If we take creationist claims about the human body at face value – that we are the special design of an omniscient, omnipotent creator god – we would have to conclude that this putative god equipped us for life in small, dispersed bands of hunter-gatherers, entirely free from the pressures of modern urban existence. That is the inescapable implication of new work by Daniel P. Longman of the School of Sport, Exercise and Health Sciences, Loughborough University, UK, and Colin N. Shaw of the Department of Evolutionary Anthropology, University of Zürich, Switzerland.
In their study, recently published in Biological Reviews, they argue that human evolutionary fitness has deteriorated markedly over the past 300 years, beginning with the Industrial Revolution. They attribute this to the escalating stresses of urban life, which are increasingly linked to counter-survival problems such as declining fertility rates and the rising prevalence of chronic inflammatory conditions, including autoimmune diseases. They also highlight impaired cognitive function in urban settings, with chronic stress playing a central role in many of these conditions.
As they note, our stress responses were shaped in environments where predators such as lions posed intermittent but existential threats. A sudden burst of adrenaline and cortisol – the classic fight-or-flight reaction – made the difference between survival and being eaten. Today, however, we summon exactly the same physiological response to traffic noise, difficult conversations with colleagues or family, and that irritatingly arrogant but ignorant creationist on the Internet. Where a lion encounter would once have been an occasional shock, we now experience the physiological equivalent of facing several lions a day.
For creationists, this poses an awkward problem. An omniscient designer should have foreseen humanity’s future circumstances and endowed us with a physiology robust enough to cope with them. Evolution, by contrast, cannot predict even the next generation, let alone the demands of life tens or hundreds of millennia later. It optimised our ancestors for survival on open African landscapes, not for navigating congested cities, chronic noise, 24-hour information streams, and the relentless stimuli of modern technology. This helps explain why our inherited design is increasingly mismatched to our environment, and why evolution cannot adjust us quickly enough to keep pace.
My own family history illustrates this accelerating mismatch. My grandparents grew up in rural Oxfordshire, before the arrival of the motor car, electricity, modern sanitation, or powered heating. Their lives were essentially unchanged from those of their parents and grandparents. My parents, by contrast, had electricity, piped water, proper sanitation, and radio; later a motor car, a television, and eventually a telephone. Now we have smartphones, laptops, air travel, satnavs, and city centres jammed with traffic. We spend hours each day staring at screens, communicating instantly across the world. My grandparents’ lives would have been recognisable to their great-grandparents, but mine would be unrecognisable to them – such has been the accelerating pace of technological change. No evolutionary process could possibly adapt a species to that speed of environmental transformation.
We are, in effect, experiencing stress levels akin to those of ancestors living among a pride of lions, not merely encountering one on rare occasions. And crucially, we have little or no time to recover before the next ‘lion’ appears.
Researchers at Cedars-Sinai have developed a synthetic RNA molecule that can help repair DNA in damaged tissues such as the myocardium following a myocardial infarction (MI). Their research is the basis for a paper just published in Science Translational Medicine
This raises a troubling question for ID creationists: if scientists can do it, why couldn’t their putative omniscient, omnipotent and, above all, omnibenevolent designer god do it? There are only a limited number of possibilities if we grant the ID proponents their designer god for the sake of argument:
It lacks the ability — in other words, it isn’t omnipotent.
It didn’t know it would be needed — in other words, it isn’t omniscient.
It doesn’t care — in other words, it isn’t omnibenevolent.
It doesn’t want us to repair damaged DNA so we continue to suffer the consequences — in other words, it is malevolent.
This is, of course, just another example of science discovering something that any intelligent, benevolent designer would have anticipated and provided, if such an entity had really designed us.
So, apart from those explanations — none of which flatter their putative designer — the only option left to creationists is that the absence of this DNA repair mechanism is the result of an unintelligent natural process in which their supposed designer played no part, such as evolution.
