Where Science and Faith Converge
  • Does Dinosaur Tissue Challenge Evolutionary Timescales? A Response to Kevin Anderson, Part 2

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Jan 18, 2017

    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.

    Resources

    Endnotes
    1. Kevin Anderson, “Dinosaur Tissue: A Biochemical Challenge to the Evolutionary Timescale,” Answers in Genesis 11 (2016): https://answersingenesis.org/fossils/dinosaur-tissue/.
    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): 34959, 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.
  • Does Dinosaur Tissue Challenge Evolutionary Timescales? A Response to Kevin Anderson, Part 1

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Jan 11, 2017

    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 are scientific 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.

    Resources

    Endnotes
    1. Kevin Anderson, “Dinosaur Tissue: A Biochemical Challenge to the Evolutionary Timescale,” Answers in Genesis 11 (2016): https://answersingenesis.org/fossils/dinosaur-tissue/.
    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, https://www.jbc.org/content/247/3/692.full.pdf.
    5. Buckley and Collins, “Collagen Survival.”
    6. Ibid.
    7. Ibid.
    8. Ibid.
    9. Anderson, “Dinosaur Tissue.
  • Duck-Billed Platypus Venom: Designed for Discovery

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Jan 04, 2017

    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.

    GLP-1

    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.
    Duckbilled platypus venom

    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.

    Resources

    Endnotes
    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.
  • Q&A: Why Would an Infinite Creator Employ the Same Designs?

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Dec 21, 2016

    Because I am a Christian, I see evidence for design in the biological realm. But for me, the converse is also true. Because I see design in the biological realm, I am a Christian. In fact, the elegant designs of biochemical systems convinced me as a graduate student that a Creator must exist and be responsible for life’s origin, paving the way for my conversion to Christianity.

    Yet, many skeptics see the features of biological systems very differently than I do. They maintain that life’s origin, design, and diversity are best explained as the outworking of evolutionary processes. As evidence for this view, biologists point to the shared biological and biochemical features (homologies) possessed by organisms that naturally group or cluster together.

    Homologous features may perform different functions and superficially appear different, yet they are fundamentally built around the same design. The quintessential example of a biological homology is the vertebrate forelimb—the human hand, the whale’s flipper, a dog’s paw, a bird’s wing, etc. Though these forelimbs are structurally distinct and perform different biological tasks, they are fundamentally built around the same design. The forelimb of every vertebrate consists of a long bone (humerus) in the arm, an elbow, two bones in the forearm (the radius and ulna), wrist bones (carpals), bones in the “hand” (metacarpals), and “fingers” (phalanges).

    blog__inline--why-would-an-infinite-creator-employ-the-same-designs-1
    Image: Homologous structures of the vertebrate forelimb. Image Credit: Wikipedia

    Evolutionary biologists interpret homologous structures as evolutionarily derived from ancestral features possessed by the common ancestor of the group. With respect to the vertebrate forelimbs, biologists maintain that the forelimb of the first tetrapods had the same design as all vertebrate forelimbs. However, through the course of evolutionary history, natural selection altered the vertebrate forelimbs to perform a variety of functional roles.

    However, as a creationist and a design proponent, I maintain that homologous structures have been designed around an archetypical plan that existed in the Creator’s mind. To put it another way, homologous structures reflect common design, not the outworking of common descent.

    My view on shared biological features led my Facebook friend Phil, a skeptic, to ask the following questions:

    “Just think about the diverse range of creatures an actual creator could have made. And yet we see creatures appearing like and acting like family cousins instead. What would compel an actual designer with unlimited power to design all creatures with the same template, as if the design was a restriction on the designer? Perhaps it was to make belief more difficult, to make only rebellious (non-credulous) hearts disbelieve?”

    Interesting questions, to be certain. This question gets to the core reason why evolutionary biologists reject the arguments for intelligent design. For these many biologists, homologous structures only make sense from within an evolutionary framework.

    The View of Biological Homologies before Darwin

    Part of the response to my friend Phil’s question can be found in the theoretical work of Sir Richard Owen, a prominent biologist from the UK who predated Darwin. One of the world’s most important anatomists in his day, Owen played a key role in discovering, describing, and interpreting biological homologies. Owen understood homologies from a design perspective. Specifically, Owen saw these mutual features as manifestations of a common blueprint that existed in the Creator’s mind, and, in turn, were physically manifested in the created order.

    Archetypes and God’s Creativity

    Instead of seeing the concept of the archetype as restricting God’s creativity, Owen regarded the archetype as reflecting teleology of the highest order. In his presentation to the Royal Institution of Great Britain, Owen lectured: “The satisfaction felt by the rightly constituted mind must ever be great in recognizing the fitness of parts for their appropriate functions; but when this fitness is gained as in the great toe of the foot of man or the ostrich, by a structure which at the same time betokens harmonious concord with a common type, the prescient operations of the One Cause of all organization becomes strikingly manifested to our limited intelligence.”1

    In other words, Owen marveled at the way the Creator generated so much functional diversity from a single template—for example, the pentadactyl architecture of the vertebrate forelimb.

    In fact, the diversity of life on Earth today—even throughout life’s history—built from 30 or so body plans (corresponding to the known animal phyla) is nothing short of mind-boggling. So, apparently creating life on Earth around design templates has done little to limit the Creator. In fact, I would argue—as Owen did— it highlights God’s ingenuity.

    Designed for Discovery

    There are a few reasons why God would have created life’s diversity using a limited set of templates. But, perhaps the most important reason is discoverability.

    The universal nature of biochemistry and the homologous and convergent biological systems allow scientists to generalize what they learn studying one organism to the entirety of the biological realm, in some instances. The universal and homologous designs in biology allow the scientific community to make use of organisms as model systems. For example: by studying DNA replication in bacteria, we have gained key insight that allows us to understand DNA replication in all life on the planet. Studying gene regulation in yeast helps us understand gene regulation in human beings. Studying the developmental pathways of the nematode C. elegans has yielded important knowledge that helps us understand growth and development in many multicellular organisms. Studying genetics in the fruit fly Drosophila has provided key understanding regarding inheritance.

    If, as my friend Phil wants, the Creator used a near infinite array of biological designs when he created, it would be virtually impossible for us to know anything about the living realm. The process of discovery in biology would become cumbersome and laborious.

    Because the living realm is intelligible, it is possible for human beings to take advantage of God’s provision for us, made available within the creation. As we study and develop an understanding of the living realm, we can deploy that knowledge to benefit humanity—in fact, all life on Earth—through agriculture, medicine, conservation efforts, and emerging biotechnologies.

    Ultimately, I believe that God has designed the biological realm for discoverability because He wants us to see, understand, and appreciate his handiwork as a Creator, so through his creation we can know him.

    “It is the glory of God to conceal a matter; to search out a matter is the glory of kings.”

    Proverbs 25:2

    Resources

    Endnotes
    1. Richard Owen, On the Nature of Limbs: A Discourse, ed. Ron Amundson (Chicago: University of Chicago Press, 2007), 38.
  • Reactive Oxygen Species: Harbingers of Evolution or Signals of Design?

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Dec 14, 2016

    Few concepts have been embraced by popular science as enthusiastically as the idea that reactive oxygen species (ROS) are harmful and that their levels should be controlled by including antioxidants in the diet or as supplements.1

    –Ulrich Theopold

    Antioxidants are the latest diet fad. Many people do whatever they can to include foods high in antioxidants in their diets. Some people even go a step further by taking antioxidant supplements. All these actions are meant to combat the harmful effects of reactive oxygen species (ROS). Produced in the mitochondria, these highly reactive chemical derivatives of molecular oxygen will destroy cellular components if left unchecked.

    Yet things aren’t always what they seem. An increasing number of studies indicate that taking dietary supplements of antioxidants has questionable health benefits.2 In fact, taking certain antioxidant supplements may be harmful. For example, studies indicate that people who supplement their diets with vitamin E and beta-carotene have higher mortality rates compared to people who don’t take antioxidant supplements at all. Other studies demonstrate that instead of slowing cancer’s spread, antioxidants, in fact, accelerate the progression of certain cancers. Antioxidant consumption also impacts development, harming certain types of stem cells.

    When it comes to antioxidants and ROS, the scientific community has made another surprising about-face. Biochemists no longer view ROS as harmful compounds, wreaking havoc on the cell’s components. Instead, they have learned that ROS play a key role in cell-signaling processes. As it turns out, consumption of excessive antioxidants interferes with ROS-based signaling pathways. And this interference explains why consuming inordinate levels of antioxidants aren’t part of a healthy lifestyle.

    The surprising implications of this new insight regarding antioxidants and ROS extend beyond dietary considerations. This new understanding has bearing on the creation vs. evolution debate by providing a response to a common objection skeptics level against intelligent design arguments.

    ROS Generation and the Case for Evolution

    ROS are primarily produced in the mitochondria by the electron transport chain (ETC). The ETC harvests energy needed to carry out the various biochemical operations that take place within the cell. For the most part, the ETC is comprised of a series of protein complexes, conceptually organized into a linear array. The first complex of the ETC receives chemically energetic electrons (ultimately, derived from the breakdown of biochemical fuels) and passes them along to the next complex in the ETC. Eventually, these electrons are handed off from complex to complex, until they reach the terminal part of the ETC. When shuttled from one complex to the other, the electrons give up some of their energy. This released energy is captured, and ultimately used to produce compounds such as ATP, which serve as energy currency inside the cell.

    blog__inline--reactive-oxygen-species-1
    Image: Illustration of electron transport chain with oxidative phosphorylation.

    One of the final steps carried out by the ETC is the conversion of molecular oxygen into water, with oxygen receiving the de-energized electrons. If the energy status of the cell is high, the movement of electrons through the ETC slows down, and, under some circumstances, becomes backed up. When this jam occurs, the electrons prematurely react with oxygen because they must go somewhere. (This usually happens between complex I and complex III). When this premature termination takes place, ROS (which include the superoxide ion, the hydroxyl free radical, and hydrogen peroxide) form instead of water.

    At face value, it appears as if ROS form as an unintended side reaction. Traditionally, biochemists regard ROS as deadly compounds that oxidize membrane components, DNA, and proteins, causing untold damage to the cell.

    For many skeptics, the apparently random, unwanted generation of ROS which terrorize the cell undermines the case for intelligent design and serves as evidence for an evolutionary origin of biochemical systems. Why? Because the seemingly unintended production of chemically destructive ROS has all the markings of a flawed system—the type of system unguided evolutionary processes would produce, not the type of design befitting a Creator.

    The Cellular Roles of ROS

    Yet in recent years, biochemists have come to see ROS differently. Instead of the product of an unwanted side reaction, biochemists have come to discover that these compounds serve as second messengers, communicating the cell’s energy status to key metabolic processes, including those that regulate stem cell development.3 These mechanisms allow the cell to coordinate various metabolic processes for the available bioenergetics sources.

    Because hydrogen peroxide has the chemical stability and capacity to dissolve through membranes, biochemists believe that it functions as the primary second messenger. Still, the other ROS do play a role in cell signaling.

    ROS can serve as second messengers because they preferentially oxidize certain amino acids in proteins, with cysteine residues often targeted. The selective oxidation of amino acid residues modifies the activity of the protein targets. Targeted proteins include transcription factors (which control gene expression), and kinases and phosphatases (which regulate different stages of the cell cycle). These protein targets explain why ROS play a critical role in stem cell renewal, stem cell proliferation, and maturation.

    Oxidative Damage by ROS Is a Trade-Off

    ROS are ideal second messengers for communicating and coordinating the cell’s metabolic pathways with respect to the cell’s energy status, because their production is closely linked to the ETC. When the energy status of the cell is high, ROS production increases. And when the cell’s energy status dips, ROS production tails off. In my view, there is an exquisite molecular logic that undergirds the use of ROS as second messengers for communicating the cell’s energy balance.

    Of course, the drawback to using ROS as second messengers is the oxidative damage these materials cause. But instead of viewing the damaging effects of these compounds as a flawed design, I maintain that it is better to think of it as a trade-off.

    Towards that end, it is important to note that the cell has an extensive and elaborate system to buffer against the harmful effects of ROS. For example, superoxide dismutase converts superoxide into hydrogen peroxide. Two other enzymes, catalase and peroxiredoxin, transform hydrogen peroxide into water. In fact, one of the targets of ROS are transcription factors that trigger the production of proteins that are part of the cell’s antioxidant defenses and proteins that take part in pathways that clear damaged proteins from the cell. This ingenious design ensures that once ROS form and play a role as second messengers, the damaged proteins are quickly destroyed and any destruction they cause is mitigated.

    It is truly remarkable how dramatically the scientific community’s views on ROS (and antioxidants) have changed in recent years. Instead of being the unwanted byproducts of metabolism that plagued the cell, ROS serve as a biochemical fuel gage, triggering processes such as quiescence and even autophagy (programmed cell death) when the energy balance is too low and the cell is experiencing starvation and cell differentiation (which impacts stem cell biology) when energy stores are sufficiently full.

    Often, skeptics point to so-called bad designs as evidence for an evolutionary history for life. But, the changed perspective of ROS serves as a cautionary tale. Many times, what is perceived as a bad design turns out to be anything but as we learn more about the system, and these discoveries undermine the best arguments for evolution while adding to the mounting case for intelligent design.

    Resources

    The Cell’s Design by Fazale Rana (book)
    30% Inefficiency by Design” by Fazale Rana (article)
    The Human Appendix: What Is It Good For?” by Fazale Rana (article)
    New Research Highlights Elegant Design in the Inverted Retina” by Fazale Rana (article)
    Wisdom Teeth Reflect the Creator’s Foresight” by Fazale Rana (article)
    Is the Whale Pelvis a Vestige of Evolution?” by Fazale Rana (article)

    Endnotes
    1. Ulrich Theopold, “Developmental Biology: A Bad Boy Comes Good, Nature 461 (September 2009): 486–87, doi:10.1038/461486a.
    2. Center for the Advancement of Health, “Antioxidant Users Don’t Live Longer, Analysis of Studies Concludes,” Science News (blog), ScienceDaily, April 16, 2008, https://www.sciencedaily.com/releases/2008/04/080415194233.htm; University of Gothenburg, “Antioxidants Cause Malignant Melanoma to Metastasize Faster,” Science News (blog), ScienceDaily, October 8, 2015, https://www.sciencedaily.com/releases/2015/10/151008131112.htm; Ed Yong, “Antioxidants Speed Up Lung Cancer,” Daily News (blog), The Scientist, January 29, 2014, https://www.the-scientist.com/?articles.view/articleNo/39022/title/Antioxidants-Speed-Up-Lung-Cancer/; University of Helsinki, “Large Doses of Antioxidants May Be Harmful to Neuronal Stem Cells,” Science News (blog), ScienceDaily, June 11, 2015, https://www.sciencedaily.com/releases/2015/06/150611091340.htm.
    3. Kira Holmström and Toren Finkel, “Cellular Mechanisms and Physiological Consequences of Redox-Dependent Signalling,” Nature Reviews Molecular Cell Biology 15 (June 2014): 411–21, doi:10.1038/nrm3801; Carolina Bigarella, Raymond Liang, and Saghi Ghaffari, “Stem Cells and the Impact of ROS Signaling,” Development 141 (November 2014): 4206–18, doi:10.1242/dev.107086.
  • Science News Flash: An Old-Earth Perspective on Dinosaur Feathers Preserved in Amber

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Dec 09, 2016

    Whenever we are in a foreign country, my wife loves to shop at local, out-of-the-way markets. She always finds some of the most interesting souvenirs.

