Unintelligent Design - Men Lose Their Y Chromosome - And Why It Matters

Men lose their Y chromosome as they age. Scientists thought it didn’t matter – but now we’re learning more

Creationists who point to the supposed 'perfection' of the human body as evidence of intelligent design have yet more evidence to ignore if they are to retain that belief. In my book, The Body of Evidence: How the Human Body Refutes Intelligent Design, I listed many of the conditions and vulnerabilities from which humans suffer precisely because our bodies are the products of evolution, not intelligent design. Viewed objectively, rather than through the rose-tinted lens of creationism, the human body is one of the strongest arguments against intelligent design and in favour of evolution.

We now have additional evidence of this. As men age, increasing numbers of their cells lose the Y chromosome — the chromosome that males normally possess alongside a single X chromosome, while females usually have two X chromosomes. It is becoming increasingly clear that this loss is implicated in several diseases that affect men disproportionately, including cardiovascular disease, Parkinsonism, and some cancers such as ocular melanoma. Together, these help to explain men's lower life expectancy.

According to the ID creationist paradigm, the human body is the supreme achievement of their god's design. So, if we assume, as they do, that this designer is the omniscient and omnibenevolent god of the Bible and Qur'an, then this male-specific vulnerability must either have been intended or be the accidental result of incompetence and lack of foresight. Traditionally, of course, ID creationists try to absolve their designer of responsibility for such flaws by blaming them on some other entity supposedly capable of thwarting the divine plan, with humans bearing the guilt because of the 'sin' of a mythical ancestral couple. This merely exposes Intelligent Design for what it really is: not science, as the Discovery Institute and its allies insist, but biblical literalism in a lab coat, forced to rely on fundamentalist superstition to explain away the failures of its own claims when the facts are examined.

How scientists are discovering this age-related loss of the Y chromosome in men's cells, and the damaging effects it has on male health, is the subject of an article in The Conversation by the distinguished geneticist Jenny Graves, Distinguished Professor of Genetics and Vice-Chancellor's Fellow at La Trobe University, Australia. Her article is reproduced here under a Creative Commons licence, reformatted for stylistic consistency.

First, some background information on the origins and function of the Y chromosome:

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.

Refuting Creationism - How The Centromere Evolved

Abstract digital DNA Helix. Purple elements represent evolutionary changes in DNA.

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26-02-19Uncovering evolution at the center of cell division | Max Planck Institute

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A paper recently published in Nature by a research team led by Andrea Musacchio, Director at the Max Planck Institute of Molecular Physiology in Dortmund, Germany, and Jef Boeke from the NYU Grossmann School of Medicine, refutes a number of creationism's sacred dogmas. It shows how evolution at the cellular level progresses through intermediate stages and how new genetic information can arise and be repurposed. It also shows how complex specified information can evolve naturally by a Darwinian process.

The paper goes some way towards solving the ‘centromere paradox’. This is the observation that although the mechanism of cell replication, which is common to all eukaryotic cells, is highly conserved, the centromere — the specialised point on a chromosome to which proteins attach and pull the chromosomes apart during cell division — appears to mutate freely. This results in a wide variety of centromeres, ranging from large, repeat-rich centromeres in some species to the tiny, minimalist ‘point centromeres’ of yeast.

The team showed that the tiny centromere in yeast evolved through intermediate stages and began as a ‘jumping gene’, or retrotransposon — an essentially parasitic chunk of DNA that can relocate within a chromosome, thereby creating new genetic material. In yeast, this appears to have been repurposed by evolution to create the precise minimalist centromere — an example of what William A. Dembski would call complex specified information and designate as evidence for a creator.

Abiogenesis News - Origin Of Complex (Eukarote) Cells - Origin Of The Cell Nucleus

Amoeba infected with a giant virus

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Ushikuvirus: A newly discovered giant virus may offer clues to the evolutionary relationships
Researchers discover a new virus called the "ushikuvirus" that provide evidence for the viral eukaryogenesis hypothesis and reveal virus-host interactions, shaping the evolution of eukaryotic cells.

Professor Masaharu Takemura.

Ushikuvirus: A Newly Discovered Giant Virus May Offer Clues to the Origin of Life | Tokyo University of Science

One of the remaining questions in evolutionary biology is how the complex (eukaryotic) cell acquired its defining feature: a membrane-bound nucleus in which the DNA is stored.

