A major difference between science and religion can be summarised as follows: science embraces reasonable uncertainty, while religion often promotes unreasonable certainty.
In practice, this means science always allows room for doubt—however small—and continually re-examines and reassesses evidence to determine whether a change of understanding is justified. Religion, by contrast, typically seeks reasons not to change its views, no matter how tenuous those reasons may be or how far removed from observable reality.
This essential feature of the scientific method is frequently misrepresented by creationists, who portray science as unreliable precisely because it revises its conclusions in light of new evidence. They contrast this with the supposed ‘eternal truths’ of the Bible, arguing that science books need constant revision while scripture remains unchanging.
One of those supposed eternal truths—about which creationists are not permitted to change their minds—is that the Earth is only a few thousand years old, and that all living things were created ex nihilo in their current forms, with no evolutionary ancestry or shared origins. Science, on the other hand, can re-evaluate the evidence from a 300-million-year-old fossil bed in Illinois and conclude that the original interpretation underestimated the complexity of the ancient ecosystem that once existed there.
A prime example of such a scientific reassessment has recently been published—open access—in the journal Paleobiology. The study was conducted by a team of palaeontologists from the University of Missouri’s College of Arts and Science, in collaboration with Gordon Baird of the Department of Geology & Environmental Sciences at the State University of New York (SUNY), Fredonia.
The work is based on a comprehensive reassessment of the rich fossil deposits from the Mazon Creek Lagerstätte in Illinois, which, during the Carboniferous Period (~300 million years ago), was part of a vast area of tropical swamps, deltas, and shallow seas. These habitats were shaped by rising sea levels that inundated earlier coal-forming wetlands.
Some 150 million years before the mythical events of ‘Creation Week’—give or take a few thousand years—our distant ancestors were small, nocturnal, rodent-like mammals eking out an existence in a world dominated by colossal reptiles. Among these dominant life forms were the dinosaurs, thriving in a variety of ecosystems and feeding on plants or other animals, depending on their species.
As they ate, they unwittingly left behind a record of their diet etched into the microscopic wear patterns on the enamel of their teeth. Today, with the help of sophisticated analytical techniques, palaeontologists can read these patterns like a diary of prehistoric meals. And with each new discovery, such as the one published by a team led by Dr Daniela E. Winkler of Kiel University, the yawning gap between ancient mythology and modern science widens ever further. Their findings provide yet another decisive refutation of the simplistic narrative crafted by Bronze Age storytellers—later compiled into what some still insist is the inerrant word of an omniscient creator.
The team focused on the teeth of sauropods—long-necked herbivorous dinosaurs such as Camarasaurus, Brachiosaurus, and Diplodocus — from the Late Jurassic Morrison Formation in North America and the Lusitanian Basin in Portugal. Using a method called Dental Microwear Texture Analysis (DMTA), they examined the microscopic wear patterns caused by feeding, revealing a fascinating spectrum of dietary strategies and environmental adaptations among different species.
What they found demolishes the notion of sauropods as a homogenous group of giant leaf-munchers. Instead, the microwear textures show distinct differences in feeding behaviour, likely linked to differences in available vegetation and habitat. For example, Camarasaurus appears to have consumed tougher, more fibrous plant material—perhaps conifers—while others such as Diplodocus may have specialised in softer vegetation like ferns or aquatic plants. These variations not only suggest niche partitioning, where species avoid direct competition by diversifying their diets, but also point to distinct ecological zones across the ancient landscapes they inhabited.
Even more telling is the comparison between North American and European sauropods. Despite being closely related, the differences in their dental microwear suggest adaptations to different environmental pressures and available flora, implying behavioural flexibility and evolutionary divergence shaped by their respective habitats.
Such complexity and diversity, preserved for over 150 million years in the microscopic textures of fossilised teeth, are a world away from the simplistic narratives of static 'kinds' created in a single week. Instead, we see a dynamic, evolving biosphere responding to ecological challenges—exactly what we’d expect in a world governed by natural selection and deep time.
I asked ChatGPT to list some of the most common fallacies used by creationists in online debates, and to design memes illustrating them.
