If God Hates Abortion Why Do So Many Occur Spontaneously in Humans?

By Fazale Rana – November 25, 2020

A common fundamentalist argument against abortion is that each human being is granted a soul at the moment of conception, and that destroying that “soul” is equivalent to murder. . . However, there’s some serious problems with the logic of ensoulation at the point of conception. The CDC as well as the March of Dimes and several fertility experts have conducted studies to see exactly how hard it is to carry a pregnancy to term. In general, less than 70% of all fertilized eggs will even implant into the mother’s womb causing pregnancy to continue. From there, there is a 25-50% chance of aborting before you even know you are pregnant. So if you look at it from the fundamentalist point of view, all those little souls are being given a home, only to be miscarried before they even know they are alive. Scientific research has compiled the following information about the rates of naturally aborted pregnancies in human beings (or, if you believe everything happens for a reason, pregnancies aborted by God himself).

RationalWiki, “Spontaneous Abortion in Humans”

Miscarriage and Troubling Questions
Perhaps nothing is more painful and confusing for a woman than when she experiences a miscarriage. My wife and I know this firsthand. Amy’s first pregnancy ended with a miscarriage early in the first trimester. Our joy and excitement were replaced by sadness and an indescribable disappointment. I don’t know if I could ever truly understand how my wife felt then or how she feels now about our loss. We wonder, all these years later, if our first child was a boy or girl. Still, we are so grateful for the wonderful children God did give to us.

Questions surrounding spontaneous abortions and miscarriages are painful, indeed. But they also expose profound philosophical and theological problems with far-reaching implications for the Christian faith. The high rate of spontaneous abortions during human pregnancies raises questions about God’s goodness and also impacts the creation/evolution controversy and the abortion debate.

  • If human beings are made in God’s image—as the crown of creation—wouldn’t a Creator have designed a less-flawed and error-prone process for human reproduction?
  • If a Creator made human beings with a soul at the point of conception, why would some of these embryos live, ever so briefly before the pregnancy—and their life—comes to an end?
  • If a Creator hates abortion, why is the rate of spontaneous abortions so great?
  • In light of the high rate of spontaneous abortions, why is it so wrong for human beings to voluntarily end a pregnancy?

Without a doubt, these questions represent a serious challenge to the Christian faith. Fortunately, new scientific insights into embryo mortality and the cause of early miscarriages help address some of these challenging and heart-wrenching concerns, even if other questions remain a troubling mystery.

Before we take a look at these new insights, it is necessary to address a broader concern about the consequences of the constancy of nature’s laws and how this feature impacts the incidences of spontaneous abortions.

Consequences of the Second Law of Thermodynamics

Given the complexity of biological systems such as human reproduction, it is unreasonable to think that these processes, no matter how well designed, will perform flawlessly every time. All the more so given the influence the second law of thermodynamics wields.

As a consequence of this law, errors will inevitably occur—at least, on occasion—during all biological processes. Because of the invariance of the laws of nature, the second law is always in operation. Hence, errors will occur during: (1) fertilization, (2) implantation of the embryo in the uterine wall, and (3) placenta formation and embryo growth and development. These errors lead to spontaneous abortions, miscarriages, and stillbirths.

While it is tempting to view entropy (the second law of thermodynamics) in a negative light, it is important to recognize that, if not for entropy, life’s existence would be impossible. Entropy enables metabolism and plays the central role in the formation and stability of cell membranes, protein higher-order structures, and the DNA double helix.

Of course, the unrelenting operation of the laws of nature leads to profound theological and philosophical issues that I have addressed elsewhere. Even if errors are inevitable in biological processes, couldn’t God have somehow designed human reproduction to be less error-prone?

Fortunately, recent scientific insights help address this issue, beginning with a detailed assessment of early embryo mortality.

What Is the Actual Rate of Spontaneous Abortions?

A survey of the scientific literature finds that the reported rates for spontaneous abortions are highly varied. Still, these rates seem to indicate human reproduction is a highly inefficient process with embryo mortality rates:

  • before and during implantation—as high as 75%
  • before the first six weeks of pregnancy—as high as 80%
  • during the first trimester—as high as 70%
  • before the first 20 weeks—as high as 50%
  • from fertilization to birth—as high as 90%

But as physiologist Gavin Jarvis from Cambridge University points out, these rates of spontaneous abortions are most certainly exaggerated and find little evidential support. These statistics are based on speculation and imprecise estimates of embryo mortality.1 In an attempt to remedy this problem, Jarvis carried out a careful reassessment of the published data on embryo mortality.

As part of this assessment, Jarvis concludes that it is impossible to know how many embryos die—or survive—during the first week of pregnancy, from the point of fertilization to the beginning stages of implantation. The earliest point that embryo survival can be realistically studied in a clinical setting is after the first week of pregnancy when the hormone human chorionic gonadotrophin (CG) can be detected. Prior to that point, the rate of embryo loss is merely a guess.

Some biomedical researchers have attempted to estimate embryo mortality during the first week of pregnancy from in vitro fertilization studies. Jarvis argues that these estimates are meaningless. He says it is hard to believe that embryo survival under laboratory conditions would reflect embryo survival rates under natural conditions. In fact, given that in vitro fertilization and subsequent embryo growth occur under nonoptimal, nonnatural conditions suggests that embryo mortality is likely much higher when carried out in the laboratory than when fertilization and early stage embryo development take place in vivo. Jarvis notes, “It’s impossible to give a precise figure for how many embryos survive in the first week but in normal healthy women, it probably lies somewhere between 60–90%.”2

Insight into embryo mortality becomes quantifiable after the first week. As it turns out, about 1 in 5 embryos die during implantation. In fact, in many of these instances the woman would not be aware she was pregnant, because she would not miss her period. Once a woman misses her period, only about 10 to 15% of the embryos die before birth. In total, about 70% of embryos make it to live birth, once implantation commences and the pregnancy is clinically confirmed from CG levels.

As Jarvis notes, “Although we can’t be precise, we can avoid exaggeration, and from reviewing the studies that do exist, it is clear that many more [embryos] survive than is often claimed.”3

Even though the rate of spontaneous abortion isn’t as high as often reported, skeptics still have grounds to question the design of human reproduction, viewing it as an error-prone, flawed process. Yet, new insight into the causes of spontaneous abortions and miscarriages suggests that a rationale undergirds pregnancy loss, especially during the early stages of pregnancy. In light of this insight it appears that spontaneous abortions may be rightly understood as a necessary part of the design of human reproduction.

Why Do Spontaneous Abortions Occur?

Most miscarriages appear to be the result of chromosomal abnormalities. Embryos with damaged chromosomes or an abnormal number of chromosomes often die. Biomedical researchers have discovered that somewhere between 50 to 80% of human embryos produced by in vitro fertilization have at least one cell that displays chromosomal abnormalities. (As mentioned, the statistics for in vitro fertilization are not likely to be reliable measures of naturally occurring fertilization, so we need to be cautious about how we interpret this finding.)4 Researchers have also learned that the leading cause of embryo mortality during in vitro fertilization appears to be associated with chromosomal abnormalities.

