Malevolent Designer News - How A Bacterium Is 'Intelligently Designed' To Spread Disease

Blacklegged tick, Ixodes scapularis

Bacteria hijack tick cell defenses to spread disease | WSU Insider

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.

This discovery was made by researchers at the College of Veterinary Medicine, Washington State University (WSU). Their findings have just been published in Proceedings of the National Academy of Sciences (PNAS) and are explained in lay terms in WSU Insider, the university's online news outlet.

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.

1. 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).
   
   
2. Disease in Humans
   • Caused mainly by Anaplasma phagocytophilum.
   • Known as Human Granulocytic Anaplasmosis (HGA).
   • Symptoms include:
     • Fever, chills, headache
     • Muscle aches
     • Malaise
     • Occasionally gastrointestinal symptoms (nausea, vomiting)
     • 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.
   
   
3. 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.
   
   
4. 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.
   
   
5. 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.
   
   
6. 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 disease

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Washington 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.

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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.

Publication:

K.A. Vosbigian,S.J. Wright,B.P. Steiert,K.L. Rosche,E.A. Fisk,E. Ramirez-Zepp,J.M. Park,E.A. Shelden,& D.K. Shaw
ATF6 enables pathogen infection in ticks by inducing stomatin and altering cholesterol dynamics
Proc. Natl. Acad. Sci. U.S.A. 122 (25) e2501045122, https://doi.org/10.1073/pnas.2501045122 (2025).

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.

K.A. Vosbigian,S.J. Wright,B.P. Steiert,K.L. Rosche,E.A. Fisk,E. Ramirez-Zepp,J.M. Park,E.A. Shelden,& D.K. Shaw
ATF6 enables pathogen infection in ticks by inducing stomatin and altering cholesterol dynamics
Proc. Natl. Acad. Sci. U.S.A. 122 (25) e2501045122, https://doi.org/10.1073/pnas.2501045122 (2025).

Copyright: ©2025 The authors.
Published by the National Academy of Sciences of the USA. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)

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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This book presents the reader with multiple examples of why, even if we accept Creationism's putative intelligent designer, any such entity can only be regarded as malevolent, designing ever-more ingenious ways to make life difficult for living things, including humans, for no other reason than the sheer pleasure of doing so. This putative creator has also given other creatures much better things like immune systems, eyesight and ability to regenerate limbs that it could have given to all its creation, including humans, but chose not to. This book will leave creationists with the dilemma of explaining why evolution by natural selection is the only plausible explanation for so many nasty little parasites that doesn't leave their creator looking like an ingenious, sadistic, misanthropic, malevolence finding ever more ways to increase pain and suffering in the world, and not the omnibenevolent, maximally good god that Creationists of all Abrahamic religions believe created everything. As with a previous book by this author, "The Unintelligent Designer: Refuting the Intelligent Design Hoax", this book comprehensively refutes any notion of intelligent design by anything resembling a loving, intelligent and maximally good god. Such evil could not exist in a universe created by such a god. Evil exists, therefore a maximally good, all-knowing, all-loving god does not.

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Malevolent Design - How Having a Bigger Brain Made Humans More Vulnerable To Cancer Than Our Chimpanzee Cousins

A Single Genetic Mutation May Have Made Humans More Vulnerable to Cancer Than Chimpanzees | Newswise

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.

It’s almost as though the 'designer' either deliberately endowed humans with a cancer-promoting mutation or failed to anticipate the consequences of the so-called "complex specified genetic information" (© William A. Dembski / Discovery Institute) introduced to facilitate brain growth—and then neglected to revise the design when the flaw became evident. But, of course, being omniscient, we have to assume, if we accept creationists dogma for the sake of argument, it knew full well what the consequences of its design would be and designed them with that consequence in mind.

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.

Malevolent Designer - How A Common Virus Sneaks Past Our Immune System And Causes Birth Defects

Scientists Uncover How a Common Herpes Virus Outsmarts the Immune System | School of Medicine | University of Pittsburgh.

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."

Malevolent Designer News - How Cold Sores Are Cleverly Designed To Maximise Suffering.

The human genome compacted inside cells
eight hours after infection.

