No Joke: New Pseudogene Function Smiles on the Case for Creation

By Fazale Rana – April 1, 2020

Time to confess. I now consider myself an evolutionary creationist. I have no choice. The evidence for biological evolution is so overwhelming…

…Just kidding! April Fool’s!

I am still an old-earth creationist. Even though the evolutionary paradigm is the prevailing framework in biology, I am skeptical about facets of it. I am more convinced than ever that a creation model approach is the best way to view life’s origin, design, and history. It’s not to say that there isn’t evidence for common descent; there is. Still, even with this evidence, I prefer old-earth creationism for three reasons.

  • First, a creation model approach can readily accommodate the evidence for common descent within a design framework.
  • Second, the evolutionary paradigm struggles to adequately explain many of the key transitions in life’s history.
  • Third, the impression of design in biology is overwhelming—and it’s becoming more so every day.

And that is no joke.

Take the human genome as an example. When it comes to understanding its structure and function, we are in our infancy. As we grow in our knowledge and insight, it becomes increasingly apparent that the structural and functional features of the human genome (and the genomes of other organisms) display more elegance and sophistication than most life scientists could have ever imagined—at least, those operating within the evolutionary framework. On the other hand, the elegance and sophistication of genomes is expected for creationists and intelligent design advocates. To put it simply, the more we learn about the human genome, the more it appears to be the product of a Mind.

In fact, the advances in genomics over the last decade have forced life scientists to radically alter their views of genome biology. When the human genome was first sequenced in 2000, biologists considered most of the sequence elements to be nonfunctional, useless DNA. Now biologists recognize that virtually every class of these so-called junk DNA sequences serve key functional roles.

If most of the DNA sequence elements in the human genome were truly junk, then I’d agree that it makes sense to view them as evolutionary leftovers, especially because these junk DNA sequences appear in corresponding locations of the human and primate genomes. It is for these reasons that biologists have traditionally interpreted these shared sequences as the most convincing evidence for common descent.

However, now that we have learned that these sequences are functional, I think it is reasonable to regard them as the handiwork of a Creator, intentionally designed to contribute to the genome’s biology. In this framework, the shared DNA sequences in the human and primate genomes reflect common design, not common descent.

Still, many biologists reject the common design interpretation, while continuing to express confidence in the evolutionary model. Their certainty reflects a commitment to methodological naturalism, but there is another reason for their confidence. They argue that the human genome (and the genomes of other organisms) display other architectural and operational features that the evolutionary framework explains best—and, in their view, these features tip the scales toward the evolutionary interpretation.

Yet, researchers continue to make discoveries about junk DNA that counterbalance the evidence for common descent, including these structural and functional features. Recent insights into pseudogene biology nicely illustrate this trend.


Most life scientists view pseudogenes as the remnants of once-functional genes. Along these lines, biologists have identified three categories of pseudogenes (unitary, duplicated, and processed) and proposed three distinct mechanisms to explain the origin of each class. These mechanisms produce distinguishing features that allow investigators to identify certain DNA sequences as pseudogenes. However, a pre-commitment to the evolutionary paradigm can influence many biologists to declare too quickly that pseudogenes are nonfunctional based on their sequence characteristics.1

The Mechanisms of Pseudogene Formation.
Image credit: Wikipedia.

As the old adage goes: theories guide, experiments decide. There is an accumulation of experimental data which indicates that pseudogenes from all three classes have utility.

A number of research teams have demonstrated that the cell’s machinery transcribes processed pseudogenes and, in turn, these transcripts are translated into proteins. Both duplicated and unitary pseudogenes are also transcribed. However, except for a few rare cases, these transcripts are not translated into proteins. Most of duplicated and unitary pseudogene transcripts serve a regulatory role, described by the competitive endogenous RNA hypothesis.

In other words, the experimental support for pseudogene function seemingly hinges on the transcription of these sequences. That leads to the question: What about pseudogene sequences located in genomes that aren’t transcribed? A number of pseudogenic sequences in genomes seemingly sit dormant. They aren’t transcribed and, presumably, have no utility whatsoever.

For many life scientists, this supports the evolutionary account for pseudogene origins, making it the preferred explanation over any model that posits the intentional design of pseudogene sequences. After all, why would a Creator introduce mutationally damaged genes that serve no function? Isn’t it better to explain the presence of functional processed pseudogenes as the result of neofunctionalization, whereby evolutionary mechanisms co-opt processed pseudogenes and use them as the raw material to evolve DNA sequence elements into new genes?

Or, perhaps, is it better to view the transcripts of regulatory unitary and duplicated pseudogenes as the functional remnants of the original genes whose transcripts played a role in regulatory networks with other RNA transcripts? Even though these pseudogenes no longer direct protein production, they can still take part in the regulatory networks comprised of RNA transcripts.

Are Untranscribed Pseudogenes Really Untranscribed?

Again, remember that support for the evolutionary interpretation of pseudogenes rests on the belief that some pseudogenes are not transcribed. What happens to this support if these DNA sequences are transcribed, meaning we simply haven’t detected or identified their transcripts experimentally?

