Editor’s note: In a multipart series, Casey Luskin has been reviewing a new book by philosopher William Lane Craig. Below is the final part. Look here for the full review.

In the previous installment of my review of William Lane Craig’s In Quest of the Historical Adam we saw that many evangelical intellectuals had accepted arguments that Adam and Eve could not have existed. These arguments, in particular the claim that human genetic diversity is too great to have been reduced to a single pair, were forcefully promoted by theistic evolutionists aka evolutionary creationists (TE/ECs) affiliated with BioLogos. Prominent among these critics was Dennis Venema, a biologist at Trinity Western University, who compared modern-day belief in Adam and Eve with adhering to the long-refuted geocentric model of the solar system. But the arguments turned out to be wrong, as even BioLogos and Venema now admit. 

To his credit, William Lane Craig is among those evangelicals who have been willing to question arguments against a historical Adam and Eve. In his book he cites the work of Ann Gauger, Ola Hössjer, and Joshua Swamidass who performed analyses showing that humanity could have originated from a single pair at least 500,000 years ago. Gauger and Hössjer noted that Adam and Eve could have lived even more recently if additional evolutionary assumptions are questioned. 

When I was reading the rhetoric used by evangelical elites who advocated abandoning a historical Adam and Eve, I was struck by how much of it seemed driven by fear — fear of looking foolish before the world because you challenged evolution and were shown to be wrong. As I discussed, the lesson from this story is that it should not be taboo for evangelicals to challenge evolutionary arguments. We need not live in fear that doing so is “anti-science” or will “bring disrepute on the Christian faith” or “shame upon the name of Jesus Christ” — as some evangelical elites have argued. 

In this final installment of my review, we’ll see that unfortunately, some prominent Christians have not fully appreciated this lesson. They seem intent upon sticking with the evolutionary consensus, repeating past mistakes and embracing certain evolutionary ideas — despite a lack of compelling evidence. To be specific:

1. BioLogos, Joshua Swamidass, and (sometimes) William Lane Craig now advocate a particular model of human origins where we are all descended from a population of hominids that evolved from a common ancestor we share with apes via standard evolutionary mechanisms — exactly as evolutionary theory proposes. Under this “Genealogical Adam and Eve” model Adam and Eve were historical people who may have been specially created, but their offspring interbred with those fully evolved hominids, eventually leading to us. This model is fundamentally evolutionary, but the evidence contradicts it or does not demand it. 
2. Craig in his book at times seems to disfavor the above model because it implies “bestial relations with nonhuman hominins.” He prefers to say that “No such appeal to interbreeding is necessary if we envision Adam and Eve as emerging from a hominin population that shared common ancestry with chimpanzees and other great apes.” (p. 378) This model is also challenged by the evidence. 
3. Whether Craig supports a standard evolutionary model where Adam and Eve are directly evolved from some common ancestor shared with apes (model 2 above), or the new model where Adam and Eve’s offspring interbred and intermixed with hominids that evolved from a common ancestor shared with apes (model 1 above), Craig is being driven by the idea that humans share a common ancestor with apes. In either case, he cites “broken” pseudogenes as evidence for human-ape common ancestry — relying on Dennis Venema as a primary source. The best science available also does not require this model to be true. 

In the models above it seems that some Christians have not fully appreciated the lesson learned from evangelical debates over Adam and Eve: We need not fear that challenging an evolutionary model necessarily goes against good science. Rather than fear, let us be driven by a desire to find the truth. So let’s dig in. 

Not Learning the Lesson on the Genealogical Adam and Eve Model 

A July 2021 article from BioLogos now acknowledges the possibility of some version of a historical Adam and Eve. They say:

Options include…postulating that Adam and Eve were a special, historical pair who were indeed the ancestors of everyone alive today, but who were part of a larger population with whom their descendants could mate.¹

Under this view, Adam and Eve were historical persons whose offspring interbred with a population of hominids which evolved from apelike ancestors. Note, however, that BioLogos distinguishes this view from what it calls the “common traditional” view where “Adam and Eve were created de novo” as our “‘sole progenitors’: they were the first two humans, and they alone gave rise to all other humans.”² BioLogos seems to still disfavor this traditional view, instead preferring that Adam and Eve did exist but their offspring interbred with a large population of humans that evolved naturally from ape-like creatures. Thus, today BioLogos seemingly proposes that we are descended from both Adam and Eve as well as evolved hominids — and we share a common ancestor with living apes. This “Genealogical Adam and Eve” (GAE) model is definitely not the “common traditional” view.

The GAE model was elaborated by Joshua Swamidass in his 2019 book The Genealogical Adam and Eve.³ As we saw in part 4 of this review, William Lane Craig at times distances himself from this proposal because it implies “bestial” relations between the descendants of Adam and Eve with non-human hominins. However, in the final analysis he seems to allow the GAE model. 

As a Christian I believe there are severe theological and scriptural problems with the GAE model, but this isn’t the place for such arguments. In any event, my main objections are scientific. Scientifically, the GAE model adopts a standard evolutionary view of human origins and says that if Adam and Eve were specially created then their offspring interbred and completely intermixed with a fully evolved population of hominids. We are the descendants of this large population. Because GAE adopts a standard evolutionary account of human origins, any scientific problems with such an account are inherited by the GAE model. Is the scientific evidence so compelling that we must accept this view?