Most creationists won’t recognise these as fallacies, of course, because their understanding of science and logic is typically on a par with that of a child of nine or ten—old enough to log onto a computer and access social media, but not yet equipped with the critical thinking skills needed to understand how debate works, what constitutes scientific evidence, and what makes a logical argument.
Many are also conspiracy theorists, as research shows (1) a strong correlation between conspiracism and creationism. Both tend to stem from the same underlying cause: a teleological mode of thinking retained from childhood and, in some individuals, carried into adulthood to such an extent that it becomes a cognitive impairment.
This makes them easy prey for the unscrupulous frauds who thrive in creationist circles—parasites who earn a living by peddling pseudoscience to those willing to pay good money for confirmation of their biases, regardless of the quality of the argument or the validity of the evidence.
The following memes are free to use, though a credit would be appreciated. To download, right click on any image and select 'save as...', or to download zipped memepack.
It's more bad news for Intelligent Design (ID) creationists who believe their putative designer is the anthropophilic, omnibenevolent God of the Bible. Hot on the heels of the discovery that some lemurs do not suffer from the age-related degenerative conditions that cause such misery for humans, comes the news that zebrafish can regenerate lost hair cells—cells that, in humans, enable hearing but cannot be replaced once lost.
These hair cells, located in the human inner ear, detect vibrations and are crucial for hearing. They can be destroyed through prolonged exposure to loud noise, resulting in permanent deafness. However, zebrafish possess homologous cells in their lateral lines—structures that allow them to detect vibrations in water, effectively functioning as a form of hearing. Remarkably, these cells can regenerate under the control of two specific genes.
It doesn't take a genius to realise that, if we accept the intelligent design argument that a divine designer deliberately created these genes, then the same designer could have endowed its supposed special creation—humans—with this regenerative ability too. Within the ID framework, the only possible conclusion is that the designer god chose *not* to give humans this ability, and instead preferred us to go deaf.
The problem for creationists deepens when one considers that these genes exemplify what William A. Dembski of the Discovery Institute cites as evidence of intelligent design: they are complex and specified, containing the genetic information to produce a defined result. Dembski insists that such "complex specified information" can only originate from an intelligent designer.
Creationists, of course, are compelled to reject the notion that these differences are simply the result of evolutionary processes. But if they also refuse to accept that this zebrafish trait—clearly underpinned by "complex specified genetic information"—constitutes evidence of intelligent design (and therefore points to a deliberate *absence* in humans), they are also undermining Dembski's single defining argument for intelligent design.
The picture of modern human (Homo sapiens) interactions with Neanderthals (H. neanderthalensis) has just become significantly richer. New evidence reveals not just a single episode of contact within the last 50,000 years, but several waves of interaction spanning much of our species’ 200,000-year history.
It was previously believed that after our last common ancestor with Neanderthals and Denisovans split into separate populations around 600,000 years ago, one lineage remained in Africa and eventually evolved into H. sapiens by about 200,000 years ago. The other migrated into Eurasia and gradually diverged into Neanderthals in the west and Denisovans in the east, with limited contact between them. According to this model, modern humans left Africa around 60,000 years ago, encountered Neanderthals in Eurasia, and interbred with them shortly afterwards—about 40,000 to 50,000 years ago.
However, a new genomic analysis provides evidence for at least three distinct episodes of interbreeding. One occurred around 200,000 to 250,000 years ago—very early in the history of H. sapiens. Another took place about 100,000 to 120,000 years ago, long before the final major migration out of Africa, and the last around 40,000 years ago, as previously believed.
These findings suggest that there may have been multiple early migrations of H. sapiens into Eurasia, followed in some cases by return migrations back into Africa, before the final, successful dispersal around 60,000 years ago.
Some of the team’s evidence comes from detecting H. sapiens DNA in the Neanderthal genome, so these ingressions could have come from earlier migrations that then failed, leaving only their DNA in the Neanderthal population.
