Malevolent Design - More Evidence That Malaria Was 'Designed' By Creationism's Putative Designer God? - Or Just Evolution Again?

A daughter parasite forms through budding from the mother cell.

As budding of the daughter parasite progresses and membrane protrusion increases (yellow), the molecular safety rope (blue) lengthens.

The images were created based on electron microscopy data and processed using AI.

© UKHD

Figure EV1: Blood-stage immunofluorescence expression profile of PfSFA2 and ultrastructure expansion microscopy (U-ExM) of PfSFA1 localization.

(A) IFA of PfSFA2-smV5 expression across the asexual blood stages, stained with an anti-V5 antibody (green), an anti-PfGAP45 antibody (magenta), and Hoechst (DNA, blue). “Ring” stage with one nucleus, trophozoite stage (“Troph”) with 2, and several stages throughout schizogony, including segmentation, are shown with the number of nuclei. The minimum and maximum displayed values for the PfSFA2-V5 and PfGAP45 channels follow the “Reset” values of the first segmentation image. Scale bars: 2 µm. (B) U-ExM of PfSFA1-smV5 schizonts stained with an anti-V5 antibody (cyan), an anti-CrCen antibody (outer-CP, magenta), SYTOX (DNA, blue), and an NHS ester-conjugated dye (grayscale). Sub-z-slices of a 7-nuclei (top) and a 14-nuclei (bottom) schizont are maximally projected and shown to the left. Representative centriolar plaque regions are numbered and shown as insets to the right. Z-depth of each maximum projection is shown to the right. Scale bars: 5 µm for full schizont; 1 µm for inset.

He, B., Ali, I., Dorner, L.P. et al. (2026).

News - Research in Germany

Creationists insist that certain biological systems are too complex to have evolved. If several interacting components are required for a system to function, they label it “irreducibly complex”; if genes encode proteins that perform a particular function, they call the DNA “complex specified information”. Both are then presented as evidence that the system must have been deliberately designed by an intelligent agent.

Curiously, however, this supposedly reliable design-detection method tends to be applied only to systems that creationists find impressive or beneficial. When comparable complexity enables a parasite to invade its host, evade its defences, reproduce rapidly and cause suffering and death, the inference to design is quietly abandoned. The parasite is instead blamed on “the Fall”, “genetic degeneration” or some other evidence-free theological excuse.

But a method that gives different answers according to whether its conclusion is theologically convenient is not a method at all. If molecular complexity, functional interdependence and genetically encoded organisation really demonstrate intelligent design, then they must do so just as reliably in a malaria parasite as in a bacterial flagellum, an eye or a blood-clotting system. And that would make them evidence not merely of intelligent design, but of intelligent malevolent design.

Two recent studies have now uncovered more of the extraordinarily elaborate machinery by which malaria parasites multiply. Instead of dividing into two daughter cells in the familiar way, Plasmodium parasites repeatedly copy their DNA and multiply their nuclei within a shared cell before producing numerous daughter parasites more or less simultaneously. The process must ensure that each viable daughter receives a nucleus and the cellular structures required to invade another host cell.

Malevolent Design - How Melanomas Are Cleverly 'Designed' To Stay Alive

Telomeres shown as white caps on the ends of the chromosome arms.

Pitt scientists discovered a key genetic step in melanoma’s race to live forever | University of Pittsburgh

Examples from nature in which, if creationist arguments for the existence of an intelligent designer are applied consistently, that designer can only be regarded as a malevolent entity intent on increasing suffering in the world, continue to accumulate. And the more examples there are, the more creationists need to ignore their own arguments, abandon any pretence that creationism is a genuine alternative science, and retreat instead into the fundamentalist biblical myths of 'The Fall' and 'Original Sin'. The evidence remains the same; only the interpretation is twisted to preserve the preferred narrative.

The latest such example concerns the genetics behind one of malignant melanoma's most dangerous properties: its ability to evade the normal cellular limit on repeated division. This had long been a missing piece in understanding how melanoma cells avoid the ordinary route to cellular senescence and continue to proliferate. Like Michael J. Behe's and William A. Dembski's supposed 'evidence' for intelligent design, it depends on a set of interacting components being in place and on genetic changes producing just the right molecular effect — precisely the kind of arrangement the Discovery Institute insists cannot arise by natural processes because, in its caricature of biology, evolution is merely 'random chance'. That claim, of course, ignores the elementary biological fact that natural selection makes evolution very much a non-random process.

The discovery, published in Science in November 2022 by Pattra Chun-on, Jonathan K. Alder and colleagues, concerns telomeres — the protective caps at the ends of chromosomes. In most normal somatic cells, telomeres gradually shorten with repeated cell division until the cell can no longer divide. This is one of the body's safeguards against uncontrolled proliferation. Cancer cells, however, often find ways to bypass this limit, and melanoma has long been known for having unusually long telomeres, even compared with many other cancers. What had not been fully understood was how melanoma achieved this.

The answer involves telomerase, the enzyme complex that lengthens telomeres. In most normal adult cells, telomerase activity is switched off or kept very low. Many melanomas carry mutations in the promoter region of TERT, the gene that encodes the catalytic component of telomerase, and these mutations increase telomerase activity. But that turned out to be only part of the story. When researchers introduced TERT promoter mutations into melanocytes, they did not reproduce the exceptionally long telomeres seen in melanoma tumours.

The missing component was TPP1, a member of the shelterin complex that helps regulate telomeres. The researchers found that mutations in the promoter region of ACD, the gene that encodes TPP1, can increase TPP1 production. When these TPP1-promoter mutations occur together with TERT promoter mutations, the two changes cooperate to produce the long telomeres characteristic of melanoma. In other words, melanoma's ability to evade normal cellular mortality depends on a coordinated interaction between altered telomerase activity and altered telomere regulation.

So, in intelligent-design creationist terms, we have a system requiring interacting molecular components, each specified by genetic changes in ordinary cellular genes, and each contributing to a result that benefits the cancer cell at the expense of the patient. If the same kind of molecular cooperation in a harmless or useful organism is to be paraded as evidence of design, then consistency demands the same conclusion here. Melanoma, on that argument, would be another product of the same intelligent designer — one whose ingenuity is directed towards helping cancer cells escape the body's normal restraints.

Of course, the scientifically honest conclusion is not that melanoma was designed, malevolently or otherwise. It is that cancer exploits the same evolved molecular machinery that normal cells use, and that mutations filtered by selection within the tumour can favour cells that divide faster, survive longer and outcompete their neighbours. The creationist problem is that the very mechanisms they claim as evidence for their designer are just as plainly at work in disease, parasitism and suffering.

Malevolent Design - A Brilliantly 'Designed' Process For Spreading Influenza - Malevolence or Evolution?