Unfortunately for them, creationists would have to abandon creationism and admit to being wrong if they accepted the naturalistic explanation. Sadly for them, creationists don’t see admitting being wrong as the intellectually honest thing to do, but as a sign of weakness and giving in to scientists and the physical evidence all ganging up to test their resolve.
This should trouble any creationist who understands the implications, so their cult leaders need to work hard to ensure none of their followers know about these things or develop the intellectual sophistication to appreciate the consequences.
Researchers from Switzerland and Japan, led by Professor Yohei Yamauchi of Eidgenössische Technische Hochschule Zürich (ETH Zürich), have developed a microscopy technique that enables real-time, high-resolution observation of how a virus gains entry to a cell. Their findings are described in the Proceedings of the National Academy of Sciences of the USA (PNAS).
The process, in which a virus exploits the pathways cells normally use to take in larger molecules such as hormones, cholesterol, or iron, involves the active cooperation of the cell as it reaches out to engulf the viral particle. This mechanism is triggered by receptors on the cell surface, to which viruses bind while ‘surfing’ along the membrane, seeking regions rich in receptors to form a stable attachment.
In other words, creationists often portray this as an “irreducibly complex” system, supposedly dependent on all components being present from the outset, requiring what they call “complex specified information” in both virus and cell to produce the receptors and binding proteins. Discovery Institute fellows Michael J. Behe and William A. Dembski present this as evidence of intelligent design.
Their argument depends on a statistical sleight of hand: they treat the entire process as though it originated in a single event involving one cell and one virus, then calculate improbabilities for each step and multiply them together, producing a vanishingly small likelihood of the whole mechanism arising spontaneously. This ignores the fact that evolution operates in populations — often large ones — across long periods, where components accumulate gradually over generations, dramatically increasing the probability of multiple features emerging together in the same lineage.
It also overlooks the billions of years during which viruses and cells have co-evolved. As multicellular organisms evolved ever more sophisticated ways of receiving and responding to external signals and substances, viruses simultaneously improved their ability to exploit those mechanisms.
But to the scientifically illiterate target audience of the ID-creationism industry, evolution is imagined as a single event rather than a continuous process, leaving them oblivious to the misuse of probability and the underlying mathematical errors.
Creationists trying to use this argument for intelligent design usually respond to biologists pointing out the obvious fact that they just presented their putative god as some sort of celestial malevolence, by retreating into Bible literalism and religious fundamentalism and invoking mythical 'Fall', so betraying the claims of the Discovery Institute and its fellows that ID is real science, not bible-literalist creationism dressed in a lab coat, as a lie.
How influenza viruses enter our cellsFor the first time, researchers have observed live and in high resolution how influenza viruses infect living cells. This was possible thanks to a new microscopy technique, which could now help to develop antiviral therapies in a more targeted manner.
In brief
For the first time, a new high-resolution microscopy technique has allowed researchers to watch live as influenza viruses infect cells.
The international team led by ETH Zurich found that the cells actively promote virus uptake.
This technique could now help to develop antiviral therapies in a more targeted manner.
Fever, aching limbs and a runny nose – as winter returns, so too does the flu. The disease is triggered by influenza viruses, which enter our body through droplets and then infect cells.
Researchers from Switzerland and Japan have now investigated this virus in minute detail. Using a microscopy technique that they developed themselves, the scientists can zoom in on the surface of human cells in a Petri dish. For the first time, this has allowed them to observe live and in high resolution how influenza viruses enter a living cell.
Led by Yohei Yamauchi, Professor of Molecular Medicine at ETH Zurich, the researchers were surprised by one thing in particular: the cells are not passive, simply allowing themselves to be invaded by the influenza virus. Rather, they actively attempt to capture it.
“The infection of our body cells is like a dance between virus and cell.
Professor Yohei Yamauchi, corresponding author.