Credit: Esther González Almela
and Álvaro Castells García

(Top) Cropped representative STORM-PAINT images of EdC-AF647 labeled hDNA (magenta), immunolabeled H3 (green), and their merge in mock and HSV-1 infected A549 cells. Scale bar: 2 µm. (Bottom) Zoomed-in regions are shown inside yellow boxes. Scale bar: 200 nm.

González-Almela, E., Castells-Garcia, A., Le Dily, F. et al. (2025)

Centre for Genomic Regulation Website

One of the many problems with Intelligent Design (ID) creationism is its complete failure to account for evolutionary arms races.

According to leading ID proponents like William A. Dembski and Michael J. Behe, living organisms and their parasites — including viruses — must have been intelligently designed because they are supposedly “irreducibly complex” and exhibit “complex specified information”. But if that were true, it would mean the same designer is deliberately crafting both parasites and the defence mechanisms their hosts use to fend them off — hardly the mark of a supremely intelligent creator.

A further problem, and one that creationists prefer to ignore, is theological: designing pathogens like viruses is fundamentally incompatible with the notion of a benevolent creator. In fact, it suggests a malevolent intelligence — one more concerned with maximising suffering than promoting life and maximising happiness. So, when science uncovers yet another example of a virus behaving with surgical precision and apparent ingenuity, ID creationists find themselves in a bind. Is irreducible complexity and complex specified genetic information not evidence of intelligent design after all? Or must they admit that the designer is, at best, morally indifferent — or worse, actively malevolent?

The latest headache for the ID camp comes courtesy of the Herpes simplex virus — the one responsible for cold sores. Researchers at the Centre for Genomic Regulation (CRG) in Barcelona, Catalunya, Spain, with colleagues in Guangdong Provincial People’s Hospital, Guangdong, China, have discovered that the virus can radically reorganise a host cell’s genetic architecture — and it does so using the host's own cellular machinery. Their findings have just been published open access in Nature Communications.

Unintelligent Designer News - Designed a Cure For COVID-19; Gave It To LLamas - Or Is It Malevolence?

How the single domain antibody locks onto the spike protein’s base

Researchers identify new antibodies against current and future coronaviruses | VIB.BE - Home

Hot on the heels of the news that the putative intelligent designer behind creationism apparently devised a method to prevent the spread of cancer cells through the body—then handed it to the sea cucumber, a group of species not especially prone to cancer—comes another remarkable revelation.

It now appears that this same designer, if we accept the claims of ID creationists, has also developed a highly effective mechanism for disabling the SARS-CoV-2 virus that causes COVID-19. And once again, rather than bestowing this gift upon humans, the species most affected by the virus, the designer gave it to llamas — creatures not exactly known for their vulnerability to coronaviruses.

The mechanism in question involves relatively simple molecules known as single-domain antibodies, or VHHs—also referred to as nanobodies. These are much smaller than the conventional antibodies produced by most animals, including humans. They work by binding tightly to the virus’s spike proteins, effectively neutralising it by preventing it from prising open host cells and initiating infection. Even more impressively, these nanobodies appear to be broadly effective against a wide range of SARS-related coronaviruses.

While creationists might marvel at the ingenuity of such a designer, they would be hard-pressed to explain — or more likely, would simply ignore — why this supposedly anthropophilic intelligence chose not to equip humans with such a defence. Instead, it stood idly by as millions suffered and economies collapsed, despite having the ‘cure’ readily available.

This unique llama-specific mechanism was discovered by a team of researchers led by Prof. Xavier Saelens and Dr. Bert Schepens at the Flemish Institute for Biotechnology (Vlaams Instituut voor Biotechnologie) – University of Ghent (VIB-UGent) Center for Medical Biotechnology.

Malevolent Designer - Creationism's Putative Desiger Designed A Way to Prevent Cancer Spreading - And Gave It To Sea Cucumbers!

A sugar compound found in sea cucumbers could hold the key to stopping the spread of cancer, according to a recent UM-led study published in Glycobiology.

