Uninteligent Design - How The Process of Germ Cell Production Goes Wrong And Creates Genetic Defects.

Paired chromosomes showing crossovers in a mouse oocyte.

Hunter lab

Left panel: short green irregular lines arranged in pairs. Right: Close up of one pair shows that the two strands form a cross shape. Paired chromosomes showing crossovers in a mouse oocyte.

Hunter lab.

Landmark Discovery Reveals How Chromosomes Are Passed From One Generation to the Next | UC Davis

This article continues my series exploring the many ways in which the human body demonstrates unintelligent design. Far from being the perfect handiwork of a benevolent creator, our anatomy and physiology are full of flaws, inefficiencies, and dangerous vulnerabilities. Each of these makes sense in light of evolution by natural selection—an opportunistic, short-term process that tinkers with existing structures—but they make no sense at all if we are supposed to be the product of an all-wise designer.

Creationists often argue from a position of ignorant incredulity, claiming that complexity implies intelligent design, when in fact the opposite is true. The hallmark of good, intelligent design is simplicity, for two very simple reasons: first, simple things are easier to construct and require fewer resources; and second, simple structures and processes have fewer potential points of failure, making them more reliable.

In short: complexity is evidence against intelligent design and in favour of a mindless, utilitarian, natural process such as evolution.

In addition to being minimally complex, another characteristic we would expect of something designed by an omniscient, maximally intelligent, and benevolent designer is that the process should work perfectly, every time, without fail.

The problem for creationists is that their favourite example of supposed intelligent design — the human body — is riddled with complexity in both its structures and processes. This complexity provides countless examples of systems that fail to perform adequately, or fail altogether, with varying frequency. Many failures occur in the layers of complexity needed to control or compensate for the inadequacies of other systems, and when those compensatory mechanisms themselves fail, the result can be a cascade of dysfunctions or processes running out of control. The consequences manifest as diseases, defects, and disabilities — hardly the work of an all-wise designer.

They are, however, exactly what we would expect from a mindless, utilitarian process like evolution, which prioritises short-term survival and reproduction, selecting only what is better — sometimes only marginally better — than what preceded it, rather than seeking optimal solutions. I have catalogued many such suboptimal compromises in the anatomy and physiology of the human body, and the problems that arise from them, in my book, The Body of Evidence: How the Human Body Refutes Intelligent Design, one of my Unintelligent Design series.

Just yesterday, I wrote about research suggesting that autism may be a by-product of the rapid evolution of intelligence in humans. Now we have another striking example of extreme biological complexity which, when it goes wrong, can have catastrophic consequences: the production of eggs in women and sperm cells in men.

Background^ How Humans Produce Eggs and Sperm. Egg production (oogenesis)

• In females, all the eggs a woman will ever have are formed before birth. During foetal development, cells in the ovaries undergo meiosis (a special type of cell division that halves the number of chromosomes).
• These immature egg cells (oocytes) remain “frozen” in an early stage until puberty, when hormones begin to stimulate their monthly maturation.
• Usually, only one egg completes development and is released each month during ovulation.
• Because oocytes are stored for decades, they accumulate damage and errors over time, which explains why fertility declines and the risk of genetic disorders rises with age.

Sperm production (spermatogenesis)

• In males, sperm are produced continuously from puberty onwards in the testes.
• Specialised stem cells divide by meiosis to create sperm cells with half the normal number of chromosomes.
• Each cell division cycle produces millions of sperm every day, but the process is intricate and vulnerable to errors.
• Defective sperm are common, though usually filtered out, and sperm quality can decline with age, illness, or environmental factors.

Why it matters
Both processes rely on precise chromosome sorting and pairing. Even small mistakes—such as an extra or missing chromosome—can lead to infertility, miscarriage, or genetic disorders such as Down syndrome. The complexity and fragility of gamete production underline how far these processes fall short of “perfect design”.

In addition, as this article exposes, the eggs are maintained in a state of partial meiosis, 'frozen' at a critical point, sometimes for several decades, until just before ovulation, requiring special processes to conserve them in that state. If this stage fails then it can result in miscarriage, or birth defects.

This research, led by Professor Neil Hunter of the Department of Microbiology and Molecular Genetics at the University of California, Davis, has been published open access in Nature and summarised in a UC Davis news article by Douglas Fox.