Prokaryotic cells — bacteria and archaea — possess a single circular DNA molecule located in the cytoplasm. By contrast, all eukaryotic cells contain their genetic material within a membrane-bound nucleus. Now scientists at the Graduate School of Science, Tokyo University of Science (TUS), Japan, led by Professor Masaharu Takemura, have provided further evidence that the eukaryotic nucleus may have originated from a giant DNA virus, similar to those that infect certain species of amoeba. Their findings suggest that the origin of the nucleus may be closely linked to the evolutionary history of this class of virus as it adapted to different hosts.

Professor Takemura and Dr Philip Bell, from the Department of Biological Sciences at Macquarie University, Sydney, independently proposed the viral eukaryogenesis theory (a term coined by Dr Bell) in 2001, suggesting that large DNA viruses — such as poxviruses — might represent plausible ancestors. Since then, beginning in 2003, the discovery of several giant DNA viruses has provided more compelling candidates. When these viruses infect a host cell, they establish so-called ‘virus factories’ within the cytoplasm. In some cases these structures are enclosed within membranes that resemble the nuclear envelope.

The hypothesis proposes that, rather than destroying its host, such a virus formed a long-term association with it. Over evolutionary time, it may have incorporated host genes and transitioned from parasite to symbiotic genetic compartment — eventually becoming the nucleus.

For advocates of “irreducible complexity”, the nucleus is often presented as an all-or-nothing structure: a fully formed membrane, nuclear pores, transport machinery, chromatin organisation and regulatory systems supposedly appearing together or not at all. Yet the viral eukaryogenesis model shows how this argument collapses once intermediate stages are recognised. Giant DNA viruses already construct membrane-bound replication compartments inside host cells; they encode components involved in DNA replication, transcription and even elements of translation.

These viral “factories” function as semi-autonomous genetic centres within the cytoplasm — in effect, simplified proto-nuclei. If such a structure entered into a stable symbiotic relationship with a host cell, incremental gene exchange and co-evolution could gradually integrate and refine the system. Each step would confer immediate functional advantages — protection of DNA, separation of transcription from translation, improved regulation — without requiring the simultaneous appearance of a fully modern nucleus. What is claimed to be irreducible instead looks like a product of stepwise evolutionary integration.

Now Professor Takemura’s team report the discovery of a new giant DNA virus infecting amoebae — the ushikuvirus, named after Lake Ushiku where it was isolated — lending further support to the viral eukaryogenesis theory. Their discovery is reported in Journal of Virology.

Abiogenesis News - Origin Of Complex (Eukaryote) Cells - Association With Mitochondria.

Beginnings of symbiosis

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A Break in a Longstanding Mystery about Origin of Complex Life | College of Natural Sciences

Here are a couple of papers published today that deal with related aspects of the origins of complex (eukaryotic) cells — all living organisms apart from Bacteria, Archaea and viruses (the prokaryotes). There is little doubt in biology that eukaryotes evolved from symbiotic associations between prokaryotes, despite the regular creationist straw man claim that scientists are naïve enough — or somehow brainwashed by evil “Darwinists” — to believe that the first complex cell arose spontaneously in a single step so fantastically improbable that magical creation becomes an almost plausible alternative.

In reality, as these two papers demonstrate, the precise details of how these symbiotic associations arose remain matters of active research and debate. I will deal with the second paper in a separate blog post. This post concerns the paper by scientists from The University of Texas at Austin, published in *Nature*, which addresses the question of how the oxygen-dependent bacterium that became the mitochondrion came together with a presumed anaerobic (oxygen-intolerant) archaeon, given that the two would not be expected to occupy the same environment.

The team propose that this apparent problem may be resolved by evidence that some archaea of the Asgard group — which today live primarily in the deep sea and other oxygen-free environments — can use, or at least tolerate, oxygen.

The Asgard archaea most closely related to eukaryotic cells are found in shallow coastal sediments or floating in the marine column. Crucially, they possess metabolic pathways that use oxygen. It is therefore possible that their ancestors did as well, meaning they could have cohabited with the bacterial ancestors of mitochondria.

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.

Refuting Creationism - How A Chance Mutation Allowed The Evolutionary Transition From Invertebrates To Vertebrates

Sea squirt, Ciona intestinalis

Credit: Shunsuke Sogabe

New discovery sheds light on evolutionary crossroads of vertebrates | University of St Andrews news

Researchers from the University of St Andrews, working with colleagues from the University of Aberdeen and the University of Oxford, have identified a pattern of gene evolution that appears to have been crucial to the origin and subsequent diversification of vertebrates from their common ancestry with invertebrates. They have just published their findings in BMC Biology.