Molecular Medicine Laboratory
Institute of Pharmaceutical Sciences
Department of Chemistry and Applied Biosciences
Eidgenössische Technische Hochschule Zürich
Zürich, Switzerland.
Viruses surf on the cell surface
Of course, our cells gain no advantage from a viral infection or from actively participating in the process. The dynamic interplay takes place because the viruses commandeer an everyday cellular uptake mechanism that is essential for the cells. Specifically, this mechanism serves to channel vital substances, such as hormones, cholesterol or iron, into the cells.
Like these substances, influenza viruses must also attach to molecules on the cell surface. The dynamics are like surfing on the surface of the cell: the virus scans the surface, attaching to a molecule here or there, until it has found an ideal entry point – one where there are many such receptor molecules located close to one another, enabling efficient uptake into the cell.
Once the cell’s receptors detect that a virus has attached itself to the membrane, a depression or pocket forms at the location in question. This depression is shaped and stabilised by a special structural protein known as clathrin. As the pocket grows, it encloses the virus, leading to the formation of a vesicle. The cell transports this vesicle into its interior, where the vesicle coating dissolves and releases the virus.
Previous studies investigating this key process used other microscopy techniques, including electron microscopy. As these techniques entailed the destruction of the cells, they could only ever provide a snapshot. Another technique that is used – known as fluorescence microscopy – only allows low spatial resolution.
Combined techniques, including for other viruses
The new technique, which combines atomic force microscopy (AFM) and fluorescence microscopy, is known as virus-view dual confocal and AFM (ViViD-AFM). Thanks to this method, it is now possible to follow the detailed dynamics of the virus’s entry into the cell.
Video: Nicole Davidson / ETH Zurich.
Accordingly, the researchers have been able to show that the cell actively promotes virus uptake on various levels. In this way, the cell actively recruits the functionally important clathrin proteins to the point where the virus is located. The cell surface also actively captures the virus by bulging up at the point in question. These wavelike membrane movements become stronger if the virus moves away from the cell surface again.
The new technique therefore provides key insights when it comes to the development of antiviral drugs. For example, it is suitable for testing the efficacy of potential drugs in a cell culture in real time. The study authors emphasise that the technique could also be used to investigate the behaviour of other viruses or even vaccines.
Significance
Influenza A viruses (IAVs) continue to cause epidemics worldwide due to their high mutability. Nevertheless, the initial step of infection, viral uptake into cells, has been challenging to observe directly with conventional microscopy techniques. Here, we developed a hybrid imaging system combining atomic force microscopy and confocal microscopy with enhanced mechanical functionality and minimal invasiveness to directly visualize nanoscale dynamics of IAV and cell membranes during viral uptake into living cells. This system enables the analysis of IAV lateral diffusion resulting from IAV–membrane interactions and characteristic membrane morphological changes induced by IAV during endocytosis. Our approach offers a method to rapidly assess the impact of viral mutations on host cell entry, which is critical for understanding emerging IAV variants.
Abstract
Influenza A virus (IAV) entry into host cells begins with interactions between the viral envelope proteins hemagglutinin (HA)/neuraminidase (NA) and sialic acid moieties on the cell plasma membrane. These interactions drive IAV’s lateral diffusion along the cell membrane and trigger membrane morphological changes required for endocytosis. However, directly visualizing these dynamic processes, which are crucial for IAV entry, has been challenging using conventional microscopy techniques. In this study, we enabled live-cell observation of nanoscale morphological dynamics of IAV and the cell membrane by reducing the mechanical invasiveness of atomic force microscopy (AFM). A customised cantilever with less than half the spring constant of conventional cantilevers enabled virus-view AFM imaging that preserved IAV–membrane interactions. By combining virus-view AFM with confocal microscopy, we performed correlative morphological and fluorescence observations of IAV lateral diffusion and endocytosis in living cells. Variations in diffusion coefficients of single virions suggested heterogeneity in sialic acid density on the cell membrane. NA inhibition decreased diffusion coefficients, while reduced sialic acid density increased them. The timing of clathrin accumulation at virion binding sites coincided with a decrease in diffusion coefficients, a relationship that was maintained independent of NA activity or sialic acid density. As clathrin assembly progressed, ~100-nm-high membrane bulges emerged adjacent to the virus, culminating in the complete membrane envelopment of the virus at peak clathrin accumulation. Our virus-view AFM will deepen our understanding of various virus–cell interactions, facilitate the evaluation of drug effects and promote future translational research.