Landmark Discovery Reveals How Chromosomes Are Passed From One Generation to the Next

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Critical Event Guides Accurate Distribution of Chromosomes To Eggs and Sperm

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When a woman becomes pregnant, the outcome of that pregnancy depends on many things — including a crucial event that happened while she was still growing inside her own mother’s womb. It depends on the quality of the egg cells that were already forming inside her fetal ovaries. The DNA-containing chromosomes in those cells must be cut, spliced and sorted perfectly. In males, the same process produces sperm in the testes but occurs only after puberty.

If that goes wrong, then you end up with the wrong number of chromosomes in the eggs or sperm. This can result in infertility, miscarriage or the birth of children with genetic diseases.

Professor Neil Hunter, corresponding author
Department of Microbiology and Molecular Genetics
University of California Davis
Davis, CA, USA.

In a paper published Sept. 24 in the journal Nature, Hunter’s team reports a major new discovery about a process that helps safeguard against these mistakes. He has pieced together the choreography of proteins that connect matching chromosome pairs — ensuring that they are sorted correctly as egg and sperm cells develop and divide.

Hunter’s discoveries required methods to watch the molecular events of chromosome recombination unfold with unprecedented detail. This involved genetic engineering in budding yeast — a model organism that has been used for decades to discover how fundamental cellular processes work.

The chromosome structures that we studied have changed very little across evolution. Every protein that we looked at in yeast has a direct counterpart in humans.

Professor Neil Hunter.

His findings could improve our understanding of fertility problems and how they are diagnosed and treated in humans.

Forming chromosome crossovers for strong connections

Humans have 46 chromosomes in each of our cells, made up of 23 pairs of matching, “homologous” chromosomes, with one of each pair inherited from each parent. Early in the process of making sperm or eggs, those chromosome pairs line up, and the parental chromosomes break and rejoin to each other. These chromosome exchanges, called “crossovers,” serve two important functions.

First, they help ensure that each chromosome that is passed on to the offspring contains a unique mixture of genes from both parents. Crossovers also keep the chromosomes connected in matching pairs. These connections guide the distribution of chromosomes when cells divide to produce eggs and sperm. Maintaining crossover connections is especially crucial in females, Hunter said.

As chromosomes pair up in developing egg or sperm cells, matching DNA strands are exchanged and twined together over a short distance to form a structure called a “double Holliday junction.” DNA strands of this structure are then cut to join the chromosomes forming a crossover.

Left panel: short green irregular lines arranged in pairs. Right: Close up of one pair shows that the two strands form a cross shape. Paired chromosomes showing crossovers in a mouse oocyte.

Hunter lab.

In males, developing immature sperm cells then immediately divide and distribute chromosomes to the sperm. In contrast, egg cells developing in the fetal ovary arrest their development after crossovers have formed. The immature egg cells can remain in suspended animation for decades after birth, until they are activated to undergo ovulation.

Only then does the process lurch back into motion: The egg cell finally divides, and the chromosome pairs that were connected by crossovers are finally separated to deliver a single set of chromosomes to the mature egg.

Maintaining the crossover connections over many years is a major challenge for immature egg cells.

Professor Neil Hunter.

If chromosome pairs aren’t connected by at least one crossover, they can lose contact with each other, like two people separated in a jostling crowd. This causes them to segregate incorrectly when the cell finally divides, producing egg cells with extra or missing chromosomes. This can cause infertility, miscarriage or genetic conditions such as Down syndrome, in which a child is born with an extra copy of chromosome 21, leading to cognitive impairment, heart defects, hearing loss and other problems.

From yeast to humans

Hunter has spent years trying to understand how crossovers form and how this process can fail and cause reproductive problems. By studying this process in yeast, researchers can directly visualize molecular events of double-Holliday junction resolution in synchronized populations of cells.

Researchers have identified dozens of proteins that bind and process these junctions. Hunter and then-postdoctoral fellow Shangming Tang (now an assistant professor of biochemistry and molecular genetics at the University of Virginia) used a technique called “real-time genetics” to investigate the function of those proteins. With this method, they made cells degrade one or more specific proteins within the junction-associated structures. They could then analyze the DNA from these cells, to see whether the junctions were resolved and if they formed crossovers. In this way, they built up a picture in which a network of proteins function together to ensure that crossovers are formed.

This strategy allowed us to answer a question that previously wasn’t possible.

Professor Neil Hunter.

They identified key proteins such as cohesin that prevent an enzyme called the STR complex (or Bloom complex in humans) from inappropriately dismantling the junctions before they can form crossovers.

They protect the double Holliday junction. That is a key discovery.

Professor Neil Hunter.

This years-long research project in yeast is broadly relevant for human reproduction because the process has changed very little during evolution. Failure to protect double-Holliday junctions may be linked to fertility problems in humans.