As we saw in part 3 of this review, the fossil evidence for human evolution from apelike creatures is weak, and neo-Darwinian mechanisms face an overwhelming mathematical obstacle to account for the origin of complex human features such as our cognitive abilities. For these reasons, many aspects of the GAE model are scientifically problematic. If humans did not evolve from apelike creatures via standard evolutionary mechanisms, I see no compelling reason to adopt the GAE hypothesis. 

Further, in part 5 of this review we saw that Gauger and Hössjer’s research — as well as Swamidass’s own modelling — show that if Adam and Eve lived far enough in the past, then modern human genetic diversity is compatible with an initial pair who were our sole ancestors. This eliminates any need to invoke thousands of evolutionary ancestors, which is a key feature of the GAE model. 

So if the scientific evidence for human evolution is weak and the GAE model not even necessarily required by the evidence, then why is it supported by BioLogos, Swamidass, and (it seems in the end) William Lane Craig? These are complex questions and there are probably many reasons. But if I had to speculate, some of them are likely the same reasons that led people to wrongly reject a historical Adam and Eve in the first place.

The GAE model allows one to retain belief in a version (albeit a non-traditional one) of a historical Adam and Eve while still adopting a fully evolutionary model of human origins. This appeals to those who (as we saw in part 5 of this review) mistakenly believe that challenging evolution “brings disrepute on the Christian faith” and “unnecessary shame upon the name of Jesus Christ.” Paul Nelson has convincingly argued that the driving philosophy behind the GAE model is a prior commitment to methodological naturalism,⁴ the idea that when studying science, one is allowed to invoke only naturalistic forces and mechanisms. Perhaps not all GAE-proponents feel strongly about methodological naturalism, but they certainly seem to feel strongly about retaining an evolutionary model, for whatever reasons. 

Yet if we care more about science and truth than about evolution, methodological naturalism, or worldly acceptance, then perhaps it is the GAE model that is “unnecessary.” I’m sure that many GAE proponents will disagree and say it is required by the science — but is the science really so clear that we must share a common ancestor with apes? We’ll get to that evidence shortly. 

Whatever the reasons for adopting the Genealogical Adam and Eve model, as BioLogos admits, it is not the “common traditional” Adam and Eve. Under the GAE scenario, Adam and Eve are not the sole progenitors of humanity, and we are not descended only from them, but also from a large population of humans that fully evolved from apelike ancestors. Thus, Christians who adhere to a traditional Adam and Eve will have difficulty with the GAE model. 

Not Learning the Lesson of Pseudogenes

Although Craig tells the story of the demise of BioLogos’s arguments against Adam and Eve, he still uses their arguments to support common ancestry. Citing Dennis Venema, Craig mentions pseudogenes as evidence for human-ape common ancestry:

One can, with Swamidass and Hössjer and Gauger, postulate instead a de novo creation of Adam and Eve. But then one faces a difficult dilemma. One must explain our genetic similarity to chimps either on the basis of repetitive divine use of a similar design plan or on the basis of considerable interbreeding with nonhumans. The first has difficulty explaining broken pseudogenes that we share with chimps… (p. 376, emphasis added)

As noted, Craig at times disfavors the GAE model because it implies bestiality between the descendants of Adam and Eve and non-human hominids. If he doesn’t accept the GAE model, and wants Adam and Eve to be our sole genetic progenitors, he seemingly has two choices: accept a version of Adam and Eve where they are miraculously created and we don’t share a common ancestor with apes, or view Adam and Eve as fully evolved hominins who did share a common ancestor with apes. Craig apparently prefers the latter option — common ancestry:

Some have appealed to interbreeding with other evolved hominin species in order to explain how Adam and Eve could have been de novo creations from inanimate material and yet their descendants bear such striking genetic similarity to chimpanzees, including broken pseudogenes that have ceased their original function (S. Joshua Swamidass, The Genealogical Adam and Eve: The Surprising Science of Universal Ancestry [Downers Grove, IL: IVP Academic, 2019]). Cf. Dennis Venema’s critique of Hössjer and Gauger’s de novo creationism on the grounds that the human genome is replete with evidence that we share common ancestors with other species, such as chimpanzees and gorillas (Dennis Venema, “Adam-Once More, with Feeling,” Jesus Creed (blog), November 4, 2019, http://www.patheos.com/blogs/jesuscreed/2019/11/04/adam -once-more-with-feeling). No such appeal to interbreeding is necessary if we envision Adam and Eve as emerging from a hominin population that shared common ancestry with chimpanzees and other great apes. Indeed, on the view proposed here, Adam and Eve could be our sole genetic progenitors, whose descendants never fell into bestial relations with nonhuman hominins or at least produced no descendants from such liaisons. (p. 378)

As we saw in part 4 of this review, the GAE model is designed to retain human-ape common ancestry and allow space for a miraculously created historical Adam and Eve, but it loses Adam and Eve as our “sole genetic progenitors.” The direct common ancestry model, which Craig seems to prefer above, views Adam and Eve as being descended from a common ancestor shared with apes, but does not allow them to be “miraculously created de novo.” Both models involve human-ape common ancestry, and although Craig isn’t clear which model he prefers, it is clear that he prefers some version of a human-chimp common ancestry model over a truly traditional model of Adam and Eve where they are our sole genetic ancestors, were miraculously created de novo, and don’t share common ancestry with apes.

