“It has been an interesting decade in Human evolutionary genetics. We have gone from hope to confidence and from confidence to despair. A series of recent studies, two of which appear in this and a recent issue of PNAS, gives new grounds for optimism.” (Rogers 2001, p. 779) 

Rogers then goes on to say:

“Various authors argued early on that the human population must have passed through a bottleneck—a period of small population size—sometime during the late Pleistocene.
    “The next few years saw improvements both in the quality of mitochondrial data available and in the statistical methods available for dealing with those data. By the mid-1990s, we were able not only to reject the hypothesis of stationary population size but also to place an upper bound on the preexpansion population size, a lower bound on the postexpansion size, and both bounds on the time of the expansion. The evidence indicated that, sometime between 30,000 and 130,000 years ago, our ancestors expanded to fill the globe from an initial population of roughly 10,000 breeding individuals. Then just as this story seemed to be gaining momentum, the bottom fell out from under it.
    “In the late 1990s, as DNA sequencing got cheaper, people began assembling large datasets from the human nuclear genome. The trouble was that each genetic locus seemed to tell a different story. The mitochondrial story received support from data from the Y chromosome and from extensive sets of short tandem repeat (STR) loci distributed throughout the genome. But other genes seemed to imply a long history of constant population size, and still others suggested the action of balancing selection or of geographic population structure. How can a single species have genes with such disparate histories? Presumably because natural selection has affected different loci in different ways. And if the pattern we see is telling us mainly about the history of selection, then it is unlikely ever to tell us much about the history of population size.
    “This was not, of course, the first time that anyone had suggested a role for natural selection in the evolution of human mitochondria. The problem is that selection and population growth can be hard to tell apart. A favorable mutation may sweep through the population under the influence of natural selection. If we focus on the carriers of this favorable mutation, the process looks just like population growth: the number of carriers is small at first, then increases, and then levels off. For practical purposes, the two processes have identical effects on genetic variation. There is still no clean way of distinguishing them except by comparing DNA from different genetic loci. Population growth should affect every locus in the same way, whereas selection should affect different loci in different ways. The disparate results that we see from different loci’ suggest that human genetic variation is influenced strongly by natural selection. If this view is correct, genetics may have little to tell us about population history.
    “This view, however may be unnecessarily gloomy. There are two aspects of the emerging pattern that are puzzling under the view that it is all a product of natural selection: First, the genetic loci that show the signature of a selective sweep are precisely the ones that, on a priori grounds, seem most likely to be neutral—the sweeps all seem to have occurred in DNA that does not code for protein. It is coding only regions that seem clearly consistent with selective neutrality and constant population size. This pattern is not as implausible as it may sound: Because of linkage, the signature of a selective sweep may extend from the coding region on which selection has acted into the noncoding regions that surround it. Nonetheless, it is surprising that the effects of selection should be most clearly visible in those portions of the genome that do not code for protein. It is also hard to imagine that selection at linked loci was responsible for the pattern seen in the STRs, because these are distributed widely throughout the genome.” (Rogers, 2001, p. 779)

The article Rogers refers to says that the coalescence time for the gene system they studied is quite long ago. The gene system was the ms205 minisatellite. They say of the variation seen among Basques, Japanese, British and Africans:

“The coalescent adds a time dimension to the phylogenetic network (tree); thus, assuming neutrality, panmixia, and constancy in population size, the depth of the tree (the time to the most recent common ancestor) is estimated as 0.72 coalescent units, or about 1.04 million years (…).” (Alonso and Armour 2001, p. 868) 

One million years ago, the only hominid on earth was H. erectus. We have his genes, which means we interbred and are descended from him. Indeed, even more important is the FACT now, that there were separate lineages over that time span which are found in modern humans. We were not, as many Christian apologists contend, the sudden creation de novo less than 120,000 years ago.

