The ministry of truth is a thing.

Mimetic Behavior in the Scientific Community

David Klinghoffer 

Yesterday I wrote about French philosopher René Girard’s idea of mimesis, and I alluded to having seen such behavior in the scientific community (here). I have been a research scientist for almost thirty years. I personally have seen persecution of scientists who support intelligent design. Some have been tossed out or denied degrees. Others see the threat, so they hide their beliefs. I have seen papers turned down because the reviewer was powerful in his or her field and often suppressed other people’s work. I have seen grants and papers turned down because the individuals writing the paper held certain scientific positions. I have repeatedly seen people lose their jobs because they hold an unpopular view. I have seen misinformation and mockery used against people with unpopular ideas. And I have seen professors pressure graduate students and postdoctoral fellows to be selective in the data they use. All these things are forbidden officially but still happen. The question is, how much do they distort scientific progress?

Just in the last month I saw a report of bad science by a scientist. He was a graduate student who tried to replicate the work of a well-known group. He could not. After careful work, he determined it was because inappropriate controls were used. Because many others were using the same assay and were publishing based on the faulty design, he wrote to the original lab to tell them, and was ignored. He then wrote up his findings and tried to publish them. He was turned down by the journals he submitted to, and rather than submit to a journal that would be ignored, he ended up publishing in a non-reviewed online site called arXiv that is seen by many. He did this just so people might not have the same difficulty he had — it had wasted months of his fellowship and prevented him from performing the work he came to do. 

It is very hard to publish negative results, even if they are important. A student was about to lose his degree because he could not change an enzyme’s activity by repeated mutation. Scientists often believe that enzymes can be modified easily. This is because the failures don’t get published. A friend who was on the student’s committee, and very knowledgeable about enzyme modification, reported that he had to demonstrate to the student’s committee that the thing the student had been assigned to do could not be done. This is another way that scientific resources of time and money are wasted.

Held Hostage Because of Propaganda

Sometimes an entire discipline can be held hostage because of propaganda. A well-known case is that of continental drift. Alfred Wegener first published his hypothesis in the early 1900s that the continents moved over geologic time. He accumulated a great deal of evidence from biology, geology, and fossils showing where the continents were originally linked. He called that super-continent Pangaea. Geologists ignored his hypothesis, despite strong evidence supporting it. It wasn’t until the 1960s that the idea was accepted, based on evidence of the movement of the northern magnetic pole.

Doctors and pharmaceutical companies are another whole category of the role of mimesis and propaganda, and I don’t have space to treat those things fairly. However, I will give one infamous example of doctors behaving badly because of resistance to change. Ignaz Semmelweis was a young doctor who was eagerly following the work of Louis Pasteur. He was aware of Pasteur’s work on the role of microbes in disease. The hospital in Vienna where he worked had a mortality rate in obstetrics of 25-30 percent, which is horrifying. He thought that maybe the childbed fever that was killing women was due to infection carried by the medical students from their dissections to the women in labor. He demanded that all the students wash their hands in a strong antiseptic before seeing women patients. The childbed fever cases dropped dramatically as a result. Some doctors took up his method, but others did not. He had seminars and consultations canceled. He had to leave Vienna and find work elsewhere after his involvement in politics turned everyone in Vienna against him. 

He found work in his native Budapest and published his research. He wrote to doctors all over Europe and beyond, but he was ignored. Women continued to die of childbed fever. Semmelweis’s mental health deteriorated, and he became angry and bitter at the medical profession’s refusal to change. He died in an insane asylum, where his colleagues had taken him two weeks before, from an infected wound inflicted by the guards (who had beaten him), probably from the same bacterium as caused childbed fever. 

Suppression by the State

Sometimes the suppression comes from the government. The restriction on doctors’ freedom to use promising treatments during the recent pandemic was unprecedented. Promising lines of research were shut down. The government of many states issued a mandate: police, firefighters, nurses, transit workers, and many others lost their jobs because for moral reasons they refused to comply with the mandate. Many had to move to other less punitive states. All these things were done to impose the agendas of Anthony Fauci’s National Institute of Allergy and Infectious Diseases, and of the CDC, on vaccine implementation. Whatever your views on the virus or the vaccines, such coercion and suppression is wrong. Uniformity of opinion cannot be imposed. As a result, we have had a significant polarization of society.

Tomorrow I will narrow my focus and discuss the treatment, in this regard, of intelligent design scientists.

File under "well said" CIII

" It is far easier to concentrate power than to concentrate knowledge. That is why so much social engineering backfires and why so many despots have led their countries into disasters."

Thomas Sowell

On the death of science?

 

Yet another miracle molecule?

 

On the Darwin of the gaps?

 An Argument from Ignorance?

William Dembski

Editor’s note: We are delighted to welcome the new and greatly expanded second edition of The design inference, by William Dembski and Winston Ewert. The following is excerpted from the Introduction.

Tacitly in the first edition of The Design Inference and explicitly in its sequel, No Free Lunch, I argued that natural selection and random variation could not create the sort of complexity we see in living things. My approach in applying the design inference to biology was to piggyback on the work of design biologists such as Douglas Axe and Michael Behe. They had identified certain subcellular systems (e.g., bacterial flagella and beta-lactamase enzymes) that proved highly resistant to Darwinian explanations. 

Our joint task was to put plausible numbers to these systems so that even factoring in Darwinian natural selection, the probability of these systems arising was exceedingly small. Note that the specification of these systems, as in their exhibiting the right sort of pattern for a design inference, was never in question. The issue was always whether the probabilities were small enough. In using specified improbability to draw a design inference for biology, I therefore needed to argue that the probabilities for Darwinian processes producing certain biological systems, such as those identified by Axe and Behe, were indeed small. 

Misguided and Irrelevant

As far as Darwinists were concerned, however, all attempts to show such biological systems to be vastly improbable were misguided and irrelevant. Any design inferences meant to defeat Darwinian evolution were, according to them, arguments from ignorance. For them, unidentified Darwinian pathways could never be decisively ruled out, so their mere possibility invalidated any design inference applied to biological evolution. In short, no calculated improbability could ever convince the Darwinian critics that the probabilities were actually small. 

It didn’t matter that Darwinists were ignorant of any detailed evidence for such Darwinian pathways, and thus had no counter-probabilities to offer. It was enough for them merely to gesture at the possibility of such pathways, as though raising a possibility could itself constitute evidence for an argument from improbability. To ID proponents critical of Darwin’s theory, the argument-from-ignorance objection seemed to apply more aptly to the Darwinists themselves for positing unsubstantiated Darwinian pathways that offered no nuts and bolts, no nitty-gritty, just hand-waving.

No matter. For Darwinists to refute ID, they merely needed to postulate unidentified, and perhaps forever unidentifiable, indirect Darwinian pathways in which structure and function coevolved and led to the complex biological features in question. Brown University biologist Kenneth Miller led the way. Michael Behe had defined a system (biological or otherwise) to be irreducibly complex if its function was lost by removing key parts. He argued that such systems resisted Darwinian explanations. Miller countered that Behe’s concept of irreducible complexity was ill-conceived because removing parts from, or otherwise simplifying, a biological system could always yield a system with a different function. To convinced Darwinists like Miller, design in biology was therefore a nonstarter. Darwinian pathways to all complex biological systems had to exist, and any inability to find them simply reflected the imperfection of our biological knowledge, not any imperfection in Darwin’s theory. 

Dawkins’s “Laziness Challenge” 

Richard Dawkins, better than anyone, has publicly championed the dogma that Darwinian pathways can and must always exist for any biological system. In a 1990s television interview he memorably took Behe to task for claiming that irreducibly complex biochemical machines, of the sort Behe popularized in Darwin’s Black Box, were beyond the reach of Darwinian processes. Dawkins charged Behe with being “lazy” (yes, he used that very word) for seeing in the irreducible complexity of these machines a reason to conclude design, and thus to rule out any further effort to discover how Darwinian processes could have formed, say, a bacterial flagellum. That is, instead of concluding that these systems were designed by a real intelligence, Behe should get back into the lab and redouble his efforts to discover how Darwinian evolution could have produced them apart from design.