In addition to Tang, the postdoc, seven undergraduates in the UC Davis College of Biological Sciences contributed to this work, including Jennifer Koo, Mohammad Pourhosseinzadeh, Emerald Nguyen, Natalie Liu, Christopher Ma, Hanyu Lu and Monica Lee.

Additional authors on the paper include Sara Hariri, Regina Bohn and John E. McCarthy, all members of the Hunter lab.

Publication:

Tang, S., Hariri, S., Bohn, R. et al.
Protecting double Holliday junctions ensures crossing over during meiosis.
Nature (2025). https://doi.org/10.1038/s41586-025-09555-1

Protecting double Holliday junctions ensures crossing over during meiosis Shangming Tang, Sara Hariri, Regina Bohn, John E. McCarthy, Jennifer Koo, Mohammad Pourhosseinzadeh, Emerald Nguyen, Natalie Liu, Christopher Ma, Hanyu Lu, Monica Lee & Neil Hunter

Abstract
Chromosomal linkages formed through crossover recombination are essential for the accurate segregation of homologous chromosomes during meiosis¹. The DNA events of recombination are linked to structural components of meiotic chromosomes². Imperatively, the biased resolution of double Holliday junction (dHJ) intermediates into crossovers^3,4 occurs within the synaptonemal complex (SC), the meiosis-specific structure that mediates end-to-end synapsis of homologues during the pachytene stage^5,6. However, the role of the SC in crossover-specific dHJ resolution remains unclear. Here we show that key SC components function through dependent and interdependent relationships to protect dHJs from aberrant dissolution into non-crossover products. Conditional ablation experiments reveal that cohesin, the core of SC lateral elements, is required to maintain both synapsis and dHJ-associated crossover recombination complexes (CRCs) during pachytene. The SC central region transverse-filament protein is also required to maintain CRCs. Reciprocally, the stability of the SC central region requires the continuous presence of CRCs effectively coupling synapsis to dHJ formation and desynapsis to resolution. However, dHJ protection and CRC maintenance can occur without end-to-end homologue synapsis mediated by the central element of the SC central region. We conclude that local ensembles of SC components are sufficient to enable crossover-specific dHJ resolution to ensure the linkage and segregation of homologous chromosomes.

Main
During meiotic prophase I, cohesin complexes connect sister chromatids and mediate their organization into linear arrays of chromatin loops tethered to a common axis^2,5,7,8,9. These cohesin-based axes define interfaces for the pairing and synapsis of homologous chromosomes that culminates in the formation of SCs. An SC is a tripartite structure comprising the two juxtaposed homologue axes, now called lateral elements, connected by a central lattice of transverse filaments^5,6. Extension of this lattice to achieve full synapsis requires an additional central element complex^5,6,10 (Extended Data Fig. 1a). Meiotic recombination facilitates pairing and synapsis between homologous chromosomes and then connects them through crossing over. These connections are necessary for accurate segregation during the first meiotic division1. To this end, the DNA events of recombination are physically and functionally linked to underlying chromosome structures2. The protein complexes that catalyse DNA double-strand breaks (DSBs) and subsequent strand exchange are tethered to homologue axes. The ensuing joint molecule intermediates and their associated recombination complexes interact with the central region of the SC. A subset of recombination events is assigned a crossover fate with a tightly regulated distribution to ensure that each chromosome pair receives at least one². At designated sites, nascent joint molecules mature into dHJs that then undergo biased resolution specifically into crossovers^3,4. These steps occur in the context of the SC central region and associated CRCs. The post-synapsis roles of SC components in crossing over remain unclear, particularly whether the SC functions after dHJ formation to facilitate crossover-specific resolution.

Tang, S., Hariri, S., Bohn, R. et al.
Protecting double Holliday junctions ensures crossing over during meiosis.
Nature (2025). https://doi.org/10.1038/s41586-025-09555-1

Copyright: © 2025 The authors.
Published by Springer Nature Ltd. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)

This study highlights how even the fundamental processes of human reproduction are fragile, failure-prone, and riddled with inefficiencies. The intricate mechanisms required to produce eggs and sperm—the most basic requirement for life to continue—are full of potential points of breakdown. These flaws make perfect sense in light of evolution, a blind tinkerer that cobbles together workable solutions from existing parts, but they are utterly inconsistent with the idea of an intelligent, purposeful designer.