    It turns out the same is true for paleontologist Lida Xing who purchased several amber pieces from a market in Myitkyina in the country of Myanmar. The amber sold at the market comes from a nearby mine in the Hukawng Valley. While most buyers are looking for amber to make jewelry, Xing was looking for amber with inclusions of plant and animal remains. The amber from the mine dates to 99 million years. Because of the amber’s age, the well-preserved plant and animal remains entombed by this fossilized tree resin offer a unique glimpse at ancient life on Earth, providing details and insight that far exceed those available from highly compressed fossil remains that typically comprise the fossil record.

    As fate would have it, one of the amber pieces Xing purchased contains a piece of a dinosaur tail (perhaps from a maniraptor) with attached feathers! This discovery is described in a paper that will appear in the December 19 issue of Current Biology.1 Yesterday the paper was published online ahead of the publication date and it has already generated headlines both in the popular news and on social media.

    This is not the first time researchers have discovered feathers preserved in amber. But it is the first time they have observed feathers associated with parts of a dinosaur, in this instance a section of the tail (near the middle or end) that includes eight vertebrae. The anatomical features clearly indicates that the preserved tail belongs to a large group of dinosaurs labeled the coelurosaurs.

    It goes without saying that this find has already caused quite a bit of a stir because of its important implications for evolutionary and creation models for bird origins.

    An Evolutionary Perspective of the Discovery

    For many in the scientific community this discovery further affirms the evolutionary link between birds and dinosaurs, with feathered dinosaurs viewed as transitional intermediates. Along these lines, the researchers describe the dinosaur feathers preserved in amber as transitional, noting that the feather’s central shaft (rachis) is poorly defined. On this basis, the researchers argue that the rachis was a late-appearing feature in feathers, forming when the barbs of the feather fused together.

    An Old-Earth Creationist Response

    As an old-earth creationist, I’m skeptical about the evolutionary account that has birds evolving from theropods. In fact, this latest discovery only adds to my skepticism.

    Paleontologists interpret feathered dinosaurs from the fossil record as transitional intermediates between theropods and birds—including the feathered dinosaur tail found in amber. Yet, each occurrence of feathered dinosaurs in the fossil record appear after the first true bird, Archaeopteryx.2 Based on the fossil record, this ancient bird appeared on Earth around 155 million years ago. Archaeopteryx’s feathers were identical to the feathers of modern birds. In fact, the same research team discovered bird feathers in 99-million-year-old amber from the same source that yielded the amber with the dinosaur feathers. The bird feathers, like those of Archaeopteryx, are identical to those found in modern birds.

    It is hard to imagine how the “primitive” feathers associated with the dinosaur tail (again, dated at 99 million years in age) could be transitional if they appear over 50 million years after Archaeopteryx and co-occur with feathers from a bird belonging to enantiornithes.

    This problem is not unique to the bird fossil record. There are several instances in which presumed transitional forms appear in the fossil record well after the first appearance of their evolutionary descendants. In fact, paleontologist have a name for this phenomenon: a temporal paradox.

    For a more complete discussion of the problems I see with the proposed evolutionary link between birds and theropod dinosaurs, see “Birds in the Fossil Record” (listed in the resource section below).

    A Young-Earth Creationist Perspective of the Discovery

    One exciting aspect of this find is the possibility that soft-tissue remnants associated with the features may be preserved in the amber. The researchers discovered iron (in the ferrous form) associated with the carbonized feather remains. They speculate that this iron derives from hemoglobin originally found in the tail muscle tissue. On this basis, the research team speculates that soft-tissue remnants derived from keratin may be present in the amber-entombed specimen.

    In recent years, young-earth creationists have made use of these types of finds to argue that it is impossible for such fossils to be millions of years old. They argue that soft tissues shouldn’t survive that long. These materials should readily degrade in a few thousand years. In their view, these finds challenge the reliability of radiometric dating methods used to determine the age of these fossils, and along with it, Earth’s antiquity. Instead, they argue that these breakthrough discoveries provide compelling scientific evidence for a young Earth and support the idea that the fossil record results from a recent global (worldwide) flood.

    An Old-Earth Creationist Response

    These types of claims prompted me to write Dinosaur Blood and the Age of the Earth. In this work (and elsewhere), I explain why the recovery of soft-tissue remnants associated with fossil finds is illegitimate evidence for a young Earth.

    Given the structural robustness of keratin, and the preservative effect of ferrous iron, it is completely reasonable to think that keratin remnants associated with the feathers could survive long enough to be completely entombed by the amber and eventually persist for nearly 100 million years.

    Though this find will be interpreted by the scientific community from an evolutionary vantage point and, more than likely, opted by young-earth creationists to challenge the antiquity of Earth and life on Earth, the dinosaur feathers entombed in amber can readily be accommodated from an old-earth creationist vantage point.

    Resources

    Creation vs. Evolution Controversy

    Is There a Controversy about Evolution?by Fazale Rana (article)
    The Creation-Evolution Controversy in Jurassic Worldby Fazale Rana (article)

    Age-of-the-Earth Controversy

    Dinosaur Blood and the Age of the Earthby Fazale Rana (book).
    Can Keratin in Feathers Survive for Millions of Years?by Fazale Rana (article)

    Endnotes
    1. Lida Xing et al., “A Feathered Dinosaur Tail with Primitive Plumage Trapped in Mid-Cretaceous Amber,” Current Biology 26 (December 19, 2016): 1–9, doi:10.1016/j.cub.2016.10.008.
    2. Some paleontologists claim that the temporal paradox for bird origins was solved based on the discovery of a feathered theropod that dates between 151 and 161 million years in age. (See Dongyu Hu et al., “A Pre-Archaeopteryx Troodontid Theropod from China with Long Feathers on the Metatarsus,” Nature 461 [October 1, 2009]: 640–43, doi:10.1038/nature08322.) However, at best, this find demonstrates the co-occurrence of feathered dinosaurs and the first true bird, when the error bars of the age-date measurements are taken into account.
    3. Lida Xing et al., “Mummified Precocial Bird Wings in Mid-Cretaceous Burmese Amber,” Nature Communications 7 (June 28, 2016): 12089, doi:10.1038/ncomms12089.
  • Pseudoenzymes Illustrate Science's Philosophical Commitments

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Dec 07, 2016

    A few months ago, I had a serious accident while shooting a compound bow in my backyard. The arrow jammed in the guide, and in my attempt to free the arrow, I caused the bow string to derail. When that happened, the string struck my left eye with such force that it fractured my orbit in five places and damaged my retina. I am now legally blind in my left eye. Thankfully, I still have some peripheral vision, but I lost all the central vision in my injured eye. (To mothers everywhere: Yes, I wasn’t careful and I shot my eye out. I should have listened.)

    Because of my injury, there is a blacked-out area in the center part of my field of vision which prevents me from focusing with my left eye. Sometimes, if something is on my left side, I can’t see it—even if it is in plain view.

    Science’s Blind Spot

    Over the years I have come to appreciate that, very often, the creation/intelligent design vs. evolution controversy has less to do with the evidence on hand, and more with how each side sees the evidence. As a case in point, when examining the features of biochemical systems, most creationists and intelligent design proponents readily see evidence of a Creator’s handiwork. Yet adherents to the evolutionary paradigm don’t see evidence for design at all. Instead, they see flawed designs. Why? Because they view biochemical systems as the outworking of an unguided evolutionary history. According to this view, evolution’s mechanisms have cobbled together biochemical systems by co-opting and repurposing existing systems to generate novel biochemical functions. As such, evolution produces kludge-job designs. Not the elegant, sophisticated systems expected if life stems from a Creator’s handiwork.

    In part, the differing perspectives are shaped by philosophical commitments and the expectations that flow from them. To expound upon this point: the philosophical framework for contemporary science is methodological naturalism. Accordingly, scientific explanations for the universe and phenomena within the universe (such as the characteristics of biochemical systems) must have a mechanistic accounting—an explanation exclusively rooted in natural processes. Any explanation that appeals to the work of supernatural agency violates the tenets of methodological naturalism and is not even entertained as a possibility.

    The consequences of methodological naturalism are far ranging for the creation/intelligent design vs. evolution controversy. The constraints of methodological naturalism exclude a priori any model that appeals to intelligent agency to explain, say, the design of biochemical systems. So although biochemical systems bear the appearance of design, the scientific community must explain the design as a product of evolutionary mechanisms. Why? Because they have no other option. If biochemical systems didn’t evolve, then they must have been created. But, the tenets of methodological naturalism forbid this explanation. Hence, biochemical systems must have evolved—by default.

    If biochemical systems arise via evolutionary mechanisms, then they must be cobbled together. They must be poorly designed. Consequently, adherents of the evolutionary paradigm are conditioned to see biochemical systems as poorly designed—even if they aren’t—because of their commitment to methodological naturalism. Many can’t see the design that is in plain view for creationists and intelligent design adherents.

    The recent discovery of pseudoenzymes helps illustrate this point.

    Pseudoenzymes: Evidence for Evolution or Intelligent Design?

    The existence of pseudoenzymes came to light about a decade ago when the human genome sequence was made available for researchers to study. It turns out that almost every enzyme family encoded by the human genome includes seemingly nonfunctioning members. (Enzymes are proteins that catalyze—or facilitate—chemical reactions in the cell.) Biochemists have dubbed these nonfunctioning enzymes pseudoenzymes. These proteins bear structural resemblances to other members of their enzyme families, yet they are unable to catalyze chemical reactions.

    Because researchers have already detected pseudoenzymes within every known enzyme family, they expect that many more pseudoenzymes await discovery. In fact, analysis of thousands of genomes has identified pseudoenzymes throughout the biological realm. To put it another way: Pseudoenzymes seem to be pervasive in biochemical systems.

    Evolutionary biologists view pseudoenzymes as a byproduct of life’s evolutionary history. Presumably, these noncatalytic enzymes arose when genes encoding their functional counterpart became duplicated. After this event, the duplicated genes experienced mutations that disabled the catalytic function of their protein products, generating pseudoenzymes.

    For adherents of the evolutionary paradigm, the widespread occurrence of pseudoenzymes serves as a prima facie (based on first impression) challenge to intelligent design, and a compelling reason to think that biochemical systems are the product of an evolutionary history. In this framework, pseudoenzymes are vestiges of life’s evolutionary past; nonfunctional biochemical scars that impede cellular functions.

    On the other hand, as a creationist and intelligent design proponent, I resist this conclusion. Why? Because I have a different set of presuppositions than most in the scientific community. I believe that life arose through a Creators direct intervention and that science has the tool kit to detect evidence of intelligent agency at work. Because of my precommitments, I would posit yet-to-be-discovered functions for pseudoenzymes and a rationale for why these enzymes bear structural similarity to catalytic counterparts within their enzyme family.

    And this is exactly what biochemists have discovered—pseudoenzymes are, indeed, functional, and there are good reasons why these biomolecules resemble their catalytic analogs.

    The Role and Rationale for Pseudoenzymes

    In a recent primer written for the open access journal BMC Biology, two biochemists surveyed recent work on pseudoenzymes, concluding that this newly recognized class of biomolecules plays a key role in cellular signaling pathways.1

    The authors reflect on the role the evolutionary paradigm played in delaying this insight. They state:

    “Because of the prejudice that focused attention on the catalytic functions of enzymes in signalling pathways, for a long time pseudoenzymes were considered to be dead—and therefore evolutionary remnants or bystanders in cell signalling networks. Contrary to this view, however, pseudoenzymes have now emerged as crucial players operating with an impressive diversity of mechanisms that we are only beginning to understand.”2

    In other words, the biases created by viewing pseudoenzymes as the byproduct of evolutionary processes hindered biochemists from identifying and characterizing the functional importance of pseudoenzymes.

    But this flawed perspective of viewing pseudoenyzmes as junk is changing. To date, biochemists have identified at least four functional roles for pseudoenzymes:

    1. They serve as protein anchors, locating cell signaling enzymes to appropriate locations within the cell.
    2. They function as scaffolds bringing enzymes of the same signaling pathway into proximity with one another, allowing the enzymes to efficiently work in conjunction with one another.
    3. They modulate the function of cell signaling proteins by binding to them, exerting an allosteric-type effect.
    4. They compete with “catalytic” cell signaling enzymes by binding the substrate without transforming it, regulating substrate transformation.

    In part, the functional significance of pseudoenzymes justifies viewing these biomolecules as the work of a Creator. But, if these biomolecules are designed, why would pseudoenzymes be so structurally like their catalytic cohorts? Evolutionary biologists maintain that these similarities reflect their evolutionary history. But, if there is reason for the structural similarities, it further justifies viewing pseudoenzymes as designed systems. As it turns out, a rationale does exist for the close similarity in structure between pseudoenzymes and other members of their enzyme family. As the authors of the survey note:

    “Enzyme structures are predisposed to mediating interactions with protein or metabolite ligands and thus these folds are the ideal templates for nature to repurpose for entirely new functions.”3

    In other words, for pseudoenzymes to influence cellular signaling pathways, they must bind substrates and interact with other proteins in the pathways with a high degree of specificity and with the identical specificity as their catalytic counterparts. Their close resemblance to their catalytic analogs allows these biomolecules to do just that.

    In short, in fulfilling their vital role as regulators of cell signaling pathways, pseudoenzymes display elegance, sophistication, and ingenuity. As a creationist, this is the reason I view these systems as a Creator’s handiwork. Because the field of pseudoenzyme biochemistry is so young, I anticipate the evidence for design to dramatically expand as we learn more about these surprising biomolecules.

    Yet, despite everything we have learned about pseudoenzymes, adherents to the evolutionary paradigm simply can’t see these biomolecules as anything other than the product of an evolutionary history.

    Because of the blind spot created by their philosophical commitments, the design of these systems is occluded from their view—and that causes them to miss the mark.

