The Female Brain: Pregnant with Design



When Jesus saw his mother there, and the disciple whom he loved standing nearby, he said to her, “Woman, here is your son.”

–John 19:26

I’ve learned the hard way: It is best to be circumspect when offering commentary about pregnancy, especially when women are around.

So, it’s with some hesitation I bring up the latest scientific insight developed by a team of researchers from Spain. These investigators discovered that pregnancy alters a woman’s brain. In fact, pregnancy reduces her grey matter.1 (Okay Fuz. Hold your tongue. Don’t say what you’re thinking.)

But, as it turns out, the loss of grey matter is a good thing. In fact, it reveals the elegant design of the human brain and adds to the growing evidence of human exceptionalism. This scientific advance also has implications for the pro-life movement.

The Spanish research team was motivated to study brain changes in pregnant women because of the effects that sex hormones have on adolescent brains. During this time, sex hormones cause extensive reorganization of the brain. This process is a necessary part of the neural maturation process. The researchers posited that changes to the female brain should take place, because of the surge of sex hormones during pregnancy. While pregnant, women are exposed to 10 to 15 times the “normal” progesterone levels. During nine months of pregnancy, women are also subjected to more estrogen than the rest of their life when not pregnant.

To characterize the effect of pregnancy on brain structure, the research team employed a prospective study design. They imaged the brains of women who wanted to become pregnant for the first time. Then, they imaged the brains of the subjects once the women had given birth. Finally, they imaged the brains of the subjects two years after birth, if they didn’t become pregnant again. As controls, they imaged the brains of women who had never been pregnant and the brains of the fathers.

The Effects of Pregnancy on Women’s Brains

While the brain’s white matter is unaffected, the researchers found that pregnancy leads to a loss of grey matter that, minimally, lasts up to two years. They also discovered that the grey matter loss was not random or arbitrary. Instead, it occurred in highly specific areas of the brain. In fact, the grey matter loss was so consistent from subject to subject that the researchers could tell if a woman was pregnant or not from brain images alone.

As it turns out, the area of the brain that loses grey matter is the region involved in social cognition that harbors the theory-of-mind neural network. This network allows human beings to display a quality anthropologists call theory of mind. Along with symbolism, our theory-of-mind capacity makes us unique compared to other animals, providing scientific justification for the idea of human exceptionalism. As human beings, we recognize that other humans possess a mind like ours. Because of that recognition, we can anticipate what others are thinking and feeling. Our theory-of-mind capability makes possible complex social interactions characteristic of our species.

Even though the pregnant women lost grey matter, they showed no loss of memory or cognitive ability. The researchers believe that the loss of grey matter stems from synaptic pruning. This process occurs in adolescents and is a vital part of brain development and maturation. Through the loss of grey matter, neural networks form. The research team posits that synaptic pruning in pregnant women establishes a neural network that plays a role in the deep attachment mothers have with their children. This attachment helps mothers anticipate their babies’ needs. The deep social connection between mother and child is critical for human survival, because human infants are so vulnerable at birth and have a prolonged childhood.

In support of this proposal, the researchers found that when they showed the pregnant women pictures of their babies, the brain areas that lost grey matter became active. On the other hand, they saw no corresponding brain activity when the mothers were shown pictures of other babies.

The Case for Human Exceptionalism Mounts

This work highlights the elegant design of human pregnancy and child rearing—features that I take as evidence for a Creator’s handiwork. It is nothing short of brilliant to have the surge of sex hormones during pregnancy, priming the brain to ensure a close attachment between mother and child, at the time of birth and throughout the first few years of childhood.

More importantly, this work adds to the mounting scientific evidence for human exceptionalism. Not only do humans uniquely possess theory of mind, but our theory-of-mind neural network is more complex and sophisticated than previously thought. It is remarkable that this neural network can be adapted and fine-tuned to ensure an intimate mother-infant attachment while maintaining relationships in the midst of complex social surroundings, typical of human interactions.

