Tuesday, April 24, 2018

News Ideas on the Evolution of Photosynthesis Reaction Centers

Pure Junk

Evolutionists do not have a clear understanding of how photosynthesis arose, as evidenced by a new paper from Kevin Redding’s laboratory at Arizona State University which states that:

After the Type I/II split, an ancestor to photosystem I fixed its quinone sites and then heterodimerized to bind PsaC as a new subunit, as responses to rising O2 after the appearance of the oxygen-evolving complex in an ancestor of photosystem II. These pivotal events thus gave rise to the diversity that we observe today.

That may sound like hard science to the uninitiated, but it isn’t.

The Type I/II split is a hypothetical event for which the main evidence is the belief that evolution is true. In fact, according to the science, it is astronomically unlikely that photosynthesis evolved, period.

And so, in typical fashion, the paper presents a teleological (“and then structure X evolved to achieve Y”) narrative to cover over the absurdity:

and then heterodimerized to bind PsaC as a new subunit, as responses to rising O2 …

First, let’s reword that so it is a little clearer: The atmospheric oxygen levels rose and so therefore the reaction center of an early photosynthesis system heterodimerized in order to bind a new protein (which helps with electron transfer).

This is a good example of the Aristotelianism that pervades evolutionary thought. This is not science, at least in the modern sense. And as usual, the infinitive form (“to bind”) provides the telltale sign. In other words, a new structure evolved as a response to X (i.e., as a response to the rising oxygen levels) in order to achieve Y (i.e., to achieve the binding of a new protein, PsaC).

But it gets worse.

Note the term: “heterodimerized.” A protein machine that consists of two identical proteins mated together is referred to as a “homodimer.” If two different proteins are mated together it is a “heterodimer.” In some photosynthesis systems, at the core of the reaction center is a homodimer. More typically, it is a heterodimer.

The Redding paper states that the ancient photosynthesis system “heterodimerized.” In other words, it switched, or converted, the protein machine from a homodimer to a heterodimer (in order to bind PsaC). The suffix “ize,” in this case, means to cause to be or to become. The ancient photosynthesis system caused the protein machine to become a heterodimer.

Such teleology reflects evolutionary thought and let’s be clear—this is junk science. From a scientific perspective there is nothing redeeming here. It is pure junk.

But it gets worse.

These pivotal events thus gave rise to the diversity that we observe today.

Or as the press release described it:

Their [reaction centers’] first appearance and subsequent diversification has allowed photosynthesis to power the biosphere for over 3 billion years, in the process supporting the evolution of more complex life forms.

So evolution created photosynthesis which then, “gave rise to” the evolution of incredibly more advanced life forms. In other words, evolution climbed an astronomical entropic barrier and created incredibly unlikely structures which were crucial for the amazing evolutionary history to follow.

The serendipity is deafening.

Religion drives science, and it matters.

Wednesday, April 18, 2018

The Dinosaur “Explosion”

As Though They Were Planted There

In the famed Cambrian Explosion most of today’s animal phyla appeared abruptly in the geological strata. How could a process driven by blind, random mutations produce such a plethora of new species? Evolutionist Steve Jones has speculated that the Cambrian Explosion was caused by some crucial change in DNA. “Might a great burst of genetic creativity have driven a Cambrian Genesis and given birth to the modern world?” [1] What explanations such as this do not address is the problem of how evolution overcame such astronomical entropic barriers. Rolling a dice, no matter how creatively, is not going to design a spaceship.

The Cambrian Explosion is not the only example of the abrupt appearance of new forms in the fossil record, and the other examples are no less easy for evolution to explain. Nor has the old saw, that it’s the fossil record’s fault, fared well. There was once a time when evolutionists could appeal to gaps in the fossil record to explain why the species appear to arise abruptly, but no more. There has just been too much paleontology work, such as a new international study on dinosaurs published this week, confirming exactly what the strata have been showing all along: new forms really did arise abruptly.

The new study narrows the dating of the rise of dinosaurs in the fossil record. It confirms that many dinosaur species appeared in an “explosion” or what “we term the ‘dinosaur diversification event (DDE)’.” It was an “explosive increase in dinosaurian abundance in terrestrial ecosystems.” As the press release explains,

First there were no dinosaur tracks, and then there were many. This marks the moment of their explosion, and the rock successions in the Dolomites are well dated. Comparison with rock successions in Argentina and Brazil, here the first extensive skeletons of dinosaurs occur, show the explosion happened at the same time there as well.

As lead author Dr Massimo Bernardi at the University of Bristol explains, “it’s amazing how clear cut the change from ‘no dinosaurs’ to ‘all dinosaurs’ was.

There just isn’t enough time, and it is another example of a failed prediction of the theory of evolution.

1. Steve Jones, Darwin’s Ghost, p. 206, Random House, New York, 2000.

h/t: The genius.

Sunday, April 15, 2018

Andreas Wagner: Genetic Regulation Drives Evolutionary Change

A Hall of Mirrors

A new paper from Andreas Wagner and co-workers argues that a key and crucial driver of evolution is changes to the interaction between transcription factor proteins and the short DNA sequences to which they bind. In other words, evolution is driven by varying the regulation of protein expression (and a particular type of regulation—the transcription factor-DNA binding) rather than varying the structural proteins themselves. Nowhere does the paper address or even mention the scientific problems with this speculative idea. For example, if evolution primarily proceeds by random changes to transcription factor-DNA binding, creating all manner of biological designs and species, then from where did those transcription factors and DNA sequences come? The answer—that they evolved for some different, independent, function; itself an evolutionary impossibility—necessitates astronomical levels of serendipity. Evolution could not have had foreknowledge. It could not have known that the emerging transcription factors and DNA sequence would, just luckily, be only a mutation away from some new function. This serendipity problem has been escalating for years as evolutionary theory has repeatedly failed, and evolutionists have applied ever more complex hypotheses to try to explain the empirical evidence. Evolutionists have had to impute to evolution increasingly sophisticated, complex, higher-order, mechanisms. And with each one the theory has become ever more serendipitous. So it is not too surprising that evolutionists steer clear of the serendipity problem. Instead, they cite previous literature as a way of legitimizing evolutionary theory. Here I will show examples of how this works in the new Wagner paper.

The paper starts right off with the bold claim that “Changes in the regulation of gene expression need not be deleterious. They can also be adaptive and drive evolutionary change.” That is quite a statement. To support it the paper cites a classic 1975 paper by Mary-Claire King and A. C. Wilson entitled “Evolution at two levels in humans and chimpanzees.” The 1975 paper admits that the popular idea and expectation that evolution occurs by mutations in protein-coding genes had largely failed. The problem was that, at the genetic level, the two species were too similar:

The intriguing result, documented in this article, is that all the biochemical methods agree in showing that the genetic distance between humans and the chimpanzee is probably too small to account for their substantial organismal differences.