There are still unresolve questions about which species migrated out of Africa, when, and whether some, such as H. rhodesiensis, had a wide distribution across African and Eurasia with regional variants, so it is entirely possible that the earliest interactions with Neanderthals could have been between, say H. rhodesiensis which brought Neanderthal genes back into Africa and then interbred with diverging H. sapiens.
See the right-hand panel for an explanation of this so-called 'muddle in the middle'.
The study, led by researchers at Harvard University and Princeton University under the direction of Professor Joshua Akey of Princeton’s Lewis-Sigler Institute for Integrative Genomics, also supports the view that Neanderthals did not simply go extinct. Instead, their dwindling populations were gradually absorbed into expanding populations of modern humans.
Where exactly the archaic hominin, Paranthropus robustus fits into the human evolutionary tree remains a subject of debate among palaeontologists. This species lived in southern Africa around 2 million years ago. They walked upright, indicating a shared ancestry with the Australopithecus and the later Homo genus. However, their comparatively small brains and massive jaws and teeth suggest a distinct evolutionary path, likely adapted for processing tough, fibrous plant material.
Determining their precise place in our evolutionary history would ideally require DNA analysis—but DNA does not survive long in the warm African climate. To overcome this limitation, a team of African and European researchers from the fields of molecular science, chemistry, and palaeoanthropology turned to a cutting-edge technique known as palaeoproteomics. By analysing proteins recovered from ancient tooth enamel, they were able to infer aspects of the underlying DNA, since the amino acid sequence in proteins is directly determined by the nucleotide sequence in DNA.
Their findings suggest that the story of early hominins is more complex than previously thought. There may have been more than one closely related species, with evidence of interbreeding or genetic divergence followed by remixing — patterns that would later come to characterise the tangled branches of the hominin family tree.
The research team included three postdoctoral scientists from the University of Copenhagen — Palesa P. Madupe, Claire Koenig, and Ioannis Patramanis — who have written about their work and its significance in the open-access magazine The Conversation.
Imaginative reconstruction of Novaculadon mirabilis. Likely this animal would have been a little larger than a mouse.
Picture credit: Hamzah Imran.
(L-R) Dr Roy Smith and University of Portsmouth student Ben Weston by the flint bed in Durlston Bay near Swanage, which is the layer of rock which the mammal fossil came out of.
When someone grows up being threatened with divine punishment for merely entertaining doubts about the literal truth of the Bible, it's hardly surprising that real-world evidence struggles to break through the psychological defences they've built to protect themselves. This phenomenon is what atheist author and philosopher, Professor Peter Boghossian refers to as doxastic closure — a mental state in which contrary ideas are shut out before they can even be considered.
Former young-Earth creationist and now science advocate and geologist Glenn Morton once described it as like having a “gatekeeper demon” perched on the edge of your consciousness—filtering out any facts or logical arguments that challenge creationist beliefs, while admitting only those misrepresentations of science that appear to support them.
In this mindset, inconvenient realities — such as the discovery of a 145-million-year-old fossil of an early mammal — are unlikely to dent the conviction that the Earth is only 6,000 to 10,000 years old, and that all animals were created in a single supernatural event. In this view, evolution is simply an illusion, no matter how well the evidence supports it.
Even so, for any creationist with the courage and intellectual honesty to read this far, the story of that inconvenient little fossil is well worth exploring. It was discovered by a palaeontology student from the University of Portsmouth, along the Dorset coast of England, and is the subject of a recent paper in Proceedings of the Geologists’ Association.
This find marks the first discovery of a multituberculate jaw at Swanage since Victorian times. Its distinct size and shape confirmed it as a completely new species.
An artist’s reconstruction of the fossilized landscape, plants and animals found preserved in a remote bonebed of Arizona’s Petrified Forest National Park
Illustration by Brian Engh
Reconstruction of life in Arizona, 200 million years ago.
Arizona’s Petrified Forest National Park is a place that many creationists might prefer to ignore—or misrepresent. It offers a vivid record of how life changed during the Triassic Period, between 252 and 201 million years ago. In other words, it documents the history of life in what is now Arizona during the vast stretch of time that predates the so-called “Creation Week,” as described in Bible-based creationist mythology.