As an interesting side note: Recent research indicates that for Neanderthals, the area of their brain devoted to maintaining social interactions was much smaller than the corresponding area in modern humans, highlighting our unique and exceptional nature even when compared to the hominids found in the fossil record.2

Pro-Life Implications

In my view, this work also has pro-life implications. I frequently hear pro-choice advocates argue that the fetus is a mass of tissue, just like a tumor. But, this study undermines this view. It is hard to think of a fetus as being just a lump of tissue, when such a sophisticated system is in place during pregnancy to form a neural network (that is, a subset of the theory-of-mind network) in the mother’s brain that generates the special capacity of the mother to bond with the fetus at birth.

It also raises concerns for the health of women who receive abortions. Though speculative, one has to wonder what effect prematurely terminating a pregnancy has on women whose brains have become fine-tuned to bond to the very infants that are destroyed by the abortion.


Placenta Optimization Shows Creator’s Handiwork” by Fazale Rana (article)
Curvaceous Anatomy of the Female Spine Reveals Ingenious Obstetric Design” by Virgil Robertson (article)
Does the Childbirth Process Represent Clumsy Evolution or Good Engineering?” by Fazale Rana (article)
Neanderthal Brains Make Them Unlikely Social Networkers” by Fazale Rana (article)


  1. Elseline Hoekzema et al., “Pregnancy Leads to Long-Lasting Changes in Human Brain Structure,” Nature Neuroscience, published electronically December 19, 2016, doi:10.1038/nn.4458.
  2. Eiluned Pearce, Chris Stringer, and R. I. M. Dunbar, “New Insights into Differences in Brain Organization between Neanderthals and Anatomically Modern Humans,” Proceedings of the Royal Society B 280 (May 2013): doi:10.1098/rspb.2013.0168.
Reprinted with permission by the author
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Does Dinosaur Tissue Challenge Evolutionary Timescales? A Response to Kevin Anderson, Part 2



What is the proper relationship between science and the Christian faith? Answering that question can be complicated, involving an interplay between science, philosophy, theology, and biblical studies. Perhaps it’s not surprising that evangelical Christians (who all take Scripture seriously) advocate disparate models, weighing differently the data and insights from science and Scripture.

The three most prominent views held by evangelical Christians are: young-earth creationism (YEC), old-earth creationism (OEC), and evolutionary creationism (EC). Each view has strengths and weaknesses. And each view accepts and rejects (or at least expresses skepticism) about certain aspects of current scientific paradigms.

It goes without saying that “in-house” discussions among adherents of these three models can become quite contentious. And for good reason: much is at stake. No one wants to undermine Scripture. And no one wants to recklessly disregard scientifically established ideas. Because to do so could compromise the Church’s ability to reach out to non-Christians. In my view, it is okay to question scientific dogma—particularly if it challenges key tenets of the Christian faith. But it is important to do so responsibly and in a scientifically credible way.

My chief motivation for writing Dinosaur Blood and the Age of the Earth was to prevent well-intentioned Christians from unwittingly undercutting their effectiveness when sharing their faith by using a seemingly compelling scientific argument for a young Earth (with the hope of demonstrating the credibility of the creation accounts from a young-Earth vantage point).

Many Christians regard the discovery of soft-tissue remnants, associated with fossilized remains age-dated to be upwards of hundreds of millions of years, as a compelling scientific evidence for a young Earth. And I can see why.

Soft tissues shouldn’t survive for millions of years. Based on common wisdom, these materials should readily degrade in a few thousand years. That being the case, the discovery of soft tissue remnants associated with fossils is a compelling reason to question the reliability of radiometric dating methods used to determine the age of these fossils, and along with it, Earth’s antiquity. Instead, YECs argue that these discoveries provide powerful scientific evidence for a young Earth and support the idea that the fossil record results from a recent global (worldwide) flood.

Yet few scientifically minded people are swayed by this argument. In Dinosaur Blood and the Age of the Earth, I explain why this increasingly prominent argument for a young Earth is invalid. First, I explain why radiometric dating methods are reliable. Secondly, I explain how it is scientifically conceivable that soft-tissue remnants could survive for upwards of hundreds of millions of years.