Graphic by Stefanie Goodwiller
University Marketing and Communications

Sea Cucumbers Could Hold Key to Stopping Cancer Spread | Ole Miss

Imagine you're a designer, and you've created a species — humans — for whom you have a particular fondness. Only, something keeps going dreadfully wrong with your blueprint. A large number of them keep dying because their cells become cancerous when they fail to replicate properly, and these cancers then spread to other organs, which ultimately give up the ghost.

Now, you can’t quite work out why these cancers start. For some reason, you've included substances called glycans on the surfaces of cells, and — just to complicate things — you’ve made cancer cells produce an enzyme called Sulf-2, which alters these glycans to help the cancer spread. Your solution? A stroke of genius: create another enzyme that inhibits Sulf-2. And lo! It works.

So, who do you give this life-saving enzyme to?

If you're creationism’s supposedly super-intelligent designer, you don’t give it to your favourite species — the one made in your own image, no less. No, instead you bestow this miracle molecule upon… sea cucumbers. A species that, incidentally, doesn’t even have a problem with cancer.

This, if they actually understood the subject properly, is what Intelligent Design creationists consider compelling evidence of a supremely intelligent designer.

The discovery that sea cucumbers possess this enzyme was made by researchers at the University of Mississippi and Georgetown University in Washington, DC. Their findings are published in the journal Glycobiology and can be read here.

It’s also neatly summarised in a University of Mississippi news article:

Refuting Creationism - Co-Evolution of Humans and Influenza Viruses - Just as the TOE Predicts

AI-generated image (ChatGPT4o)

H3N2 virus is a respiratory viral infection of the influenza A virus.

Large-scale immunity profiling grants insights into flu virus evolution | For the press | eLife

In a striking confirmation of evolutionary theory—and a clear rebuttal of several fundamental creationist claims—scientists have demonstrated a close correlation between population-level immunity and the evolution of influenza viruses to evade that immunity. The findings, reported in eLife, align perfectly with predictions made by evolutionary biology: as the immune landscape of a population shifts, so too does the genetic makeup of viruses in an ongoing evolutionary arms race.

Disappointingly for creationists hoping for signs that biomedical science is abandoning evolution in favour of supernatural explanations, there is no such evidence. Nowhere in the study is there a hint that scientists are retreating from evolutionary principles or embracing a non-falsifiable belief system involving mysterious, unexplained entities. On the contrary, the researchers are clear and unequivocal: their results reinforce the view that viral evolution is a dynamic, adaptive process shaped by natural selection in response to host immunity.

Even more troubling for proponents of Intelligent Design (ID) is the unavoidable implication that the viral mutations observed in this study constitute what William A. Dembski calls "complex specified information"—which he argues can only arise through the intervention of an intelligent designer. If one follows that line of reasoning, the logical (if deeply uncomfortable) conclusion is that this designer is actively modifying viruses to undermine the very immune systems it supposedly created to protect us. Such behaviour can hardly be described as intelligent and is incompatible with the benevolent deity so often associated with the Intelligent Design movement.

Malevolent Or Incompetent Design? - Or Just Mindless Evolution?

Chikungunya virus has become a disease of global concern due to its potentially disabling consequences and its efficient transmission.

The Aedes mosquito is the primary vector for the Chikungunya virus

LJI scientists uncover clues to how a viral infection can lead to arthritis-like disease – lji.org

Scientists believe they have uncovered a mechanism by which a viral infection can trigger a persistent autoimmune response, leading to chronic and often severe pain.

If fully understood, this discovery poses a significant challenge to Intelligent Design (ID) creationism. Under the ID paradigm, such an outcome leaves us with two unpalatable options: either the designer is incompetent, having failed to foresee the consequences of a poorly calibrated immune system, or the suffering inflicted on random individuals is intentional—engineered by design.

This finding also reignites a long-standing issue for creationism: the existence of parasites, particularly viruses. According to criteria promoted by Discovery Institute fellows William A. Dembski ("complex specified information") and Michael J. Behe ("irreducible complexity"), viruses must be regarded as the product of intelligent design. Yet these same entities are responsible for making us ill—seemingly by the same designer who supposedly crafted our immune system to protect us from them. The contradiction is striking.

The explanation stems from recent work by a research team at the La Jolla Institute for Immunology and is published in Cell Reports Medicine.