Indeed, there is evidence that non-Africans have a genetic history going back at least 600,000 years—much longer ago than the Out of Africa view would allow. Consider a paper published last year which said:

"Human DNA sequence variation data are useful for studying the origin, evolution, and demographic history of modern humans and the mechanisms of maintenance of genetic variability in human populations, and for detecting linkage association of disease. Here, we report worldwide variation data from a 10-kilobase noncoding autosomal region. We identified 75 variant sites in 64 humans (128 sequences) and 463 variant sites among the human, chimpanzee, and orangutan sequences. Statistical tests suggested that the region is selectively neutral. The average nucleotide diversity ( p [pi]) across the region was 0.088% among all of the human sequences obtained, 0.085% among African sequences, and 0.082% among non-African sequences, supporting the view of a low nucleotide diversity (0.1%) in humans. The comparable p [pi] value in non-Africans to that in Africans indicates no severe bottleneck during the evolution of modern non-Africans; however, the possibility of a mild bottleneck cannot be excluded because non-Africans showed considerably fewer variants than Africans. The present and two previous large data sets all show a strong excess of low frequency variants in comparison to that expected from an equilibrium population, indicating a relatively recent population expansion. The mutation rate was estimated to be

1.15 × 10^9 per nucleotide per year. Estimates of the long-term effective population size Ne by various statistical methods were similar to those in other studies. The age of the most recent common ancestor was estimated to be 1.29 million years ago among all of the sequences obtained and 634,000 years ago among the non-African sequences, providing the first evidence from a noncoding autosomal region for ancient human histories, even among non-Africans. (Zhao et al, 2000, p. 11354-11358)

http://www.pnas.org/cgi/content/abstract/97/21/11354

This article gives the time to the most recent common ancestors in Table 5 (reproduced below). Note that the 95% confidence interval on both sides of the mean are ALL PRIOR TO THE TIME THAT ANATOMICALLY MODERN MAN WAS ON EARTH. This data demonstrates the high likelihood of independent genetic lineages stretching back long before the Out of Africa view would allow. And it is the Out of Africa view that many Christian apologists like Ross, Newman, Weister and Wilcox have incorporated into their apologetical schemes. And they are wrong. Here is table 5 — (Ne is the effective breeding population)

“Table 5. The age (T, 10^3 years) of the MRCA of human sequences

Sequences      Ne        Tmode          Tmean        95% Interval

All samples    10,000   1,288           1,356         712~2,112
               12,000   1,104           1,203         605~1,949
               15,000     924           1,034         504~1,728
Africans        6,000   1,204           1,256         694~1,882
                8,000   1,158           1,203         646~1,843
               10,000   1,032           1,105         576~1,752
Non-Africans    6,000     747             806         384~1,330
                7,000     678             756         353~1,277
                8,000     634             713         333~1,229

The average mutation rate (2.28 × 10⁴ per sequence per generation) was used. “ source  Zhao, et al, 2000, p. 11354-11358)

Note above that the upper limits of the 95% confidence interval incorporates the earliest H. erecti.

The paper says:

“The TMRCA [The Most Recent Common Ancestor--grm] of Africans was about 0.4 Myr older than that of non-Africans (1,032,000 versus 634,000) (Table 5). However, the TMRCA of non-Africans from our data are older than the fossils for modern humans (see ref. 3) and is also older than those of non-Africans estimated from PDHA1, the ß[beta]-globin gene, and mitochondrial DNA (1, 3, 8, 27). It indicates that even non-Africans have ancient genetic histories, at least at some regions. Of course, a substantial or large part of the genetic diversity in non-Africans at the region we studied might be due to migration from Africa. However, the genealogical depths at this region and the ß[beta]-globin gene region (1) in non-Africans and the long separation time between African and non-African sequences at the PDHA1 region (3) suggest that the transformation from archaic to modern humans might have occurred in a subdivided population. This does not contradict the assumption of the African origin of modern humans and also does not imply independent evolution of modern characteristics in separate populations as implied by the multiregional model, because the transformation could have occurred through gene flow and natural selection (3). However, it does suggest that the origin and evolution of modern humans is more complex than depicted by the simple out of Africa model (1, 3), especially the assumption of a complete replacement of all indigenous populations outside of Africa by the African stock.  Zhao, et al, 2000, p. 11354-11358)

A note that unfortunately must be said in this day of racial sensitivity. One can not use this data to say that the races were genetically distinct. We aren't. The data accumulated by Alonso and Armour studied the DNA of 50 people, meaning that here were 100 individual strands of nuclear DNA sequenced. The most popular allele (48) was shared by 13 Basques, 11 Japanese, 14 Brits, 8 Kenyans and 2 Pygmies (see p. 865 of Alonso and Armour). Among other ethnically shared lineages are one each for the Basque and Japanese; the Basques, Brits and Kenyans; the Basques and the Kenyans; the Basques Japanese, Kenyans and Pygmies; and the Pygmies and Kenyans. That being said, each of the populations sampled contained several unique sequences. The pygmies had 8 unique lineages; the Japanese, 3; the Brits, 4; the Basques, 1; and the Kenyans, 4. Clearly, while the unique genetic lineages indicate a long time span back to the most recent common ancestor, the lineages shared by various populations are widely enough shared to know that we humans are clearly one interbreeding population and have been for the past 1 million years.