    Resources
    The Cell’s Design: How Chemistry Reveals the Creator’s Artistry by Fazale Rana (book)
    Pseudoenzymes Make Real Case for Intelligent Design” by Fazale Rana (article)
    Q&A: Is Christianity a Science Showstopper?” by Fazale Rana (article)
    Does the Evolutionary Paradigm Stymie Scientific Advance?” by Fazale Rana (article)
    Q&A: Is Evolution Falsifiable?” by Fazale Rana (article)

    Endnotes
    1. Patrick Eyers and James Murphy, “The Evolving World of Pseudoenzymes: Proteins, Prejudice, and Zombies,” BMC Biology 14 (November 2016): 98, doi:10.1186/s12915-016-0322-x.
    2. Ibid.
    3. Ibid.
  • Ancient Muds Bog Down Evolutionary Explanation for Life’s Origin

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Nov 30, 2016

    When I was a kid, I played a lot of sandlot football. And nothing was more fun than playing football after a hard rain on a muddy field. It was a blast to slosh around in the mud. But if the field was too muddy, it was hard to run, making it difficult to advance the ball down the field.

    Scientists like playing in the mud, too. And recently, a scientist from the University of Washington had a good time working with ancient mud from early Earth (dating to 3.8 billion years in age). As a result of her efforts, Eva Stüeken now argues that the nitrogen in some of the oldest muddy sediments on Earth was produced by microorganisms.

    Her interpretation of the nitrogen in ancient muds adds to the mounting evidence for an early and rapid origin of life, making it more difficult for the scientific community to advance an evolutionary explanation for life’s start.1

    In earlier studies, geochemists measured about 430 parts per million (ppm) nitrogen in biotite minerals recovered from 3.8-billion-year-old sediments of the Isua Formation of Greenland. Typically, the highest levels of nitrogen co-occur with graphite granules. (Some geochemists regard the graphite granules as a biomarker.) Because nitrogen is an integral component of biomolecules such as DNA and proteins, the occurrence of this element in the biotite can be taken as a biosignature.

    Unfortunately, it is not that straightforward. Some geochemists claim that the nitrogen in the ancient mud comes from abiotic sources. For example, lightning and volcanism can fix atmospheric nitrogen, conceivably accounting for its presence in the biotite grains.

    To test this idea, University of Washington earth scientist Eva Stüeken modeled the amount of abiotic nitrogen that would be expected in ancient muds if it came exclusively from abiotic processes. She determined that abiotic pathways were insufficient to explain nitrogen levels, meaning that some of the nitrogen must be biogenic.

    Early Life on Earth

    The presence of nitrogen in ancient muds adds to the mounting geochemical and fossil evidence that points to the presence of life on early Earth. (See the Resources section below to learn about other evidences for early life on Earth.) It looks like life appeared on Earth as soon as our planet could sustain it. In fact, a case can be made that life could not have originated and persisted on Earth prior to 3.8 billion years ago. This constraint means that life must have originated within a geological instant.

    Both the geochemical and fossil evidence indicate that Earth’s first life was microbial in nature. Though morphologically simple, the geochemical data indicates this life was biochemically diverse and complex. There are good reasons to think that the first life-forms could engage in a wide range of metabolic activities including: photosynthesis, methanogenesis, methanotrophism, and sulfur disproportionation. While far from conclusive, the biogenic nitrogen in the ancient muds suggests that Earth’s first life also had the capacity to fix nitrogen.

    Evidence for Evolution or Creation?

    As discussed in Origins of Life, the sudden, early appearance of metabolically sophisticated life on Earth is difficult to accommodate within an evolutionary framework. Traditionally, origin-of-life researchers have maintained that the origin-of-life process would have required hundreds of millions of years—maybe even a billion years. To put it another way, when viewed from an evolutionary standpoint, no one would have expected that lifes origin would have happened so rapidly.

    This latest insight about the ancient muds creates an additional problem for evolutionary models. It argues against the existence of a prebiotic soup on early Earth. This idea is a cornerstone for most origin-of-life models. Accordingly, life emerged on early Earth out of a prebiotic soup—a complex chemical mixture—as the molecules in the soup became more complex and, eventually, self-organized into the first cellular entities.

    If a prebiotic soup existed on Earth, it should leave behind a geochemical signature in the oldest rocks on Earth. Geochemists have uncovered chemical residues in the oldest rock formations on Earth—including the nitrogen in the ancient muds—but inevitably, these residues turn out to be biogenic in origin, not abiotic. In other words, there is no geochemical evidence for a prebiotic soup. This idea is all covered with the mud.

    On the other hand, the sudden appearance of biochemically complex life on early Earth bears the signature of the Creator’s handiwork. They are also key predictions for the RTB model for life’s origin.

    Resources

    Origins of Life: Biblical and Evolutionary Models Face Off by Fazale Rana and Hugh Ross (book)
    Creating Life in the Lab: How New Discoveries in Synthetic Biology Make a Case for the Creator by Fazale Rana (book)
    Science News Flash: 3.7-Billion-Year-Old Fossils Perplex Origin-of-Life Researchers” by Fazale Rana (article)
    Early Life was More Complex than We Thought” by Fazale Rana (article)
    When Did Life First Appear on Earth?” by Fazale Rana (article)
    Origin-of-Life Predictions Face Off: Evolution vs. Biblical Creation” by Fazale Rana (article)
    Fossils Indicate Early Life Was Metabolically Complex and Diverse” by Fazale Rana (podcast)
    Life May Have Begun 300 Million Years Earlier Than We Thought” by Fazale Rana (podcast)

    Endnotes
    1. Eva Stüeken, “Nitrogen in Ancient Mud: A Biosignature?” Astrobiology 16 (September 2016): 730–35, doi:10.1089/ast.2016.1478.
  • Can a Creation Model Explain the Origin of Mitochondria?

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Nov 23, 2016

    Some called her a scientific heretic. Others were a bit more kind, describing her as a maverick.

    Lynn Margulis (1938–2011) earned her reputation in the late 1960s when she proposed the endosymbiont hypothesis for the origin of eukaryotic cells. Because her ideas about evolution didn’t conform to Darwinian principles, evolutionary biologists summarily dismissed her idea out of hand and then went on to ignore her work for a couple of decades. She was ultimately vindicated, however, as the endosymbiont hypothesis gradually gained acceptance.

    Today, Margulis’s proposal has become a cornerstone idea of the evolutionary paradigm and is taught in introductory high school and college biology courses. This classroom exposure explains why I am often asked about the endosymbiont hypothesis when I speak on university campuses. Many first-year biology students and professional life scientists alike find the evidence for this idea compelling, and consequently view it as providing broad support for an evolutionary explanation for the history and design of life.

    Yet, new work by biochemists from Cambridge University make it possible to account for the origin of eukaryotic cells from a creation model perspective, providing a response to the endosymbiont hypothesis.1

    The Endosymbiont Hypothesis

    According to this hypothesis, complex cells originated when symbiotic relationships formed among single-celled microbes after free-living bacterial and/or archaeal cells were engulfed by a “host” microbe. (Ingested cells that take up permanent residence within other cells are referred to as endosymbionts.)

    Accordingly, organelles, such as mitochondria, were once endosymbionts. Once taken inside the host cell, the endosymbionts presumably took up permanent residency within the host, with the endosymbionts growing and dividing inside the host. Over time, the endosymbionts and the host became mutually interdependent, with the endosymbionts providing a metabolic benefit for the host cell. The endosymbionts gradually evolved into organelles through a process referred to as genome reduction. This reduction resulted when genes from the endosymbionts genomes were transferred into the genome of the host organism. Eventually, the host cell evolved both the machinery to produce the proteins needed by the former endosymbiont and the processes needed to transport those proteins into the organelle’s interior.

    Evidence for the Endosymbiont Hypothesis

    The main line of evidence for the endosymbiont hypothesis is the similarity between organelles and bacteria. For example, mitochondria—which are believed to be descended from a group of α-proteobacteria—are about the same size and shape as a typical bacterium and have a double membrane structure like gram-negative cells. These organelles also divide in a way that is reminiscent of bacterial cells.

    There is also biochemical evidence for the endosymbiont hypothesis. Evolutionary biologists view the existence of the diminutive mitochondrial genome as a vestige of this organelle’s evolutionary history. Additionally, the biochemical similarities between mitochondrial and bacterial genomes are taken as further evidence for the evolutionary origin of these organelles.

    The presence of the unique lipid called cardiolipin in the mitochondrial inner membrane also serves as evidence for the endosymbiont hypothesis. Cardiolipin is an important lipid component of bacterial inner membranes, yet it is not found in the membranes of eukaryotic cells—except for the inner membranes of mitochondria. In fact, biochemists consider it a signature lipid for mitochondria and a vestige of this organelle’s evolutionary history.

    A Creation Model Perspective on Mitochondria

    So, as a creationist, how do I make sense of the evidence for the endosymbiont hypothesis?

    Instead of focusing my efforts on refuting the endosymbiont hypothesis, here, I take a different approach. I maintain that it is reasonable to view eukaryotic cells as the work of a Creator, with the shared similarities between mitochondria and bacteria reflecting common design rather than common descent.

    However, to legitimately interpret mitochondrial origins from a creation model perspective, there must be a reason for the biochemical similarities between mitochondria and bacteria. Previously, I wrote about discoveries that provide a rationale for why mitochondria have their own genomes. (See “Resources.”) Thanks to recent research advances, an explanation now exists for why the mitochondrial inner membranes harbor cardiolipin.

    Cardiolipin’s Function

    Previous studies identified close associations between cardiolipin and a number of proteins found in the mitochondrial inner membrane. These proteins play a role in harvesting energy for the cell to use. Compared to other lipid components found in the inner membrane, cardiolipin appears to preferentially associate with these proteins. Evidence indicates that cardiolipin helps to stabilize the structures of these proteins and serves to organize the proteins into larger functional complexes within the membrane.2 In fact, several studies have implicated defects in cardiolipin metabolism in the onset of a number of neuromuscular disorders.

    The work of the Cambridge University investigators adds to this insight. These researchers were using computer simulations to model the interactions between cardiolipin and a protein complex called F1-F0 ATPase. Embedded within the inner membrane of mitochondria, this complex is a biomolecular rotary motor that produces the compound ATP—an energy storage material the cell’s machinery uses to power its operations.

    Like other proteins found in the inner membrane, cardiolipin forms a close association with F1-F0 ATPase. However, instead of permanently binding to the surface of the protein complex, cardiolipin dynamically interacts with this membrane-embedded protein complex. The researchers think that this dynamic association and the unusual chemical structure of cardiolipin (which gives it the flexibility to interact with a protein surface) are critical for its role within the mitochondrial inner membrane. As it turns out, cardiolipin not only stabilizes the F1-F0 ATPase complex (as it does for other inner membrane proteins), but it also lubricates the protein’s rotor, allowing it to turn in the viscous cell membrane environment. Also, its unique structure helps move protons through the F1-F0 ATPase motor, providing the electrical power to operate this biochemical motor.

    The bottom line: There is an exquisite biochemical rationale for why cardiolipin is found in mitochondrial inner membranes (and bacterial membranes). In light of this new insight, it is reasonable to view the shared similarities between these organelles and bacteria as reflecting common design—the product of the Creator’s handiwork. Like most biological systems, this organelle appears to be designed for a purpose.

    Resources
    Why Do Mitochondria Have DNA?” by Fazale Rana (article)
    Mitochondrial Genomes: Evidence for Evolution or Creation?” by Fazale Rana (article)
    Complex Protein Biogenesis Hints at Intelligent Designby Fazale Rana (article)
    Archetype or Ancestor? Sir Richard Owen and the Case for Designby Fazale Rana (article)
    Nanodevices Make Megascopic Statementby Fazale Rana (article)

    Endnotes
    1. Anna Duncan, Alan Robinson, and John Walker, “Cardiolipin Binds Selectively but Transiently to Conserved Lysine Residues in the Rotor of Metazoan ATP Synthases,” Proceedings of the National Academy of Sciences USA 113 (August 2016): 8687–92, doi:10.1073/pnas.1608396113.
    2. Giuseppe Paradies et al., “Functional Role of Cardiolipin in Mitochondrial Bioenergetics,” Biochimica et Biophysica Acta—Bioenergetics 1837 (April 2014): 408–17, doi:10.1016/j.bbabio.2013.10.006.
  • Science News Flash: Chimps Use Tools to Fish for Algae

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Nov 16, 2016

    Some of my fondest memories as a little kid are the summer afternoons I spent with my grandfather fishing in the Missouri River, near Mandan, North Dakota.

    I don’t remember catching many fish, but that didn’t matter. I enjoyed spending time with my grandpa. I’m sure the experience was a bit trying for him though. If I detected even the slightest movement, I would reel in my line, hoping there would be a fish on the end. Inevitably, my excitement would give way to disappointment when I discovered that all I had caught was a clump of algae. And, of course, grandpa would have to clean up the mess I created and then recast my line.

    But my response to reeling in an algae clump would have been different if I was a chimpanzee—if the field observations of primatologists from Germany are to be believed. Instead of disappointment, I would have been excited by my green, slimy, catch. As it turns out, chimpanzees will eat algae. It can be a valuable food source for them, rich in protein, carbohydrates, and minerals.

    The German primatologists recently generated headlines when they published a report in the American Journal of Primatology describing 15 months of field work in the Bakoun Classified Forest of Guinea.1 Using camera footage from 11 different sites, the research team observed both male and female chimpanzees of every age using sticks (ranging from 6 inches to 12 feet in length) to “fish” algae out of rivers, streams, and ponds during the dry season.

    The chimpanzees’ fishing efforts could last for up to an hour, with the average duration being around nine minutes. The chimps typically collected around a tenth of a pound of algae for each fishing expedition.

    Evolutionary anthropologists point to these types of observations as shedding important light on the evolution of human behavior. They maintain that the use of tools by chimpanzees is an antecedent to the advanced behaviors displayed by modern humans.

    However, I take a different view, maintaining that these types of discoveries actually undermine the standard models of human evolution. How so? These insights place chimpanzee behavior closer to hominid behavior (inferred from the fossil record). The temptation is to see hominid tool use as transitional, a way station on the path to modern human behavior. Yet the newly recognized behavior of chimpanzees distances the hominids from modern humans. Just because hominids such as habilines and erectines made tools and engaged in other remarkable behaviors doesn’t mean that they were becoming human. Instead, their behavior appears to be increasingly animal-like, particularly in light of the newly discovered chimp activities.

    Resources
    Who Was Adam? by Fazale Rana with Hugh Ross (book)
    Chimpanzee Behavior Supports RTB’s Model for Humanity’s Origin” by Fazale Rana (article)
    Chimpanzees’ Sleeping Habits Closer to Hominid Behavior than to Humans‘” by Fazale Rana (article)
    Chimpanzees Respond to Death like Humans: Evidence for Evolution or Creation? Part 1 (of 2)” by Fazale Rana (article)
    Chimpanzees Respond to Death like Humans: Evidence for Evolution or Creation? Part 2 (of 2)” by Fazale Rana (article)

    Endnotes
    1. Christophe Boesch et al,. “Chimpanzees Routinely Fish for Algae with Tools during the Dry Season in Bakoun, Guinea,” American Journal of Primatology, published electronically November 3, 2016, doi:10.1002/ajp.22613.
  • The Logic of DNA Replication Makes a Case for Intelligent Design

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Nov 09, 2016

    Why do I think God exists?

