Evolutionary Story Tells the Tale of Creation


By Fazale Rana – December 4, 2019

Story Telling in the Evolutionary Paradigm

Storytelling isn’t just the purview of a mischievous kid facing the music in the principal’s office, it is part of the construct of science.

Recent work by a team of scientific investigators from the University of Florida (UF) highlights the central role that storytelling plays in evolutionary biology.1 In fact, it is not uncommon for evolutionary biologists to weave grand narratives that offer plausible evolutionary stories for the emergence of biological or behavioral traits. And, though these accounts seem scientific, they are often unverifiable scientific explanations.

Inspired by Rudyard Kipling’s (1865–1936) book of children’s origin stories, the late evolutionary biologist Stephen Jay Gould (1941–2002) referred to these evolutionary tales as just-so stories. To be fair, others have been critical of Gould’s cynical view of evolutionary accounts, arguing that, in reality, just-so stories in evolutionary biology are actually hypotheses about evolutionary transformations. But still, more often than not, these “hypotheses” appear to be little more than convenient fictions.

An Evolutionary Just-So Story of Moths and Bats

The traditional evolutionary account of ultrasonic sound detection in nocturnal moths serves as a case in point. Moths (and butterflies) belong to one of the most important groups of insects: lepidoptera. This group consists of about 160,000 species, with nocturnal moths comprising over 75 percent of the group.

Moths play a key role in ecosystems. For example, they serve as one of the primary food sources for bats. Bats use echolocation to help them locate moths at night. Bats emit ultrasonic cries that bounce off the moths and reflect back to the bats, giving these predators the pinpoint location of the moths, even during flight.

Many nocturnal moth species have defenses that help them escape predation by bats. One defense is ears (located in different areas of their bodies) that detect ultrasonic sounds. This capability allows the moths to hear the bats coming and get out of their way.

For nearly a half century, evolutionary biologists explained moths’ ability to hear ultrasonic sounds as the outworking of an “evolutionary arms race” between echolocating bats and nocturnal moths. Presumably, bats evolved the ability to echolocate, allowing them to detect and prey upon moths at night by plucking them out of the air in mid-flight. In response, some groups of moths evolved ears that allowed them to detect the ultrasonic screeches emitted by bats, helping them to avoid detection.


Figure: Flying Pipistrelle bat. Image credit: Shutterstock

For 50 years, biologists have studied the relationship between echolocating bats and nocturnal moths with the assumption that this explanation is true. (I doubt Mr. Reynolds ever assumed my stories were true.) In fact, evolutionary accounts like this one provide evidence for the idea of coevolution. Advanced by Paul Ehrlich and Peter Raven in 1964, this evolutionary model maintains that ecosystems are shaped by species that affect one another’s evolution.

If the UF team’s work is to be believed, then it turns out that the story recounting the evolutionary arms race between nocturnal moths and echolocating bats is fictional. As team member Jesse Barber, a researcher who has studied bats and moths, complains, “Most of the introductions I’ve written in my papers [describing the coevolution of bats and moths] are wrong.”2

An Evolutionary Study on the Origin of Moths and Butterflies

To reach this conclusion, the UF team generated the most robust evolutionary tree (phylogeny) for lepidopterans to date. They also developed an understanding of the timing of events in lepidopteran natural history. They were motivated to take on this challenge because of the ecological importance of moths and butterflies. As noted, these insects play a central role in terrestrial ecosystems all over the world and coevolutionary models provide the chief explanations for their place in these ecosystems. But, as the UF researchers note, “These hypotheses have not been rigorously tested, because a robust lepidopteran phylogeny and timing of evolutionary novelties are lacking.”3

To remedy this problem, the researchers built a lepidopteran evolutionary tree from a data set of DNA sequences that collectively specified 2,100 protein-coding genes from 186 lepidopteran species. These species represented all the major divisions within this biological group. Then, they dated the evolutionary timing of key events in lepidopteran natural history from the fossil record.

Based on their analysis, the research team concluded that the first lepidopteran appeared around 300 million years ago. This creature fed on nonvascular plants. Around 240 million years ago, lepidopterans with tubelike proboscises (long, sucking mouthpiece) appeared, allowing these insects to extract nectar from flowering plants.

These results cohere with the coevolutionary model that the first lepidopterans fed internally on plants and, later, externally, as they evolved the ability to access nectar from plants. Flowering plants appear around 260 million years ago, which is about the time that the tubelike proboscis appears in lepidopterans.

But perhaps the most important and stunning finding from their study stems from the appearance of hearing organs in moths. It looks as if these organs arose independently 9 separate times—around 80 to 90 million years ago—well before bats began to echolocate. (The earliest known bat from the fossil record with the capacity to echolocate is around 45 to 50 million years old.)

The UF investigators uncovered another surprising result related to the appearance of butterflies. They discovered that butterflies became diurnal (active in the daytime) around 98 million years ago. According to the traditional evolutionary story, butterflies (which are diurnal) evolved from nocturnal moths when they transitioned to daytime activities to escape predation of echolocating bats, which feed at night. But as with the origin of hearing organs in moths, the transition from nocturnal to diurnal behavior occurred well before the first appearance of echolocating bats and seems to have occurred independently at least two separate times.

It Just Isn’t So

The UF evolutionary biologists’ study demonstrates that the coevolutionary models for the origin of hearing organs in moths and diurnal behavior of butterflies—dominant for over a half century in evolutionary thought—are nothing more than just-so stories. They appear to make sense on the surface but are no closer to the truth than the tales I would weave in Mr. Reynolds’ office.

In light of this discovery, the research team posits two new evolutionary models for the origin of these two traits, respectively. Now scientists think that the evolutionary emergence of hearing organs in moths may have provided these insects the capacity for auditory surveillance of their environment. Their capacity to hear may have helped them detect the low-frequency sounds of flapping bird wings, for example, and avoid predation. Presumably, these same hearing organs later evolved to detect the high-frequency cries of bats. As for the evolutionary origin of diurnal behavior characteristic of butterflies, researchers now speculate that butterflies became diurnal to take advantage of flowers that bloom in the daytime.

Again, on the surface, these explanations seem plausible. But one has to wonder if these models, like their predecessors, are little more than just-so stories. In fact, this study raises a general concern: How much confidence can we place in any evolutionary account? Could it be that other evolutionary accounts are, in reality, good stories, but in the end will turn out to be just as fanciful as the stories written by Rudyard Kipling?

In and of itself, recognizing that many evolutionary models could just be stories doesn’t provide sufficient warrant for skepticism about the evolutionary paradigm. But it does give pause for thought. Plus, two insights from this study raise real concerns about the capacity of evolutionary processes to account for life’s history and diversity:

  1. The discovery that ultrasonic hearing in moths arose independently nine separate times
  2. The discovery that diurnal behavior in butterflies appeared independently in at least two separate instances


Evolutionary biologists use the term convergence to refer to the independent origin of identical or nearly identical biological and behavioral traits in organisms that cluster into unrelated groups.

Convergence isn’t a rare phenomenon or limited to the independent origin of hearing organs in moths and diurnal behavior in butterflies. Instead, it is a widespread occurrence in biology, as evolutionary biologists Simon Conway Morris and George McGhee document in their respective books Life’s Solution and Convergent Evolution. It appears as if the evolutionary process routinely arrives at the same outcome, time and time again.4 In fact, biologists observe these repeated outcomes at the ecological, organismal, biochemical, and genetic levels.

From my perspective, the widespread occurrence of convergent evolution is a feature of biology that evolutionary theory can’t explain. I see the widespread occurrence of convergence as a failed scientific prediction of the evolutionary paradigm.

Convergence Should Be Rare, Not Widespread

In effect, chance governs biological and biochemical evolution at its most fundamental level. Evolutionary pathways consist of a historical sequence of chance genetic changes operated on by natural selection, which, too, consists of chance components. The consequences are profound. If evolutionary events could be repeated, the outcome would be dramatically different every time. The inability of evolutionary processes to retrace the same path makes it highly unlikely that the same biological and biochemical designs should appear repeatedly throughout nature.5

In support of this view, consider a 2002 landmark study carried out by two Canadian investigators who simulated macroevolutionary processes using autonomously replicating computer programs. In their study, the computer programs operated like digital organisms.6 The programs could be placed into different “ecosystems” and, because they replicate autonomously, they could evolve. By monitoring the long-term evolution of these digital organisms, the two researchers determined that evolutionary outcomes are historically contingent and unpredictable. Every time they placed the same digital organism in the same environment, it evolved along a unique trajectory.

In other words, given the historically contingent nature of the evolutionary mechanisms, we would expect convergence to be rare in the biological realm. Yet, biologists continue to uncover example after example of convergent features—some of which are quite astounding.

Bat Echolocation and Convergence

Biologists have discovered one such example of convergence in the origin of echolocating bats. Echolocation appears to have arisen two times independently: once in microbats and once in Rhinolophidae, a superfamily of megabats.7 Prior to this discovery, reported in 2000, biologists classified Rhinolophidae as a microbat based on their capability to echolocate. But DNA evidence indicates that this superfamily has greater affinity to megabats than to microbats. This result means that echolocation must have originated separately in the microbats and Rhinolophidae. Researchers have also shown that the same genetic and biochemical changes occurred in microbats and megabats to create their echolocating ability. These changes appear to have taken place in the gene prestin and in its protein-product, prestin.8

In other words, we observe two outcomes: (1) the traditional evolutionary accounts for coevolution among echolocating bats, nocturnal moths, and diurnal butterflies turned out to be just-so stories, and (2) the convergence observed in these three groups stands as independent and separate instances of failed predictions of the evolutionary paradigm.

Convergence and the Case for Creation

If the widespread occurrence of convergence can’t be explained through evolutionary theory, then how can it be explained?

It is not unusual for architects and engineers to redeploy the same design features, sometimes in objects, devices, or systems that are completely unrelated to one another. So, instead of viewing convergent features as having emerged through repeated evolutionary outcomes, we could understand them as reflecting the work of a divine mind. From this perspective, the repeated origins of biological features equate to the repeated creations by an intelligent Agent who employs a common set of solutions to address a common set of problems facing unrelated organisms.

Now that’s a story even Mr. Reynolds might believe.