Malevolent Designer News - How an Intelligent Designer COULD Have Made us all Immune to HIV but Chose not to

Researchers map 7,000-year-old genetic mutation that protects against HIV – University of Copenhagen

Let’s step into the mindset of an Intelligent Design (ID) creationist for a moment, as we examine a recent scientific study investigating why a small minority of people are immune to the Human Immunodeficiency Virus (HIV), while the vast majority are not.

A research team from the Novo Nordisk Foundation Center for Basic Metabolic Research (CBMR) at the University of Copenhagen, led by Professor Simon Rasmussen, has discovered that this immunity is conferred by a genetic mutation. This mutation originated in a single individual who lived near the Black Sea between 6,700 and 9,000 years ago.

According to Discovery Institute Fellow William A. Dembski, this mutation would represent what he calls “complex specified information”, a concept he attributes to an intelligent designer. Dembski argues that only such a designer could create the necessary genetic information, as mutation and natural selection alone are not goal-directed and therefore cannot produce the desired specificity. However, Dembski is notably vague about how we can objectively determine what genetic information is “specified” and what is not. He appears to rely on subjective judgement, essentially deeming any beneficial mutation as “specified”, while dismissing deleterious mutations as irrelevant.

Even granting Dembski his biased subjectivity, we are left with the implication that the mutation which conferred HIV immunity to this individual's descendants must have been “specified” by his proposed intelligent designer.

This raises an obvious question: if the intelligent designer of humans could have provided our species with immunity to HIV, why did it choose not to do so from the outset? Why rely on what appears to be a slow, natural evolutionary process to spread this mutation through the population—one that depends on people dying of HIV while those with the mutation survive and reproduce, creating the selection pressure for its spread? A process so gradual that, to this day, it remains a rare trait in the human gene pool, with only 18-25% of Danes carrying the mutated gene.

It also raised a couple of theological question for creationists: why would an omnibenevolent creator create HIV with its 'designed' ability to bypass our immune system the same designer allegedly designed to protect us and how is that an intelligent act by an omnibenevolent deity?

Malevolent Designer - How The Influenza Virus Appears To Be Intelligently Designed to Make Us Sick

Confocal microscopy of a cell (magenta, cell nucleus in blue) of the A549 cell line on immobilized influenza viruses (green).

© HZI / Broich

Influenza virus. 3D illustration showing surface glycoprotein spikes hemagglutinin purple and neuraminidase orange.

Image Credit: Kateryna Kon / Shutterstock.

HZI | How influenza viruses communicate with cells

In their attempts to pass creationism off as legitimate science, Discovery Institute fellows William A. Dembski and Michael J. Behe have unwittingly undermined their own case. Their arguments—largely based on a classic god-of-the-gaps fallacy and a false dichotomy—can just as easily be turned against the very idea that their supposed intelligent designer is the God of the Christian Bible.

While they stop short of making that claim explicitly, the infamous Wedge Document [1.1], which outlines the political aims and strategy of the Discovery Institute, leaves no doubt: their ultimate goal is a fundamentalist Christian theocracy governed by so-called "Christian principles" and that selling the idea that 'Intelligent Design' creationism is real science, is a fundamental aspect of that strategy because it would enable them to teach creationism to children at taxpayers' expense, under the guise of real science.

And yet, even within their own paradigm, the evidence points not to a benevolent deity but to something far more disturbing.

Take, for example, recent research from the Helmholtz Centre for Infection Research, which offers a striking illustration of what Dembski might call "complex specified information" and what Behe might regard as "irreducible complexity". The study reveals how the influenza virus is 'designed'—if one accepts their terminology—with remarkable sophistication to circumvent our defences and invade human cells. Ironically, these very defences are what the same creationists insist were intelligently designed to protect us—against, among other things, intelligently designed viruses. We are left, according to this worldview, with the absurd spectacle of a designer who engineers both the pathogens and the immune system meant to defend us from them—a system that, demonstrably, does not always work.

And this is held up as evidence of a supreme intelligence!