As I noted, these abnormalities inevitably arise as a consequence of the complexity of human reproduction and the second law of thermodynamics. In light of this inevitability, biomedical investigators now think that spontaneous abortions serve as the means to prevent embryos with chromosomal abnormalities from developing once they begin the process of implantation. By studying the interactions between embryos created via in vitro fertilization with cells cultured from the endometrium (the cell layers that line the uterine wall), investigators have discovered that when healthy embryos are introduced to endometrial cells in a Petri dish, they cluster around the embryo, releasing chemicals that promote implantation. On the other hand, endometrial cells eschew embryos with chromosomal abnormalities, halting the release of chemicals that prompt implantation.5 These investigators also discovered that endometrial cells exposed to embryos with chromosomal abnormalities underwent a stress response, whereas healthy embryos activated gene networks in the endometrial cells that led to the production of metabolic enzymes and the secretion of implantation factors. Researchers confirmed this result by exposing the uteri of mice to cell culture media that was used to grow abnormal human embryos and they observed the same response in the mouse cells in vivo as the human cells in vitro.

In other words, it appears as if the endometrium serves as a gatekeeper rejecting embryos with chromosomal abnormalities and embracing developmentally viable embryos. Because the rejection of abnormal embryos happens so early in the pregnancy, most women are unaware that they were pregnant.

Ironically, some researchers believe the widespread occurrence of miscarriages actually led to the success of our species. Compared to other mammals, humans have an unusually high rate of spontaneous abortions (even when we consider Jarvis’s revised estimates). For the most part, humans give birth to a single child that requires nine months of gestation. Other mammals have shorter pregnancies, some birthing litters. For these mammals, a process that allows a few abnormal embryos to grow and develop has relatively little consequences because a significant number of the litter will be healthy. But for humans, allowing a single ill-fated pregnancy to go to full-term is a flawed strategy. As biologist Shawn Chavez notes, “In the case of animals that have litters, maybe they make 10 embryos a month and only eight make it to live birth, but that’s still eight. Whereas we typically can only make one embryo per month, so if it isn’t a good one, maybe it’s better to try again next month.”6 Biologist Tim Bruckner makes a similar point. He states, “According to the theory of natural selection, we want to have children that survive infancy and grow up and have children of their own so they can pass on our genes. There’s this idea that human reproduction is inefficient because so many pregnancies are lost, but overall it may have led to the preservation of our species.”7

These insights into the cause of miscarriage also contribute to our understanding of infertility. Women with a hypervigilant endometrium may struggle to get pregnant because the endometrium rejects both abnormal and healthy embryos. By the same token, these insights explain why some women are prone to miscarriages. In this case, their endometrium isn’t selective enough, allowing embryos to develop which otherwise “biologically” shouldn’t.

Spontaneous Abortions: A Necessary Design Feature of Human Reproductions

On the surface, the high rate of spontaneous abortions appears to be a flawed design. In reality, this feature of human reproduction reflects an exquisite biological rationale. Though emotionally brutal, miscarriages are a necessary feature of the human reproduction process that arises from the complexity of human reproduction and the second law of thermodynamics. If not for the high rate of spontaneous abortions we would have a reduced likelihood of having healthy children.

Though this scientific insight doesn’t answer all the difficult questions associated with spontaneous abortions, it can offer some source of comfort knowing that a rationale exists for pregnancy loss. As science journalist Alice Klein writes:

As traumatic as my own miscarriage was, it is comforting to learn that it probably wasn’t because of anything I did or anything that was wrong with me. On the contrary, it was most likely due to a random genetic error that I had no control over. Instead of my body failing me, it may have protected me from investing further in a pregnancy that probably wasn’t going to produce a healthy baby.8

All these years later, I find comfort, too, in knowing that there is a reason why my wife suffered a miscarriage. Still, Amy and I are left with many questions—questions for which we may never receive answers. Though it may sound odd to nonreligious people, in the midst of this uncertainty, we choose to rely on the fact that God is just and merciful and sovereign over all things.


The Fixed Laws of Nature

The Elegant Design of Human Reproduction

Disabilities and the Image of God

Pro-Life Argument

  1. Gavin E. Jarvis, “Early Embryo Mortality in Natural Human Reproduction: What the Data Say,” F1000Research 5 (June 12, 2017): 2765, doi:10.12688/f1000research.8937.2.
  2. University of Cambridge, “Human Reproduction Likely to Be More Efficient Than Previously Thought,” ScienceDaily (June 13, 2017), sciencedaily.com/releases/2017/06/170613101932.htm.
  3. University of Cambridge, “Human Reproduction.”
  4. Lucia Carbone and Shawn L. Chavez, “Mammalian Pre-Implantation Chromosomal Instability: Species Comparison, Evolutionary Considerations, and Pathological Correlations,” Systems Biology in Reproductive Medicine 61, no. 6 (2015): 321–35, doi:10.3109/1939638.2015.1073406.
  5. Gijs Teklenburg et al., “Natural Selection of Human Embryos: Decidualizing Endometrial Stromal Cells Serve as Sensors of Embryo Quality upon Implantation,” PLoS One 5 (April 21, 2010): e10258, doi:10.1371/journal.pone.0010258; Jan J. Brosens et al., “Uterine Selection of Human Embryos at Implantation,” Scientific Reports 4 (February 6, 2014): 3894, doi:10.1038/srep03894.
  6. Alice Klein, “The Real Reasons Miscarriage Exists—And Why It’s So Misunderstood,” New Scientist (August 5, 2020), https://www.newscientist.com/article/mg24732940-900-the-real-reasons-miscarriage-exists-and-why-its-so-misunderstood/.
  7. Klein, “The Real Reasons Miscarriage Exists.”
  8. Klein, “The Real Reasons Miscarriage Exists.”

Reprinted with permission by the author

Original article at:

Do Goosebumps Send a Chill Down the Spine of the Creation Model?

By Fazale Rana – September 2, 2020

I think few would be surprised to learn that J. K. Rowling’s Harry Potter titles are the best-selling children’s books of all time, but do you know which works take second place in that category? It’s the Goosebumps series by R. L. Stine.

From 1992 to 1997, Stine wrote and published 62 Goosebumps books. To date, these books have been printed in over 3o languages, with over 400 million copies sold worldwide (this does not include Stine’s numerous spin-off books) and adapted for television and film. Each book in the Goosebumps lineup features different child characters who find themselves in scary situations that often involve encounters with the bizarre and supernatural.

The title of the series is apropos. Humans get goosebumps whenever we are afraid. We also get goosebumps when we are moved by something beautiful and awe-inspiring. And, of course, we get goosebumps when we are cold.

Goosebumps are caused by a process dubbed piloerection. When we feel cold, tiny smooth muscles (called the arrector pili) deep within our skin contract. Because these muscles are attached to hair follicles, this contraction causes our hairs to stand on end. Getting goosebumps is one of our quirks as human beings. Most biologists don’t think this phenomenon serves any useful purpose, making it that much more of an oddity. So, if goosebumps have no obvious utility, then why do we experience them at all?

Evolutionary Explanation for Goosebumps

Many life scientists view goosebumps as a vestige of our evolutionary history. So, while goosebumps serve no apparent function in modern humans, evolutionary biologists believe they did have utility for our evolutionary ancestors, who were covered with a lot of hair. Presumably, when our ancestors were cold, the contraction of the arrector pili muscles created pockets of air near the surface of the skin when the hairs stood on end, serving as insulation from the chill. And when our ancestors were frightened, contraction of the arrector pili muscles caused their hair to puff up, making them seem larger and more menacing.