Why is Craig willing to give up core aspects of a traditional Adam and Eve in favor of some model which requires human-ape common ancestry? The answer can be summed up in two words he uses in both quotes above: “broken pseudogenes.”

The logic goes as follows: Pseudogenes are broken genes which once had function but were inactivated by some mutation. God would never put broken DNA into two species in the same place, the argument goes. Therefore, if humans and apes share nonfunctional pseudogenes in the same location of our respective genomes, then we must have acquired those pseudogenes through some natural non-designed mechanism — namely, inheritance from a common ancestor.

Intelligent design is compatible with common ancestry, so in discussing this topic we’re not necessarily testing ID on the macro-scale. But on the small-scale the logic seems correct that broken DNA shared by two species is better explained by material evolutionary causes than by intelligent causation. But if pseudogenes aren’t broken non-functional junk DNA, then this raises the possibility that they are important functional parts of our genome. In that case, the reason we share “pseudogenic” DNA with apes isn’t common ancestry, but for functionally important reasons reflecting common design.

So are pseudogenes really “broken” and non-functional junk DNA? Well, what does the literature say?

A Rapidly Growing Trend in the Technical Literature: Pseudogene Function

In fact, the number of papers reporting extensive function for pseudogenes is impressive. Many prominent peer-reviewed scientific papers have said things like (my paraphrase), “We used to think pseudogenes were junk DNA, but this is just because we really didn’t have the technology to understand them. We still barely understand pseudogenes. But now that we’re developing methods of studying them, we’re discovering that functionality is quite common.” This means that it might be wiser to adopt a “wait and see” approach to pseudogenes, and not prematurely conclude they are just broken DNA reflecting our common ancestry with apes. 

Consider the arguments of a BioEssays paper, “Processed pseudogenes: A substrate for evolutionary innovation,” just published in September 2021: 

The implication of pseudogenes in biological processes including neurogenesis, inflammatory responses and cancer necessitates revisitation of the notion that pseudogenes are evolutionary ‘junk’. However, the extent of pseudogene activity remains poorly investigated, in part perhaps due the bias inherent to the term ‘pseudogene’, which presumes non-functionality. Furthermore, technical shortcomings have impeded unambiguous distinction of pseudogene activity from their near identical parental counterparts.⁵ [Emphasis added.]

The paper explains that although pseudogenes have been traditionally “labelled functionless en masse,” the truth is that “comparatively little is known” about them:

Following Ohno’s assumption that most duplicated genes are destined for degeneracy, Jacq and co-workers concluded that the identified 5S ribosomal RNA ‘pseudo’ genes were artefacts of evolution. These remarks provided the foundation for a framework that categorises apparently defective sequences with similarity to another gene as pseudogenes. The genomics revolution subsequently saw regions of the genome with pseudogene hallmarks labelled functionless en masse. Although pseudogenes are almost as numerous as protein-coding genes (14 767, of which, 72% are processed, 24% duplicated, 1.6% duplicated, 2.4% other, and 19 957, respectively), comparatively little is known about the contribution of pseudogenes to the evolution of the human genome.

Christian intellectuals who believe that pseudogenes are non-functional junk are adopting assumptions directly grown out of an evolutionary paradigm — and these are assumptions about an aspect of the genome that we actually know very little about. Neither Christians nor anyone else needs to fear that they are denying good science by anticipating function for pseudogenes, or at least by being cautious about jumping on the bandwagon that they are genetic “junk.”.

Many other authoritative papers argue similarly. A 2018 paper published in a Springer biochemistry journal comments:

For a long time, pseudogenes have been considered as “junk DNA” that inevitably arises as a result of ongoing evolutionary process. However, experimental data obtained during recent years indicate this understanding of the nature of pseudogenes is not entirely correct, and many pseudogenes perform important genetic functions. … pseudogenes are integral components of extensive regulatory networks of interacting genes.⁷

The paper continues:

Development of new generation DNA sequencing (NGS) has led to an unforeseen discovery of the pervasive transcription phenomenon. Although protein-encoding exon sequences represent only a small fraction of animal and plant genomes (<2% of human genome), the majority of them are transcribed. Therefore, it is not surprising that pseudogene RNAs (psRNAs) are significantly represented in the studied transcriptomes. Thus, about 10% of all identified (~15,000-18,000) human pseudogenes appear to be transcribed. According to available experimental data, transcribed pseudogenes may be divided into three groups: (1) universally transcribed, (2) non-specifically transcribed, and (3) transcribed in a strict tissue-specific manner. Universally expressed pseudogenes are related to housekeeping genes that usually have the largest number of pseudogenes. The second group of pseudogenes, in particular CYP4Z2P and derivatives of Oct-4, Connexin-43, and BRAF genes, are highly expressed in one or two tissue types, but demonstrate low expression levels in other tissues. Finally, strictly tissue-specific transcription was shown for ~150 human pseudogenes, including derivatives of the AURKA (kidneys) and RHOB (intestine) genes. The tissue-specific character of transcription suggests that these pseudogenes perform tissue specific functions. In general, the majority of transcribed pseudogenes have been detected in the testicles, whereas the muscle tissue has the least number of transcribed pseudogenes.

