sub-Saharan Africa (Lemonick, 1987). A
year later, that speculation became a major Newsweek production titled, The
Search for Adam and Eve (Tierney, et al., 1988). The provocative front cover
presented a snake, tree, and a nude African couple in a Garden of Eden type
setting. The biblical-story imagery was reinforced by showing the woman offering an
apple to the man.
A word of explanation is in order. For decades, evolutionists had been trying to
determine the specific geographical origin of humanswhether we all came from one
specific locale, or whether there were many small pockets of people placed around the
globe. When they set out to determine the specific geographical origin of humans, a
curious piece of data came to light. As they considered various human populations,
Africans seemed to show much more genetic variation than non-Africans (i.e., Asians,
Europeans, Native Americans, Pacific Islanders, et al.). According to molecular
biologists, this increased variability is the result of African populations being older,
thus, having had more time to accumulate mutations and diverge from one
another. This assumption led some researchers to postulate that Africa was the
ancient cradle of civilization from which all of humanity had emerged.
The genetic material (DNA) in a cells nucleus controls the functions of the cell,
bringing in nutrients from the body and making hormones, proteins, and other
chemicals. Outside the nucleus is an area known as the cytoplasmic matrix (generally
referred to simply as the cytoplasm), which contains, among other things, tiny beanshaped organelles known as mitochondria. These often are described as the energy
factories of the cell.

Mitochondria contain their own DNA, which they use to make certain proteins; the
DNA in the nucleus oversees production of the rest of the proteins necessary for life
and its functions. However, mitochondrial DNA (mtDNA) was thought to be special
for two reasons. First, it is short and relatively simple in comparison to the DNA
found within the nucleus, containing only thirty-seven genes instead of the 70,000+
genes located in the nuclear DNA. This makes it relatively easy to analyze. Second,
unlike nuclear DNA, which each person inherits in a jumbled form from both parents,
mitochondrial DNA was thought to be passed on only through the mothers line (more
about this later). Working from the assumption that mtDNA is passed to the progeny
only by the mother, Dr. Cann and her coworkers believed that each new cell should
contain copies of only the eggs mitochondria. In trying to draw the human family
tree, therefore, researchers took a special interest in these minute strands of genetic
code. What they really were interested in, of course, was the variations in
mitochondrial DNA from one group of people to another.
Although our mtDNA should be, in theory at least, the same as our mothers mtDNA,
small changes (or mutations) in the genetic code can, and do, arise. On rare
occasions, mutations are serious enough to do harm. More frequently, however, the
mutations have no effect on the proper functioning of either the DNA or the
mitochondria. In such cases, the mutational changes will be preserved and carried on
to succeeding generations.
Theoretically, if scientists could look farther and farther into the past, they would find
that the number of women who contributed the modern varieties of mitochondrial
DNA gets less and less until, finally, we arrive at one original mother. She, then,
would be the only woman out of all the women living in her day to have a daughter in
every generation till the present. Coming forward in time, we would see that the
mtDNA varieties found within her female contemporaries were gradually eliminated
as their daughters did not have children, had only sons, or had daughters who did not
have daughters. This does not mean, of course, that we wouldlook like this putative
ancestral mother; rather, it means only that we would have gotten our mitochondrial
DNA from her.
To find this woman, researchers compared the different varieties of mtDNA in the
human family. Since mtDNA occurs in fairly small quantities, and since the
researchers wanted as large a sample as possible from each person, they decided to
use human placentas as their source of the mtDNA. So, Rebecca Cann and her
colleagues selected 145 pregnant women and two cell lines representing the five
major geographic regions: 20 Africans, 34 Asians, 46 Caucasians, 21 aboriginal
Australians, and 26 aboriginal New Guineans (Cann, et al., 1987, 325:32). All
placentas from the first three groups came from babies born in American
hospitals. Only two of the 20 Africans were born in Africa.