These two behaviors are observed in other mammals and even in some bird species. For evolutionary biologists, this shared behavior attests to our evolutionary connection to animal life.

In other words, many life scientists see goosebumps as compelling evidence that human beings have an evolutionary origin because: (1) goosebumps serve no useful purpose in humans today and (2) the same physiological process that causes goosebumps in humans causes hair and fur of other animals to stand erect when they feel cold or threatened.

So, one theological question creationists need to address is this: Why would God create human beings to have a useless response to the cold or to being frightened? For those of us who hold to a creation model/design perspective, goosebumps in humans cause us a bit of a fright. But is there any reason to be scared?

What if goosebumps in humans serve a useful function? If they do, that function undermines the idea that goosebumps are a vestige of our evolutionary history and, at the same time, makes it reasonable to think that human beings are the handiwork of a Creator. Accordingly, all facets of our anatomy and physiology are intentionally designed for a purpose, including goosebumps. And this is precisely what a research team from Harvard University has discovered. These investigators identified an unexpected function performed by arrector pili muscles, beyond causing hairs to stand erect.1 This new insight suggests a reason why humans get goosebumps, making it reasonable to interpret this physiological feature of human beings within a creation model/design framework.

Multiple Roles of the Arrector Pili Muscle

To carry out its function, the arrector pili muscle forms an intimate association with nerves in the sympathetic nervous system. This component of the nervous system contributes to homeostasis, allowing the bodies of animals (including humans) to maintain constant and optimal conditions. As part of this activity, animals receive sensory input from their surroundings and respond to environmental changes. So, in this case, when a mammal experiences cold the sympathetic nervous system transmits the sensation to the arrector pili muscles, causing them to contract, helping the animal to stay warm.

Recently, the Harvard research team, working with mice, discovered that the arrector pili muscle also plays a structural role, with the individual nerve fibers of the sympathetic nervous system wrapping around the muscle. This architecture positions the nerves next to a bed of stem cells near hair follicles, providing the sympathetic nervous system with a direct connection to the hair follicle stem cells.

Normally, the hair follicle stem cells are in a quiescent (inactive) state. Under conditions of prolonged cold, however, the sympathetic nerves release the neurotransmitter norepinephrine. This release stimulates the stem cells to replicate and develop into new hair. In other words, the interplay between the arrector pili and the sympathetic nerves provides both a short-term (contraction of the arrector pili) and a long-term (hair growth) response to cold.

The researchers discovered that when they removed the arrector pili muscles the sympathetic nerves retracted, losing their connection to the hair follicle stem cells. In the retracted state, the sympathetic nerves could not stimulate the activity of the hair follicle stem cells. In short, the arrector pili plays an integral role in coupling stem cell regeneration and, hence, hair growth to changes in the environment by functioning as scaffolding.

Goosebumps and the Case for Creation

In mammals (which have a coat of fur or bodies heavily covered with hair), the dual role played by the arrector pili muscles in mounting both rapid and long-term responses to the cold highlights the elegance, sophistication, and ingenuity of biological systems—features befitting the work of a Creator. But does this insight have any bearing on why humans experience goosebumps if they are created by God?

Toward this end, if the arrector pili muscles served no true function, evolutionary theory predicts that they should atrophy, maybe even disappear. Yet, the work of the Harvard scientists makes it plain that if the arrector pili muscles became more diminutive or were lost, it could very well compromise the overall function of the sympathetic nervous system in human skin, because the scaffolding for nerves of the sympathetic system would be lost.

The recognition that the arrector pili muscles prevent the sympathetic nerves from retracting away from hair follicles in mice suggests that this muscle functions in the same way in human skin. In mice and other mammals, the positioning of the sympathetic nerve is critical to stimulate the growth of new hair in response to ongoing exposure to cold. The same should be true in humans. Still, it is not clear at this juncture if hair growth in humans under these conditions would have any real benefit. On the other hand, there is no evidence to the contrary. We don’t know.

What we do know is that without the arrector pili muscles the sympathetic nerves would lose their positioning anchor in human skin. It seems perfectly reasonable to think that the proper positioning of the sympathetic nerve in the skin, in general, plays an overarching role in communicating changes in the environment to our bodies, helping us to maintain a homeostatic state.

In other words, because the muscle serves multiple purposes, it helps explain why these intact, fully functional muscles are found in human skin, with goosebumps produced as a by-product of the arrector pili’s association with hair follicles and sympathetic nerves. And who knows, maybe these muscles have added functions yet to be discovered.

There may be other reasons why we get goosebumps. They help us to pay close attention to the happenings in our environment. And, of course, this heightened awareness provides a survival advantage. On top of that use, goosebumps also provide social cues to others, signaling to them that we are cold or frightened, with the hope that these cues would encourage them to step in and help us—again, a survival advantage.

The cold truth is this: gaining a better understanding about the anatomy and physiology of the skin makes goosebumps less frightening for those of us who embrace a creation model approach to humanity’s origin.


  1. Yuli Schwartz et al., “Cell Types Promoting Goosebumps Form a Niche to Regulate Hair Follicle Stem Cells,” Cell 182, no. 3 (August 6, 2020): 578–93, doi:10.1016/j.cell.2020.06.031.

Reprinted with permission by the author

Original article at:

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

By Fazale Rana – April 1, 2020

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

…Just kidding! April Fool’s!

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

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

And that is no joke.

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

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

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

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

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

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


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

The Mechanisms of Pseudogene Formation.
Image credit: Wikipedia.

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

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

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

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

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

Are Untranscribed Pseudogenes Really Untranscribed?

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

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

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

Are Untranscribed Pseudogenes Really Nonfunctional?

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

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

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

Common Design or Common Descent?

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

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

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


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

Reprinted with permission by the author

Original article at:


Does Evolutionary Bias Create Unhealthy Stereotypes about Pseudogenes?

By Fazale Rana – March 18, 2020

Truth be told, we all hold to certain stereotypes whether we want to admit it or not. Though unfair, more often than not, these stereotypes cause little real damage.

Yet, there are instances when stereotypes can be harmful—even deadly. As a case in point, researchers have shown that stereotyping disrupts the healthcare received by members of so-called disadvantaged groups, such as African Americans, Latinos, and the poor.1

Healthcare providers are frequently guilty of bias towards underprivileged people. Often, the stereotyping is unconscious and unintentional. Still, this bias compromises the medical care received by people in these ethnic and socioeconomic groups.

Underprivileged patients are also guilty of stereotyping. It is not uncommon for these patients to perceive themselves as the victims of prejudice, even when their healthcare providers are genuinely unbiased. As a result, these patients don’t trust healthcare workers and, consequently, withhold information that is vital for a proper diagnosis.

Fortunately, psychologists have developed best practices that can reduce stereotyping by both healthcare practitioners and patients. Hopefully, by implementing these practices, the impact of stereotyping on the quality of healthcare can be minimized over time.

Recently, a research team from Australia identified another form of stereotyping that holds the potential to negatively impact healthcare outcomes.2 In this case, the impact of this stereotyping isn’t limited to disadvantaged people; it affects all of us.