As a case in point, in a piece for Nature Reviews, a team of collaborators from Australia argue that failure to detect pseudogene transcripts experimentally does not confirm the absence of a transcription.2 For example, the transcripts for a pseudogene transcribed at a low level may fall below the experimental detection limit. This particular pseudogene would appear inactive to researchers when, in fact, the opposite is the case. Additionally, pseudogene expression may be tissue-specific or may take place at certain points in the growth and development process. If the assay doesn’t take these possibilities into account, then failure to detect pseudogene transcripts could just mean that the experimental protocol is flawed.

The similarity of the DNA sequences of pseudogenes and their corresponding “sister” genes causes another complication. It can be hard to experimentally distinguish between a pseudogene and its “intact” sister gene. This limitation means that, in some instances, pseudogene transcripts may be misidentified as the transcripts of the “intact” gene. Again, this can lead researchers to conclude mistakenly that the pseudogene isn’t transcribed.

Are Untranscribed Pseudogenes Really Nonfunctional?

These very real experimental challenges notwithstanding, there are pseudogenes that indeed are not transcribed, but it would be wrong to conclude that they have no role in gene regulation. For example, a large team of international collaborators demonstrated that a pseudogene sequence contributes to the specific three-dimensional architecture of chromosomes. By doing so, this sequence exerts influence over gene expression, albeit indirectly.3

Another research team determined that a different pseudogene plays a role in maintaining chromosomal stability. In laboratory experiments, they discovered that deleting the DNA region that harbors this pseudogene increases chromosomal recombination events that result in the deletion of pieces of DNA. This deletion is catastrophic and leads to DiGeorge/velocardiofacial syndrome.4

To be clear, these two studies focused on single pseudogenes. We need to be careful about extrapolating the results to all untranscribed pseudogenes. Nevertheless, at minimum, these findings open up the possibility that other untranscribed pseudogene sequences function in the same way. If past history is anything to go by when it comes to junk DNA, these two discoveries are most likely harbingers of what is to come. Simply put, we continue to uncover unexpected function for pseudogenes (and other classes of junk DNA).

Common Design or Common Descent?

Not that long ago, shared nonfunctional, junk DNA sequences in the human and primate genomes were taken as prima facia evidence for our shared evolutionary history with the great apes. There was no way to genuinely respond to the challenge junk DNA posed to creation models, other than to express the belief that we would one day discover function for junk DNA sequences.

Subsequently, discoveries have fulfilled a key scientific prediction made by creationists and intelligent design proponents alike. These initial discoveries involved single, isolated pseudogenes. Later studies demonstrated that pseudogene function is pervasive, leading to new scientific ideas such as the competitive endogenous RNA hypothesis, that connect the sequence similarity of pseudogenes and “intact” genes to pseudogene function. Researchers are beginning to identify functional roles for untranscribed pseudogenes. I predict that it is only a matter of time before biologists concede that the utility of untranscribed pseudogenes is pervasive and commonplace.

The creation model interpretation of shared junk DNA sequences becomes stronger and stronger with each step forward, which leads me to ask, When are life scientists going to stop fooling around and give a creation model approach a seat at the biology table?


  1. Seth W. Cheetham, Geoffrey J. Faulkner, and Marcel E. Dinger, “Overcoming Challenges and Dogmas to Understand the Functions of Pseudogenes,” Nature Reviews Genetics 21 (December 17, 2019): 191–201, doi:10.1038/s41576-019-0196-1.
  2. Cheetham et al., 191–201.
  3. Peng Huang, et al., “Comparative Analysis of Three-Dimensional Chromosomal Architecture Identifies a Novel Fetal Hemoglobin Regulatory Element,” Genes and Development 31, no. 16 (August 15, 2017): 1704–13, doi: 10.1101/gad.303461.117.
  4. Laia Vergés et al., “An Exploratory Study of Predisposing Genetic Factors for DiGeorge/Velocardiofacial Syndrome,” Scientific Reports 7 (January 6, 2017): id. 40031, doi: 10.1038/srep40031.

Reprinted with permission by the author

Original article at:

Biochemical Synonyms Restate the Case for a Creator

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Sometimes I just can’t help myself. I know it’s clickbait but I click on the link anyway.

A few days ago, as a result of momentary weakness, I found myself reading an article from the ScoopWhoop website, “16 Things Most of Us Think Are the Same but Actually Aren’t.”

OK. OK. Now that you saw the title you want to click on the link, too.

To save you from wasting five minutes of your life, here is the ScoopWhoop list:

  • Weather and Climate
  • Turtle and Tortoise
  • Jam and Jelly
  • Eraser and Rubber
  • Great Britain and the UK
  • Pill and Tablet
  • Shrimp and Prawn
  • Butter and Margarine
  • Orange and Tangerine
  • Biscuits and Cookies
  • Cupcakes and Muffins
  • Mushrooms and Toadstools
  • Tofu and Paneer
  • Rabbits and Hares
  • Alligators and Crocodiles
  • Rats and Mice

And there you have it. Not a very impressive list, really.

If I were putting together a biochemist’s version of this list, I would start with synonymous mutations. Even though many life scientists think they are the same, studies indicate that they “actually aren’t.”

If you have no idea what I am talking about or what this insight has to do with the creation/evolution debate, let me explain by starting with some background information, beginning with the central dogma of molecular biology and the genetic code.