After analyzing a portion of the mtDNA in the cells of each placenta, they found that
the differences grouped the samples by region. In other words, Asians were more
like each other than they were like Europeans, people from New Guinea were more
like each other than they were like people from Australia, and so on.
Next, they saw two major branches from in their computer-generated tree of recent
human evolution. Seven African individuals formed one distinct branch, which
started lower on the trunk than the other four. This was because the differences
among these individuals were much greater than the differences between other
individuals and other groups. More differences mean more mutations, and hence
more time to accumulate those changes. If the Africans have more differences, then
their lineage must be older than all the others. The second major branch bore the nonAfrican groups and, significantly, a scattering of the remaining thirteen Africans in the
sample. To the researchers, the presence of Africans among non-Africans meant an
African common ancestor for the non-African branches, which, likewise, meant an
African common ancestor for both branches. The nickname Eve stuck to this
hypothetical common ancestral mother, and later, then, fired the medias imagination.
Having concluded that the African group was the oldest, Dr. Cann and her colleagues
wanted to find out justhow old the group might be. To do this, they used what is
known as a molecular clock that, in this case, was based on mutations in the
mtDNA. The rate at which the clock ticked was determined from the accumulation of
changes over a given period of time. As we note below in our discussion of the socalled molecular clock, if the assumption was made that there was one mutation every
1,000 years, and if scientists found a difference of 10 mutations between us and our
ancient hypothetical ancestor, they then could infer that that ancestor lived 10,000
years ago.
The researchers looked in two places for their figures. First, they compared mtDNA
from humans with that from chimpanzees, and then used paleontology and additional
molecular data to determine the age of the supposed common ancestor. This (and
similar calculations on other species) revealed a mutation rate in the range of 2% to
4% per million years. Second, they compared the groups in their study that were
close geographically, and took the age of the common ancestor from estimated times
of settlement as indicated by anthropology and archaeology. Again, 2% to 4% every
million years seemed reasonable to them.
Since the common mitochondrial ancestor diverged from all others by 0.57%, she
must have lived sometime between approximately 140,000 (0.57 4 1,000,000) and
290,000 (0.57 2 1,000,000) years ago. The figure of 200,000 was chosen as a
suitable round number.

The results obtained from analysis of mitochondrial DNA eventually led to what is
known in evolutionary circles as the Out of Africa theory. This is the idea that the
descendants of mitochondrial Eve were the only ones to colonize Africa and the rest
of the world, supplanting all other hominid populations in the process. Many (though
not all) evolutionists claim that such an interpretation is in accord with archaeological,
paleontological, and other genetic data (see Stringer and Andrews, 1988; for an
opposing viewpoint, see the written debate in the April 1992 issue of Scientific
American).
While many evolutionists have accepted the mitochondrial DNA tree, they differ
widely in their views regarding both the source of the nuclear DNA and the
humanity of Eve. Some believe that Eve contributedall the nuclear DNA, in
addition to the mitochondrial DNA. Some believe she was an archaic Homo
sapiens, while others believe she was fully human. The exact interpretation is hotly
debated because mitochondrial DNA is something of a passenger in the genetic
processes that lead to the formation of new species: it therefore neither contributes to
the formation of a new species nor reveals anything about what actually happened
(Lewin, 1987, 238:24).

The Demise of Mitochondrial Eve

Things change rapidly in science. What is popular one day, is not the next. Theories
come, and theories go. And so it is with mitochondrial Eve. She once was in vogue
as the woman of the moment, so to speak. Now, she has become virtually the
crazy aunt in the attic that no one wants to admit even exists.
But it was not forbidden fruit that caused her demise this time around. The passing
of one of evolutions most familiar icons is due to new scientific facts that have
surfaced since her introduction in 1987. If humans received mitochondrial DNA only
from their mothers, then researchers could map a family tree using that
information. And, if the mutations affecting mtDNA had indeed occurred at constant
rates, then the mtDNA could serve as a molecular clock for timing evolutionary
events and reconstructing the evolutionary history of extant species. It is the ifs in
these two sentences that are the problem.
Mitochondrial Eve is alleged to have lived in Africa at the beginning of the Upper
Pleistocene period (between 100,000 and 200,000 years ago). She has been described
as the most-recent common ancestor of all humans on Earth today, with respect to
matrilineal descent. The validity of these assertions, however, is dependent upon two
critically important assumptions: (1) that mtDNA is, in fact, derived exclusively from
the mother; and (2) that the mutation rates associated with mtDNA have remained

