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The Naked Ape: An Open Letter to BioLogos on the Genetic Evidence, Cont.

Cornelius Hunter

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In a previous article I reviewed BioLogos Fellow Dennis Venema‘s articles (here and here) which claimed that the genomes of different species are what we would expect if they evolved. For instance, allied species have similar genomes, and genetic features fall into evolution’s common descent pattern. I argued that this claim is inaccurate and that the scientific evidence tells a very different message.

In a later article Venema focused his claim on the specific case of human evolution, and the similarity between the human and chimpanzee genomes. As before, Venema finds this genetic evidence to be a compelling confirmation of evolution:

The first line of evidence in favor of humans sharing ancestry with other forms of life is straightforward — there are other species that have a genome that is nearly identical to our own — the genomes found in great apes such as chimpanzees, gorillas and orangutans. Compared to our “book,” the “books” of these species match at the chapter and paragraph level — all three species have DNA sequences that have the same genes in the same basic order as we do. There are subtle differences, of course — blocks of sequence that have been rearranged through breakage and rejoining of chromosomes, as expected — but the overall pattern is clear.

Taken together, what we observe when comparing the overall structure of the human genome to other primates is that (a) our genomes do indeed have the features one would predict them to have if they are copies of a shared ancestral genome, and (b) the differences we do observe are easily accounted for by well-known mechanisms. These observations strongly support the hypothesis that our species arose through an evolutionary process.

It does not seem that the evidence supports evolutionary theory as Venema concludes. In fact, there appear to be several significant problems with this claim, as I will explain.

First, as we saw in my previous article, the genetic data from the different species do not fall into the expected evolutionary pattern. Here Venema focuses on the high genetic similarity between the primates, claiming it confirms evolution. But if this is what is required to confirm evolutionary relationships, then the substantial genetic differences that are so often found between otherwise similar species must falsify evolutionary relationships in those cases.

But evolutionists have never entertained any such doubts. Those evolutionary relationships are intact, according to evolutionists, and this suggests that the high similarity between the primate genomes never was required for evolutionists to believe they evolved from a common ancestor.

So it appears that Venema’s claim, that the high genetic similarity between the primates confirms their evolutionary relationship, is more of an “after the fact” claim rather than a confirmation of a genuine evolutionary prediction. In fact, given the substantial morphological differences between humans and the other primates, evolutionists had indeed expected greater genetic differences:

The chimpanzee is our closest living relative. The morphological differences between the two species are so large that there is no problem in distinguishing between them. However, the nucleotide difference between the two species is surprisingly small.

So it does not appear that the high similarity between the chimp and human genomes was predicted by evolution, or is required by evolution. Beyond that, given the high similarity between the chimp and human genomes, there are many inconsistencies with evolution, as we shall see next.

The Gorilla Genome Is Strangely Similar to Both the Chimp and Human Genomes

When the human and chimpanzee genomes were compared a few years ago, the human genes showed some surprising differences in a few places, such as in genes thought to be related to hearing. Evolutionists called it “accelerated” evolution and they said that it was due to the development of human language. However it turns out that the gorilla genome has a similar pattern. And that doesn’t make sense since gorillas don’t have our advanced verbal skills:

Much of the 15% is in sections of the genome that do not code for proteins. But the researchers also looked at functional gene changes. They found that certain genes — including some involved in hearing and brain development — had gone through more rapid changes than expected in both the gorilla and human lineage. Some of these rapid changes are puzzling: the gene LOXHD1 is involved in hearing in humans and was therefore thought to be involved in speech, but the gene shows just as much accelerated evolution in the gorilla. “But we know gorillas don’t talk to each other–if they do they’re managing to keep it secret,” says [lead author] Scally.

So now evolutionists are calling it “parallel accelerated” evolution, because the same accelerated evolution, by random mutation, must have happened independently, in the human and gorilla genomes. But why would the same “accelerated evolution” occur in the gorilla? It wasn’t developing human language. Perhaps there is some other reason, but why then wouldn’t that “accelerated evolution” occur in the chimpanzee? It doesn’t make sense with evolution, for we must say that random mutations just happened to create the same pattern twice.

The gorilla genome also shows similarities to the chimp genome, including duplications that are not present in the other primates. Evolutionists say these various chimp-gorilla similarities were coincidences, occurring repeatedly by chance in the two different species:

We show that both the gorilla and chimpanzee genomes have experienced independent yet convergent patterns of structural mutation that have not occurred in humans, including the formation of subtelomeric heterochromatic caps, the hyperexpansion of segmental duplications, and bursts of retroviral integrations.