A Bias Against Pseudogenes

These researchers have uncovered a bias in the way life scientists view the human genome (and the genomes of other organisms). Too often they regard the human genome as a repository of useless, nonfunctional DNA that arises as a vestige of evolutionary history. Because of this view, life scientists and the biomedical research community eschew studying regions of the human genome they deem to be junk DNA. This posture is not unreasonable. It doesn’t make sense to invest precious scientific resources to study nonfunctional DNA.

Many life scientists are unaware of their bias. Unfortunately, this stereotyping hinders scientific advance by delaying discoveries that could be translated into the clinical setting. Quite often, supposed junk DNA has turned out to serve a vital purpose. Failure to recognize this function not only compromises our understanding of genome biology, but also hinders biomedical researchers from identifying defects in these genomic regions that contribute to genetic diseases and disorders.

As psychologists will point out, acknowledging bias is the first step to solving the problems that stereotyping causes. This is precisely what these researchers have done by publishing an article in Nature Review Genetics.3 The team focused on DNA sequence elements called pseudogenes. Traditionally, life scientists have viewed pseudogenes as the remnants of once functional genes. Biologists have identified three categories of pseudogenes: (1) unitary, (2) duplicated, and (3) processed.

Researchers categorize DNA sequences as pseudogenes based on structural features. Such features indicate to the investigators that these sequence elements were functional genes at one time in evolutionary history, but eventually lost function due to mutations or other biochemical processes, such as reverse transcription and DNA insertion. Once a DNA sequence is labeled a pseudogene, bias sets in and researchers just assume that it lacks function—not because it has been experimentally demonstrated to be nonfunctional, but because of the stereotyping that arises out of the evolutionary paradigm.

The authors of the piece acknowledge that “the annotation of genomics regions as pseudogenes constitutes an etymological signifier that an element has no function and is not a gene. As a result, pseudogene-annotated regions are largely excluded from functional screen and genomic analyses.”4 In other words, the “pseudogene” moniker biases researchers to such a degree that they ignore these sequence elements as they study genome structure and function without ever doing the hard, experimental work to determine whether it is actually nonfunctional.

This approach is clearly misguided and detracts from scientific discovery. As the authors admit, “However, with a growing number of instances of pseudogene-annotated regions later found to exhibit biological function, there is an emerging risk that these regions of the genome are prematurely dismissed as pseudogenic and therefore regarded as void of function.”5

Discovering Function Despite Bias

The harmful effects of this bias become evident as biomedical researchers unexpectedly stumble upon function for pseudogenes, time and time, again, not because of the evolutionary paradigm, but despite it. These authors point out that many processed pseudogenes are transcribed and, of those, many are translated to produce proteins. Many unitary and duplicated pseudogenes are also transcribed. Some are also translated into proteins, but a majority are not. Instead they play a role in gene regulation as described by the competitive endogenous RNA hypothesis.

Still, there are some pseudogenes that aren’t transcribed and, thus, could rightly be deemed nonfunctional. However, the researchers point out that the current experimental approaches for identifying transcribed regions are less than ideal. Many of these methods may fail to detect pseudogene transcripts. However, as the researchers point out, even if a pseudogene isn’t transcribed it still may serve a functional role (e.g., contributing to chromosome three-dimensional structure and stability).

This Nature article raises a number of questions and concerns for me as a biochemist:

  • How widespread is this bias?
  • If this type of stereotyping exists toward pseudogenes, does it exist for other classes of junk DNA?
  • How well do we really understand genome structure and function?
  • Do we have the wrong perspective on the genome, one that stultifies scientific advance?
  • Does this bias delay the understanding and alleviation of human health concerns?

Is the Evolutionary Paradigm the Wrong Framework to Study Genomes?

Based on this article, I think it is safe to conclude that we really don’t understand the molecular biology of genomes. We are living in the midst of a scientific revolution that is radically changing our view of genome structure and function. 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 question if the evolutionary paradigm is the proper framework for thinking about genome structure and function. From my perspective, treating biological systems as the Creator’s handiwork provides a superior approach to understanding the genome. A creation model approach promotes scientific advance, particularly when the rationale for the structure and function of a particular biological system is not apparent. This expectation forces researchers to keep an open mind and drives further study of seemingly nonfunctional, purposeless systems with the full anticipation that their functional roles will eventually be uncovered.

Over the last several years, I have raised concerns about the bias life scientists have harbored as they have worked to characterize the human genome (and genomes of other organisms). It is gratifying to me to see that there are life scientists who, though committed to the evolutionary paradigm, are beginning to recognize this bias as well.

The first step to addressing the problem of stereotyping—in any sector of society—is to acknowledge that it exists. Often, this step is the hardest one to take. The next step is to put in place structures to help overcome its harmful influence. Could it be that part of the solution to this instance of scientific stereotyping is to grant a creation model approach access to the scientific table?


Pseudogene Function

The Evolutionary Paradigm Hinders Scientific Advance

  1. For example, see Joshua Aronson et al., “Unhealthy Interactions: The Role of Stereotype Threat in Health Disparities,” American Journal of Public Health 103 (January 1, 2013): 50–56, doi:10.2105/AJPH.2012.300828.
  2. Seth W. Cheetham, Geoffrey J. Faulkner, and Marcel E. Dinger, “Overcoming Challenges and Dogmas to Understand the Functions of Pseudogenes,” Nature Reviews Genetics 21 (March 2020): 191–201, doi:10.1038/s41576-019-0196-1.
  3. Cheetham, Faulkner, and Dinger, 191–201.
  4. Cheetham, Faulkner, and Dinger, 191–201.
  5. Cheetham, Faulkner, and Dinger, 191–201.

Reprinted with permission by the author

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But Do Watches Replicate? Addressing a Logical Challenge to the Watchmaker Argument

By Fazale Rana – January 22, 2020

Were things better in the past than they are today? It depends who you ask.

Without question, there are some things that were better in years gone by. And, clearly, there are some historical attitudes and customs that, today, we find hard to believe our ancestors considered to be an acceptable part of daily life.

It isn’t just attitudes and customs that change over time. Ideas change, too—some for the better, some for the worst. Consider the way doing science has evolved, particularly the study of biological systems. Was the way we approached the study of biological systems better in the past than it is today?

It depends who you ask.

As an old-earth creationist and intelligent design proponent, I think the approach biologists took in the past was better than today for one simple reason. Prior to Darwin, teleology was central to biology. In the late 1700s and early to mid-1800s, life scientists viewed biological systems as the product of a Mind. Consequently, design was front and center in biology.

As part of the Darwinian revolution, teleology was cast aside. Mechanism replaced agency and design was no longer part of the construct of biology. Instead of reflecting the purposeful design of a Mind, biological systems were now viewed as the outworking of unguided evolutionary mechanisms. For many people in today’s scientific community, biology is better for it.

Prior to Darwin, the ideas shaped by thinkers (such as William Paley) and biologists (such as Sir Richard Owen) took center stage. Today, their ideas have been abandoned and are often lampooned.

But, advances in my areas of expertise (biochemistry and origins-of-life research) justify a return to the design hypothesis, indicating that there may well be a role for teleology in biology. In fact, as I argue in my book The Cell’s Design, the latest insights into the structure and function of biomolecules bring us full circle to the ideas of William Paley (1743-1805), revitalizing his Watchmaker argument for God’s existence.