constant over time. However, we now know that both of these assumptions are
wrong!
First, let us examine the assumption that mtDNA is derived solely from the
mother. In response to a paper that appeared in Science in 1999, anthropologist Henry
Harpending of the University of Utah lamented: There is a cottage industry of
making gene trees in anthropology and then interpreting them. This paper will
invalidate most of that (as quoted in Strauss, 1999, 286:2436). Just as women
thought they were getting their fair shake in science, the tables turned. As one study
noted:
Women have struggled to gain equality in society, but biologists have long thought
that females wield absolute power in a sphere far from the public eye: in the
mitochondria, cellular organelles whose DNA is thought to pass intact from mother to
child with no paternal influence. On page 2524 however, a study by Philip Awadalla
of the University of Edinburgh and Adam Eyre-Walker and John Maynard Smith of
the University of Sussex in Brighton, U.K. finds signs of mixing between maternal
and paternal mitochondrial DNA (mtDNA) in humans and chimpanzees. Because
biologists have used mtDNA as a tool to trace human ancestry and relationships,
the finding has implications for everything from the identification of bodies to
the existence of a mitochondrial Eve 200,000 years ago (Strauss, 286:2436,
emphasis added).
One year later, researchers made this startling admission:
Mitochondrial DNA (mtDNA) is generally assumed to be inherited exclusively from
the mother. Several recent papers, however, have suggested that elements of
mtDNA may sometimes be inherited from the father. This hypothesis is based on
evidence that mtDNA may undergo recombination. If this does occur, maternal
mtDNA in the egg must cross over with homologous sequences in a different DNA
molecule; paternal mtDNA seems the most likely candidate. If mtDNA can
recombine, irrespective of the mechanism, there are important implications for
mtDNA evolution and for phylogenetic studies that use mtDNA (Morris and
Mightowlers, 2000, 355:1290, emphasis added).
In 2002, a study was conducted that concluded:
Nevertheless, even a single validated example of paternal mtDNA transmission
suggests that the interpretation of inheritance patterns in other kindreds thought to
have mitochondrial disease should not be based on the dogmatic assumption of
absolute maternal inheritance of mtDNA. The unusual case described by Schwartz

and Vissing is more than a mere curiosity (Williams, 2002, 347:611, emphasis
added).
And now we know that these are more than small fractional amounts of mtDNA
coming from fathers. The August 2002 issue of the New England Journal of
Medicine contained the results of one study, which concluded:
Mammalian mitochondrial DNA (mtDNA) is thought to be strictly maternally
inherited. Very small amounts of paternally inherited mtDNA have been detected
by the polymerase chain reaction (PCR) in mice after several generations of
interspecific backcrosses. We report the case of a 28-year-old man with
mitochondrial myopathy due to a novel 2-bp mtDNA deletion. We determined that
the mtDNA harboring the mutation was paternal in origin and accounted for 90
percent of the patients muscle mtDNA (Schwartz and Vissing, 2002, 347:576,
emphasis added).
Ninety percent! And all this time, evolutionists have been selectively shaping our
family tree using what was alleged to be only maternal mtDNA!
As scientists have begun to comprehend the fact, and significance, of the death of
mitochondrial Eve, many have found themselves searching for alternatives that can
help them maintain their current beliefs regarding human origins. But this
recombination ability in mtDNA makes the entire discussion a moot point. As Strauss
noted:
Such recombination could be a blow for researchers who have used mtDNA to trace
human evolutionary history and migrations. They have assumed that the mtDNA
descends only through the mother, so they could draw a single evolutionary tree of
maternal descentall the way back to an African mitochondrial Eve, for
example. But with recombination there is no single tree, notes
Harpending. Instead, different parts of the molecule have different
histories. Thus,theres not one woman to whom we can trace our
mitochondria, says Eyre-Walker (1999, 286:2436, emphasis added).
Our thoughts on the matter exactly.