Dead cells after the self-destruction and fragmentation process. The large green areas are the “eat me” signals which alert immune cells to kick-start clean-up and recycling process, while the small green circles are the “Footprint of Death” F-ApoEVs left behind by the dying cell.

’Footprint of Death’ gives new clues to cell life, News, La Trobe University

My previous post was about the discovery, reported in Cell Host & Microbe in May 2026, that a single amino-acid change in a coronavirus protein can alter how a bat-related coronavirus interacts with the immune systems of bats and humans. In the case of SARS-CoV-2, the virus that causes COVID-19, such changes help to explain how a virus that may be relatively benign in its natural host can become a serious pathogen when it crosses the species barrier into humans. By creationists' own criteria, this should qualify as intelligent design.

This post concerns another example which, if creationists applied their criteria for intelligent design consistently, would be further evidence of malevolent design. It is the finding, reported in Nature Communications, that influenza A virus can exploit part of the normal process of programmed cell death to help infect neighbouring cells.

Applied consistently, these discoveries would portray creationists' putative designer god as a malevolent entity that designs ways to increase suffering. But, since creationists need to portray this alleged designer as the omnibenevolent god of the Bible, this supposed 'evidence of intelligent design' somehow ceases to be evidence of design at all and becomes evidence of 'Sin' and 'The Fall', as creationists abandon any pretence of science and retreat into Biblical mythology to explain away inconvenient facts.

The discovery, by a team led by PhD candidate Stephanie Rutter in Professor Ivan Poon’s lab at the La Trobe Institute for Molecular Science (LIMS), shows how each step in the process of cell death and renewal is important in helping a dying cell break down and be cleared away by the body’s immune system. The team found that, as cells self-destruct, they change shape, lift away from their surroundings, and leave behind a residue which the researchers dubbed the 'footprint of death'. This contains a previously undescribed type of extracellular vesicle (EV). EVs are small packages used by cells to transport proteins, lipids, DNA and RNA to other cells, acting as an important means of communication between cells.

These new vesicles, known as FOOD-derived apoptotic extracellular vesicles, or F-ApoEVs, normally mark the site of a dead cell and help the immune system identify and clear away the remaining fragments, preventing inflammation and other harmful consequences. But this useful clean-up process can also be turned into a weakness. The researchers found that, when dying cells are infected with influenza A virus, viral proteins and even virus particles can be carried in these F-ApoEVs, providing another route by which infection can spread to neighbouring cells.

Had this process been beneficial to humans, rather than to influenza viruses, creationists would doubtless hail it as a marvel of intelligent design by their god. Yet, because the benefit is to a virus and the result can be disease, suffering and death, the same kind of complexity somehow ceases to count as evidence of design and is quietly reclassified as a mysterious consequence of 'The Fall'.

Creationists get into this bind because they are trying to force the evidence into their preferred mythology. Science has no such problem. The immune system, cell-death pathways and the pathogens that exploit them are all products of evolutionary history, not foresight. They are parts of a continuing arms race in which every useful biological process presents opportunities for parasites, viruses and other pathogens to exploit. An influenza virus that stumbles upon a weakness in a host system does not need to understand it, plan it, or design it; it merely needs to leave more copies of itself than viruses that did not.

Malevolent Design - How SARS-CoV-2 Was Cleverly Designed to Jump From Bats To Humans - Evolution Or Malevolence

A Single Molecular Change May Help Viruses Jump from Bat to Human | UC San Francisco

Two recent papers should delight admirers of creationism's putative intelligent designer, because both show the sort of biochemical ingenuity they normally rush to claim as evidence of design. One, published in Cell Host & Microbe in May 2026 and reported by UCSF in June, shows how a single molecular change can alter the way a coronavirus interacts with bat and human immune systems, helping to explain how viruses related to SARS-CoV-2, the virus that caused the COVID-19 pandemic, can cross the species barrier. The other, published in October 2025 in Nature Communications, which will be the subject of my next blog post, shows how influenza A virus can exploit the remnants of dying cells to help spread infection to neighbouring healthy cells.

However, that excitement is likely to be tempered somewhat when it dawns on them that, if these systems are the products of intelligent design, their designer can only be regarded as malevolent, since the result is an increase in the sum total of suffering in the world. But this does not seem to trouble ID proponents who cite Michael J. Behe's favourite examples — the Escherichia coli flagellum and anti-malarial drug resistance in Plasmodium falciparum — as evidence of irreducible complexity and hence of intelligent design, while ignoring the awkward fact that these supposed examples of design help microorganisms survive, move, infect, or evade human attempts to control them.

This puts creationists in a familiar bind. On the one hand, they like to claim any useful biological complexity as evidence of their Biblical god. On the other, when the same logic points to a designer of pathogens, parasites, immune evasion, drug resistance and viral spread, they retreat into vague claims about 'Sin', 'The Fall', or some mysterious corruption of nature, thereby absolving their god of responsibility for the very mechanisms they were praising as designed only moments earlier.

The first paper, in Cell Host & Microbe, was by a large team of researchers from the University of California San Francisco (UCSF) Quantitative Biosciences Institute, the Icahn School of Medicine at Mount Sinai, the Institut Pasteur and the Fred Hutchinson Cancer Center. It showed that a single amino-acid change in a viral protein can alter how coronaviruses interact with bat and human immune systems, changing the host's response to infection.

Bats are important viral reservoirs because their immune systems and physiology can allow them to tolerate viruses that might cause serious disease in other mammals. They can therefore harbour viruses for long periods, providing opportunities for viral lineages to persist, diversify and acquire mutations that may matter greatly when those viruses encounter a new host species. The UCSF-led study helps to explain how relatively small genetic differences can make the difference between a virus that remains associated with a bat reservoir and one that is better able to evade human immune defences.

This is precisely the sort of thing creationists should, by their own logic, have to call 'complex specified information'. The change is functional; it affects a specific biological outcome; and it is beneficial from the point of view of the viral lineage. The problem, of course, is that creationists usually smuggle in the assumption that 'beneficial' must mean beneficial to humans. If it benefits a virus, a bacterium, a parasite or a cancer cell, they suddenly decide it does not count.

Comparing SARS-CoV-2 with a related bat coronavirus, RaTG13, the researchers found that a viral protein called ORF9b was a key factor. The SARS-CoV-2 and RaTG13 versions of ORF9b are very similar, but behave very differently. In human cells, the SARS-CoV-2 version helped disable an innate immune alarm system, allowing the virus to multiply more effectively. In bat cells, the RaTG13 version interacted with a restriction factor that helped suppress infection.