It’s important to appreciate what you just read: We already see evidence of function for about 10 percent of pseudogenes — something that evolutionists once thought impossible. But many pseudogenes are expressed only in specific tissues and at specific times. This suggests that it may be very difficult to detect the function and purpose of these pseudogenes. Why? Because they may be active just rarely during the human life cycle. You can’t keep a human being in a lab for a lifetime to see what’s going on in every tissue type. As the paper explains:

Although it has already been 40 years since the discovery of pseudogenes, investigation of these genomic components by modern methods is only at its beginning. [Emphasis added.]

Even so, as a paper in Annual Review of Genetics observed: “pseudogenes that have been suitably investigated often exhibit functional roles.”⁷ Likewise, a 2012 paper in RNA Biology states that “pseudogenes were long considered as junk genomic DNA” but “pseudogene regulation is widespread in eukaryotes.” The paper concludes that “the study of functional pseudogenes is just at the beginning” and predicts “more and more functional pseudogenes will be discovered as novel biological technologies are developed in the future.”⁸

These new technologies are already bearing fruit. The literature is full of papers reporting specific functions in sections of DNA previously labeled as “pseudogenes.”⁹ The ENCODE project reported over 850 human pseudogenes that are “transcribed and associated with active chromatin.”¹⁰ A paper in Molecular Biology and Evolution found that “656 human–macaque orthologous pseudogenes…are transcribed.”¹¹ And a study of the human proteome published in Nature reported “more than 200 peptides that are encoded by 140 pseudogenes.”¹²

Mass-functionality for pseudogenes is no longer difficult to believe. They can yield functional proteins, functional RNA transcripts, or perform a function without producing any transcript. In RNA interference, a pseudogene yields an “anti-sense” RNA transcript which cannot produce a protein, but can bind with transcripts of protein-coding versions of the gene. When such binding occurs, the protein-coding transcript cannot be translated, reducing protein production.¹³ In target mimicry, small RNAs bind to a protein-coding mRNA transcript, inhibiting translation. If a pseudogene produces decoy mRNA transcripts which mimic the “target” sequence of the protein-coding counterparts, these small RNAs can bind to the pseudogene transcripts instead. This prevents inhibition of translation, increasing protein production.¹⁴ One of the papers quoted above lists multiple types of function for pseudogene RNA, which they call “psRNA”:

psRNAs participate in the regulation of parental gene expression at both transcriptional and translational levels. The sense strand of DNA serves as a template for the synthesis of sense mRNA (sRNA), whereas transcription of the antiparallel strand produces complementary antisense RNA (asRNA). As both sRNA and asRNA are synthesized during pseudogene transcription, we will further discuss the functional relevance of the pseudogene transcripts taking into account this structural difference.

Functions of sRNAs. Typically, sequences of pseudogene sRNAs only slightly differ from parental gene mRNAs. Due to the high similarity, they share miRNA-binding sites (miRNA response elements, MRE), whose binding to miRNAs ensures regulatory functions of these RNA molecules in both the nucleus and the cytoplasm. … The higher the pseudogene transcription activity, the higher the number of miRNA molecules that bind to its sRNA, which depletes their intracellular pool and reduces suppression of the parental gene expression, i.e., the ratio between the amounts of gene and pseudogene transcripts tunes gene expression….

Functions of asRNAs. Antisense transcription has been found in all studied living organisms. The NGS (next generation sequencing) data suggest that >70% RNAs in the mouse transcriptome overlap with complementary sequences, thus representing natural antisense transcripts. The same is true for the human transcriptome. In mice and humans, the majority of asRNAs are strictly conserved, which indicates their functional relevance, which has been experimentally confirmed. By now, many functions of asRNAs have been identified. asRNAs can affect their target genes both in cis and in trans. Some of these activities have been also observed for pseudogene asRNAs.

Pseudogene asRNAs in the formation of duplexes with parental gene sRNAs. Discovery of the involvement of pseudogene asRNAs in the inhibition of translation of parental gene mRNAs was one of the first indications of their functional role in living organisms. This mechanism is realized through the formation of RNA-RNA duplexes between highly homologous regions of the pseudogene asRNA and translated mRNA with subsequent suppression of the corresponding genes at the translation level….

Pseudogene asRNAs in the formation of short interfering RNAs (siRNAs). Pseudogene asRNAs participating in the formation of RNARNA duplexes may give rise to siRNAs. The structure and mechanism of action of regulatory siRNAs are similar to those of miRNAs….