The Molecular ClockDating Mitochondrial Ancestors

Second, let us examine the assumption that the mutations affecting mtDNA did indeed
occur at constant rates. The researchers who made the initial announcement about
Eve not only gave a location for this amazing female, but also proposed the time
period during which she was supposed to have lived. However, in order for the

mtDNA theory to be of any practical use, those scientists had to assume that random
mutations in the DNA occurred at documented, steady rates. For example, if they
speculated that there was one mutation every 1,000 years, and they found a difference
of 10 mutations between us and our ancient hypothetical ancestor, they then could
infer that that ancestor lived 10,000 years ago. Scientistswho used this concept to
determine the age of mitochondrial Everefer to this proposed mutation rate as a
molecular clock. One group of researchers described the process as follows:
The hypothesis of the molecular clock of evolution emerged from early observations
that the number of amino acid replacements in a given protein appeared to change
linearly with time. Indeed, if proteins (and genes) evolve at constant rates they could
serve as molecular clocks for timing evolutionary events and reconstructing the
evolutionary history of extant species (Rodriguez-Trelles, et al., 2001, 98:11405,
parenthetical item in orig.).
It sounds good in theory, but the actual facts tell an entirely different story. As these
same researchers went on to admit:
The neutrality theory predicts that the rate of neutral molecular evolution is constant
over time, and thus that there is a molecular clock for timing evolutionary events. It
has been observed thatthe variance of the rate of evolution is generally larger than
expected according to the neutrality theory, which has raised the question of how
reliable the molecular clock is or, indeed, whether there is a molecular clock at
all. The observations are inconsistent with the predictions made by various
subsidiary hypotheses proposed to account for the overdispersion of the molecular
clock (98:11405, emphasis added).
Another study that was published in 2002 pointed out a built-in, natural bias for older
ages that result from use of the molecular clock. The researchers who carried out the
study noted:
There is presently a conflict between fossil- and molecular-based evolutionary time
scales. Molecular approaches for dating the branches of the tree of life frequently
lead to substantially deeper times of divergence than those inferred by
paleontologists. Here we show that molecular time estimates suffer from a
methodological handicap, namely that they are asymmetrically bounded random
variables, constrained by a nonelastic boundary at the lower end, but not at the higher
end of the distribution. This introduces a bias toward an overestimation of
time since divergence, which becomes greater as the length of the molecular sequence
and the rate of evolution decrease. Despite the booming amount of sequence
information, molecular timing of evolutionary events has continued to yield
conspicuously deeper dates than indicated by the stratigraphic data. Increasingly, the

discrepancies between molecular and paleontological estimates are ascribed to

deficiencies of the fossil record, while sequence-based time tables gain credit. Yet,
we have identified a fundamental flaw of molecular dating methods, which leads
to dates that are systematically biased towards substantial overestimation of
evolutionary times (Rodriguez-Trelles, et al., 2002, 98:8112,8114, emphasis added).
Until approximately 1997, we did not have good empirical measures of mutation rates
in humans. However, that situation greatly improved when geneticists were able to
analyze DNA from individuals with well-established family trees going back several
generations. One study found that mutation rates in mitochondrial DNA
were eighteen times higher than previous estimates (see Parsons, et al., 1997).
Science writer Ann Gibbons authored an article for the January 2, 1998 issue of
Science titled Calibrating the Mitochondrial Clock, the subheading of which read as
follows: Mitochondrial DNA appears to mutate much faster than expected,
prompting new DNA forensics procedures and raising troubling questions about the
dating of evolutionary events. In that article, she discussed the new data which
showed that the mutation rates used to obtain mitochondrial Eves age no longer could
be considered valid, and concluded:
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 peoplelived 100,000 to
200,000 years ago in Africa. Using the new clock, she would be a mere 6,000 years
old (1998: 279:29, emphasis added).
Gibbons quickly went on to note, of course, that no one thinks thats the case,
(279:29). She concluded her article by discussing the fact that many test results are
(to use her exact word) inconclusive. She then noted: And, for now, so are some of
the evolutionary results gained by using the mtDNA clock (279:29).
We now know that the two key assumptions behind the data used to establish the
existence of mitochondrial Eve are not just flawed, but wrong. The assumption
that mitochondrial DNA is passed down only by the mother is completely incorrect (it
also can be passed on by the father). And, the mutation rates used so calibrate the socalled molecular clock are now known to have been in error. (To use the words of
Rodriguez-Trelles and his coworkers, the method contains a fundamental flaw.)
Philip Awadalla and his coworkers noted in Science: Many inferences about the
pattern and tempo of human evolution and mtDNA evolution have been based on the
assumption of clonal inheritance. There inferences will now have to be reconsidered
(1999, 286:2525). However, rather than merely reconsidering their theory and