Their solution was to resort to a monumental shift in evolutionary theory: evolution would occur via the tweaking of gene regulation.

We suggest that evolutionary changes in anatomy and way of life are more often based on changes in the mechanisms controlling the expression of genes than on sequence changes in proteins. We therefore propose that regulatory mutations account for the major biological differences between humans and chimpanzees.

In other words, evolution would have to occur not by changing proteins, but by changing protein regulation. What was left unsaid was that highly complex, genetic regulation mechanisms would now have to be in place, a priori, in order for evolution to proceed.

Where did those come from?

Evolution would have to create highly complex, genetic regulation mechanisms so that evolution could occur.

Not only would this ushering in of serendipity to evolutionary theory go unnoticed, it would, incredibly, be cited thereafter as a sort of evidence, in its own right, showing that evolution occurs by changes to protein regulation.

But of course the 1975 King-Wilson paper showed no such thing. The paper presupposed the truth of evolution, and from there reasoned that evolution must have primarily occurred via changes to protein regulation. Not because anyone could see how that could occur, but because the old thinking—changes to proteins themselves—wasn’t working.

This was not, and is not, evidence that changes in the regulation of gene expression can be “adaptive and drive evolutionary change,” as the Wagner paper claimed.

But this is how the genre works. The evolution literature makes unfounded claims that contradict the science, and justifies those claims with references to other evolution papers which do the same thing. It is a web of deceit.

Ultimately it all traces back to the belief that evolution is true.

The Wagner paper next cites a 2007 paper that begins its very first sentence with this unfounded claim:

It has long been understood that morphological evolution occurs through alterations of embryonic development.

I didn’t know that. And again, references are provided. This time to a Stephen Jay Gould book and a textbook, neither of which demonstrate that “morphological evolution occurs through alterations of embryonic development.”

These sorts of high claims by evolutionists are ubiquitous in the literature, but they never turn out to be true. Citations are given, and those in turn provide yet more citations. And so on, in a seemingly infinite hall of mirrors, where monumental assertions are casually made and immediately followed by citations that simply do the same thing.

Religion drives science, and it matters.

Saturday, April 14, 2018

IC: We Can Say It, But You Can’t

Pre Adaptation

In contrast [to trait loss], the gain of genetically complex traits appears harder, in that it requires the deployment of multiple gene products in a coordinated spatial and temporal manner. Obviously, this is unlikely to happen in a single step, because it requires potentially numerous changes at multiple loci.

If you guessed this was written by an Intelligent Design advocate, such as Michael Behe describing irreducibly complex structures, you were wrong. It was evolutionist Sean Carroll and co-workers in a 2007 PNAS paper.

When a design person says it, it is heresy. When an evolutionist says it, it is the stuff of good solid scientific research.

The difference is the design person assumes a realist view (the genetically complex trait evinces design) whereas the evolutionist assumes an anti-realist view (in spite of all indications, the genetically complex trait must have arisen by blind causes).

To support their position, evolutionists often appeal to a pre adaptation argument. This argument claims that the various sub components (gene products, etc.), needed for the genetically complex trait, were each needed for some other function. Therefore, they evolved individually and independently, only later to serendipitously fit together perfectly and, in so doing, form a new structure with a new function that just happened to be needed. As Richard Dawkins once put it:

The bombardier beetle’s ancestors simply pressed into different service chemicals that already happened to be lying around. That’s often how evolution works.

The problem, of course, is that this is not realistic. To think that each and every one of the seemingly unending, thousands and thousands, of genetically complex traits just happened to luckily arise from parts that just happened to be lying around, is to make one’s theory dependent on too much serendipity.

Religion drives science, and it matters.

Wednesday, April 11, 2018

Leyden and Teixeira: Political “Civil War” Coming Because of Global Warming

The Politicization of Science

Twitter CEO Jack Dorsey recently tweeted that Peter Leyden’s and Ruy Teixeira’s article, “The Great Lesson of California in America’s New Civil War,” is a “Great read.” The article both urges and forecasts a blue-state takeover of America where our current political divide gives way to a Democrat dominion. This new “Civil War” is to begin this year and, like the last one will have an economic cause. Unfortunately, the thinking of Leyden and Teixeira is steeped in scientific ignorance which drives their thesis.

According to Leyden and Teixeira both the last, and now upcoming, Civil Wars are about fundamentally different economic systems that cannot coexist. In the mid nineteenth century it was an agrarian economy dependent on slaves versus a capitalist manufacturing economy dependent on free labor. Today, the conflict is between (i) the red states which are dependent on carbon-based energy systems like coal and oil, and (ii) the blue states that are shifting to clean energy and weaning themselves off of carbon. Granting this dubious thesis, why are these two economies so irreconcilable? Because of global warming and the terrible natural disasters it brings:

In the era of climate change, with the mounting pressure of increased natural disasters, something must give.

You read that right. Leyden’s and Teixeira’s thesis is driven by anthropogenic global warming, or AGW, which they sprinkle throughout the article. Red states are bad because they deny it, blue states are good because they face the truth and reckon with it with progressive policies. After all, it is “the scientific consensus that climate change is happening, that human activity is the main cause, and that it is a serious threat.”

It must be nice to go through life with such certainty. Ignorance, as they say, is bliss.

We can begin with the most obvious mistake. While it certainly revs people up to hear that global warming is “a serious threat,” we have little evidence for this. Even those “consensus” scientists agree that we are not justified in claiming the sky is falling. And, no, in spite of what you may have heard, the recent hurricanes were probably not products of global warming.

But what about that scientific consensus that Leyden and Teixeira speak of? Doesn’t that make their case?

Unfortunately, Leyden and Teixeira are the latest example of how historians have utterly failed. In spite of their best efforts, historians, and especially historians of science, have not been able to disabuse people of the myths of science.

In science, as in politics, majorities are majorities until they aren’t. A scientific consensus can occur both for theories that end up enshrined in museums and for theories that end up dumped in the trash bin.

Once upon a time the scientific consensus held the Earth was the center of the universe. Only later did the scientific consensus shift to the Sun as the center of the universe.

Both were wrong.

What Mr. Nelson taught you in seventh grade history class was right after all: If you don’t understand history you will repeat its mistakes. And Leyden and Teixeira are today’s poster children of such naiveté.

A scientific consensus for a theory means just one thing: That the majority of scientists accept the theory. Nothing more, nothing less. The problem with science, as Del Ratzsch once explained, is that it is done by people.