This discovery will be a major disappointment for creationists who cling to the notion that there is no evidence for what they call “macroevolution” — a term so ill-defined that it can be stretched to mean whatever a creationist happens to need at the time. Sometimes it is invoked to mean the origin of a new species, at other times a new genus, an entire new order, or even the biologically absurd idea of one species giving birth to an individual belonging to a completely different order. More often, though, “macroevolution” is said to mean the origin of entirely new anatomical structures.

Even that definition collapses immediately under scrutiny. Asked what novel structure humans possess that chimpanzees lack, “macroevolution” abruptly becomes the evolution of anything creationists choose to label a “kind” — another conveniently nebulous term, defined precisely nowhere and flexibly everywhere.

Yet if the origin and diversification of vertebrates does not qualify as “macroevolution”, it is difficult to imagine what possibly could. The St Andrews–led team has shown that this transition was enabled by gene evolution — that is, mutation acted upon by natural selection — affecting the genetic control of cell signalling during embryonic development. These changes influence when and where new cell types arise as a developing embryo progresses from a single-celled zygote to a complex multicellular organism, complete with differentiated tissues and specialised organs.

As this gene regulatory system evolved, it allowed the vertebrate phylum to diversify into the many classes and orders that now dominate marine and terrestrial ecosystems. No doubt this will require yet another round of misrepresentation by creationists, along with further blurring of the already elastic definitions of “macroevolution” and “kinds”.

Unintelligent Design - One Design Blunder Led To Another And Ended Up Causing Cancer - Or Was It Deliberate?

A broken DNA repair tool accelerates aging | News from Goethe University Frankfurt

Researchers from Goethe University, Frankfurt am Main, Germany, have shown how a faulty DNA repair mechanism triggers inflammation and leads to accelerated ageing, developmental abnormalities, and cancer.

Their findings are published in Science.

As I explained in my book, The Unintelligent Designer: Exposing the Intelligent Design Hoax, one of the hallmarks of an evolved system — and one which creationists have been conditioned to mistake for evidence of intelligent design — is complexity. In reality, the opposite is true: intelligently designed objects and processes are typically *minimally

complex, doing exactly what is required and no more.

One reason complexity arises in evolved systems is the need for additional layers of processes to compensate for the suboptimal designs that evolution inevitably produces. An intelligently designed process — especially one devised by a designer endowed with foresight — would require no such compensatory mechanisms. It would function reliably every time and be robust enough to withstand environmental stressors and other causes of malfunction. Nor would a perfectly designed copying process be prone to copying errors.

What we observe in reality, however, is an excessively complex system that still malfunctions — and when it does, it can do so unpredictably and catastrophically, leading to increased suffering and even death. The equivalent, in engineering terms, would be an aircraft manufacturer producing planes that were mostly safe most of the time, yet costly to build because they relied on intricate back-up systems to compensate for other components prone to failure — and which nevertheless suffered unpredictable mid-flight failures when those back-ups failed, causing aircraft to fall from the sky. Such an incompetent aircraft manufacturer would not remain in business for long.

In contrast to evolved systems which are overly complex and still prone to errors, an intelligently designed organism would be minimally complex, maximally efficient, robust enough to withstand environmental stressors and work perfectly every time. As so often, what ID predicts is not what we actually observe. In normal science, the falsification of a hypothesis is regarded as confirmation that the hypothesis was wrong, but in creationism the reverse holds; if the facts fail to confirm the hypothesis the facts must be wrong. The hypothesis must be clung to with grim determination, come what may.

Unintelligent Design - Why Some People Suffer More From The Common Cold Than Others - Incompetent or Malevolent Design - Or Evolution?

Electron micrograph showing a human nasal epithelial cell releasing rhinovirus (blue).

Credit: Julien Amat, Bao Wang

Electron micrograph of differentiated human nasal epithelial organoids with cilia of multiciliated cells accentuated in blue.

Credit: Julien Amat, Bao Wang.

Why the same cold can be a sniffle for some and a crisis for others | Yale News

You might expect an intelligently designed system, created by an omnibenevolent designer, to work just as effectively for everybody and not badly for some and only just adequately for others. And yet, as so often with creationism, the facts are not at all what the theory predicts. In science this would be called falsification, but for creationists it is just another inconvenient fact to be ignored or blamed on ‘the Fall’ — or even on the victim.