In addition to the petrified remains of ancient conifers, the site preserves fossils of long-extinct crocodile-like reptiles and some of the earliest dinosaurs known from North America. Now, a new study of a fossil-rich bone bed from the late Triassic—around 09 million years ago—has revealed new insights into stream ecosystems of that time, including the discovery of the largest pterosaur yet found in North America.
Creationists frequently argue that macroevolution without divine involvement is impossible because it supposedly requires the creation of new genetic information to code for novel structures. They assert that such new genetic information cannot arise through natural processes, claiming this would violate the Second Law of Thermodynamics. However, try getting a creationist to explain what the Second Law of Thermodynamics actually is, how it relates to genetic information, and why it supposedly forbids gene duplication, and it quickly becomes apparent that they haven’t the faintest idea what they’re talking about.
Of course, this entire argument hinges on a distorted definition of macroevolution, namely the claim that it must involve the appearance of entirely new structures not present in ancestral forms. Like so many creationist arguments, it is built on misinformation and the misrepresentation of fundamental biological concepts. Macroevolution refers to evolutionary changes above the species level, while evolution more broadly is defined as a change in allele frequencies in a population over time.
Another familiar plank in the creationist propaganda platform is the patently absurd claim that evolution cannot occur through a loss of genetic information, on the grounds that lost genetic material is always deleterious—if not fatal—and therefore cannot be passed on to subsequent generations. This claim, too, wilfully ignores well-established mechanisms in evolutionary biology.
So, a recent paper from an international team including researchers from the University of Vienna and the University of Wisconsin–Madison (USA) should present a problem for that narrative. The study shows that the bizarre body plan of marine arthropods known as sea spiders (Pycnogonida) is the result of a lost gene.
If creationists were intellectually honest, they might take this as a cue to question why creationist ‘scientists’ (to use the term loosely) are misleading them. More likely, however, they’ll claim that it’s the mainstream biologists who are doing the lying—despite the fact that the latter group provide empirical evidence to support their conclusions.
Here we have yet another example demonstrating that, if we apply Discovery Institute fellow William A. Dembski's criteria for proving intelligent design — namely the presence of complex specified genetic information — then we must conclude that creationism's supposed intelligent designer is, in fact, a malevolent force devising ever more sophisticated ways to inflict suffering on the world.
Once again, honest creationists are left with a stark dilemma: either complex specified information is indeed evidence of design, in which case the designer is malevolent, or it is not, in which case a central tenet of Intelligent Design creationism collapses. The dishonest ones, of course, will simply dismiss the evidence, likely misrepresent the science, and continue to bear false witness against scientists. In neither case should we expect creationists to admit that the theory of evolution fully accounts for the appearance of "malevolent" design, arising naturally without conscious intent or divine interference.
It’s a curious paradox that people who claim to worship the God of the Bible as an omnibenevolent, anthropophilic being are so often willing to see that deity cast in the role of a malevolent agent—so long as they can reject the theory of evolution. This strongly suggests that their opposition to evolution is not primarily theological, but political.
The latest example comes from the tick-borne pathogen Anaplasma, which causes anaplasmosis and contributes to Lyme disease. This bacterium hijacks the cellular machinery of ticks to ensure its own survival and transmission to new hosts, including humans. Although Dembski has famously avoided providing a rigorous, testable definition of "complex specified genetic information," any such definition would surely encompass genetic adaptations that promote survival and reproduction.
What information do you have on Anaplasma and the tick that transmits it?
Anaplasma is a genus of bacteria that includes several species capable of causing disease in humans and animals. The most medically relevant species is Anaplasma phagocytophilum, which causes anaplasmosis—a tick-borne disease that affects both humans and various mammals.
Overview of Anaplasma
Anaplasma are obligate intracellular bacteria in the family Anaplasmataceae.
They primarily infect white blood cells (especially neutrophils in the case of A. phagocytophilum).
Disease is often seasonal, peaking during the months of high tick activity (late spring to early autumn in temperate zones).
In severe cases: respiratory failure, organ failure, neurological symptoms
Incubation period: ~5–14 days after a tick bite.