Influenza A virus (IAV) is an enveloped RNA virus with two key surface glycoproteins: hemagglutinin (HA) and neuraminidase (NA). The virus surface contains 300 to 400 HA and 40 to 50 NA molecules (1). IAV envelope proteins comprise at least 18 HA and 11 NA subtypes (2), which enable IAV to infect various host species including humans, birds, pigs, bats, and other animals (3). These envelope proteins play crucial roles in IAV infection of host cells.
They interact with sialic acids on cell surface glycolipids and glycoproteins (4) or with major histocompatibility complex class II (MHC class II) molecules (5–7). HA binds to sialic acids at the terminal ends of glycan chains on the cell surface. The HA–sialic acid interactions are inherently weak, with dissociation constants typically in the millimolar range (0.9 to 68.4 × 10−3 M) (8–10). However, multivalent binding of multiple HAs to sialic acids enables IAV to stably adhere to the cell membrane (11, 12). Meanwhile, NA catalyzes the cleavage of sialic acids (13), inhibiting stable adhesion of IAV to the cell membrane. Through these mechanisms, HA and NA effectively regulate the attachment and detachment of IAV to the cell membrane.
The competitive action between HA and NA allows IAV to diffuse laterally along the cell membrane surface topology (). This lateral diffusion represents a critical dynamic macroscopic phenomenon reflecting virus–membrane interactions. However, conventional microscopy techniques have struggled to detect IAV movement on the 10-nm-thick cell membrane, resulting in limited visualization success (15–18).
HA-NA-sialic acid interactions also trigger endocytosis involving morphological changes of the cell membrane. When diffusing IAV binds to functional receptors such as EGFR (19) and Cav1.2 (20) through sialic acids, it initiates the recruitment and assembly of the endocytic machinery including clathrin, actin, and dynamin. IAV utilizes multiple entry pathways including clathrin-mediated endocytosis (CME), macropinocytosis, and both clathrin-independent and dynamin-independent mechanisms (16, 21–23).
IAV primarily utilizes CME for cellular entry (16, 21). Previous imaging of membrane dynamics using atomic force microscopy (AFM) has revealed that in IAV-free CME, clathrin-coated membrane invaginations (pits) larger than 100 nm in diameter form (24, 25). This is accompanied by the emergence of actin-dependent membrane bulges that develop on one side of the pit and eventually lead to its closure. Although electron microscopy has provided morphological snapshots of pits during IAV internalization (26), the membrane dynamics during IAV internalization via CME have yet to be successfully visualized.
AFM enables mechanical imaging of sample morphology with nanometer-scale resolution (27, 28). Since the development of high-speed AFM in 2001 (29), this technique has contributed significantly to molecular dynamics analysis (30–36). Additionally, the advent of cell-imaging AFM in 2013 has enabled advances in membrane dynamics analysis (37, 38). The integration of cell-imaging AFM combined with confocal microscopy has provided unique capabilities for observing nanoscale membrane morphological changes in living cells (24, 25). Despite these advances, a major challenge persists: the mechanical interference of the cantilever with biological samples. Visualizing the dynamic processes of IAV lateral diffusion and internalization requires an innovative technology capable of simultaneously observing the nanoscale morphology of the 10-nm-thick cell membrane and the 100-nm spherical IAV interacting with cell surface sialic acid-bearing glycolipids and proteins. Given that multivalent IAV–membrane interaction forces are relatively weak, ranging from 10 to 25 pN (39), achieving low-invasive imaging capabilities is critical.