According to a paper just published in Cell Press Blue, the reason some people suffer more from a cold caused by a rhinovirus is not so much because of differences in the virus, but because their bodies react differently. Some take control and prevent the spread of viruses to adjacent cells of the mucous membrane lining the nasal passages, whereas other people’s bodies fail to prevent the virus spreading.

The paper is by a team at Yale School of Medicine, New Haven, CT, USA, led by Associate Professor Dr Ellen F. Foxman, PhD.

By growing organoids in vitro and infecting them with rhinoviruses, the team were able to show that whether the infection spreads depends on how quickly the infected cells are able to mount an interferon response. A good response limits the infection to just a few cells and the cold does not develop beyond a ‘sniffle’. Where the response is weak, the infection spreads and, in cases where the victim has an underlying respiratory condition such as asthma or COPD, the cold can develop into a serious illness.

Why the interferon response differs between individuals is not known with any certainty, but it could be due to a number of factors, including genetics. However, it is known that in patients with pre-existing respiratory conditions, the interferon response is inhibited.

That, of course, begs the question for ID creationists: why a system supposedly designed to protect us gets downgraded when it is most needed, and, if the difference is due to underlying genetics, why some people got better genes in this respect than others. Under the ID creationist paradigm, genes that produce any given output are deemed to hold ‘complex specified genetic information’ and, as such, are evidence for intelligent design.

Leaving aside the question of why any omnibenevolent designer would design viruses to make us sick and then design an immune response to prevent them doing so, we are left with the question of why this immune system does not always work very well and why some people have a worse version than others. If an omnibenevolent designer can design an effective immune system, why did it not give it to everyone? Does it actually want those people to suffer more from the viruses it supposedly designed?

The evolutionary explanation is, of course, straightforward, with none of the theological conundrums that plague creationism. Evolution does not seek out perfection and has no interest in equity. In the environment of an evolutionary arms race with viruses, the results are inevitably suboptimal and unevenly distributed throughout the population unless there is particularly strong selection pressure to drive the ‘best’ solution to fixation. It is also in the survival interests of viruses to tone down their victim’s responses, thereby reducing that selection pressure. The resulting trade-off and compromise is what we see today in the different responses to the same virus.

Malevolent Design - How The Herpes Virus Entered Our Genome Then Co-Evolved With Us

Source: BioLogos

First ancient human herpesvirus genomes document their deep history with humans

An international research team led by the University of Vienna and the University of Tartu (Estonia) — in collaboration with the University of Cambridge and University College London — has shown that ancient genomes of human betaherpesvirus 6A and 6B (HHV-6A/B) entered the human genome and then co-evolved with humans over the last 2,000 years. Their study, published in Science Advances a few days ago, confirms that these viruses have been evolving with, and within, humans since at least the Iron Age.

A common creationist claim, rooted in ignorance of what genetic information actually is, is that new genetic information cannot be created. Claims that new genetic information cannot arise because it would violate the laws of thermodynamics rely on a fundamental category error. The second law applies to closed systems, whereas every biological system on Earth is emphatically open, continuously exchanging energy and matter with its environment. Local decreases in entropy are not only permitted but expected in open systems supplied with external energy — which, on Earth, is overwhelmingly provided by the Sun. Crystals grow, snowflakes form, embryos develop, and genomes increase in length and complexity without violating any physical law.

Moreover, information is not a conserved physical quantity like energy. Shannon information theory concerns the statistical properties of signals in communication channels; it says nothing about biological meaning, function, or heredity. Treating genetic information as though it were interchangeable with thermodynamic entropy is simply a misuse of terminology. When genomes gain duplicated genes, viral insertions, or transferred sequences, no atoms are created, no laws are broken, and no special pleading is required — just chemistry operating under well-understood physical principles.

The creationist claim is flatly contradicted by straightforward observations of several well-understood mechanisms by which new genetic information can enter a species’ genome. These include gene duplication or whole-genome duplication, horizontal gene transfer from one species to another (particularly common in parasite–host relationships), and — as demonstrated by the research discussed here — the insertion of viral DNA into the genome. This last process gives rise to endogenous viral elements that are ubiquitous in biology and which precisely match evolutionary trees established independently from multiple other lines of evidence.

Endogenous viral insertions are especially devastating for the creationist concept of immutable “created kinds”. Viral DNA does not insert itself independently at exactly the same genomic locations in unrelated lineages by chance. When identical viral sequences are found embedded at the same chromosomal positions in different populations — and when their accumulated mutations form nested hierarchical patterns — they provide a precise historical record of shared ancestry.