Far from supporting creationist claims, these findings align far more convincingly with what we would expect from a blind, indifferent process of evolution—one that requires no designer at all. Once again, creationists are faced with an uncomfortable dilemma: either accept the notion of a malevolent and inept designer or acknowledge the explanatory power of natural selection and evolutionary biology.

Unintelligent Design - The Design Defect That Can Cause a Cleft Palate - Incompetence, Malevolence or Evolution?

Medical science corrects a design defect.

Source

New study reveals how cleft lip and cleft palate can arise | MIT News | Massachusetts Institute of Technology

In my book, The Body of Evidence: How the Human Body Refutes Intelligent Design, I present numerous examples demonstrating that the human body is not the product of intelligent design, but rather the outcome of an evolutionary process characterised by compromises and suboptimal solutions. Evolution is constrained by what it has to work with and must continually balance competing demands—for instance, short-term reproductive success versus long-term health and well-being, which often contribute little or nothing to the long-term propagation of genes.

The result is an error-prone and overly complex system built upon earlier suboptimal compromises. This complexity gives rise to the many defects and medical problems to which humans are prone—problems that would not exist if the human body were the creation of an intelligent and benevolent designer, such as the deity posited by creationist belief systems. Such a deity would surely have designed a body so robust that there would be little need for a medical profession, save perhaps for treating accidental trauma. The very existence of hospitals and medical science stands as a testament to the failure of the human body's design to approach anything resembling the perfection many creationists claim.

Now, researchers at the Massachusetts Institute of Technology (MIT) have identified yet another example of this flawed complexity: a defect in transfer RNA (tRNA) linked to babies being born with a cleft lip and palate. The defect lies in the DDX1 gene, which is essential for proper tRNA function. Without it, tRNA cannot deliver amino acids to ribosomes to synthesise proteins. In the absence of this crucial process, the cells that form the upper lip and the roof of the mouth cannot fuse correctly during development.

The findings, by a team led by Michaela Bartusel, are published in The American Journal of Human Genetics.

Malevolent Design - Why Did Bats Get a Better Immune System Than We Did?

A Carollia perspicillata bat from a colony that had been maintained at WSU Vancouver.

Photo: WSU

Seba's short-tailed bat, Carollia perspicillata

By Desmodus - Own work, CC BY-SA 4.0, Link

Bat cells could aid in fighting humans’ most deadly diseases | WSU Insider | Washington State University

Creationists assert that humans are the special creation of their designer god, placing humanity at the pinnacle of 'creation'. Even those theists who accept the Theory of Evolution but believe it was guided by God with humans as the intended ultimate outcome, regard humanity as their deity's supreme achievement.

If this claim were accurate, it would be reasonable to expect humans to possess the optimal anatomical and physiological characteristics across all biological systems. In reality, numerous species exhibit superior traits and abilities compared to humans—traits which, had they been bestowed upon humans, would have significantly improved our wellbeing and survival capabilities.

For instance, birds have a respiratory system far superior to mammals, including humans, enabling efficient oxygen exchange during flight. Raptors possess remarkable eyesight, allowing them precise vision at speeds that would render nearby objects a mere blur to human vision. Elephants, sharks, and naked mole rats exhibit extraordinary resistance to cancer. Furthermore, many mammals experience lower perinatal mortality rates than humans even with modern medical intervention.

As highlighted in a recent study published in PLOS Biology, bats tolerate viral infections that are often fatal to humans, so they can harbour evolving viruses that, when they find their way into humans, can result in serious pandemics such as the recent COVID-19 pandemic.

If we entertain the creationist argument, their purported intelligent designer had already perfected these advantageous traits in other species. Yet, paradoxically, humans were deprived of these beneficial adaptations. This scenario suggests a designer whose decisions could only be interpreted as either incompetent or malevolent. It is the equivalent of a car manufacturer having designed a super-efficient, low-emission and cheap engine in one of its models, continuing to fit an old, expensive, wasteful and polluting engine to its top of the range model.

However, the evolutionary explanation — that different species evolved distinct traits adapted specifically to their environmental pressures — fully clarifies why humans possess adequate but not necessarily optimal traits. Unfortunately for creationists, adherence to their dogma forces them to dismiss this rational explanation, instead endorsing a narrative that inadvertently portrays their intelligent designer as either incompetent, malevolent, or potentially both.