In this study, we address and overcome the challenge of mechanical interference by enhancing the low invasiveness of AFM through the use of a customised soft cantilever. In combination with confocal microscopy, low-invasive AFM enables simultaneous live-cell imaging of both morphology and fluorescence. The redesigned cantilever minimizes disruption of IAV–membrane interactions, allowing accurate observation of viral dynamics. Using this system, we investigated the lateral diffusion of single IAV particles under various conditions, including NA inhibition, reduced cell surface sialic acid density, and different viral subtypes. We also analyzed membrane morphological changes before and during IAV endocytosis. While fluorescently labeled IAV was primarily used, we also demonstrate our AFM’s capability to track unlabeled viruses. This virus-view dual confocal and AFM, called ViViD-AFM, enables correlative morphological and fluorescence imaging of IAV–membrane dynamics, providing nanoscopic insights into HA-NA-sialic acid interactions.
What ID advocates never seem to notice is that, in arguing that such mechanisms must have been deliberately engineered, they are attributing to their designer a system in which viruses are given exquisitely tailored tools for invading the very cells it supposedly created. If one insists that this is intentional design, then one must also accept that the designer crafted the molecular equivalent of lockpicks and battering rams, optimised for breaching living tissue. It is difficult to reconcile this with any notion of benevolence.
Indeed, by rejecting evolution as the explanation for viral entry, ID proponents corner themselves into an uncomfortable theological stance: their designer not only equipped viruses with the machinery to exploit cellular signalling, but also ensured that cells remained vulnerable to such exploitation. The result is an ecosystem in which suffering, disease, and death are not unfortunate consequences of natural processes but deliberate design choices.
This is, of course, why mainstream biology requires no such designer. Co-evolution naturally explains why cells have receptors essential for communication and nutrient uptake, while viruses have, over immense timescales, adapted to hijack those same pathways. No malevolent architect is required—only the simple, iterative logic of variation, selection, and replication.
Yet the ID movement persistently overlooks this simpler, evidence-based account, preferring instead an argument that—if taken seriously—presents their putative creator as either unable to prevent viral parasitism or fully complicit in engineering it. Neither option supports the benevolent, omnipotent designer they hope to defend.
You would think that a planet designed specifically for humans would be safe—one with an abundant supply of clean water to drink and wholesome food to eat.
Sadly, that is far from the case. As recent research has shown, on top of the pathogens and parasites that abound in nature—and which seem almost purpose-built to cause suffering, not just to humans but to virtually every other life form—there now exists yet another threat. Wherever you look in the natural world, every species has one or more parasites adapted to live in or on it, and even parasites themselves often fall prey to their own parasites. To this long list we can now add a group of cyanobacteria capable of turning fresh water into a deadly neurotoxin during warm weather. It is almost as though Earth wasn’t designed by an intelligent, benevolent creator after all.
In science, this is what’s known as a falsified hypothesis. You begin with an idea—in this case, that Earth was designed for humans by an omnibenevolent, omniscient deity—then you consider what predictions would logically follow. One such prediction might be that a planet designed for human well-being would contain no natural hazards or harmful organisms that routinely inflict suffering. Then you examine the evidence. If the facts contradict the prediction, the hypothesis is falsified.
And that is precisely what the existence of harmful organisms does. The evidence directly contradicts the creationist claim of an intelligently designed planet optimally crafted for humans. This does not, in itself, disprove the existence of such a deity; rather, it falsifies the specific claim that the deity is all-loving and all-knowing, or that it intentionally designed Earth and its myriad pathogens and parasites. The alternative is that the god described in the Bible and Qur’an is not as advertised—or does not exist and played no role in designing the world. The pathogens and parasites appear to have arisen from entirely different processes while this supposed designer either looked away or was not involved at all. Such outcomes are not the work of a benevolent creator.