Who in their right mind would consider designing a critical function such as the production of reproductive gametes, that needs to be suspended at a critical point for decades, requiring more complexity to minimise the risk of it failing - and then designing that process so it sometimes fails with serious, even fatal consequences for the resulting child?

Gamete production is just one of many such examples: from reproductive bottlenecks to skeletal weaknesses and brain vulnerabilities, our bodies bear the unmistakable stamp of compromise and accident, not foresight or perfection. This is the reality I explore in detail in my book, The Body of Evidence: How the Human Body Refutes Intelligent Design, part of my Unintelligent Design series.

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Refuting Creationism - How Autism May Be The Result Of Compromise In The Evolution Of Human Intelligence

Trump 'fact checking' his autism claim

How evolution explains autism rates in humans | EurekAlert!

If the human genome had been intelligently designed by an omniscient, omnibenevolent, omnipotent supernatural deity, as creationists insist, it should be perfect and free from defects of any sort. In fact, it is difficult to see why there would be any variance in such an intelligently designed genome, let alone variance that causes genetic defects—unless those were intentionally included by the designer, who then cannot reasonably be described as omnibenevolent or omniscient.

If, however, the human genome is the product of hundreds of millions of years of gradual evolutionary processes — processes that prioritise survival and reproduction, with all the sub-optimal compromises that a utilitarian form of ‘design’ entails — then variance and defects are exactly what we would expect.

Creationists traditionally ignore questions about the origin of variance in a supposedly ‘perfect’ intelligently designed genome. The existence of genetic defects is usually explained away by resorting to Bible-literalist mythology about ‘The Fall’ — an abandonment of the Discovery Institute’s Wedge Strategy, which seeks to present creationism as real science rather than a fundamentalist religion dressed in a lab coat. News that autism may in fact be a by-product of the evolution of intelligence in humans will therefore be an even greater problem for creationists, who insist that our high intelligence sets us apart as the special creation of a perfect god.

Ironically, as well as possessing high intelligence, humans — unlike any other primates — also have autism and schizophrenia. It is this correlation that provides a clue to their shared evolutionary origins.

My book, The Body of Evidence: How the Human Body Refutes Intelligent Design, lists lots of examples of how the human body is the result of these sub-optimal evolutionary compromises with all the problems that has produced. This example is just another instance and more evidence of the lack of intelligence in the process.

Malevolent Designer News - How Candida Albicans (Thrush) Is Cleverly Designed to Infect Your Mouth - Evolution Or Malevolent Design?

The yeast fungus Candida albicans (blue) breaks out of human immune cells (red) by forming long thread-like cells called hyphae. The part of the hypha that has already left the immune cells is coloured yellow.

© Erik Böhm, Leibniz-HKI

The dose makes the difference - Leibniz-HKI

As has often been pointed out in these blog posts, the "evidence" offered by Discovery Institute fellows William A. Dembski and Michael J. Behe for an intelligent designer can, by the same logic and using the same evidence, be interpreted as pointing to a theologically awkward malevolent designer. This is a line of reasoning routinely ignored by the "Cdesign proponentcists", who prefer to overlook the many examples of parasites and pathogens—and the evolutionary traits that make them so successful at invading and surviving within their hosts.

A fresh example that creationists will either have to ignore or blame on "The Fall" comes from researchers at the Leibniz Institute for Natural Product Research and Infection Biology. They have shown that the fungus Candida albicans, which causes thrush, has evolved a highly sophisticated and "finely tuned" mechanism for infecting the human mouth while evading the immune system.

The stock creationist response is to shift responsibility onto the biblical myth of "The Fall," retreating into Bible literalism. Yet this is precisely the kind of literalism the Discovery Institute has been at pains to insist is not essential to the notion of intelligent design, which it markets as a scientific alternative to evolutionary theory—or "Darwinism," as they prefer to call it. This rhetorical sleight of hand was central to the Institute’s "Wedge Strategy," devised after the 1987 US Supreme Court ruling in Edwards v. Aguillard, which confirmed that teaching creationism in public schools violated the Establishment Clause of the First Amendment.

The new research reveals that C. albicans produces a toxin called candidalysin in carefully regulated doses that allow it to infiltrate the mucous lining of the mouth. Too little candidalysin, and the fungus would fail to establish itself; too much, and it would trigger an immune response strong enough to destroy it. Normally, C. albicans exists in a round, yeast-like form, but under the "right" conditions it can switch into the filamentous hyphal form typical of fungi. This transformation allows it to penetrate host tissues and, in immune-compromised patients, become life-threatening. It is in this invasive hyphal state that C. albicans produces candidalysin.