    In short: The elegance, sophistication, and ingenuity of biochemical systems—and their astonishing similarity to man-made systems—convinces me that God is responsible for life’s origin and design.

    While many skeptics readily acknowledge the remarkable designs of biochemical systems, they would disagree with my conclusion about God’s existence. Why? Because for every biochemical system I point to that displays beauty and elegance, they can point to one that seems to be poorly designed. In their view, these substandard designs reflect life’s evolutionary origin. They argue that evolutionary mechanisms kludged together the cell’s chemical systems through a historically contingent process that co-opted preexisting systems, cobbling them together to form new biochemical systems.

    According to skeptics, one doesn’t have to look hard to find biochemical systems that seem to have been put together in a haphazard manner, and DNA replication appears to be an example of this. In many respects, DNA replication lies at the heart of the cell’s chemical operations. If designed by a Creator, this biochemical system, above all others, should epitomize intelligent design. Yet the DNA replication process appears to be unwieldy, inefficient, and unduly complex—the type of system evolution would generate by force, not the type of system worthy to be designated the product of the Creator’s handiwork.

    Yet new work by Japanese researchers helps explain why DNA replication is the way it is.1 Instead of reflecting the cumbersome product of an unguided evolutionary history, the DNA replication process displays an exquisite molecular logic.

    To appreciate the significance of the Japanese study and its implication for the creation/evolution controversy, a short biochemistry primer is in order. For readers who are familiar with DNAs structure and the DNA replication process, you can skip the next two sections.

    DNA

    DNA consists of chain-like molecules known as polynucleotides. Two polynucleotide chains align in an antiparallel fashion to form a DNA molecule. (The two strands are arranged parallel to one another with the starting point of one strand in the polynucleotide duplex located next to the ending point of the other strand and vice versa.) The paired polynucleotide chains twist around each other to form the well-known DNA double helix. The cell’s machinery forms polynucleotide chains by linking together four different subunit molecules called nucleotides. The nucleotides used to build DNA chains are adenosine, guanosine, cytidine, and thymidine, famously abbreviated A, G, C, and T, respectively.

    The nucleotide molecules that make up the strands of DNA are, in turn, complex molecules consisting of both a phosphate moiety, and a nucleobase (either adenine, guanine, cytosine, or thymine) joined to a 5-carbon sugar (deoxyribose).

    blog__inline--logic-of-dna-replication-makes-case-for-intelligent-design-1

    Image 1: Adenosine Monophosphate, a Nucleotide

    Repeatedly linking the phosphate group of one nucleotide to the deoxyribose unit of another nucleotide forms the backbone of the DNA strand. The nucleobases extend as side chains from the backbone of the DNA molecule and serve as interaction points when the two DNA strands align and twist to form the double helix.
    blog__inline--logic-of-dna-replication-makes-case-for-intelligent-design-2

    Image 2: The DNA Backbone

    When the two DNA strands align, the adenosine (A) side chains of one strand always pair with thymidine (T) side chains from the other strand. Likewise, the guanosine (G) side chains from one DNA strand always pair with cytidine (C) side chains from the other strand.

    DNA Replication

    Biochemists refer to DNA replication as a template-directed, semi-conservative process. By template-directed, biochemists mean that the nucleotide sequences of the “parent” DNA molecule function as a template, directing the assembly of the DNA strands of the two “daughter” molecules. By semi-conservative, biochemists mean that after replication, each daughter DNA molecule contains one newly formed DNA strand and one strand from the parent molecule.

    blog__inline--logic-of-dna-replication-makes-case-for-intelligent-design-3

    Image 3: Semi-Conservative DNA Replication

    Conceptually, template-directed, semi-conservative DNA replication entails the separation of the parent DNA double-helix into two single strands. By using the base-pairing rules, each strand serves as a template for the cell’s machinery to use when it forms a new DNA strand with a nucleotide sequence complementary to the parent strand. Because each strand of the parent DNA molecule directs the production of a new DNA strand, two daughter molecules result. Each one possesses an original strand from the parent molecule and a newly formed DNA strand produced by a template-directed synthetic process.

    DNA replication begins at specific sites along the DNA double helix, called replication origins. The DNA double helix unwinds locally at the origin of replication to produce what biochemists call a replication bubble. The bubble expands in both directions from the origin during the course of DNA replication. Once the individual strands of the DNA double helix unwind and are exposed within the replication bubble, they are available to direct the production of the daughter strand. The site where the DNA double helix continuously unwinds is called the replication fork. Because DNA replication proceeds in both directions away from the origin, there are two replication forks within each bubble.

    blog__inline--logic-of-dna-replication-makes-case-for-intelligent-design-4

    Image 4: DNA Replication

    DNA replication can only proceed in a single direction, from the top of the DNA strand to the bottom. Because the strands that form the DNA double helix align in an antiparallel fashion with the top of one strand juxtaposed to the bottom of the other strand, only one strand at each replication fork has the proper orientation (bottom-to-top) to direct the assembly of a new strand, in the top-to-bottom direction. For this strand—referred to as the “leading strand”—DNA replication proceeds rapidly and continuously in the direction of the advancing replication fork.

    DNA replication can’t proceed along the strand with the top-to-bottom orientation until the replication bubble has expanded enough to expose a sizable stretch of DNA. When this happens, DNA replication moves away from the advancing replication fork. DNA replication can only proceed a short distance for the top-to-bottom oriented strand before the replication process has to stop and wait for more of the parent DNA strand to be exposed. When a sufficient length of the parent DNA template is exposed for a second time, DNA replication can proceed again, but only briefly before it has to stop again and wait for more DNA to be exposed. The process of discontinuous DNA replication takes place repeatedly until the entire strand is replicated. Each time DNA replication starts and stops, a small fragment of DNA is produced. Biochemists refer to these pieces of DNA (that will eventually comprise the daughter strand) as “Okazaki fragments,” named after the biochemist who discovered them. Biochemists call the strand produced discontinuously the “lagging strand,” because DNA replication for this strand lags behind the more rapidly produced leading strand.

    One additional point: The leading strand at one replication fork is the lagging strand at the other replication fork, since the replication forks at the two ends of the replication bubble advance in opposite directions.

    Before the newly formed daughter strands can be produced, a small RNA primer must be produced. The protein that synthesizes new DNA by reading the parent DNA template strand—DNA polymerase—can’t start production from scratch. It has to be primed. A massive protein complex, called the primosome, which consists of more than 15 different proteins, produces the RNA primer needed by DNA polymerase.

    Once primed, DNA polymerase will continuously produce DNA along the leading strand. However, for the lagging strand, DNA polymerase can only generate DNA in spurts to produce Okazaki fragments. Each time DNA polymerase generates an Okazaki fragment, the primosome complex must produce a new RNA primer.

    Once DNA replication is completed, the RNA primers are removed from the continuous DNA of the leading strand and the Okazaki fragments that make up the lagging strand. A protein called a 3’–5’ exonuclease removes the RNA primers. A different DNA polymerase fills in the gaps created by the removal of the RNA primers. Finally, a protein called a ligase connects all the Okazaki fragments together to form a continuous piece of DNA out of the lagging strand.

    DNA Replication and the Case for Evolution

    This cursory description of DNA replication clearly illustrates the complexity of this biochemical operation. (Many details of the process were left out of the discussion.) This description also reveals why biochemists view this process as cumbersome and unwieldy. There is no obvious reason why DNA replication proceeds as a semi-conservative, RNA primer-dependent, unidirectional process involving leading and lagging strands to produce DNA daughter molecules. Because of this uncertainty, skeptics view DNA replication as a chance outcome of a historically contingent process, kludged together from the biochemical leftovers of the RNA world.

    If there is one feature of DNA replication that is responsible for the complexity of the process, it is the directionality of DNA replication—from top to bottom. At first glance, it would seem as if the process would be simpler and more elegant if replication could proceed in both directions. Skeptics argue that the fact that it doesn’t reflects the evolutionary origin of the replication process.

    Yet work by the team from Sapporo, Japan indicates that there is an exquisite molecular rationale for the directionality of DNA replication.

    Why DNA Replication Proceeds in a Single Direction

    These researchers recognized an important opportunity to ask why DNA replication proceeds only in a single direction with the discovery of a class of enzymes that add nucleotides to the ends of transfer RNA (tRNA) molecules. (tRNA molecules ferry amino acids to the ribsosome during protein synthesis.) If damaged, tRNA molecules cannot properly carry out their role in protein production. Fortunately, there are repair enzymes that can fix damaged tRNA molecules. One of them is called Thg-1-like protein (TLP).

    TLP adds nucleotides to damaged ends of tRNA molecules. But instead of adding the nucleotides top to bottom, the enzyme adds these subunit molecules to the tRNA bottom to top, the opposite direction of DNA replication.

    By determining the mechanism employed by TLP during bottom-to-top nucleotide addition, the researchers gained important insight into the constraints of DNA replication. As it turns out, bottom-to-top addition is a much more complex process than the normal top-to-bottom nucleotide addition. Bottom-to-top addition is a cumbersome two-step process that requires an enzyme with two active sites that have to be linked together in a precise way. In contrast, top-to-bottom addition is a simple, one-step reaction that proceeds with a single active site. In other words, DNA replication proceeds in a single direction (top-to-bottom) because it is mechanistically simpler and more efficient.

    One could argue that the complexity that arises by the top-to-bottom DNA replication process is a trade-off for a mechanistically simpler nucleotide addition reaction. Still, if DNA replication proceeded in both directions the process would be complex and unwieldy. For example, if replication proceeded in two directions, the cell would require two distinct types of primosomes and DNA polymerases, one set for each direction of DNA replication. Employing two sets of primosomes and DNA polymerases is clearly less efficient than employing a single set of enzymes.

    Ironically, if DNA replication could proceed in two directions, there still would be a leading and a lagging strand. Why? Because bottom-to-top replication is a two-step process and would proceed more slowly than the single step of top-to-bottom replication. In other words, the assembly of the DNA strand in a bottom-to-top direction would lag behind the assembly of the DNA strand that traveled in a top-to-bottom direction.

    Bidirectional DNA replication would also cause another complication due to a crowding effect. Once the replication bubble opens, both sets of replication enzymes would have to fit into the replication bubble’s constrained space. This molecular overcrowding would further compromise the efficiency of the replication process. Overcrowding is not an issue for unidirectional DNA replication that proceeds in a top-to-bottom direction.

    The bottom line: In light of this new insight, it is hard to argue that DNA replication has been cobbled together via a historically contingent pathway. Instead, it is looking more and more like a process ingenuously designed by a Divine Mind.

    Resources
    The Cell’s Design: How Chemistry Reveals the Creator’s Artistry by Fazale Rana (book)
    DNA Soaks Up Sun’s Rays” by Fazale Rana (article)
    DNA: Designed for Flexibility” by Fazale Rana (article)
    How the Central Dogma of Molecular Biology Points to Design” by Fazale Rana (article)
    Why I Believe God Exists: Evidences from a Biochemist” by Fazale Rana (video)

    Endnotes
    1. Shoko Kimura et al., “Template-Dependent Nucleotide Addition in the Reverse (3–5) Direction by Thg1-like Protein,” Science Advances 2 (March 2016): e1501397, doi:10.1126/sciadv.1501397.
  • Can New Medical Technology Boldly Go Where No Man Has Gone Before?

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Nov 02, 2016

    When I was in junior high, I would rush home every day after school to tune in to the afternoon reruns of Star Trek.

    Fascinated by the technology possessed by the crew of the Enterprise, I often imagined what it would be like if I had their high-tech devices.

    I was particularly intrigued by the tricorder Spock used to collect readings when the team beamed down to a planet’s surface. As a professional biochemist, I really came to appreciate the powerful technology Spock had at his fingertips. Gaining even cursory insight into a biochemical sample can take weeks of hard work in the lab. But for Spock, pointing the tricorder in the direction of the alien life-form was all he had to do. Of course, Spock didn’t get to have all the fun.

    Dr. McCoy had a tricorder too. His instrument could be used to diagnose sick and injured crew members by simply passing a wand over the patients. Wouldn’t it be great if physicians could diagnosis our ailments so quickly and easily? No more trips to the doctor’s office. No more late-night excursions to the emergency room.

    Well, science fiction is about to become science fact, thanks to work by engineers from Washington University. These researchers developed a smart phone app that can measure hemoglobin concentration in a patient’s blood after the patient presses his/her finger against the phone’s camera.1

    This new technology represents an important advance in medical screening, allowing physicians to quickly test for anemia. This blood disorder is rampant in the developing world, caused by malnutrition and parasite infections.

    Measuring the blood’s oxygen-carrying capacity is key for diagnosing anemia. Detecting and monitoring anemia can be difficult in a third-world context, because the most reliable method for determining the oxygen-carrying capacity of blood involves drawing blood and counting red blood cells. This procedure: (1) exposes medical workers to the patient’s blood; (2) runs the risk of being unsanitary, introducing the risk of infection; and (3) requires access to a laboratory to count the red blood cells.

    Noninvasive methods exist, but they require expensive medical instruments.

    These limitations motivated the University of Washington team to develop the smart phone app to measure hemoglobin content in blood. This technology is relatively inexpensive, mobile, and can yield rapid results—ideal for screening for anemia in the field.

    HemaApp

    The University of Washington team dubbed their app: HemaApp. The app makes use of an algorithm that converts video images of the patient’s finger into a series of oscillating curves corresponding to different wavelengths of light. The form of these curves is influenced by the absorption of light by hemoglobin in the blood (which causes blood’s red color). The more hemoglobin, the greater the blood’s light absorption at certain wavelengths of light.

    In a pilot study (involving men and women, patients of all ages, and several ethnicities), the researchers showed that HemaApp performed as well as the leading noninvasive blood monitoring technologies, paving the way to use this technology in the field.

    These researchers think that their accomplishments are the first step toward broader usage of smart phones for medical screening. It is conceivable that the technology can be adapted to screen for sickle-cell anemia, which is caused by mutations to the gene encoding hemoglobin. These mutations lead to hemoglobin with a distorted structure, which alters its light absorption spectrum.

    This technology will also be a benefit to people living in the first world. Patients with anemia can monitor the hemoglobin level of their blood at home, providing them with a tool to more effectively manage their health issues. Because the hemoglobin measurements are made with a smart phone, the data can be easily sent to the patient’s physician.