In fact, the deity’s reputation would fare better if it didn’t exist, because then it could not be held responsible.
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.
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.
High-resolution imaging of yellow fever virus reveals structural secrets that could power next-generation vaccines.
UQ scientists uncover secrets of yellow fever - News - The University of Queensland
Scientists at the University of Queensland, Australia, have produced near atomic-level 3D images of the yellow fever virus. These reveal the remarkable complexity that Michael J. Behe and William A. Dembski of the Discovery Institute insist constitutes evidence of intelligent design – a theme almost universally endorsed by creationists and forming the central plank of their advocacy for creationism.
So, the obvious question for intelligent design advocates is this: is the irreducible complexity and complex specificity of the yellow fever virus evidence that it was intelligently designed to kill people? Or, when complex specified information and irreducible complexity do harm to humans, do these supposed ‘evidences’ for the existence of an intelligent designer (i.e. a god) somehow cease to apply, even though they benefit the virus? If so, how can a supposedly scientific definition change its meaning depending on the subjective judgement of what is being specified and how much or how little it benefits humans?
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.
An open-access report in the journal Biocontaminant [PDF] describes a sudden, large increase in the number of infections with the chikungunya virus in southern China, with more than 4,000 cases in Foshan City, Guangdong Province, and over 3,600 cases in Shunde District. The initial spread of the outbreak was observed in this region and quickly escalated into a major public health concern. These cases have not only been documented in Guangzhou, Shenzhen, Yangjiang, and Zhanjiang within Guangdong Province but have also emerged in Macao and Hong Kong.
Let’s pretend for a moment that Intelligent Design Creationism accurately describes reality — that a supernatural entity, indistinguishable from the supposedly omnibenevolent god of the Bible, is continually intervening in living organisms to ensure they conform to a divine plan for the world, particularly for human life.
Let’s also assume that William A. Dembski, Michael J. Behe, and other “CDesign proponentsists” are correct in asserting that the presence of “irreducible complexity” and particularly “complex specified genetic information” is evidence of the work of this putative designer.
How, then, does this announcement about the increase in cases of chikungunya in southern China fit into that worldview?
Chikungunya is a virus transmitted to humans only through the bite of a female Aedes mosquito when she takes a blood meal — in much the same way that Zika, yellow fever, and malaria are transmitted. Once infected, a person develops a sudden-onset fever with painful joints and acts as a reservoir for the virus, enabling the next mosquito to pick it up and continue the chain of infection.
The recent increase in cases is believed to be due to two main factors:
More viruses circulating in the population
More Aedes mosquitoes, with a northward spread driven by global warming
The genetic information in the chikungunya virus genome is clearly enabling the virus population to increase in response to environmental change. If this doesn’t qualify as “complex specified information”, it’s difficult to imagine what would.
Furthermore, the feeding strategy of the Aedes mosquito is a striking example of a finely tuned process: if any part of it fails, the entire transmission cycle collapses. By Michael J. Behe’s own definition, this appears to meet the criteria for “irreducible complexity” and, within that framework, would be touted as conclusive evidence of “intelligent design”.
The inescapable conclusion, then — if we accept the Intelligent Design worldview, in which a divine intelligence is the only possible explanation for such genetic information and irreducibly complex systems — is that both the virus and the mosquito have been intelligently designed to cause human suffering. They seem to have no other purpose than to reproduce themselves and increase infection levels within the population. In other words, according to the logic of ID creationism, this virus was designed with malevolent intent.
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.
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.
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.
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.
Creationists often imagine the human body as the handiwork of a supreme intelligence, carefully engineered for optimal function. Yet the reality revealed by biology is far messier. Our anatomy and physiology are riddled with compromises, inefficiencies, and vulnerabilities that make far more sense as the outcomes of evolutionary processes than as the products of intelligent design. I give multiple examples of the results of these sub-optimal evolutionary compromises in my book, The Body of Evidence: How the Human Body Refutes Intelligent Design. One striking example lies in the complex relationship between mother and foetus during pregnancy, where cooperation and conflict are locked in an evolutionary arms race.