Convergence of Echolocation

The Historical Contingency of the Evolutionary Process

  1. Akito Y. Kawahara et al., “Phylogenomics Reveals the Evolutionary Timing and Pattern of Butterflies and Moths,” Proceedings of the National Academy of Sciences, USA 116, no. 45 (November 5, 2019): 22657–63, doi:10.1073/pnas.1907847116.
  2. Ed Yong, “A Textbook Evolutionary Story about Moths and Bats Is Wrong,” The Atlantic (October 21, 2019), https://www.theatlantic.com/science/archive/2019/10/textbook-evolutionary-story-wrong/600295/.
  3. Kawahara et al., “Phylogenomics.”
  4. Simon Conway Morris, Life’s Solution: Inevitable Humans in a Lonely Universe (New York: Cambridge University Press, 2003); George McGhee, Convergent Evolution: Limited Forms Most Beautiful (Cambridge, MA: MIT Press, 2011).
  5. Stephen Jay Gould, Wonderful Life: The Burgess Shale and the Nature of History (New York: W. W. Norton & Company, 1990).
  6. Gabriel Yedid and Graham Bell, “Macroevolution Simulated with Autonomously Replicating Computer Programs,” Nature 420 (December 19, 2002): 810–12, doi:10.1038/nature01151.
  7. Emma C. Teeling et al., “Molecular Evidence Regarding the Origin of Echolocation and Flight in Bats,” Nature 403 (January 13, 2000): 188–92, doi:10.1038/35003188.
  8. Gang Li et al., “The Hearing Gene Prestin Reunites Echolocating Bats,” Proceedings of the National Academy of Sciences, USA 105, no. 37 (September 16, 2008): 13959–64, doi:10.1073/pnas.0802097105.

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Evolution of Antibiotic Resistance Makes the Case for a Creator


By Fazale Rana – November 27, 2019

It isn’t that hard to imagine, because antibiotics weren’t readily available for medical use until after World War II. And since that time, widespread availability of antibiotics has revolutionized medicine. However, the ability to practice modern medicine is being threatened because of the rise of antibiotic-resistant bacteria. Currently, there exists a pressing need to understand the evolution of antibiotic-resistant strains and to develop new types of antibiotics. Surprisingly, this worthy pursuit has unwittingly stumbled upon evidence for a Creator’s role in the design of biochemical systems.

Alexander Fleming (1881–1955) discovered the first antibiotic, penicillin, in 1928. But it wasn’t until Ernst Chain, Howard Florey, and Edward Abraham purified penicillin in 1942 and Norman Heatley developed a bulk extraction technique in 1945 that the compound became available for routine medical use.


Figure 1: Alexander Fleming. Image Credit: Wikipedia

Prior to this time, people often died from bacterial infections. Complicating this vulnerability to microbial pathogens was the uncertain outcome of many medical procedures. For example, patients often died after surgery due to complications arising from infections.


Figure 2: A generalized structure for penicillin antibiotics. Image credit: Shutterstock

Bacterial Resistance Necessitates New Antibiotics

Unfortunately, because of the growing threat of superbugs—antibiotic-resistant strains of bacteria—health experts around the world worry that we soon will enter into a post-antibiotic era in which modern medicine will largely revert to pre-World War II practices. According to Dr. David Livermore, laboratory director at Public Health England, which is responsible for monitoring antibiotic-resistant strains of bacteria, “A lot of modern medicine would become impossible if we lost our ability to treat infections.”1

Without antibiotics, people would routinely die of infections that we easily treat today. Abdominal surgeries would be incredibly risky. Organ transplants and chemotherapy would be out of the question. And the list continues.

The threat of entering into a post-antibiotic age highlights the desperate need to develop new types of antibiotics. It also highlights the need to develop a better understanding of evolutionary processes that lead to the emergence of antibiotic resistance in bacteria.

Recently, a research team from Michigan State University (MSU) published a report that offers insight into the latter concern. These researchers studied the evolution of antibiotic resistance in bacteria that had been serially cultured in the laboratory for multiple decades in media that was free from antibiotics.2 Through this effort, they learned that the genetic history of the bacterial strain plays a key role in its acquisition of resistance to antibiotics.

This work has important implications for public health, but it also carries theological implications. The decades-long experiment provides evidence that the elegant designs characteristic of biochemical and biological systems most likely stem from a Creator’s handiwork.

The Long-Term Evolution Experiment

To gain insight into the role that genetic history plays in the evolution of antibiotic resistance, the MSU researchers piggy-backed on the famous Long-Term Evolution Experiment (LTEE) at Michigan State University. Inaugurated in 1988, the LTEE is designed to monitor evolutionary changes in the bacterium E. coli, with the objective of developing an understanding of the evolutionary process.


Figure 3: A depiction of E. coli. Image Credit: Shutterstock

The LTEE began with a single cell of E. coli that was used to generate twelve genetically identical lines of cells. The twelve clones of the parent E. coli cell were separately inoculated into a minimal growth medium containing low levels of glucose as the only carbon source. After growing overnight, an aliquot (equal fractional part) of each of the twelve cultures was transferred into fresh growth media. This process has been repeated every day for about thirty years. Throughout the experiment, aliquots of cells have been frozen every 500 generations. These frozen cells represent a “fossil record” of sorts that can be thawed out and compared to current and other past generations of cells.

Relaxed Selection and Decay of Antibiotic Resistance

In general, when a population of organisms no longer experiences natural selection for a particular set of traits (antibiotic resistance, in this case), the traits designed to handle that pressure may experience functional decay as a result of mutations and genetic drift. This process is called relaxed selection.

In the case of antibiotic resistance, when the threat of antibiotics is removed from the population (relaxed selection), it seems reasonable to think that antibiotic resistance would decline in the population because in most cases antibiotic resistance comes with a fitness cost. In other words, bacterial strains that acquire antibiotic resistance face a trade-off that makes them less fit in environments without the antibiotic.

Genetic History and the Re-Evolution of Antibiotic Resistance

In light of this expectation, the MSU researchers wondered how readily bacteria that have experienced relaxed selection can overcome loss of antibiotic resistance when the antibiotic is reintroduced to the population.

To explore this question, the researchers examined the evolution of antibiotic resistance in the LTEE ancestor by exposing it to a set of different antibiotics and compared its propensity to acquire antibiotic resistance with four strains of E. coli derived from the LTEE ancestor (that underwent 50,000 generations of daily growth and transfer into fresh media in the absence of exposure to antibiotics).

As expected, the MSU team discovered that 50,000 generations of relaxed selection rendered the four strains more susceptible to four different antibiotics (ampicillin, ceftriaxone, ciprofloxacin, and tetracycline) compared to the LTEE ancestor. When they exposed these strains to the different antibiotics, the researchers discovered that acquisition of antibiotic resistance was idiosyncratic: some strains more readily evolved antibiotic resistance than the LTEE ancestor and others were less evolvable.

Investigators explained this difference by arguing that during the period of relaxed selection some of the strains experienced mutations that constrained the evolution of antibiotic resistance, whereas others experienced mutations that potentiated (activated) the evolution of antibiotic resistance. That is, historical contingency has played a key role in the acquisition of antibiotic resistance. Different bacterial lineages accumulated genetic differences that influence their capacity to evolve and adapt in new directions.

Historical Contingency

This study follows on the heels of previous studies that demonstrate the historical contingency of the evolutionary process.3 In other words, chance governs biological and biochemical evolution at its most fundamental level. As the MSU researchers observed, evolutionary pathways consist of a historical sequence of chance genetic changes operated on by natural selection (or that experience relaxed selection), which, too, consists of chance components.

Because of the historically contingent nature of the evolutionary process, it is highly unlikely that the same biological and biochemical designs should appear repeatedly throughout nature. In his book Wonderful Life, Stephen Jay Gould used the metaphor of “replaying life’s tape.” If one were to push the rewind button, erase life’s history, and then let the tape run again, the results would be completely different each time.4

The “Problem” of Convergence

And yet, we observe the opposite pattern in biology. From an evolutionary perspective, it appears as if the evolutionary process independently and repeatedly arrived at the same outcome, time and time again (convergence). As evolutionary biologists Simon Conway Morris and George McGhee point out in their respective books Life’s Solution and Convergent Evolution, identical evolutionary outcomes are a widespread feature of the biological realm.5

Scientists see these repeated outcomes at ecological, organismal, biochemical, and genetic levels. To illustrate the pervasiveness of convergence at the biochemical level, I describe 100 examples of convergence in my book The Cell’s Design.6

From my perspective, the widespread occurrence of convergent evolution is a feature of biology that evolutionary theory can’t genuinely explain. In fact, given the clear-cut demonstration that the evolutionary process is historically contingent, I see the widespread occurrence of convergence as a failed scientific prediction for the evolutionary paradigm.


Evolution in Bacteria Doesn’t Equate to Large-Scale Evolution

The evolution of E. coli in the LTEE doesn’t necessarily validate the evolutionary paradigm. Just because such change is observed in a microbe doesn’t mean that evolutionary processes can adequately account for life’s origin and history, and the full range of biodiversity.


Convergence and the Case for Creation

Instead of viewing convergent features as having emerged through repeated evolutionary outcomes, we could understand them as reflecting the work of a divine Mind. In this scheme, the repeated origins of biological features equate to the repeated creations by an intelligent Agent who employs a common set of solutions to address a common set of problems facing unrelated organisms.

Sadly, many in the scientific community are hesitant to embrace this perspective because they are resistant to the idea that design and purpose may play a role in biology. But, one can hope that someday the scientific community will be willing to move into a post-evolution future as the evidence for a Creator’s role in biology mounts.


The Historical Contingency of the Evolutionary Process

Microbial Evolution and the Validity of the Evolutionary Paradigm

  1. Sarah Bosley, “Are You Ready for a World without Antibiotics?” The Guardian, August 12, 2010, https://www.theguardian.com/society/2010/aug/12/the-end-of-antibiotics-health-infections.
  2. Kyle J. Card et al., “Historical Contingency in the Evolution of Antibiotic Resistance after Decades of Relaxed Selection,” PLoS Biology 17, no. 10 (October 23, 2019): e3000397, doi:10.1371/journal.pbio.3000397.
  3. Zachary D. Blount et al., “Historical Contingency and the Evolution of a Key Innovation in an Experimental Population of Escherichia coli,” Proceedings of the National Academy of Sciences USA 105, no. 23 (June 10, 2008): 7899-7906, doi:10.1073/pnas.0803151105.
  4. Stephen Jay Gould, Wonderful Life: The Burgess Shale and the Nature of History (New York: W.W. Norton & Company, 1990).
  5. Simon Conway Morris, Life’s Solution: Inevitable Humans in a Lonely Universe (New York: Cambridge University Press, 2003); George McGhee, Convergent Evolution: Limited Forms Most Beautiful (Cambridge, MA: MIT Press, 2011).
  6. Fazale Rana, The Cell’s Design: How Chemistry Reveal the Creator’s Artistry (Grand Rapids, MI: Baker, 2008).