That bats have superior immune system to humans has long been known, but why that is in terms of their cell physiology is still something of a mystery. Now, however, a team of researchers led by Washington State University molecular virologist Michael Letko has developed two lines of bat cell cultures which can be used to study how their immune system responds to different viruses, for example, the ebola virus, with a view to utilising that information to treat infections in humans.

Their findings are the subject of a research paper in PLOS Biology and are explained in a Washington State University (WSU) news item:

Malevolent Design - How Dembski's 'Complex Specified Information' Causes Acute Myeloid Leukemia

Rapid growth of blood cancer driven by a single genetic ‘hit’

William A. Dembski’s concept of complex specified information (CSI) remains ambiguous—arguably by design. His use of the word specified is particularly opaque: is he referring to information that produces outcomes he wishes his readers to believe are purposeful and intelligently designed by a particular deity, or is the term intended to encompass any genetic information that results in any outcome—beneficial, neutral, or harmful?

Taken at face value, and in the absence of a clear, testable definition, there appears to be no reason Dembski’s concept could not apply to information that is ultimately detrimental, either to the organism itself, or to another organism in the case of parasites or cancer. Why, for instance, should we conclude that the complex information in a gene enabling the expansion of the human brain and the enhancement of cognitive function was specified, but that the equally complex genetic information enabling a cell to become a malignant cancer, or allowing the Plasmodium falciparum parasite to evade anti-malarial drugs, was not also specified by the same intelligent designer?

Given that Dembski is a senior fellow of the Discovery Institute — an organisation notorious for its Wedge Strategy, which seeks to undermine public trust in science through disinformation and misrepresentation while promoting creationism under the guise of scientific legitimacy — it is unsurprising that complex specified information remains a nebulous and ill-defined term. The strategy’s aim has never been to engage in genuine scientific discourse or subject its claims to critical scrutiny, but rather to advance a religious agenda while avoiding the accountability that comes with reasoned analysis and empirical testing. A cynic might conclude that the leading ID advocates know their claim has no scientific basis but want their target audience to believe otherwise.

So, I invite Intelligent Design creationists to explain why the recent discovery of a gene that promotes the rapid early development of acute myeloid leukaemia should not be an example of Dembski's 'complex specified information' and so evidence that Dembski's intelligent designer designed acute myeloid leukaemia, or whether Dembski's term is deliberately vague so as to appeal to people looking for confirmation of existing bias.

Unintelligent Design - If Scientists Can Do It, Why Can't an Intelligent, Omnipotent Designer - If It Wanted To?

Treatment for mitochondrial diseases within reach | University of Gothenburg

If the human body had truly been intelligently designed by an omnibenevolent, omniscient deity, it would operate flawlessly under all conditions, free from the compromises and constraints inherent in evolutionary history.

Were this the case, much of modern medicine would be unnecessary, limited perhaps to the management and repair of traumatic injuries. Parasites, should they exist at all, would be effortlessly repelled by a perfect immune system. Genetic and structural defects, such as hernias, atherosclerosis, autoimmune disorders, blindness, deafness, neurodegenerative diseases, and complications in childbirth would simply not occur.

However, as I showed in my book, The Body of Evidence: How the Human Body Refutes Intelligent Design, the human body is not the product of intelligent design; it has evolved through a process marked by trial and error, adaptation to existing structures, and the utilitarian pressures of survival and reproduction. This explains the vast array of medical conditions that keep healthcare systems busy, often stretched to their limits. It also drives the extensive scientific research dedicated to discovering the causes and developing cures for various illnesses—achievements that an omnipotent and omnibenevolent creator, if one existed, presumably would have provided already.

Recent news highlights this contrast starkly. Scientists may have discovered a groundbreaking cure for a rare mitochondrial disease caused by mutations in the POLG gene, a condition that leads to severe disability or even early death. This advancement prompts a critical question for creationists: If human scientists can find solutions to such devastating genetic problems, why can't—or won't—your purported intelligent designer? And perhaps, more to the point, why was this defect designed in the first place?