These events must have occurred independently and in parallel.

Viruses

Human uniqueness is expansive. Relative brain size, hairless sweaty skin, striding bipedal posture, long-distance running, ability to learn to swim, innate ability to learn languages in childhood, prolonged helplessness of the young, ability to imitate and learn, inter-generational transfer of complex cultures, awareness of self and of the past and future, theory of mind, increased longevity, provisioning by post-menopausal females, difficult childbirth, and cerebral cortical asymmetry are just a few from a long list of features that make humans exceptional.

Another such unique feature is at the genome level: the lack of endemic infectious retroviruses in humans. The problem is that these viruses are present in the other primates, and so according to evolution these viruses must be present in their common ancestor which, again according to evolution, would be an ancestor of humans as well. Therefore this lack of endemic infectious retroviruses in humans is inconsistent with evolution:

Other than the recent introductions of HIV and human T leukaemia virus (HTLV) into humans from other animals, humans seem to be devoid of species-wide endemic infectious retroviruses. By contrast, like most other mammals studied, other hominids and non-human primates (NHPs) do have such viruses. Indeed, given the remarkable corroboration between the phylogenetic trees of primates and their lineage-specific simian foamy viruses (SFVs) our common ancestors with other hominids almost certainly had SFVs. The same is probably true of the lineage-specific simian infectious retroviruses (SIVs) found in most NHPs. Assuming that the common ancestors of hominids carried multiple endemic infectious retroviruses, how did the human lineage eliminate them? Given that humans remain susceptible to re-infection with both SFVs and SIVs from other hominids, this seems unlikely to be explained solely on the basis of more efficient host restriction systems. Rather, there seems to have been an episode in which the ancestral human lineage was somehow ‘purged’ of these endemic viruses.

In other words, the endemic infectious retroviruses do not align with the expected evolutionary pattern. The human lineage must, somehow, have been purged of these endemic viruses. Perhaps such a purging occurred, and future research may be able to strengthen that hypothesis. But as it stands, this evidence is not consistent with evolution.

Chimp-Human Genome Beneficial Differences Are Few

As noted above, evolutionists were surprised by the high similarity between the chimp and human genomes. With so few differences, how could evolution construct such tremendous differences? But not only is evolution limited to a relatively few genetic modifications to create the human, but according to evolution the majority of even those modifications would likely have had little or no consequence or even would have been slightly harmful. Here is how a 2005 paper on the chimpanzee-human genome comparisons put it:

In particular, we find that the patterns of evolution in human and chimpanzee protein-coding genes are highly correlated and dominated by the fixation of neutral and slightly deleterious alleles.

The paper is written from an evolutionary perspective, assuming that humans and chimpanzees share a common ancestor. Given that a priori assumption, they were forced to conclude that most of the mutations affecting protein-coding genes led to “neutral and slightly deleterious alleles.” So not only are evolution’s random mutation resources meager, in terms of both quality and quantity as explained above, but even worse, those mutations mostly led to “neutral and slightly deleterious alleles.”

In fact the beneficial mutations in protein-coding genes, which presumably would be important in evolving the human from a small, primitive ape, literally number only in the hundreds. It would be astonishing if the human could be evolved from so few mutations.

Chimp-Human Genome Differences Have Discrepancies

Furthermore, the chimp-human genome differences show some strange patterns, with unexplainable variation towards the ends of most chromosomes, and with the chromosomal banding patterns.

A common response from evolutionists is that these discrepancies are small in magnitude. That is true, they are small in magnitude. But that is not what counts. Molecular spectra that make magnetic resonance imaging (MRI) possible are also small in magnitude. That doesn’t mean they don’t count. What is important is that the chimp-human genome differences show patterns that evolutionary theory struggles to account for. The evidence is not consistent with the theory, by a wide margin.

The chimp-human genome differences have also been described using sliding 1-Mb windows. Those results also showed nonrandom variations, but later research found that those variations correlate with the observed de novo human mutation rate patterns. The research paper concluded that the variation in chimp-human genome differences “is only partly explained” by the mutation rate patterns. But these results raise the specter that the variations in the chimp-human genome differences seen in 1-Mb windows may be explainable by a known phenomenon.

This suggests the possibility that future research may also explain the variation towards the ends of chromosomes, and with the chromosomal banding patterns. But that was not the claim. Evolutionists such as Venema claim that today’s evidences “strongly support the hypothesis that our species arose through an evolutionary process.”