When I published Dinosaur Blood and the Age of the Earth, I expected responses by YECs. And there have been a few. Generally, I won’t engage in tit-for-tat when my ideas are criticized. But, I am making an exception in the case of Kevin Anderson’s recent technically rigorous article for Answers in Depth, the journal of Answers in Genesis, titled: “Dinosaur Tissue: A Biochemical Challenge to the Evolutionary Timescale.” Because Anderson is a scholar, and because his approach is fair-minded, it is important to pay attention to his critiques of my work and to engage his ideas.

In part one (of this two-part blog series), I addressed Anderson’s dismissal of the biomolecular durability argument I present in Dinosaur Blood and the Age of the Earth as part of the explanation for collagen (and keratin) survivability in fossils. In this second part, I engage Anderson’s challenges to what he refers to as “the most popular explanation for prolonged preservation” of soft tissue. Namely, the “iron model.”1

The Iron Model for Soft Tissue Preservation

As described in Dinosaur Blood and the Age of the Earth, paleontologists have noted iron deposits associated with preserved soft-tissue remnants in a number of fossilized specimens. (In fact, iron deposits were associated with the recently discovered dinosaur feathers preserved in amber, age-dated to 99 million years.2) On this basis, they speculate that the iron in conjunction with oxygen help to preserve soft-tissue materials through a variety of possible mechanisms, including: killing off microbes, inhibiting enzymes, and causing cross-linking reactions that function as a fixative (like formaldehyde), at least until mineral entombment takes place.3 The researchers posit that iron associated with hemoglobin (the protein that binds and carries oxygen found in red blood cells) is the primary source of iron. Presumably, when the organism dies, the red blood cells lyse, releasing hemoglobin and iron into the tissue.

To demonstrate the validity of this idea, researchers from North Carolina State University exposed ostrich blood vessels dispersed in an aqueous solution of ruptured blood cells. They observed iron deposits forming on the blood vessels. The blood cell lysate stabilized the soft tissue. Compared to blood vessels dispersed in water (in the presence and absence of oxygen) which lasted only a few days, blood vessels exposed to red blood lysates persisted for upwards of two years (and counting).

Yet, Anderson questions the iron model for a variety of reasons.

  • He raises doubts about the relevancy of the laboratory experiments on the ostrich blood vessels.
  • He expresses concern that the iron level in dinosaurs is insufficient for it to achieve adequate preservation, even if the iron model is valid.
  • He notes that the reactions that promote cross-linking also destroys amino acids. (Even though amino acids have been recovered from dinosaur and bird fossils.)

In my view, none of these criticisms bears much weight.

To be fair, Anderson rightly highlights a problem constantly confronting scientists studying the origin and history of life. Namely, how do chemical and physical processes identified in the laboratory under highly controlled conditions (and the auspices of researchers) translate to the uncontrolled conditions of Earth’s past environment? Though granting Anderson this point—in fact, I have raised a similar criticism toward work in prebiotic chemistry in my book Creating Life in the Lab—it is important to acknowledge that the stability experiments with ostrich blood vessels demonstrate that, in principle, the iron model has merit. It is also worth noting that the conditions employed by the researchers in the lab experiments represent a worst-case scenario, because the vessels were dispersed in water which promotes hydrolysis and microbial growth. In other words, under “real-life” conditions, iron-mediated preservation of soft tissue has an even greater likelihood than in the experiments conducted in the laboratory.

Concerning Anderson’s second point about iron abundances in dinosaurs (or ancient birds), it is noteworthy that iron from the lysed red blood cells binds to the ostrich blood vessels, suggesting some type of concentrating mechanism that localizes the iron to the soft tissue. Also, as Anderson acknowledges, there may be environmental sources of iron that could contribute to the iron pool. Even if there are still questions as to the source and available levels of iron for tissue preservation, this mechanism appears to be significant. As already noted, paleontologists have discovered iron associated with soft tissue remnants found in fossils.