The production of hyphae, and therefore candidalysin, is controlled by the gene EED1. By any definition, EED1 would qualify as an example of "complex specified information" according to Dembski’s own formulation — evidence, according to the Discovery Institute, of supernatural intelligent design.

Refuting Creationism - The Lengths Plants Will Go To Just To Get Pollinated - No Intelligence Needed

chloropid flies on a Vincetoxicum nakaianum flower.

The grass fly visiting the flowers (A) and kleptoparasiting spider hunting ant (B)

Press Releases - SCHOOL OF SCIENCE THE UNIVERSITY OF TOKYO

The driving force behind evolution is reproductive success, so in a broad sense every adaptation can be seen as a reproductive strategy. Few, however, are as peculiar as that of Vincetoxicum nakaianum, a dogbane species native to Japan. Rather than relying on nectar rewards or visual lures to attract pollinators, this plant enlists the services of kleptoparasitic chloropid flies — insects that usually home in on the scent of injured prey in order to steal a meal.

In a remarkable twist, the flowers of V. nakaianum release chemical signals that closely mimic the odour of ants under attack by predators, especially spiders. Drawn in by what they perceive as the scent of a potential victim to exploit, the flies inadvertently collect and deposit pollen as they move from flower to flower. This unusual strategy has now been documented in detail in a study led by Ko Mochizuki of the University of Tokyo, published in Current Biology, and described in a University of Tokyo School of Science press release.

What makes this particularly striking is how roundabout and intricate the mechanism is. If an intelligent designer had set out to ensure pollination, far simpler methods are available — from bright colours and nectar rewards to direct reliance on wind. Instead, V. nakaianum has evolved a convoluted route, exploiting the specialised behaviour of flies that themselves depend on the predation of ants by spiders. Such elaborate, contingent solutions are precisely what we expect from evolution by natural selection acting over countless generations, not from foresightful design.

Malevolent Design - How Our Gut Microbiome is 'Designed' to Destroy Our Kidneys - Malevolence or Evolution?

Kidney fibrosis linked to molecule made by gut bacteria – News Bureau

Mostly, our gut microbes are beneficial or at least neutral because we have co-evolved and reached an accommodation. One benefit we derive from their presence is that they make life difficult for potentially harmful organisms, if only by monopolising the available resources and occupying the niches in our gut.

There is a downside, of course, as in any evolved system, which is inevitably a compromise and can tip over into pathology under certain circumstances. But overall, because the disadvantages are more than compensated for by the benefits, the system has evolved and been maintained.

However, a newly discovered downside is that a Staphylococcus species may be implicated in one of the serious complications of diabetes mellitus (DM) — kidney fibrosis and ultimately kidney failure. The discovery was made by researchers at the University of Illinois Urbana-Champaign and Mie University in Japan, co-led by Professor Isaac Cann of Illinois and Professor Esteban Gabazza of Mie University. The bacterium is believed to produce corisin — a small peptide — which is found at high levels in patients with diabetic kidney fibrosis. The researchers have just published their findings, open access, in Nature Communications.

For creationists, this sort of discovery is always a problem, one they normally ignore or blame on “Eve’s sin,” revealing ID creationism for what it is — Bible literalism in a lab coat — which must retreat into mystical theology when faced with problems ID cannot address. Yet creationists also claim that their omniscient creator god is personally responsible for the design of organisms such as Staphylococcus. That would mean it knowingly endowed Staphylococcus with the genes to make corisin, along with all the harmful consequences.

Taking William A. Dembski’s “complex specified genetic information,” which supposedly produces a specific outcome, at face value, the staphylococcal genes are equally “proof” of intelligent design. And so we end up with an unresolved paradox for ID creationism: “complex specified” genes that do us harm, standing as evidence of malevolent design.

Malevolent Design - How The Poxvirus is 'Intelligently Designed' To Rapidly Multiply

A Survival Kit for Smallpox Viruses - Universität Würzburg

The tRNA ensures the cohesion of the polymerase and the associated factors; without it, they would not arrange themselves in this way.

Image: Clemens Grimm.

Researchers at Julius Maximilian University of Würzburg (JMU) have discovered that poxviruses have developed a unique strategy to multiply rapidly after infecting a host cell. They achieve this by assembling a large protein complex with the help of a transfer RNA (tRNA) molecule. Remarkably, this is the first known example of a ‘chaperone’ function being carried out by a tRNA rather than a protein. Each component of the assembly plays a specific role in the production of new poxviruses. Crucially, the complex only functions when all parts are correctly assembled, and the tRNA is indispensable for this construction.