What we do know about AGW is that the data have been massaged, predictions have failed, publications have been manipulated, enormous pressure to conform has been applied, and ever since Lynn White’s 1966 AAAS talk the science has been thoroughly politicized.

None of this means that AGW is false, but the theories that end up in textbooks and museums don’t usually need enormous social and career pressures for sustenance.

As it stands scientists have been walking back the hype (it’s climate change, not global warming anymore), and trying to explain the lack of a hockey stick temperature rise (the ocean is temporarily absorbing the heat); insiders are backing out (see here and here), and new papers are showing current temperatures have not been so out of the ordinary (e.g., here).

AGW is certainly an important theory to study. And perhaps it is true. But its track record of prediction is far more important than the number of people voting for it.

The idea that AGW is the driver behind a new Civil War in America to start, err, later this year is simply absurd. I’m less concerned about Leyden’s and Teixeira’s political desires as I am about the mythologies they are built on.

Religion drives science, and it matters.

Sunday, April 8, 2018

Ethan Siegel Updates the Drake Equation

Not Even Wrong

Astrophysicist Ethan Siegel may not have been aware of the phosphorous problem when he wrote his article on fixing the Drake Equation which appeared at Forbes last week. But he certainly should have known about origin of life problem. His failure to account for the former is a reasonable mistake, but his failure to account for the latter is not.

The Drake Equation is simply the product of a set of factors, estimating the number of active, technologically-advanced, communicating civilizations in our galaxy—the Milky Way. Siegel brings the Drake Equation up to date with a few modifications.

He is careful to ensure that his final result is not too large and not too small. Too large an estimate would contradict the decades-long SETI (search for extraterrestrial intelligence) project which, err, has discovered precisely zero radio signals in the cosmos that could be interpreted as resulting from an intelligent civilization. Too small an estimate would signal an end to Siegel’s investigations of extraterrestrial intelligence.

What is needed is a Goldilocks numbers—not too large and not too small. Siegel optimistically arrives at a respectable 10,000 worlds in the Milky Way “teeming with diverse, multicellular, highly differentiated forms of life,” but given the length of time any such civilization is likely to exist, there is only a 10% chance of such a civilization existing co-temporally with us.

Ahh, just right. Small enough to avoid contradicting SETI, but large enough to be interesting.

But Siegel’s value of 25% for the third factor, the fraction of stars with the right conditions for habitability, seems much too high give new research indicating phosphorus is hard to come by in the cosmos.

The problem, it seems, is that phosphorus (the P in the ubiquitous energy-carrying ATP molecule you learned about in high school biology class) is created only in the right kind of supernovae, and there just isn’t enough to go around. As one of the researchers explained:

The route to carrying phosphorus into new-born planets looks rather precarious. We already think that only a few phosphorus-bearing minerals that came to the Earth—probably in meteorites—were reactive enough to get involved in making proto-biomolecules. If phosphorus is sourced from supernovae, and then travels across space in meteoritic rocks, I'm wondering if a young planet could find itself lacking in reactive phosphorus because of where it was born? That is, it started off near the wrong kind of supernova? In that case, life might really struggle to get started out of phosphorus-poor chemistry, on another world otherwise similar to our own.

This could be trouble for Siegel. The problem in his goal-seeked 10% result he has committed to specific values. The wiggle room is now gone, and new findings such as the phosphorus problem will only make things worse. Siegel’s 10% result could easily drop by 10 orders of magnitude or more on the phosphorus problem alone.

That would be devastating, but it would be nothing compared to a realistic accounting for the origin of life problem. That is Siegel’s fifth factor and he grants it a value of 1-in-10,000. That is, for worlds in habitable zones, there is a 1/10,000 probability of life arising from non-life, at some point in the planet’s history.

That is absurd. Siegel pleads ignorance, and claims 1-in-10,000 is “as good a guess as any,” but of course it isn’t.

We can begin by dispelling the silly proclamations riddling the literature, that the origin of life problem has been essentially solved. As the National Academy of Sciences once declared:

For those who are studying the origin of life, the question is no longer whether life could have originated by chemical processes involving nonbiological components. The question instead has become which of many pathways might have been followed to produce the first cells [1]

Fortunately the National Academy of Sciences has since recanted that non-scientific claim, and admitted there is no such solution at hand. Such scientific realism can now be found elsewhere as well.

The origin of life problem has not been solved, not even close. But that doesn’t mean we are left with no idea of how hard the problem is, and that 1-in-10,000 (i.e., 10^-4) is “as good a guess as any,” as Siegel claims. Far from it. Even the evolution of a single protein has been repeatedly shown to be far, far less likely than 10^-4.

As for something more complicated than a single protein, one study estimated the chances of a simple replicator evolving at 1 in 10^1018. It was a very simple calculation and a very rough estimate. But at least it is a start.

One could argue that the origin of life problem is more difficult than that, or less difficult than that. But Siegel provided no rational at all. He laughably set the bounds at 1-in-ten and one-in-a-million, and then with zero justification arbitrarily picked 1-in-10,000.

In other words, Siegel set the lower and upper limits at 10^-1 and 10^-6, when even a single protein has been estimated at about 10^-70, and a simple replicating system at 10^-1018.

Siegel’s estimate is not realistic. With zero justification or empirical basis, Siegel set the probability of the origin of life at a number that is more than 1,000 orders or magnitude less than what has been estimated.

Siegel’s estimate was not one thousand times too optimistic, it was one thousand orders of magnitude too optimistic. It was not too optimistic by three zeros; it was too optimistic by one thousand zeros. Siegel is not doing science. He is goal-seeking, using whatever numbers he needs to get the right answer.

Religion drives science, and it matters.

Brochosome Proteins Encoded By Orphan Genes

A Pattern Problem

A few years ago Paul Nelson debated Joel Velasco on the topic of design and evolution. Nelson masterfully demonstrated design in nature. For his part Velasco also provided an excellent defense of evolution. But the Epicurean claim that the world arose via random chance is not easy to defend, and Velasco’s task would be challenging. Consider, for example, the orphans which Nelson explained are a good example of taxonomically-restricted designs. Such designs make no sense on evolution, and though Velasco responded with many rebuttals, none were very convincing. Since that debate the orphan problem has become worse, as highlighted by a new study of brochosomes.


The term orphan refers to a DNA open reading frame, or ORF, without any known similar sequence in other species or lineages, and hence ORFan or “orphan.” Since orphans are unique to a particular species or lineage, they contradict common ancestry’s much celebrated nested hierarchy model.