    HemaApp isn’t quite as impressive as a medical tricorder, but it sure is a big step in that direction.

    Yet, as promising as the biomedical implications are for this advance, the bioethical implications are even more exciting.

    Biomedical Technology, Bioethics, and Social Justice

    Many Christians are vigilant about the ethical implications associated with biomedical advances, raising concerns when technologies undermine the sanctity of human life.

    Yet, a neglected area of bioethics relates to the accessibility of medical care and emerging biomedical technologies. Many diagnostic tools and medical procedures require highly specialized equipment and highly trained personnel. These requirements sometimes render even the most basic medical care so costly that only a relatively small percentage of the world’s population has access to life-saving biomedical technologies.

    In my view, the inequitable distribution of medical care should be considered as much a pro-life issue as the destruction of human embryos associated with many emerging biotechnologies or euthanasia. Like all Christians, I hold the view that all human life has immeasurable value—inherent worth and dignity—because all human beings are made in God’s image. If so, then it is reasonable to think that all human beings have fundamental human rights. And, in my view, that includes equal access to basic medical care. And ideally, beyond that, all human beings should be able to equally benefit from biomedical advances.

    The use of smartphones as a medical screening tool moves us one step closer to realizing this ideal. HemaApp stands as a powerful new biomedical technology, but it is affordable and portable. These features make it possible for the wealthiest and poorest people on the planet to benefit from this advance. In fact, this technology could be transformative for some of the poorest parts of the world by helping medical workers quickly identify and treat those people suffering from anemia.

    The University of Washington researchers bring us one step closer to the dream of a young teenager who loved to watch Star Trek. They are also making it possible to envision how, as human beings, we can boldly go where no one has gone before—to a world where biotechnology provides treatments and therapies for many horrible diseases and injuries and also makes basic medical care accessible to the worlds poor.

    Resources

    Embryonic Stem Cell Research: An Interview with Dr. Fazale ‘Fuz Rana” (article)
    Q&A: Is a New in vitro Fertilization Method Ethical?” by Fazale Rana (article)
    GNINOLC: We Have It All Backwards” by Fazale Rana (article)
    Advance Holds Potential to Resolve Cloning’s Ethical Challenges” by Fazale Rana (article)

    Endnotes
    1. Edward Jay Wang et al., “HemaApp: Noninvasive Blood Screening of Hemoglobin Using Smartphone Cameras,” Proceedings of the 2016 ACM International Joint Conference on Pervasive and Ubiquitous Computing (September 2016): 593–604, doi:10.1145/2971648.2971653.
  • Placenta Optimization Shows Creator's Handiwork

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Oct 19, 2016

    The Creator of the universe desires an intimate relationship with each of us.

    It is one of the more outrageous claims of the Christian faith. And no passage of Scripture expresses the intimacy between Creator and creature more than Psalm 139:13.

    A fresh perspective on this passage of Scripture comes from recent work by researchers from Cambridge University in the UK. This study reveals the central role the placenta plays in properly allocating nutritional resources between mother and child, illustrating the intimate care God provided for us through the elegant design of embryological development.1

    This research also has important pro-life implications, providing a response to the claim that the fetus is nothing more than a harmful mass of tissue.

    Nutritional Demands of the Fetus and the Mother

    For a pregnancy to be successful, nutrients must be carefully distributed between the fetus and the mother. Yet sharing nutrients runs contrary to the biological tendencies of the mother and the unborn baby. The fetus has a genetic drive for growth and craves all the nutrients it can get. So does the mother. But for the fetus to grow and develop, the mother must provide it with the nutrients it needs, setting up a potential tug of war between the mother and the developing baby in her womb.

    Ironically, if the fetus hoards nutrients excessively, the hoarding can backfire. If the mother doesn’t have access to sufficient nutrients during the pregnancy, it can negatively impact lactation and the mother’s long-term health, which, in turn, compromises her ability to care for the child after birth.

    As it turns out, the placenta plays a critical role in managing this trade-off. Instead of being passive tissue that absorbs available nutrients from the mother, the placenta dynamically distributes nutrients between mother and fetus, optimally ensuring the health of both mother and developing baby. To do this, the placenta receives metabolic signals from both the mother and fetus and responds to this input by regulating the nutrient amounts made available to the fetus.

    One of the key genes involved in nutrient regulation is called p110α. This gene codes for a protein that integrates the metabolic signals from mother and fetus. The Cambridge University researchers wanted to understand the role that the maternal and fetal versions of this gene play in parsing the nutrient supply between mother and developing baby.

    What Happens When p110α Is Defective in Mother and Child?

    What happens when p110α is defective in mother and child? To answer this question, the research team used mice as a model system, preparing genetic mutants, so that either the mother or fetus had a defective version of the p110α gene. If the mother had a healthy p110α gene, but the fetus a defective version, the placenta developed abnormally. But in spite of its defective appearance, the placenta compensated so that it would still take up the nutrients the fetus needed to develop. However, if the mother had a defective version of the p110α gene, the placenta (which formed abnormally even though the fetus had a healthy version of the p110α gene) transported fewer nutrients to the fetus.

    In adult tissue, the p110α gene plays a role in regulating growth in relationship to nutrient supply and mediates the metabolic effects of insulin and insulin-like growth factors. That means that a defective version of this gene models conditions in which the mother’s health is compromised due to disease, poor nutrition, stress, or other factors.

    On the basis of this study, it appears that when the mother is healthy, the placenta readily transports nutrients to the fetus and dynamically adjusts, even if it forms abnormally. On the other hand, if the mother’s health is compromised, the placenta restricts nutrient flow to the fetus to ensure the mother’s long-term health, with the prospects that the fetus can still grow and develop.

    This insight has important biomedical implications. In the developing world, one in five pregnancy complications involve the placenta. In the developed world, this number is one in eight. The researchers hope that this insight will help them understand the etiologies behind problem pregnancies and also help them identify biomarkers that will alert physicians to problems earlier in the pregnancy.

    This work also has important apologetics implications, as well.

    Indeed, We Are Fearfully and Wonderfully Made

    This work highlights the elegance of embryological development. It seems an exquisite rationale—a biological logic, if you will—undergirds every aspect of development. The optimal way the placenta partitions resources between mother and fetus, carefully managing trade-offs, evinces the handiwork of the Creator, and reveals the Creator’s intimate care for the fetus.

    The devastating effects caused by mutations to the p110α gene raises questions about the capacity of evolutionary mechanisms to explain the origin of the reproductive system in placental mammals. Because the placenta is not a passive conduit for nutrients between mother and fetus, the challenges of explaining its genesis via unguided evolutionary process become insurmountable. If the placenta lacks the capability to effectively allocate resources between the mother and fetus—or even if this process operates in a suboptimal manner—the fetus may not survive, or the mother may not be healthy enough to nurse and rear the child once it’s born. In other words, it becomes difficult to imagine how the placenta’s role in embryological development could evolve from an imperfect system to an optimal system under the influence of natural selection because of the critical, dynamic role the placenta plays in embryological development. If this role isn’t properly executed, the child isn’t likely to make it to reproductive age.

    Is the Fetus Like a Tumor?

    This work also has implications for the pro-life debate. I have often heard pro-choice advocates argue that abortion is not murder, because the fetus is like a tumor. But the work by the scientists from Cambridge University makes this view impossible. Because the placenta dynamically allocates resources between the mother and the fetus in a way that preserves the mother’s health, the fetus cannot be viewed as a tumor robbing the mother of nutrients. Instead, it looks as if the placenta’s function has been designed in such a way to ensure optimal health for both the mother and the fetus. This study also shows that if the mothers health is in jeopardy, the placenta actually compromises the health of the fetus so that the mother’s health is not unduly harmed by the pregnancy.

    Resources
    Curvaceous Anatomy of the Female Spine Reveals Ingenious Obstetric Design” by Virgil Robertson (article)
    What Are the Odds of You Being You? by Matthew McClure (article)
    Morning Sickness May Protect Embryos from Toxins with Fazale Rana (podcast)

    Endnotes
    1. Amanda Sferruzzi-Perri et al., “Maternal and Fetal Genomes Interplay through Phosphoinositol 3-Kinase (PI3K)-p110α Signaling to Modify Placental Resource Allocation,” Proceedings of the National Academy of Sciences, USA 113 (October 2016): 11255–60, doi:10.1073/pnas.1602012113.
  • Does Oxytocin Cause Spiritual Experiences?

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Oct 12, 2016

    Why do people believe in God?

    In 1998, Michael Shermer, the founding publisher of Skeptic magazine, and sociologist Frank Sulloway sought to answer this “Why?” question. Surveying 10,000 individuals from the United States, Shermer and Sulloway learned that nearly 30 percent said the beauty, design, and complexity of the universe justified belief in God, and nearly 20 percent said they were convinced of God’s existence because they experienced God in everyday lives.

    In many ways, this finding isn’t surprising—if Christianity is true. Both the Old and New Testaments teach that God has made himself known through creation. This revelation would be reflected in the beauty, design, and complexity of the natural realm. Scripture also teaches that the Holy Spirit draws nonbelievers to Christ and intervenes in the life of believers.

    In other words, according to this survey, many people hold to belief in God for both rational and experiential reasons.

    Still, a number of skeptics argue that belief in God is a biological phenomenon, exclusively. They maintain that people who believe in God delude themselves into thinking that they hold their belief for rational reasons. Skeptics argue that belief in God instead has to do more with our biology than anything else.

    In 2005, human geneticist Dean Hamer created quite a stir when he published The God Gene. In this book, he claims to have discovered an association between the VMAT2 gene and self-transcendence, a composite of three psychological attributes that presumably reflect an individual’s propensity toward spirituality. As a result of his research, Hamer dubbed VMAT2 “the God gene.” (The VMAT2 gene encodes a membrane-embedded protein that transports monoamines, such as serotonin and dopamine, from the cytosol of nerve cells into synaptic vesicles.) Hamer claims this discovery helps explain why spirituality is heritable and suggests there is a genetic, and, hence, strictly biological basis for why some people believe in God and why others don’t. In other words, our spirituality is biologically determined.

    Added to this claim is recent work by researchers from the University of North Carolina at Chapel Hill (UNC).1 These investigators claim that when men are administered oxytocin, they develop a heightened orientation toward spirituality and enhanced positive experiences during religious practices, such as meditation. (They define spirituality as the feeling of being connected to other living things and to a higher power.) These responses to oxytocin occurred for both believers and nonbelievers alike, and most closely correlate to variants of two genes that encode proteins involved in the release of oxytocin from the hypothalamus and its transmission between neurons. In other words, the subjects’ responses to oxytocin had more to do with their genetics than their beliefs about God’s existence. The researchers conclude that the growing evidence indicates that “humans—and perhaps some more than others—are biologically predisposed to be receptive to spiritual experiences.”2

    Prior to this study, neuroscientists had indirect evidence that oxytocin release impacted spirituality. For example, researchers observed that people who had transformative religious experiences had elevated levels of oxytocin in their blood. But, thanks to this latest study, a causal connection between oxytocin release and spiritual experience has been established.

    Oxytocin’s Physical Effects

    Oxytocin is a peptide produced by the hypothalamus. This compound serves as a hormone when released into the bloodstream and a neurotransmitter when released into the forebrain.

    Oxytocin has been nicknamed the “love hormone” and the “cuddle chemical.” Exposure to oxytocin enhances empathy and trust. Exposure also reduces self-focus and elicits altruistic responses. To put it another way, oxytocin exposure promotes social bonding.

    This compound is also released during childbirth and breast-feeding, helping mothers and infants to bond. It is also released during sex, promoting a connection between lovers.3

    Does Oxytocin’s Role in Spiritual Experiences Invalidate the Christian Faith?

    Does oxytocin’s role in spiritual experiences invalidate the Christian faith? Hardly. In fact, this discovery and previous work identifying the role oxytocin plays in social bonding, mother-infant bonding, and bonding between mates makes perfect sense within a Christian worldview.

    In his book The Biology of Sin, neuroscientist Matthew Stanford presents a model that helps make sense of these types of discoveries.4 Stanford points out that Scripture teaches that human beings are created as both material and immaterial beings, possessing a physical body and nonphysical mind and spirit. Instead of being a “ghost in the machine,” our material and immaterial natures are intertwined, interacting with each other. It is through our bodies (including our brain), that we interact with the physical world around us. The activities of our brain influence the activities of our mind (where our thoughts, feelings, and emotions are housed), and vice versa. It is through our spirit that we have union with God. Spiritual transformation can influence our brain’s activities and how we think, and how and what we think can influence our spirit.

    If God created human beings to (1) be in a relationship with him, (2) form monogamous relationships with the opposite sex, (3) multiply and fill the Earth, and (4) be in community with one another, wouldn’t it make sense that he would have created biological mechanisms to ensure bonding between members of a community, between mother and child, between husband and wife, and between each of us and God? Oxytocin appears to be just such a mechanism. Having a biological mechanism that promotes bonding between members of a community, between mothers and children, and between husbands and wives makes added sense when considering how difficult these relationships are. Oxytocin’s influence ensures that parents won’t abandon their children when they become a burden. It helps marriages remain intact during challenging times in the relationship.

    But what about the observation that some people seem to have a greater biological propensity for spiritual experiences than others? Doesn’t that seem unfair? Does that mean that God created some people to respond to him and others not to?

    This question assumes that the only basis for belief is spiritual experience. There are rational reasons to think God exists. Scholars have developed compelling philosophical and scientific arguments for God’s existence. There is historical and archaeological evidence that supports the credibility of the Old and New Testaments. A powerful case can be made for the historicity of Christ, including his death and resurrection. Scripture also teaches that God has written his law on our hearts. We know there is an inherent right and wrong, and we are well aware that we don’t conform to that standard. In other words, even if we don’t have a propensity for spiritual experiences at all, we still have the capacity to recognize the truth of the Christian faith and our desperate need for forgiveness. Whether we have spiritual experiences or not, we all have the ability to understand and respond to the gospel.

    Scripture teaches that each person possesses a unique set of gifts. Each of us has distinct strengths and weakness. Scripture also teaches that when we come together, each of our gifts contribute to the community, and our collective strengths and weaknesses complement each other. If what Scripture teaches on this point is true, wouldn’t we expect God to create humans (as a population) with biological variability? I know many Christians for whom the life of the mind is far more important to their faith than spiritual experiences. I also know many Christians for whom religious experiences are central to their faith. Both types of people play critical roles in the church. To put it another way, our Creator may have had good reasons to design humans with varying biological propensities to spirituality.

    One final point: Skeptics need to be careful when they assert that oxytocin release into the forebrain causes spiritual experiences, and, ultimately, conclude that belief is a biological phenomenon. The knife cuts both ways. If belief in God has a strictly biological basis, that means so does atheism. In other words, atheists can’t claim that they reject belief in God for rational reasons, or because they have superior intellect. In their model, they are just as much victims of their biology as they claim Christians are.