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Analysis of Genomes Converges on the Case for a Creator

By Fazale Rana – November 13, 2019

Are you a Marvel or a DC fan?

Do you like the Marvel superheroes better than those who occupy the DC universe? Or is it the other way around for you?

Even though you might prefer DC over Marvel (or Marvel over DC), over the years these two comic book rivals have often created superheroes with nearly identical powers. In fact, a number of Marvel and DC superheroes are so strikingly similar that their likeness to one another is obviously intentional.1

Here are just a few of the superheroes Marvel and DC have ripped off each other:

  • Superman (DC, created in 1938) and Hyperion (Marvel, created in 1969)
  • Batman (DC, created in 1939) and Moon Knight (Marvel, created in 1975)
  • Green Lantern (DC, created in 1940) and Nova (Marvel, created in 1976)
  • Catwoman (DC, created in 1940) and Black Cat (Marvel, created in 1979)
  • Atom (DC, created in 1961) and Ant-Man (Marvel, created in 1962)
  • Aquaman (DC, created in 1941) and Namor (Marvel, created in 1939)
  • Green Arrow (DC, created in 1941) and Hawkeye (Marvel, created in 1964)
  • Swamp Thing (DC, created in 1971) and Man Thing (Marvel, created in 1971)
  • Deathstroke (DC, created in 1980) and Deadpool (Marvel, created in 1991)

This same type of striking similarity is also found in biology. Life scientists have discovered countless examples of biological designs that are virtually exact replicas of one another. Yet, these identical (or nearly identical) designs occur in organisms that belong to distinct, unrelated groups (such as the camera eyes of vertebrates and octopi). Therefore, they must have an independent origin.



Figure 1: The Camera Eyes of Vertebrates (left) and Cephalopods (right); 1: Retina; 2: Nerve Fibers; 3: Optic Nerve; 4: Blind Spot. Image credit: Wikipedia

From an evolutionary perspective, it appears as if the evolutionary process independently and repeatedly arrived at the same outcome, time and time again. As evolutionary biologists Simon Conway Morris and George McGhee point out in their respective books, Life’s Solution and Convergent Evolution, identical evolutionary outcomes are a widespread feature of the biological realm.2 Scientists observe these repeated outcomes (known as convergence) at the ecological, organismal, biochemical, and genetic levels.

From my perspective, the widespread occurrence of convergent evolution is a feature of biology that evolutionary theory can’t genuinely explain. In fact, I see pervasive convergence as a failed scientific prediction—for the evolutionary paradigm. Recent work by a research team from Stanford University demonstrates my point.3

These researchers discovered that identical genetic changes occurred when: (1) bats and whales “evolved” echolocation, (2) killer whales and manatees “evolved” specialized skin in support of their aquatic lifestyles, and (3) pikas and alpacas “evolved” increased lung capacity required to live in high-altitude environments.

Why do I think this discovery is so problematic for the evolutionary paradigm? To understand my concern, we first need to consider the nature of the evolutionary process.

Biological Evolution Is Historically Contingent

Essentially, chance governs biological and biochemical evolution at its most fundamental level. Evolutionary pathways consist of a historical sequence of chance genetic changes operated on by natural selection, which, too, consists of chance components. The consequences are profound. If evolutionary events could be repeated, the outcome would be dramatically different every time. The inability of evolutionary processes to retrace the same path makes it highly unlikely that the same biological and biochemical designs should appear repeatedly throughout nature.

The concept of historical contingency embodies this idea and is the theme of Stephen Jay Gould’s book Wonderful Life.4 To help illustrate the concept, Gould uses the metaphor of “replaying life’s tape.” If one were to push the rewind button, erase life’s history, and then let the tape run again, the results would be completely different each time.

Are Evolutionary Processes Historically Contingent?

Gould based the concept of historical contingency on his understanding of the evolutionary process. In the decades since Gould’s original description of historical contingency, several studies have affirmed his view.

For example, in a landmark study in 2002, two Canadian investigators simulated macroevolutionary processes using autonomously replicating computer programs, with the programs operating like digital organisms.5 These programs were placed into different “ecosystems” and, because they replicated autonomously, could evolve. By monitoring the long-term evolution of the digital organisms, the two researchers determined that evolutionary outcomes are historically contingent and unpredictable. Every time they placed the same digital organism in the same environment, it evolved along a unique trajectory.

In other words, given the historically contingent nature of the evolutionary mechanisms, we would expect convergence to be rare in the biological realm. Yet, biologists continue to uncover example after example of convergent features—some of which are quite astounding.

The Origin of Echolocation

One of the most remarkable examples of convergence is the independent origin of echolocation (sound waves emitted from an organism to an object and then back to the organism) in bats (chiropterans) and cetaceans (toothed whales). Research indicates that echolocation arose independently in two different groups of bats and also in the toothed whales.



Figure 2: Echolocation in Bats. Image credit: Shutterstock

One reason why this example of convergence is so remarkable has to do with the way some evolutionary biologists account for the widespread occurrences of convergence in biological systems. Undaunted by the myriad examples of convergence, these scientists assert that independent evolutionary outcomes result when unrelated organisms encounter nearly identical selection forces (e.g., environmental, competitive, and predatory pressures). According to this idea, natural selection channels unrelated organisms down similar pathways toward the same endpoint.

But this explanation is unsatisfactory because bats and whales live in different types of habitats (terrestrial and aquatic). Consequently, the genetic changes responsible for the independent emergence of echolocation in the chiropterans and cetaceans should be distinct. Presumably, the evolutionary pathways that converged on a complex biological system such as echolocation would have taken different routes that would be reflected in the genomes. In other words, even though the physical traits appear to be identical (or nearly identical), the genetic makeup of the organisms should reflect an independent evolutionary history.

But this expectation isn’t borne out by the data.

Genetic Convergence Parallels Trait Convergence

In recent years, evolutionary biologists have developed interest in understanding the genetic basis for convergence. Specifically, these scientists want to understand the genetic changes that lead to convergent anatomical and physiological features (how genotype leads to phenotype).

Toward this end, a Stanford research team developed an algorithm that allowed them to search through entire genome sequences of animals to identify similar genetic features that contribute to particular biological traits.6 In turn, they applied this method to three test cases related to the convergence of:

  • echolocation in bats and whales
  • scaly skin in killer whales
  • lung structure and capacity in pikas and alpacas

The investigators discovered that for echolocating animals, the same 25 convergent genetic changes took place in their genomes and were distributed among the same 18 genes. As it turns out, these genes play a role in the development of the cochlear ganglion, thought to be involved in echolocation. They also discovered that for aquatic mammals, there were 27 identical convergent genetic changes that occurred in same 15 genes that play a role in skin development. And finally, for high-altitude animals, they learned that the same 25 convergent genetic changes occurred in the same 16 genes that play a role in lung development.

In response to this finding, study author Gill Bejerano remarked, “These genes often control multiple functions in different tissues throughout the body, so it seems it would be very difficult to introduce even minor changes. But here we’ve found that not only do these very different species share specific genetic changes, but also that these changes occur in coding genes.”7

In other words, these results are not expected from an evolutionary standpoint. It is nothing short of amazing that genetic convergence would parallel phenotypic convergence.

On the other hand, these results make perfect sense from a creation model vantage point.

Convergence and the Case for Creation

Instead of viewing convergent features as having emerged through repeated evolutionary outcomes, we could understand them as reflecting the work of a Divine Mind. In this scheme, the repeated origins of biological features equate to the repeated creations by an Intelligent Agent who employs a common set of solutions to address a common set of problems facing unrelated organisms.

Like the superhero rip-offs in the Marvel and DC comics, the convergent features in biology appear to be intentional, reflecting a teleology that appears to be endemic in living systems.


Convergence of Echolocation

The Historical Contingency of the Evolutionary Process

  1. Jamie Gerber, “15 DC and Marvel Superheroes Who Are Strikingly Similar,” ScreenRant (November 12, 2016), screenrant.com/marvel-dc-superheroes-copies-rip-offs/.
  2. Simon Conway Morris, Life’s Solution: Inevitable Humans in a Lonely Universe (New York: Cambridge University Press, 2003); George McGhee, Convergent Evolution: Limited Forms Most Beautiful (Cambridge, MA: MIT Press, 2011).
  3. Amir Marcovitz et al., “A Functional Enrichment Test for Molecular Convergent Evolution Finds a Clear Protein-Coding Signal in Echolocating Bats and Whales,” Proceedings of the National Academy of Sciences, USA 116, no. 42 (October 15, 2019), 21094–21103, doi:10.1073/pnas.1818532116.
  4. Stephen Jay Gould, Wonderful Life: The Burgess Shale and the Nature of History (New York: W. W. Norton & Company, 1990).
  5. Gabriel Yedid and Graham Bell, “Macroevolution Simulated with Autonomously Replicating Computer Programs,” Nature 420 (December 19, 2002): 810–12, doi:10.1038/nature01151.
  6. Marcovitz et al., “A Functional Enrichment Test.”
  7. Stanford Medicine, “Scientists Uncover Genetic Similarities among Species That Use Sound to Navigate,” ScienceDaily, October 4, 2019, sciencedaily.com/releases/2019/10/191004105643.htm.

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Original article at:

Can Dinosaurs Be Resurrected from Extinction?


By Fazale Rana – September 25, 2019

If you could visit a theme park that offered you a chance to view and even interact with real-life dinosaurs, would you go? I think I might. Who wants to swim with dolphins when you can hang out with dinosaurs? Maybe even ride one?

Well, if legendary paleontologist Jack Horner has his way, we just might get our wish—and, it could be much sooner than any of us realize. Horner is a champion of the scientific proposal to resurrect dinosaurs from extinction. And it looks like this idea might have a real chance at success.

Horner’s not taking the “Jurassic Park/World” approach of trying to clone dinosaurs from ancient DNA (which won’t work for myriad technical reasons). He wants to transform birds into dinosaur-like creatures by experimentally manipulating their developmental processes in a laboratory setting.

The Evolutionary Connection between Birds and Dinosaurs

The basis for Horner’s idea rises out of the evolutionary paradigm. Most paleontologists think that birds and dinosaurs share an evolutionary history. These scientists argue that shared anatomical features (a key phrase we’ll return to) between birds and certain dinosaur taxa demonstrate their evolutionary connection. Currently, paleontologists place dinosaurs into two major groups: avian and nonavian dinosaurs. Accordingly, paleontologists think that birds are the evolutionary descendants of dinosaurs.

So, if Horner and others are successful, what does this mean for creation? For evolution?