As for Anderson’s third point, it is true that the reaction mediated by iron and oxygen (which drives cross-linking) alters amino acids. And it is true that unaltered amino acids are found in the fossil specimens. But these two results are not mutually exclusive. How is that possible? Because chemical reactions don'[t necessarily go to completion. To put it another way, during the preservation process, it is unlikely that all the amino acids comprising dinosaur proteins reacted via the iron and oxygen mediated reactions. Some of the amino acids will remain unaltered—even highly reactive ones. It is noteworthy that the molecular profiles of materials extracted from dinosaur fossils show a relative dearth of less stable amino acids and an abundance of more durable amino acids, exactly as expected if the amino acids come from the remnants of ancient protein specimens.4

Ultimately, my complaint with Anderson’s critiques have less to do with his scientific points, and more to do with his “either-or” posture. Even if Anderson’s critique of the iron model stands, it doesn’t mean that there is no way to account for soft-tissue preservation. As I argue in Dinosaur Blood and the Age of the Earth, there is probably no single preservation mechanism that accounts for the survival of soft tissue materials. In reality, it is a combination of mechanisms working additively (maybe, synergistically) that accounts for the persistence of soft tissue in fossils, with the iron-oxygen mechanism working in conjunction with other processes.

Other Preservation Mechanisms

In Dinosaur Blood and the Age of the Earth, I argue that many of the mechanisms that affect soft-tissue decomposition (hydrolysis via exposure to water, oxidation caused by oxygen exposure, breakdown by environmental enzymes, and microbial decomposition) can actually protect soft-tissue remnants under some circumstances.

In response to this point, Anderson argues that these claims are “self-contradictory.”5 But this is exactly my point. Conditions traditionally thought to drive soft-tissue breakdown, preserve soft tissues under certain sets of conditions. In other words, traditional views about soft-tissue decomposition aren’t likely correct.

In fact, the iron model illustrates this point. In keeping with common wisdom, exposure to oxygen drives soft-tissue destruction. Conversely, excluding oxygen during the fossilization process should aid in preservation by preventing oxidative decomposition of the soft-tissue materials. But oxidation reactions also drive cross-linking of proteins. So, exposure to oxygen also preserves soft tissues. Whether decomposition or preservation occurs depends on the specific circumstances surrounding the fossilization process, with some conditions “tipping the scale” in favor of decomposition and other conditions “moving the needle” toward preservation. And, of course, iron released from hemoglobin (or from environmental sources) accelerates the cross-linking reactions, helping to stabilize the soft-tissue materials.

Are Fossils Thousands of Years Old or Millions of Years Old?

Anderson concludes his argument by lamenting the bias of the scientific community. He says, “The problem is that the evolutionary community does not really consider the first alternative [dinosaurs aren’t as old as we think they are] as a possibility. Thus, it really is not an ‘either/or’ option. In their view the fossils must be old, therefore the tissue must somehow have survived (biochemical contradictions not withstanding). . . . No one has ever observed multi-millions of years of animal tissue preservation. The only reason there is even a quest for an unknown preservation mechanism is because evolutionary assumptions require dinosaur fossils to be at least 65 million years old.”6

Anderson’s protests not withstanding, the scientific community does not assume the fossils to be millions of years old, but has measured fossils to be millions of years old using sound, scientifically established radiometric methods. Consequently, the scientific community has observed soft tissue preserved for millions of years, with the recovery of blood vessels remnants, and protein fragments from the fossils of dinosaurs (and other organisms).

Finally, while it is true that the scientific community lacks full understanding of the mechanisms involved, preservation of soft tissues in fossils does not stand as a “biochemical contradiction.” Instead, there are sound explanations for the persistence of soft-tissue remnants in fossils. And as work continues, I predict that the scientific community will identify new preservation mechanisms. In fact, this has already happened. Researchers now think that eumelanin released from melanosomes can serve as a fixative assisting in the preservation of keratin associated with fossilized feathers, claws, and skin.7

I appreciate Kevin Anderson’s thoughtful engagement with my ideas regarding soft-tissue preservation, but I disagree with his conclusions. Simply put, soft-tissue preservation in fossils is not a valid scientific argument for a young Earth, nor does it provide evidence that the fossil record was laid down as a result of a recent, global flood.