In a paper published in the Proceedings of the National Academy of Sciences (PNAS), Associate Professor Kshitiz of the Department of Biomedical Engineering, University of Connecticut, together with postdoctoral fellows Yasir Suhail and Wenqiang Du, Gunter Wagner of Yale, and Junaid Afzal of the University of California San Francisco (UCSF), have shown how the interface between mother and foetus in the placenta is the product of evolutionary arms races—not the result of intelligent design, as creationists like to imagine.
Firstly, there is the need for the developing foetus to obtain an adequate supply of nutrients, which requires its placental cells to penetrate into the lining of the mother’s uterus.
Secondly, there is the need for the mother to defend herself against invasion by what her body recognises as a ‘foreign’ organism, part of her evolved immune response. Finally, there is the overarching evolutionary imperative of successful reproduction, which entails the birth of healthy offspring.
What the team discovered is that the inevitable evolutionary compromise involves the foetus’s placental cells producing a protein that suppresses the mother’s immune response. This suppression works only because the mother’s cells have evolved to cooperate, allowing the foetal protein to function.
In other words, the mother’s cells have evolved a strategy for permitting the foetus to dampen her immune system—an immune system that itself evolved in the ancestors of placental mammals. This situation can hardly be credited to the act of a supreme intelligence.
Parasite–host relationships are a nightmare for creationists. Their usual escape hatch is “The Fall”, but that undermines the Discovery Institute’s claim that intelligent design is science rather than Bible-literalist dogma in a lab coat. It also raises the obvious question: if parasites only appeared 6,000–10,000 years ago, how did they spread so quickly—and why do we find fossil evidence of parasitism millions of years old?
Creationists cope by dismissing science as a conspiracy, waving away radiometric dating, or pushing myths such as dinosaur fossils being “carbon-dated” [sic] to a few thousand years old. So creationism persists, despite the vast amount of evidence against it, by a combination of wilful ignorance, disinformation and a lack of critical thinking skills.
Now creationists must also ignore new research from Stockholm University, where scientists isolated bacterial DNA from the teeth of woolly and steppe mammoths. They showed these bacteria evolved into the ancestors of those infecting modern elephants—evidence of parasites a million years before “Creation Week”, and of co-evolution continuing right up to today’s elephants, the descendants of those mammoths.
Incidentally, neither mammoths nor modern elephants are mentioned in the Bible, reflecting the parochial ignorance of its authors - a fact often overlooked in depictions of animals boarding Noah's Ark, which usually includes a pair of elephants!
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.
The notion of intelligent design — the current flagship of creationism’s attempt to replace scientific realism with magical superstitions and Bible literalism dressed up as “alternative science” — contains a blatant paradox its advocates must ignore: the very same “logic” used to argue that the God of the Bible created living organisms can just as easily be used to argue that any such designer is a malevolent sadist who deliberately increases suffering in the world while ignoring countless ways to reduce it.
The theological problems this raises are never discussed in polite creationist circles, except for the lazy fallback of blaming everything on “The Fall.” But this move exposes intelligent design for what it really is — Bible-literalist religion in disguise. And that sits awkwardly against over half a century of insistence by the Discovery Institute that ID is not a religious idea, but rather a scientific one that should be taught in American public schools at taxpayer expense — a direct violation of the Establishment Clause and the U.S. Supreme Court’s ruling in Edwards v. Aguillard (1987).