The team found that changing just one of ORF9b's roughly 100 amino acids reversed its ability to evade the immune response. In creationist thinking, if the phrase is to mean anything at all, this would be new functional genetic information. Yet the actual explanation requires no magic, no designer and no supernatural intervention: a mutation changed an amino acid; that change altered protein interactions; and the result affected viral fitness in different host-cell environments. In other words, ordinary chemistry and physics, operating through mutation, selection and host-virus interaction, produced exactly the kind of functional change creationists insist cannot happen naturally.

The paper in Cell Host & Microbe was accompanied by a news item from UCSF by Levi Gadye:

Unintelligent Design - What Happens when A Badly 'Designed' Process Goes Rogue - Cancer - Malevolent Design Or Evolution?

Dr. Alexandra Nusawardhana, the lead author of the study and who earned her doctorate in biomedical sciences this year from Penn State College of Medicine, conducts research to understand genomic instability and cancer treatment response.

Credit: Jason Plotkin / Penn State. Creative Commons

DNA repair protein gene gone rogue may unlock new cancer treatments | Penn State University

A characteristic of evolved biological systems, and one that distinguishes them from systems designed from first principles, is that they are often unnecessarily complex, vulnerable to failure and dependent on layers of patchwork compensation. This is what we should expect from systems produced by utilitarian, suboptimal compromises built from whatever was available at the time.

With no plan, no foresight and no predetermined objective, natural selection can only favour whatever leaves more descendants in a particular environment. The result is not an ideal solution, but merely a workable one — one that is better than what preceded it, even if it remains a very long way from perfection. An intelligent designer, such as the one proposed by advocates of intelligent design, would be under no such historical constraints and could, in principle, rebuild a system from scratch to arrive at the optimal solution.

To illustrate this, this post and the next will look at two recent papers that incidentally demonstrate how many human health problems arise from these over-complex, error-prone systems — systems that would not exist if the human body were the pinnacle of created perfection that creationists imagine it to be. Unless, of course, the designer intended us to suffer when its systems failed.

The first concerns a paper published in February 2026 in Nature Communications by researchers at Penn State College of Medicine. It shows how one component of the DNA repair machinery — a system needed because DNA replication and maintenance are themselves vulnerable to error and damage — can itself go wrong and produce a pattern of genomic instability resembling that seen when the BRCA1 and BRCA2 tumour-suppressor pathway is defective.

The culprit is EXO1, a gene that encodes an exonuclease involved in DNA processing and repair. In normal cells, EXO1 helps trim and process damaged or mismatched DNA so that repair can proceed. But when EXO1 is overexpressed, as the researchers found in a significant proportion of several cancers, including about 20–30% of breast and ovarian cancers as well as melanoma, testicular, cervical and hepatobiliary cancers, too much of this normally useful protein becomes destructive. Instead of helping to preserve genome integrity, excessive EXO1 activity can degrade newly synthesised DNA during replication stress, expanding single-stranded DNA gaps and degrading reversed replication forks.

The result is a BRCA-like pattern of genomic instability even in cells whose BRCA pathway is still functional. In other words, the cell behaves in some important respects like a BRCA-mutant tumour cell, not because BRCA1 or BRCA2 is mutated, but because too much EXO1 has overwhelmed the normal protective system. This matters clinically because such tumours may respond to some of the same treatments used against BRCA-mutant cancers, including drugs that target DNA repair vulnerabilities.

So, we have a DNA replication and maintenance system that needs elaborate repair machinery because the genome is constantly vulnerable to damage; then we have the catastrophic consequences when that repair machinery itself goes rogue. Compare that with the simpler, more robust system we might expect from an intelligent designer endowed with foresight and unconstrained by evolutionary history. Complexity is not the hallmark of intelligent design that creationists claim it to be. In biology, it is very often the accumulated consequence of failure-prone, suboptimal compromises produced by evolutionary tinkering without a predetermined objective.

Malevolent Design - We Have The Ability To Regenerate An Amputated Limb - But It's Turned Off And Hidden

A conceptual graphic shows how growth factors BMP2 and FGF2 are applied to the injury site to stimulate tissue regeneration, highlighting new research into restoring damaged digits.

Credit: Melissa Bristow/Texas A&M University College of Veterinary Medicine and Biomedical Sciences

A–C Representative longitudinal sections and μCT images (insets) of control and FGF2 treated digits 21 days post treatment (DPT). A Control BSA treated digits do not display a regenerative response and are truncated. B The majority of FGF2 treated digits are truncated without displaying a regenerative response. C A minority of FGF2 treated digits produce an ectopic skeletal element distal to the amputation that articulates with the stump bone.

Yu, L., Yan, M., Scaturro, K.Z. et al. (2026).

What if humans could regrow tissue? Texas A&M study moves science closer – Texas A&M Stories.

Although the Discovery Institute and its Fellows who advocate for Intelligent Design are usually careful not to identify their putative “intelligent designer” explicitly with the God of the Christian Bible, the dog-whistle signals they use leave their target audience in little doubt. The designer is understood to be the Christian god, merely relabelled for legal and tactical convenience. That being so, and if that god were actively interfering in the design and evolution of living systems — with humans as the supposed pinnacle of creation and occupying a special place in it — we might reasonably expect humans to have been given the best design available.

Instead, nature looks exactly as an unplanned evolutionary process would lead us to expect: a patchwork of compromises, contingencies and inherited limitations. As I describe in my book, The Malevolent Designer: Why Nature's God is not Good, humans are remarkable in some respects, particularly in our relatively large brains and consequent cognitive abilities, but in most other respects we are not especially impressive. We are not the strongest animals, nor the fastest. Birds of prey have far better eyesight; barn owls and dogs have far better hearing in relevant ranges; dogs have a vastly superior sense of smell; elephants and some other long-lived animals have evolved impressive cancer-resistance mechanisms; and the immune systems of many bats are tuned in ways that make our own look distinctly ordinary.

But perhaps the most striking contrast is in the ability of some animals to regenerate lost or damaged body parts. Several species can regenerate structures that humans simply cannot replace. Salamanders can regrow limbs; fish can replace fins and repair tissues that would leave mammals permanently damaged; and some invertebrates can regenerate astonishing portions of the body. Yet, noticeably, all the prayers, incantations and appeals to divine mercy have never once been shown to regrow an amputated human limb, replace a lost eye, repair a severed spinal cord, or restore dead heart muscle after an infarction. Nor do we see cancerous sections of colon removed by surgery obligingly regrowing as healthy tissue in answer to prayer. These are not impossible biological feats in principle; they are just things our lineage cannot normally do.