The Nelson-Valasco Debate

Velasco addressed the orphan problem with several arguments. First, Velasco reassured the audience that there isn’t much to be concerned with here because “Every other puzzle we’ve ever encountered in the last 150 years has made us even more certain of a fact that we already knew, that we’re all related.”

Second, Velasco argued that the whole orphan problem is contrived, as it is nothing more than a semantic misunderstanding—a confusion of terms. These are nothing more than open reading frames without significant similarity to any known sequence.

Third, Velasco argued that many of the orphans are so categorized merely because the search for similar sequence is done only in “very distantly related” species.

Furthermore, and fourth, Velasco argued that orphans are really nothing more than a gap in our knowledge. For the more we know about a species, the more the orphan problem goes away. And which species do we know the most about? Ourselves of course. And we have no orphans: “Well what about humans, we know a lot about humans. How many orphan genes are in humans? What do you think? Zero.”

In fact, and fifth, Velasco argued that while new orphans are discovered with each new genome that is decoded, the trend is slowing and is suggestive that in the long run relatives for these orphans will be found: “In fact if you trend the absolute number going up, as opposed to the percentage of orphan genes in organisms, that number is going down.”

So to summarize Velasco’s position, the orphan problem will be solved so don’t worry about, but actually orphans are not a problem at all but rather a semantic misunderstanding, but on the other hand the orphan problem is a consequence of incomplete genomic data, but actually on the other hand the problem is a consequence of insufficient knowledge about the species, and in any case even though the number of known orphans keeps on rising, they will eventually go away because the orphans, as a percentage of the overall genomic data (which has been exploding exponentially) is going down.

This string of evolution arguments reminds us of the classic dog-owner’s defense: He’s not my dog, he didn’t bite you, and besides you hit the dog first anyway. Not surprisingly, each of Velasco’s arguments fails, as I explained here.

In fact, there are many orphans, and while function can be difficult to identify, it has been found for many orphans. As science writer Helen Pilcher explained:

In corals, jellyfish and polyps, orphan genes guide the development of explosive stinging cells, sophisticated structures that launch toxin-filled capsules to stun prey. In the freshwater polyp Hydra, orphans guide the development of feeding tentacles around the organism’s mouth. And the polar cod’s orphan antifreeze gene enables it to survive life in the icy Arctic.

Up to a third of genomes have been found have been found to be unique, as this review explains:

Comparative genome analyses indicate that every taxonomic group so far studied contains 10–20% of genes that lack recognizable homologs in other species. Do such ‘orphan’ or ‘taxonomically-restricted’ genes comprise spurious, non-functional ORFs, or does their presence reflect important evolutionary processes? Recent studies in basal metazoans such as Nematostella, Acropora and Hydra have shed light on the function of these genes, and now indicate that they are involved in important species-specific adaptive processes. 

And this is yet another failed prediction of evolution, as this paper explains:

The frequency of de novo creation of proteins has been debated. Early it was assumed that de novo creation should be extremely rare and that the vast majority of all protein coding genes were created in early history of life. However, the early genomics era lead to the insight that protein coding genes do appear to be lineage-specific. Today, with thousands of completely sequenced genomes, this impression remains.

Why then was Velasco so confident and almost nonchalant in his argumentation? Why was he so assured that, one way or another, the orphan problem was not a problem? And why did he believe there are zero orphans in humans, and so it merely is a matter of studying biology, and the orphans will go away?

Lander Orphan Study

It could be due to a significant 2007 study from Eric Lander’s group which rejected most of the large number (several thousands) of orphans that had been tentatively identified in the human genome. The study confidently concluded that “the vast majority” of the orphans were “spurious”:

The analysis here addresses an important challenge in genomics— determining whether an ORF truly encodes a protein. We show that the vast majority of ORFs without cross-species counterparts [i.e., orphans] are simply random occurrences. The exceptions appear to represent a sufficiently small fraction that the best course is would be [sic] consider such ORFs as noncoding in the absence of direct experimental evidence.

The authors went on to propose that “it is time to undertake a thorough revision of the
human gene catalogs by applying this principle to filter the entries.”

That peer-reviewed paper, in a leading journal, was well received (e.g., Larry Moran called it an “excellent study”) and it certainly appeared to be authoritative. So it is not surprising that Velasco would be confident about orphans. For all appearances, they really were no problem for evolution.

There was just one problem. This was all wrong.

There was no scientific evidence that those human sequences, identified as orphans, were “spurious.” The methods used in the Lander study were full of evolutionary assumptions. The results entirely hinged on evolution. Although the paper did not explicitly state this, without the assumption of evolution no such conclusions could have been made.

This is what philosophers refer to as theory-ladenness. Although the paper authoritatively concluded the vast majority of the orphans in the human genome were spurious, this was not an empirical observation or inference, as it might seem to some readers. Their data (and proposed revisions to human gene catalogs), methods, and conclusions were all laden, at their foundation, with the theory of evolution.

So Velasco’s argument was circular. To defend evolution he claimed there were zero orphans in the human genome, but that “fact” was a consequence of assuming evolution is true in the first place. If the assumption of evolution is dropped, then there is no evidence for that conclusion.


Since the Nelson-Velasco debate the orphan problem has just gotten worse. Consider, for example, brochosomes which are intricate, symmetric, secretory granules forming super-oily coatings on the integuments of leafhoppers. Brochosomes develop in glandular segments of the leafhopper’s Malpighian tubules.

The main component of brochosomes, as shown in a recent paper, is proteins. And these constituent proteins, as well as brochosome-associated proteins, are mostly encoded by orphan genes.

As the paper explains, most of these proteins “appear to be restricted to the superfamily Membracoidea, adding to the growing list of cases where taxonomically restricted genes, also called orphans, encode important taxon-specific traits.”

And how did all these orphan genes arise so rapidly? The paper hypothesizes that “It is possible that secreta exported from the organism may evolve especially rapidly because they are not strongly constrained by interactions with other traits.”

That evolutionists can so easily reach for just-so stories, such as this, is yet another example of how false predictions have no consequence for evolutionary theory. Ever since Darwin evolutionists have proclaimed how important it is that the species fall into the common descent pattern. This has especially been celebrated at the molecular level.

But of course the species fall into no such pattern, and when obvious examples present themselves, such as the brochosome proteins, evolutionists do not miss a step.

There is no empirical content to this theory. Predictions hailed as great successes and confirmations of the truth of evolution suddenly mean nothing and have no consequence when the falsification becomes unavoidable.