The HHV-6A/B insertions documented in this study behave exactly as evolutionary theory predicts: they enter the genome at a particular point in time, are inherited by descendants, accumulate mutations at measurable rates, and track human population history. There is no coherent creationist explanation for why a designer would place broken, mutating viral sequences into genomes in patterns that perfectly mirror evolutionary trees derived independently from anatomy, archaeology, and population genetics.

If humans were created as a distinct “kind”, there is no reason for their genomes to contain time-stamped viral relics tracing population divergence over millennia. But if humans evolved — and if viruses have co-evolved with us — this is precisely the pattern we expect to find. The data fit evolution effortlessly, while creationism is left inventing ad hoc excuses to deny what the genome itself records.

Malevolent Design - How Cancer Perfectly Illustrates ID Creationism's 'Proof' of Intelligent Design

Creationism's God at work

Creationism's intelligent designer creating cancer.

AI-generated image (ChatGPT 5.2).

Dresden research group uncovers new key mechanism in cancer cells | TU Dresden

ID advocates should be thrilled to learn that a team of researchers from Technische Universität Dresden (TUD), Germany, together with colleagues from Charles University, Prague, Czechia, have discovered a perfect example of what Discovery Institute fellows William A. Dembski and Michael J. Behe claim is proof of intelligent design—namely complex specified information and irreducible complexity. The team have just published their findings, open access, in Nature Communications.

There is one slight problem, however: this supposed ‘proof of intelligent design’ turns out to be one of the mechanisms that makes cancer so effective at increasing pain and suffering — and at killing people.

This presents creationists with a theological conundrum. Either there is more than one intelligent designer, which comes close to—or even crosses—the line into blasphemy, or the intelligent designer is actively and knowingly creating a cause of pain and suffering, and is therefore not the omnibenevolent deity portrayed in the Bible.

The stark alternative to these theologically insurmountable problems is equally problematic for ID creationism: admitting that their ‘proof of intelligent design’ is nothing of the sort, and is better explained as the result of a natural process in which no intelligence was involved—thereby absolving their god of any culpability.

The TUD-led team discovered that the protein MCL1 not only inhibits programmed cell death, or apoptosis, but also plays a central role in tumour metabolism. Normal, non-cancerous cells will usually self-destruct if their DNA becomes corrupted beyond repair, but when this process fails, a tumour can develop through the proliferation of cells carrying damaged DNA. In cancers, this self-destruct mechanism is suppressed by MCL1.

The team also found that MCL1 is not only responsible for preventing apoptosis, but also dysregulates cellular energy metabolism. In other words, a single factor ensures both cancer cell survival and the functioning of key metabolic and signalling pathways for the benefit of the tumour.

In Michael J. Behe’s terms, all the components of this survival mechanism must be present for the cancer to persist; and in William A. Dembski’s terms, the genetic information coding for MCL1 must constitute highly specified complex information.

Unintelligent Design - The Design Blunder That Causes Cancer - Or Was It Malevolent Design?

Graphical abstract

Scientists find cancer weak spot in backup DNA repair system | Scripps Research

Scientists at the Scripps Institute have discovered a defective DNA repair mechanism that would normally trigger cell death but which, paradoxically, keeps cancer cells alive. They have recently published their findings, open access, in Cell Reports. It is exactly the sort of biochemical complexity that creationists routinely mistake for evidence of intelligent design, having been led to believe that well-designed systems must be highly complex. In reality, good intelligent design is minimally complex: complexity increases the risk of failure, is harder to maintain, and is more energetically costly.

The DNA “code” is one of creationism’s favourite props for its familiar ignorance-plus-incredulity-therefore-God-did-it argument — a textbook god-of-the-gaps false dichotomy. Yet even a superficial look beneath the metaphor reveals that DNA replication and repair are very far from the flawless perfection we would expect from an omniscient, omnipotent and omnibenevolent deity — especially when it comes to its supposedly special creation, humankind. What we actually observe is a fragile, error-prone system patched together by evolutionary history rather than foresight.

The system is only needed in the first place because cell replication in multicellular organisms remains essentially identical to that of single-celled organisms. Despite the fact that the benefits of multicellularity arise from cell specialisation into tissues and organs with discrete functions — each requiring only a tiny fraction of the genome — every cell is forced to copy the entire DNA complement every time it divides. This vast waste of energy and resources serves only to multiply the probability of error, and errors are not rare anomalies but routine occurrences. This is not the signature of intelligent design.