  1. Kevin Anderson, “Dinosaur Tissue: A Biochemical Challenge to the Evolutionary Timescale,” Answers in Genesis 11 (2016):
  2. Lida Xing et al., “A Feathered Dinosaur Tail with Primitive Plumage Trapped in Mid-Cretaceous Amber,” Current Biology 26 (December 19, 2016): 3352–60, doi:10.1016/j.cub.2016.10.008.
  3. Mary Schweitzer et al., “A Role for Iron and Oxygen Chemistry in Preserving Soft Tissues, Cells and Molecules from Deep Time,” Proceedings of the Royal Society B 281 (January 2014): 20132741, doi:10.1098/rspb.2013.2741.
  4. Mary Schweitzer et al., “Preservation of Biomolecules in Cancellous Bone of Tyrannosaurus Rex,” Journal of Vertebrate Paleontology 17 (June 1997): 349–59, doi:10.1080/02724634.1997.10010979.
  5. Kevin Anderson, “Dinosaur Tissue.”
  6. Ibid.
  7. Alison Moyer, Wenxia Zheng, and Mary Schweitzer, “Keratin Durability Has Implications for the Fossil Record: Results from a 10 Year Feather Degradation Experiment,” PLoS One 11 (July 2016): e0157699, doi:10.1371/journal.pone.0157699.
Reprinted with permission by the author
Original article at:

Does Dinosaur Tissue Challenge Evolutionary Timescales? A Response to Kevin Anderson, Part 1



Is there a bona fide scientific challenge to the age of the Earth, which is measured to be 4.5 billion years old? As an old-earth creationist (OEC), I would answer no. But, there has been one scientific argument for a young Earth that has given me some pause for thought: the discovery of soft tissue remnants in the fossilized remains of dinosaurs (and other organisms). Paleontologists have discovered the remnants of blood vessels, red blood cells, bone cells, and protein fragments, such as collagen and keratin, in the fossilized remains of dinosaurs that age-date older than 65 million years.

These unexpected finds have become central to the case made by young-earth creationists (YEC) for a 6,000-year-old Earth. In effect, the argument goes like this: Soft tissues shouldn’t survive for millions of years. Instead, these materials should readily degrade in a few thousand years. Accordingly, the discovery of soft tissue remnants associated with fossils is a prima facie challenge to the reliability of radiometric dating methods used to determine the age of these fossils, and along with it, Earth’s antiquity. YECs argue that these discoveries provide compelling scientific evidence for a young Earth and support the idea that the fossil record results from a recent global (worldwide) flood.

As I detail in my book Dinosaur Blood and the Age of the Earth, there are good reasons to think that radiometric dating methods are reliable. And, that being the case, then there must be an explanation for soft tissue survival. Despite the claims made by YECs, there arescientific mechanisms that can account for the survival of soft-tissue materials for millions of years, as discussed in Dinosaur Blood and the Age of the Earth.

In response to my book (and other recent challenges) to the soft-tissue argument for a young Earth, YEC Kevin Anderson wrote a piece for Answers in Depth, the journal of Answers in Genesis, titled: “Dinosaur Tissue: A Biochemical Challenge to the Evolutionary Timescale.”

In this technically rigorous piece, Anderson argues that paleontologists now view soft-tissue remnants associated with the fossilized remains of dinosaur (and other organisms) as commonplace. On this point, Anderson and I would agree. However, Anderson complains that the scientific community ignores the troubling implications of the soft-tissue finds. He states: “Despite a large body of evidence for the authenticity of the tissue, there remains a pattern of denial within the evolutionist community—presumably to downplay the ramifications of this discovery. . . . Apparently many find the soft-tissue evidence much easier to dismiss than to understand and explain. Perhaps this should not be too surprising. The tissue is certainly difficult to account for within the popular geologic timescale.”1

Yet, in Dinosaur Blood and the Age of the Earth, I explain how soft-tissue remnants associated with fossils are accounted for within “the popular geologic timescale.”

Soft-Tissue Survival in Fossils

Once entombed within a mineral “encasement” (which occurs as the result of the fossilization process), soft-tissue remnants can survive for vast periods of time. The key: the soft tissues must be preserved until entombment happens. In Dinosaur Blood and the Age of the Earth, I identify several factors that promote soft-tissue preservation during the fossilization process. One relates to the structure of the molecules comprising the soft tissues. Some molecules are much more durable than others, making them much more likely to survive until entombment.