Treatment: Responds well to doxycycline, especially if started early.
If untreated, it can lead to complications, especially in the elderly or immunocompromised.
Tick Vectors
The primary vector in the United States is the blacklegged tick (Ixodes scapularis), also called the deer tick.
In Europe, the main vector is the castor bean tick (Ixodes ricinus).
These are the same ticks that transmit Lyme disease (Borrelia burgdorferi) and Babesia (babesiosis), leading to frequent co-infections.
Hosts and Reservoirs
Main animal reservoirs include:
White-tailed deer
Rodents
Small mammals
Ticks acquire the bacteria when feeding on an infected host and then transmit it during subsequent feedings.
Biological Strategy of the Pathogen
Recent research (such as the 2025 WSU referenced) shows that Anaplasmacan:
Hijack the tick's cellular defence mechanisms, particularly its oxidative stress response, allowing the bacteria to survive within the tick's gut.
Manipulate the cell death pathways of tick cells, suppressing apoptosis (programmed cell death) to extend the viability of the cells it infects.
Modify gene expression in the tick to enhance its own survival and transmission potential.
These mechanisms qualify as highly sophisticated biological strategies—precisely the sort of adaptations that Intelligent Design proponents would struggle to explain without appealing to either special pleading or malevolent intent.
Ecological and Public Health Impact
Geographic spread is increasing, partly due to climate change, which expands the habitat range of ticks.
Public health monitoring is challenged by co-infections and misdiagnosis (HGA is often confused with Lyme disease or viral infections).
Preventative strategies include tick checks, repellents, and public awareness campaigns.
Bacteria hijack tick cell defenses to spread diseaseWashington State University researchers have discovered how the bacteria that cause anaplasmosis and Lyme disease hijack cellular processes in ticks to ensure their survival and spread to new hosts, including humans.
Based in the College of Veterinary Medicine, the team found that the bacteria can manipulate a protein known as ATF6, which helps cells detect and respond to infection, to support its own growth and survival inside the tick. The findings, published in the journal Proceedings of the National Academy of Sciences, could serve as a launching point for developing methods to eliminate the bacteria in ticks before they are transmitted to humans and other animals.
Most research has looked at how these bacteria interact with humans and animals and not how they survive and spread in ticks. What we have found could open the door to targeting these pathogens in ticks, before they are ever a threat to people.
Kaylee A. Vosbigian, lead author
Department of Veterinary Microbiology and Pathology
College of Veterinary Sciences
Washington State University, Pullman, WA, USA.
Vosbigian and her advisor, Dana Shaw, the corresponding author of the study and an associate professor in the Department of Veterinary Microbiology and Pathology, focused their research on Ixodes scapularis, also known as the black-legged tick, which is responsible for spreading both Anaplasma phagocytophilum and Borrelia burgdorferi, the causative agents of anaplasmosis and Lyme disease. Both diseases are becoming increasingly common and can cause serious illness in humans and animals.
The team discovered that when ATF6 is activated in tick cells, it triggers the production of stomatin, a protein that helps move cholesterol through cells as part of a normal cellular processes. The bacteria exploit this process against their tick hosts, using the cholesterol — which they need to grow and build their own cell membranes but cannot produce themselves — to support their own survival and success.
Stomatin plays a variety of roles in the cell, but one of its key functions is helping shuttle cholesterol to different areas. The bacteria take advantage of this, essentially stealing the cholesterol they need to survive.
Kaylee A. Vosbigian
When the researchers blocked the production of stomatin, restricting the availability of cholesterol, bacterial growth is significantly reduced. The researchers believe this shows targeting the ATF6-stomatin pathway could lead to new methods for interrupting the disease cycle in ticks before transmission occurs.
As part of the study, Vosbigian also developed a new research tool called ArthroQuest, a free, web-based platform hosted by WSU that allows scientists to search the genomes of ticks, mosquitoes, lice, sand flies, mites, fleas and other arthropod vectors for transcription factor binding sites — genetic switches like ATF6 that control gene activity.