The paradox lies in the fact that the very same so-called evidence — Michael J. Behe’s “irreducible complexity” and William A. Dembski’s “complex specified genetic information” — can be found in the genomes, structures, and processes of parasites and pathogens, making them devastatingly effective at exploiting and destroying their hosts. In fact, Behe himself has, probably without realising it, used precisely such examples. The bacterial flagellum he highlights enables E. coli to move efficiently through our gut, causing sometimes fatal food poisoning. And his example of resistance to anti-malarial drugs in Plasmodium parasites illustrate how evolution equips them to continue killing hundreds of thousands of children every year while condemning millions more to cycles of malarial fever.
Now, new research has highlighted another gruesome example. The bacterium Yersinia pestis — responsible for multiple waves of plague throughout the Middle Ages — has been shown to have evolved into its highly lethal form only in relatively recent human history. Beginning with the “Plague of Justinian” about 1,500 years ago, Y. pestis unleashed pandemics that killed between 30% and 50% of Europe’s population.
An interdisciplinary team at the University of South Florida (USF) and Florida Atlantic University (FAU), with collaborators in India and Australia, has now confirmed genomically that the Justinian plague was indeed caused by Y. pestis, as long assumed. Analysing DNA from plague victims buried in a mass grave at the ancient city of Jerash, Jordan — the epicentre of that pandemic — one group identified the culprit, while another team traced the bacterium’s evolutionary changes that made it one of history’s most notorious killers.
Here’s one of those discoveries in biological science that should have ID creationists jumping up and down yelling, "Told you so!". It’s news that the parasite that causes malaria shows both what they call 'irreducible complexity' and 'complex specified genetic information'. According to Discovery Institute fellows Michael J. Behe and William A. Dembski, that would mean it is intelligently designed and, by implication, designed to do exactly what it does — by the Christian God.
But, for reasons which can only be guessed at — and probably not a million miles from the fact that this conclusion would mean the Christian god is actively designing ways to kill people, particularly children, and especially in Africa — creationists tend to ignore it. After all, that’s the very antithesis of the compassionate, benevolent, loving god of the Bible.
Instead, they quietly sidestep the inconvenient reality that examples of their supposed 'proof of intelligent design' are found just as often in parasites and pathogens as in their hosts. This is precisely what evolutionary biology predicts: a host–parasite relationship invariably leads to an evolutionary arms race, producing sophisticated and complex systems that equip the parasite to survive in the host and to infect new victims.
And, true to form, we now have another such example in the major cause of malaria, Plasmodium falciparum, which killed some 569,000 people in Africa in 2023:
Key Facts:
Globally in 2023, there were an estimated 263 million malaria cases and 597,000 malaria deaths in 83 countries.
The WHO African Region carries a disproportionately high share of the global malaria burden.
In 2023, the WHO African Region was home to 94% of malaria cases (246 million) and 95% (569,000) of malaria deaths (432,400 children under 5).
Children under 5 accounted for about 76% of all malaria deaths in the Region.
It gets tedious repeating this point so often, but so long as creationists keep using what they claim is irreducible complexity and/or complex specified genetic information as evidence for intelligent design, they need to be reminded that the same argument can also be used as evidence of their putative designer’s malevolence.
Creationists, of course, ignore the fact that parasites are no less “designed” than humans and have structures and processes that are “irreducibly complex” and depend on “complex specified information” in order to succeed in their environments. Yet their existence, and how they interact with and even manipulate their hosts, inevitably increases suffering in the world – a theological problem that creationist disinformation organisations such as the Discovery Institute avoid like the plague.
Parasite–host relationships also inevitably involve evolutionary arms races – the antithesis of intelligence if both “sides” are supposedly designed by the same designer.
So, to keep reminding them: if their justification for designating their god as the designer of living systems holds true, then it is also justification for designating the same god as the cause of suffering. Here is another example of a parasite that falls within their definition of an organism “designed” to do what it does and to participate in an arms race with its host in order to do so. This concerns the discovery that the parasitic worm Schistosoma mansoni, which causes schistosomiasis, is able to suppress neurons in the skin to evade detection as it burrows into its victim’s body (usually the leg).
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.
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.