In my view, many examples of molecular-level biomachinery stand as strict analogs to human-made machinery in terms of architecture, operation, and assembly. The biomachines found in the cell’s interior reveal a diversity of form and function that mirrors the diversity of designs produced by human engineers. The one-to-one relationship between the parts of man-made machines and the molecular components of biomachines is startling (e.g., the flagellum’s hook). I believe Paley’s case continues to gain strength as biochemists continue to discover new examples of biomolecular machines.

The Skeptics’ Challenge

Despite the powerful analogy that exists between machines produced by human designers and biomolecular machines, many skeptics continue to challenge the revitalized watchmaker argument on logical grounds by arguing in the same vein as David Hume.1 These skeptics assert that significant and fundamental differences exist between biomachines and human creations.

In a recent interaction on Twitter, a skeptic raised just such an objection. Here is what he wrote:

“Do [objects and machines designed by humans] replicate with heritable variation? Bad analogy, category mistake. Same one Paley made with his watch on the heath centuries ago.”

In other words, biological systems replicate, whereas devices and artefacts made by human beings don’t. This difference is fundamental. Such a dissimilarity is so significant that it undermines the analogy between biological systems (in general) and biomolecular machines (specifically) and human designs, invalidating the conclusion that life must stem from a Mind.

This is not the first time I have encountered this objection. Still, I don’t find it compelling because it fails to take into account manmade machines that do, indeed, replicate.

Von Neumann’s Universal Self-Constructor

In the 1940s, mathematician, physicist, and computer scientist John von Neumann (1903–1957) designed a hypothetical machine called a universal constructor. This machine is a conceptual apparatus that can take materials from the environment and build any machine, including itself. The universal constructor requires instructions to build the desired machines and to build itself. It also requires a supervisory system that can switch back and forth between using the instructions to build other machines and copying the instructions prior to the replication of the universal constructor.

Von Neumann’s universal constructor is a conceptual apparatus, but today researchers are actively trying to design and build self-replicating machines.2 Much work needs to be done before self-replicating machines are a reality. Nevertheless, one day machines will be able to reproduce, making copies of themselves. To put it another way, reproduction isn’t necessarily a quality that distinguishes machines from biological systems.

It is interesting to me that a description of von Neumann’s universal constructor bears remarkable similarity to a description of a cell. In fact, in the context of the origin-of-life problem, astrobiologists Paul Davies and Sara Imari Walker noted the analogy between the cell’s information systems and von Neumann’s universal constructor.3 Davies and Walker think that this analogy is key to solving the origin-of-life problem. I would agree. However, Davies and Walker support an evolutionary origin of life, whereas I maintain that the analogy between cells and von Neumann’s universal constructor adds vigor to the revitalized Watchmaker argument and, in turn, the scientific case for a Creator.

In other words, the reproduction objection to the Watchmaker argument has little going for it. Self-replication is not the basis for viewing biomolecular machines as fundamentally dissimilar to machines created by human designers. Instead, self-replication stands as one more machine-like attribute of biochemical systems. It also highlights the sophistication of biological systems compared to systems produced by human designers. We are a far distance away from creating machines that are as sophisticated as the machines found inside the cell. Nevertheless, as we continue to move in that direction, I think the case for a Creator will become even more compelling.

Who knows? With insights such as these maybe one day we will return to the good old days of biology, when teleology was paramount.


Biomolecular Machines and the Watchmaker Argument

Responding to Challenges to the Watchmaker Argument

  1. “Whenever you depart, in the least, from the similarity of the cases, you diminish proportionably the evidence; and may at last bring it to a very weak analogy, which is confessedly liable to error and uncertainty.” David Hume, “Dialogues Concerning Natural Religion,” in Classics of Western Philosophy, 3rd ed., ed. Steven M. Cahn, (1779; repr., Indianapolis: Hackett, 1990), 880.
  2. For example, Daniel Mange et al., “Von Neumann Revisited: A Turing Machine with Self-Repair and Self-Reproduction Properties,” Robotics and Autonomous Systems 22 (1997): 35-58, https://doi.org/10.1016/S0921-8890(97)00015-8; Jean-Yves Perrier, Moshe Sipper, and Jacques Zahnd, “Toward a Viable, Self-Reproducing Universal Computer,” Physica D: Nonlinear Phenomena
    97, no. 4 (October 15, 1996): 335–52, https://doi.org/10.1016/0167-2789(96)00091-7; Umberto Pesavento, “An Implementation of von Neumann’s Self-Reproducing Machine,” Artificial Life 2, no. 4 (Summer 1995): 337–54, https://doi.org/10.1162/artl.1995.2.4.337.
  3. Sara Imari Walker and Paul C. W. Davies, “The Algorithmic Origins of Life,” Journal of the Royal Society Interface 10 (2013), doi:10.1098/rsif.2012.0869.

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The Flagellum’s Hook Connects to the Case for a Creator

By Fazale Rana – January 8, 2020

What would you say is the most readily recognizable scientific icon? Is it DNA, a telescope, or maybe a test tube?


Figure 1: Scientific Icons. Image credit: Shutterstock

Marketing experts recognize the power of icons. When used well, icons prompt consumers to instantly identify a brand or product. They can also communicate a powerful message with a single glance.

Though many skeptics question if it’s science at all, the intelligent design movement has identified a powerful icon that communicates its message. Today, when most people see an image the bacterial flagellum they immediately think: Intelligent Design.

This massive protein complex powerfully communicates sophisticated engineering that could only come from an Intelligent Agent. And along these lines, it serves as a powerful piece of evidence for a Creator’s handiwork. Careful study of its molecular architecture and operation provides detailed evidence that an Intelligent Agent must be responsible for biochemical systems and, hence, the origin of life. And, as it turns out, the more we learn about the bacterial flagellum, the more evident it becomes that a Creator must have played a role in the origin and design of life—at least at the biochemical level—as new research from Japan illustrates.1

The Bacterial Flagellum

This massive protein complex looks like a whip extending from the bacterial cell surface. Some bacteria have only a single flagellum, others possess several flagella. Rotation of the flagellum(a) allows the bacterial cell to navigate its environment in response to various chemical signals.


Figure 2: Typical Bacteria with Flagella. Image credit: Shutterstock

An ensemble of 30 to 40 different proteins makes up the typical bacterial flagellum. These proteins function in concert as a literal rotary motor. The flagellum’s components include a rotor, stator, drive shaft, bushing, universal joint, and propeller. It is essentially a molecular-sized electrical motor directly analogous to human-produced rotary motors. The rotation is powered by positively charged hydrogen ions flowing through the motor proteins embedded in the inner membrane.


Figure 3: The Bacterial Flagellum. Image credit: Wikipedia

The Bacterial Flagellum and the Revitalized Watchmaker Argument

Typically, when intelligent design proponents/creationists use the bacterial flagellum to make the case for a Creator, they focus the argument on its irreducibly complex nature. I prefer a different tact. I like to emphasize the eerie similarity between rotary motors created by human designers and nature’ bacterial flagella.

The bacterial flagellum is just one of a large number of protein complexes with machine-like attributes. (I devote an entire chapter to biomolecular machines in my book The Cell’s Design.) Collectively, these biomolecular machines can be deployed to revitalize the Watchmaker argument.