Now researchers from Texas A&M College of Veterinary Medicine and Biomedical Sciences (VMBS) have found something that should be even more disturbing for Intelligent Design creationists. In a paper recently published in Nature Communications, they report that non-regenerating mouse digit wounds can be induced to move part-way towards regeneration. In other words, the relevant mammalian cells may not be entirely incapable of regeneration; their capacity appears to be suppressed or obscured by the normal wound-healing response. Creationists who reject the evolutionary explanation now need to explain why an intelligent, omnibenevolent designer would leave mammals, including humans, with a latent capacity for regeneration, while allowing that capacity to be overridden by scarring.

The researchers’ explanation makes perfect sense as the outcome of a utilitarian, unplanned evolutionary process. In mammals, rapid wound closure by scar-forming fibroblasts can be life-saving. A quick patch reduces blood loss, closes a route for infection and gives the injured animal a better chance of surviving long enough to reproduce. Regeneration, by contrast, is slower and more complex. Evolution has no foresight and no obligation to produce perfection; it merely preserves what works well enough under the circumstances. The injury is patched up with a near-enough-is-good-enough solution, and the animal lives to pass on its genes.

That, of course, should not have been beyond the wit of an intelligent designer to improve upon. A competent designer could have given us both abilities: rapid wound closure to prevent fatal bleeding and infection, followed by orderly regeneration of the missing structures. Instead, we have the familiar evolutionary compromise: survival first, elegance later — and often not at all.

The problem centres on fibroblast cells, which can follow different developmental routes. In ordinary mammalian wound-healing, they rapidly close the wound and form scar tissue. In strongly regenerative animals, similar cells can organise into a blastema — a temporary structure that seals the wound while also providing the cellular basis for rebuilding missing tissues. The Texas A&M team showed that, after the wound had first closed, applying fibroblast growth factor 2 (FGF2), followed later by bone morphogenetic protein 2 (BMP2), could redirect the response. The result was imperfect regeneration, but it included bone, tendon, ligament and joint-like structures.

The conclusion is not that humans are about to start regrowing limbs, nor that a mouse digit is the same as a human arm or leg. It is more interesting than that. The potential for regeneration in mammals may not have vanished completely. It may still be there, hidden beneath the faster, rougher, scar-forming response that natural selection has favoured. For creationists, that raises the awkward question of why their supposed designer would equip other animals with regenerative abilities, leave traces of the same capacity in mammals, and then arrange matters so that, when humans most need it, the system normally fails.

Malevolent Design - Fungi That Turn Spiders Into 'Zombies'

Spider infected with Gibellula pseudosolita

Chang, Chen-xin, et al (2026)

Spider infected with Gibellula pseudosolita

Chang, Chen-xin, et al (2026)

Inside the Hidden World of Spider-Attacking Fungi | Blog


Parasites are hard enough for creationists to force-fit into their predetermined belief that all things were created by an omnibenevolent god, short of resorting to the near-blasphemous claim that 'Sin' somehow gave a rival creator unfettered access to their god's supposedly perfect creation in order to corrupt and destroy it. That rather undermines the claim of perfection in the first place, because a perfect creation, by definition, ought not to be corruptible.

But even harder for creationists to explain are parasites which, judged by their own favourite pseudo-scientific slogans — 'complex specified information' and 'irreducible complexity' — appear exquisitely adapted not merely to parasitise a living organism, but to consume it from within and then use its body as a platform for producing more parasites. In Pensoft's own popular description, these are "zombie" fungi: araneopathogenic fungi that parasitise spiders, mummify them, and then grow spore-producing structures from their bodies.

For example, newly identified spider-attacking fungi have recently been reported in two papers, published respectively in IMA Fungus and MycoKeys. Together, they add to the growing picture of a hidden diversity of highly specialised fungal parasites adapted to exploit spiders in different habitats.

The first is a new species of Purpureocillium fungus, belonging to the Purpureocillium atypicola group: Purpureocillium atlanticum. It was discovered in Brazil's Atlantic Forest, where it infects trapdoor spiders hidden in their burrows in the forest floor. The fungus covers the spider in cotton-white mycelium and eventually sends a purple fruiting structure up from the spider's cephalothorax, allowing spores to be released above the burrow. This discovery also shows that Purpureocillium atypicola, originally discovered in Japan in 1897 and thought to be a single species, is actually a global complex of multiple species.

The second paper reports three new species of Gibellula fungi — Gibellula pseudopigmentosa, Gibellula pseudosolita, and Gibellula sinensis — discovered on spiders in China and Laos. These fungi erupt from spider bodies in stalked, branch-like structures, and the species were distinguished from one another by differences in their reproductive structures, spore-forming bodies and phylogenetic relationships.

Malevolent Designer News - How The Malaria Parasite Is Cleverly Designed to Maximise Suferring

Immune response to
Plasmodium falciparum infection

AI-generated image (ChatGPT 5.4 Thinking)

Plasmodium falciparum parasite.

Malaria’s mRNA: Messages that Mess with the Immune System | Weizmann USA

Research is continually revealing just how efficient the human malaria parasite, Plasmodium falciparum, is at making people sick — and, all too often, killing them. There can be few better examples of the sort of intricate, information-rich biological machinery that Discovery Institute Fellows such as Michael J. Behe and William A. Dembski insist points to an intelligent designer. Although they are careful never to say so plainly, their dog-whistle signals leave their followers in little doubt that this putative designer is meant to be the god of the Bible and Qur’an. That ambiguity gives them enough wriggle-room to tell courts and educators that Intelligent Design is science, not creationism in a lab coat, while still presenting it to supporters as a moral crusade against “Darwinism”.

Now researchers at the Weizmann Institute of Science, in a paper published recently in Cell Reports, have shown yet another reason why this parasite is so successful. Malaria caused an estimated 610,000 deaths in 2024; the WHO African Region accounted for about 95% of those deaths, and children under five made up about three-quarters of the deaths in that region, according to the World Health Organization.

The researchers, led by Professor Neta Regev-Rudzki, discovered that the parasite exports tiny vesicles containing messenger RNA (mRNA), not only into the red blood cells it infects, but also into the host’s monocytes — immune-system cells that should be helping to fight the infection. Once inside the monocyte, the parasite’s mRNA enters the cell nucleus and binds to two essential human proteins, ACIN1 and PNN, which are normally involved in cutting and splicing RNA transcripts so they can be translated into proteins. With this splicing machinery disrupted, crucial immune-related transcripts are misprocessed and degraded, suppressing the production of proteins needed for an effective immune response.

In other words, P. falciparum is not merely hiding from the immune system; it is actively sabotaging part of the host’s cellular communication network from inside the nucleus. The result is a neat evolutionary trick: the immune system is distracted and disrupted while the real threat — parasites multiplying inside red blood cells — continues to spread.