In other words, the tRNA provides the essential element of the complex, which some might describe—using the Discovery Institute’s own terms—as containing “complex specified information” and forming an “irreducibly complex” system essential to the virus’s success.

By that same logic, it follows that the viruses responsible for smallpox and mpox (monkeypox) must have been intelligently designed. This leaves creationists with an unenviable dilemma:

• Accept the Discovery Institute’s definitions and admit their designer created deadly viruses — theologically awkward.
• Claim another intelligence designs life, beyond their god’s control — even more awkward.
• Abandon the Institute’s “evidence” for intelligent design — politically awkward.

Unintelligent Design - When Snakes Borrow Genes from the Sea - It's Fatal To Creationism

Tiger Snake, Notechis scutatus

Credit: Max Tibby- Snake Catchers Adelaide

A Western Brown snake, Pseudonaja nuchalis

By Andy - originally posted to Flickr as Western Brown, CC BY-SA 2.0, Link

New study unlocks mystery origin of iconic Aussie snakes | Newsroom | University of Adelaide

Intrigued by the information I unearthed while researching for my recent blog post about Australia's elapsid snakes and how skinks have evolved resistance to their venom, I discovered that these snakes have evolved from a common ancestor that once lived in the sea, and, while there, picked up a number of 'jumping genes' that are only found in marine animals as diverse as fish, sea squirts, sea urchins, bivalve molluscs and turtles.

The more we learn about genomes, the clearer it becomes that evolution is not a neat or predictable process—it is messy, opportunistic, and deeply influenced by historical contingency. A striking example of this comes from a recent genomic study that traced the origins of Australia’s iconic elapid snakes—not just through their DNA, but through the foreign DNA embedded within it. Researchers have identified at least 14 distinct horizontal gene transfer (HGT) events in these snakes, in which transposable elements—“jumping genes” — from unrelated marine organisms such as fish, tunicates, molluscs, and turtles have been incorporated into the snake genome.

This is compelling evidence that the ancestors of modern Australian elapids passed through a marine environment, acquiring genetic material from the organisms they encountered there. The transfers are not random. They show ecological specificity, temporally sequenced occurrence, and a nested pattern of inheritance — hallmarks of an evolutionary process rather than the actions of an intelligent designer.

For proponents of Intelligent Design creationism, this presents a serious interpretive problem. The idea that different species share features because of a “common designer” does not explain why Australian elapids should contain such a unique suite of genes from marine animals—genes absent in closely related snakes that remained on land. Nor does it account for the fact that many of these sequences serve no obvious function, are neutral or even mildly deleterious, and resemble the genetic detritus typical of unguided evolution.

ID advocates will likely claim this is just more evidence of “design reuse” or “genetic toolkits.” But such claims are not only ad hoc; they fail to explain the clear environmental and phylogenetic patterns observed in the data. The evolutionary explanation, by contrast, is both predictive and parsimonious: snakes dispersed through a marine environment, interacted with marine organisms, and as a result, their genomes bear the signature of that history.
In what follows, we will explore how this discovery not only sheds light on the evolutionary past of Australian elapids, but also exposes the weaknesses in ID’s core explanatory framework. The genome of a snake tells a story—and it's not the story of design.

Malevolent Design - We COULD Have Been Designed To Re-Grow Lost Or Damaged Eyes - Malevolence Or Evolution?

Golden apple snail, Pomacea canaliculata

This Snail’s Eyes Grow Back: Could They Help Humans do the Same? | UC Davis

First, we had the example of Australian lizards which, unlike humans, have been endowed with immunity to snake venom through a simple mutation — the kind of change that creationists like William A. Dembski of the Discovery Institute would insist is the result of "intelligent design" because it is both complex and specified.

Now we have the example of the aquatic golden apple snail, Pomacea canaliculata, which — again, unlike humans — can regenerate a lost or damaged eye. The snail’s eye is genetically and structurally similar to the mammalian eye, so there appears to be no reason why an omnibenevolent, omniscient intelligent designer could not have endowed humans and other animals with that ability too. And of course, according to William A. Dembski and Michael J. Behe, the irreducibly complex eye and the complex, specified genetic information are both evidence for intelligent design by the same intelligent designer that designed the mammalian eye and it genetic underpinning.

Creationists, of course, believe that humans are the pinnacle of their putative intelligent designer’s work. So, from their viewpoint, the only reasons it didn't grant us the ability to regenerate eyes — or to resist snake venom — must be that it either didn’t want to, didn’t think to, or didn’t know how to. Yet all of those options are inconsistent with the claimed attributes of being omnipotent, omniscient, and omnibenevolent.