The reaction of the ID community to Dawkins’s “laziness challenge” was that he might just as well have recommended to physicists that they keep trying to construct a perpetual motion machine. Yet why did one task seem futile (constructing a perpetual motion machine) but not the other (discovering Darwinian pathways to irreducibly complex biochemical machines)? Physicists had the second law of thermodynamics to rule out the charge of laziness. That’s why Dawkins would never have said to a physicist, “You’re just being lazy for giving up on inventing a machine that can run itself forever.” 

Even so, Dawkins’s “laziness challenge” was and remains misguided because Behe’s skepticism is based not on ignorance but on careful study of the obstacles that Darwinian evolution must overcome and its consistent failure to do so. To seal the deal, however, the ID research community still needed something like the second law for biology. We found it in the law of conservation of information. This law logically completes the design inference. We’ll address this law in the epilogue.

Time to take the hint re:quantum gravity?

 

The sword Rome lived(and died) by?

 

On Father Charles Coughlin.

 

The Cambrian explosion was nuclear?

 Fossil Friday: Protists Add to the Cambrian Explosion

Gunter Bechly

When talking about the Cambrian Explosion, the focus is usually on the abrupt appearance of bilaterian animal phyla with their distinct body plans, which has been called a Big Bang of life. However, the Cambrian Explosion is not restricted to these animals. As I have shown in previous articles, non-bilaterian animals like true sponges and jellyfish also first appeared in the Lower Cambrian (Bechly 2020, 2023). Today we will have a look at a largely ignored part of the Cambrian Explosion. That is the abrupt appearance of several major groups of protists (Lipps 1993, Wikipedia 2023).

Radiolarians represent an important group of marine zooplankton with beautiful siliceous mineral skeletons that were famously featured in wonderful drawings by the German pioneer Darwinist Ernst Haeckel. Their oldest fossil record is from the Earliest Cambrian (Ediacaran-Cambrian boundary) to Middle Cambrian of China (Braun et al. 2007, Maletz 2017, Chang et al. 2018, Zhang & Feng 2019, Zhang et al. 2021). Thus, they appear right together with the Cambrian Explosion of animal phyla.

Tentative Determinations

oraminiferans are amoeboid marine protists, which mostly live in the seafloor sediment and have a calcium carbonate skeleton. Their oldest uncontroversial fossil record is again from the Early Cambrian (e.g., Culver 1991, McIlroy et al. 2001, Streng et al. 2005). Pawlowski et al. (2003) therefore concluded that “Fossil Foraminifera appear in the Early Cambrian, at about the same time as the first skeletonized metazoans.” More recent evidence for late Ediacaran foraminiferans suggests that this group may have originated already with the Avalon Explosion rather than the Cambrian Explosion (Gaucher & Sprechermann 1999, Hua et al. 2010, Pazio 2012, Chai et al. 2021), but even Hua et al. (2010) admitted that “the oldest unambiguous foraminifers are from Early Cambrian Atdabanian Stage strata.” Possible testate amoebae and possible foraminiferans (Rhizaria) have even been reported from 716-635 million-year-old carbonate rocks in Namibia and Mongolia, which date to a time right after the Sturtian glaciation of the Cryogenian “Snowball Earth” (Bosak et al. 2011, 2012, Parry 2011). However, these determinations are only tentative and far from established. At least the tintinnid determinations in the same work have been strongly disputed by Lipps et al. (2012) (see below).

Dinoflagellates are another important group of planktonic protists. Even though the oldest fossil dinoflagellates are known from middle Triassic sediments, there is indirect evidence from geochemical markers that these protists also first appeared in the Lower Cambrian period (Moldowan & Talyzina 1998).

“Darwin’s Dilemma Still Holds”

Other groups of protists appeared at other periods in Earth history, but they also originated abruptly without gradual transition from assumed precursors. For example, diatoms suddenly appear in the fossil record of the Early Jurassic about 182 million years ago (Kooistra & Medlin 1996, Bryłka et al. 2023). Coccolithophores (Hapotophyta), which form the chalk of the famous White Cliffs of Dover, appear at the Norian-Rhaetian boundary about 208.5 million years ago (Gardin et al. 2012). Uncontroversial tintinnids (Ciliata) are first recorded from Upper Triassic to Lower Cretaceous sediments, while several alleged Proterozoic records about 1.600-580 million years ago as well as Paleozoic records are all very doubtful and disputed (Lipps et al. 2012). Lipps et al. (2012) commented that “no solid evidence of Proterozoic tintinnids or other ciliates comes from the Precambrian rock record. Darwin’s dilemma of the lack of fossils for this ancient age (Schopf 2001; Knoll 2004) therefore still holds for at least the ciliates. If there are tintinnid fossils from this ancient time, they have yet to be discovered.”

Not even the tiniest and most abundant organisms seem to confirm the gradualist predictions of Darwinian evolution. Whenever empirical data from the actual fossil record are used to test this crucial part of the theory, it simply fails. Since gradualism is strongly refuted by the evidence, the theory must be false, because even Richard Dawkins, arguably the most ardent modern popularizer of Darwinism, clearly stated in his bestselling book The Greatest Show on Earth (Dawkins 2009) that “evolution not only is a gradual process as a matter of fact; it has to be gradual if it is to do any explanatory work.” Clinging to a refuted paradigm, in spite of the accumulated conflicting evidence, is not science but rather irrational dogmatic belief.

The great war: the end of a world?

 

An interlude XI

 The Lord JEHOVAH is the living embodiment of hope itself.

The war of the Titans rages on

 

The cold war 2.0?

 

The resistance is brought to you by...

 

The argument from common sense?

 Bill Dembski Reflects on the Origins of a Classic

Andrew McDiarmid

Hailed as “sparklingly original” and an “important contribution,” mathematician William Dembski’s 1998 book The Design Inference gave the modern design hypothesis a firm empirical footing and quickly inspired demonization and dismissal from disgruntled Darwinists. Twenty-five years later, Dembski’s arguments stand firm, and a second edition with fresh analysis and insight is now available to a new generation of truth seekers. On a new episode of ID the Future, physicist Brian Miller invites Dr. Dembski to take us back to the 1980s to tell us the story of how The Design Inference came to life. 

What is the nature of randomness? It was a question very much in vogue in academic circles in the late Eighties. Dembski was just finishing a dissertation in mathematics and was intrigued by the relationship between order and disorder, randomness and design. “Randomness is fundamentally a question of design,” he wrote in his 1991 essay “Randomness by Design”. Dembski continued to develop these ideas, and not even a second PhD in philosophy could pull him away from the question of design. Here, Dembski tells the story of how his ideas eventually became a book and how the book got published by one of the most respected publishing houses in academia. 

Dembski also discusses the influence on his work of another man who was weighing up the design hypothesis in the 1980s: evolutionary biologist Richard Dawkins. His 1986 book, The Blind Watchmaker, argued against Paley’s design argument in favor of an evolutionary story of life on earth. The book inspired Dembski to pursue design. “What I was doing in The Design Inference was in dialectical conversation with Darwin and Dawkins,” recalls Dembski. “Whereas Darwin and Dawkins needed that every aspect of biology be un-designed, it was enough for me to say, is there a method for reliably detecting design, and if that method is applied to some biological systems, could it reliably tell us that we’re dealing with an effective intelligence?”

Download the podcast or listen to it here. 

Yet more common ground?

 

Common ground?

 

The antiRome?

 

Chance and necessity can be counted out?

 Dembski Won the Argument with His Critics; New Edition of The Design Inference Shows How

Brian Miller

One of the foundational books undergirding the intelligent design research program is The Design Inference: Eliminating Chance through Small Probabilities, by mathematician and philosopher William Dembski. He developed a rigorous methodology for design detection. His work was initially praised by esteemed scholars. Then, he applied his design-detection apparatus to biology and demonstrated that life displays clear evidence for design. After making this connection, he faced enormous opposition for daring to challenge the sacred dogma of secular society that life is an unintended product of the blind forces of nature. 