Central Dogma of Molecular Biology

According to this tenet of molecular biology, the information stored in DNA is functionally expressed through the activities of proteins. When it is time for the cell’s machinery to produce a particular protein, it copies the appropriate information from the DNA molecule through a process called transcription and produces a molecule called messenger RNA(mRNA). Once assembled, mRNA migrates to the ribosome, where it directs the synthesis of proteins through a process known as translation.


Figure 1: The central dogma of molecular biology. Image credit: Shutterstock

The Genetic Code

At first glance, there appears to be a mismatch between the stored information in DNA and the information expressed in proteins. A one-to-one relationship cannot exist between the four different nucleotides that make up DNA and the twenty different amino acids used to assemble proteins. The cell handles this mismatch by using a code comprised of groupings of three nucleotides, called codons, to specify the twenty different amino acids.



Figure 2: Codons. Image credit: Wikipedia

The cell uses a set of rules to relate these nucleotide triplet sequences to the twenty amino acids that comprise proteins. Molecular biologists refer to this set of rules as the genetic code. The nucleotide triplets represent the fundamental units of the genetic code. The code uses each combination of nucleotide triplets to signify an amino acid. This code is essentially universal among all living organisms.

Sixty-four codons make up the genetic code. Because the code only needs to encode twenty amino acids, some of the codons are redundant. That is, different codons code for the same amino acid. In fact, up to six different codons specify some amino acids. Others are specified by only one codon.1


Figure 3: The genetic code. Image credit: Shutterstock

A little more background information about mutations will help fill out the picture.


A mutation refers to any change that takes place in the DNA nucleotide sequence. DNA can experience several different types of mutations. Substitution mutations are one common type. When a substitution mutation occurs, one (or more) of the nucleotides in the DNA strand is replaced by another nucleotide. For example, an A may be replaced by a G, or a C may be replaced by a T. This substitution changes the codon. Interestingly, the genetic code is structured in such a way that when substitution mutations take place, the resulting codon often specifies the same amino acid (due to redundancy) or an amino acid that has similar chemical and physical properties to the amino acid originally encoded.

Synonymous and Nonsynonymous Mutations

When substitution mutations generate a new codon that specifies the same amino acid as initially encoded, it’s referred to as a synonymous mutation. However, when a substitution produces a codon that specifies a different amino acid, it’s called a nonsynonymous mutation.

Nonsynonymous mutations can be deleterious if they affect a critical amino acid or if they significantly alter the chemical and physical profile along the protein chain. If the substituted amino acid possesses dramatically different physicochemical properties from the native amino acid, it may cause the protein to fold improperly. Improper folding impacts the protein’s structure, yielding a biomolecule with reduced or even lost function.

On the other hand, biochemists have long thought that synonymous mutations have no effect on protein structure and function because these types of mutations don’t change the amino acid sequences of proteins. Even though biochemists think that synonymous mutations are silent—having no functional consequences—evolutionary biologists find ways to use them, including using patterns of synonymous mutations to establish evolutionary relationships.

Patterns of Synonymous Mutations and the Case for Biological Evolution

Evolutionary biologists consider shared genetic features found in organisms that naturally group together as compelling evidence for common descent. One feature of particular interest is the identical (or nearly identical) DNA sequence patterns found in genomes. According to this line of reasoning, the shared patterns arose as a result of a series of substitution mutations that occurred in the common ancestor’s genome. Presumably, as the varying evolutionary lineages diverged from the nexus point, they carried with them the altered sequences created by the primordial mutations.

Synonymous mutations play a significant role in this particular argument for common descent. Because synonymous mutations don’t alter the amino acid sequence of proteins, their effects are considered to be inconsequential. So, when the same (or nearly the same) patterns of synonymous mutations are observed in genomes of organisms that cluster together into the same group, most life scientists interpret them as compelling evidence of the organisms’ common evolutionary history.

It is conceivable that nonsynonymous mutations, which alter the protein amino acid sequences, may impart some type of benefit and, therefore, shared patterns of nonsynonymous changes could be understood as evidence for shared design. (See the last section of this article.) But this is not the case when it comes to synonymous mutations, which raises the question: Why would a Creator intentionally introduce new codons that code for the same amino acid into genes when these changes have no functional utility?

Apart from invoking a Creator, the shared patterns of synonymous mutations make perfect sense if genomes have been shaped by evolutionary processes and an evolutionary history. However, this argument for biological evolution (shared ancestry) and challenge to a creation model interpretation (shared design) hinges on the underlying assumption that synonymous mutations have no functional consequence.

But what if this assumption no longer holds?

Synonymous Mutations Are Not Interchangeable

Biochemists used to think that synonymous mutations had no impact whatsoever on protein structure and, hence, function, but this view is changing thanks to studies such as the one carried out by researchers at University of Colorado, Boulder.2

These researchers discovered synonymous mutations that increase the translational efficiency of a gene (found in the genome of Salmonella enterica). This gene codes for an enzyme that plays a role in the biosynthetic pathway for the amino acid arginine. (This enzyme also plays a role in the biosynthesis of proline.) They believe that these mutations alter the three-dimensional structure of the DNA sequence near the beginning of the coding portion of the gene. They also think that the synonymous mutations improve the stability of the messenger RNA molecule. Both effects would lead to greater translational efficiency at the ribosome.