Religion drives science, and it matters.

h/t: El Hombre

Sunday, April 1, 2018

The Unauthorized Answers to Jerry Coyne’s Blog

What Your Biology Teacher Didn’t Tell You

Jerry Coyne’s website (Why Evolution Is True) has posed study questions for learning about evolution. Evolutionists have responded in the “Comment” section with answers to some of the questions (see here, here, and here). But when I posted a few relevant thoughts, they were quickly deleted after briefly appearing. That’s unfortunate because those facts can help readers to understand evolution. Here is what I posted:

Well the very first question is question begging:

“Why is the concept of homology crucial for even being able to talk about organic structure?”

It isn’t. We are “able to talk about organic structure” without reference to homology. In fact, if you are interested in biology, you can do more than mere talk. Believe it or not you actually can investigate how organic structure works, without even referencing homology. The question reveals the underlying non-scientific Epicureanism at work. This is not to say homology is not an important concept and area of study. Of course it is. But it is absurd to claim it is required even merely to talk about organic structure. Let’s try another:

“What is Darwin’s explanation for homology?”

Darwin’s explanation for homology is that it is a consequence of common descent. He repeatedly argues that homologous structures provide good examples of non-adaptive patterns as well as disutility, thus confirming common descent by virtue of falsifying the utilitarianism-laden doctrine of creation. See for example pp. 199-200, where Darwin concludes:

“Thus, we can hardly believe that the webbed feet of the upland goose or of the frigate-bird are of special use to these birds; we cannot believe that the same bones in the arm of the monkey, in the fore leg of the horse, in the wing of the bat, and in the flipper of the seal, are of special use to these animals. We may safely attribute these structures to inheritance.”

Pure metaphysics, and ignoring the enormous problem that non-adaptive patterns cause for evolutionary theory. Oh my. Well, let’s try another:

“How does Darwin’s account of serial homology (the resemblance of parts within an organism, for example, the forelimbs to the hindlimbs, or of a cervical vertebra to a thoracic vertebra) depend on the repetition of parts or segmentation?”

Hilarious. It’s a wonderful example of teleology, just-so-stories, and metaphysics, so characteristic of the genre, all wrapped up in a single passage (pp. 437-8). Darwin goes into a typical rant of how designs and patterns (serial homologies in this case) absolutely refute utilitarianism. “How inexplicable are these facts on the ordinary view of creation!,” he begins. Pure metaphysics.

He then provides a just-so story about how “we may readily believe that the unknown progenitor of the vertebrata possessed many vertebræ,” etc., and that like any good breeder, natural selection “should have seized on a certain number of the primordially similar elements, many times repeated, and have adapted them to the most diverse purposes.”

Seized on? Wow, that natural selection sure is good—long live Aristotelianism. Gotta love this mythology.

Monday, February 19, 2018

This Didn’t Evolve a Few Mutations At a Time

Action Potentials

Are there long, gradual, pathways of functional intermediate structures, separated by only one or perhaps a few mutations, leading to every single species, and every single design and structure in all of biology? As we saw last time, this has been a fundamental claim and expectation of evolutionary theory which is at odds with the science.* If one mutation is rare, a lot of mutations are astronomically rare. For instance, if a particular mutation has a one-in-a-hundred million (one in 10^8) chance of occurring in a new individual, then a hundred such particular mutations have a one in 10^800 chance of occurring. It’s not going to happen. Let’s have a look at an example: nerve cells and their action potential signals.

[* Note: Some evolutionists have attempted to get around this problem with the neutral theory, but that just makes matters worse].

Nerve cells have a long tail which carries an electronic impulse. The tail can be several feet long and its signal might stimulate a muscle to action, control a gland, or report a sensation to the brain.

Like a cable containing thousands of different telephone wires, nerve cells are often bundled together to form a nerve. Early researchers considered that perhaps the electronic impulse traveled along the nerve cell tail like electricity in a wire. But they soon realized that the signal in nerve cells is too weak to travel very far. The nerve cell would need to boost the signal along the way for it to travel along the tail.

After years of research it was discovered that the signal is boosted by membrane proteins. First, there is a membrane protein that simultaneously pumps two potassium ions into the cell and three sodium ions out of the cell. This sets up a chemical gradient across the membrane. There is more potassium inside the cell than outside, and there is more sodium outside than inside. Also, there are more negatively charged ions inside the cell so there is a voltage drop (50-100 millivolt) across the membrane.

In addition to the sodium-potassium pump, there are also sodium channels and potassium channels. These membrane proteins allow sodium and potassium, respectively, to pass through the membrane. They are normally closed, but when the decaying electronic impulse travels along the nerve cell tail, it causes the sodium channels to quickly open. Sodium ions outside the cell then come streaming into the cell down the electro-chemical gradient. As a result, the voltage drop is reversed and the decaying electronic impulse, which caused the sodium channels to open, is boosted as it continues on its way along the nerve cell tail.

When the voltage goes from negative to positive inside the cell, the sodium channels slowly close and the potassium channels open. Hence the sodium channels are open only momentarily, and now with the potassium channels open, the potassium ions concentrated inside the cell come streaming out down their electro-chemical gradient. As a result the original voltage drop is reestablished.

This process repeats itself as the electronic impulse travels along the tail of the nerve cell, until the impulse finally reaches the end of the nerve cell. Although we’ve left out many details, it should be obvious that the process depends on the intricate workings of the three membrane proteins. The sodium-potassium pump helps set up the electro-chemical gradient, the electronic impulse is strong enough to activate the sodium channel, and then the sodium and potassium channels open and close with precise timing.

How, for example, are the channels designed to be ion-selective? Sodium is about 40% smaller than potassium so the sodium channel can exclude potassium if it is just big enough for sodium. Random mutations must have struck on an amino acid sequence that would fold up just right to provide the right channel size.

The potassium channel, on the other hand is large enough for both potassium, and sodium, yet it is highly efficient. It somehow excludes sodium almost perfectly (the potassium to sodium ratio is about 10000), yet allows potassium to pass through almost as if there were nothing in the way.

Nerve cells are constantly firing off in your body. They control your eyes as you read these words, and they send back the images you see on this page to your brain. They, along with chemical signals, control a multitude of processes in our bodies, and there is no scientific reason to think they gradually evolved, one mutation at time.

Indeed, that idea contradicts everything we know from the science. And yet this is what evolutionists believe. Let me repeat that: evolutionists believe nerve cells and their action potential designs evolved one mutation at time. Indeed, evolutionists believe this is a proven fact, beyond all reasonable doubt.

It would be difficult to imagine a more absurd claim. So let’s have a look at the details of this line of thinking. Here is a recent paper from the Royal Society, representing the state of the art in evolutionary thinking on this topic. The paper claims to provide a detailed explanation of how early evolution produced action potential technology.