This durability partially explains the chemical profile of the compounds associated with soft-tissue remnants. For example, paleontologists have uncovered collagen and keratin fragments associated with dinosaur fossils. These finds make sense because these molecules are heavily cross-linked. And they occur at high levels in bones (collagen) and feathers, skin, and claws (keratin). Researchers also believe that iron released from hemoglobin, and eumelanin released from melanosomes associated with feathers, function as fixatives to further stabilize these molecules, delaying their decomposition.

But What about Measured Collagen Decomposition Rates?

Kevin Anderson agrees that some molecules, such as collagen, resist rapid degradation. However, he rejects the durability argument I present in Dinosaur Blood and the Age of the Earth as part of the explanation for collagen (and keratin) survivability, citing work published in 2011 by researchers from the University of Manchester in the UK.2

In this study, investigators monitored collagen loss in cattle and human bones at 90 °C (194 °F). Even though this high temperature doesn’t directly apply to the fossilization process, the researchers employed a temperature close to the boiling point of water to gather rate data in a reasonable time frame. Still, it took them about one month to generate the necessary data, even at this high temperature. In turn, they used this data to calculate the bone loss at 10 °C (50 °F), which corresponds to the average temperature of a typical archaeological site in a country such as Great Britain. These calculations made use of the Arrhenius rate equation. This equation allows scientists to calculate the rate for a chemical process (such as the breakdown of collagen) at any temperature, once the rate has been experimentally determined for a single temperature. The only assumption is that the physical and chemical properties of the system (in this case, collagen) are the same as the temperature used to measure the reaction rate and the temperature used to calculate the reaction rate.

But, as I discuss in Dinosaur Blood and the Age of the Earth, if the conditions differ, then a phenomenon known as an Arrhenius plot break occurs. This discontinuity makes it impossible to calculate the reaction rate.

On this basis, I questioned if the data generated by the University of Manchester scientists for collagen breakdown in bone near the boiling point of water is relevant to breakdown rates for temperatures that would be under 100 °F, let alone to temperatures near 50 °F. I speculated that at such high temperatures, the collagen would undergo structural changes (for example, breaking of inter-chain hydrogen bonds that cross-link collagen chains together) making this biomolecule much more susceptible to chemical degradation than at lower temperatures where collagen would remain in its native state. In other words, the conditions employed by the research team from the University of Manchester may not be relevant to collagen preservation in fossil remains.

Kevin Anderson challenged my claim, stating, “Dr. Rana speculates that high temperatures may unexpectedly alter how collagen will degrade, so perhaps the Arrhenius equation cannot be properly applied. However, he fails to offer any experimental support for his conclusion. If he wants to challenge these decay studies, he needs to provide experimental evidence that collagen decay is somehow an exception to this equation.”3

Fair enough. Yet, it was relatively easy for me to find the experimental data he requires. A quick literature search produced work published in the early 1970s by a team of researchers from the USDA in Beltsville, MD describing the thermal denaturation profiles of intact collagen from a variety of animal sources.4 The onset temperatures for the denaturation process typically begin near 60 °C (140 °F), reach the mid-point of the denaturation around 70 °C (158 °F), and end around 80 °C (176 °F). In other words, collagen denaturation occurs at temperatures well below the temperatures used by the University of Manchester scientists in their study.

From the denaturation profiles, these researchers determined that the loss of native structure primarily entails the unraveling of the collagen triple helix. This unraveling would expose the protein backbone, making it much easier to undergo chemical degradation.

In Dinosaur Blood and the Age of the Earth, I discuss another reason why the study results obtained by the University of Manchester scientists don’t contradict the recovery of collagen from 70–80 million-year-old dinosaur remains. In effect, this research team was addressing a different question. Namely, how long can collagen last in animal remains in a form that can be isolated and used as a source of genetic information about the organisms found at archaeological and fossil sites?