The Scripps Institute team have shown that some cancer cells survive precisely because the normal high-fidelity repair system fails. When that happens, a crude backup mechanism takes over — an emergency repair process that is little more than a biological kludge and which introduces further errors as it works. It is rather like calling out an emergency plumber who fixes one leak by installing a long section of pipe riddled with smaller leaks. Would anyone describe that as intelligent workmanship?

Malevolent Design - How Breast Cancer is 'Designed' to Survive

Cell culture plates in the Roeder lab where scientists recently studied gene expression in breast cancer.

Credit: Lori Chertoff.

The Rockefeller University » This molecular switch helps cancer cells survive harsh conditions

Researchers at The Rockefeller University's Laboratory of Biochemistry and Molecular Biology have uncovered the mechanism that enables breast cancer cells not only to withstand environmental stress, but to turn it to their advantage. They have just published their findings in Nature Chemical Biology.

For ID creationists, these findings pose yet another challenge—one typically ignored or waved away as the consequence of ‘sin’, neatly exposing the Discovery Institute’s attempt to persuade US legislators and educators that ID is a genuine scientific alternative. No real science explains inconvenient evidence by invoking fundamentalist doctrine or unevidenced forces inherited from ancient superstition.

The Rockefeller University team has shown that breast cancer cells can override a regulatory factor that normally controls gene expression. The transcription of DNA into mature messenger RNA involves the enzyme RNA polymerase II (POL II), whose activity depends on around 30 subunits. One of these, MED1, normally carries acetyl groups. Without those acetyl groups, MED1 loses its ability to regulate POL II, allowing the enzyme to transcribe genes that help cancer cells survive. Environmental stress deacetylates MED1. In essence, conditions such as low oxygen or elevated temperature—deadly to normal cells—can instead make cancer cells more resilient.

Incompetent Design - How Sunlight Turns Off Cancer Protection in Skin

Schematic of the role of YTHDF2 in regulating U6 snRNA decay and interaction with TLR3 to control UVB-induced inflammation and tumorigenesis.

Seungwon Yang, Yan-Hong Cui, Haixia Li, et al.(2025), Fig.7 P

New study reveals how controlling sunburn-triggered inflammation may prevent skin cancer - UChicago Medicine

Researchers at the University of Chicago have uncovered how prolonged exposure to ultraviolet (UV) radiation can lead to skin cancer by disabling a vital protective mechanism in skin cells. They have just published their findings, open access, in Nature Communications.

This protective mechanism relies on a protein called YTHDF2, which plays a key role in regulating RNA metabolism and maintaining cellular health. Sunlight degrades this protein, removing that safeguard and allowing damage to accumulate.

For advocates of Intelligent Design (ID) creationism, this research presents several awkward questions—questions they will either ignore or attribute to ‘sin’.

First, why is this protection needed at all? If life were intentionally and intelligently designed, why would RNA metabolism require an additional, failure-prone layer of regulation to keep cells functioning? Why not design it to be robust in the first place?

Second, why create a system so fragile that sunlight—an unavoidable feature of life on Earth—can disable it? Designing a repair mechanism that breaks down precisely when it is needed most hardly inspires confidence in the designer’s competence.

And then there is the broader problem: ID creationism equates its designer with the supposedly omniscient and omnipotent god of the Bible or Qur’an. If that is true, why design a mechanism that predictably causes cancer? Was this an act of malevolence or oversight?

If YTHDF2 were flawless and impervious to degradation, Discovery Institute fellow William A. Dembski would no doubt present it as an example of “complex specified information,” a supposed indicator of intelligent purpose. But its vulnerability raises uncomfortable possibilities: Is this an unsuccessful attempt to patch over earlier design flaws in RNA metabolism? A sign of competing designers beyond the control of ID’s putative omnipotent creator? Or evidence that the designer is actively introducing harm and suffering?

The answer, of course, is that this problem arises because the human body is not the product of intelligent design at all, but of a long evolutionary process that modifies existing processes and structures to produce workable—though often imperfect—solutions. Evolution favours whatever improves short-term reproductive success, even if it introduces compromises and sub-optimal outcomes that undermine long-term survival and health. These sub-optimal systems then drive the evolution of an additional layers of complexity to minimise the results of failure.