There aren’t many tools out there for studying gene regulation in arthropods. Most are built for humans or model species like fruit flies, which are genetically very different from ticks.
Kaylee A. Vosbigian
Using ArthroQuest, the team found that ATF6-regulated control of stomatin appears to be prevalent in blood-feeding arthropods. Since the hijacking of cholesterol and other lipids is common among arthropod-borne pathogens, the researchers suspect many may also exploit ATF6.
We know many other vector-borne pathogens, like Borrelia burgdorferi and the malaria-causing parasite Plasmodium, rely on cholesterol and other lipids from their hosts. So, the fact that this ATF6-stomatin pathway exists in other arthropods could be relevant to a wide range of disease systems.
Assistant Professor Dana K. Shaw, corresponding author.
Department of Veterinary Microbiology and Pathology
College of Veterinary Sciences
Washington State University, Pullman, WA, USA.
Significance
Infection dynamics for tick-borne pathogens like Anaplasma have primarily been studied in mammals. Comparatively less is known about tick–pathogen interactions. We found that Anaplasma activates the stress response receptor, ATF6, in ticks. Activated ATF6 functions as a transcriptional regulator. Using a custom script in R, we identified stomatin as an ATF6-regulated target that supports Anaplasma by modulating cholesterol trafficking. Our custom tool “ArthroQuest” revealed that the ATF6-regulated nature of stomatin is unique to arthropods. Given that lipid hijacking is common among arthropod-borne microbes, ATF6-mediated induction of stomatin may be exploited in many vector–pathogen relationships. In addition, our findings predict that there are many ATF6-regulated genes unique to ticks, highlighting that there is still much to be uncovered.
Abstract
How tick-borne pathogens interact with their hosts has been primarily studied in vertebrates where disease is observed. Comparatively less is known about pathogen interactions within the tick. Here, we report that Ixodes scapularis ticks infected with either Anaplasma phagocytophilum (causative agent of anaplasmosis) or Borrelia burgdorferi (causative agent of Lyme disease) show activation of the ATF6 branch of the unfolded protein response (UPR). Disabling ATF6 functionally restricts pathogen survival in ticks. When stimulated, ATF6 functions as a transcription factor, but is the least understood out of the three UPR pathways. To interrogate the Ixodes ATF6 transcriptional network, we developed a custom R script to query tick promoter sequences. This revealed stomatin as a potential gene target, which has roles in lipid homeostasis and vesical transport. Ixodes stomatin was experimentally validated as a bona fide ATF6-regulated gene through luciferase reporter assays, pharmacological activators, RNA interference transcriptional repression, and immunofluorescence microscopy. Silencing stomatin decreased A. phagocytophilum colonization in Ixodes and disrupted cholesterol dynamics in tick cells. Furthermore, blocking stomatin restricted cholesterol availability to the bacterium, thereby inhibiting growth and survival. Taken together, we have identified the Ixodes ATF6 pathway as a contributor to vector competence through Stomatin-regulated cholesterol homeostasis. Moreover, our custom, web-based transcription factor binding site search tool “ArthroQuest” revealed that the ATF6-regulated nature of stomatin is unique to blood-feeding arthropods. Collectively, these findings highlight the importance of studying fundamental processes in nonmodel organisms.
The North American deer tick, Ixodes scapularis, can transmit up to seven different pathogens that impact human and animal health including Anaplasma phagocytophilum (causative agent of anaplasmosis) and Borrelia burgdorferi (causative agent of Lyme disease) (1). The continuous rise in reported cases of tick-borne disease (2–10) underscores the need for novel intervention strategies. Although the intricacies of mammalian host–pathogen interactions have been well studied, comparatively little is known about tick–pathogen interactions.