A recent study of several nuclear gene localities have shown that the polymorphism observed among modern humans is such that the time to the most recent common ancestor for these genetic systems is much longer ago than merely 100,000 years, meaning that there must have been considerable genetic input to modern humans from hominids who were not themselves modern.  While the authors argue for an Out of Africa viewpoint, to me it really doesn't matter where the non-modern hominids lived, be it in Africa or Eurasia.  The data clearly shows that we have lots of diversity in our nuclear genome which clearly indicates that there is genetic input from non-modern hominids. Here is the data:

Gene                 TMRCA 
                                                          (Myr)

Plp                  1.28
Hprt                 0.53
Gk                   0.41
Pdha1                1.05
dys44                1.35
Zfx                  0.93
Xq13.3               0.56
Ace                  1.11
Lpl                  0.91
Beta-globin          1.36
Mclr                 0.71

(Takahata et al, 2001, p. 178)

Several other studies present the same problem for apologetics. Huang et al (1998) have analyzed the ZDF gene and estimated that this gene has been evolving in human populations for approximately 306,000 years with a 95% confidence interval of 162,000 to 975,000 years. Kaessmann, Wiebe and Paabo (1999) analyzed a non-coding region of the human X chromosome and determined that the region requires 675,000 years for coalescence to occur with a 95% confidence interval from 525,000-975,000 years.

Ayala et al,(1994, p. 6793) describes two different indications of ancient genetic input to modern humanity. They write:

	"Two recent molecular studies favor some degree of regional
continuity over complete African replacement.  The first study
concerns polymorphisms in the genes for green and red visual
pigments.   Color vision in animals is mediated by light-
sensitive pigments consisting of a chromophore covalently linked
to  a protein moiety (opsin).  The genes coding for opsins in the
red and green pigments are located on the long arm of chromosome
X, whereas the one for the blue pigment is on chromosome 7.  In
humans, the red and green opsin genes are highly homologous and
consist of six exons.  The duplication of these two genes has
been dated to 30-40 Myr B. P., shortly after the divergence of
the Old-and New-World primates.
	"The green and red opsin genes have now been sequenced in a
sample of 16 chimpanzees, 7 gorillas, and 4 orangutans, yielding
a total of 14 biallelic polymorphic sites (all in either exon 2
or 4).  Six of these polymorphisms are also found in humans,
which indicates that they are of ancient origin predating the
divergence of humans and apes.
	"One of these trans-specific polymorphisms involves the
amino acid residue 65, which in the green opsin gene of
orangutans and humans can be either threonine or isoleucine.  The
relevant results is that this polymorphism has been found in
Caucasians (the Ile-65 allele in 4 out of 120 individuals) but
not in a sample of 56 individuals of African ancestry and 49 of
Asian ancestry.  It is possible that the Ile-65 allele may
eventually be found in African populations.  It is also possible
that it may have been lost from African and Asian populations in
recent times, that is, after the emergence of modern humans.  But
since this polymorphism is millions of years old, loss of the
allele over the long period since the migration of H. erectus out
of Africa is more likely than a recent loss.  In the replacement
model, migrants from Africa colonize other parts of the world and
replace any preexisting populations within the last 200,000
years.  It would seem unlikely that the polymorphism would have
been passed on to Caucasian populations and become thereafter
lost in the larger African population.  Thus, the opsin
polymorphism argues (mildly) against a complete replacement of
the Caucasian gene pool by African populations.
	"The second example concerns an autosomal recessive disorder
in lipid metabolism due to the absence of apolipoprotein C-II,
the physiological activator of lipoprotein lipase, a key enzyme
in very low density lipoprotein metabolism.  Two deleterious
alleles, one from a Venezuelian Caucasian family and one from a
Japanese family, share a frameshift mutation suggesting common
ancestry.  These two mutants diverged from the normal allele at
least 2 Myr B. P.  The persistence of two defective alleles over
such a long time is a puzzle, perhaps a consequence of small
heterozygote advantage.  But this persistence (i) argues against
extremely small population bottlenecks throughout the Pleistocene
human history, and (ii) favors the conclusion that European and
Asian H. erectus  have contributed to the gene pool of modern H.
sapiens." ~ Francisco J. Ayala, Ananias Escalante, Colm O'hUigin
and Jan Klein, "Molecular Genetics of Speciation and Human
Origins," Proc. Natl. Acad. Sci, USA, 91:6787-6794, July 1994, p.
6793.