Sounds promising, but when evolutionists speak of “details,” they have something slightly different in mind. Here are several passages from the paper which reveal that not only is there a lack of details, but that the study is thoroughly unscientific.

We propose that the next step in the evolution of eukaryote DCS [membrane depolarization (through uncontrolled calcium influx), contraction and secretion] coupling has been the recruitment of stretch-sensitive calcium channels, which allow controlled influx of calcium upon mechanical stress before the actual damage occurs, and thus anticipate the effects of membrane rupture.

The recruitment of calcium channels? And exactly who did the recruiting? Here the authors rely on vague terminology to paper over a host of problematic details of just how random mutations somehow performed this recruiting.

To prevent the actual rupture, the first role of mechanosensory Ca++ channels might have been to pre-activate components of the repair pathway in stretched membranes.

“To prevent”? Let’s spell out the logic a little more clearly. The authors are hypothesizing that these calcium channels evolved the ability to pre-activate the repair pathway “to prevent” actual rupture. By spelling out the logic a bit more clearly, we can see more easily the usual teleology at work. The evolution literature is full of teleology, and for good reason. Evolutionists are unable to formulate and express their ideas without it. The ever-present infinitive form is the tell-tale sign. Aristotelianism is dead—long live Aristotelianism.

As another anticipatory step, actomyosin might have been pre-positioned under the plasma membrane (hence the cortical actomyosin network detected in every eukaryotic cell) and might have also evolved direct sensitivity to stretch … Once its cortical position and mechanosensitivity were acquired, the actomyosin network could automatically fulfil an additional function: cell-shape maintenance—as any localized cell deformation would stretch the cortical actomyosin network and trigger an immediate compensatory contraction. This property would have arisen as a side-effect (a ‘spandrel’) of the presence of cortical actomyosin for membrane repair, and quickly proved advantageous.

An “anticipatory step”? “Pre-positioning”? Actomyosin “evolved” sensitivity to stretch? The position and mechanosensitivity “were acquired”? The network could “fulfil an additional function”? Sorry, but molecular machines (such as actomyosin) don’t “evolve” anything. There is more teleology packed into these few sentences than any medieval tract. And for good measure the authors also add the astonishing serendipity that this additional function “would have arisen as a side-effect.” That was lucky.

Once covering the cell cortex, the actomyosin network acquired the ability to deform the cell by localized contraction.

The actomyosin network “acquired the ability” to deform the cell by localized contraction? Smart move on the part of the network. But may we ask just how did that happen?

Based on the genomic study of the protist Naegleria which has a biphasic life cycle (alternating between an amoeboid and a flagellated phase), amoeboid locomotion has been proposed to be ancestral for eukaryotes. It might have evolved in confined interstitial environments, as it is particularly instrumental for cells which need to move through small, irregularly shaped spaces by exploratory deformation.

Amoeboid locomotion evolved “as it is particularly instrumental.” No infinitive form but this is no less teleological. Things don’t evolve because they are “instrumental.” What the authors fail to inform their readers of is that this would require an enormous number of random mutations.

One can hypothesize that, if stretch-sensitive calcium channels and cortical actomyosin were part of the ancestral eukaryotic molecular toolkit (as comparative genomics indicates), membrane deformation in a confined environment would probably trigger calcium influx by opening of stretch-sensitive channels, which would in turn induce broad actomyosin contraction across the deformed part of the cell cortex, global deformation and cell movement away from the source of pressure.

The concept of a “molecular toolkit” is standard in evolutionary thought, and another example teleological thinking.

One can thus propose that a simple ancestral form of amoeboid movement evolved as a natural consequence of the scenario outlined above for the origin of cortical actomyosin and the calcium–contraction coupling; once established, it could have been further elaborated.

Amoeboid movement evolved “as a natural consequence,” and “once established” was “further elaborated”? This is nothing more than teleological story-telling with no supporting evidence.

It is thus tempting to speculate that, once calcium signalling had gained control over primitive forms of amoeboid movement, the same signalling system started to modify ciliary beating, possibly for ‘switching’ between locomotor states.

Calcium signaling “gained control” and then “started to modify” ciliary beating “for ‘switching’ between locomotor states”? The “for switching” is yet another infinitive form, and “gained control” is an active move by the calcium signaling system. Pure, unadulterated, teleology.

Possibly, in ancestral eukaryotes calcium induced a relatively simple switch (such as ciliary arrest, as still seen in many animal cells and in Chlamydomonas in response to high Ca++ concentrations), which was then gradually modified into more subtle modulations of beating mode with a fast turnover of molecular actors mediated by differential addition, complementation and loss.

“Calcium induced a relatively simple switch”? Sorry, ions don’t induce switches, simple or otherwise. And the switch “was then gradually modified into more subtle modulations”? Note how the passive voice obviates those thorny details. The switch “was modified” conveniently omits the fact that such modification would have to occur via random mutation, one mutation at a time.

Alternatively, control of cilia by calcium could have evolved convergently—but such convergence would then have been remarkably ubiquitous, as there seems to be no eukaryotic flagellum that is not controlled by calcium in one way or another.

“Could have evolved convergently”? And exactly how would that happen? At least the authors then admit to the absurdity of that alternative.

Unfortunately, they lack such sensibility for the remainder of the paper. As we saw above, the paper is based on a sequence of teleological thinking. It falls into the evolutionary genre where evolution is taken, a priori, as a given. This going in assumption underwrites vast stretches of teleological thought, and cartoon-level story telling. Not only is there a lack of empirical support, but the genre is utterly unscientific, as revealed by even a mildly critical reading.

And needless to say, the paper does absolutely nothing to alleviate the problem we began with. The many leaps of logic and reasoning in the paper reveal all manner of monumental changes evolution requires to construct nerve cells and the action potential technology. We are not looking at a narrative of minute, gradual changes, each contributing to the overall fitness. Many, many simultaneous mutations are going to be needed. Even a conservative minimum number of 100 simultaneous mutations leads to the untenable result of a one in 10^800 chance of occurring.

It’s not going to happen. Religion drives science, and it matters.

Saturday, February 10, 2018

Here is How Evolutionists Respond to the Evidence


Mutations are rare and good ones are even more rare. One reason mutations are rare is because there are sophisticated error correction mechanisms in our cells. So according to evolution random mutations created correction mechanisms to suppress random mutations. And that paradox is only the beginning. Because error correction mechanisms, as with pretty much everything else in biology, require many, many mutations to be created. If one mutation is rare, a lot of mutations are astronomically rare. For instance, if a particular mutation has a one-in-a-million (one in 10^6) chance of occurring in a new individual, then a hundred such particular mutations have a one in 10^600 chance of occurring. It’s not going to happen.