Recently we have shown that A. phagocytophilum and B. burgdorferi activate the unfolded protein response (UPR) in ticks, which influences microbial colonization and persistence in the arthropod (11, 12). The UPR is a cellular response network that is initiated by three endoplasmic reticulum (ER) transmembrane receptors IRE1α, PERK, and ATF6. Each branch of the UPR initiates a signaling cascade and coordinates gene expression networks by activating specific transcription factors. We have shown that the IRE1α-TRAF2 pathway leads to microbe-restricting immune responses in arthropods by activating the NF-κB-like molecule, Relish (11). We have also demonstrated that stimulating PERK activates the antioxidant transcription factor, Nrf2, which facilitates pathogen persistence in ticks (12). Out of the three UPR receptors, ATF6 is the least understood (13). When activated, site-1 and site-2 proteases cleave the cytosolic portion of ATF6, which allows it to translocate to the nucleus and act as a transcriptional regulator (nATF6) (14). The role of ATF6 has never been explored in arthropod vectors.
Here, we demonstrate that Ixodes ATF6 is activated by tick-borne pathogens and supports A. phagocytophilum colonization in ticks. To determine how ATF6 impacts vector competence, we used protein modeling and a custom transcription factor binding site query to probe the ATF6 regulatory network in I. scapularis. Gene ontology (GO) and Reactome analyses identified Stomatin, a lipid homeostasis and vesical transport protein, as a potential gene regulated by ATF6 in ticks. Using pharmacological manipulations, RNA interference (RNAi), quantitative fluorescent assays, and immunofluorescence microscopy, we found that Stomatin supports pathogen colonization in ticks by facilitating cholesterol acquisition by the bacterium. These findings demonstrate that stomatin is induced during the arthropod-phase of the pathogen life cycle to enable survival and persistence in the vector.
Programs that predict transcription factor regulatory networks are generally restricted to model organisms, leaving out many arthropod vectors. We used our custom R script to develop a publicly available, web-based tool termed “ArthroQuest” that currently allows users to query 20 different arthropod vector genomes, in addition to Drosophila and humans. Queries with ArthroQuest revealed that the ATF6-regulated nature of stomatin appears to be unique to arthropods. Given that lipid hijacking and cholesterol incorporation is common in many arthropod-borne microbes (15), ATF6-mediated induction of stomatin may be a shared phenomenon among many vector–pathogen relationships that is exploited for the survival and persistence of transmissible pathogens.
This discovery poses a significant problem for proponents of Intelligent Design (ID) creationism because it challenges one of their core assertions: that complex specified information (CSI) within genetic material is a reliable indicator of an intelligent, purposeful designer. If we accept this premise, then we are compelled to ask why such intelligence would devote itself to crafting mechanisms that cause suffering, disease, and death—such as the ability of Anaplasma to hijack tick cell defences and ensure its own propagation at the expense of both ticks and mammalian hosts, including humans.
The usual ID response is to insist that their designer is benevolent — typically equated with the God of the Bible. But here, we are faced with a biological system so well-adapted to spreading infection that it must either be acknowledged as a product of evolutionary processes or attributed to a designer with malevolent intent. This is not a fringe example; it is one of many cases where nature reveals a level of intricate adaptation that ID advocates would normally cite as evidence for design, were it not so profoundly disturbing.
What this ultimately reveals is the theological inconsistency at the heart of ID creationism. The refusal to acknowledge the explanatory power of evolution, even when confronted with examples like Anaplasma, indicates that ID is not a scientific theory but a religious or ideological stance. The selective application of their own criteria — applauding "design" in butterflies but ignoring it in parasites — exposes the intellectual dishonesty behind the movement. Evolution, by contrast, provides a consistent and naturalistic framework that explains both the beautiful and the brutal features of the living world — without invoking a morally compromised designer.
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According to creationists, humans are the designer’s special creation, and the Universe, Earth, and all life upon it were created solely for our benefit.
If that were the case, one might reasonably expect human design to be uniquely perfect—free from disease and physical defects. Yet, paradoxically, we are more prone to cancer than our closest evolutionary relatives, the other great apes. Recent research from the UC Davis Comprehensive Cancer Center suggests that this heightened cancer susceptibility may be linked to the very mutation that enabled us to develop our comparatively large brains.
The theory of evolution, of course, precisely predicts these kinds of suboptimal trade-offs and their consequences. As an undirected, uncaring process, evolution is concerned solely with reproductive success—not with long-term health, perfection, or ideal design.