Many of the attacks were little more than knee-jerk reactions, but some raised legitimate concerns and asked relevant questions. In the decades that followed, Dembski responded to critics and refined his model. He also collaborated with computer scientists Robert J. Marks and Winston Ewert, along with other scholars, to expand upon his initial ideas and further apply them to biology (here, here, here).

Most recently, Dembski partnered with Ewert to write a second, greatly expanded edition of The Design Inference, which is being released today. The new edition represents the culmination of decades of thought and research. It presents a rigorous and reliable procedure for detecting design in any context. The esteemed Princeton University mathematician Sergiu Klainerman welcomed the book as follows:

Well argued and eminently readable… I don’t see how any open-minded scientist can ignore this important book.

Here I will present a primer on design detection that will aid readers in appreciating the genius behind Dembski and Ewert’s accomplishment. 

The Logic Behind Design Detection

The fundamental goal of any approach to design detection is identifying patterns, events, or artifacts that (1) are extremely unlikely to have occurred through chance and natural processes and (2) show signs that they were deliberate acts of a mind. The challenge is rigorously meeting both criteria. Nearly everyone recognizes that the criteria have been properly met in certain contexts. Forensic experts can often clearly distinguish between a death resulting from natural causes and homicide. Archaeologists readily distinguish between naturally occurring rocks and an arrowhead. And tourists easily differentiate between patterns on mountains resulting from wind and erosion and the faces of the Presidents on Mount Rushmore. 

In every context, the first criterion entails identifying, at least qualitatively, the probability for the occurrence of some event or outcome solely due to chance and natural processes. For instance, the probability of any number between 1 and 6 appearing on a well-constructed six-sided die is 1 in 6. The outcome is purely the result of chance. In contrast, the probability of rolling a 6 on a loaded die could be close to 100 percent. The outcome is a direct result of gravity. 

The outcome could also be the product of chance and natural processes. The structure of a snowflake displays a hexagonal pattern due to the physical properties of water molecules. It also displays its own unique features due to chance molecular interactions. Determining the probability of undesigned outcomes must take into consideration both factors. 

The second criterion entails a mind assigning significance or value to some outcomes independently of any law-like process. As a thought experiment, imagine Bill Gates deciding on a whim to give one billion dollars to five specific people scattered throughout the world. In addition, the day after the money was dispersed, you were one of six people invited to a dinner party. If you discovered that four of the five recipients of Gate’s generosity were also invited, you would know that the invitees were not chosen randomly. You would also know that the invitations were not primarily based on any factors independent of the invitees’ newfound wealth, such as their height or weight or nationality. The guests were deliberately chosen for some premeditated purpose, such as raising money for a charity or a political campaign. 

The key elements for this conclusion are (1) the number of combinations of six people chosen out of the entire human population being extremely high and (2) and the number of combinations of six people possessing such wealth being much lower. The disparity between the probability of choosing randomly a specific set of six people and the probability of randomly choosing a set out of all sets of six people with at least that much wealth is what points to design.  

Application to Biology

The argument for design in biology follows the same logic. The number of configurations of atoms resulting from chance and natural laws is unimaginably large. By comparison, the number of configurations is vastly smaller that correspond to life or anything to which a mind would attribute the same significance as life, or nearly so, such as a computer with an advanced AI or an automated space shuttle capable of colonizing mars.  

Stated differently, the probability of a configuration of atoms corresponding to life occurring through chance and natural processes is unimaginably small. By comparison, the probability is vastly larger of choosing life out of a pool of entities that are as significant, or nearly as significant, as life.   

Understanding the Design Debate

The design debate centers on one of the two criteria. Design proponents have described the exceedingly low probability of some biological system or structure emerging, such as a random sequence of amino acids folding into a functional protein. They also point out the significance of biological components, such as folded proteins, in the context of life. 

Some critics challenge the first criterion by arguing either that biological structures are not as rare as design proponents believe, or that natural processes such as self-organization and natural selection dramatically improve the odds of their forming. Others challenge the second criterion by arguing that a specific structure might be extremely unlikely to occur by chance and natural processes, but biological structures are not as special as design proponents believe. Critics assert that life could have used many other structures to accomplish the same tasks, so the probability of finding anything that serves a particular purpose is tractable. 

The second edition of The Design Inference lays out the theoretical framework and practical methodology for addressing all these objections. In addition, advances in biology over the past few decades allow the methodology to be rigorously applied. Such analyses demonstrate evidence for design that is now so clear and rigorous that, for intellectually honest and sincere seekers of the truth, denying it is no longer feasible.   

The multicultural third reich?

 

On the pursuit of happiness

 

James Tour vs. The Sphinx?

 

On giving up Darwin.

 Wisdom Wednesday: Yale Polymath David Gelernter’s Farewell to Darwinism

Emily Sandico

Afew years ago, the brilliant Yale University polymath David Gelernter wrote an essay entitled “Giving Up Darwin — A fond farewell to a brilliant and beautiful theory,” in which he made a stunning confession: “Stephen Meyer’s thoughtful and meticulous 𝘋𝘢𝘳𝘸𝘪𝘯’𝘴 𝘋𝘰𝘶𝘣𝘵 convinced me that Darwin has failed.”

Is Gelernter a creationist? No. Is he a proponent of intelligent design? No. “There’s no reason,” Gelernter wrote in the Claremont Review of Books, “to doubt that Darwin successfully explained the small adjustments by which an organism adapts to local circumstances: changes to fur density or wing style or beak shape. Yet there are many reasons to doubt whether he can answer the hard questions and explain the big picture — not the fine-tuning of existing species but the emergence of new ones. The origin of species is exactly what Darwin cannot explain.”

Gelernter summarizes: “𝘋𝘢𝘳𝘸𝘪𝘯’𝘴 𝘋𝘰𝘶𝘣𝘵 is one of the most important books in a generation. Few open-minded people will finish it with their faith in Darwin intact.”

That might sound like a scary thought. Some may not be willing to read Meyer’s book and risk losing their faith in the science we’ve been told is all settled. But don’t you wonder why a brilliant guy like Professor Gelernter would give up Darwin? Read his true confession here

One atheist says the quiet part out loud?

 

Micah Chapter 3 New World Translation (2013 edition)

 3.1 I said: “Hear, please, you heads of Jacob

And you commanders of the house of Israel.+

Should you not know what is just?

 2 But you hate what is good+ and love what is bad;+

You tear off the skin from my people and the flesh from their bones.+

 3 You also eat the flesh of my people+

And strip off their skin,

Smashing their bones, crushing them to pieces,+

Like what is cooked in a pot,* like meat in a cooking pot.

 4 At that time they will call to JEHOVAH for help,

But he will not answer them.

He will hide his face from them at that time,+

Because of their wicked deeds.+

 5 This is what JEHOVAH says against the prophets who are leading my people astray,+

Who proclaim ‘Peace!’+ while they bite* with their teeth+

But who declare* war against him who puts nothing into their mouths:

 6 ‘You will have night;+ there will be no vision;+

There will only be darkness for you, no divination.

The sun will set on the prophets,

And the day will turn dark for them.+

 7 The visionaries will be put to shame,+

And the diviners will be disappointed.

All of them will have to cover over the mustache,*

For there is no answer from God.’”

 8 As for me, I am filled with power by the spirit of JEHOVAH,

And with justice and might,

To tell to Jacob his revolt and to Israel his sin.

 9 Hear this, please, you heads of the house of Jacob

And you commanders of the house of Israel,+

Who detest justice and who make crooked all that is straight,+

10 Who build Zion with bloodshed and Jerusalem with unrighteousness.+

11 Her leaders* judge for a bribe,+

Her priests instruct for a price,+

And her prophets practice divination for money.*+

And yet they lean on JEHOVAH,* saying:

“Is not JEHOVAH with us?+

No calamity will come upon us.”+

12 So because of you,

Zion will be plowed up as a field,

Jerusalem will become heaps of ruins,+

And the mountain of the House* will become like high places in a forest.*+

Not to be outdone we have Catholicism's civil war.