Reverse Evolution

In effect, Horner and other interested scientists seek to reverse what they view as the evolutionary process, converting birds into an evolutionarily ancestral state. Dubbed reverse evolution, this approach will likely become an important facet of paleontology in the future. Evolutionary biologists believe that they can gain understanding of how biological transformations took place during life’s history by experimentally reverting organisms to their ancestral state. Reverse evolution experiments fuse insights from paleontology with those from developmental biology, molecular biology, comparative embryology, and genomics. Many life scientists are excited, because, for the first time, researchers can address questions in evolutionary biology using an experimental strategy.

Proof-of-Principle Studies

The first bird that researchers hope to reverse-evolve into a dinosaur-like creature is the chicken (Gallus gallus). This makes sense. We know a whole lot about chicken biology, and life scientists can leverage this understanding to precisely manipulate the embryonic progression of chicks so that they develop into dinosaur-like creatures.

As I described previously (see Resources for Further Exploration), in 2015 researchers from Harvard and Yale Universities moved the scientific community one step closer to creating a “chickenosaurus” by manipulating chickens in ovo to develop snout-like structures, instead of beaks, just like dinosaurs.1

Now, two additional proof-of-principle studies demonstrate the feasibility of creating a chickenosaurus. Both studies were carried out by a research team from the Universidad de Chile.

In one study, the research team coaxed chicken embryos to develop a dinosaur-like foot structure, instead of the foot structure characteristic of birds.2 A bird’s foot has a perching digit that points in the backward direction, in opposition to the other toes. The perching digit allows birds to grasp. In contrast, the corresponding toe in dinosaurs is nonopposable, pointing forward.


Figure 1: Dinosaur Foot Structure. Image credit: Shutterstock


Figure 2: Bird Foot Structure. Image credit: Shutterstock

The researchers took advantage of the fact that vertebrate skeletons are plastic, meaning that their structure can be altered by muscle activity. These types of skeletal alterations most commonly occur during embryonic and juvenile stages of growth and development.

Investigators discovered that muscle activity causes the perching toe of birds to reorient during embryonic development from originally pointing forward to adopting an opposable orientation. Specifically, the activity of three muscles (flexor hallucis longus, flexor hallucis brevis, and musculus extensor hallucis longus) creates torsion that twists the first metatarsal, forcing the perching digit into the opposable position.

The team demonstrated that by injecting the compound decamethonium bromide into a small opening in the eggshell just before the torsional twisting of the first metatarsal takes place, they could prevent this foot bone from twisting. The compound causes muscle paralysis, which limits the activity of the muscles that cause the torsional stress on the first metatarsal. The net result: the chick developed a dinosaur-like foot structure.

In a second study, this same research team was able to manipulate embryonic development of chicken embryos to form a dinosaur-like leg structure.3 The lower legs of vertebrates consist of two bones: the tibia and the fibula. In most vertebrates, the fibula is shaped like a tube, extending all the way to the ankle. In birds, the fibula is shorter than the tibia and has a spine-like morphology (think chicken drumsticks).


Figure 3: The Lower Leg of a Chicken. Image credit: Shutterstock

Universidad de Chile researchers discovered that the gene encoding the Indian Hedgehog protein becomes active at the distal end of the fibula during embryonic development of the lower leg in chicks, causing the growth of the fibula to cease. They also learned that the event triggering the increased activity of the Indian Hedgehog gene likely relates to the depletion of the Parathyroid Hormone-Related Protein near the distal end of the fibula. This protein plays a role in stimulating bone growth.

The researchers leveraged this insight to experimentally create a chick with dinosaur-like lower legs. Specifically, they injected the amniotic region of the chicken embryo with cyclopamine. This compound inhibits the activity of Indian Hedgehog. They discovered that this injection altered fibula development so that it was the same length as the tibia, contacting the ankle, just like in dinosaurs.

These two recent experiments on foot structure along with the previous one on snout structure represent science at its best. While the experiments reside at the proof-of-principle stage, they still give scientists like Jack Horner reason to think that we just might be able to resurrect dinosaurs from extinction one day. These experiments also raise scientific and theological questions.

Do Studies in Reverse Evolution Support the Evolutionary Paradigm?

On the surface, these studies seemingly make an open-and-shut case for the evolutionary origin of birds. It is impressive that researchers can rewind the tape of life and convert chickens into dinosaur-like creatures.

But deeper reflection points in a different direction.

All three studies highlight the amount of knowledge and insight about the developmental process required to carry out the reverse evolution experiments. The ingenious strategy the researchers employed to alter the developmental trajectory is equally impressive. They had to precisely time the addition of chemical agents at the just-right levels in order to influence muscle activity in the embryo’s foot or gene activity in the chick’s developing lower legs. Recognizing the knowledge, ingenuity, and skill required to alter embryological development in a coherent way that results in a new type of creature forces the question: Is it really reasonable to think that unguided, historically contingent processes could carry out such transformations when small changes in development can have profound effects on an organism’s anatomy?

It seems that the best the evolutionary process could achieve would be the generation of “monsters” with little hope of survival. Why? Because evolutionary mechanisms can only change gene expression patterns in a random, haphazard manner. I would contend that the coherent, precisely coordinated genetic changes needed to generate one biological system from another signals a Creator’s handiwork, not undirected evolutionary mechanisms, as the explanation for life’s history.

Can a Creation Model Approach Explain the Embryological Similarities?

Though the work in reverse evolution seems to fit seamlessly within an evolutionary framework, observations from these studies can be explained from a creation model perspective.

Key to this explanation is the work of Sir Richard Owen, a preeminent biologist who preceded Charles Darwin. In contemporary biology, scientists view shared features possessed by related organisms as evidence of common ancestry. Birds and theropod dinosaurs would be a case in point. But for Owen, shared anatomical features reflected an archetypal design that originated in the Mind of the First Cause. Toward this end, the anatomical features shared by birds and theropods can be understood as reflecting common design, not common descent.

Though few biologists embrace Owen’s ideas today, it is important to note that his ideas were not tried and found wanting. They simply were abandoned in favor of Darwin’s theory, which many biologists preferred because it provided a mechanistic explanation for life’s history and the origin of biological systems. In fact, Darwin owes a debt of gratitude to Owen’s thinking. Darwin coopted the idea of the archetype, but then replaced the canonical blueprint that existed in the Creator’s Mind (per Owen) with a hypothetical common ancestor.

This archetypal approach to biology can account for the results of reverse-evolution studies. Accordingly, the researchers have discovered differences in the developmental program that affect variations in the archetype, yielding differences in modern birds and long-extinct dinosaurs.

The idea of the archetype can extend to embryonic growth and development. One could argue that the Creator appears to have developed a core (or archetypal) developmental algorithm that can be modified to yield disparate body plans. From a creation model standpoint, then, the researchers from Harvard and Yale Universities and the Universidad de Chile didn’t reverse the evolutionary process. They unwittingly reverse-engineered a dinosaur-like developmental algorithm from a bird-like developmental program.

Why Would God Create Using the Same Design Templates?

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.

Shared anatomical and physiological features, as well as shared features of embryological development make it possible to apply what we learn by studying one organism to others. This shared developmental program makes it possible to use our understanding of embryological growth and development to reengineer a bird into a dinosaur-like creature. Discoverability makes it easier to appreciate God’s glory and grandeur, as evinced in biochemical systems by their elegance, sophistication, and ingenuity.

Discoverability also reflects 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 chickens? And where would our efforts to re-create dinosaurs be if not for the biological designs they share with birds?

Resources for Further Exploration

Reverse Evolution

Shared Biological Designs and the Creation Model

  1. Bhart-Anjan S. Bhullar et al., “A Molecular Mechanism for the Origin of a Key Evolutionary Innovation, the Bird Beak and Palate, Revealed by an Integrative Approach to Major Transitions in Vertebrate History,” Evolution 69, no. 7 (2015): 1665–77, doi:10.1111/evo.12684.
  2. João Francisco Botelho et al., “Skeletal Plasticity in Response to Embryonic Muscular Activity Underlies the Development and Evolution of the Perching Digit of Birds,” Scientific Reports 5 (May 14, 2015): 9840, doi:10.1038/srep09840.
  3. João Francisco Botelho et al., “Molecular Developments of Fibular Reduction in Birds and Its Evolution from Dinosaurs,” Evolution 70, no. 3 (March, 2016): 543–54, doi:10.1111/evo.12882.

Reprinted with permission by the author

Original article at:

Does Old-Earth Creationism Make God Deceptive?


By Fazale Rana – July 17, 2019

“Are [vestigial structures] unequivocal evidence of evolution?

No. Are they reasonable evidence of evolution? Yes.

Ditto gene sequences.

Appearance of evolution is no more a valid deflection [for the overwhelming evidence for evolution] than the appearance of age is a valid dodge of the overwhelming confluence of evidence of antiquity.

Both are sinking ships. I got off before going under with you on this one.”

—Hill R. (a former old-earth creationist who now espouses theistic evolution/evolutionary creationism)

Most people who follow my work at Reasons to Believe know I question the grand claim of the evolutionary paradigm; namely, that evolutionary processes provide the exclusive explanation for the origin, design, and history of life. In light of my skepticism, friends and foes alike often ask me how I deal with (what many people perceive to be) the compelling evidence for the evolutionary history of life, such as vestigial structures and shared genetic features in genomes.

As part of my response, I point out that this type of evidence for evolution can be accommodated by a creation model, with the shared features reflecting common design, not common descent—particularly now that we know that there is a biological rationale for many vestigial structures and shared genetic features. This response prompted my friend Hill R. to level his objection. In effect, Hill says I am committing the “appearance of evolution” fallacy, which he believes is analogous to the “appearance of age” fallacy committed by young-earth creationists (YECs).

Hill is not alone in his criticism. Other people who embrace theistic evolution/evolutionary creation (such as my friends at BioLogos) level a similar charge. According to these critics, both appearance of age and appearance of evolution fallacies make God deceptive.

If biological systems are designed, but God made them appear as if they evolved, then the conclusions we draw when we investigate nature are inherently untrustworthy. This is a problem because, according to Scripture, God reveals himself to us through the record of nature. But if we are misled by nature’s features and, consequently, draw the wrong conclusion, then it makes God deceptive. However, God cannot lie or deceive. It is contrary to his nature.

So, how do I respond to this theological objection to RTB’s creation model?

Before I reply, I want to offer a little more background information to make sure that anyone who is unfamiliar with this concern can better appreciate the seriousness of the charge against our creation model. If you don’t need the background explanation, then feel free to skip ahead to A Response to the Appearance of Evolution Challenge.