    Resources

    Magnets and Morality” by Fazale Rana (article)
    Does Human Morality Arise from Brain Chemistry?” by Fazale Rana (article)
    Is There a Biological Basis for Belief?” by Fazale Rana (article)
    Is There a Biological Basis for Belief? A Follow Up” by Fazale Rana (article)
    Epigenetics—Sins of the Father” by Fazale Rana (article)
    Sex Does Bring a Man Closer to God—Science Is Proving It!” with Fazale Rana (a Wenz World radio interview)

    Endnotes
    1. Patty Van Cappellen et al., “Effects of Oxytocin Administration on Spirituality and Emotional Responses to Meditation,” Social, Cognitive, and Affective Neuroscience 11 (June 2016): 1579–87, doi:10.1093/scan/nsw078.
    2. Ibid.
    3. This observation prompted the headline “Having Sex Makes Men More Likely to Believe in God.” It is tempting to inquire if the converse is true.
    4. Matthew Stanford, The Biology of Sin: Grace, Hope, and Healing for Those Who Feel Trapped (Downers Grove, IL: InterVarsity Press, 2010), 15–19.
  • Q&A: Is Evolution Falsifiable?

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Oct 05, 2016

    I expected to get a reaction—and I did.

    Last week I posted the below ‘meme’ on my Facebook page and Twitter account, claiming that the evolutionary paradigm is unfalsifiable because of the stranglehold that methodological naturalism has on the operation of science.

    blog__inline--is-evolution-falsifiable-1

    And of course, it elicited a rather negative reaction by at least one atheist who listed a number of ways to falsify biological evolution, delineated by evolutionary biologist Jerry Coyne.

    So, is biological evolution falsifiable? Was it unwarranted on my part to claim that biological evolution is unfalsifiable? Am I “full of it,” as this skeptic asserted?

    My response: In principle, chemical and biological evolution are falsifiable, as are all scientific theories. But in reality, the evolutionary paradigm is unfalsifiable—because of the influence of methodological naturalism.

    In effect, methodological naturalism restricts the available explanations for the universe and phenomena within the universe such as the origin and history of life. Certain explanations are off the table, a priori. As a consequence, intelligent design/creationism cannot be part of the construct of science.

    The Effect of Methodological Naturalism on Scientific Inquiry

    Methodological naturalism provides the philosophical framework for science. This concept is distinct, yet related to philosophical naturalism. According to philosophical naturalism, all that exists is the material, physical universe. There is no supernatural. There is no reality outside of the universe itself. There is no God. As the late astronomer Carl Sagan once quipped, “The cosmos is all that is, or ever was, or ever will be.”

    In contradistinction to philosophical naturalism, methodological naturalism claims to be metaphysically neutral on the question of God’s existence. According to the tenets of methodological naturalism, when one engages in the scientific enterprise it is necessary to suspend belief in God, regardless of one’s personal convictions. The only allowed explanations for the universe and phenomena within the universe are natural process, mechanistic explanations. One cannot appeal to the supernatural. But that doesn’t mean the supernatural doesn’t exist. Simply put, the supernatural is not given a place in the scientific project.

    In other words, if you believe that God exists, your views cannot influence the way in which you conduct science. Methodologically speaking, you must function as if God does not exist. Sometimes methodological naturalism is called provisional atheism or benchtop atheism. This restriction makes methodological naturalism functionally equivalent to philosophical naturalism, rendering science an inherently atheistic enterprise, though, again, its practitioners may well believe God exists.

    In effect, methodological naturalism restricts the available explanations for the universe and phenomena within the universe such as the origin and history of life. Certain explanations are off the table, a priori. As a consequence, intelligent design/creationism cannot be part of the construct of science. Any explanation that states an intelligent agent is responsible for, say, the origin of life, is prohibited. As a result, chemical and biological evolution are the only available alternatives for someone who’s trying to scientifically account for the origin and history of life.

    The net effect is this: Chemical and biological evolution are true by default, regardless of the evidence at hand. No matter how much evidence exists challenging the evolutionary paradigm, it cannot be supplanted because there is no other alternative explanation that is allowed.

    A Failed Prediction for the Evolutionary Paradigm

    As it turns out, discordant phylogenies plague evolutionary biologists. On this basis alone, one could conclude that the evolutionary paradigm has been falsified.

    As an illustration of this point, consider one of the ways that Jerry Coyne thinks biological evolution can be falsified:

    “Complete discordance between phylogenies based on morphology/fossils and on DNA. While individual genes can show discordance by lateral transfer—rotifers, for example, have incorporated into their genome from DNA from very unrelated organisms, and this is also common for bacteria. But lateral transfer of genes, as opposed to their direct descent from parent to offspring, is relatively uncommon. So, for example, if we sequenced the genome of a blue whale and found that on the whole the species was more closely related to fish than to mammals, we’d have a serious problem for the theory of evolution.”

    Coyne’s prediction is similar to one made by the late evolutionary biologist Morris Goodman. According to Goodman, one of the founders of the discipline of molecular anthropology:

    “If the biblical account of creation were true, then independent features of morphology, proteins, and DNA sequences would not be expected to be congruent with each other. Chaotic patterns, with different proteins and different DNA sequences failing to indicate any consistent set of species relationships, would contradict the theory of evolution.”1

    As it turns out, discordant phylogenies plague evolutionary biologists. It is not uncommon for evolutionary trees built from morphological features to disagree with evolutionary trees built from DNA sequence data. Again, it is not uncommon for molecular phylogenies to disagree with one another when constructed using different regions of the genome. (For examples, see the articles listed below under Resources.) On this basis alone, one could conclude that the evolutionary paradigm has been falsified—or at minimum one would be justified to express skepticism about the capacity of the evolutionary paradigm to account for the origin, history, and design of life.

    Again, these are not predictions made by intelligent design proponents or creationists. These are predictions made by evolutionary biologists, both of whom are (or were) skeptics. And on the basis of these predictions, the evolutionary paradigm has failed.

    But Wait—Not So Fast

    How do evolutionary biologists respond to the pervasive problem of discordant phylogenies?

    By arguing that the discordance can be dismissed because morphological data is an unreliable indicator of evolutionary history. How do they know this is the case? Because morphological and molecular phylogenies disagree.

    Or they claim that the discordance results from incomplete lineage sorting. How do they know incomplete lineage sorting has occurred? Because evolutionary trees built using different genes (or genomic regions) disagree.

    Another way evolutionary biologists dismiss the discordant trees is to assert that some regions of the genomes are phylogenetically uninformative. That is, these regions of the genome don’t issue a phylogenetically reliable signal. How do evolutionary biologists know this to be the case? Because evolutionary trees built from certain regions of the genome don’t yield the expected results—and consequently, produce discordant phylogenies.

    These responses are classical instances of circular reasoning. In effect, evolutionary biologists are using discordant evolutionary trees as a way to explain why discordant evolutionary trees result when they attempt to build phylogenies using different data sets.

    Is Evolution Falsifiable?

    Why the circular reasoning? Because if one adheres to methodological naturalism, the only valid scientific explanation for the origin and history of life is through some type of evolutionary process. Evolution must be true by default. Why? Because if the evolutionary paradigm is falsified, then the only other alternative is intelligent design/creationism. And this approach to biology is prohibited, a priori, because of philosophical commitments to a materialistic approach to the life sciences. This state of affairs can only lead to tautologies when failed predictions arise, though the tautologies are draped in scientific jargon.

    So, is biological evolution falsifiable? Yes, in principle. But no, in reality.

    I suspect that when evolutionary biologists list “if-they-are-true” observations that would disprove biological evolution, it doesn’t mean they are necessarily willing to consider another paradigm. Because if they were, they would readily see the evolutionary paradigm’s many shortcomings.

    Resources

    Origin of Complex Cells: A Big Event for Evolution or Creation?” by Fazale Rana (article)
    DNA Sequences: More Is Not Better” by Fazale Rana (article)
    Birds Terrorize Evolutionary Biologists” by Fazale Rana (article)

    Endnotes
    1. Morris Goodman, “Reconstructing Human Evolution from Proteins,” chap. 8.4 in The Cambridge Encyclopedia of Human Evolution, Steve Jones et al., eds. (New York: Cambridge University Press, 1993), 307–13.
  • Science News Flash: First Three-Parent Baby Born

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Sep 29, 2016

    Shocking headlines from around the world have announced the first-ever birth of a baby with three parents (two mothers and one father)!

    The research team who carried out this work will report the details about the conception and birth of this child at next month’s meeting of the American Society for Reproductive Medicine, to be held in Salt Lake City.1

    Born to Muslim parents, this baby was conceived without destroying any embryos in the process. Fertilization took place in a test tube using the father’s sperm cells and a donor’s egg. Prior to fertilization, the researchers removed the nucleus from the donor’s egg and replaced it with the nucleus from one of the mother’s egg cells. In other words, the fertilized egg had genetic material from two women. The nuclear DNA came from the mother-to-be and the DNA in the egg’s mitochondria came from the donor.

    This procedure ensured that the child would be free from the devastating effects of a mutated gene in the mother’s mitochondrial DNA that causes Leigh syndrome.

    This procedure holds the potential to eradicate hundreds of genetic disorders caused by mutations to mitochondrial DNA. Mitochondria play a key role in energy production for the cell. If these organelles aren’t healthy, it can lead to a number of devastating neurodegenerative and muscular degenerative disorders.

    How should Christians think about this exciting new biotechnology? Is it ethical? Will it lead to designer babies? Should we play God?

    My answers to these questions might surprise you…

    For details about this technique and my thoughts on how Christians should respond to this biomedical discovery, check out the February 25, 2014 edition of Science News Flash (podcast).

    Resources

    Designer Babies?” by Fazale Rana (podcast)

    Endnotes
    1. J. Zhang et al., “First Live Birth Using Human Oocytes Reconstituted by Spindle Nuclear Transfer for Mitochondrial DNA Mutation Causing Leigh Syndrome,” Fertility and Sterility 106 (September 2016): e375–e376, doi:10.1016/j.fertnstert.2016.08.004.
  • Did Neanderthals Make Jewelry?

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Sep 28, 2016

    I was a troublemaker in high school. And that meant I spent more than my fair share of time in Mr. Reynold’s office—our school’s vice principal.

    It wasn’t long before we developed a bit of a dance that played out each time I was summoned to his office. Mr. Reynolds would accuse me of some misdeed (for which he usually had ample evidence) and I would respond with an elaborate defense, hoping to convince him of my innocence. I quickly learned that if my excuse was to stick, every detail of my story had to hang together.

    A few days ago, I was reminded of my conversations with Mr. Reynolds when I learned about recent work by a large team of collaborators from the US, UK, Germany, and France. Based on their research efforts, these paleoanthropologists claim to have new evidence that Neanderthals produced body ornaments and, hence, possessed the capacity for symbolism and advanced cognitive abilities—just like us.1 Yet, this story doesn’t hang together when considering other details about Neanderthal biology and natural history.

    Take it from someone who has experience concocting stories—the claim that Neanderthals displayed symbolism doesn’t pan out.

    The Grotte du Renne Cave Site

    During a recent visit to the well-studied Grotte du Renne cave site in central France, these research collaborators unearthed previously unknown hominid bone fragments. These pieces of bones were morphologically nondescript. Yet these investigators found the bones to be highly informative, thanks to the application of newly developed, sophisticated techniques that allowed them to characterize ancient protein and mitochondrial DNA fragments associated with the bones. These ancient biomolecules indicated that the bones came from a Neanderthal infant.

    This discovery is significant because these newly discovered bone fragments were recovered in the same layers that contain beads made from animal teeth, shells, and ivory. These “necklaces” serve as markers for symbolic capacity—a property that many people think defines modern humans. Symbolic capacity is a behavioral feature that causes a number of anthropologists to think that modern humans are behaviorally unique and exceptional.

    The Grotte du Renne site contains 15 archaeological layers spanning about 12 feet in depth. Neanderthals and modern humans occupied this cave at various times between 28,000–45,000 years ago. The top layers—which are the most recent—contain artifacts produced by modern humans. However, the most interesting layers are VIII, IX, and X. These layers contain Neanderthal remains, with layer X harboring markers for symbolism. This layer dates to about 40,000 years in age. If this data is accepted at face value, it indicates that these hominids evolved the capacity for symbolic behavior and possessed advanced cognitive abilities just before their extinction.

    Neanderthals appeared about 250,000 years ago and became extinct around 40,000+ years ago. The archaeological record indicates that for most of their existence Neanderthals behaved in a relatively unsophisticated manner compared to modern humans. (This behavior is described as the Mousterian culture.) However, based on the findings from the Grotte du Renne, some paleoanthropologists have argued that around 40,000 years ago—the time of modern humans’ arrival in Europe and right before Neanderthals’ disappearance—these hominids evolved the capacity for modern behavior and with it, symbolic thought. (Paleoanthropologists refer to this behavior as the Châtelperronian culture.)

    Neanderthal Symbolism and the RTB Human Origins Model

    The existence of the Châtelperronian culture means that modern humans aren’t behaviorally unique. From an evolutionary vantage point, it implies that advanced cognitive abilities evolved independently in modern humans and Neanderthals (with the antecedents for symbolism residing with the direct evolutionary ancestor of modern humans and Neanderthals).

    If this insight stands, it undermines the view of humanity espoused by Scripture—namely, that human beings uniquely bear God’s image—and, specifically the RTB human origins model (detailed in the expanded and updated edition of Who Was Adam?), which regards symbolism as an aspect of the image of God.

    So what did this research team discover and what conclusions can they legitimately draw from their discoveries?

    It is also worth noting that every previous claim for Neanderthal symbolism from the archaeological record has failed to withstand scientific scrutiny.

    Characterization of the Grotte du Renne Bone Fragments

    The research team saw the discovery of the morphologically indistinct bone fragments in layer X as an opportunity to try out new methods they recently developed, designed to recover and characterize ancient protein fragments from fossil specimens. They hope that these fragments (which are much more likely to be present in ancient bones than DNA) will provide insight into the taxonomic identity of the bone fragments, but also help scientists gain insight into the biology and natural history of ancient organisms. (The study of ancient proteins is called paleoproteomics).

    Early work in paleoproteomics demonstrates that fragments of certain forms of collagen can be used to identify large bodied genera. These researchers extracted proteins from 196 bone fragments found in layer X. Of those, 28 possessed a collagen fingerprint that identified them as coming from a hominid.