Chimp-Human Alternate Splicing Differences

You may have learned in your high school biology class that genes are segments of DNA, but it is a bit more complicated than that. For starters, in the higher species a gene is often not a simple continuous segment of DNA but rather is interrupted several times by intervening segments. So there are the coding segments (called exons for expressed regions) and then there are the intervening segments (called introns for intervening regions).

When a gene is transcribed, the transcript contains both the exons and introns. It is then spliced by a complicated spliceosome machine that removes the introns from the gene copy and glues the exons together.

One of the features of the exon/intron genetic architecture is that it allows for alternative splicing schemes. In fact, incredibly, a given gene can have thousands of different forms depending on how the spliceosome machine edits the gene.

When it was discovered that the human genome contained about twenty five thousand genes it seemed too few. Are not more genes required for a human body? More recently it has been discovered that we make up for that small number of genes with alternative splicing schemes. Most of our genes may undergo such editing, and the result can be a completely different function for the resulting protein.

We have an enormous alternative splicing program in our cells, far more than chimps have. And this is another inconsistency with evolutionary theory.

Given the high similarity between the chimp and human genomes, and the relatively few beneficial mutations in protein-coding genes (discussed above), evolutionists have considered the possibility of evolution by splicing. In other words, our enormous alternative splicing program may have been an important factor in our evolving from a small, primitive ape.

But there are many thousands of these gene-splicing changes that would have to evolve. And unlike bacteria whose populations are large and generation times are short, our gene splicing changes would have to evolve in smaller populations with longer generation times.

It is difficult to see how evolution would have the resources to make this happen. The problem quickly becomes astronomically improbable if groups of genes would need to implement their new splicing logic together. And how could that not be the case?

In fact, even if only the order of implementing splicing for a small number of genes is important, the problem quickly becomes astronomically improbable. And again, how could that not be the case?

But this is only the beginning. In addition to the fact that the evolution of our enormous gene splicing changes is unlikely, it also represents an enormous serendipity problem. We would have to say that random mutations constructed complicated genes, with exons and introns and splicing codes, and the incredible splicing machinery, which, it would just so happen, would luckily be just what was needed to evolve humans.

It is even worse than this when one considers the exons themselves. Those random mutations would have divided the genetic instructions into so many exons, and it just so happened that they would be the right building blocks that, when rearranged, would lead to humans. The serendipity is astronomical here.

Imagine if you were building a tricycle and your friend modified each part you had crafted (not adding anything), and now the parts fit together to construct the space shuttle rocket motor.

The Kangaroo-Human Genomes

In my previous article I explained that, in addition to striking differences in otherwise allied species, striking similarities in otherwise distant species are also inconsistent with evolution. This problem arises also with the human genome. Consider the kangaroo genome, which turned out to be similar to the human genome. As one evolutionist explained:

There are a few differences, we have a few more of this, a few less of that, but they are the same genes and a lot of them are in the same order. Which really surprised us, we thought they’d be completely scrambled, but they’re not, there’s great chunks of the human genome which is sitting right there in the kangaroo genome.

It was a surprise because under evolution humans and kangaroos must be quite distant relatives. Evolutionists believe a small mouse-like species split into two lineages — the marsupials and the placentals — about 150 million years ago. And according to evolutionists that mouse-like species eventually evolved by random mutations into, among other things, a kangaroo in the one lineage and into a human in the other. With that much evolutionary distance the kangaroo and human genomes should have evolved substantial differences.

Conclusion

The genomes of primates do not support evolutionary theory. As we have discussed, there are always speculations for whatever evidence is discovered. Perhaps evolution did this, perhaps it did that. But that does not change the fact that the primate genomes do not “strongly support the hypothesis that our species arose through an evolutionary process,” as Venema and fellow evolutionists claim. There are a wide variety of substantial contradictions and problems with this theory.

Image credit: © Fotos 593 — stock.adobe.com.

Cross-posted at Darwin’s God.

Cornelius G. Hunter

Fellow, Center for Science and Culture
Cornelius G. Hunter is a graduate of the University of Illinois where he earned a Ph.D. in Biophysics and Computational Biology. He is Adjunct Professor at Biola University and author of the award-winning Darwin’s God: Evolution and the Problem of Evil. Hunter’s other books include Darwin’s Proof, and his newest book Science’s Blind Spot (Baker/Brazos Press). Dr. Hunter's interest in the theory of evolution involves the historical and theological, as well as scientific, aspects of the theory. His blog is Darwin's God.

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