Which leaves us with only one other explanation: that it wants us to suffer when we damage or lose an eye.

All rather strange, really — especially considering that, according to the Bible, God views blemishes such as blindness as a form of profanity:

And the Lord spake unto Moses, saying, Speak unto Aaron, saying, Whosoever he be of thy seed in their generations that hath any blemish, let him not approach to offer the bread of his God.

For whatsoever man he be that hath a blemish, he shall not approach: a blind man, or a lame, or he that hath a flat nose, or any thing superfluous, Or a man that is brokenfooted, or brokenhanded, Or crookbackt, or a dwarf, or that hath a blemish in his eye, or be scurvy, or scabbed, or hath his stones broken;

No man that hath a blemish of the seed of Aaron the priest shall come nigh to offer the offerings of the Lord made by fire: he hath a blemish; he shall not come nigh to offer the bread of his God.

He shall eat the bread of his God, both of the most holy, and of the holy. Only he shall not go in unto the vail, nor come nigh unto the altar, because he hath a blemish; that he profane not my sanctuaries: for I the Lord do sanctify them.

And Moses told it unto Aaron, and to his sons, and unto all the children of Israel.

Leviticus 21:16-24

Almost as an added insult to the humans it denied this regenerative ability to, while giving it to golden apple snails, the golden apple snail is a major invasive agricultural pest which causes widespread damage to rice crops, when it gets into paddy fields.

Malevolent Designer - We COULD Have Been Designed To Resist Snake Venom - Malevolence Or Evolution?

Major Skink, Bellatorias frerei

Major Skink, Bellatorias frerei

How Aussie skinks outsmart lethal snake venom - News - The University of Queensland

As though the recent news from the biological sciences wasn't already bad enough for creationists, we now have two examples demonstrating how—if an omnibenevolent, omniscient deity really had designed humans as the pinnacle of creation—it could have done a far better job. Yet, apparently, it chose not to.

The first, which is the subject of this blog post, involves a seemingly humble Australian lizard, the major skink (Bellatorias frerei), which possesses a simple mutation that renders it immune to Australian snake venom.

The second example, which I’ll cover in my next post, concerns the apple snail. This remarkable mollusc has an eye that is structurally and genetically similar to the mammalian eye—but unlike ours, it can regenerate if damaged or lost. But more on that later.

Australia is infamous for its venomous snakes—many of them deadly. Yet thanks to the widespread availability of antivenoms, there are only one or two fatalities annually, out of hundreds of snakebite cases.

However, if humans had been endowed with the same mutation as the skink, there would be no deaths at all—and no need for antivenoms. Interestingly, this is the same mutation that grants immunity to cobra venom in some mammals, such as mongooses and honey badgers. So, from a creationist perspective, there appears to be no good reason to deprive humans of this mutation — unless the designer was malevolent, indifferent, or just lazy.

It would pose an interesting challenge to intelligent design (ID) creationists to explain the "intelligence" in designing snakes to kill lizards with neurotoxic venom, only to then design lizards that are immune to it. Of course, creationists invariably avoid addressing these sorts of paradoxes—paradoxes which evolutionary biology easily explains as the outcome of an unintelligent evolutionary arms race.

These neurotoxic venoms work by binding to receptors on the surface of muscle cells and blocking the action of the neurotransmitter acetylcholine. This prevents muscle contraction, ultimately stopping respiration. The simple mutation in the skinks alters these receptors so that the venom can no longer bind effectively, neutralising its effects.

Creationism Refuted - Complex Specified Information in 'Spanish Flu' Virus Makes ID Creationists Sick

Emergency hospital in Zurich’s Tonhalle during the so-called “Spanish flu” in November 1918

Image: Schweizerisches Nationalmuseum, Inventarnummer LM-102737.46

Swiss Genome of the 1918 Influenza Virus Reconstructed | UZH

A major stumbling block that non-biologist Christian fundamentalist theologian William A. Dembski has blundered into is that his so-called ‘proof of intelligent design’ (i.e., the Christian god) also, by the same reasoning, constitutes evidence for malevolent design — something found in virtually every genome of every parasite and pathogen. This presents CDesign proponentsists with a fatal paradox: either their ‘proof of intelligent design’ also proves the existence of an evil designer, or ‘complex specified information’ is not the definitive evidence for design they like to claim it is.