As radical (and unexpected) as this finding may seem to be, it follows on the heels of other recent discoveries that also recognize the functional importance of synonymous mutations.3Generally speaking, biochemists have discovered that synonymous mutations function to influence not only the rate and efficiency of translation (as the scientists from the University of Colorado, Bolder learned) and the folding of the proteins after they are produced at the ribosome.

Even though synonymous mutations leave the amino acid sequence of the protein unchanged, they can exert influence by altering the:

  • regulatory regions of the gene that influence the transcription rate
  • secondary and tertiary structure of messenger RNA that influences the rate of translation
  • stability of messenger RNA that influences the amount of protein produced
  • translation rate that influences the folding of the protein as it exits the ribosome

Biochemists are just beginning to come to terms with the significance of these discoveries, but it is already clear that synonymous mutations have biomedical consequences.They also impact models for molecular evolution. But for now, I want to focus on the impact these discoveries has on the creation/evolution debate.

Patterns of Synonymous Mutations and the Case for Creation

As noted, many people consider the most compelling evidence for common descent to be the shared genetic features displayed by organisms that naturally cluster together. But if life is the product of a Creator’s handiwork, the shared genetic features could be understood as shared designs deployed by a Creator. In fact, a historical precedent exists for the common design interpretation. Prior to Darwin, biologists viewed shared biological features as manifestations of archetypical designs that existed in the Creator’s mind.

But the common design interpretation requires that the shared features be functional. (Or, that they arise independently in a nonrandom manner.) For those who view life from the framework of the evolutionary paradigm, the shared patterns of synonymous mutations invalidate the common design explanation—because these mutations are considered to be functionally insignificant.

But in the face of mounting evidence for the functional importance of synonymous mutations, this objection to common design has begun to erode. Though many life scientists are quick to dismiss the common design interpretation of biology, advances in molecular biology continue to strengthen this explanation and, with it, the case for a Creator.


  1. As I discuss in The Cell’s Design, the rules of the genetic code and the nature of the redundancy appear to be designed to minimize errors in translating information from DNA into proteins that would occur due to substitution mutations. This optimization stands as evidence for the work of an intelligent Agent.
  2. JohnCarlo Kristofich et al., “Synonymous Mutations Make Dramatic Contributions to Fitness When Growth Is Limited by Weak-Link Enzyme,” PLoS Genetics 14, no. 8 (August 27, 2018): e1007615, doi:10.1371/journal.pgen.1007615.
  3. Here are a few representative studies that ascribe functional significance to synonymous mutations: Anton A. Komar, Thierry Lesnik, and Claude Reiss, “Synonymous Codon Substitutions Affect Ribosome Traffic and Protein Folding during in vitro Translation,” FEBS Letters 462, no. 3 (November 30, 1999): 387–91, doi:10.1016/S0014-5793(99)01566-5; Chung-Jung Tsai et al., “Synonymous Mutations and Ribosome Stalling Can Lead to Altered Folding Pathways and Distinct Minima,” Journal of Molecular Biology 383, no. 2 (November 7, 2008): 281–91, doi:10.1016/j.jmb.2008.08.012; Florian Buhr et al., “Synonymous Codons Direct Cotranslational Folding toward Different Protein Conformations,” Molecular Cell Biology 61, no. 3 (February 4, 2016): 341–51, doi:10.1016/j.molcel.2016.01.008; Chien-Hung Yu et al., “Codon Usage Influences the Local Rate of Translation Elongation to Regulate Co-translational Protein Folding,” Molecular Cell Biology 59, no. 5 (September 3, 2015): 744–55, doi:10.1016/j.molcel.2015.07.018.
  4. Zubin E. Sauna and Chava Kimchi-Sarfaty,” Understanding the Contribution of Synonymous Mutations to Human Disease,” Nature Reviews Genetics 12 (August 31, 2011): 683–91, doi:10.1038/nrg3051.

Reprinted with permission by the author
Original article at:

Discovery of Intron Function Interrupts Evolutionary Paradigm

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Nobody likes to be interrupted when they are talking. It feels disrespectful and can be frustrating. Interruptions derail the flow of a conversation.

The editors tell me that I need to interrupt this lead to provide a “tease” for what is to come. So, here goes: Interruptions happen in biochemical systems, too. Life scientists long thought that these interruptions disrupted the flow of biochemical information. But, it turns out these interruptions serve an important function, offering a rejoinder a common argument against intelligent design.

Now back to the lead.

Perhaps it is no surprise that some psychologists study interruptions1 with the hope of discovering answers to questions such as:

  • Why do people interrupt?
  • Who is most likely to interrupt?
  • Do we all perceive interruptions in the same way?

While there is still much to learn about the science of interruptions, psychologists have discovered that men interrupt more often than women. Ironically, men often view women who interrupt as ruder and less intelligent than men who interrupt during conversations.

Researchers have also found that a person’s cultural background influences the likelihood that he or she will interrupt during a discourse. Personality also plays a role. Some people are more sensitive to pauses in conversation and, therefore, find themselves interrupting more often than those who are less uncomfortable with periods of silence.

Psychologists have learned that not all interruptions are the same. Some people interrupt because they want the “floor.” These people are called intrusive interrupters. Cooperativeinterrupters help move the conversation along by agreeing with the speaker and finishing the speaker’s thoughts.