Popularized by William Paley in the eighteenth century, this argument states that as a watch requires a watchmaker, so too, life requires a Creator. Following Paley’s line of reasoning, a machine is emblematic of systems produced by intelligent agents. Biomolecular machines display the same attributes as human-crafted machines. Therefore, if the work of intelligent agents is necessary to explain the genesis of machines, shouldn’t the same be true for biochemical systems?

Skeptics inspired by atheist philosopher David Hume have challenged this simple, yet powerful, analogy. They argue that the analogy would be compelling only if there is a high degree of similarity between the objects that form the analogy. Skeptics have long argued that biochemical systems and machines are too dissimilar to make the Watchmaker argument work.

However, the striking similarity between the machine parts of the bacterial flagellum and human-made machines cause this objection to evaporate. New work on flagella by Japanese investigators lends yet more support to the Watchmaker analogy.

New Insights into the Structure and Function of the Flagellum’s Universal Joint

The flagellum’s universal joint (sometimes referred to as the hook) transfers the torque generated by the motor to the propeller. The research team wanted to develop a deeper understanding of the relationship between the molecular structure of the hook and how the structural features influence its function as a universal joint.

Comprised of nearly 100 copies (monomers) of a protein called FlgE, the hook is a curved, tube-like structure with a hollow interior. FlgE monomers stack on top of each other to form a protofilament. Eleven protofilaments organize to form the hook’s tube, with the long axis of the protofilament aligning to form the long axis of the hook.

Each FlgE monomer consists of three domains, called D0, D1, and D2. The researchers discovered that when the FlgE monomers stack to form a protofilament, the D0, D1, and D2 domains of each of the monomers align along the length of the protofilament to form three distinct regions in the hook. These layers have been labeled the tube layer, the mesh layer, and the spring layer.

During the rotation of the flagellum, the protofilaments experience compression and extension. The movement of the domains, which changes their spatial arrangement relative to one another, mediates the compression and extension. These domain movements allow the hook to function as a universal joint that maintains a rigid tube shape against a twisting “force,” while concurrently transmitting torque from the motor to the flagellum’s filament as it bends along its axis.

Regardless of one’s worldview, it is hard not to marvel at the sophisticated and elegant design of the flagellum’s hook!

The Bacterial Flagellum and the Case for a Creator

If the Watchmaker argument holds validity, it seems reasonable to think that the more we learn about protein complexes, such as the bacterial flagellum, the more machine-like they should appear to be. This work by the Japanese biochemists bears out this assumption. The more we characterize biomolecular machines, the more reason we have to think that life stems from a Creator’s handiwork.

Dynamic properties of the hook assembly add to the Watchmaker argument (when applied to the bacterial flagellum). This structure is much more sophisticated and ingenious than the design of a typical universal joint crafted by human designers. This elegance and ingenuity of the hook are exactly the attributes I would expect if a Creator played a role in the origin and design of life.

Message received, loud and clear.


The Bacterial Flagellum and the Case for a Creator

Can Intelligent Design Be Part of the Scientific Construct?

  1. Takayuki Kato et al., “Structure of the Native Supercoiled Flagellar Hook as a Universal Joint,” Nature Communications 10 (2019): 5295, doi:10.1038/s4146.

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Original article at:


Genome Code Builds the Case for Creation

By Fazale Rana – December 18, 2019

A few days ago, I was doing a bit of Christmas shopping for my grandkids and I happened across some really cool construction kits, designed to teach children engineering principles while encouraging imaginative play. For those of you who still have a kid or two on your Christmas list, here are some of the products that caught my eye:

These building block sets are a far cry from the simple Lego kits I played with as a kid.

As cool as these construction toys may be, they don’t come close to the sophisticated construction kit cells use to build the higher-order structures of chromosomes. This point is powerfully illustrated by the insights of Italian investigator Giorgio Bernardi. Over the course of the last several years, Bernardi’s research teams have uncovered design principles that account for chromosome structure, a set of rules that he refers to as the genome code.1

To appreciate these principles and their theological implications, a little background information is in order. (For those readers familiar with chromosome structure, skip ahead to The Genome Code.)


DNA and proteins interact to make chromosomes. Each chromosome consists of a single DNA molecule wrapped around a series of globular protein complexes. These complexes repeat to form a supramolecular structure resembling a string of beads. Biochemists refer to the “beads” as nucleosomes.


Figure 1: Nucleosome Structure. Image credit: Shutterstock

The chain of nucleosomes further coils to form a structure called a solenoid. In turn, the solenoid condenses to form higher-order structures that constitute the chromosome.


Figure 2: Chromosome Structure Image credit: Shutterstock

Between cell division events (called the interphase of the cell cycle), the chromosome exists in an extended diffuse form that is not readily detectable when viewed with a microscope. Just prior to and during cell division, the chromosome condenses to form its readily recognizable compact structures.

Biologists have discovered that there are two distinct regions—labeled euchromatin and heterochromatin for chromosomes in the diffuse state. Euchromatin is resistant to staining with dyes that help researchers view it with a microscope. On the other hand, heterochromatin stains readily. Biologists believe that heterochromatin is more tightly packed (and, hence, more readily stained) than euchromatin. They have also learned that heterochromatin associates with the nuclear envelope.


Figure 3: Structure of the Nucleus Showing the Distribution of Euchromatin and Heterochromatin. Image credit: Wikipedia

The Genome Code

Historically, biologists have viewed chromosomes as consisting of compositionally distinct units called isochores. In vertebrate genomes, five isochores exist (L1, L2, H1, H2, and H3). The isochores differ in the composition of guanine- and cytosine-containing deoxyribonucleotides (two of the four building blocks of DNA). The GC composition increases from L1 to H3. Gene density also increases, with the H3 isochore possessing the greatest number of genes. On the other hand, the size of DNA pieces of compositional homogeneity decreases from L1 to H3.

Bernardi and his collaborators have developed evidence that the isochores reflect a fundamental unit of chromosome organization. The H isochores correspond to GC-rich euchromatin (containing most of the genes) and the L isochores correspond to GC-poor heterochromatin (characterized by gene deserts).

Bernardi’s research teams have demonstrated that the two groups of isochores are characterized by different distributions of DNA sequence elements. GC-poor isochores contain a disproportionately high level of oligo A sequences while GC-rich isochores harbor a disproportionately high level of oligo G sequences. These two different types of DNA sequence elements form stiff structures that mold the overall three-dimensional architecture of chromosomes. For example, oligo A sequences introduce curvature to the DNA double helix. This topology allows the double helix to wrap around the protein core that forms nucleosomes. The oligo G sequence elements adopt a topology that weakens binding to the proteins that form the nucleosome core. As Bernardi points out, “There is a fundamental link between DNA structure and chromatin structure, the genomic code.”2

In other words, the genomic code refers to a set of DNA sequence elements that:

  1. Directly encodes and molds chromosome structure (while defining nucleosome binding),
  2. Is pervasive throughout the genome, and
  3. Overlaps the genetic code by constraining sequence composition and gene structure.

Because of the existence of the genomic code, variations in DNA sequence caused by mutations will alter the structure of chromosomes and lead to deleterious effects.