Like other organism's the human body is full of these examples of evolutionary compromises and sub-optimal solutions that cause diseases and health problems that illustrate the difference between an intelligently designed system and an evolved system. Looked at in detail, the human body is evidence against intelligent design and strongly supports the Theory of Evolution, as I show in my book, The Body of Evidence: How the Human Body Refutes Intelligent Design.

Unintelligent Design - The Design Blunder That Causes Many Diseases - Malevolence or Incompetence?

Glutathionylated mtDNA

AI-generated image (ChatGPT 5.1)

New type of DNA damage found in our cells’ powerhouses | UCR News | UC Riverside

Scientists led by the University of California, Riverside (UC Riverside) have identified a previously unknown form of DNA damage in mitochondria that may underlie a wide range of disorders linked to mitochondrial dysfunction. Their findings have just been published in the Proceedings of the National Academy of Sciences (PNAS).

Mitochondria contain their own DNA (mtDNA), which is essential for the proper functioning of these organelles that convert glucose into ATP, supplying cells with the energy needed to power metabolic processes.

The culprit is a large molecule, glutathionylate, which attaches to DNA and, if left unrepaired, can cause mutations. Researchers at UC Riverside, working with colleagues at the University of Texas MD Anderson Cancer Center, found that glutathionylated mtDNA accumulates in mitochondria at levels up to 80 times higher than in the cell nucleus. In short, the nuclear DNA repair system is vastly more efficient than its mitochondrial counterpart.

For advocates of Intelligent Design (ID), this discovery—if they understood it rather than dismissing it as part of an imagined conspiracy to undermine their faith—creates an acute theological problem. If we temporarily grant the core assumption of ID creationism, that a supernatural designer indistinguishable from the allegedly omniscient, omnipotent, and omnibenevolent god of the Bible and Qur’an is responsible for the design of mitochondrial DNA and its replication machinery, then only two coherent conclusions follow:

• the designer is incompetent, having failed to produce fault-free mtDNA and an adequate repair mechanism, despite supposedly managing this for nuclear DNA; or
• the designer could have produced fault-free mtDNA but chose instead to create error-prone mtDNA and a weak repair process, thereby intentionally designing disease and suffering—in other words, malevolence.

Moreover, the very need for a repair system betrays the absence of omnipotent, intelligent engineering. It is characteristic instead of the layered complexity produced by cumulative, unplanned evolutionary processes, which inevitably yield sub-optimal compromises.

The notion of an omniscient designer also rules out the excuse that the harmful consequences were unforeseeable. An all-knowing creator would have foreseen them; yet, according to ID logic, the designer implemented them regardless—designing mitochondrial DNA to fail and cause disease.

Thus, a biological phenomenon that fits seamlessly within the framework of evolutionary theory becomes an insurmountable theological obstacle for ID advocates, who must contort the evidence to suit a predetermined conclusion while catering to a scientifically illiterate and credulous audience.

Unintelligent Design - The Defect that Causes Alzheimer's - Incompetence or Malevolence?

Exosomes

Researchers discover cell defect linked to the development of Alzheimer’s

Researchers at Aarhus University in Denmark have identified a defect in the production of exosomes within cells, linked to a mutation found in patients with dementia. Their findings are published in the journal of the Alzheimer’s Association, *Alzheimer’s & Dementia*.

Advocates of Intelligent Design argue that all genetic information must originate from an intelligent agent, claiming that anything both complex and specified cannot arise without deliberate design. Their proposed designer is invariably indistinguishable from the god of the Bible and Qur’an: an all-knowing, all-powerful and supposedly benevolent creator.

What they never address is why a system attributed to such a being should fail at all—let alone in ways that cause profound suffering. It is akin to a human engineer producing an aircraft with engines that randomly fail or wings that detach mid-flight. And because this designer is held to be omniscient, the failure cannot be inadvertent. It must have been foreseen and deliberately incorporated, making such mutations part of the intended plan rather than unfortunate accidents.

Following the internal logic of ID creationism, Alzheimer’s dementia would therefore count as an intended outcome—meeting William Dembski’s own criteria for “complex specified genetic information”. This provides yet another instance, alongside the cancer example I discussed recently, of biological processes that appear designed to destroy. It sits comfortably among the many parasites and pathogens explored in The Malevolent Designer: Why Nature’s God is Not Good, all pointing to a distinctly malign pattern in the supposed “design”.