Malevolent Design - Science is Close To Combatting Another Of Creationism's Divine Malevolence's Nasties

AI-generated image (ChatGPT Latest)

Scientists develop first-of-its-kind antibody to block Epstein-Barr virus - Fred Hutch

A recent paper in the Cell Press journal Cell Reports Medicine by researchers at the Fred Hutch Cancer Center in Seattle reports the development of monoclonal antibodies against Epstein-Barr virus (EBV), a pathogen carried by an estimated 95% of the global human population. The mere existence of such a virus, together with the fact that human scientists have now produced what looks like a promising way of blocking it, should be acutely embarrassing to any creationist prepared to follow the evidence where it leads.

For devotees of creationism’s putative intelligent designer, EBV is an awkward example of its supposed handiwork. It is superbly adapted for what it does: infecting human cells, evading immune defences, and contributing to a range of diseases, including several cancers. If one were looking for something that appears exquisitely “designed” to do harm, EBV would be a strong candidate.

It is especially effective at finding and entering its target cells. The viral glycoprotein gp350 helps it bind to receptors on human cells, while gp42 helps it fuse with and enter them. In other words, it possesses precisely the sort of functional complexity that Intelligent Design advocates such as William Dembski and Michael Behe habitually point to as evidence of design. By their own argument, a system so finely tuned to perform a specific task should count as “specified complexity” or even “irreducible complexity”. The problem, of course, is that the task in question is the infection of human beings by a cancer-associated virus.

Creationists who lean on these arguments are therefore trapped by them. If complexity and functional integration are proof of a designer, then they must also account for the obvious implication: a designer responsible for EBV would have to be, at best, indifferent to human suffering and, at worst, positively malevolent. To escape that conclusion, they usually have to abandon Intelligent Design’s own logic and retreat instead to the theological fallback of “The Fall” and “sin” from the Abrahamic creation myths. In doing so, they quietly concede that their alleged scientific proof of design proves far more than they want it to.

This paper adds a further layer of discomfort. Human scientists have begun to do what any competent and benevolent designer should have done in the first place: devise antibodies capable of blocking the virus from infecting human cells. The study reports monoclonal antibodies against gp350 and gp42, with one anti-gp42 antibody preventing infection in mice with human immune systems. So the obvious question for intellectually honest creationists is this: if human science can engineer a way to interfere with such a pathogen, why was an all-powerful designer unable, or unwilling, to equip us with protection from the outset?

Predictably, most will not confront that question. They will retreat into the familiar refuge of mystery: “we cannot know the mind of God”. But that is precisely where religion and science part company. Science does not declare a problem solved by calling it unknowable. It treats mysteries as challenges to be investigated, understood and, where possible, overcome. That is exactly what these researchers have done with EBV.

Malevolent Design - How Epigenetics Helps Pancreatic Cancer To Spread

Representation of KLF5 expression patterns in lab-grown human pancreatic cancer cells (left) and their patterns of migration from the primary tumor (right). Credit: Andrew Feinberg laboratory, Johns Hopkins Medicine. Originally published in Molecular Cancer.

Growth of Spreading Pancreatic Cancer Fueled By “Under-Appreciated” Epigenetic Changes | Johns Hopkins Medicine

A new paper in Molecular Cancer from Johns Hopkins Medicine describes yet another discovery that should be deeply uncomfortable for Intelligent Design creationists. The researchers found that the spread of pancreatic cancer is driven not chiefly by fresh mutations in DNA sequence, but by epigenetic reprogramming — changes in chromatin organisation and gene activity. In particular, they identified KLF5 as a major driver of metastatic growth, with higher expression in most metastatic lesions than in the matched primary tumours. The paper in Molecular Cancer shows that KLF5 promotes metastatic proliferation through epigenetic modifier genes including NCAPD2 and MTHFD1, helping switch on programmes involved in migration, plasticity and invasion. [1]

What makes this especially important is that epigenetics is not some magical extra layer of “specified information” inserted into life by a supernatural designer. Its roots are ancient. In bacteria, DNA methylation is a major form of epigenetic regulation, involved in gene expression, chromosome replication and DNA repair. In archaea, histone-based chromatin already exists in a form strikingly similar to that of eukaryotes, and studies show that chromatin architecture and its role in regulating gene expression long predate complex multicellular life. In other words, the basic machinery was already there in simpler organisms, doing ordinary cellular housekeeping long before animals and plants ever appeared. [2]

Multicellular organisms did not receive a brand-new control system from an intelligent agent; they inherited this ancient molecular toolkit and elaborated it. As multicellularity evolved, epigenetic regulation expanded and became central to cell differentiation, allowing cells with the same DNA to adopt different stable identities by opening some regions of the genome and closing others. Work on the transition from unicellular to multicellular states in Dictyostelium, for example, shows that chromatin reorganisation and histone modifications are closely tied to the shift into multicellularity, while evolutionary reviews note that epigenetic diversity expanded rapidly with multicellular life and that epigenetic marks are crucial in development and long-lived cell lineages. [3]

And that is exactly why this Johns Hopkins work is such bad news for ID creationists. The same ancient, repurposed system that multicellular organisms rely on for cell specialisation can also be subverted to drive one of the deadliest features of cancer: metastasis. That is what evolved systems do. They are modified from older parts, good enough to work, but never perfect and never immune to catastrophic failure. What this study reveals is not elegant, flawless engineering, but the vulnerability of a historically evolved regulatory system — one that natural selection adapted for development and tissue specialisation, but which disease can hijack with lethal consequences. That is entirely consistent with evolution, and profoundly at odds with the notion of a competent, benevolent designer. [1]

Malevolent Design - How Brain Cells Promote Brain Cancer

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Scientists uncover hidden cells fuelling brain cancer — and a drug that could stop them - McMaster News

Scientists at McMaster University and The Hospital for Sick Children have discovered how a type of brain cell that normally supports healthy brain function can instead go rogue, helping glioblastoma grow and spread. Their findings were recently published in the Cell Press journal Neuron. The prognosis for glioblastoma remains grim, with survival often measured in months.

As putative examples of intelligent design, cells like these should be acutely embarrassing for any creationist willing to follow the evidence where it leads, because within the ID creationist paradigm the only logical conclusion is that the designer is malevolent. By contrast, as examples of how evolution produces workable but imperfect, error-prone systems, they are entirely consistent with the Theory of Evolution and yet another vindication of the science.

Glioblastoma is not simply a mass of malignant cells, but an organised ecosystem sustained by a network of interacting cells. In that sense, it is indistinguishable from the sort of irreducibly complex system that Michael J. Behe claims is evidence of intelligent design. What the researchers found is that a type of cell called an oligodendrocyte, normally responsible for supporting and insulating nerve fibres, can switch roles and actively support tumour growth. These helper cells communicate with cancer cells through a specific signalling system, creating conditions in which the tumour can flourish.