The bottomline: Most of the genomic sequence plays a role in establishing the higher-order structures necessary for chromosome formation.

Genomic Code Challenges the Junk DNA Concept

According to Bernardi, the discovery of the genomic code explains the high levels of noncoding DNA sequences in genomes. Many people view such sequences as vestiges of an evolutionary history. Because of the existence and importance of the genomic code, the vast proportion of noncoding DNA found in vertebrate genomes must be viewed as functionally vital. According to Bernardi:

Ohno, mostly focusing on pseudo-genes, proposed that non-coding DNA was “junk DNA.” Doolittle and Sapienza and Orgel and Crick suggested the idea of “selfish DNA,” mainly involving transposons visualized as molecular parasites rather than having an adaptive function for their hosts. In contrast, the ENCODE project claimed that the majority (~80%) of the genome participated “in at least one biochemical RNA-and/or chromatin-associated event in at least one cell type.”…At first sight, the pervasive involvement of isochores in the formation of chromatin domains and spatial compartments seems to leave little or no room for “junk” or “selfish” DNA.3

The ENCODE Project

Over the last decade or so, ENCODE Project scientists have been seeking to identify the functional DNA sequence elements in the human genome. The most important landmark for the project came in the fall of 2012 when the ENCODE Project reported phase II results. (Currently, ENCODE is in phase IV.) To the surprise of many, the project reported that around 80 percent of the human genome displays biochemical activity—hence, function—with many scientists anticipating that that percentage would increase as phases III and IV moved toward completion.

The ENCODE results have generated quite a bit of controversy, to say the least. Some researchers accept the ENCODE conclusions. Others vehemently argue that the conclusions fly in the face of the evolutionary paradigm and, therefore, can’t be valid. Of course, if the ENCODE Project conclusions are correct, then it becomes a boon for creationists and intelligent design advocates.

One of the most prominent complaints about the ENCODE conclusions relates to the way the consortium determined biochemical function. Critics argue that ENCODE scientists conflated biochemical activity with function. These critics assert that, at most, about ten percent of the human genome is truly functional, with the remainder of the activity reflecting biochemical noise and experimental artifacts.

However, as Bernardi points out, his work (independent of the ENCODE Project) affirms the project’s conclusions. In this case, the so-called junk DNA plays a critical role in molding the structures of chromosomes and must be considered functional.

Function for “Junk DNA”

Bernardi’s work is not the first to recognize pervasive function of noncoding DNA. Other researchers have identified other functional attributes of noncoding DNA. To date, researchers have identified at least five distinct functional roles that noncoding DNA plays in genomes.

  1. Helps in gene regulation
  2. Functions as a mutational buffer
  3. Forms a nucleoskeleton
  4. Serves as an attachment site for mitotic apparatus
  5. Dictates three-dimensional architecture of chromosomes

A New View of Genomes

These types of insights are forcing us to radically rethink our view of the human genome. It appears that genomes are incredibly complex, sophisticated biochemical systems and most of the genes serve useful and necessary functions.

We have come a long way from the early days of the human genome project. Just 15 years ago, many scientists estimated that around 95 percent of the human genome consists of junk. That acknowledgment seemingly provided compelling evidence that humans must be the product of an evolutionary history. Today, the evidence suggests that the more we learn about the structure and function of genomes, the more elegant and sophisticated they appear to be. It is quite possible that most of the human genome is functional.

For creationists and intelligent design proponents, this changing view of the human genome provides reasons to think that it is the handiwork of our Creator. A skeptic might wonder why a Creator would make genomes littered with so much junk. But if a vast proportion of genomes consists of functional sequences, then this challenge no longer carries weight and it becomes more and more reasonable to interpret genomes from within a creation model/intelligent design framework.

What a Christmas gift!


Junk DNA Regulates Gene Expression

Junk DNA Serves as a Mutational Buffer

Junk DNA Serves a Nucleoskeletal Role

Junk DNA Plays a Role in Cell Division

ENCODE Project

Studies that Affirm the ENCODE Results

  1. Giorgio Bernardi, “The Genomic Code: A Pervasive Encoding/Molding of Chromatin Structures and a Solution of the ‘Non-Coding DNA’ Mystery,” BioEssays 41, no. 12 (November 8, 2019), doi:10.1002/bies.201900106.
  2. Bernardi, “The Genomic Code.”
  3. Bernardi, “The Genomic Code.”

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Original article at:


Mutations, Cancer, and the Case for a Creator

By Fazale Rana – December 11, 2019

Cancer. Perhaps no other word evokes more fear, anger, and hopelessness.

It goes without saying that cancer is an insidious disease. People who get cancer often die way too early. And even though a cancer diagnosis is no longer an immediate death sentence—thanks to biomedical advances—there are still many forms of cancer that are difficult to manage, let alone effectively treat.

Cancer also causes quite a bit of consternation for those of us who use insights from science to make a case for a Creator. From my vantage point, one of the most compelling reasons to think that a Creator exists and played a role in the origin and design of life is the elegant, sophisticated, and ingenious designs of biochemical systems. And yet, when I share this evidence with skeptics—and even seekers—I am often met with resistance in the form of the question: What about cancer?

Why Would God Create a World Where Cancer Is Possible?

In effect, this question typifies one of the most common—and significant—objections to the design argument. If a Creator is responsible for the designs found in biochemistry, then why are so many biochemical systems seemingly flawed, inelegant, and poorly designed?

The challenge cancer presents for the design argument carries an added punch. It’s one thing to cite inefficiency of protein synthesis or the error-prone nature of the rubisco enzyme, but it’s quite another to describe the suffering of a loved one who died from cancer. There’s an emotional weight to the objection. These deaths feel horribly unjust.

Couldn’t a Creator design biochemistry so that a disease as horrific as cancer would never be possible—particularly if this Creator is all-powerful, all-knowing, and all-good?

I think it’s possible to present a good answer to the challenge that cancer (and other so-called bad designs) poses for the design argument. Recent insights published by a research duo from Cambridge University in the UK help make the case.1

A Response to the Bad Designs in Biochemistry and Biology

Because the “bad designs” challenge is so significant (and so frequently expressed), I devoted an entire chapter in The Cell’s Design to addressing the apparent imperfections of biochemical systems. My goal in that chapter was to erect a framework that comprehensively addresses this pervasive problem for the design argument.

In the face of this challenge it is important to recognize that many so-called biochemical flaws are not genuine flaws at all. Instead, they arise as the consequences of trade-offs. In their cellular roles, many biochemical systems face two (or more) competing objectives. Effectively managing these opposing objectives means that it is impossible for every aspect of the system to perform at an optimal level. Some features must be carefully rendered suboptimal to ensure that the overall system performs robustly under a wide range of conditions.

Cancer falls into this category. It is not a consequence of flawed biochemical designs. Instead, cancer reflects a trade-off between DNA repair and cell survival.

DNA Damage and Cancer

The etiology (cause) of most cancers is complex. While about 10 percent of cancers have a hereditary basis, the vast proportion results from mutations to DNA caused by environmental factors.

Some of the damage to DNA stems from endogenous (internal) factors, such as water and oxygen in the cell. These materials cause hydrolysis and oxidative damage to DNA, respectively. Both types of damage can introduce mutations into this biomolecule. Exogenous chemicals (genotoxins) from the environment can also interact with DNA and cause damage leading to mutations. So does exposure to ultraviolet radiation and radioactivity from the environment.