Evidence for Evolution: Vestigial Structures

Evolutionary biologists often point to vestigial structures—such as the pelvis and hind limbs of whales and dolphins (cetaceans)—as compelling evidence for biological evolution. Evolutionary biologists view vestigial structures this way because they are also homologous (structurally similar) structures. Vestigial structures are rudimentary body parts that are smaller and simpler than the corresponding features possessed by the other members of a biological group. As a case in point, the whale pelvis and hind limbs are homologous to the pelvis and hind limbs of all other mammals.


Figure 1: Whale Pelvis. Image credit: Shutterstock

Evolutionary biologists believe that vestigial structures were fully functional at one time but degenerated over the course of many generations because the organisms no longer needed them to survive in an ever-changing environment—for example, when the whale ancestor transitioned from land to water. From an evolutionary standpoint, fully functional versions of these structures existed in the ancestral species. The structures’ form and function may be retained (possibly modified) in some of the evolutionary lineages derived from the ancestral species, but if no longer required, the structures become diminished (and even lost) in other lineages.

Evidence for Evolution: Shared Genetic Features

Evolutionary biologists also 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. (In a sense, they are analogous to vestigial anatomical features.) 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.

A Response to the Evidence for Evolution

As a rejoinder to this evidence, I point out that we continue to uncover evidence that vestigial structures display function (see Vestigial Structures are Functional in the Resources section.) Likewise, evidence is beginning to accumulate that synonymous mutations have functional consequences. (see Shared Genetic Features Reflect Design in the Resources section.) Again, if these features have functional utility, then they can reasonably be interpreted as the Creator’s handiwork.

But, even though these biological features bear function, many critics of the RTB model think that the shared features of these biological systems still bear the hallmarks of an evolutionary history. Therefore, they argue that these features look as if they evolved. And if so, we are guilty of the “appearance of evolution” fallacy.

Appearance of Age and the Appearance of Evolution

In 1857, Philip Gosse, a biologist and preacher from England, sought to reconcile the emerging evidence for Earth’s antiquity with Scripture. Gosse was convinced that the earth was old. He was also convinced that Scripture taught that the earth was young. In an attempt to harmonize these disparate stances, he proposed the appearance of age argument in a book titled Omphalos. In this work, Gosse argued that God created Earth in six days, but made it with the appearance of age.


Figure 2: Philip Henry Gosse, 1855. Image credit: Wikipedia

This idea persists today, finding its way into responses modern-day YECs make to the scientific evidence for Earth’s and life’s antiquity. For many people (including me), the appearance of age argument is fraught with theological problems, the chief one being that it makes God deceptive. If Earth appears to be old, and it measures to be old, yet it is young, then we can’t trust anything we learn when we study nature. This problem is not merely epistemological; it is theological because nature is one way that God has chosen to make himself known to us. But if our investigation of nature is unreliable, then it means that God is untrustworthy.

In other words, on the surface, both the appearance of age and the appearance of evolution arguments made by YECs and old-earth creationists (OECs), respectively, seem to be equally problematic.

But does the RTB position actually commit the appearance of evolution fallacy? Does it suffer from the same theological problems as the argument first presented by Gosse in Omphalos? Are we being hypocritical when we criticize the appearance of age fallacy, only to commit the appearance of evolution fallacy?

A Response to the Appearance of Evolution Challenge

This charge against the RTB creation model neglects to fully represent the reasons I question the evolutionary paradigm.

First, my skepticism is not theologically motivated but scientifically informed. For example, I point out in an article I recently wrote for Sapientia that a survey of the scientific literature makes it clear that evolutionary theory as currently formulated cannot account for the key transitions in life’s history, including:

  • the origin of life
  • the origin of eukaryotic cells
  • the origin of body plans
  • the origin of human exceptionalism

Additionally, some predictions that flow out of the evolutionary paradigm have failed (such as the widespread prevalence of convergence), further justifying my skepticism. (See Scientific Challenges to the Evolutionary Paradigm in the Resources section.)

In other words, when we interpret shared features as a manifestation of common design (including vestigial structures and shared genetic patterns), it is in the context of scientifically demonstrable limitations of the evolutionary framework to fully account for life’s origin, history, and design. To put it differently, because of the shortcomings of evolutionary theory, we don’t see biological systems as having evolved. Rather, we think they’ve been designed.

Appearance of Design Fallacy

Even biologists who are outspoken atheists readily admit that biological and biochemical systems appear to be designed. Why else would Nobel Laureate Francis Crick offer this word of caution to scientists studying biochemical systems: “Biologists must keep in mind that what they see was not designed, but rather evolved.”1 What other reason would evolutionary biologist Richard Dawkins offer for defining biology as “the study of complicated things that give the appearance of having been designed for a purpose”?2

Biologists can’t escape the use of design language when they describe the architecture and operation of biological systems. In and of itself, this practice highlights the fact that biological systems appear to be designed, not evolved.

To sidestep the inexorable theological implications that arise when biologists use design language, biologist Colin Pittendrigh coined the term teleonomy in 1958 to describe systems that appear to be purposeful and goal-directed, but aren’t. In contrast with teleology—which interprets purposefulness and goal-directedness as emanating from a Mind— teleonomy views design as the outworking of evolutionary processes. In other words, teleonomy allows biologists to utilize design language— when they describe biological systems—without even a tinge of guilt.

In fact, the teleonomic interpretation of biological design resides at the heart of the Darwinian revolution. Charles Darwin claimed that natural selection could account for the design of biological systems. In doing so, he supplanted Mind with mechanism. He replaced teleology with teleonomy.

Prior to Darwin, biology found its grounding in teleology. In fact, Sir Richard Owen—one of England’s premier biologists in the early 1800s—produced a sophisticated theoretical framework to account for shared biological features found in organisms that naturally cluster together (homologous structures). For Owen (and many biologists of his time) homologous structures were physical manifestations of an archetypal design that existed in the Creator’s mind.

Thus, shared biological features—whether anatomical, physiological, biochemical, or genetic—can be properly viewed as evidence for common design, not common descent. In fact, when Darwin proposed his theory of evolution, he appropriated Owen’s concept of the archetype but then replaced it with a hypothetical common ancestor.

Interestingly, Owen (and other like-minded biologists) found an explanation for vestigial structures like the pelvis and hind limb bones (found in whales and snakes) in the concept of the archetype. They regarded these structures as necessary to the architectural design of the organism. In short, a model that interprets shared biological characteristics from a design/creation model framework has historical precedence and is based on the obvious design displayed by biological systems.

Given the historical precedence for interpreting the appearance of design in biology as bona fide design and the inescapable use of design language by biologists, it seems to me that RTB’s critics commit the appearance of design fallacy when they (along with other biologists) claim that things in biology look designed, but they actually evolved.

Theories Are Underdetermined by Data

A final point. One of the frustrating aspects of scientific discovery relates to what’s called the underdetermination thesis.3 Namely, two competing theories can explain the same set of data. According to this idea, theories are underdetermined by data. This limitation means that two or more theories—that may be radically different from one another—can equally account for the same data. Or, to put it another way, the methodology of science never leads to one unique theory. Because of this shortcoming, other factors—nonscientific ones—influence the acceptance or rejection of a scientific theory, such as a commitment to mechanistic explanations to explain all of biology.

As a consequence of the underdetermination theory, evolutionary models don’t have the market cornered when it comes to offering an interpretation of biological data. Creation models, such as the RTB model—which relies on the concept of common design—also makes sense of the biological data. And given the inability of current evolutionary theory to explain key transitions in life’s history, maybe a creation model approach is the better alternative.

In other words, when we interpret vestigial structures and shared genetic features from a creation model perspective, we are not committing an appearance of age type of fallacy, nor are we making God deceptive. Instead, we are offering a common sense and scientifically robust interpretation of the elegant designs so prevalent throughout the living realm.

Far from a sinking ship one should abandon, a creation model offers a lifeline to scientific and biblical integrity.


Vestigial Structures Are Functional

Shared Genetic Features Reflect Design

Scientific Challenges for the Evolutionary Paradigm

Archetype Biology

  1. Francis Crick, What Mad Pursuit: A Personal View of Scientific Discovery (New York: Basic Books, 1988), 138.
  2. Richard Dawkins, The Blind Watchmaker: Why the Evidence for Evolution Reveals a Universe without Design (New York: W. W. Norton, 1996), 4.
  3. Val Dusek, Philosophy of Technology: An Introduction (Malden, MA: Blackwell Publishing, 2006), 12.

Reprinted with permission by the author

Original article at:

Membrane Biochemistry Challenges Route to Evolutionary Origin of Complex Cells


By Fazale Rana – July 10, 2019

Unfortunately, the same thing could be said to biologists trying to discover the evolutionary route that led to the emergence of complex, eukaryotic cells. No matter the starting point, it seems as if you just can’t get there from here.

This frustration becomes most evident as evolutionary biologists try to account for the biochemical makeup of the membranes found in eukaryotic cells. In my opinion, this struggle is not just an inconvenient detour. As the following paragraphs show, obstacles line the roadway, ultimately leading to a dead end that exposes the shortcomings of the endosymbiont hypothesis—a cornerstone idea in evolutionary biology.

Endosymbiont Hypothesis

Most biologists believe that the endosymbiont hypothesis stands as the best explanation for the origin of complex cells. According to this hypothesis, complex cells originated when symbiotic relationships formed among single-celled microbes after free-living bacterial and/or archaeal cells were engulfed by a “host” microbe.

The mitochondrion represents the “poster child” of the endosymbiont hypothesis. Presumably, this organelle started as an endosymbiont. Evolutionary biologists believe that once engulfed by the host cell, the microbe took up permanent residency, growing and dividing inside the host. Over time, the endosymbiont and host became mutually interdependent, with the endosymbiont providing a metabolic benefit—such as a source of ATP—for the host cell. In turn, the host cell provided nutrients to the endosymbiont. Presumably, the endosymbiont gradually evolved into an organelle through a process referred to as genome reduction. This reduction resulted when genes from the endosymbiont’s genome were transferred into the genome of the host organism.

Evidence for the Endosymbiont Hypothesis
1. Most of the evidence for the endosymbiont hypothesis centers around mitochondria and their similarity to bacteria. Mitochondria are about the same size and shape as a typical bacterium and have a double membrane structure like gram-negative cells. These organelles also divide in a way that is reminiscent of bacterial cells.

2. Biochemical evidence also exists for the endosymbiont hypothesis. Evolutionary biologists view the presence of the diminutive mitochondrial genome as a vestige of this organelle’s evolutionary history. They see the biochemical similarities between mitochondrial and bacterial genomes as further evidence for the evolutionary origin of these organelles.