Pseudogene asRNAs in the generation of piRNAs. Pseudogene-encoded RNAs that interact with PIWI proteins (piRNAs) were recently found among short noncoding RNAs in human and animal spermatozoa and germline cells….

Pseudogene asRNA in the regulation of transcription of target genes. By now, the role of lncRNAs in epigenetic genome modifications accompanied with the establishment of gene expression patterns in cells has been demonstrated and extensively studied. Similar properties were also observed for some pseudogene RNAs….¹⁵

Many other papers have warned against dismissing pseudogenes as mere junk. A 2012 paper in Science Signaling noted that although “pseudogenes have long been dismissed as junk DNA,” recent advances have established that “the DNA of a pseudogene, the RNA transcribed from a pseudogene, or the protein translated from a pseudogene can have multiple, diverse functions and that these functions can affect not only their parental genes but also unrelated genes.”¹⁶ Their homology to the protein-coding versions of the gene is necessary for this regulatory function, as “pseudogenes, due to their high-sequence homology, can act as legitimate bona fide microRNA competitors, thereby actively competing with their ancestral protein-coding genes for the same pool of microRNAs through sets of conserved MREs [microRNA response elements].”¹⁷ The Science Signalingpaper concludes that “pseudogenes have emerged as a previously unappreciated class of sophisticated modulators of gene expression.” A 2011 paper in the journal RNA concurs:

Pseudogenes have long been labeled as ‘junk’ DNA, failed copies of genes that arise during the evolution of genomes. However, recent results are challenging this moniker; indeed, some pseudogenes appear to harbor the potential to regulate their protein-coding cousins.¹⁸

As a 2013 paper in eLife states, “Pseudogenes are thought to be inactive gene sequences, but recent evidence of extensive pseudogene transcription raised the question of potential function.”¹⁹ Another paper in eLife from 2015 states, “Using a new bioinformatic method to analyze ribosome profiling data, we show that 40% of lncRNAs and pseudogene RNAs expressed in human cells are translated [into proteins].”²⁰ The paper continues:

The experiments show that thousands of non-coding RNAs in the human genome are, in fact, translated. This is many more than anticipated and represents approximately 40% of the lncRNAs and pseudogene RNAs, and 35% of untranslated regions in messenger RNAs.

Sequence conservation can also imply pseudogene functionality even when a specific function has not yet been detected. A 2014 study in Proceedings of the National Academy of Sciences compared pseudogenes in humans, C. elegans, and fruit flies. It found direct evidence of function as well as conserved sequencing, suggesting function: “Overall, we identify a broad spectrum of biochemical activity for pseudogenes, with the majority in each organism exhibiting varying degrees of partial activity. In particular, we identify a consistent amount of transcription (∼15%) across all species, suggesting a uniform degradation process. Also, we see a uniform decay of pseudogene promoter activity relative to their coding counterparts and identify a number of pseudogenes with conserved upstream sequences and activity, hinting at potential regulatory roles.”²¹ A 2011 paper in Celllikewise infers functions in many pseudogenes: “Sequencing efforts have revealed ~19,000 pseudogenes in humans, many of which are transcribed and are often well conserved, suggesting that selective pressure to maintain pseudogenes exists.”²²

One of the most profound and prominent statements on the subject came in a 2020 paper in Nature Reviews Genetics. This paper warned that pseudogene function is “Prematurely Dismissed” due to “dogma,” where “The dominant limitation in advancing the investigation of pseudogenes now lies in the trappings of the prevailing mindset that pseudogenic regions are intrinsically non-functional.” Instead the paper finds that “Where pseudogenes have been studied directly they are often found to have quantifiable biological roles.” Some of these functions are “protein-based,” meaning the pseudogene generates a functional protein. But other functions can be “RNA-based” or “DNA-based.” For example, evolutionists typically presume that a pseudogene that does not produce a protein can’t be functional. But the paper observes that pseudogenes that cannot be translated into a protein may still have a function through their RNA transcript:

Many pseudogenes contain a frequency of mutations that render them unlikely to be (or incapable of being) translated into proteins. However, such mutations do not necessarily preclude pseudogenes from performing a biological function.

A variety of other non-transcriptional functions are documented in the paper, including stabilizing chromosomes, mediating transcript-splicing, and regulating recombination. Thus, in many cases copy numbers of pseudogenes seem to have functional importance, where deviations from the normal genetic state cause disease. They predict: “It is expected that further links between human pseudogene polymorphisms and complex diseases will be identified in the coming years.”

The typical response from evolutionists would be that these examples are just isolated rare cases, and that the bulk of pseudogenes are nonetheless junk. The authors of the Nature Reviews Genetics paper — who give no indication of sympathy for intelligent design —  are aware of this objection. They say the following in direct rebuttal to it: 

The examples of pseudogene function elaborated on here should not imply that pseudogene functionality is likely to be confined to isolated instances. At least 15% of pseudogenes are transcriptionally active across three phyla, many of which are proximal to conserved regulatory regions. It is estimated that at least 63 new human-specific protein-coding genes were formed by retrotransposition since the divergence from other primates. Numerous ‘retrogenes’ continue to be recognized as functional protein-coding genes rather than pseudogenes across species. High-throughput mass spectrometry and ribosomal profiling approaches have identified hundreds of pseudogenes that are translated into peptides. Although the functions of these peptides remain to be experimentally determined, such examples illustrate the challenge in substantiating a gene–pseudogene dichotomy.