Infectious agents such as viruses can also cause cancer. Again, these infectious agents cause genomic instability, which leads to DNA mutations.


Figure: Tumor Formation Process. Image credit: Shutterstock

In effect, DNA mutations are an inevitable consequence of the laws of nature, specifically the first and second laws of thermodynamics. These laws make possible the chemical structures and operations necessary for life to even exist. But, as a consequence, these same life-giving laws also undergird chemical and physical processes that damage DNA.

Fortunately, cells have the capacity to detect and repair damage to DNA. These DNA repair pathways are elaborate and sophisticated. They are the type of biochemical features that seem to support the case for a Creator. DNA repair pathways counteract the deleterious effects of DNA mutation by correcting the damage and preventing the onset of cancer.

Unfortunately, these DNA repair processes function incompletely. They fail to fully compensate for all of the damage that occurs to DNA. Consequently, over time, mutations accrue in DNA, leading to the onset of cancer. The inability of the cell’s machinery to repair all of the mutation-causing DNA damage and, ultimately, protect humans (and other animals) from cancer is precisely the thing that skeptics and seekers alike point to as evidence that counts against intelligent design.

Why would a Creator make a world where cancer is possible and then design cancer-preventing processes that are only partially effective?

Cancer: The Result of a Trade-Off

Even though mutations to DNA cause cancer, it is rare that a single mutation leads to the formation of a malignant cell type and, subsequently, tumor growth. Biomedical researchers have discovered that the onset of cancer involves a series of mutations to highly specific genes (dubbed cancer genes). The mutations that cause cells to transform into cancer cells are referred to as driver mutations. Researchers have also learned that most cells in the body harbor a vast number of mutations that have little or no biological consequence. These mutations are called passenger mutations. As it turns out, there are thousands of passenger mutations in a typical cancer cell and only about ten driver mutations to so-called cancer genes. Biomedical investigators have also learned that many normal cells harbor both passenger and driver mutations without ever transforming. (It appears that other factors unrelated to DNA mutation play a role in causing a cancer cell to undergo extensive clonal expansion, leading to the formation of a tumor.)

What this means is that mutations to DNA are quite extensive, even in normal, healthy cells. But this factor prompts the question: Why is the DNA repair process so lackluster?

The research duo from Cambridge University speculate that DNA repair is so costly to cells—making extensive use of energy and cell resources—that to maintain pristine genomes would compromise cell survival. These researchers conclude that “DNA quality control pathways are fully functional but naturally permissive of mutagenesis even in normal cells.”2 And, it seems as if the permissiveness of the DNA repair processes generally have little consequence given that a vast proportion of the human genome consists of noncoding DNA.

Biomedical researchers have uncovered another interesting feature about the DNA repair processes. The processes are “biased,” with repairs taking place preferentially on the DNA strand (of the double helix) that codes for proteins and, hence, is transcribed. In other words, when DNA repair takes place it occurs where it counts the most. This bias displays an elegant molecular logic and rationale, strengthening the case for design.

Given that driver mutations are not in and of themselves sufficient to lead to tumor formation, the researchers conclude that cancer prevention pathways are quite impressive in the human body. They conclude, “Considering that an adult human has ~30 trillion cells, and only one cell develops into a cancer, human cells are remarkably robust at preventing cancer.”3

So, what about cancer?

Though cancer ravages the lives of so many people, it is not because of poorly designed, substandard biochemical systems. Given that we live in a universe that conforms to the laws of thermodynamics, cancer is inevitable. Despite this inevitability, organisms are designed to effectively ward off cancer.

Ironically, as we gain a better understanding of the process of oncogenesis (the development of tumors), we are uncovering more—not less—evidence for the remarkably elegant and ingenious designs of biochemical systems.

The insights by the research team from Cambridge University provide us with a cautionary lesson. We are often quick to declare a biochemical (or biological) feature as poorly designed based on incomplete understanding of the system. Yet, inevitably, as we learn more about the system we discover an exquisite rationale for why things are the way they are. Such knowledge is consistent with the idea that these systems stem from a Creator’s handiwork.

Still, this recognition does little to dampen the fear and frustration associated with a cancer diagnosis and the pain and suffering experienced by those who battle cancer (and their loved ones who stand on the sidelines watching the fight take place). But, whether we are a skeptic or a believer, we all should be encouraged by the latest insights developed by the Cambridge researchers. The more we understand about the cause and progression of cancers, the closer we are to one day finding cures to a disease that takes so much from us.

We can also take added encouragement from the powerful scientific case for a Creator’s existence. The Old and New Testaments teach us that the Creator revealed by scientific discovery has suffered on our behalf and will suffer alongside us—in the person of Christ—as we walk through the difficult circumstances of life.


Examples of Biochemical Trade-Offs

Evidence that Nonfunctional DNA Serves as a Mutational Buffer

  1. Serena Nik-Zainal and Benjamin A. Hall, “Cellular Survival over Genomic Perfection,” Science 366, no. 6467 (November 15, 2019): 802–03, doi:10.1126/science.aax8046.
  2. Nik-Zainal and Hall, 802–03.
  3. Nik-Zainal and Hall, 802–03.

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Have You Got God Right Where You Want Him?

Once there was a time when man believed that the earth was the center of all there is.

Once there was a time when man believed the sun was the center of all there is.

Once there was a time when man believed the earth was flat and if you traveled too far, you would fall off the edge… to somewhere… evidently little regard was ever given to exactly what ‘somewhere’ would be, other than an ancient map I once studied containing words along the edges that said, “Here be Dragons”.

Now, most of humanity realizes that the sun, earth and the rest of the solar system are neither at the center of anything, but in addition, we’re so minuscule as to not even show up within one spiral arm of our ‘sombrero’ galaxy… and that the universe is an endless sea of such galaxies.

We now say that everything our Hubble Space Telescope sees is ‘The Known Universe’.

Of those of you who believe in an Intelligent Design… and are of the belief that just because what we can now peer into the vastness of space, that now that’s all there is… I’ve got something quite intriguing for you to ponder and for you to compare yourself with those ancient people of the past who thought their intelligence had it all figured out too.

Just what does the word ‘Create’ mean to you, and how would you describe someone who enjoys making things, or even just painting or sculpting?

Do you actually think an all-powerful Creator would only make something once? And then sit down… cross His arms, and declare, That’s it! I’m done! I’m never going to make anything else again!

I’m just going to sit here for eternity and retire from being creative! I’ve lost all interest, and there’s nothing you can say that will make me change my mind!”

If you really believe that way… as the ancients did, then all I can conclude is that you have tied your God’s hands behind his back, and that you are as jealous as the child who has discovered there’s a new baby in the house.

I’ve got news for you brothers and sisters… There very well could be an endless sea of beautiful universes, dangling like crystal prisms, along a great corridor that the Creator frequents, and adds yet another whenever He pleases.

And to top it off… if it is His will, there could be life inside every single one of those gems.

It’s called The Multiverse Theory… and unless you’re an astrophysicist, you don’t even want to attempt comprehending it… but leave it to say, it certainly removes the rope that some people have used to tie God’s ‘Creative’ hands.

Start thinking bigger.


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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