The team discovered that a crucial part of this communication system involves cell-surface receptors called CCR5. By blocking this receptor, tumour growth can be significantly slowed. CCR5 is already the target of the anti-HIV medication Maraviroc, a drug that has already been clinically tested and approved, so it offers a potentially promising treatment for glioblastoma, even if not yet a cure.

Malevolent Design - A Parasitic Fly With All Creationism's Hall Marks for Intelligent Design Is Heading For The USA

Lava of the New World screwworm, Cochliomyia hominivorax.

By John Kucharski - via Wikipedia

The New World screwworm, Cochliomyia hominivorax.

Judy Gallagher, CC BY

An article in The Conversation by Richard Wall, Emeritus Professor in the School of Biological Sciences at the University of Bristol, should remind creationists—if they had the wit to understand why—of the theological quagmire into which their favourite leaders have led them.

The Discovery Institute and its fellows, with their reliance on notions such as irreducible complexity and complex specified genetic information, have taken creationism to a point where the only escape lies in three almost equally unacceptable options:

• They can abandon the very arguments they present as proof of intelligent design, and so admit that they have no proof at all.
• They can accept that the designer god they traditionally equate with the god of the Bible and Qur'an is in fact an evil god, relentlessly designing ever more ingenious ways to increase suffering in the world.
• Or they can retreat into theology and Bible-literalist fundamentalism, abandoning any pretence that intelligent design is genuine science rather than simply rebranded creationism, by blaming everything on 'The Fall'. But in doing so they must also admit the existence of some other creative force with powers sufficient to rival their creator god—one to which their god is either powerless or indifferent. That, of course, destroys the basic principle of Judeo-Christian monotheism: a single omnipotent ruling deity. Ironically, the Discovery Institute was established for the very purpose of persuading US legislators and state education officials that intelligent design is real science.

This problem for creationism arises because the notions of irreducible complexity and complex specified genetic information apply just as well—if not better—to parasites and pathogens as they do to those aspects of nature that creationists like to present as evidence of their god's existence and benevolence; in other words, anything that happens to benefit them.

Professor Wall's article concerns a parasitic fly, the New World screwworm, Cochliomyia hominivorax, whose larvae feed on open wounds in cattle and sometimes humans, often with fatal consequences. The fly is currently extending its range northwards through Mexico and has now reached states bordering Texas. His article is reproduced here under a Creative Commons licence, reformatted for stylistic consistency:

Malevolent Design - How Mosquitoes Are Perfectly Designed to Spread Diseases.

Hundreds of Hungry Mosquitoes, a Student Volunteer and a Mesh Suit

What are mosquitoes for?

According to creationist dogma, everything was designed by an intelligent creator for a purpose. So what, exactly, is the purpose of mosquitoes? Because, judged by what they actually do, they appear to have been designed to spread disease. Mosquitoes are among the deadliest animals on Earth, acting as vectors for malaria, dengue, yellow fever, Zika virus and other infections. If an omnipotent, omniscient designer created them, then that designer must have known exactly what they would do. By the logic of creationism itself, mosquitoes were designed for that purpose.

Creationists usually try to escape the implications of this by retreating into theology and blaming “The Fall”. But taken seriously, that excuse creates more problems than it solves. It implies the existence of a second creative force, independent of and apparently beyond the control of creationism’s god, which can redesign living things for harm and produce pathogens capable of exploiting them. In other words, it requires a rival designer with powers alarmingly similar to those creationists reserve for their own deity - something any serious Christian theologian would regard as a serious blasphemy, carrying the risk of eternal damnation.

What creationist leaders dare not admit is that the far better explanation is evolution. There is no need to invent a second supernatural being to explain why mosquitoes are so well adapted to finding human hosts and transmitting disease. Evolution by natural selection explains it perfectly well, without tying theology in knots or making their designer look either incompetent, malevolent, or powerless against a rival entity with god-like creative powers.

This is especially awkward for intelligent design creationists, because they insist that the hallmarks of design are “complex specified information” and “irreducible complexity”. Yet mosquitoes plainly possess precisely those features — at least by creationist standards. Without their finely tuned sensory systems and behavioural adaptations, they could not locate humans so efficiently or spread infection so effectively. In other words, the very traits creationists cite as proof of design would, in this case, be evidence of a designer producing one of the world’s most efficient disease-delivery systems.

That problem was highlighted in a paper published in Science Advances by researchers from the Georgia Institute of Technology, the Massachusetts Institute of Technology, and the University of California, Riverside, led by Professor David Hu.

They showed that mosquitoes use a combination of visual cues and the detection of carbon dioxide exhaled by humans to home in on a target. Of the roughly 3,500 mosquito species, around 100 are anthropophilic, meaning they preferentially feed on humans. Some can even detect a single human in a herd of cattle — all with a brain containing only about 200,000 neurones. The team set out to understand how mosquitoes are so extraordinarily effective at locating a human host from which to take a blood meal, and in the process, transmit disease.

How the team conducted their experiments is described in an article in The Conversation by lead author David Hu. His article is reproduced below under a Creative Commons licence, reformatted for stylistic consistency.

Unintelligent Design - The DNA Design Blunder That Causes Cancers and Dementia - Malevolence, Incompetence or Evolution?

New research discovers dementia-linked protein’s role in DNA mistakes | Houston Methodist Newsroom

Scientists have discovered that a protein responsible for regulating DNA repair can itself become a source of genomic instability, contributing to cancers and neurodegenerative diseases. The finding provides another example of the fragile and failure-prone complexity that characterises biological systems shaped by evolutionary tinkering rather than the work of a competent designer.

The research, reported in an open access paper published in the journal Nucleic Acids Research, was carried out by a team led by Professor Muralidhar L. Hegde, PhD, professor of neurosurgery at the Houston Methodist Research Institute's Center for Neuroregeneration and Department of Neurosurgery. The team describe how a key regulatory protein, TDP43, which controls the genes involved in DNA repair, can itself become a major cause of genomic instability.

When the regulation of TDP43 fails, the consequences can include cancers, amyotrophic lateral sclerosis (ALS), and frontotemporal dementia (FTD). The difficulty is that this protein can either be absent or overproduced, and both conditions cause the DNA repair genes it regulates to become overactive, resulting in a destabilised genome. This sort of delicate regulatory balance is exactly what evolutionary biologists expect from systems assembled gradually through natural selection, where new control mechanisms are added to existing processes rather than engineered from scratch.

This presents an awkward problem for creationists who claim that biological complexity is evidence of intelligent design. For those with the intellectual integrity to confront the implications, the findings present a difficult choice. Either accept that evolution provides a coherent explanation for such biological paradoxes, or accept that what is claimed to be evidence of intelligent design instead suggests a designer who is incompetent, malevolent, or possibly both—certainly nothing like the allegedly omnibenevolent god of the Bible and Qur'an.