A classic example — and another blow to creationist reasoning—has just been described in a study by researchers from the Swiss universities of Basel and Zurich. They have recovered and analysed the genome of the virus responsible for the 1918–1920 ‘Spanish flu’ pandemic, which killed more people than were killed in the First World War. In fact, the term ‘Spanish flu’ is a misnomer; the virus is now believed to have originated in a U.S. military base in Kansas and was brought to Europe by American soldiers.

The Swiss team discovered that from the outset, the virus appears to have been pre-adapted for infectivity and immune evasion. They identified three key mutations that remained unchanged as the virus evolved over the course of the pandemic. Two of these mutations made the virus resistant to an antiviral component of the human immune system, while the third enabled it to bind more effectively to receptors on the surface of human cells, allowing it to enter and infect them more readily. These mutations were so effective that victims frequently died within hours of the onset of symptoms.

Malevolent Designer - Does The Designer Favour Zebrafish Or Just Hate Humans?

Two zebrafish genes hold the key to regenerating inner ear cells, offering hope for future human therapies.

Stowers Institute for Medical Research

Regrowing hearing cells: New… | Stowers Institute for Medical Research

It's more bad news for Intelligent Design (ID) creationists who believe their putative designer is the anthropophilic, omnibenevolent God of the Bible. Hot on the heels of the discovery that some lemurs do not suffer from the age-related degenerative conditions that cause such misery for humans, comes the news that zebrafish can regenerate lost hair cells—cells that, in humans, enable hearing but cannot be replaced once lost.

These hair cells, located in the human inner ear, detect vibrations and are crucial for hearing. They can be destroyed through prolonged exposure to loud noise, resulting in permanent deafness. However, zebrafish possess homologous cells in their lateral lines—structures that allow them to detect vibrations in water, effectively functioning as a form of hearing. Remarkably, these cells can regenerate under the control of two specific genes.

It doesn't take a genius to realise that, if we accept the intelligent design argument that a divine designer deliberately created these genes, then the same designer could have endowed its supposed special creation—humans—with this regenerative ability too. Within the ID framework, the only possible conclusion is that the designer god chose *not* to give humans this ability, and instead preferred us to go deaf.

The problem for creationists deepens when one considers that these genes exemplify what William A. Dembski of the Discovery Institute cites as evidence of intelligent design: they are complex and specified, containing the genetic information to produce a defined result. Dembski insists that such "complex specified information" can only originate from an intelligent designer.

Creationists, of course, are compelled to reject the notion that these differences are simply the result of evolutionary processes. But if they also refuse to accept that this zebrafish trait—clearly underpinned by "complex specified genetic information"—constitutes evidence of intelligent design (and therefore points to a deliberate *absence* in humans), they are also undermining Dembski's single defining argument for intelligent design.

This striking discovery was made by researchers at the Stowers Institute for Medical Research and has just been published open access in Nature Communications.

Malevolent Design - What A Benevolent Designer Could Have Given Us, But Chose Not To, Apparently.

Coquerel's sifaka,Propithecus coquereli.

Ring-tailed Lemur, Lemur catta.

Study Suggests Lemurs Age Differently Than Humans | Duke Today

According to creationist superstition, humans were specially created by a perfect, anthropophilic, omnibenevolent creator god. If that were true, it would be reasonable to expect humans to be perfectly designed—free from defects or anything likely to cause long-term suffering.

However, the facts do not support this view. For example, as humans age, they increasingly suffer from a condition known as inflammaging — low-grade, chronic inflammation that contributes to a range of health problems, including heart disease, strokes, diabetes, cancer, and osteoarthritis.

Properly understood, this should give creationists cause for concern. The same designer god apparently gave some other primates—most notably, certain species of lemur—the ability to avoid this consequence of ageing. In fact, these lemurs even show a reduced tendency toward inflammatory conditions as they grow older.

This raises a serious question for Intelligent Design creationists: if the same designer god was capable of creating such a mechanism for lemurs, why did it not see fit to bestow the same gift upon its supposed favourite creation—humans? Or are these inflammatory conditions intended to cause suffering and disease as we age?

The discovery that some lemurs appear to have been specially favoured by a creator god—if we accept the ID creationist premise for the sake of argument—was made by a team of researchers led by Elaine Elizabeth Gomez Guevara, a biological anthropologist in the Department of Evolutionary Anthropology at Duke University, Durham, USA. As a scientist and biologist, however, she attributes the differences between lemurs and humans to evolution — not to indifference or malevolence on the part of a designer god.

The team has just published their findings in the Journal of Comparative Physiology B.

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.