    The researchers then extracted more than 70 different proteins from 3 of the 28 bone pieces. As is true for all studies involving ancient biomolecules, contamination by biomolecules from the environment and human handlers is a real concern. Because of this complication, the researchers employed an elaborate set of steps to discriminate endogenous proteins from contaminants, including:

    • Analyzing extraction blanks: Proteins found in both the blanks and samples must be contaminants introduced in the handling of the bones.
    • Assessing chemical alteration of proteins: As proteins age, they undergo characteristic chemical changes (such as glutamine and asparagine deamidation). Proteins that don’t show these transformations must be contaminants.
    • Searching protein databases: The researchers compared the amino acid sequences of the extracted proteins with amino acid sequences of proteins produced by nonhuman animals. Matches were taken as contaminants.

    Through this process, the researchers discovered a number of collagens and non-collagen proteins that appeared to be authentic. Many of these extracted proteins are produced by cells during bone growth. Isotope analysis of collagen extracted from the hominid bones indicate that they came from an individual whose chief diet was breast milk. On this basis, the researchers concluded that the fragments were from an infant. They then found that the amino acid sequences of the extracted collagens matched collagen amino acid sequences found in both Neanderthals and Denisovans. (The researchers deduced the amino acid sequences of hominid collagens from the Neanderthal and Denisovan genomes.)

    Additionally, the researchers recovered mitochondrial DNA (mtDNA) from one of the bone pieces. The sequence of this DNA aligns with Neanderthal mtDNA, providing confirmatory evidence that the bone fragments came from a Neanderthal.

    Finally, the researchers used carbon-14 dating of extracted collagen to determine the age of the bone pieces at 37,000–39,000 years bp (before the present).

    On the basis of all of these results, they concluded that the bone pieces came from a Neanderthal infant that was buried in the cave around 38,000 years ago, and more broadly that Neanderthals produced the “necklace beads” found in layer X.

    It is important to point out that this is not the first time anthropologists have arrived at this conclusion. Anthropologists have long had evidence from morphologically informative fossils for the co-occurrence of Neanderthal remains and symbolic artifacts in layer X. The novelty of this work centers around the power of paleoproteomics and ancient DNA analysis to provide key insight into the identity of fossil remains and the natural history of ancient creatures.

    Did Neanderthals Display Symbolism?

    Does the co-occurrence of Neanderthal remains and symbolic artifacts in layer X provide evidence for Neanderthal behavior on par with modern humans? It can, but this conclusion has to align with everything else we know about Neanderthal biology and behavior—and it doesn’t.

    For example, previous work by other archaeologists at the Grotte du Renne has demonstrated that the layers in this cave have been mixed. It appears as if past occupants dug into the cave floor, turning over the cave layers. This activity means that the association between Neanderthal remains and symbolic artifacts could merely be coincidental.

    In the face of this challenge, paleoanthropologists could argue that the 37,000–39,000-year-old date of the remains in layer X (determined in the latest study)—which matches the age of the symbolic artifacts—indicates that mixing didn’t impact layer X. Yet within the past few years, paleoanthropologists have shown that carbon-14 dating of Neanderthal remains has been plagued by carbon-14 contaminants, which renders their measured ages younger than they actually are. Improved methodology (designed to remove these contaminants) places Neanderthal extinction around 45,000+ years bp. This well-known contamination issue raises questions about the dating of the Grotte du Renne specimens, leaving open the real possibility that the Neanderthal remains are much older than 38,000 years in age. If so, it makes it likely that mixing of the cave layers did, indeed, occur.

    Apart from the mixing of the Grotte du Renne cave layers and questions about the dating of the Neanderthal remains in layer X, the most significant reason for skepticism about claims regarding Neanderthals’ symbolic capabilities centers around what we have learned about the anatomy and physiology of this hominid’s brain.

    Collectively, these observations indicate that Neanderthals were cognitively inferior to modern humans. It is hard to square these biological differences with claims that Neanderthals displayed symbolism.

    It is true: Neanderthals had a brain size comparable to modern humans (maybe even slightly larger), but as I point out in Who Was Adam?, the body mass of Neanderthals was larger than modern humans. Anthropologists think that the ratio of brain size to body mass is a better indicator of intelligence than brain size alone. This ratio is called the encephalization quotient (EQ). The EQ of modern humans is greater than that of Neanderthals, indicating that these hominids were cognitively inferior to modern humans.

    More importantly, the brain structures of modern human and Neanderthals differ. As discussed in Who Was Adam?, Neanderthals possessed an underdeveloped parietal lobe compared to modern humans. This part of the brain plays a role in processing information that supports language and mathematical reasoning. Also, Neanderthals devoted a greater region of their brain to vision and body control than modern humans. This would have left a smaller portion of the brain available for advanced cognition. Paleoanthropologists have determined that blood flow to Neanderthal brains was significantly lower compared to modern humans, implying that these hominids inherently lacked the capacity to support the same high level of interneuronal connectivity and synaptic activity as modern humans.

    As discussed in Who Was Adam?, comparisons of modern human and Neanderthal genomes also reveal differences in genes involved in neuronal development. This result helps explain the morphological differences between modern human and Neanderthal brains.

    I also point out that studies of Neanderthal dental microanatomy reveal that these creatures had a rapid, practically nonexistent adolescence. This rapid maturation leaves little time for brain development to occur after birth like it does in modern humans.

    Collectively, these observations indicate that Neanderthals were cognitively inferior to modern humans. It is hard to square these biological differences with claims that Neanderthals displayed symbolism.

    Finally, it is worth noting that every previous claim for Neanderthal symbolism from the archaeological record has failed to withstand scientific scrutiny.2 It is unclear if Neanderthals buried their dead, and if they did, these burials most certainly were not ritualistic. Claims of Neanderthal music and art haven’t panned out, and there is no concrete evidence that Neanderthals had language capacity.

    Take it from someone who has experience concocting stories, the claim that Neanderthals displayed symbolism doesn’t hang together. Anthropologists who claim otherwise should be sent to detention during their lunch hour.

    What if the association between Neanderthal remains and symbolic artifacts proves true? There are other ways to explain their co-occurrence. Because Neanderthals and modern humans coexisted for a brief period of time in Europe, it could be that Neanderthals “appropriated” modern human artifacts and carried them to their cave sites. Given everything we know about Neanderthal brain anatomy, this is a much better story than one that has Neanderthals possessing symbolic capabilities.

    Resources
    Who Was Adam? by Fazale Rana with Hugh Ross (book)
    Paleoanthropologists Mixed Up about Neanderthal Behavior” by Fazale Rana (article)
    The Latest on Neanderthal Extinctions” by Fazale Rana (article)
    Did Neanderthals Make Art?” by Fazale Rana (article)
    Did Neanderthals Bury Their Dead with Flowers?” by Fazale Rana (article)
    Do Neanderthal Cave Structures Challenge Human Exceptionalism?” by Fazale Rana (article)
    Neanderthal Brains Make Them Unlikely Social Networkers” by Fazale Rana (article)
    Blood Flow to Brain Contributes to Human Exceptionalism” by Fazale Rana (article)
    Human, Neanderthal Brains Only Differ after Birth” by Fazale Rana (podcast)

    Endnotes
    1. Frido Welker et al., “Palaeoproteomic Evidence Identifies Archaic Hominins Associated with the Châtelperronian at the Grotte du Renne,” Proceedings of the National Academy of Sciences, USA, published electronically September 16, 2016, doi:10.1073/pnas.1605834113.
    2. For more details, see the articles listed in the resource section of this piece and the expanded and updated edition of Who Was Adam?: A Creation Model Approach to the Origin of Humanity.
  • Blood Flow to Brain Contributes to Human Exceptionalism

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Sep 21, 2016

    Are human beings exceptional? Are we unique, as the Bible teaches?

    Recent work by paleoanthropologists from Australia adds to the mounting scientific evidence for human exceptionalism. These scientists demonstrate that modern humans have an unusually high rate of blood flow to our brains, compared to other primates, including the hominids represented in the fossil record.1 They argue that the increased blood flow to the human brain reflects an unusually high level of: (1) neuron-neuron connectivity; and (2) synaptic activity. Ultimately, these enhanced capabilities support the uniquely advanced cognitive capacity displayed by modern humans. To put it differently, the increased blood flow to the modern human brain helps account for the cognitive differences between humans and the other hominids, including Neanderthals.

    This research helps support a key prediction of RTB’s human origins model (derived from the biblical text) by demonstrating a fundamental difference between humans and Neanderthals.

    Measuring Blood Flow to Hominid Brains

    To establish the relative blood flow to the brains of modern humans and hominids, the researchers measured the radius of the opening of two holes at the base of the skull that serve as the entryway for the internal carotid arteries. These blood vessels accommodate about 85 percent of the blood flow to the human brain. These arteries also give rise to the middle cerebral arteries (which supply the lateral portions of the frontal, parietal, and temporal lobes) and the anterior cerebral arteries (which supply the medial parts of the frontal, and parietal lobes).

     

    blog__inline--blood-flow-to-brain-contributes-to-human-exceptionalism-1

    Image: Internal Carotid Artery. Credit: Wikipedia

    These holes in the skull exclusively provide the conduits for the internal carotid arteries. No accompanying nerves or veins pass through these openings. Blood flow and blood pressure controls the radius and the wall thickness of the arteries, making the size of these openings a reasonable proxy for blood flow to the brain.

    Performing measurements only for complete and undamaged skull openings, the researchers determined the radius of the carotid openings for 34 hominid specimens, representing 12 species, including:

    • africanus (8 specimens)
    • afarensis (3 specimens)
    • boisei (1 specimen)
    • habilis (1 specimen)
    • naledi (1 specimen)
    • rudolfensis (1 specimen)
    • georgicus (1 specimen)
    • erectus (5 specimens)
    • heidelbergensis (2 specimens)
    • neanderthalensis (5 specimens)
    • floresiensis (1 specimen)
    • Archaic sapiens (5 specimens)

    Brain Blood Flow in Hominids

    In lower primates, neuron numbers increase with brain mass in a linear manner (because neurons occupy a constant volume). Measurements made in a previous study for 34 haplorhine primates saw brain blood flow scaling with brain volume.

    But the researchers observed something different for the hominids. While the blood flow to the brain scaled with increases in brain volume for the Australopithecines and early Homo species, a different pattern was observed for H. erectus, H. heidelbergensis, and Neanderthals. Increases in cerebral blood grew at a faster pace than expected based on increases in brain size.

    For modern humans, the increase in cerebral blood flow maxes out, even departing further from the trend line observed for the late appearing Homo species. To put it another way, modern humans (H. sapiens sapiens) stand as an outlier, with an unusually high cerebral blood flow, even compared to Neanderthals.

    Differences in Brain Blood Flow between Humans and Neanderthals

    The primate brain possesses an extremely high aerobic demand, requiring prodigious amounts of oxygen. For modern humans, the brain is responsible for 25 percent of our resting metabolic activity. The brain needs a constant supply of oxygen and nutrients (such as glucose). The disproportionate blood flow to the human brain reflects the high level of interneuronal activity and synaptic transmissions between nerve cells.

    Even though Neanderthals had roughly the same brain size as modern humans, the cerebral blood flow to their brain was significantly lower. This observation implies that these hominids inherently lacked the capacity to support the same high level of interneuronal connectivity and synaptic activity as modern humans. This result lines up with a wide range of other findings (detailed in the expanded and updated edition of Who Was Adam?) indicating Neanderthals had limited cognitive capacity compared to modern humans. Collectively, these results justify skepticism regarding claims that these creatures possessed symbolic capability (language, art, music, body ornamentation, etc.).

    Brain Blood Flow and Implications for Human Uniqueness

    This research helps support a key prediction of RTB’s human origins model (derived from the biblical text) by demonstrating a fundamental difference between humans and Neanderthals. Instead of viewing hominids as evolutionary transitional forms, RTB’s biblical model holds that hominids, including Neanderthals, were animals made by God. They possessed intelligence and emotional capacity, but lacked the image of God—a quality associated only with anatomically modern humans (Genesis 1:26–27). Therefore, we expect that Neanderthals would have displayed behavior that is qualitatively different from, and inferior to, that of modern humans. This study provides confirmation of this expectation.

    This study also provides scientific support for the biblical teaching that human beings are uniquely made in God’s image. If human beings truly are image bearers, then we should expect that scientific data would emerge for human exceptionalism, and it has in a way that aligns with the biblical perspective of humanity’s unique cognitive and behavioral capacities.

    Resources
    Who Was Adam?: A Creation Model Approach to the Origin of Humanity by Fazale Rana with Hugh Ross (book)
    Neanderthal Brains Make Them Unlikely Social Networkers” by Fazale Rana (article)
    Did Neanderthals Make Art?” by Fazale Rana (article)
    Did Neanderthals Bury Their Dead with Flowers?” by Fazale Rana (article)
    Do Neanderthal Cave Structures Challenge Human Exceptionalism?” by Fazale Rana (article)
    Human, Neanderthal Brains Only Differ after Birth” by Fazale Rana (podcast)

    Endnotes
    1. Roger Seymour, Vanya Bosiocic, and Edward Snelling, “Fossil Skulls Reveal that Blood Flow Rate to the Brain Increased Faster than Brain Volume during Human Evolution,” Royal Society Open Science 3 (August 2016): 160305, doi:10.1089/rsos.160305.
  • Does the Evolutionary Paradigm Stymie Scientific Advance?

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Sep 12, 2016

    A common challenge I often hear is that creationism and intelligent design are showstoppers for science. If we conclude that “God did it,” skeptics complain, “wouldn’t that shut down scientific inquiry?”

    A few years ago, I had a brief email exchange with a prominent origin-of-life researcher who sincerely raised that concern:

    “I would be interested in how you think the creation model approach . . . will lead to scientific advance. Your book Origins of Life clearly showed that science does not have all the answers to how life may have begun, and of course I agree with that conclusion. What this means to me is that we have some beautiful open questions to work on to try to find the answers. But in your book, at the end of each chapter, you typically ended with the creationist answer to open questions: God did it. This is what I meant by stopping the questioning process. If the answer is that God did it, where do we go from there?”

    I responded to this concern elsewhere, but, at this juncture, I would like to point out that the evolutionary paradigm can also shut down scientific inquiry, delaying the discovery of key scientific insights, and often with important biomedical implications.

    The evolutionary paradigm can also shut down scientific inquiry, delaying the discovery of key scientific insights, and often with important biomedical implications.

    This point is powerfully illustrated by the latest work by a team of researchers from Duke University.1 These investigators demonstrated that the highly repetitive satellite DNA associated with centromeres displays function.

    Repetitive DNA in Evolutionary and Creation Models

    From within the evolutionary framework, this discovery was unexpected. Most molecular biologists have long viewed highly repetitive DNA sequences as nonfunctional. In fact, much of the satellite DNA sequences in the human genome (which comprise 10 percent of the genetic makeup of humans) have been ignored by the research community, because of the influence of the evolutionary paradigm. These sequences have long been regarded as the leftover vestiges of an unguided, evolutionary history.