Interruptions are not confined to conversations. They are a part of life, including the biochemical operations that take place inside the cell.

In fact, biochemists have discovered that the information harbored in genes, which contains the instructions to build proteins—the workhorse molecules of the cell—experience interruptions in their coding sequences. These intrusive interruptions would disrupt the flow of information in the cell during the process of protein synthesis if the interrupting sequences weren’t removed by the cell’s machinery.

Molecular biologists have long viewed these genetic “interruptions” (called introns) as serving no useful purpose for the cell, with introns comprising a portion of the junk DNA found in the genomes of eukaryotic organisms. But it turns out that introns—like cooperative interruptions during a conversation—serve a useful purpose, according to the recent work of two independent teams of molecular biologists.

Introns Are Abundant

Noncoding regions within genes, introns consist of DNA sequences that interrupt the coding regions (called exons) of a gene. Introns are pervasive in genomes of eukaryotic organisms. For example, 90 percent of genes in mammals consists of introns, with an average of 8 per gene.

After the information stored in a gene is copied into messenger RNA, the intron sequences are excised, and the exons spliced together by a protein-RNA complex known as a spliceosome.


Figure 1: Drawing of pre-mRNA to mRNA. Image credit: Wikipedia

Molecular biologists have long wondered why eukaryotic genes would be riddled with introns. Introns seemingly make the structure and expression of eukaryotic genes unnecessarily complicated. What possible purpose could introns serve? Researchers also thought that once the introns were spliced out of the messenger RNA sequences, they were discarded as genetic debris.

Introns Serve a Functional Purpose

But recent work by two independent research teams from Sherbrooke University in Quebec, Canada, and MIT, respectively, indicates that molecular biologists have been wrong about introns. They have learned that once spliced from messenger RNA, these fragments play a role in helping cells respond to stress.

Both research teams studied baker’s yeast. One advantage of using yeast as a model organism relates to the relatively small number of introns (295) in its genome.


Figure 2: A depiction of baker’s yeast. Image credit: Shutterstock

Taking advantage of the limited number of introns in baker’s yeast, the team from Sherbrooke University created hundreds of yeast strains—each one missing just one of its introns. When grown under normal conditions with a ready supply of available nutrients, the strains missing a single intron grew normally—suggesting that introns aren’t of much importance. But when the researchers grew the yeast cells under conditions of food scarcity, the yeast with the deleted introns frequently died.2

The MIT team observed something similar. They noticed that during the stationary phase of growth (when nutrients become depleted, slowing down growth), introns spliced from RNA accumulated in the growth medium. The researchers deleted the specific introns that they found in the growth medium from the baker’s yeast genome and discovered that the resulting yeast strains struggled to survive under nutrient-poor conditions.3

At this point, it isn’t clear how introns help cells respond to stress caused by a lack of nutrients, but they have some clues. The Sherbrooke University team thinks that the spliced-out introns play a role in repressing the production of proteins that help form ribosomes. These biochemical machines manufacture proteins. Because protein synthesis requires building block materials and energy, during periods when nutrients are scarce, protein production slows down in cells. Ratcheting down protein synthesis impedes cell growth but affords them a better chance to survive a lack of nutrients. One way cells can achieve this objective is to stop making ribosomes.

The MIT team thinks that some spliced-out introns interact with spliceosomes, preventing them from splicing out other introns. When this disruption happens, it slows down protein synthesis.

Both research groups believe that in times when nutrients are abundant, the spliced-out introns are broken down by the cell’s machinery. But when nutrients are scarce, that condition triggers intron accumulation.

At this juncture, it isn’t clear if the two research teams have uncovered distinct mechanisms that work collaboratively to slow down protein production, or if they are observing facets of the same mechanism. Regardless, it is evident that introns display functional utility. It’s a surprising insight that has important ramifications for our understanding of the structure and function of genomes. This insight has potential biomedical utility and theological implications, as well.

Intron Function and the Case for Creation

Scientists who view biology through the lens of the evolutionary paradigm are quick to conclude that the genomes of organisms reflect the outworking of evolutionary history. Their perspective causes them to see the features of genomes, such as introns, as little more than the remnants of an unguided evolutionary process. Within this framework, there is no reason to think that any particular DNA sequence element, including introns, harbors function. In fact, many life scientists regard the “evolutionary vestiges” in the genome as junk DNA. This clearly has been the case for introns.

Yet, a growing body of data indicates that virtually every category of so-called junk DNA displays function. We can now add introns—cooperative interrupters—to the list. And based on the data on hand, we can make a strong case that most of the sequence elements in genomes possess functional utility.

Could it be that scientists really don’t understand the biology of genomes? Or maybe we have the wrong paradigm?

It seems to me that science is in the midst of a revolution in our understanding of genome structure and function. Instead of being a wasteland of evolutionary debris, most of the genome appears to be functional. And the architecture and operations of genomes appear to be far more elegant and sophisticated than anyone ever imagined—at least within the confines of the evolutionary paradigm.

But what if the genome is viewed from a creation model framework?

The elegance and sophistication of genomes are features that are increasingly coming into scientific view. And this is precisely what I would expect if genomes were the product of a Mind—the handiwork of a Creator.

Now that is a discovery worth talking about.