 

A functional protein ab initio would necessitate a miracle?

 To Create Functional Proteins, Evolution Would Need a Miracle

Brian Miller

Theologian Rope Kojonen claims that God designed the laws of nature, which then gave rise to “fine-tuned” preconditions and smooth fitness landscapes. He says, among other things, that these conditions allow proteins to evolve by natural processes. Is he right?

At Evolution News, philosopher Stephen Dilley has already written two articles in a series (here) introducing an evaluation of Kojonen’s argument. Dilley summarized his contribution to a review article he wrote with Casey Luskin, Emily Reeves, and myself titled “On the Relationship Between Design and Evolution,” in the peer-reviewed journal Religions. In the article we critique Kojonen’s book The Compatibility of Evolution and Design, which argues that evolutionary theory can be reconciled with the belief that life demonstrates evidence of design. Dilley commended the book for the sophistication and comprehensiveness of its philosophical arguments. 

However, Dilley noted that the viability of Kojonen’s thesis depends on the scientific details. Even though the proposal is primarily a philosophical analysis, its strength or weakness hinges largely upon empirical evidence. As we state in our article:

It is true that KEBDA [Kojonen’s evolution-friendly biological design argument] is a philosophical argument. And, of course, the conceptual and epistemological elements of the argument are important. But some philosophical arguments also depend in part upon scientific evidence. In this case, much depends on whether there is a good case for fine-tuned preconditions and suitable fitness landscapes (as Kojonen envisions them). Indeed, Kojonen situates design precisely in those fine-tuned preconditions which yield smooth fitness landscapes that allow evolution to succeed. His case for marrying design with evolution therefore depends on the existence of this fine-tuning. So, it is crucial to assess whether this fine-tuning is real. And this question can be assessed scientifically: are fitness landscapes smooth? Are there open pathways between functional proteins, for example? Or are there impassible barriers between such proteins?

Thus, to assess Kojonen’s conception of design (and its compatibility with evolution) involves careful empirical analysis of “preconditions” and fitness landscapes. We examine Kojonen’s account of these phenomena, especially his claim that preconditions and landscapes are set up to allow proteins to evolve.

Kojonen’s Argument

We summarize Kojonen’s argument as follows:

To his credit, Kojonen acknowledges that the weight of empirical evidence affirms that functional proteins are often exceptionally rare — an exceedingly small percentage of amino acid sequences in sequence space fold into complex three-dimensional structures that can perform biological tasks (Kojonen 2021, pp. 119–20). (Sequence space is the multidimensional map of all possible amino acid sequences.) Finding a viable protein sequence is akin to finding a needle in a haystack. Yet Kojonen then argues that protein rarity is not a barrier for evolution because functional proteins are sufficiently close to each other in sequence space such that one protein could plausibly transform into another. He argues that, because of the fine-tuning of natural laws, there are otherwise unexpected functional pathways through sequence space to link up functional amino acid sequences such that one protein sequence could traverse to another through sequence-space via evolutionary mechanisms. Proteins might be rare, but they are not isolated. There is a proverbial cluster of needles lumped together in the haystack: when one is found, another is close at hand.

Andreas Wagner’s Contribution

Kojonen justifies this assertion by citing the research of Andreas Wagner and his team. Wagner claims to have demonstrated that every protein can evolve into another protein through a limited number of mutations. In addition, every protein in biology is interconnected through a continuous series of traversable steps.

We respond as follows:

Yet Wagner’s research is significantly limited. In particular, Wagner never directly studied the feasibility of one protein evolving into another. Instead, he compared the metabolic pathways of different organisms and identified enzymes (a type of protein) that are present in multiple pathways, and he also identified enzymes that are missing (Rodrigues and Wagner 2009). In addition, Wagner studied how mutations can change the regulatory regions of proteins to alter when (and to what extent) proteins are expressed (Aguilar-Rodríguez et al. 2017, 2018). Wagner argued that such changes could direct proteins to enter or leave metabolic pathways. But he did not study the more fundamental question of the plausibility (or implausibility) of the evolutionary origin of proteins in the first place. 

To be sure, Wagner has performed notable research that bears some (limited) relevance on protein evolvability. For example, in addition to the studies above, he surveyed numerous proteins’ relative locations in sequence space (Ferrada and Wagner 2010). He identified which proteins with the same structures perform different functions and which functions could be performed by proteins with different structures. He also tallied the functions performed by proteins in pairs of local regions in sequence space, noting these regions’ specific sizes and distances from each other. In addition, he mapped the percentage of functions performed in paired local regions as a function of the regions’ size and separation (i.e., amino acid differences). Based on this analysis, Wagner extrapolated the conclusion that mutations could change a protein (with a particular function) into another protein (with a different function) in the same region. In Wagner’s view, this allowed proteins to evolve in organic history. Yet again, he did not actually empirically demonstrate that such transformations were ever possible. Instead, he simply mapped interesting correlations between protein sequences, functions, and structures.

In fact, Wagner’s own research suggests that protein evolution is exceedingly difficult. He acknowledged, for example, that many proteins correspond to extremely rare sequences. Moreover, he identified highly separated regions of sequence space where the proteins in the different regions possessed different structures and performed different functions. This observation suggests that many proteins are not simply rare but also isolated — they are strikingly different from all other proteins in distant regions of sequence space. Wagner did not demonstrate that a series of short steps (or smooth evolutionary pathways) connect these distinct types of proteins. Even if mutations might transform some proteins into other close-at-hand proteins — which Wagner did not show — his own data strongly indicate impassable chasms between many other types of proteins. To borrow Wagner’s metaphor: many proteins appear to be separated from each other like stars in the universe.

The State of the Field

We then describe how research by leading experts in the field of protein evolution reinforces the view that distinct proteins are so isolated from each other that one could never evolve into another. From an article referencing the late Dan Tawfik:

“Once you have identified an enzyme that has some weak, promiscuous activity for your target reaction, it’s fairly clear that, if you have mutations at random, you can select and improve this activity by several orders of magnitude”, says Dan Tawfik at the Weizmann Institute in Israel. “What we lack is a hypothesis for the earlier stages, where you don’t have this spectrum of enzymatic activities, active sites, and folds from which selection can identify starting points. Evolution has this catch-22: Nothing evolves unless it already exists.” (Mukhopadhyay 2013)

We also reference a lecture by Tawfik where he states that proteins can only be modified to the point where their structure does not significantly change. He describes how different protein structures appear completely isolated from each other, and biologists have zero knowledge of how they emerged. The vast preponderance of the evidence indicates that novel complex proteins could never have evolved through an undirected process. This conclusion completely overturns Kojonen’s thesis about the compatibility of evolution and design. 

So, Kojonen’s model of design is empirically testable: are preconditions fine-tuned and fitness landscapes smooth such that proteins can readily evolve? Or does the empirical data indicate that fitness landscapes are not smooth and that distinct proteins are isolated from each other? As we show in our article, there is good evidence for the latter view. If we are correct, then Kojonen’s account of design is mistaken. This severely damages his attempt to harmonize “design” with “evolution.”

How about we just stick to the plain reading of the text?

 1John ch.4:12NIV"No one has ever seen God; but if we love one another, God lives in us and his love is made complete in us."

John Ch.6:46NIV"No one has seen the Father except the one who is from God; only he has seen the Father."

Exodus Ch.33:20NIV"But,” he said, “you cannot see my face, for no one may see me and live.”"

Colossians Ch.1:15NIV"The Son is the image of the INVISIBLE God(Not merely father), the firstborn over all creation. "

An interlude X

 

The epigenome:The kingmaker?

 Epigenetics: Performing the Genome

David Coppedge

Epigenetics has been rising in esteem contemporaneously with the decline of the Central Dogma of genetics (that DNA is the master control in the cell). Just as the pianist gets the applause and not the piano, the epigenome is now being considered the artist behind the instrument. It’s not that the genome has lost any of its aura, but it cannot do anything without a performer.