And finally, Harris and Hey studied  the PDHA1 gene on the X chromosome and concluded that it would take 1.86 million years for the variation we see in this gene to accumulate in the human population. Clearly, this is evidence that the common apologetical scheme is flawed, false and flimsy. They say:

"The base of the PDHA1 gene tree is relatively ancient, with an estimated age of  1.86 million years, a late Pliocene time associated with early species of Homo." (Harris and Hey, 1999)

These data fits well with other recent studies, such as the fact that anatomically modern Mungo Man has an archaic form of mtDNA requiring breeding with the archaics. [Proc. Natl. Acad. Sci. USA 98(2001):537-542]

These data fits well with the recent work by Wolpoff et al in which they showed that early European anatomically modern people shared more traits with Neanderthal than with the supposed African invaders (Wolpoff, et al, 2001, p. 293-297)

These data fit well with the discovery of a putative (but contested) Neanderthal-human hybrid child at Lagar Velho (Duarte et al, 2000; Trinkaus and Duarte, 2000, p. 102). See http://www.glenn.morton.btinternet.co.uk/hybrid.htm

These data fit well with the recent descriptions of SM3, a fossil erectus skull from Java, that displays both modern human and Homo erectus features. A recent article says:

"But SM3 seems to straddle the divide, appearing even at a glance to combine features of both H. erectus and H. sapiens. It fell to Eric Delson, an anthropologist affiliated with the museum, to classify her. He decided to try a new technique that essentially creates a 3D computer representation of an object, which can then be analysed using statistical methods.

Halfway human

First Delson recreated the shape of SM3's skull using coordinates from some 200 points on its surface. He did the same for 23 other specimens--11 H. erectus, 10 modern H. sapiens, and 2 archaic H. sapiens. With this information, his computer program arranged the specimens according to their similarity, placing SM3 just about squarely between the erectus and modern humans--while even the archaic H. sapiens fell in among the erectus specimens. " Christine Soares, "Talking Heads", New Scientist, April 14, 2001, p. 27-28 

This data fits well with the data of Wallace et al in which the mutation that may cause Alzheimer's disease was inserted into the human genome 770,000 years ago.(Wallace, et al., 1997, p. 14900) 

In my opinion, Christians are tying themselves to a sinking ship by placing such apologetical emphasis on the supposed recent (<120,000 year) creation of man. There are two reasons for this belief. First, the new genetic evidence is changing the landscape. It is changing the viability of the most popular Christian view of human origins and it is providing a means of dating the very creation of man which is also inconsistent with the other popular view, the YEC view (already falsified many times over but what is one more falsification between friends?). Secondly, Christians have tied themselves with the epistemologically weakest view of human origins. It has long been known that if the time to the most recent common mitochondrial ancestor was around 200,000 years, then the time to the most recent nuclear genomic ancestor would be 4-9 times that long. Christian apologists have long ignored the warning about this that I have been giving for the past several years (http://www.asa3.org/archive/ASA/199806/0083.html). Templeton states:

"If the coalescence time of mtDNA is truly about 200,000 years ago, then the expected coalescence time of almost all nuclear genes are going to be commonly greater than one or two million years. This places the expected coalescence times of much nuclear DNA into a period in which all humans probably lived in Africa. Hence, studies on nuclear DNA are expected to have an African root under all hypotheses of modern human evolution." (Templeton, 1997, p. 353) 

In order for the recent origin of man, as envisioned by Christian apologists, to be true, ALL GENETIC SYSTEMS MUST BE LESS THAN THAT AGE. That means that no genes can have coalescence times of greater than 200,000 years. This clearly is falsified by the new data (and we should have seen it coming). Christian apologists have tied themselves to the mitochondrial data hoping that it would win the day for them. Unfortunately, to falsify this position required only one genetic system be found with a coalescence time longer than 200,000 years, which we now have. Obviously the concept of a recent origin of man is less defendable than the ancient origin of man.