There are also a couple of additional problems here for ID creationists. First, well-designed DNA should not require an additional layer of complexity in the form of a suite of repair genes, followed by yet another regulatory system to control them. Secondly, a well-designed repair mechanism should not itself require such delicate regulation, and the regulatory system should certainly not fail—let alone fail catastrophically. Within the ID creationist paradigm, this is difficult to reconcile with the idea of a competent and benevolent designer.

Malevolent Design - Yet More Evidence Of Intelligently Designed Cancer?

Scientists Uncover Key Driver of Treatment-Resistant Cancer

These images show the beginnings of chromothripsis in colorectal cancer cells. The N4BP2 enzyme (green) infiltrates a micronucleus (zoomed in square selections), where it induces DNA damage (red). Blue represents the main cell nucleus.

Credit: UC San Diego Health Sciences

At the risk of labouring the point I made in my post yesterday — that the exact same arguments ID creationists use as ‘proof’ of intelligent design can also be applied to cancers, parasites, pathogens, and genetic diseases, thereby ‘proving’, in ID terms, that these too were intelligently designed by the same deity — we have yet another example of complex specified genetic information driving the evolution of cancers as they rapidly develop resistance to treatments.

This is reported in a research paper in Science by researchers at the University of California, San Diego (UC San Diego).

The researchers discovered an enzyme responsible for breaking up a chromosome in cancer cells and rearranging it into a scrambled version, enabling the tumour to evolve rapidly. The process is quite simple and closely mimics evolution by natural selection, or the development of antibiotic resistance in bacteria. Shuffling genes in this way increases the likelihood that a small number of cancer cells will survive the treatment aimed at destroying them. The tumour then regrows from these resistant cells, producing a treatment-resistant cancer.

This ability, known as chromothripsis, is found in about 24% of human cancers.

The key to this process is the protein enzyme N4BP2, and the complex, specified gene that produces it. The process begins when an error in DNA replication causes individual chromosomes to become trapped inside tiny, fragile structures called micronuclei. When these micronuclei burst, the chromosome is exposed to nucleases — enzymes capable of breaking DNA.

Within the ID creationist paradigm, there are no such things as mistakes: everything works exactly as it was designed to work. So we are left to assume that these fragile micronuclei, with their entrapped chromosomes, are a deliberate design feature.

The researchers showed that N4BP2 is uniquely capable of entering micronuclei and breaking the trapped chromosome.

To test the hypothesis that N4BP2 is the culprit, they eliminated it in brain cancer cells and observed a reduction in chromothripsis. They then introduced it into healthy cell nuclei and found that it caused chromosomes to break even in otherwise normal cells.

This is, of course, just as much compelling evidence of intelligent design as anything traditionally cited by ID creationists as proof of an intelligent designer. By contrast, the theory of evolution provides an explanation with none of the problems that force creationists to retreat into contradictory theology, Bronze Age origin myths, and appeals to ‘mystery’.

Malevolent Design - More Evidence Of Intelligently Designed Cancer?

Pancreatic cancers co-opt nerve cells to assist them to develop.

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Let’s get on pancreatic cancer’s nerves | Cold Spring Harbor Laboratory

Creationists seem to have pinned all their hopes of justification for their evidence-free beliefs on a false dichotomy and a classic “god of the gaps” fallacy: the claim that complex specified information and irreducible complexity are proof of design by an intelligent entity. This argument relies heavily on the parochial ignorance of its intended audience, who are expected to assume that this “designer” must be the Christian god of the Bible — or, depending on geography and cultural background, the god of the Qur’an — and that therefore those holy books must be the inerrant word of the supposed creator.

However, the problem this raises for creationists is an obvious one: who or what, within their framework, designed all the many examples of irreducible complexity and complex specified information that cause suffering, sickness, and death?

Another striking example has just been published in Cancer Discovery by Professor Jérémy Nigri and colleagues from Cold Spring Harbor Laboratory, New York, USA.

In this paper, the researchers use advanced 3D imaging to show how, even before tumours form, tumour-promoting fibroblasts — known as myCAFs — send out signals that attract nerve fibres. The myCAFs and nerve cells then work together within pancreatic lesions to create a microenvironment favourable for cancer growth. Embarrassingly for Intelligent Design advocates, this system depends entirely on the genetic capacity of myCAFs to send the correct molecular signals, and for nerve fibres to respond appropriately — a finely tuned interaction requiring precisely the sort of “irreducible complexity” they insist can only arise through intentional design.

Within the ID paradigm, these facts should be indisputable evidence of their god’s involvement — but only when the outcome is something they find beneficial, such as eyes, blood clotting, or a brain capable of abstract thought. When the very same logic points instead to cancers, parasites, and congenital diseases, it is suddenly no evidence at all, and certainly not evidence of malevolent intent on the part of the designer. The argument collapses into childish special pleading: design is invoked when convenient, but denied when morally awkward.

Malevolent Design - How Cancer Reprograms The Immune System To Work For It, Not Against It - Malevolence or Evolution?

Tumour containing infiltrating neutrophils. In light grey, tumour cells. Among the infiltrating neutrophils, some do not express CCL3 (blue), while others are CCL3 positive (red). CCL3-positive neutrophils are highly conserved across tumour types and promote the growth of growing tumours.

© Mikaël Pittet – UNIGE

Immune 'hijacking' predicts cancer evolution - Medias - UNIGE

A recent research paper in Cancer Cell, published by a team from the Université de Genève (Unige), Switzerland, led by Professor Mikaël Pittet, describes how neutrophils — key cells of the immune system — can be reprogrammed by cancer cells and then co-opted to drive the cancer’s progression.

This process depends entirely on the presence of multiple interacting components and on specific genes being expressed in both the tumour cells and the neutrophils. Without such irreducible complexity and so-called complex specified genetic information, these cancers would fail to progress.

Regular readers of this blog will be aware that, if we accept the Intelligent Design creationists’ argument for design — namely irreducible complexity and complex specified information — then the inescapable conclusion is that this putative designer must also be the evil genius behind cancers, parasites, pathogens, genetic disorders, congenital diseases, and all the suffering they entail, along with the vast medical resources required to combat them.

Far from being the reputedly omnibenevolent and compassionate god of the Bible, creationism’s designer becomes the exact opposite: randomly mendacious and obsessively sadistic, toiling relentlessly to devise ever more ways to increase suffering in the world.

And yet creationists appear to prefer us to adopt that view of their favourite deity rather than accept the evidence that such systems have evolved — and that what we see in cancers, parasites, and pathogens is precisely what the Theory of Evolution predicts, with no supernatural malice or intent involved. For some reason, Intelligent Design creationists often seem more concerned with disproving “Darwinism” for political purposes than with promoting the god of the Bible or Qur’an.