attempting to revamp it accordingly, evolutionists need to admit, honestly and

forthrightly, that mitochondrial Eve, as it turns out, has existed only in their minds,
not in the facts of the real world. Science works by analyzing the data and forming
hypotheses based on those data. Science is not supposed to massage the data until
they fit a certain preconceived hypothesis. All of the conclusions that have been
drawn from research on mitochondrial Eve via the molecular clock must now be
discarded as unreliable. A funeral and interment are in order for mitochondrial Eve.

References
Awadalla Philip, Adam Eyre-Walker, and John Maynard Smith (1999), Linkage Disequilibrium and
Recombination in Hominid Mitochondrial DNA, Science, 286:2524-2525, December 24.
Cann, Rebecca L., Mark Stoneking, and Allan C. Wilson (1987), Mitochondrial DNA and Human
Evolution,Nature, 325:31-36, January 1.
Gibbons, Ann (1998), Calibrating the Mitochondrial Clock, Science, 279:28-29, January 2.
Lemonick, Michael D. (1987), Everyones Genealogical Mother, Time, p. 66, January 26.
Lewin, Roger (1987), The Unmasking of Mitochondrial Eve, Science, 238:24-26, October 2.
Morris, Andrew A. M., and Robert N. Lightowlers (2000), Can Paternal mtDNA be Inherited?, The
Lancet,355:1290-1291, April 15.
Parsons, Thomas J., et al. (1997), A High Observed Substitution Rate in the Human Mitochondrial DNA Control
Region, Nature Genetics, 15:363.
Rodriguez-Trelles, Francisco, Rosa Tarrio, and Francisco J. Ayala (2001), Erratic Overdispersion of Three
molecular Clocks: GPDH, SOD, and XDH, Proceedings of the National Academy of Sciences, 98:11405-11410,
September 25.
Rodriguez-Trelles, Francisco, Rosa Tarrio, and Francisco J. Ayala (2002), A Methodological Bias Toward
Overestimation of Molecular Evolutionary Time Scales, Proceedings of the National Academy of
Sciences,99:8112-8115, June 11.
Schwartz, Marianne and John Vissing (2002), Paternal Inheritance of Mitochondrial DNA, New England Journal
of Medicine, 347:576-580, August 22.
Strauss, Evelyn (1999), mtDNA Shows Signs of Paternal Influence, Science, 286:2436, December 24.
Stringer, C.B. and P. Andrews (1988), Genetic and Fossil Evidence for the Origin of Modern
Humans, Science,239:1263-1268, March 11.
Tierney, John, Lynda Wright, and Karen Springen (1988), The Search for Adam and Eve, Newsweek, pp. 46-52,
January 11.

Williams, R. Sanders (2002), Another Surprise from the Mitochondrial Genome, New England Journal of
Medicine, 347:609-611, August 22.

Brad Harrub is a graduate of Kentucky Wesleyan College, where he earned a B.S.

degree in biology. He also earned a Ph.D. in neurobiology and anatomy from the
College of Medicine at the University of Tennessee in Memphis. He is a member of
the Society for Neuroscience, and was listed in the 2001-2002 edition of Whos Who
Among Scientists and Researchers. He was an invited speaker to the 2003
International Conference on Creationism. He currently serves as the Director of
Scientific Information at Apologetics Press, and as associate editor of Reason &
Revelation. [RETURN TO TEXT]
Bert Thompson is a graduate of Abilene Christian University, where he earned a B.S.
degree in biology. He also is a graduate of Texas A&M University, where he earned
both M.S. and Ph.D. degrees in microbiology. Dr. Thompson is a former professor in
the College of Veterinary Medicine at Texas A&M, where he taught for several
years. While at Texas A&M, he served as Coordinator of the Cooperative Education
Program in Biomedical Science. Currently, Dr. Thompson is the Executive Director
of Apologetics Press and editor of Reason & Revelation. [RETURN TO TEXT]