  1. Teal Burrell, “The Science behind Interrupting: Gender, Nationality and Power, and the Roles They Play,” Post Magazine (March 14, 2018),; Alex Shashkevich, “Why Do People Interrupt? It Depends on Whom You’re Talking To,” The Guardian (May 18, 2018),
  2. Julie Parenteau et al., “Introns Are Mediators of Cell Response to Starvation,” Nature 565 (January 16, 2019): 612–17, doi:10.1038/s41586-018-0859-7.
  3. Jeffrey T. Morgan, Gerald R. Fink, and David P. Bartel, “Excised Linear Introns Regulate Growth in Yeast,” Nature 565 (January 16, 2019): 606–11, doi:10.1038/s41586-018-0828-1.

Reprinted with permission by the author
Original article at:

Mitochondria’s Deviant Genetic Code: Evolution or Creation?



When I was in high school, I had the well-deserved reputation of being a wise guy—though the people who knew me then might have preferred to call me a wise—, instead. Either way, for being a wise guy, I sure didn’t display much wisdom during my teenage years.

I would like to think that I am wiser today. But, the little wisdom I do possess didn’t come easy. To quote singer and songwriter, Helen Reddy, “It’s wisdom born of pain.”

Life’s hardships sure have a way of teaching you lessons. But, I also learned that there is a shortcut to gaining wisdom—if you are wise enough to recognize it. (See what I did there?) It is better to solicit the advice of wise people than to gain wisdom through life’s bitter experiences. And, perhaps there was no wiser person ever than Solomon. Thankfully, Solomon’s wisdom was captured in the book of Proverbs. Many of life’s difficulties can be sidestepped if we are willing to heed Solomon’s advice.

Solomon gained his wisdom through observation and careful reflection. But, his wisdom also came through divine inspiration, and according to Solomon, it was through wisdom that God created the world in which we live (Proverbs 8:22–31). And, it is out of this wisdom that the Holy Spirit inspired Solomon to offer the insights found in the Proverbs.

In Psalm 104, the Psalmist (presumably David) echoes the same idea as Solomon: God created our world through wisdom. The Psalmist writes:

How many are your works, Lord!

In wisdom you made them all;

Based on Proverbs 8 and Psalm 104, I would expect God’s wisdom to be manifested in the created order. The Creator’s fingerprints—so evident in nature—should not only reflect the work of intelligent agency but also display undeniable wisdom. In my view, that wisdom should be reflected in the elegance, cleverness, and ingenuity of the designs seen throughout nature. Designs that reflect an underlying purpose. And these features are exactly what we observe when we study the biological realm—as demonstrated by recent work on aquatic mammal body size conducted by investigators from Stanford University.1

Body Sizes of Aquatic Mammals

Though the majority of the world’s mammals live in terrestrial habitats, the most massive members of this group reside in Earth’s oceans. For evolutionary biologists, common wisdom has it that the larger size of aquatic mammals reflects fewer evolutionary constraints on their body size because they live in the ocean. After all, the ocean habitat is more expansive than those found on land, and aquatic animals don’t need to support their weight because they are buoyed by the ocean.

As it turns out, common wisdom is wrong in this case. Through the use of mathematical modeling (employing body mass data from about 3,800 living species of aquatic mammals and around 3,000 fossil species), the research team from Stanford learned that living in an aquatic setting imposes tight constraints on body size, much more so than when animals live on land. In fact, they discovered (all things being equal) that the optimal body mass for aquatic mammals is around 1,000 pounds. Interestingly, the body mass distributions for members of the order Sirenia (dugongs and manatees), and the clades Cetacea (whales and dolphins), and Pinnipeds (sea lions and seals) cluster near 1,000 pounds.

Scientists have learned that the optimal body mass of aquatic mammals displays an underlying biological rationale and logic. It reflects a trade-off between two opposing demands: heat retention and caloric intake. Because the water temperatures of the oceans are below mammals’ body temperatures, heat retention becomes a real problem. Mammals with smaller bodies can’t consume enough food to compensate for heat loss to the oceans, and they don’t have the mass to retain body heat. The way around this problem is to increase their body mass. Larger bodies do a much better job at retaining heat than do smaller bodies. But, the increase in body mass can’t go unchecked. Maintaining a large body requires calories. At some point, metabolic demands outpace the capacity for aquatic mammals to feed, so body mass has to be capped (near 1,000 pounds).

The researchers noted a few exceptions to this newly discovered “rule.” Baleen whales have a body mass that is much greater than 1,000 pounds. But, as the researchers noted, these creatures employ a unique feeding mechanism that allows them to consume calories needed to support their massive body sizes. Filter feeding is a more efficient way to consume calories than hunting prey. The other exception is creatures such as otters. The researchers believe that their small size reflects a lifestyle that exploits both aquatic and terrestrial habitats.

Argument for God’s Existence from Wisdom

The discovery that the body mass of aquatic mammals has been optimized is one more example of the many elegant designs found in biological systems—designs worthy to be called the Creator’s handiwork. However, from my perspective, this optimization also reflects the Creator’s sagacity as he designed mammals for the purpose of living in the earth’s oceans.