One further implication of this data must be noted. Either the Bible is totally false in what it says about Adam or one must do what I am doing--extend the Biblical chronology. To claim, in the face of this evidence, that modern man was a de novo creation within the past 200,000 years is to do the same thing the young-earth creationists do--ignore the data and believe what we want to believe regardless of the observational data.

The above data absolutely falsifies the idea that humanity had no genetic relationship to Homo erectus and the more ancient primates. Like it or not, we Christians need to deal with this data.

References

Alonso, Santos and John A. L. Armour, 2001, “A Highly Variable Segment of Human Subterminal 16p Reveals a History of Population Growth for Modern Humans Outside Africa,” Proc. Natl. Acad. Sci., USA, 98:3:864-869, p. 868.

Ayala, Francisco J., Ananias Escalante, Colm O'hUigin, and Jan Klein, "Molecular Genetics of Speciation and Human Origins," Proc. Natl. Acad. Sciences, USA, Vo. 91:6787-6794.

Duarte Cidália, et al, "The early Upper Paleolithic human skeleton from the Abrigo do Lagar Velho (Portugal) and Modern Human Emergence in Iberia " Proc. Natl. Acad. Sciences, USA, Vol. 96, Issue 13, 7604-7609; 

Harding, Rosalind M. et al, 1997, "Archaic African and Asian Lineages in the Genetic Ancestry of Modern Humans," Am. Journal of Human Genetics, 60:772-789.

Harding, Rosalind M., et al, 2000. “Evidence for Variable Selective Pressures at MC1R,” Am. J. Human Genetics, 66(2000):1351-1361.

Harris, Eugene and Jody Hey, "X Chromosome Evidence for Ancient Human Histories" Proceedings Nat'l Academy of Sciences, U.S.A. 96:3320-3324

Huang, W., Fu Y-X, Chang BHG, Gu X, Jorde L.B. and Li W-H, 1998, "Sequence Variation in ZFX Introns in Human Populations," Molecular BIology and Evolution 15:138-142 cited in John Relethford, 2001, Genetics and the Search for Modern Human Origins, (New York: John Wiley).

Johnson, Welkin E. and Jon M. Coffin, 1999 "Constructing Primate Phylogenies from Ancient Retrovirus Sequences," Proc. Natl. Acad. Sci., USA, 96:10254-10260.

Kaesmann, H., V. Wiebe and S. Paabo, 1999, "Extensive Nuclear DNA sequence Diversity Among Chimpanzees,  Science 286:1159-1162 cited by John Relethford, 2001, Genetics and the Search for Modern Human Origins, (New York: John Wiley).

Morris, Henry M. and Gary E. Parker,1987. What is Creation Science?, (El Cajon: Master Books, 1987)

Rogers, Alan R., 2001, “Order Emerging from Chaos in Human Evolutionary Genetics,” PNAS, 93:3:779-780.

Takahata et al, "Testing Multiregionality of Modern Human Origins," Mol. Biol. Evol., 18(2001):2:172-183

Templeton, Alan R.  "Testing the Out of Africa Replacement Hypothesis with Mitochondrial DNA Data," in G. A. Clark and C. M. Willermet, ed., Conceptual Issues in Modern Human Origins Research, (New York: Aldine de Gryuter, 1997), pp. 329-360.

Trinkaus, Erik and Cidalia Duarte, “The Hybrid Child from Portugal,” Scientific American April 2000.

Douglas C. Wallace, et al, “Ancient mtDNA sequences in the Human Nuclear Genome: A Potential Source of Errors in Identifying Pathogenic Mutations,” Proc. Natl. Acad. Sci., 94(1997):14900-14905.

 Wolpoff, Milford H. John Hawks, David W. Frayer, and Keith Hunley, “Modern Human Ancestry at the Peripheries: A Test of the Replacement Theory,” Science 291(2001):293-297

 Zhao, Zhongming et al, “Worldwide DNA sequence variation in a 10-kilobase noncoding region on human chromosome 22” Proc. Natl. Acad. Sci. USA, Vol. 97, Issue 21, 11354-11358, October 10, 2000

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Last Revised 12-2-2001