Frank Gannon wrote a most interesting essay in the journal EMBO Reports, titled, “The piano and the pianist.” Gannon, an Australian who was the former director of a medical research institute in Brisbane, was not writing about the performing arts. He wanted to introduce a new analogy to overcome “the ubiquitous ‘DNA is the blueprint of life’ interpretation of biology,” repeated by some who downplay the elements in the cell that give an organism its dynamic responsiveness to the environment.

The image of inevitability and of a rigorous design plan, and the notion of the dominating importance of DNA are misleading messages, however, that do not represent reality.

I suggest that the piano and the pianist is a better analogy as to how our lives and our health unfold.

Gannon denies that our health is genetically determined: i.e., if we have a certain genetic defect, we will get the disease. That is not entirely true, he says as he details the analogy.

The function of each piano is defined by its 88 keys, but different pianos have different tones and timbres.Some pianos have defects that distort some notes. These could be at the little-used periphery of the keyboard or they could be more central. If the middle C was out of tune, it could be very jarring for the listener in a solo lyrical piece but it may be more subtle if it is part of complex chords. More importantly, though, it is the way the pianist plays the piano that will define the outcome as a pleasure or as discordant. Each pianist selects the tempo and the mood and may even compensate for a dud note.

How Does the Analogy Relate to Biology? 

Writes Gannon, “If the keyboard is the genetic code, the piano is the epigenetic context that interprets the blueprint of life and varies the outcome.” He discusses specific ways cells “perform” the genome. DNA is wrapped in chromatin made of histone proteins that can be tagged with markers like methyl or acetyl groups. Parts can be phosphorylated or tagged with ubiquitin proteins. A host of accessory proteins switch genes on and off, responding to cues from the environment. Indeed, “a growing number of regulatory RNAs create a bewildering combination of possibilities that define the performance of the cell and ultimately of the individual.” 

No analogy is perfect, and one must understand that most of these regulatory agents are coded in DNA themselves. In music, we don’t see pianists emerging from the keys of a piano. Still, the “defining role of epigenetics” deserves more attention, Gannon argues. We are not slaves of our genes. Lifestyle choices, such as diet, exercise, and mental habits, can improve the quality of the performances played on our genetic instruments. 

Most of Gannon’s one-page essay deals with epigenetic targets for treating genetic diseases. While surprised at the lack of attention given to epigenetics, he understands the difficulties involved. “Compared to the neat linearity of the genome,” he notes, “epigenetic regulation is a mess that is hard to reduce into a defined sequence.” Targeting the correct epigenetic regulator is correspondingly difficult. If the dud note is middle C, a carelessly targeted drug might inadvertently put a different note out of tune.

In biology, additional factors other than the genome and epigenome come into play, such as the microbiome — all those microbial and viral partners in and on the organism. These, in turn, respond to the habits of the organism in its habitat. Gannon ends with a cadenza and coda:

As we analyze the beneficial effects of a healthy microbiome and lifestyle, we are looking for answers to why these work. What does the microbiome in the gut provide the organism with to improve health? What are the molecular consequences of exercise such that the total organism and not just the muscles work better? How does diet modify the health of individuals? How does excess fat impact functions in other tissues? More results and more insights will inevitably highlight the crucial role of the epigenome as the connection between the environment and the genome. The piano remains important, but the pianist will finally move into the limelight.

Other Epigenetic News

Researchers at the John Innes Centre explored “intricate mechanisms of epigenetic silencing” (the suppression of gene activity) that impact vernalization in plants. Researchers identified several accessory proteins that trigger epigenetic switches when Arabidopsis plants feel the cold snap that indicates the time for flowering is coming. The switch turns off the floral repressor gene FLC, allowing the genes for bud formation to activate.

At the University of Georgia, researchers investigated the ticking of epigenetic clocks that are biomarkers for aging. “While these clocks work accurately from birth until death,” the press release says, “they are set back to zero in each new generation.” The team confirmed that such epigenetic clocks work in plants, including Arabidopsis and poplar trees, and that these clocks “keep ticking accurately over many generations.”

Remember “Intelligent Design at High Altitudes”? Another paper in Current Biology examined genetic changes in 2,252 Tibetan women who live at high elevations. The authors claim the gene modifications show evidence of positive natural selection. It appears though, that instead of finding new adaptive genes, they found existing genes that were downregulated — i.e., epigenetic responses to the low oxygen atmosphere rather than naturally selected mutations. 

Putting Life Back into Performance

Gannon’s piano analogy suggests opportunities for design theorists. If the genome is like the piano keyboard, it cannot be that the epigenome is as static and determined as the sheet music on the stand. There is dynamic responsiveness in the performance. The pianist (if by that we mean the organism) might have to play the same piece as another individual within its species, but can alter the tempo and quality of the performance depending on the occasion: the audience, the venue, the number of broken keys, the amount of stress on the player, the player’s age and experience, and other factors. 

Every zebra, zebra finch, or zebrafish may resemble its conspecifics, but no two individuals will follow the exact same path. A plains zebra in South Africa may face fewer predators than one in the Serengeti but will endure wider swings in seasonal temperatures. Many individual organisms, such as snowshoe hares, change their appearance from summer to winter. Deciduous trees cycling through seasonal changes offer another example. Epigenetic responses in different tissues of the body will also behave according to local conditions despite having the same genome. The epigenome tunes each performance using its built-in mechanisms to detect the conditions in the environment. It switches on internal controls that adapt cell processes appropriately to the conditions they are sensing. Design theorists are keen on elucidating the mechanisms by which organisms track the environment and actively switch on applicable responses.

Beyond Histones

If epigenetics plays the genome, who plays the epigenome? What tells the epigenome to add a methyl group to a particular histone on a particular gene? Is epigenetics just another layer of information written in matter, cycling mindlessly, amenable to philosophical naturalism? What breathes fire into a piano piece, putting the soul into a rendition by Van Cliburn or Vladimir Horowitz? Even a paper roll with dots on it, running through a mechanical player piano, had to be originally performed by a live pianist. The same is true with digital recording: the soul of the performance is not in the bumps on a CD or the bits in an MP3 file.

If scientists were ever to put together all the parts of a cell, I’m not convinced it would come alive. Information by itself is sterile. All the codes and epi-codes for all the parts could be present, but they would exist as mere fancy arrangements of dumb matter without an additional spark. A spark-discharge apparatus wouldn’t do it. Dr. Frankenstein’s Tesla-coil bolts wouldn’t make his monster sit up except in the movies. To be or not to be is a metaphysical question, but the animating factor that switches on life itself — whether in microbe or man — appears to be an endowment from the ultimate Mind

Why 536c.e would scoff at 2023c.e's idea of a climate catastrophe.

 

On why the physical universe cannot be its own God

 

The speed of light demystified(?)

 

Why the coming apocalypse is the best news

 Genesis Ch.8:21NIV"The LORD smelled the pleasing aroma and said in his heart: “NEVER again will I curse the ground because of humans, even though a every inclination of the human heart is evil from childhood. And NEVER again will I destroy all living creatures, as I have done."

The Lord JEHOVAH Will never destroy (nor will he permit anyone to destroy) his earthly Creation. Especially the human race. JEHOVAH'S Messiah the Lord Jesus Christ will return to usher in a glorious millennium in which the promise of peace on earth announced by Holy Angels at his birth will be fulfilled.

Luke Ch.2:12-14NIV"“Today in the town of David a Savior has been born to you; he is the Messiah, the Lord. 12This will be a sign to you: You will find a baby wrapped in cloths and lying in a manger.”

13Suddenly a great company of the heavenly host appeared with the angel, praising God and saying,Glory to God in the highest heaven,

and on earth PEACE to those on whom his favor rests.”"

This peace is not the enforced quiet that passes for peace in the less unfortunate parts of our global civilisation. JEHOVAH Has higher standards than that.