3. The presence of the unique lipid, cardiolipin, in the mitochondrial inner membrane also serves as evidence for the endosymbiont hypothesis. This important lipid component of bacterial inner membranes is not found in the membranes of eukaryotic cells—except for the inner membranes of mitochondria. In fact, biochemists consider it a signature lipid for mitochondria and a vestige of the organelle’s evolutionary history. So far, the evolutionary route looks well-paved and clear.

Discovery of Lokiarchaeota

Evolutionary biologists have also developed other lines of evidence in support of the endosymbiont hypothesis. For example, biochemists have discovered that the genetic core (DNA replication and the transcription and translation of genetic information) of eukaryotic cells resembles that of the archaea. This similarity suggests to many biologists that a microbe belonging to the archaeal domain served as the host cell that gave rise to eukaryotic cells.

Life scientists think they may have determined the identity of that archaeal host. In 2015, a large international team of collaborators reported the discovery of Lokiarchaeota, a new phylum belonging to the archaea. This phylum clusters with eukaryotes on the evolutionary tree. Analysis of the genomes of Lokiarchaeota identifies a number of genes involved in membrane-related activities, suggesting that this microbe may well have possessed the ability to engulf other microbes.1 At this point, it looks like “you can get there from here.”

Challenges to the Endosymbiont Hypothesis

Despite this seemingly compelling evidence, the evolutionary route to the first eukaryotic cells is littered with potholes. I have written several articles detailing some of the obstacles. (See Challenges to the Endosymbiont Hypothesis in the Resources section.) Also, a divide on the evolutionary roadway called the lipid divide compounds the problem for the endosymbiont hypothesis.

Lipid Divide

The lipid divide refers to the difference in the chemical composition of the cell membranes found in bacteria and archaea. Phospholipids comprise the cell membranes of both sorts of microbes. But the similarity ends there. The chemical makeup of the phospholipids is distinct in bacteria and archaea.

Bacterial phospholipids are built around a d-glycerol backbone, which has a phosphate moiety bound to the glycerol in the sn-3 position. Two fatty acids are bound to the d-glycerol backbone at the sn-1 and sn-2 positions. In water, these phospholipids assemble into bilayer structures.


Figure: Difference between archaeal (top) and bacterial (middle and bottom) phospholipids. Features include 1: isoprene chains, 2: ether linkage, 3: l-glycerol, 4 and 8: phosphate group, 5: fatty acid chains, 6: ester linkages, 7: d-glycerol, 9: lipid bilayer of bacterial membranes, 10: lipid monolayer found in some archaea. Image credit: Wikipedia

Archaeal phospholipids are constructed around an l-glycerol backbone (which produces membrane lipids with different stereochemistry than bacterial phospholipids). The phosphate moiety is attached to the sn-1 position of glycerol. Two isoprene chains are bound to the sn-2 and sn-3 positions of l-glycerol via ether linkages. Some archaeal membranes are formed from phospholipid bilayers, while others are formed from phospholipid monolayers.

Presumably, the structural features of the archaeal phospholipids serve as an adaptation that renders them ideally suited to form stable membranes in the physically and chemically harsh environments in which many archaea find themselves.

Lipid Divide Frustrates the Origin of Eukaryotic Cell Membranes

In light of the lipid divide and the evidence that seemingly indicates that the endosymbiotic host cell likely belonged to Lokiarchaeota, it logically follows that the membrane composition of eukaryotic cells should be archaeal-like. But, this expectation is not met and the evolutionary route encounters another pothole. Instead, the cell membranes of eukaryotic cells closely resemble bacterial membranes.

One way to repair the roadway is to posit that during the evolutionary process that led to the emergence of eukaryotic cells, a transition from archaeal-like membranes to bacterial-like membranes took place. In fact, supporting evidence comes from laboratory studies demonstrating that stable bilayers can form from a mixture of bacterial and archaeal phospholipids, even though the lipids from the two sources have opposite stereochemistry.

Evolutionary biologists Purificación López-García and David Moreira question if evidence can be marshaled in support of this scenario for two reasons.2 First, mixing of phospholipids in the lab is a poor model for cell membranes that function as a “dynamic cell-environment interface.”3

Second, they question if this transition is feasible given how exquisitely optimized membrane proteins must be to fit into cell membranes. The nature of protein optimization is radically different for bacterial and archaeal membranes. Because cell membrane systems are optimized, the researchers question if an adequate driving force for this transition exists.

In other words, these two scientists express serious doubts about the biochemical viability of a transitional stage between archaeal membranes. In light of these obstacles, López-García and Moreira write, “The archaea-to-bacteria membrane shift remains the Achilles’ heel for these models [that propose an archaeal host for endosymbionts].”4

In other words, you can’t get there from here.

Can Lokiarchaeota Traverse the Lipid Divide?

In the midst of this uncertain evolutionary route, a recent study by investigators from the Netherlands seems to point the way toward the evolutionary origin of eukaryotic membranes.5 Researchers screened the Lokiarchaeota genome for enzymes that would take part in phospholipid synthesis with the hope of finding clues about how this transition may have occurred. They conclude that this group of microbes could not make l-glycerol-1-phosphate (a key metabolic intermediate in the production of archaeal phospholipids) because it lacked the enzyme glycerol-1-phosphate dehydrogenase (G1PDH). They also discovered evidence that suggests that this group of microbes could make fatty acids and chemically attach them to sugars. The researchers argue that Lokiarchaeota could make some type of hybrid phospholipid with features of both archaeal and bacterial phospholipids.

The team’s approach to understanding how evolutionary processes could bridge the lipid divide and account for the origin of eukaryotic membranes is clever and inventive, to be sure. But it is far from convincing for at least four reasons.

1. Absence of evidence is not evidence of absence, as the old saying goes. Just because the research team didn’t find the gene for G1PDH in the Lokiarchaeota genetic material doesn’t mean this microbe didn’t have the capacity to make archaeal-type phospholipids. Toward this end, it is important to note that researchers have not cultured any microbe that belongs to this group organisms. The group’s existence is inferred from metagenomic analysis, which involves isolating small fragments of DNA from the environment (in this case a hydrothermal vent system in the Atlantic Ocean, called Loki’s Castle) and stitching them together into a genome. The Lokiarchaeota “genome” is low quality (1.4-fold coverage) and incomplete (8 percent of the genome is missing). Around one-third (32 percent) of the genome codes for proteins with unknown function. Could it be that an enzyme capable of generating l-glycerol-1-phosphate exists in the mysterious third of the genome? Or in the missing 8 percent?

2. While the researchers discovered that genes could conceivably work together to make d-glycerol-3-phosphate (though the enzymes encoded by these genes perform different metabolic functions), they found no direct evidence that Lokiarchaeota produces d-glycerol-3-phosphate. Nor did they find evidence for glycerol-3-phosphate dehydrogenase (G3PDH) in the Lokiarchaeota genetic material. This enzyme plays a key role in the synthesis of phospholipids in bacteria.

3. Though the researchers found evidence that Lokiarchaeota had the capacity to make fatty acids, some of the genes required for the process seem to have been acquired by these microbes via horizontal gene transfer with genetic material from bacteria. (It should be noted that 29 percent of the Lokiarchaeota genome comes from the bacteria.) It is not clear when Lokiarchaeota acquired these genes and, therefore, if this metabolic capability has any bearing on the origin of eukaryotes.

4. The researchers present no evidence that Lokiarchaeota possessed the protein machinery that would chemically attach isoprenoid lipids to d-glycerol-3-phosphate via ether linkages.

Thus, the only way to establish Lokiarchaeota membranes as a transitional evolutionary pathway between those found in Archaea and Bacteria is to perform chemical analysis of its membranes. At this juncture, such analysis is impossible to perform because no one has been able to culture Lokiarchaeota. In fact, other evidence suggests that this group of microbes possessed archaeal-type membranes. Researchers have recovered archaeal lipids in the sediments surrounding Loki’s Castle, but they have not recovered bacterial-like lipids.

More Lipid Divide Frustration

Given these problems, could it be that the host microbe for the endosymbiont was a member of Bacteria, not Archaea? While this model would solve the problem of the lipid divide, it leaves unexplained the similarity between the genetic core of eukaryotes and the Archaea. Nor does it account for the grouping of eukaryotes with the Archaea.

It doesn’t look like you can get there from here, either.

Evolutionary biologists Jonathan Lombard, Purificación López-García and David Moreira sum things up when they write, “The origin of eukaryotic membranes is a problem that is rarely addressed by the different hypotheses that have been proposed to explain the emergence of eukaryotes.”6 Yet, until this problem is adequately addressed, the evolutionary route to eukaryotes will remain obscure and the endosymbiont hypothesis noncompelling.

In light of this challenge and others, maybe a better way to make sense of the origin of eukaryotic cells is to view them as the Creator’s handiwork. For many scientists, it is a road less traveled, but it accounts for all of the data. You can get there from here.


Challenges to the Endosymbiont Hypothesis

Support for a Creation Model for the Origin of Eukaryotic Cells

  1. Anja Spang et al., “Complex Archaea that Bridge the Gap between Prokaryotes and Eukaryotes,” Nature 521 (May 14, 2015): 173–79, doi:10.1038/nature14447; Katarzyna Zaremba-Niedzwiedzka et al., “Asgard Archaea Illuminate the Origin of Eukaryotic Cellular Complexity,” Nature 541 (January 19, 2017): 353–58, doi:10.1038/nature21031.
  2. Purificación López-García and David Moreira, “Open Questions on the Origin of Eukaryotes,” Trends in Ecology and Evolution 30, no. 11 (November 2015): 697–708, doi:10.1016/j.tree.2015.09.005.
  3. López-García and Moreira, “Open Questions.”
  4. López-García and Moreira, “Open Questions.”
  5. Laura Villanueva, Stefan Schouten, and Jaap S. Sinninghe Damsté, “Phylogenomic Analysis of Lipid Biosynthetic Genes of Archaea Shed Light on the ‘Lipid Divide,’” Environmental Microbiology 19, no. 1 (January 2017): 54–69, doi:10.1111/1462-2920.13361.
  6. Jonathan Lombard, Purificación López-García, and David Moreira, “The Early Evolution of Lipid Membranes and the Three Domains of Life,” Nature Reviews Microbiology 10 (June 11, 2012): 507–15, doi:10.1038/nrmicro2815.

Reprinted with permission by the author

Original article at:

Satellite DNA: Critical Constituent of Chromosomes

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By Fazale Rana – June 26, 2019

Let me explain.

Recently, I wound up with a disassembled cabinet in the trunk of my car. Neither my wife Amy nor I could figure out where to put the cabinet in our home and we didn’t want to store it in the garage. The cabinet had all its pieces and was practically new. So, I offered it to a few people, but there were no takers. It seemed that nobody wanted to assemble the cabinet.