They continue: “As the abundance of such [non-coding-DNA] acquired functions does not appear to be an especially rare or isolated phenomenon, it would seem remiss to take the default perspective that processed pseudogenes are functionless. Instead, it is probable that pseudogene-containing regions of the genome harbour important biological functions that are yet to be revealed.”

However, at present, the authors note, “due in part to the experimental challenge of investigating their function and expression, pseudogenes are typically excluded from genome-wide functional screens and expression analyses.” In other words, one of the main reasons we aren’t finding function for pseudogenes is because we aren’t looking for it. One complication is that pseudogene transcription shows “cell-type specificity and dynamic expression” — meaning they may only be transcribed in particular places at particular times. This is all the more reason not to assume that lack of evidence for the function of a pseudogene is evidence that the pseudogene has no function! It very likely may be functional in a cell-type or a situation that we just haven’t properly investigated yet. As they put it, “The use of assays ill-suited to analysis of pseudogenes has arguably stymied elucidation of their biological roles.” But they are hopeful: “CRISPR-based approaches, carefully applied, have the potential to revolutionize our ability to dissect the functions of pseudogenes.”

The paper cautions that there are many instances where DNA that was dismissed as pseudogene junk was later found to be functional: “with a growing number of instances of pseudogene-annotated regions later found to exhibit biological function, there is an emerging risk that these regions of the genome are prematurely dismissed as pseudogenic and therefore regarded as void of function.”²³

Pseudogene Mistakes of the Past

There is precedent for Christians prematurely dismissing pseudogenes as broken DNA, only to be later proven wrong. The same thing happened in earlier, high-profile situations. During the 2005 Kitzmiller v. Dover trial, leading theistic evolutionist biologist Kenneth Miller testified that the human beta-globin pseudogene is “broken” because “it has a series of molecular errors that render the gene non-functional.” Since humans, chimpanzees, and gorillas share “matching mistakes” in the pseudogene, he told the court, this “leads us to just one conclusion … that these three species share a common ancestor.”²⁴ He was wrong. A 2013 study in Genome Biology and Evolution reported that the beta-globin pseudogene is functional.²⁵

Humans have six copies of the beta-globin gene. Five produce beta-globin proteins, but the sixth, the pseudogene copy, has a premature stop codon that prevents proper translation. The researchers compared all six genes across humans and chimpanzees, and found the beta-globin pseudogene exhibits fewer differences than would be expected if it were non-functional and accumulating random mutations at a constant rate. This “conserved” sequence suggests the beta-globin pseudogene has a selectable function, making it less tolerant of mutations. The beta-globin pseudogene’s inability to produce a translatable RNA transcript does not preclude it from being functional. The researchers argue that the pseudogene works as an on/off switch, regulating expression of protein-coding beta-globin genes during embryonic development. 

Relearning the Lesson of Pseudogenes

Despite all this evidence, most evolutionists still assume that pseudogenes are junk DNA. This remains the “consensus” view. Meanwhile, many Christian intellectuals don’t see the assumptions or appreciate the rapidly growing evidence of pseudogene function. They only see the consensus, and think we must not oppose it. But the trendline of the evidence shows that pseudogenes should not be assumed to be “broken” DNA. To summarize, there are many reasons to adopt a “wait and see” approach on pseudogenes:

• Pseudogene non-functionality is an assumption stemming from an evolutionary mindset, not a conclusion from careful studies of the evidence.
• In fact, pseudogenes have barely been studied — largely because technology has not yet been developed to study them. Our lack of technical ability to study pseudogenes stems directly from widespread evolutionary assumptions that they do nothing and that we shouldn’t waste our time trying to figure out what they do.
• Although entirely unanticipated under an evolutionary “junk” DNA mindset, many specific examples of pseudogene function have been found. In other cases pseudogene function has been inferred based upon biochemical activity of pseudogenic DNA or conservation of sequence. 
• This evidence of pseudogene function is unsurprising because we know there are many ways that pseudogenes can have function: Pseudogenes can yield functional proteins, functional RNA transcripts, or perform a function without producing any transcript. Many pseudogene RNAs seem to have gene regulatory functions, often in an epigenetic context. 
• We’re just at the beginning of developing technology to understand pseudogenes. Many pseudogenes may be active only in one tissue type or at certain stages of the life cycle, making their functions difficult to detect. So it’s not surprising that we don’t yet have an overwhelming number of examples of functional pseudogenes. But as we develop better technologies to study pseudogenes, functionality is showing itself to be more and more prevalent.

True, the precise functions of many pseudogenes remain unknown. For example, the Vitamin C “gulo” pseudogene, a unitary pseudogene shared by humans and many primates, is not yet known to have function (although it’s been argued that this pseudogene is active in utero). That is why it has become a popular argument against intelligent design among proponents of TE/EC. Prior to 2013, the same could have been said about the beta-globin pseudogene, now understood to have function.