But, instead of relying on intuition alone to make a case for a Creator, I want to present a formal argument for God’s existence based on the wisdom of biology’s designs. To make this argument, I follow after philosopher Richard Swinburne’s case for God’s existence based on beauty. Swinburne argues, “If God creates a universe, as a good workman he will create a beautiful universe. On the other hand, if the universe came into existence without being created by God, there is no reason to suppose that it would be a beautiful universe.”2 In other words, the beauty in the world around us signifies the Divine.

In like manner, if God created the universe, including the biological realm, we should expect to see wisdom permeating the designs in nature. On the other hand, if the universe came into being without God’s involvement, then there is no reason to think that the designs in nature would display a cleverness and ingenuity that affords a purpose—a sagacity, if you will. In fact, evolutionary biologists are quick to assert that most biological designs are flawed in some way. They argue that there is no purpose that undergirds biological systems. Why? Because evolutionary processes do not produce biological systems from scratch, but from preexisting systems that are co-opted through a process dubbed exaptation (by the late evolutionary biologist Stephen Jay Gould), and then modified by natural selection to produce new designs.3 According to biologist Ken Miller:

“Evolution . . . does not produce perfection. The fact that every intermediate stage in the development of an organ must confer a selective advantage means that the simplest and most elegant design for an organ cannot always be produced by evolution. In fact, the hallmark of evolution is the modification of pre-existing structures. An evolved organism, in short, should show the tell-tale signs of this modification.”4

And yet we see designs in biology that are not just optimized, but characterized by elegance, cleverness, and ingenuity—wisdom.

Truly, God is a wise guy.



  1. William Gearty, Craig R. McClain, and Jonathan L. Payne, “Energetic Tradeoffs Control the Size Distribution of Aquatic Mammals,” Proceedings of the National Academy of Sciences USA (March 2018): doi:10.1073/pnas.1712629115.
  2. Richard Swinburne, The Existence of God, 2nd ed. (New York: Oxford University Press, 2004), 190–91.
  3. Stephen Jay Gould and Elizabeth S. Vrba, “Exaptation: A Missing Term in the Science of Form,” Paleobiology8 (January 1, 1982): 4–15, doi:10.1017/S0094837300004310.
  4. Kenneth R. Miller, “Life’s Grand Design,” Technology Review 97 (February/March 1994): 24–32.
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Duck-Billed Platypus Venom: Designed for Discovery



I wouldn’t classify it as a bucket-list experience, but it was off-the-charts cool to see a duck-billed platypus up close a few years ago when my wife and I visited Tasmania. This little creature reminded me of a beaver as he swam around in the water.

But as cute and cuddly as the duck-billed platypus appears to be, I came to learn (not by experience but by listening to the zookeeper) that you don’t want to mess with this egg-laying mammal. The platypus has spurs on its hind feet, and for males, the spurs are loaded with venom. Being struck by a platypus’s spurs is no pleasant thing. The venom can kill a small animal (such as a dog) and cause excruciating pain for humans.

Not only does the duck-billed platypus fascinate animal lovers, it has captured the attention of the scientific community. This creature is neither a placental nor a marsupial mammal. Instead, it belongs to an unusual group called the monotremes. Biologists regard monotremes as primitive mammals. And because they group apart from other mammals, many life scientists believe that they can learn a lot about the mammalian biology (including human biology) through comparative studies of the monotremes.

Recently, researchers from Australia demonstrated the value of studying platypus biology when they discovered that a gut hormone (GLP-1) which regulates blood sugar levels doubles as a component in the duck-billed platypus’s venom.1 They believe that this insight may lead to a new drug treatment for type 2 diabetes.

To appreciate why this research team thinks that the platypus GLP-1 hormone may have use in treating diabetes, a little background is in order.


Found in all mammals, glucagon-like peptide-1 (GLP-1) belongs to a family of biomolecules called incretins. These compounds serve as metabolic hormones that stimulate a decrease in blood glucose levels. Secreted in the gut, GLP-1 ultimately lowers blood sugar levels by making its way through the blood stream to the pancreas. GLP-1 stimulates the beta-cells in the pancreas to release insulin. In turn, insulin causes the liver, muscles, and adipose tissues to take up glucose from the blood.

GLP-1 is named after glucagon. A blood hormone, glucagon has the opposite effect as insulin. When released by the alpha-cells of the pancreas, glucagon stimulates the liver to break down glycogen and then release glucose into the blood stream. Glucagon exerts its effect when the blood sugar level drops. Like GLP-1, glucagon also stimulates insulin release, so when the blood sugar level rises (because of glucagon’s release from the alpha-cells), the sugar is quickly taken up by muscle and adipose tissues.

Image: Insulin and glucagon regulate blood glucose levels in the human anatomy, specifically the liver and pancreas.

Eating food stimulates the release of GLP-1 in the gut. This ingenious design ensures that insulin is released and the liver, muscles, and fat tissues are poised to take up glucose even before blood sugar levels rise as nutrients are absorbed into the bloodstream via the digestion process. This preparation is vital, because elevated levels of blood sugar have dangerous long-term consequences.

Platypus Venom

To the surprise of the Australian researchers, the venom of the duck-billed platypus contains GLP-1. Other animals, such as the Gila monster, have venom components that are structurally analogous to GLP-1, but are distinct molecules. (In the Gila monster, this bio-compound is called exendin-4.) Again, an ingenious design. Including incretins in venom causes blood sugar levels to drop after the venom is injected into the victim. Lowered blood sugar levels create confusion and lethargy.