ID proponents typically fall back on blaming “The Fall”, implying the existence of another creative force beyond the control of their designer. This manoeuvre only further undermines their claim that ID is a scientific enterprise rather than creationism thinly disguised, since it relies on biblical literalism to rescue the argument from the conclusion of an incompetent or malevolent designer—an outcome that is theologically awkward and, for many believers, outright heretical.

Malevolent Design - How Some Cancers Are Designed to Win - Incompetence or Malevolence?

Cancer cells dividing

Shapeshifting cancers’ masters, unmasked | Cold Spring Harbor Laboratory

Scientists led by Cold Spring Harbor Laboratory (CSHL) Professor Christopher Vakoc have uncovered a mechanism by which certain cancers manage to evade modern medical treatments: they can disguise themselves as ordinary cells from entirely different tissues, such as those of the skin. In two recent papers — one in Nature Communications and another in Cell Reports — Vakoc’s team identify the proteins that determine whether pancreatic cancer cells retain their pancreatic identity or slip into a skin-cell-like state. They also highlight a different set of proteins with a pivotal role in tuft-cell lung cancer.

Proteins, of course, are specified by genetic information, and if that information is altered, so too is the protein’s function. In the language of ID creationists, proteins are products of “complex, specified genetic information”.

This presents intelligent design creationists with a familiar problem — one they usually address, as with parasites and pathogens, by ignoring it and relying on the scientific illiteracy of their followers. If complex, specified information were genuinely evidence of an intelligent designer, then that same designer would be implicated in the origin of the proteins that maintain and diversify cancers. Their “specified information” is neither less complex nor less specific than the proteins involved in cognition, immunity, or embryonic development.

Only by refusing to define “complex specificity” in scientific terms — or to explain how it might be distinguished from information that is supposedly non-complex or non-specified — do ID advocates manage to maintain the fiction that all beneficial traits are the work of their designer, while harmful traits must arise from some other agency. This selective attribution, based entirely on subjective human preference, underscores the religious foundations of intelligent design creationism and its distance from genuine science.

The team’s findings are summarised in a Cold Spring Harbor Laboratory news release by Jen A. Miller.

Unintelligent Design - Flatworms Can Regenerate Body Parts - So Why Can't Humans?

The planarian Schmidtea mediterranea

Credit: FLI / Anna Schroll

Schmidtea mediterranea

New research shows a tiny, regenerative worm could change our understanding of healing Stowers Institute for Medical Research

Researchers at the Stowers Institute for Medical Research have uncovered new details explaining how the planarian flatworm, Schmidtea mediterranea, can regenerate not just a missing body part, but an entire organism from a tiny tissue fragment. Their findings have just been published in Cell Reports and represent a major advance in our understanding of regeneration at the cellular and genetic level.

This little worm continues to surprise scientists. Remove its head? It grows a new one. Slice it into pieces? Each piece becomes a complete worm. Such astonishing powers naturally prompt two very different kinds of questions – one scientific, one theological.

If one temporarily accepts creationist premises for the sake of argument, we are forced into a series of uncomfortable and contradictory conclusions.

Why would a supposedly omniscient, omnipotent, and omnibenevolent designer grant a humble flatworm the ability to regenerate an entire body, yet deny this life-saving ability to humans and virtually all other organisms? If this designer could abolish suffering, disease, and limb loss – and knowingly chose not to – what does that imply about its nature?

Creationists are left defending a worldview in which their designer appears either: unwilling to prevent suffering; unable to create beneficial traits consistently; or deliberately designing suffering into its creation. None of these options are theologically tidy – and they certainly do not align with the claim of a universally benevolent designer. The creationist framework produces contradictions, apologetics acrobatics, and moral dilemmas rather than answers.

By contrast, when we ask the evolutionary question – “How did this ability evolve?” – the picture becomes coherent.

Planarians have followed a unique evolutionary trajectory in which extreme regeneration conferred a significant survival advantage. Natural selection acted on stem-cell behaviour, gene regulation, and patterning networks over deep time, refining a mechanism that happens to be far beyond the needs of most other species.

Other organisms have regenerative abilities too – salamanders, zebrafish, sea stars, even humans to a limited extent – but the selective pressures and biological constraints differed. Regeneration is complex, energetically costly, and evolution works from what already exists. Most lineages simply did not follow that path. To borrow Michael Behe’s favourite term, planarian regeneration may appear “irreducibly complex” – and yet, as usual, complexity proves to be a testament to gradual evolutionary refinement, not evidence for supernatural assembly.