Christian intellectuals who presume that pseudogenes are broken DNA are betting on a horse that has barely begun to run its race — and as the horse is starting to run we’re seeing that it’s not doing so well. Just as a paper in Nature Reviews Genetics cited above argued that pseudogene function is “Prematurely Dismissed,” some Christians are prematurely dismissing orthodox Christian doctrines. Even for those who don’t feel ready to endorse the view that pseudogenes are functional, at the very least an agnostic “wait and see” approach seems prudent, given the poverty of our knowledge and the trendline of the evidence. 

Let’s talk about that trendline. Pseudogenes are just one type of DNA thought to be “junk.” Back in the 1990s and early 2000s, over 90 percent of the genome was commonly thought to be genetic junk — a view that is now rejected by most biologists. Intelligent design theorists predicted that much of junk DNA would turn out to have function. They were right: a revolution has largely taken over biological thinking. While there’s still a lot we don’t know about the genome, the trendline is strongly against the “junk” view. If you don’t believe me, look at the orange line in the top graph of this image from the journal Nature. It shows the rapid, even exponential rate at which functions are being discovered for non-coding genetic elements — which Nature says was “previously called junk DNA.” 

Don’t bet on the wrong horse. Be cautious about throwing away millennia-old doctrines because you’re being told that the consensus demands you must believe that pseudogenes are “broken” genes inherited from our apelike ancestors. The consensus may say this but the evidence doesn’t. If you want to question or fully break with the consensus on pseudogene functionality, the evidence is there to support you. Challenging the consensus shouldn’t be done lightly and requires taking a risk based upon what you think the evidence says. But it was the right thing to do when it came to rejecting evolutionary arguments against a historical Adam and Eve. Let’s be willing to take a risk on pseudogene functionality and follow the evidence where it is leading.