How do evolutionists reckon with this scientific problem?

First, one common answer is to dismiss the question altogether. Evolution is a fact, don’t worry about the details. Obviously this is not very compelling.

Second, another common answer is to cast the problem as a strawman argument against evolution, and appeal to gradualism. Evolutionists going back to Darwin have never described the process as “poof.” They do not, and never have, understood the process as the simultaneous origin of tens or hundreds, or more mutations. Instead, it is a long, slow, gradual process, as Darwin explained:

If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down. But I can find out no such case […] Although the belief that an organ so perfect as the eye could have been formed by natural selection, is enough to stagger any one; yet in the case of any organ, if we know of a long series of gradations in complexity, each good for its possessor, then, under changing conditions of life, there is no logical impossibility in the acquirement of any conceivable degree of perfection through natural selection

The Sage of Kent could find “no such case”? That’s strange, because they are ubiquitous. And with the inexorable march of science, it is just getting worse. Error correcting mechanisms are just one example of many. Gradualism is not indicated.

What if computer manufacturers were required to have a useful, functional electronic device at each step in the manufacturing process? With each new wire or solder, what must emerge is a “long series of gradations in complexity, each good for its possessor.”

That, of course, is absurd (as Darwin freely confessed). From clothing to jet aircraft, the manufacturing process is one of parts, tools, and raw materials strewn about in a useless array, until everything comes together at the end.

The idea that every single biological structure and design can be constructed by one or two mutations at a time, not only has not been demonstrated, it has no correspondence to the real world. It is just silly.

What evolution requires is that biology is different, but there is no reason to believe such a heroic claim. The response that multiple mutations is a “strawman” argument does not reckon with the reality of the science.

Third, some evolutionists recognize this undeniable evidence and how impossible evolution is. Their solution is to call upon a multiverse to overcome the evidence. If an event is so unlikely it would never occur in our universe, just create a multitude of universes. And how many universes are there? The answer is, as many as are needed. In other words, when confronted with an impossibility, evolutionist simply contrive a mythical solution.

Forth, another common response that evolutionists make is to appeal to the fitness of the structure in question. Biological designs, after all, generally work pretty well, and therefore have high fitness. Is this not enough to prove that it evolved? For evolutionists, if something helps, then it evolves. Presto.

To summarize, evolutionists have four different types of responses to the evidence, and none of the responses do the job.

Religion drives science, and it matters.

Saturday, January 27, 2018

Early Complexity: A Case Study of Evolutionary Theory

No Matter How Perplexing

Nature does not make jumps. That old canon of natural history, as Darwin called it, goes back centuries and was heartily endorsed and adopted by evolutionary theory. Here are representative quotes from Origin, 1st edition, explaining important this doctrine was to Darwin:

I have been astonished how rarely an organ can be named, towards which no transitional grade is known to lead. The truth of this remark is indeed shown by that old canon in natural history of "Natura non facit saltum." We meet with this admission in the writings of almost every experienced naturalist; or, as Milne Edwards has well expressed it, nature is prodigal in variety, but niggard in innovation. Why, on the theory of Creation, should this be so? [194]

On the theory of natural selection we can clearly understand the full meaning of that old canon in natural history, "Natura non facit saltum." This canon, if we look only to the present inhabitants of the world, is not strictly correct, but if we include all those of past times, it must by my theory be strictly true. [206]

The canon of "Natura non facit saltum" applies with almost equal force to instincts as to bodily organs. [210]

the canon in natural history, of "natura non facit saltum" is applicable to instincts as well as to corporeal structure, and is plainly explicable on the foregoing views, but is otherwise inexplicable,—all tend to corroborate the theory of natural selection. [243]

As natural selection acts solely by accumulating slight, successive, favourable variations, it can produce no great or sudden modification; it can act only by very short and slow steps. Hence the canon of "Natura non facit saltum," which every fresh addition to our knowledge tends to make more strictly correct, is on this theory simply intelligible. We can plainly see why nature is prodigal in variety, though niggard in innovation. But why this should be a law of nature if each species has been independently created, no man can explain. [471]

In these and other passages Darwin explained the fundamental evolutionary view and prediction that evolution and natural selection produce gradual change with no sudden changes or jumps.

At this point, more than a century and a half later, that fundamental prediction of evolution has been falsified so many times by the empirical evidence it is a wonder there is anyone left believing in the theory.

One way that this prediction has been falsified, among many, is in the finding of early complexity. Evolutionists of course expected that the history of life would reveal a gradual increase in complexity. But as I have discussed many times here, life does not fit this evolutionary expectation. Instead the very earliest life forms reveal high complexity.

For example, as science writer (and evolutionist) Amy Maxmen explains, Amoebas contain hundreds of times more DNA than humans, and this “just didn’t make sense.”

amoebas date back farther in time than humans, and simplicity is considered an attribute of primitive beings. It just didn’t make sense.

The amoeba versus human comparison was just one example of how genome size contradicts evolutionary theory. What about the number of genes? Here again, evolution makes a clear prediction, as Maxmen explains:

Simple, early organisms would have fewer genes than complex ones, they [evolutionists] predicted

And here again, the evolution prediction was demolished by the science. For example, evolutionists were surprised to find sea anemones have more genes than insects, in spite of arising earlier. That, admits Maxmen, “meant animals might have been genetically complex from the start.”

These sorts of findings also contradict the evolutionary tree. Your high school biology book said that the new genetic data perfectly corroborated the traditional morphological data. Evolutionists have triumphantly celebrated the confirmation that the molecular sequence data provided to pre-existing evolutionary trees.

But that celebration was premature. In fact, study after study have found there is no such corroboration. In fact, as I have documented many times, morphological data across the species contradict the evolutionary tree (i.e., they do not fall into an evolutionary common descent pattern), and the new molecular data simply continued that trend.

Then molecular analyses did something else. They rearranged the order of branches on evolutionary trees. Biologists pushed aside trees based on how similar organisms looked to one another, and made new ones based on similarities in DNA and protein sequences. The results suggested that complex body parts evolved multiple times and had also been lost.

In other words, the scientific data contradict the theory. The result is that evolutionists have had to concoct increasingly complex and bizarre epicycles to try to explain the data. This includes complex structures evolving, then disappearing, then re-evolving, all in the same lineage, as well as independently evolving in a separate lineage. As Maxmen explains:

Furthermore, the idea that complex parts like a brain and nervous system—including nerve cells, synapses, and neurotransmitter molecules—could evolve separately multiple times perplexes evolutionary biologists because parts are gained one at a time. The chance of the same progression happening twice in separate lineages seems unlikely—or so biologists thought.