In other words, they weren’t interested in how long chemically and physically altered collagen fragments would persist in fossil remains, but, instead, how long collagen will retain a useful form that can yield insight into the natural history of past organisms. Specifically, they were interested in the survival of “the non-helical collagen telopeptides located at the very ends of each chain and recently considered potentially useful for species identification in archaeological tissues.”5

The researchers lament that this region of the collagen molecules is “lost to the burial environment within a relatively short period of geologic time.”6 As they point out, the parts of the collagen molecule most useful to characterize the natural history of past organisms and their relationships to extant creatures, unfortunately, are “regions of the protein that do not benefit from as many interchain hydrogen bonds as the helical region, and thus will likely be the first to degrade.”7

The researchers also point out that they expect collagen to persist for much longer than 700,000 years, but in a chemically altered state due to cross-linking reactions and other types of chemical modifications. They state, “Collagen could plausibly be detected at lower concentrations [than 1 percent of the original amounts] in much older material but likely in a diagenetically-altered state and at levels whereby separation from endogenous and exogenous contaminations is much more time-consuming, costly and perhaps applicable only to atypically large taxa that can offer sufficient fossil material for destructive analysis.”8

In other words, chemically altered forms of collagen will persist in animal remains well beyond a million years, particularly if they are large creatures such as dinosaurs. And this is precisely what paleontologists have discovered associated with dinosaur fossils—fragments of diagentically altered collagen (and keratin).

But What about Molecular Fragments Derived from Non-Durable Proteins Isolated from Dinosaur Remains?

Another related challenge raised by Anderson relates to the recovery of molecular fragments of other proteins from dinosaur fossils that are much less durable than collagen. Anderson writes: “Several of these proteins (e.g., myosin, actin, and tropomyosin) are not nearly as structurally ‘tough’ as collagen. . . . Even if there were a biochemical basis that enabled collagen fragments to survive millions of years, this cannot be said about all these other dinosaur proteins.”9

As I point out in Dinosaur Blood and the Age of the Earth, in addition to molecular durability, there are several other factors that contribute to soft-tissue preservation. One relates to abundance. Biomolecules that occur at high levels in soft tissue will be more likely to leave behind traces in fossilized remains than molecules that occur at relatively low levels.

Along these lines, collagen and keratin would have been some of the most abundant proteins in dinosaurs and ancient birds, making up connective tissue and feathers, skin, and claws, respectively. Likewise, actin, myosin, and tropomyosin would also have occurred at high levels in dinosaurs and ancient birds, because these proteins are the major components of muscle. So even though these proteins aren’t as durable as collagen or keratin, it still makes sense that fragments of these biomolecules would be associated with dinosaur fossils because of their abundances.

In short, the durability and abundances of proteins provide a credible explanation for the occurrence of soft-tissue remnants in the fossilized remains of dinosaurs. But these two features don’t fully account for soft-tissue preservation. As it turns out, there are additional factors to consider.

In his article, Anderson also challenges what he refers to as “the most popular explanation for prolonged preservation” of soft tissue. Namely, the “iron model.”10 In part 2 of my response to Kevin Anderson, I will describe and respond to his critique of the iron model and other preservation mechanisms.



  1. Kevin Anderson, “Dinosaur Tissue: A Biochemical Challenge to the Evolutionary Timescale,” Answers in Genesis 11 (2016):
  2. Mike Buckley and Matthew James Collins, “Collagen Survival and Its Use for Species Identification in Holocene-Lower Pleistocene Bone Fragments from British Archaeological and Paleontological Sites,” Antiqua 1 (2011): e1, doi:10.4081/antiqua.2011.e1.
  3. Anderson, “Dinosaur Tissue.”
  4. Philip E. McClain and Eugene R. Wiley, “Differential Scanning Calorimeter Studies of the Thermal Transitions of Collagen: Implications on Structure and Stability,” Journal of Biological Chemistry 247 (February 1972): 692–97,
  5. Buckley and Collins, “Collagen Survival.”
  6. Ibid.
  7. Ibid.
  8. Ibid.
  9. Anderson, “Dinosaur Tissue.”
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Duck-Billed Platypus Venom: Designed for Discovery



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

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

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

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

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


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

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

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

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

Platypus Venom

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

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

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

Type 2 Diabetes

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

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

Platypus GLP-1 as an Anti-Diabetic Medication

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

The Case for Evolution, the Case for Creation

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

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

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

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

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

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

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

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



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