Notes

1. Stephen Schaffner, “What Genetics Says About Adam and Eve,” BioLogos (July 11, 2021), https://biologos.org/articles/what-genetics-say-about-adam-and-eve.
2. “Were Adam and Eve historical figures?,” BioLogos, https://biologos.org/common-questions/were-adam-and-eve-historical-figures/ (accessed October 26, 2021). Biologos notes that this “common traditional” view might be rejected if “the results of scientific inquiry … conflict with traditional interpretations.”
3. S. Joshua Swamidass, The Genealogical Adam and Eve: The Surprising Science of Universal Ancestry (IVP Academic, 2019).
4. See Paul Nelson, “Which Game? Whose Rules?” (August 24, 2020), https://henrycenter.tiu.edu/2020/08/which-game-whose-rules/; Paul Nelson, “Trapped in the Naturalistic Parabola” (June 17, 2020), https://evolutionnews.org/2020/06/trapped-in-the-naturalistic-parabola/; Paul Nelson, “Nelson: Parabolas and Methodological Naturalism (Again)” (June, 2020),https://discourse.peacefulscience.org/t/nelson-parabolas-and-methodological-naturalism-again/10956/2.
5. Robin-Lee Troskie, Geoffrey J. Faulkner, Seth W. Cheetham, “Processed pseudogenes: A substrate for evolutionary innovation,” BioEssays, 2021 (43): 2100186.
6. T. F. Kovalenko and L. I. Patrushev, “Pseudogenes as Functionally Significant Elements of the Genome,” Biochemistry, Vol. 83, No. 11, pp. 1332-1349.
7. Evgeniy S. Balakirev, and Francisco J. Ayala, Pseudogenes, “Are They “Junk” or Functional DNA?,” Annual Review of Genetics, Vol. 37:123–51 (2003).
8. Yan-Zi Wen et al., “Pseudogenes are not pseudo any more,” RNA Biology 9 (January, 2012): 27-32.
9. S. Hirotsune et al. “An expressed pseudogene regulates the messenger-RNA stability of its homologous coding gene,” Nature 423 (May 1, 2003): 91-96; Oliver H. Tam et al., “Pseudogene-derived small interfering RNAs regulate gene expression in mouse oocytes,” Nature 453 (2008): 534-538; D. Zheng and M. B. Gerstein, “The ambiguous boundary between genes and pseudogenes: the dead rise up, or do they?,” Trends in Genetics 23 (May, 2007): 219-224; D. Pain et al., “Multiple Retropseudogenes from Pluripotent Cell-specific Gene Expression Indicates a Potential Signature for Novel Gene Identification,” The Journal of Biological Chemistry 280 (February 25, 2005): 6265-6268; J. Zhang et al., “NANOGP8 is a retrogene expressed in cancers,” FEBS Journal 273 (2006): 1723-1730; Habib et al., “Microdeletion in a FAAH pseudogene identified in a patient with high anandamide concentrations and pain insensitivity,” British Journal of Anaesthesia, Volume 123, Issue 2, August 2019, pp. e249-e253; Lucia L. Prieto-Godino, “Olfactory receptor pseudo-pseudogenes,” Nature, Vol. 539, pp. 93-97 (November 3, 2016); Poliseno et al. “A coding-independent function of gene and pseudogene mRNAs regulates tumour biology.” Nature 465 (2010): 1033-1038; Zhe Ji, Ruisheng Song, Aviv Regev, Kevin Struhl, “Many lncRNAs, 5’UTRs, and pseudogenes are translated and some are likely to express functional proteins,” eLife, 2015, 4:e08890 DOI: 10.7554/eLife.08890; Enrique M. Muro, Nancy Mah, Miguel A. Andrade-Navarro, “Functional evidence of post-transcriptional regulation by pseudogenes,” Biochimie, 93 (2011): 1916-1921; Armin P Piehler, Marit Hellum, Jürgen J Wenzel, Ellen Kaminski, Kari Bente Foss Haug, Peter Kierulf, and Wolfgang E Kaminski, “The human ABC transporter pseudogene family: Evidence for transcription and gene-pseudogene interference,” BMC Genomics, 2008, 9:165; Nicole A Rapicavoli, Kun Qu, Jiajing Zhang, Megan Mikhail, Remi-Martin Laberge, Howard Y Chang, “A mammalian pseudogene lncRNA at the interface of inflammation and anti-inflammatory therapeutics,” eLife, 2013, 2:e00762; Suzuki et al., “Human-Specific NOTCH2NL Genes Expand Cortical Neurogenesis through Delta/Notch Regulation,” Cell, 173: 1370-1384; Fiddes et al, “Human-Specific NOTCH2NL Genes Affect Notch Signaling and Cortical Neurogenesis,” Cell, 173: 1356-1369; Hayashi et al., “The OCT4 pseudogene POU5F1B is amplified and promotes an aggressive phenotype in gastric cancer,” Oncogene, 34: 199-208.
10. ENCODE Project Consortium. “An integrated encyclopedia of DNA elements in the human genome.” Nature, 489 (September 6, 2012): 57-74.
11. Jinrui Xu and Jianzhi Zhang, “Are Human Translated Pseudogenes Functional?,” Molecular Biology and Evolution, Vol. 33(3): 755-760 (2015).
12. Kim et al., “A draft map of the human proteome,” Nature, Vol. 509: 575-581 (May 29, 2014).
13. Oliver H. Tam et al., “Pseudogene-derived small interfering RNAs regulate gene expression in mouse oocytes,” Nature 453 (2008): 534-538
14. Poliseno et al. “A coding-independent function of gene and pseudogene mRNAs regulates tumour biology.” Nature 465 (2010): 1033-1038.
15. T. F. Kovalenko and L. I. Patrushev, “Pseudogenes as Functionally Significant Elements of the Genome,” Biochemistry, Vol. 83, No. 11, pp. 1332-1349.
16. Laura Poliseno, “Pseudogenes: Newly Discovered Players in Human Cancer,” Science Signaling 5 (242) (September 18, 2012).
17. Leonardo Salmena, Laura Poliseno, Yvonne Tay, Lev Kats, and Pier Paolo Pandolfi, “A ceRNA Hypothesis: The Rosetta Stone of a Hidden RNA Language?,” Cell, 146: 353-358 (August 5, 2011).
18. R. C. Pink et al., “Pseudogenes: Pseudo-functional or key regulators in health and disease?” RNA 17 (2011): 792-798.
19. Nicole A Rapicavoli, Kun Qu, Jiajing Zhang, Megan Mikhail, Remi-Martin Laberge, Howard Y Chang, “A mammalian pseudogene lncRNA at the interface of inflammation and anti-inflammatory therapeutics,” eLife, 2013, 2:e00762.
20. Zhe Ji, Ruisheng Song, Aviv Regev, Kevin Struhl, “Many lncRNAs, 5’UTRs, and pseudogenes are translated and some are likely to express functional proteins,” eLife, 2015, 4:e08890 DOI: 10.7554/eLife.08890.
21. Cristina Sisu et al., “Comparative analysis of pseudogenes across three phyla,” Proceedings of the National Academy of Sciences, September 16, 2014, vol. 111, no. 37, pp. 13361-13366.
22. Leonardo Salmena, Laura Poliseno, Yvonne Tay, Lev Kats, and Pier Paolo Pandolfi, “A ceRNA Hypothesis: The Rosetta Stone of a Hidden RNA Language?,” Cell, 146: 353-358 (August 5, 2011).
23. Seth W. Cheetham, Geoffrey J. Faulkner, and Marcel E. Dinger, “Overcoming challenges and dogmas to understand the functions of pseudogenes,” Nature Reviews Genetics, 21: 191–201 (2020)
24. Kenneth Miller, Testimony in Kitzmiller v. Dover Trial. M.D. Pa, Day 1 AM (September 26, 2005).
25. A. Moleirinho, Susana Seixas, Alexandra M. Lopes, Celeste Bento, Maria J. Prata, and Antonio Amorim, “Evolutionary Constraints in the β-Globin Cluster: The Signature of Purifying Selection at the δ-Globin (HBD) Locus and Its Role in Developmental Gene Regulation,” Genome Biology and Evolution 5 (2013): 559-571.

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