Unlike GLP-1, GLP-1-like venom components of, say, the Gila monster, are long-lived in the bloodstream because they have structural features that make them resistant to digestive enzymes such as dipeptidyl peptidase. This enzyme targets GLP-1 after its release to ensure it is quickly destroyed once this gut hormone triggers insulin release. If not quickly removed, insulin release would persist, thereby causing blood sugar to plummet to dangerously low levels.

The structure of the GLP-1 produced by the duck-billed platypus appears to be fine-tuned so that this biomolecule can balance its two roles as a gut hormone and a venom component. And this property makes the platypus GLP-1 an intriguing molecule to biomedical scientists looking for more effective ways to treat type 2 diabetes. The duck-billed platypus GLP-1 is an actual gut hormone (as opposed to an analog), but is much longer lasting, which makes it an ideal anti-diabetic drug.

Type 2 Diabetes

The most common form of the disease, type 2 diabetes results primarily from lifestyle effects: namely, obesity and lack of exercise. (Although there also appears to be a genetic contribution to this form of diabetes.) In type 2 diabetes, the capacity of beta-cells in the pancreas to secrete insulin becomes impaired, usually because of the accumulation of amylose in their interior. Reduced insulin secretion causes blood sugar levels to remain elevated at dangerously high levels. Persistently elevated blood sugar levels can lead to heart disease, stroke, loss of vision, kidney failure, and impaired blood circulation to the extremities.

Treatment for type 2 diabetes centers around dietary changes designed for keeping blood sugar levels low, weight loss, and increased exercise. Anti-diabetic medications also play an important role in managing type 2 diabetes. Pharmacologists have developed an arsenal of drugs, but all of them have their shortcomings.

Platypus GLP-1 as an Anti-Diabetic Medication

Because of the limitations of current anti-diabetic medications, pharmacologists are intrigued by the platypus version of GLP-1. Like all variants found among mammals, this gut hormone lowers blood glucose levels, but because it doubles as a venom component, it has a longer half-life than the GLP-1 hormones produced by other mammals—an ideal set of properties for an anti-diabetic drug. In fact, there is already a precedent for using venom components to treat diabetes. Exendin-4 from the Gila monster has been developed into a last resort anti-diabetic drug called Exenatide.

The Case for Evolution, the Case for Creation

It’s provocative that the biology of a creature, such as the duck-billed platypus, could provide such important insight into human biology that it can drive new drug development, positively impacting human health.

This study highlights the clever designs that characterize biochemical systems. The function of GLP-1 as an incretin and, in turn, its employ as a venom component are nothing less than genius. The elegance and sophistication of biochemical systems are precisely the characteristics I, a Christian biochemist, would expect to see, if, indeed, life stems from a Creator’s handiwork. In contrast, sophistication and ingenuity aren’t the features I would expect if evolutionary mechanisms—which are unguided, co-opting preexisting designs and cobbling them together to produce new designs—have generated biochemical systems.

Still, many people in the scientific community would argue that as hard as it may be to believe that biochemical systems evolved, it must be the case. Why? Because of the shared features that characterize these systems. As a case in point, the GLP-1 gut hormone is found in all mammals. So, presumably, this biomolecule emerged in the evolutionary ancestor of mammals and persists in all mammals today. Likewise, the shared features of GLP-1 and exendin-4 found in the Gila monster venom indicate to many biologists that the venom component must be evolutionarily derived from GLP-1.

Yet, as a creationist and an intelligent design proponent, I choose to interpret the universal nature of the cell’s chemistry and shared features of biochemical systems as manifestations of archetypical designs that emanate from the Creator’s mind—inspired by the thinking of Sir Richard Owen. To put it differently, for me, the shared features reflect common design, not common descent.

Of course, this leads to the follow-up rebuttal: Why would God create using the same template? Why not create each biochemical system from scratch to be ideally suited for its function? As I pointed out recently, there may well be several reasons why a Creator would design living systems around a common set of templates. In my estimation, the most significant reason is discoverability. The shared features of biochemical systems make it possible to apply what we learn by studying one organisms to all others, in some cases. As a case in point: The occurrence of GLP-1 in all mammals and the shared features of GLP-1 and exendin-4 make it possible to gain insight into human biology by studying the duck-billed platypus.

This discoverability makes it easier to appreciate God’s glory and grandeur, as evinced in biochemical systems by their elegance, sophistication, and ingenuity.

Discoverability of biochemical systems also reflect God’s providence and care for humanity. If not for the shared features, it would be nearly impossible for us to learn enough about the living realm for our benefit. Where would biomedical science be without the ability to learn fundamental aspects about our biology by studying model organisms such as yeast, fruit flies, and mice? How would it be possible to identify new medications if not for the biochemical similarities between humans and other creatures, such as the duck-billed platypus?

Far from making no sense, the shared features in biochemistry are a manifestation of the Creator’s care and love for humanity.



  1. Enkhjargal Tsend-Ayush et al., “Monotreme Glucagon-Like Peptide-1 in Venom and Gut: One Gene—Two Very Different Functions,” Scientific Reports 6 (November 29, 2016): id. 37744, doi:10.1038/srep37744.
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