Isaiah Ch.55:8,9NIV"“For my thoughts are not your thoughts,

neither are your ways my ways,”

declares the LORD.

9“As the heavens are higher than the earth,

so are my ways higher than your ways

and my thoughts than your thoughts."

The coming kingdom of JEHOVAH is not going to be a police state  characterized by a peace maintained by the threat of armed violence.

The examiner of hearts himself will be the guarantor of humanity's enduring peace and security.

Psalms Ch.37:7-11ASV"Rest in JEHOVAH, and wait patiently for him: Fret not thyself because of him who prospereth in his way, Because of the man who bringeth wicked devices to pass.

8Cease from anger, and forsake wrath: Fret not thyself, it tendeth only to evil-doing.

9For evil-doers shall be cut off; But those that wait for JEHOVAH they shall inherit the land.

10For yet a little while, and the wicked shall not be: Yea, thou shalt diligently consider his place, and he shall not be.

11But the meek shall inherit the land, And shall delight themselves in the abundance of peace."

Politics cannot bring about this promised peace. The only "peace" the politicians and political activists can give us is the temporary quiet while they restock their arms and ammunition. 

So even if our anger is justified JEHOVAH urges us to patiently wait on him rather than look to the politicians of the present age and their enablers. How many "revolutions" have proved to be nothing more than an exchanging of one tyrant for another. Indeed the exchanging of one tyrant for several tyrants.

But the faith we place in JEHOVAH is not mere credulity . It is indeed no different from the faith we put in any other trusted companion or counselor. We become acquainted with the character and expertise of said person and our confidence is a fruit of that acquaintance. So too with our Lord JEHOVAH We can let others make up our mind for us or we can choose to investigate for ourselves.

Acts ch.17:26,27ASV"and he made of one every nation of men to dwell on all the face of the earth, having determined their appointed seasons, and the bounds of their habitation; 27that they should seek God, if haply they might feel after him and find him, though he is not far from each one of us:"

Try our free bible course

Why no amount of Chance and necessity is sufficient.

 Dembski and Tour: Why Chance Doesn’t Have a Chance

Andrew McDiarmid

Are life and the universe products of chance, necessity, or design? In anticipation of a new updated second edition of his seminal book The Design Inference, out this coming week, ID the Future features Rice University synthetic organic chemist James Tour and intelligent design pioneer William Dembski concluding a discussion about the origin and role of information in living things. Here in Part 2, Dr. Dembski tackles questions from Dr. Tour’s audience on topics like information theory, probability theory, the origin of life, evolution, the multiverse hypothesis, and Dembski’s contributions to the theory of intelligent design. 

Proponents of an evolutionary explanation for life and the universe often credit natural processes with a seemingly unlimited amount of time and boundless creativity. But the discovery in the 20th century that the universe had a beginning showed that evolution does not have unlimited resources. Dembski has calculated a universal probability bound — the finite limit of available resources and opportunities in the history of the universe — and argues that the complexity of the living cell, the foundational unit of all life on Earth, is leaps and bounds beyond the reach of chance. Download the podcast or listen to it here.

ID is still in the fight?

 

ITimothy Chapter 6 New International Version

 

6.1All who are under the yoke of slavery should consider their masters worthy of full respect, so that God’s name and our teaching may not be slandered. 2Those who have believing masters should not show them disrespect just because they are fellow believers. Instead, they should serve them even better because their masters are dear to them as fellow believers and are devoted to the welfare a of their slaves.

These are the things you are to teach and insist on. 3If anyone teaches otherwise and does not agree to the sound instruction of our Lord Jesus Christ and to godly teaching, 4they are conceited and understand nothing. They have an unhealthy interest in controversies and quarrels about words that result in envy, strife, malicious talk, evil suspicions 5and constant friction between people of corrupt mind, who have been robbed of the truth and who think that godliness is a means to financial gain.

6But godliness with contentment is great gain. 7For we brought nothing into the world, and we can take nothing out of it. 8But if we have food and clothing, we will be content with that. 9Those who want to get rich fall into temptation and a trap and into many foolish and harmful desires that plunge people into ruin and destruction. 10For the love of money is a root of all kinds of evil. Some people, eager for money, have wandered from the faith and pierced themselves with many griefs.

11But you, man of God, flee from all this, and pursue righteousness, godliness, faith, love, endurance and gentleness. 12Fight the good fight of the faith. Take hold of the eternal life to which you were called when you made your good confession in the presence of many witnesses. 13In the sight of God, who gives life to everything, and of Christ Jesus, who while testifying before Pontius Pilate made the good confession, I charge you 14to keep this command without spot or blame until the appearing of our Lord Jesus Christ, 15which God will bring about in his own time—God, the blessed and only Ruler, the King of kings and Lord of lords, 16who alone is immortal and who lives in unapproachable light, whom no one has seen or can see. To him be honor and might forever. Amen.

17Command those who are rich in this present world not to be arrogant nor to put their hope in wealth, which is so uncertain, but to put their hope in God, who richly provides us with everything for our enjoyment. 18Command them to do good, to be rich in good deeds, and to be generous and willing to share. 19In this way they will lay up treasure for themselves as a firm foundation for the coming age, so that they may take hold of the life that is truly life.

20Timothy, guard what has been entrusted to your care. Turn away from godless chatter and the opposing ideas of what is falsely called knowledge, 21which some have professed and in so doing have departed from the faith.

Grace be with you all.

On why artificial intelligence will remain subordinate to actual intelligence.

 Must AI Inevitably Degenerate into Nonsense, through “Model Collapse”?

Casey Luskin

Discovery Institute’s recent COSM 2023 conference hosted a panel on “The Quintessential Limits and Possibilities of AI,” addressing one of the fundamental questions that COSM seeks to investigate: “Is artificial intelligence ‘generative’ or degenerative?” If these experts are right, AI might be doomed to eventually degenerate into nonsense.

George Montañez, Assistant Professor of Computer Science at Harvey Mudd College, opened the session by explaining how AI works. Modern AIs and their “large language models” (LLMs) are trained on huge sets of real-world data — namely text and images generated by humans. Panelist William Dembski, a mathematician and philosopher, pointed out that these LLMs “require a lot of input data and training” in order to work. For example, he notes that it took an immense amount of data, time, money, and collateral damage to humans, to train AI to recognize and reject pornography. Similarly, software engineer Walter Myers noted on the panel that ChatGPT had to train on millions of images of cats and dogs before it could reliably recognize them. In contrast, Montañez points out that a human child can see a few pictures of an animal and they’re immediately able to recognize that species as life.

Montañez further explained that after enough training, AI can interpret data “beyond the things it’s seeing” — but this is only due to “biases and assumptions” provided by humans who program AI with these capabilities. This means that “human fingerprints are all over” the capabilities of AI, and “as impressive as these systems are,” they are “highly parasitic on human rationality and creativity.” Montañez gave the example of an AI that remixes rap with Shakespeare. You “might think it’s amazing” but the reality is “it’s all based upon human programming.”

Model Collapse

But there’s a pitfall to training AI on large datasets — something Denyse O’Leary recently wrote about — called “model collapse.” In short, AI works because humans are real creative beings, and AIs are built using gigantic amounts of diverse and creative datasets made by humans on which they can train and start to think and reason like a human. Until now, this has been possible because human beings have created almost everything we see on the Internet. As AIs scour the entire Internet, they can trust that virtually everything they find was originally made by intelligent and creative beings (i.e., humans). Train AI on that stuff, and it begins to appear intelligent and creative (even if it really isn’t).

But what will happen as humans become more reliant on AI, and more and more of the Internet becomes populated with AI-generated material? If AI continues to train on whatever it finds on the Internet, but the web is increasingly an AI-generated landscape, then AI will end up training on itself. We know what happens when AIs train on themselves rather than the products of real intelligent humans — and it isn’t pretty. This is model collapse.