    A press release from Duke University describing this latest work acknowledges this omission: “Even though the sequence of the human genome was declared complete more than a decade ago, it retains several glaring gaps, especially in the repetitive sequences around centromeres.”2

    Sequencing highly repetitive DNA sequences is extremely challenging, to be sure. And this is part of the reason for the gaps in the human genome sequence. But, because of the influence of the evolutionary paradigm, few, if any, biologists thought these repetitive sequences were anything other than junk. Viewing satellite DNA as junk took away any motivation on the part of molecular biologists to “plow ahead” and try to determine these recalcitrant DNA sequences.

    On the other hand, a creation model/intelligent design perspective predicts that nearly all of the DNA sequences found within the human genome would display function—including highly repetitive satellite DNA sequences. And this prediction is satisfied by the latest insights from the Duke research team.

    To be fair, the Duke researchers were working from an evolutionary framework. So, why were they studying satellite DNA, if other life scientists chose to ignore these sequences? The researchers from Duke University were trying to understand the structure-function relationships of centromeres.

    Centromeres

    These chromosomal regions are made up of highly repetitive DNA dubbed alpha satellite DNA and comprise about 5 percent of the human genomes. Centromeres serve as the attachment site for replicated chromosomes during the cell division process.

    blog__inline--does-evolutionary-paradigm-stymie-scientific-advance-1

    Image: 3-D Chromosome Illustration.

    The alpha satellite DNA of centromeres displays several layers of organization that are built upon a 171 base pair (bp) unit called a monomer. In turn, these monomers are repeated numerous times to form higher order repeats (HORs). The size of the HOR is specific for each of the 22 autosomes and 2 sex chromosomes that comprise the human genome. For example, the HOR of chromosome X consists of 12 monomers, while the HOR of chromosome 8 is made up of six monomers. The next level of organization, called HOR arrays, arises from the extensively repeated occurrence of HORs.

    There can be two or more HOR arrays within centromeres. For example, chromosome 17—the subject of the Duke University study—possesses two HOR arrays, dubbed D17Z1 and D17Z1-B.

    Proteins comprising the kinetochore bind to one or the other HOR array on chromosome 17. (The kinetochore protein complex binds to the centromere, serving as an attachment site for the mitotic spindle, which pulls apart the sister chromosomes during cell division.)

    blog__inline--does-evolutionary-paradigm-stymie-scientific-advance-2

    Image: Mitotic Spindle. Credit: Wikimedia Commons

    As it turns out, for 70 percent of people, the centromere assembles at the D17Z1 site of chromosome 17 for both sister chromosomes. For 30 percent, centromere assembly occurs at the D17Z1 site for one of the sister chromosomes and at the D17Z1-B site of the other.

    Variations in the Repetitive DNA of Centromeres

    In an attempt to determine why one site is used for centromere assembly as opposed to the other, the researchers from Duke University discovered sequence and size variations for the monomers used to build the HOR arrays. And this variation plays a key role in dictating the site for centromere assembly. They also discovered that some sequence and size variants display a loss of functional competency. In other words, this variability can cause the chromosome to become unstable and/or the mitotic spindle fails to properly form. The researchers think that these failures may lead to increased risks of cancer, birth defects, and infertility.

    If the instability becomes too great, the centromere will assemble at alternate HOR array sites, explaining why (for 30 percent of the population) centromere assembly occurs at different sites for the sister chromosomes of human chromosome 17.

    Repetitive DNA Displays Function

    This work indicates that repetitive DNA sequences within the human genome do, indeed, possess functional attributes, just as creationists and intelligent design adherents have predicted. And the researchers think that their insight is only the beginning. Beth Sullivan, the senior researcher for the project stated:

    “What we found in this study is probably the tip of the iceberg. There could be all sorts of functional consequences to having variation within the complex, repetitive portion of the genome that we don’t know about yet.”3

    Implications for Evolutionary and Creation Models

    Many regard the shared “junk DNA” sequences in the genomes of humans and the Great Apes as the most compelling evidence for evolution. When the human genome sequence was first reported in the early 2000s, geneticists estimated that at least 95 percent of human DNA sequences are junk.

    Over the last decade, discovery after discovery has demonstrated that many classes of junk DNA display function. In fact, the ENCODE project indicates that a vast proportion of the human genome is functional, not junk.

    Yet, many evolutionary biologists reject the results of the ENCODE project, insisting that this research effort has mistakenly assigned function to many of the human genome DNA sequences. Why are evolutionary biologists skeptical of the ENCODE project results? Because, if these results are valid, then the evolutionary paradigm can’t be correct.

    Recent work by Duke University scientists demonstrates that, in spite of skepticism over the ENCODE project results, researchers continue to discover new functions for junk DNA. It turns out that these repetitive sequences serve a role in the process of cell division, expanding the role of junk DNA beyond regulating gene expression.

    But in spite of these discoveries, many evolutionary biologists doggedly cling to the view that junk DNA must be nonfunctional because of their deep-seated commitment to the evolutionary paradigm. All of this makes me wonder:

    Is the skepticism about the functional utility of junk DNA—fueled by the demands of the evolutionary paradigm—a science stopper?

    Resources

    Who Was Adam?: A Creation Model Approach to the Origin of Humanity by Fazale Rana with Hugh Ross (book)
    Q&A: Is Christianity a Science Showstopper?” by Fazale Rana (article)
    Responding to ENCODE ‘Skeptics‘” by Fazale Rana (article)
    Do Scientists Accept the Results of the ENCODE Project?” by Fazale Rana (article)
    Is Most of Our DNA Garbage?” by Fazale Rana (podcast)

    Endnotes
    1. Megan E Aldrup-MacDonald et al., “Genomic Variation within Alpha Satellite DNA Influences Centromere Location on Human Chromosomes with Metastable Epialleles,” Genome Research, published electronically August 10, 2016, doi:10.1101/gr.206706.116.
    2. Marla Vacek Broadfoot, “Variation in ‘Junk’ DNA Leads to Trouble,” Duke Today (blog), Duke University, August 30, 2016, https://today.duke.edu/2016/08/variation-%E2%80%9Cjunk%E2%80%9D-dna-leads-trouble.
    3. Ibid.
  • Science News Flash: 3.7-Billion-Year-Old Fossils Perplex Origin-of-Life Researchers

    by Telerik.Sitefinity.DynamicTypes.Model.Authors.Author | Sep 07, 2016

    Good things can come from bad circumstances.

    This idea is beautifully illustrated by the research efforts of a team of Australian scientists. Climate change has triggered the excessive melting of ice and snow in western Greenland. This loss of snow and ice concerns many people, but, on the other hand, it has been a boon for the scientific community. It has exposed a new outcropping of rocks, giving geologists first-time access to a rare window of the earth’s distant past. As it turns out, these rocks harbor what appears to be the oldest fossils on Earth—stromatolites that date to around 3.7 billion years in age.1

    Billion year old fossils 

    Image: Stromatolites in western Australia

    This latest insight has important implications for understanding the origin of life. In fact, on the day researchers from Australia reported this discovery in scientific literature, it made headlines in news outlets around the world.2

    Evidence for Early Life on Earth

    As Hugh Ross and I discuss in Origins of Life, geochemists have unearthed a number of chemical markers in the Isua Supracrustal Belt (ISB) of western Greenland that strongly hint at microbial life on Earth between 3.7 and 3.8 billion years ago. But origin-of-life researchers debate the bio-authenticity of these geochemical signatures, because a number of potential abiotic processes can produce similar geochemical profiles.

    Most scientists doubted that fossils would ever be unearthed in the Isua rock formations because these outcrops have undergone extensive metamorphosis, experiencing high temperatures and pressures—conditions that would destroy fossils. But these newly exposed formations contain regions that have experienced only limited metamorphosis, making it possible for fossils to survive.

    Careful microscopic and chemical characterization of the Isua stromatolites affirms their biogenecity. These analyses also indicate that they formed in shallow water marine environments.

    These recently discovered stromatolites (and the previously detected geochemical life signatures in the Isua formations) indicate that a complex and diverse ecology of microorganisms existed on Earth as far back as 3.7 billion years ago.

    Prior to the discovery of 3.7 billion-year-old stromatolites, origin-of-life researchers widely agreed that microbial life existed on Earth around 3.4–3.5 billion years ago, based on the recovery of stromatolites, microbial mats, microfossils, and geochemical signatures in rock formations found in western Australia. Many origin-of-life researchers have expressed amazement that complex microbial ecologies were present on Earth as early as 3.4 billion years ago. For example, paleontologist J. William Schopf marveled:

    “No one had foreseen that the beginning of life occurred so astonishingly early.”3

    The researchers who recovered and analyzed the Isua stromatolites expressed similar surprise:

    “The complexity and setting of the Isua stromatolites points to sophistication in life systems at 3,700 million years ago, similar to that displayed by 3,480–3,400 million-year-old Pilbara stromatolites.”4

    From a naturalistic perspective, the only way for these researchers to make sense of this discovery is to conclude that life must have originated prior to 4 billion years ago. They state: “This implies that by ~3,700 million years ago life already had a considerable prehistory, and supports model organism chronology that life arose during the Hadean (>4,000 million years ago).”5

    Implications for Evolutionary Models

    However, the researchers’ explanation for the appearance of a complex, diverse microbial ecosystem at 3.7 billion years ago is problematic, when the natural history of early Earth is considered.

    Traditionally, planetary scientists have viewed the early Earth as hot and molten, from the time of its formation (4.5 billion years ago) until ~3.8 billion years ago. This era of Earth’s history is called the Hadean. Accordingly, oceans were not present on early Earth until around 3.8 billion years ago. They believe a number of factors contributed to the hellish environment of our early planet, chief of which were the large impactors striking the earth’s surface. Some of these impact events would have been so energetic that they would have volatilized any liquid water on the planet’s surface and rendered the surface and subsurface as a molten state. In light of this scenario, it would be impossible for life to originate much earlier than 3.8 billion years ago. To put it another way, if the traditional understanding of early Earth history is correct, then it looks as if complex microbial ecologies appeared on Earth suddenly—within a geological instant. It is impossible to fathom how the explosive appearance of early life could happen via evolutionary mechanisms.

    More recently, a number of planetary scientists have proposed that early Earth only remained molten for the first 200–300 million years of its history. After which time, oceans became permanent (or maybe semi-permanent) features on the planet’s surface. The basis for this view has been the discovery of zircon crystals that date between 4.2–4.4 billion years ago. Geochemical signatures within these crystals are consistent with their formation in an aqueous setting, implying that oceans were present on Earth prior to 3.8 billion years ago.

    But this revised scenario doesn’t help the evolutionary approach to life’s origin. Around 3.8 billion years ago, a gravitational perturbation in the early solar system sent asteroids towards Earth. Some estimates have the earth experiencing over 17,000 impact events during this time. This event, called the late heavy bombardment (LHB), was originally regarded as a sterilization event. If so, then any life present on Earth prior to the LHB would have been obliterated. That being the case, again, it appears as if complex microbial ecologies appeared on Earth suddenly, within a geological instant.

    Recently, some planetary scientists have challenged the notion that the LHB was a sterilization event. They argue that life on the planet’s surface would have been destroyed, but life in some environments, such as hydrothermal vents, could have survived. In other words, there would have been refugiums on Earth that served as “safe houses” for life, ushering it through the LHB.

    Yet the latest discovery by the Australian scientists doesn’t fit this scenario. The Isua stromatolites formed at the earth’s surface in a shallow water environment. In fact, the research team generated data that effectively ruled out stromatolite formation near hydrothermal vents. But if the refugium model has validity, the Isua fossils should have formed in a high-temperature milieu.

    Finally, pushing life’s origin back to more than 4 billion years ago doesn’t solve the problem of a sudden origin-of-life—it merely displaces it to another window of time in Earth’s history. Origin-of-life researchers have geochemical evidence suggesting that life was present on Earth between 4.2–4.4 billion years ago. Given that the earth was molten for the first 200–300 million years of its existence (minimally), that doesn’t leave much time for life to originate.

    No matter the scenario, a naturalistic, evolutionary approach to the origin-of-life can’t seem to accommodate the sudden appearance of life on Earth. On the other hand, if a Creator brought life into being, this is precisely the mode and tempo expected for life’s appearance on Earth.

    Implications for Creation Models

    While the discovery of 3.7 billion-year-old stromatolites confounds evolutionary explanations for life’s origins, it affirms RTB’s origin-of-life model. This model is derived from the biblical creation accounts and make two key and germane predictions: (1) life should appear on Earth soon after the planet’s formation; and (2) first life should possess intrinsic complexity. And both of these predictions are satisfied by this latest advance.

    Resources
    Origins of Life: Biblical and Evolutionary Models Face Off by Fazale Rana and Hugh Ross (book)
    Creating Life in the Lab: How New Discoveries in Synthetic Biology Make a Case for the Creator by Fazale Rana (book)
    Life May Have Begun 300 Million Years Earlier Than We Thought” by Fazale Rana (podcast)
    Early Life Was More Complex Than We Thought” by Fazale Rana (article)
    When Did Life First Appear on Earth?” by Fazale Rana (article)
    Insight into the Late Heavy Bombardment and RTB’s Creation Model” by Fazale Rana (article)
    Origin-of-Life Predictions Face Off: Evolution vs. Biblical Creation” by Fazale Rana (article)

    Endnotes
    1. Allen P. Nutman et al., “Rapid Emergence of Life Shown by Discovery of 3,700-Million-Year-Old Microbial Structures,” Nature, published electronically August 31, 2016, doi:10.1038/nature19355.
    2. For a detailed discussion of this discovery and its implications for the creation/evolution controversy, listen to “Fossils Indicate Early Life Was Metabolically Complex and Diverse,” Apologia (Ex Libris), podcast audio, August 31, 2016, https://www.reasons.org/podcasts/apologia-premium/fossils-indicate-early-life-was-metabolically-complex-and-diverse.
    3. J. William Schopf, Cradle of Life: The Discovery of Earth’s Earliest Fossils (Princeton, NJ: Princeton University Press, 1999), 3.
    4. Allen P. Nutman, “Rapid Emergence of Life.”
    5. Ibid.

About Reasons to Believe

RTB's mission is to spread the Christian Gospel by demonstrating that sound reason and scientific research—including the very latest discoveries—consistently support, rather than erode, confidence in the truth of the Bible and faith in the personal, transcendent God revealed in both Scripture and nature. Learn More »

Support Reasons to Believe

Your support helps more people find Christ through sharing how the latest scientific discoveries affirm our faith in the God of the Bible.

Donate Now

U.S. Mailing Address
818 S. Oak Park Rd.
Covina, CA 91724
  • P (855) 732-7667
  • P (626) 335-1480
  • Fax (626) 852-0178
Reasons to Believe logo