Getting Rid of the Junk

After driving around with the cabinet pieces in my trunk for a few days, I channeled my inner Marie Kondo. This cabinet wasn’t giving me any joy by taking up valuable space in the trunk. So, I made a quick detour on my way home from the office and donated the cabinet to a charity.

When I told Amy what I had done, she expressed surprise and a little disappointment. If she had known I was going to donate the cabinet, she would have kept it for its glass doors. In other words, if I hadn’t donated the cabinet, it would have eventually wound up in our garage because it has nice glass doors that Amy thinks she could have repurposed.

There is a point to this story: The cabinet was designed for a purpose and, at one time, it served a useful function. But once it was disassembled and put in the trunk of my car, nobody seemed to want it. Disassembling the cabinet transformed it into junk. And since my wife loves to repurpose things, she saw a use for it. She didn’t perceive the cabinet as junk at all.

The moral of my little story also applies to the genomes of eukaryotic organisms. Specifically, is it time that evolutionary scientists view some kinds of DNA not as junk, but rather as purposeful genetic elements?

Junk in the Genome

Many biologists hold the view that a vast proportion of the genomes of other eukaryotic organisms is junk, just like the disassembled cabinet I temporarily stored in my car. They believe that, like the unwanted cabinet, many of the different types of “junk” DNA in genomes originated from DNA sequences that at one time performed useful functions. But these functional DNA sequences became transformed (like the disassembled cabinet) into nonfunctional elements.

Evolutionary biologists consider the existence of “junk” DNA as one of the most potent pieces of evidence for biological evolution. According to this view, junk DNA results when undirected biochemical processes and random chemical and physical events transform a functional DNA segment into a useless molecular artifact. Junk pieces of DNA remain part of an organism’s genome, persisting from generation to generation as a vestige of evolutionary history.

Evolutionary biologists highlight the fact that, in many instances, identical (or nearly identical) segments of junk DNA appear in a wide range of related organisms. Frequently, the identical junk DNA segments reside in corresponding locations in these genomes—and for many biologists, this feature clearly indicates that these organisms shared a common ancestor. Accordingly, the junk DNA segment arose prior to the time that the organisms diverged from their shared evolutionary ancestor and then persisted in the divergent evolutionary lines.

One challenging question these scientists ask is, Why would a Creator purposely introduce nonfunctional, junk DNA at the exact location in the genomes of different, but seemingly related, organisms?

Satellite DNA

Satellite DNA, which consists of nucleotide sequences that repeat over and over again, is one class of junk DNA. This highly repetitive DNA occurs within the centromeres of chromosomes and also in the chromosomal regions adjacent to centromeres (referred to as pericentromeric regions).


Figure: Chromosome Structure. Image credit: Shutterstock

Biologists have long regarded satellite DNA as junk because it doesn’t encode any useful information. Satellite DNA sequences vary extensively from organism to organism. For evolutionary biologists, this variability is a sure sign that these DNA sequences can’t be functional. Because if they were, natural selection would have prevented the DNA sequences from changing. On top of that, molecular biologists think that satellite DNA’s highly repetitive nature leads to chromosomal instability, which can result in genetic disorders.

A second challenging question is, Why would a Creator intentionally introduce satellite DNA into the genomes of eukaryotic organisms?

What Was Thought to Be Junk Turns Out to Have Purpose

Recently, a team of biologists from the University of Michigan (UM) adopted a different stance regarding the satellite DNA found in pericentromeric regions of chromosomes. In the same way that my wife Amy saw a use for the cabinet doors, the researchers saw potential use for satellite DNA. According to Yukiko Yamashita, the UM research head, “We were not quite convinced by the idea that this is just genomic junk. If we don’t actively need it, and if not having it would give us an advantage, then evolution probably would have gotten rid of it. But that hasn’t happened.”1

With this mindset—refreshingly atypical for most biologists who view satellite DNA as junk—the UM research team designed a series of experiments to determine the function of pericentromeric satellite DNA.2 Typically, when molecular biologists seek to understand the functional role of a region of DNA, they either alter it or splice it out of the genome. But, because the pericentromeric DNA occupies such a large proportion of chromosomes, neither option was available to the research team. Instead, they made use of a protein found in the fruit fly Drosophila melanogaster, called D1. Previous studies demonstrated that this protein binds to satellite DNA.

The researchers disabled the gene that encodes D1 and discovered that fruit fly germ cells died. They observed that without the D1 protein, the germ cells formed micronuclei. These structures reflect chromosomal instability and they form when a chromosome or a chromosomal fragment becomes dislodged from the nucleus.

The team repeated the study, but this time they used a mouse model system. The mouse genome encodes a protein called HMGA1 that is homologous to the D1 protein in fruit flies. When they damaged the gene encoding HMGA1, the mouse cells also died, forming micronuclei.

As it turns out, both D1 and HMGA1 play a crucial role, ensuring that chromosomes remain bundled in the nucleus. These proteins accomplish this feat by binding to the pericentromeric satellite DNA. Both proteins have multiple binding sites and, therefore, can simultaneously bind to several chromosomes at once. The multiple binding interactions collect chromosomes into a bundle to form an association site called a chromocenter.

The researchers aren’t quite sure how chromocenter formation prevents micronuclei formation, but they speculate that these structures must somehow stabilize the nucleus and the chromosomes housed in its interior. They believe that this functional role is universal among eukaryotic organisms because they observed the same effects in fruit flies and mice.

This study teaches us two additional lessons. One, so-called junk DNA may serve a structural role in the cell. Most molecular biologists are quick to overlook this possibility because they are hyper-focused on the informational role (encoding the instructions to make proteins) DNA plays.

Two, just because regions of the genome readily mutate without consequences doesn’t mean these sequences aren’t serving some kind of functional role. In the case of pericentromeric satellite DNA, the sequences vary from organism to organism. Most molecular biologists assume that because the sequences vary, they must not be functionally important. For if they were, natural selection would have prevented them from changing. But this study demonstrates that DNA sequences can vary—particularly if DNA is playing a structural role—as long as they don’t compromise DNA’s structural utility. In the case of pericentromeric DNA, apparently the nucleotide sequence can vary quite a bit without compromising its capacity to bind chromocenter-forming proteins (such as D1 and HMGA1).

Is the Evolutionary Paradigm the Wrong Framework to Study Genomes?

Scientists who view biology through the lens of the evolutionary paradigm are often 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 satellite DNA, 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 harbors function. In fact, many life scientists regard these “evolutionary vestiges” as junk DNA. This clearly was the case for satellite DNA.

Yet, a growing body of data indicates that virtually every category of so-called junk DNA displays function. In fact, based on the available data, a strong case can be made that most sequence elements in genomes possess functional utility. Based on these insights, and the fact that pericentromeric satellite DNA persists in eukaryotic genomes, the team of researchers assumed that it must be functional. It’s a clear departure from the way most biologists think about genomes.

Based on this study (and others like it), I think it is safe to conclude that we really don’t understand the molecular biology of genomes.

It seems to me that we live in the midst of a revolution in our understanding of genome structure and function. Instead of being a wasteland of evolutionary debris, 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.

This insight also leads me to wonder if we have been using the wrong paradigm all along to think about genome structure and function. I contend that viewing biological systems as the Creator’s handiwork provides a superior framework for promoting scientific advance, particularly when the rationale for the structure and function of a particular biological system is not apparent. Also, in addressing the two challenging questions, if biological systems have been created, then there must be good reasons why these systems are structured and function the way they do. And this expectation drives further study of seemingly nonfunctional, purposeless systems with the full anticipation that their functional roles will eventually be uncovered.

Though committed to an evolutionary interpretation of biology, the UM researchers were rewarded with success when they broke ranks with most evolutionary biologists and assumed junk regions of the genome were functional. Their stance illustrates the power of a creation model approach to biology.

Sadly, most evolutionary biologists are like me when it comes to old furniture. We lack vision and are quick to see it as junk, when in fact a treasure lies in front of us. And, if we let it, this treasure will bring us joy.


  1. University of Michigan, “Scientists Discover a Role for ‘Junk’ DNA,” ScienceDaily (April 11, 2018), www.sciencedaily.com/releases/2018/04/180411131659.htm.
  2. Madhav Jagannathan, Ryan Cummings, and Yukiko M. Yamashita, “A Conserved Function for Pericentromeric Satellite DNA,” eLife 7 (March 26, 2018): e34122, doi:10.7554/eLife.34122.

Why Would God Create a World Where Animals Eat Their Offspring?

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What a book a Devil’s chaplain might write on the clumsy, wasteful, blundering, low and horridly cruel works of nature!

–Charles Darwin, “Letter to J. D. Hooker,” Darwin Correspondence Project

You may not have ever heard of him, but he played an important role in ushering in the Darwinian revolution in biology. His name was Asa Gray.

Gray (1810–1888) was a botanist at Harvard University. He was among the first scientists in the US to adopt Darwin’s theory of evolution. Asa Gray was also a devout Christian.


Asa Gray in 1864. Image credit: John Adams Whipple, Wikipedia

Gray was convinced that Darwin’s theory of evolution was sound. He was also convinced that nature displayed unmistakable evidence for design. For this reason, he reasoned that God must have used evolution as the means to create and, in doing so, Gray may have been the first person to espouse theistic evolution.

In his book Darwinia, Asa Gray presents a number of essays defending Darwin’s theory. Yet, he also expresses his deepest convictions that nature is filled with indicators of design. He attributed that design to a type of God-ordained, God-guided process. Gray argued that God is the source of all evolutionary change.


Gray and Darwin struck up a friendship and exchanged around 300 letters. In the midst of their correspondence, Gray asked Darwin if he thought it possible that God used evolution as the means to create. Darwin’s reply revealed that he wasn’t very impressed with this idea.

I cannot persuade myself that a beneficent & omnipotent God would have designedly created the Ichneumonidæ with the express intention of their feeding within the living bodies of caterpillars, or that a cat should play with mice. Not believing this, I see no necessity in the belief that the eye was expressly designed. On the other hand I cannot anyhow be contented to view this wonderful universe & especially the nature of man, & to conclude that everything is the result of brute force. I am inclined to look at everything as resulting from designed laws, with the details, whether good or bad, left to the working out of what we may call chance. Not that this notion at all satisfies me. I feel most deeply that the whole subject is too profound for the human intellect. A dog might as well speculate on the mind of Newton. Let each man hope & believe what he can.1

Darwin could not embrace Gray’s theistic evolution because of the cruelty he saw in nature that seemingly causes untold pain and suffering in animals. Darwin—along with many skeptics today—couldn’t square a world characterized by that much suffering with the existence of a God who is all-powerful, all-knowing, and all-good.