This is a tautology. Whatever we observe, evolution somehow created it, no matter how ridiculous the narrative becomes. An unfair criticism? Consider Maxmen’s conclusion:

When new data suggests a rearrangement, it must be considered no matter how perplexing the conclusion seems.

In other words, the plausibility of evolution is not a consideration. No matter “how perplexing” are the data, we must find a way to force fit it into the theory.

Religion drives science, and it matters.

Tuesday, January 23, 2018

Embryonic Development Reveals Staggering Complexity

Oh My

I recently cited a paper on the evolution of embryonic development and how the evidence contradicts evolutionary theory and common descent. Even the evolutionists, though in understated terms, admitted there were problems. Evolutionary analyses are “reaching their limits,” it is difficult to “conclude anything about evolutionary origins,” genetic similarities “do not necessarily imply common ancestry,” and “conserved regulatory networks can become unrecognizably divergent.” In other words, like all other disciplines within the life sciences, embryonic development is not working. The science contradicts the theory.

But there is much more to the paper, and as a reader noticed, the authors give a rather blunt admission of the magnitude of the problem, not often seen in the literature:

One of the main reasons for Duboule’s pessimism about the return of the EvoDevo comet is the staggering complexity and diversity of cellular and developmental regulatory processes. The configuration space for realistic models of such systems is vast, high dimensional, and potentially infinitely complex.

Staggering complexity? Staggering diversity? The configuration space is vast and high-dimensional?

And it is potentially infinitely complex?

And we are to believe this is the product of random mutations?

Religion drives science, and it matters.

Sunday, January 21, 2018

About That RNA World Hypothesis

It Just Doesn’t Make Sense

Given its widespread popularity and acceptance you might not have realized that the so-called RNA-World hypothesis suffers from some dramatic problems. At the top of the list is the rather awkward fact that there is, err, no evidence for it. While skeptics have pointed this out for years, we now see evolutionists coming clean on this inconvenient truth as well. To wit, here is how Peter Wills and Charles Carter open their recent BioSystems paper:

The RNA World is a widely-embraced hypothetical stage of molecular evolution, devoid of protein enzymes, in which all functional catalysts were ribozymes. Only one fact concerning the RNA World can be established by direct observation: if it ever existed, it ended without leaving any unambiguous trace of itself.

Even this is a bit of an understatement. Because without the prior assumption of evolution, which can and has underwritten a wide range of speculation, there is precisely zero reason to believe this wild hypothesis. No organisms have ever been discovered that demonstrate the RNA World hypothesis in action. Nor have scientists ever constructed any such organisms in their laboratories. This is not too surprising because no one has even produced anything remotely close to a detailed design of how such organisms could function.

Wills and Carter also point out negative evidences such as catalysis (RNA enzymes lack the ability to function over a wide range of temperatures) and the “impossible obstacles” to the hypothetical yet necessary transition from the RNA World to something resembling today’s extant cells. As Carter explains:

Such a rise from RNA to cell-based life would have required an out-of-the-blue appearance of an aaRS [aminoacyl-tRNA synthetase]-like protein that worked even better than its adapted RNA counterpart. That extremely unlikely event would have needed to happen not just once but multiple times—once for every amino acid in the existing gene-protein code. It just doesn’t make sense.

Indeed, it just doesn’t make sense. And yet in spite of these obvious problems, the RNA World has been a textbook staple, presented as a plausible and likely example of how early life evolved.

Religion drives science, and it matters.

Friday, January 19, 2018

How Embryonic Development Bears on Evolution

Follow the Theory

In order for evolution to have occurred, the intricate embryonic development stages of species must have evolved. Indeed, the developmental pathways of the species would be crucial in such a process. If we are to believe the evolutionary claim that the species spontaneously arose, then untold embryonic development pathways must have somehow undergone massive change. But while evolutionists expected the study of such evolution of development to yield great insight into the evolutionary process and history, it has underwhelmed. This shortcoming is well known, as exemplified in this 2015 paper:

First, traditional comparative approaches to the evolution of development—whether focused on the morphological or on the molecular/genetic level—are reaching their limits in terms of explanatory power.

Except that this is an overstatement. To say that comparative approaches “are reaching their limits in terms of explanatory power” is to suggest that there was, at one time, some significant level of explanatory power provided. That would be a very optimistic interpretation of the data.

The paper continues:

The more we learn about the evolution of pattern-forming gene networks, or the ontogeny of complex morphological traits, the more it becomes clear that it is less than straightforward to conclude anything about evolutionary origins or dynamics based on such comparisons alone.

“Less than straightforward”? Let’s be clear—a more accurate descriptor would be “impossible.” In fact, the evidence does not reveal an evolutionary history, but rather is supported by the theory. Evolutionary theory does not follow the data, as Huxley prescribed, but rather the data follow the theory.

The paper continues:

On the one hand, homoplasy or convergent evolution abounds at all levels of investigation. One of the most lauded major insights of EvoDevo is that a common toolkit of genes and signaling pathways is reused over and over again to create a large diversity of different body plans, shapes, and organs.

Most lauded major insights? That would be the mother of all euphemisms. Evolutionists are always rationalizing devastating contradictions as teachable moments, and here we have yet another example. To cast the nonsensical finding of a “common toolkit” as a “major insight” is laughable.

This becomes clear as the paper continues:

Because of this, similarities in gene expression patterns or morphological structure often do not necessarily imply common ancestry, since they may as well reflect the frequent reuse of the same regulatory or morphogenetic modules.

Profound similarities “do not necessarily imply common ancestry.” We have now entered a Lewis Carroll world, as Sober would put it. The whole point of evolution was that such similarities revealed and mandated common descent. But now, we have the exact opposite, as similarities cannot be due to common descent, but must have arisen independently. And this is an “insight”? A fundamental prediction is demolished and evolutionists do not skip a beat. This is not science.

But it gets worse:

On the other hand, developmental system drift allows conserved networks to change considerably in terms of their component genes and regulatory interactions without changing the phenotypic outcomes such systems produce. This means that even functionally conserved regulatory networks can become unrecognizably divergent at the molecular and genetic level, especially across large evolutionary time spans.

We have now reached the height of absurdity. First, profound developmental similarities were found which could not be ascribed to common descent. Now we find that those developmental pathways which can (theoretically) be ascribed to common descent are profoundly different.

When will this bad dream end? The science contradicts the theory. Over. And over. And over. And over.

It never ends. Religion drives science, and it matters.

[h/t: El Hombre]