This apparent paradox goes a long way towards explaining why they have so little hesitation in bearing false witness against scientists, misleading their followers with disinformation, and spreading blatant falsehoods. There is no pro-truth agenda in creationism. There is, however, a thinly veiled political agenda: the establishment of theocratic government — first in the USA, then elsewhere — dragging society back towards the pre-Enlightenment world of the so-called Dark Ages, when ignorance, fear, and superstition allowed unelected and unaccountable religious clerics to rule unchecked, and for most people at the lower strata of a hierarchical society, life was nasty, brutish and short.

Malevolent Design - How Ovarian Cancer Looks Intelligently Designed to Spread Rapidly

Creationism's intelligent designer at work

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Cancer cells (red) stick to mesothelial cells (green) and form hybrid spheres that cut into surrounding abdominal tissue.

Credit: Uno et al., 2026

Scientists now know why ovarian cancer spreads so rapidly in the abdomen | Nagoya University

If intelligent design advocates were honest enough to follow the logic of their own arguments and apply it consistently to the real world, they ought to be acutely embarrassed by the deity they are presenting to the public. Their putative designer god, judged by the evidence they themselves cite, looks less like a benevolent engineer and more like the author of suffering, disease, and death.

That uncomfortable reality is illustrated by yet another research paper showing that pain and mortality can be the direct result of the very things ID proponents celebrate as hallmarks of design: irreducible complexity and “complex specified information”.

This latest example comes from scientists at Nagoya University, Japan, who have shown how ovarian cancer forms an alliance with healthy cells that enables it to spread rapidly to other organs in the abdomen. Their paper has just been published in Science Advances.

As regular readers will be aware, a recurring theme of this blog is that ID advocates conspicuously ignore the vast number of examples from parasitology, oncology, and genetics where the very evidence they cite for an intelligent designer applies just as readily to diseases caused by parasites, pathogens, and genetic malfunctions. Applying ID’s own logic, these are not signs of benevolent craftsmanship but evidence of something far darker — a malevolent intent behind the supposed designer.

The paper in Science Advances is yet another case in point, and doubtless there will be many more soon.

The authors discovered that ovarian cancer cells gather clusters of mesothelial cells from the peritoneum and form hybrid spheres. These protect the cancer cells, help them invade other organs, and create a pathway for metastasis throughout the abdomen. Worse still, these hybrid spheres resist chemotherapy more effectively than cancer cells alone.

If something this complex resulted in something beneficial for humans, Discovery Institute fellows Michael J. Behe and William A. Dembski would doubtless have produced one or more books about it, written magazine articles, and embarked on television tours explaining how the finding devastates “Darwinism” and constitutes scientific proof of an intelligent designer — leaving their audiences in no doubt that the locally favoured god is the only entity capable of producing such complexity.

As it is, we can expect only a deafening silence from the Discovery Institute, while their hapless supporters cast about for a fundamentalist religious excuse such as “the Fall”, or perhaps invoke some other evil agent — anything, in fact, except the god of the Bible, who is apparently only credited with designing good things.

Malevolent Design - The Malaria Parasite Is Irreducibly Complex And Has Complex Specified Genetic Information - Oops!

Blood smear showing P. falciparum parasites.

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Malaria: Newly Identified “Crown” Stage Controls Parasite Reproduction

Researchers from the Hebrew University of Jerusalem have uncovered yet another layer of exquisite molecular sophistication in one of humanity’s most persistent and lethal parasites, Plasmodium falciparum, the chief cause of malignant malaria. Their findings, reported in a recent press release and published in the peer-reviewed Journal of Cell Biology, describe a newly identified regulatory “crown” checkpoint that controls parasite reproduction with remarkable precision.

It is difficult to imagine a discovery more awkward for Intelligent Design creationists, because Plasmodium falciparum is precisely the sort of organism that embodies everything Michael Behe and William Dembski insist cannot arise by evolution. Here is complex specified genetic information, tightly regulated developmental choreography, and interlocking biochemical machinery operating across multiple life stages — the very definition, we are told, of “irreducible complexity”.

Unfortunately for the Discovery Institute, this irreducible complexity does not produce a bird’s wing, a human eye, or some uplifting example of divine craftsmanship. It produces malaria — a parasite responsible for immense suffering and hundreds of thousands of deaths every year, mostly children. If complexity is meant to be a hallmark of intelligent design, then the designer’s portfolio includes some rather grim specialities.

The problem is compounded by the fact that Michael Behe has already made malaria central to his arguments. In The Edge of Evolution, he famously pointed to the parasite’s resistance to anti-malarial drugs as an example of the supposed limits of Darwinian evolution, claiming that multiple coordinated mutations were beyond the reach of natural selection. Yet malaria has since become one of the clearest demonstrations that evolution not only occurs, but does so rapidly and repeatedly, exploiting enormous population sizes and intense selection pressures to produce exactly the adaptations Behe claimed were improbable.

As Kenneth Miller pointed out, Behe's mathematical sleight of hand was to assume resistance had to evolve as a single event in a single cell, not across a large population over time - a fallacy of which any good microbiologists should have been aware.

This newly described “crown” stage is simply the latest reminder that biological complexity is not evidence of supernatural design. Evolution predicts complexity wherever it confers survival advantage — including in parasites, pathogens, and diseases. The only real surprise is that creationists continue to present complexity as a theological virtue, when nature so often deploys it in the service of exploitation rather than benevolence.

As ever, none of this will deter creationists from repeating their familiar articles of faith. Faced with an organism whose life cycle resembles a biochemical symphony — regulated checkpoints, specialised invasion machinery, host-cell remodelling, immune evasion, and reproductive stages split between mosquito and human — they will insist that this is not evidence for evolution but evidence against it. The argument, such as it is, runs that complexity must have been present from the start, because it could not have arisen gradually.

But this is simply the old “irreducible complexity” claim in a new disguise: the assertion that because creationists personally cannot imagine intermediate stages, no such stages could have existed. Science, of course, is not obliged to conform to the limits of anyone’s imagination. Evolution does not require that complex systems appear in a single leap. It proceeds by modification of what already exists — co-option, duplication, repurposing, and incremental refinement over deep time — producing the layered complexity we observe today.

Another common retreat is the insistence that this is merely “microevolution”, the trivial shuffling of genes within some mythical created “kind”. Yet Plasmodium falciparum is not merely adjusting the colour of its spots. It is evolving novel biochemical strategies, repeatedly acquiring drug resistance, fine-tuning developmental regulation, and exploiting host environments with extraordinary efficiency. If this is “only microevolution”, then the term has been drained of all meaning.