Filial Cannibalism

The widespread occurrence of filial cannibalism (when animals eat their young or consume their eggs after laying them) and abandonment (leading to death) exemplify such cruelty in animals. It seems such a low and brutal feature of nature.

Why would God create animals that eat their offspring and abandon their young?

Is Cruelty in Nature Really Evil?

But what if there are good reasons for God to allow pain and suffering in the animal kingdom? I have written about good scientific reasons to think that a purpose exists for animal pain and suffering (see “Scientists Uncover a Good Purpose for Long-Lasting Pain in Animals” by Fazale Rana).

And, what if animal death is a necessary feature of nature? Other studies indicate that animal death promotes biodiversity and ecosystem stability (see “Of Weevils and Wasps: God’s Good Purpose in Animal Death” by Maureen Moser, and “Animal Death Prevents Ecological Meltdown” by Fazale Rana).

There also appears to be a reason for filial cannibalism and offspring abandonment, at least based on a study by researchers from Oxford University (UK) and the University of Tennessee.2 These researchers demonstrated that filial cannibalism and offspring abandonment comprise a form of parental care.

What? How is that conclusion possible?

It turns out that when animals eat their offspring or abandon their young, the reduction promotes the survival of the remaining offspring. To arrive at this conclusion, the researchers performed mathematical modeling of a generic egg-laying species. They discovered that when animals sacrificed a few of their young, the culling led to greater fitness for their offspring than when animals did not engage in filial cannibalism or egg abandonment.

These behaviors become important when animals lay too many eggs. In order to properly care for their eggs (protect, incubate, feed, and clean), animals confine egg-laying to a relatively small space. This practice leads to a high density of eggs. But this high density can have drawbacks, making the offspring more vulnerable to diseases and lack of sufficient food and oxygen. Filial cannibalism reduces the density, ensuring a greater chance of survival for those eggs that are left behind. So, ironically, when egg density is too high for the environmental conditions, more offspring survive when the parents consume some, rather than none, of the eggs.

So, why lay so many eggs in the first place?

In general, the more eggs that are laid, the greater the number of surviving offspring—assuming there are unlimited resources and no threats of disease. But it is difficult for animals to know how many eggs to lay because the environment is unpredictable and constantly changing. A better way to ensure reproductive fitness is to lay more eggs and remove some of them if the environment can’t sustain the egg density.

So, it appears as if there is a good reason for God to create animals that eat their young. In fact, you might even argue that filial cannibalism leads to a world with less cruelty and suffering than a world where filial cannibalism doesn’t exist at all. This feature of nature is consistent with the idea of an all-powerful, all-knowing, and all-good God who has designed the creation for his good purposes.


  1. To Asa Gray 22 May [1860],” Darwin Correspondence Project, University of Cambridge, accessed May 15, 2019, https://www.darwinproject.ac.uk/letter/DCP-LETT-2814.xml.
  2. Mackenzie E. Davenport, Michael B. Bansall, and Hope Klug, “Unconventional Care: Offspring Abandonment and Filial Cannibalism Can Function as Forms of Parental Care,” Frontiers in Ecology and Evolution 7 (April 17, 2019): 113, doi:10.3389/fevo.2019.00113.

Reprinted with permission by the author
Original article at:

Origins of Monogamy Cause Evolutionary Paradigm Breakup

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Gregg Allman fronted the Allman Brothers Band for over 40 years until his death in 2017 at the age of 69. Writer Mark Binelli described Allman’s voice as “a beautifully scarred blues howl, old beyond its years.”1

A rock legend who helped pioneer southern rock, Allman was as well known for his chaotic, dysfunctional personal life as for his accomplishments as a musician. Allman struggled with drug abuse and addiction. He was also married six times, with each marriage ending in divorce and, at times, in a public spectacle.

In a 2009 interview with Binelli for Rolling Stone, Allman reflected on his failed marriages: “To tell you the truth, it’s my sixth marriage—I’m starting to think it’s me.”2

Allman isn’t the only one to have trouble with marriage. As it turns out, so do evolutionary biologists—but for different reasons than Greg Allman.

To be more exact, evolutionary biologists have made an unexpected discovery about the evolutionary origin of monogamy (a single mate for at least a season) in animals—an insight that raises questions about the evolutionary explanation. Based on recent work headed by a large research team of investigators from the University of Texas (UT), Austin, it looks like monogamy arose independently, multiple times, in animals. And these origin events were driven, in each instance, by the same genetic changes.3

In my view, this remarkable example of evolutionary convergence highlights one of the many limitations of evolutionary theory. It also contributes to my skepticism (and that of other intelligent design proponents/creationists) about the central claim of the evolutionary paradigm; namely, the origin, design, history, and diversity of life can be fully explained by evolutionary mechanisms.

At the same time, the independent origins of monogamy—driven by the same genetic changes—(as well as other examples of convergence) find a ready explanation within a creation model framework.

Historical Contingency

To appreciate why I believe this discovery is problematic for the evolutionary paradigm, it is necessary to consider the nature of evolutionary mechanisms. According to the evolutionary biologist Stephen Jay Gould (1941–2002), evolutionary transformations occur in a historically contingent manner.This means that the evolutionary process consists of an extended sequence of unpredictable, chance events. If any of these events were altered, it would send evolution down a different trajectory.

To help clarify this concept, Gould used the metaphor of “replaying life’s tape.” If one were to push the rewind button, erase life’s history, and then let the tape run again, the results would be completely different each time. In other words, the evolutionary process should not repeat itself. And rarely should it arrive at the same end point.

Gould based the concept of historical contingency on his understanding of the mechanisms that drive evolutionary change. Since the time of Gould’s original description of historical contingency, several studies have affirmed his view. (For descriptions of some representative studies, see the articles listed in the Resources section.) In other words, researchers have experimentally shown that the evolutionary process is, indeed, historically contingent.

A Failed Prediction of the Evolutionary Paradigm

Given historical contingency, it seems unlikely that distinct evolutionary pathways would lead to identical or nearly identical outcomes. Yet, when viewed from an evolutionary standpoint, it appears as if repeated evolutionary outcomes are a common occurrence throughout life’s history. This phenomenon—referred to as convergence—is widespread. Evolutionary biologists Simon Conway Morris and George McGhee point out in their respective books, Life’s Solution and Convergent Evolution, that identical evolutionary outcomes are a characteristic feature of the biological realm.5 Scientists see these repeated outcomes at the ecological, organismal, biochemical, and genetic levels. In fact, in my book The Cell’s Design, I describe 100 examples of convergence at the biochemical level.

In other words, biologists have made two contradictory observations within the evolutionary framework: (1) evolutionary processes are historically contingent and (2) evolutionary convergence is widespread. Since the publication of The Cell’s Design, many new examples of convergence have been unearthed, including the recent origin of monogamy discovery.

Convergent Origins of Monogamy

Working within the framework of the evolutionary paradigm, the UT research team sought to understand the evolutionary transition to monogamy. To achieve this insight, they compared the gene expression profiles in the neural tissues of reproductive males for closely related pairs of species, with one species displaying monogamous behavior and the other nonmonogamous reproduction.

The species pairs spanned the major vertebrate groups and included mice, voles, songbirds, frogs, and cichlids. From an evolutionary perspective, these organisms would have shared a common ancestor 450 million years ago.

Monogamous behavior is remarkably complex. It involves the formation of bonds between males and females, care of offspring by both parents, and increased territorial defense. Yet, the researchers discovered that in each instance of monogamy the gene expression profiles in the neural tissues of the monogamous species were identical and distinct from the gene expression patterns for their nonmonogamous counterparts. Specifically, they observed the same differences in gene expression for the same 24 genes. Interestingly, genes that played a role in neural development, cell-cell signaling, synaptic activity, learning and memory, and cognitive function displayed enhanced gene expression. Genes involved in gene transcription and AMPA receptor regulation were down-regulated.

So, how do the researchers account for this spectacular example of convergence? They conclude that a “universal transcriptomic mechanism” exists for monogamy and speculate that the gene modules needed for monogamous behavior already existed in the last common ancestor of vertebrates. When needed, these modules were independently recruited at different times in evolutionary history to yield monogamous species.

Yet, given the number of genes involved and the specific changes in gene expression needed to produce the complex behavior associated with monogamous reproduction, it seems unlikely that this transformation would happen a single time, let alone multiple times, in the exact same way. In fact, Rebecca Young, the lead author of the journal article detailing the UT research team’s work, notes that “Most people wouldn’t expect that across 450 million years, transitions to such complex behaviors would happen the same way every time.”6

So, is there another way to explain convergence?

Convergence and the Case for a Creator

Prior to Darwin (1809–1882), biologists referred to shared biological features found in organisms that cluster into disparate biological groups as analogies. (In an evolutionary framework, analogies are referred to as evolutionary convergences.) They viewed analogous systems as designs conceived by the Creator that were then physically manifested in the biological realm and distributed among unrelated organisms.

In light of this historical precedence, I interpret convergent features (analogies) as the handiwork of a Divine mind. The repeated origins of biological features equate to the repeated creations by an intelligent Agent who employs a common set of solutions to address a common set of problems facing unrelated organisms.

Thus, the idea of monogamous convergence seems to divorce itself from the evolutionary framework, but it makes for a solid marriage in a creation model framework.


  1. Mark Binelli, “Gregg Allman: The Lost Brother,” Rolling Stone, no. 1082/1083 (July 9–23, 2009), https://www.rollingstone.com/music/music-features/gregg-allman-the-lost-brother-108623/.
  2. Binelli, “Gregg Allman: The Lost Brother.”
  3. Rebecca L. Young et al., “Conserved Transcriptomic Profiles underpin Monogamy across Vertebrates,” Proceedings of the National Academy of Sciences, USA 116, no. 4 (January 22, 2019): 1331–36, doi:10.1073/pnas.1813775116.
  4. Stephen Jay Gould, Wonderful Life: The Burgess Shale and the Nature of History (New York: W. W. Norton & Company, 1990).
  5. Simon Conway Morris, Life’s Solution: Inevitable Humans in a Lonely Universe (New York: Cambridge University Press, 2003); George McGhee, Convergent Evolution: Limited Forms Most Beautiful (Cambridge, MA: MIT Press, 2011).
  6. University of Texas at Austin, “Evolution Used Same Genetic Formula to Turn Animals Monogamous,” ScienceDaily (January 7, 2019), www.sciencedaily.com/releases/2019/01/1901071507.htm.

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.

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