Enter Robert J. Marks, Distinguished Professor of Electrical and Computer Engineering at Baylor University. He noted that on the first day of COSM 23, computer scientist and AI pioneer Stephen Wolfram warned that we’re at the edge of available training data for AI — essentially we’re hitting the limits of what we can feed AI to make it smart. Once AI runs out of training data, what will it do — train itself?

After taking the audience through a brief history of computing and the development of AI, Marks noted that “each jump [in computing ability] was done by humans, not AI. Each jump in AI happened due to human ingenuity.” But when AI runs out of human ingenuity to train on, will it itself hit a limit — i.e., model collapse? As Montañez put it, “After we’ve scraped the web of all human training data” then “it starts to scrape AI-generated data” because “that’s all you have.” That’s when you get model collapse, and we might be getting close to it.

Marks cited a newly posted study at Arxiv.org, “The Curse of Recursion: Training on Generated Data Makes Models Forget,” which shows model collapse in action. An initial “generation” of AI is trained directly on human-created data and its output generally makes sense. But after multiple generations of AI training on itself, the result is gibberish that’s obsessed with nonsensically colored jackrabbits:

A similar phenomenon happens with images. Marks showed how an AI trained to creatively make variations of the Mona Lisa painting initially provides some interesting if perhaps disturbing images. But eventually, as it trains on its own material, you end up not with art but with nonsensical lines and smudges.

Digital Inbreeding

The problem of model collapse is not entirely unlike human genetics, where siblings or cousins are warned never to marry because they both carry the same deleterious mutations which, when combined, will yield malformed offspring. Better to marry someone outside your immediate gene pool, because they will likely have “fresh genetic material” that can be combined with yours to make healthy children.

In a similar way, AI training on itself needs fresh creative material on which to train or else the algorithms will end up feeding on themselves in recursive cycles that degenerate into nonsense. As Popular Mechanics put it recently, AI will end up “eating its own tail.” 

To mix metaphors, the threat of model collapse is akin to digital inbreeding, and it guarantees that without humans constantly providing fresh creative material for AIs to train on, AIs are doomed to deteriorate. Their creativity may therefore be limited by the human datasets they’re given, meaning there are basic limits to what AI can do. AI will never surpass humans in fundamental ways, and will always be limited by what they can learn from us.

The antiZionism faction of evangelicalism's civil war(s)?

 

There are no good guys V

 

MAGA : South Africa edition?

 

Darwinists can't show their work because the caterpillar ate it?

 Fossil Friday: How the Caterpillar Got Its Legs, or Not

Gunter Bechly

This Fossil Friday features a caterpillar trapped in 45-million-year-old tree resin of Eocene Baltic amber. A caterpillar of course looks very much different from the butterfly into which it eventually develops. The wonderful metamorphosis of caterpillars into butterflies was first discovered by the British physician William Harvey (1651) and Dutch biologist Jan Swammerdam (1669), and famously featured in paintings by the pioneer entomologist Maria Sybilla Merian in her book Metamorphosis insectorum Surinamensium (Merian 1705).

The more primitive groups of insects like roaches, locusts, cicadas, and bugs have a so-called hemimetabolous development, where the nymph is similar in body plan to the adult insect, and with each molting grows in size and especially in length of the wing sheaths. However, most insect species, and indeed most animals on our planet, belong to Holometabola, the clade of insects with complete metamorphosis, which includes lace wings, beetles, bees and wasps, mosquitoes and flies, scorpionflies and fleas, as well as caddisflies and butterflies. In these insects the larva has a very different body plan from the adult insect. After the final larval stage there is a resting stage called pupa or chrysalis, in which the larval body is mostly dissolved into a kind of cell soup and rearranged into the adult body plan. This miraculous development was featured in the Illustra Media documentary Metamorphosis (Illustra Media 2011, Klinghoffer 2011) and poses a considerable conundrum for evolutionary biologists.

The Nature of the Conundrum

Only three hypotheses for the evolution of metamorphosis in insects have been presented: one, which suggests that the holometabolan larva is equivalent to the hemimetabolan nymph, fell out of favor decades ago. Another hypothesis suggested that the holometabolan caterpillar originated from a weird hybridization event of an insect with a velvet worm (Williamson 2009), which is generally considered as preposterous nonsense (Giribet 2009; also see Evolution News 2011). The currently preferred hypothesis is based on very old ideas of Harvey (1651) and Berlese (1913), which were further developed and elaborated by Truman & Riddiford (1999, 2002, 2019, 2022). Their so-called pronymph hypothesis suggests that the juvenile stages of hemimetabolous and holometabolous insects are not homologous, but that only the hemimetabolan pronymph is equivalent to the caterpillar larva, and the multiple nymphal instars are all equivalent to the pupal stage (also see Grimaldi & Engel 2005). However this hypothesis faces two formidable challenges:

The proymph is a non-feeding final embryonic stage, lacking functional mouth parts, which hatches from the egg and immediately molts into the first nymphal instar. The caterpillar larva is a pure feeding stage, basically a gut with legs. How could one evolve into the other with functional and advantageous intermediate forms?

Likewise, how could a single pupal stage, in which the complete body plan is dissolved and rearranged (including even the brain, see Truman et al. 2023 and Saplakoglu 2023), evolve via viable transitional forms from a normal series of nymphal instars that gradually transform into the adult with each molting? This appears to be not just unlikely but inconceivable and virtually impossible. Therefore, this hypothesis is controversial even among mainstream biologists, who have raised many objections to the interpretation of the pupa as only nymphal stage (e.g., DuPorte 1958). All that evolutionists have to offer are vague speculations such as this: “Perhaps 280 million years ago, through a chance mutation, some pro-nymphs failed to absorb all the yolk in their eggs, leaving a precious resource unused. In response to this unfavorable situation, some pro-nymphs gained a new talent: the ability to actively feed” (Jabr 2012). Easy peasy.

Anyway, we should expect that such a marvellous mode of development evolved from normal nymphal stages, if at all, after hundreds of millions of years of gradual change. However, that is not at all what the fossil record shows.

Actually, the first holometabolan insects are recorded from the same Pennsylvanian period as the first flying insects. Molecular clock data even suggest that Holometabola are at least as ancient (about 328-318 mya) as the earliest fossil record of flying insects (Labandeira 2011), or place “the origin of Holometabola in the Carboniferous (355 Ma), a date significantly older than previous paleontological and morphological phylogenetic reconstructions” (Wiegmann et al. 2009a, 2009b, Misof et al. 2014). My dear colleague and frequent co-author André Nel (2019) recently commented that “the late Carboniferous was also the time of the oldest known holometabolous insects, with complete metamorphosis (wasps, beetles, scorpionflies).” Indeed, fossils from larval and adult holometabolous insects of different orders have been found in late Carboniferous layers (see Kukalová-Peck 1997, Nel et al. 2007, 2013, Béthoux 2009, Kirejtshuk & Nel 2013, Kirejtshuk et al. 2014).

Early and Abrupt Appearance

This very early and abrupt appearance of the highly complex holometabolan metamorphosis represents one of the many examples of the waiting time problem, because it certainly required many coordinated mutations, which again required orders of magnitude more time to originate and spread than was available.

But any theory for the origin of the caterpillar larva needs to explain a lot more than that. While hemimetabolan nymphs and all adult winged insects have only three pairs of thoracic legs, the caterpillar larvae of butterflies and plant wasps additionally possess several pairs of chubby abdominal leglets called prolegs. “These prolegs pose an evolutionary mystery, and scientists have long grappled over how and why they got them” (Pallardy 2023). Where did those prolegs come from? There are three alternative hypotheses on the table:

Prolegs are serially homologous with thoracic legs, and thus derived from reactivated abdominal legs of crustaceans. This alternative was challenged and arguably refuted by previous evo-devo studies like Yue & Hua (2010) and Oka et al. (2010).

Prolegs are novel adaptations without immediate precursor structures.

Prolegs are derived from endites, internally facing structures of the crustacean limbs (e.g., Oka et al. 2010).