Intelligent (sic) Design creationists have painted themselves into a corner.
Two of their most prominent arguments—irreducible complexity (Michael J. Behe) and complex specified information (William A. Dembski)—are intended to demonstrate the involvement of an intelligent designer in the natural world. But when these same criteria are applied to harmful parasitic organisms, such as the common herpesvirus (cytomegalovirus), which is the leading infectious cause of birth defects in the United States, the implication is that this virus too is the product of intentional design by the same creator that ID proponents insist is responsible for all life.
Within the framework of Intelligent Design creationism, the conclusion is inescapable: their designer deity—typically equated with the omniscient, omnibenevolent god of the Christian Bible—knowingly and deliberately created a pathogen that causes immense suffering. If ID logic is followed consistently, their deity is not a benevolent creator but a malevolent force that engineers disease and deformity with full foreknowledge of the consequences.
The only escape from this theological and philosophical bind is for ID creationists to refute their own criteria—to claim that irreducible complexity and complex specified information are compelling proof of design when found in beneficial biological systems, but somehow irrelevant or invalid when found in destructive pathogens. In doing so, they are forced to hold two mutually exclusive beliefs simultaneously.
In reality, these hallmarks of design touted by ID advocates are common outcomes of natural evolutionary processes — especially arms races between host defences and parasitic invaders. These processes are inherently unguided and wasteful, which in itself refutes the idea of intelligent planning.
Another striking example of this evolutionary struggle has just been published in Nature Microbiology by researchers from the University of Pittsburgh School of Medicine and the La Jolla Institute for Immunology. Their study sheds light on how the herpesvirus has evolved sophisticated strategies to evade the immune system — a feature that ID logic would classify as evidence of "design."
Graphical representation of urea formation in a droplet.
Figure: Luis Quintero / ETH Zürich.
Creationism's ever-shrinking, gap-shaped creator god has just lost a little more ground. New research suggests that the formation of basic organic molecules may have been far easier under early Earth conditions than previously thought. Remarkably, scientists have found that urea—a key organic compound—can form spontaneously from ammonia and carbon dioxide on the surface of water droplets. This process requires no catalysts, no high pressure or heat, and consumes minimal energy.
Although vitalism was refuted as early as 1828 — decades before Darwin — creationists still claim that life cannot arise from non-living matter. Yet they quickly retreat when asked how dead food becomes living tissue, or what exactly they mean by ‘life’: a substance, a process, or some kind of magical force. In reality, life is a set of chemical processes, and at its core, it’s about managing entropy—using energy to maintain order against the natural drift toward disorder.
The discovery was made by researchers at Eidgenössische Technische Hochschule (ETH) Zürich in collaboration with colleagues from Auburn University in Alabama, USA. Their findings have just been published in Science.
The knee-jerk response from any creationist worth his or her salt, when shown evidence of observed instances of evolution, is to demand a redefinition of the term *evolution*—away from its scientific meaning of a change in allele frequency in a population over time, and towards the creationist’s caricature: a species instantaneously transforming into an entirely unrelated taxon. This is, of course, something evolutionary biologists have never claimed, and which—if it ever occurred—would actually refute the Theory of Evolution.
This is the all-too-familiar, disingenuous tactic of setting the bar impossibly high for one’s opponent, while keeping it at ground level for one’s own evidence-free superstition.
So, for those creationists more interested in finding workarounds to ease the cognitive dissonance between what they would like the facts to be and what science actually shows, than learning the truth about the world around us, the news that researchers at Chicago’s Field Museum have demonstrated evolutionary change in the city’s rodent populations over the last 125 years will likely present little difficulty. They can always chant, “But it’s still a chipmunk/vole/etc., so not evolution!”
However, for those with the intellectual integrity and humility to base their opinions on observable evidence, rather than dismissing any evidence that doesn't conform to their preconceived alternative reality, this finding is a compelling vindication of a basic principle of the Theory of Evolution: that species change over time in response to environmental pressures.
The researchers have recently published their findings in the journal Integrative & Comparative Biology.