Now, a new study by Matsuoka et al. (2023) tested these three hypotheses with evo-devo data. The authors suggest that prolegs are novel traits, but based on the re-activation of pre-existing endite genes. The press release makes it very clear: prolegs “seem to be modified endites. As crustaceans evolved into insects, endites were largely lost. But in butterflies and moths, the gene for them got reactivated, providing caterpillars with their prolegs.” (Pallardy 2023).

To evaluate the feasibility of this hypothesis we first have to look at the distribution of prolegs within holometabolan insects, because this character is not hierarchically distributed as would be predicted by Darwinism, but instead is very incongruent (homoplastic): prolegs occur in the larvae of plant wasps, scorpionflies and fleas, caddisflies and butterflies, and some families of flies, but are absent in all other holometabolan groups. This incongruent pattern implies that prolegs were either reduced multiple times, or instead originated independently as a convergence, which is also suggested by developmental data (Suzuki & Palopoli 2001). Actually, Hinton (1955) proposed an independent origin of prolegs 27 times within Diptera. This alone is a grandiose empirical failure of Darwinian theory, because the unique anatomical similarity does not seem to be plausibly based on inheritance from a common ancestor. For the sake of the argument we will let this pass and just look at the new study.

Assessing the new study

As we have seen above, Darwinists now explain the origin of caterpillar leglets with the reactivation of a crustacean gene, that was dormant for maybe 100 million years. Seriously? After such a long period without function and without adaptive pressure to eliminate deleterious mutations, this gene should still have remained functional instead of been degraded by random genetic noise? This would be akin to a genuine miracle and arguably would violate an assumed law of evolution known as Dollo’s Law, which is based on the simple fact that history does not repeat itself (Gould 1970). Could this law be broken on some realistic time scale?

As shown by Rana (2017), there were several studies that evaluated the time frame in which the function of a gene is degraded and lost, so that it cannot be reactivated:

The study by Marshall et al. (1994) suggested that reactivation is reasonable over time scales of 0.5-6 million years. The authors concluded that “the reactivation of long (>10 million years)-unexpressed genes and dormant developmental pathways is not possible unless function is maintained by other selective constraints.”

Lynch & Conery (2000) showed that duplicated genes lose function by stochastic silencing within a few million years. Rana (2017) mentions that such duplicated genes can serve as proxy for dormant genes, because they are no longer under the influence of selection. Lynch and Conery found a half-life of 4 million years, which implies that function is lost after 16-24 million years.

Protas et al. (2007) showed that such a loss of function happens much more quickly, in about 1 million years, if it is advantageous and thus influenced by selection.

Horne (2010) studied the reactivation of eye sight in blind ostracods and commented that “there appear to be several well-documented examples of the reactivation of dormant genes, allowing the reappearance of ‘lost’ characters, in some cases after several [my emphasis] million years.” 

So, we have a realistic time frame of roughly 1-24 million years for the reactivation of a dormant gene. Indeed, short term reversals can be observed in lab experiments, e.g., concerning drug resistance among germs (Gouda et al. 2019). Anything longer than the mentioned time constraint is prohibited by Dollo’s Law of irreversibility (Gould 1970, Bull & Charnov 1985). Any apparent reactivation on longer time frames (see examples mentioned by Fryer 1999, Dingle 2003, Cruickshank & Paterson 2006, Horne 2010, and Rana 2017) cannot be reasonably explained with Darwinian processes, but requires intelligent design as more plausible and causally adequate explanation. Rana (2017) correctly emphasized that “it is not unusual for engineers to reuse the same design or to revisit a previously used design feature in a new prototype.”

But There Might Be a Loophole

Lynch (2022) recently found that “the long half‐life of enhancers, transcription factor binding sites, and protein−protein interaction motifs suggest that evolutionary reversals are possible after much longer periods of loss than previously suspected.” He concluded that “these data indicate that reactivation of these smaller functional units is possible after many millions of years and suggest that re-evolution of complex traits may occur through their loss and regain. Thus these data suggest that organisms need not surmount “the sheer statistical improbability … of evolution ever arriving at the same complex genic end‐result twice” (Müller in Gould 1970), rather “organisms might only need to retrace a single step such as the reacquisition of a transcription factor binding site in a cis‐regulatory element of a protein−protein interaction motif.”

However, there is a caveat, because the longer half-life does not apply to silenced protein coding genes, which would degrade much faster. Lynch (2022) explicitly admitted that “it seems unlikely that the genetic information for the development and function of the character can be maintained for long periods of time in the absence of the character (Bull & Charnov, 1985).” This could only be avoided in cases of serially homologous characters, when at least one instance of expression of this character would remain, so that selection could work against the deterioration of function by random copy errors. Therefore, Lynch (2022) suggested as a loophole for the violation of Dollo’s law “that the developmental programs required for the establishment of serially homologous characters may never really be lost so long as a single instance of the character remains.”

How Would Darwinists Argue?

So, let’s have a look at the possibility that this loophole could allow for the reactivation of the endite gene in caterpillars as suggested in the new study by Matsuoka et al. (2023). Probably, Darwinists would argue as follows: putative homologs of abdominal leg endites are present as pairs of eversible vesicles on the abdomen in some primitive wingless insects (apterygotes) like diplurans, bristletails, and silverfish that are known from (controversial) Devonian and Carboniferous fossils. Such vesicles are absent in all known winged insects and thus were reduced in the stem species of crown group pterygotes, which lived at least 323 million years ago in the earliest Pennsylvanian (Namurian) period according to the oldest fossil record (Brauckmann et al. 1994, Brauckmann & Schneider 1996, Prokop et al. 2005, Prokop & Hörnschemeyer 2016, Wolfe et al. 2016), and 410 million years ago in the Late Devonian period according to molecular clock estimates (Wiegmann et al. 2009b, Misof et al. 2014). This is 10 million years prior to the oldest fossil record of holometabolans (313.7 mya, Wolfe et al. 2016) and 60 million years prior to molecular clock estimates of their origin (350 mya, Wiegmann et al. 2009a, 2009b, Misof et al. 2014 / 328-318 mya according to Labandeira 2011). Therefore, the transformation would have occurred after 60-10 million years of gene suppression if the prolegs would belong to the ground plan of holometabolan insects. This would still reach or exceed the above mentioned limits imposed by Dollo’s law.

But it gets much worse for the evolutionist hypothesis. As we have seen above, larval prolegs do not belong to the ground plan of holometabolan insects (Peters et al. 2014), but developed independently multiple times in several crown groups among them. Therefore, we have to look at the age of those crown groups and not the age of Holometabola as a whole to evaluate the available window of time. Let’s be maximally generous and assume that larval prolegs are at least homologous in caddisflies (Trichoptera) and butterflies (Lepidoptera), so that they could belong to the ground plan of their common amphiesmenopteran ancestor. According to The Timetree of Life (Wiegmann et al. 2009a, 2009b) the relevant crown groups originated in Permian and Triassic periods: Lepidoptera, for example, about 230 million years ago and Amphiesmenoptera (the clade of Trichoptera+Lepidoptera) 282 million years ago. This molecular dating roughly agrees with the early fossil record of these groups. This implies that the reactivation of the dormant gene would have occurred after 128-41 million years (410/323-282 mya) of absence of any instantiated serially homologous character, which is simply impossible according to the limits proposed by mainstream evolutionary biology itself.

Is This Hard Science? Really?

Of course, such inconvenient facts do not bother evolutionary biologists at all, because the law obviously must have been broken, because we know it happened. Apparently laws do not mean much in evolutionary biology and can be suspended whenever a just-so story requires it. Sounds like hard science — not!

Why is it that you cannot find such simple calculations as we just made above anywhere in the mainstream scientific literature, to check if a scenario is plausible and compatible with other claims of evolutionary theory? Are the scientists really interested in testing their hypotheses and eventually finding out that they don’t hold water? It certainly doesn’t look like that to me. In spite of all the scientific efforts by Darwinists, the origin of complete metamorphosis in holometabolan insects remains an unsolved mystery, which is much better and causally more adequately explained by intelligent design.