The “All Outcomes Are Equiprobable” Argument

I Had to Write “Evolution Is True” 500 Times

I’ve been busy lately with a big landscaping job for the neighborhood evolutionist. He wanted a massive set of stones to be carefully arranged in his backyard. He wanted stones of different colors, and the careful arrangement would spell out “Evolution Is True.”

Unfortunately, the day I finished this big job there was an earthquake in the neighborhood which jumbled the stones I had carefully arranged. I had to go back to the evolutionist’s property and put the stones back in order.

To makes matters worse, the evolutionist wouldn’t pay me for the job. When I sued him he told the judge that I was lying. He said I didn’t do the job, but instead the arrangement of the stones was due to the recent earthquake.

I explained to the judge that such an event would be unlikely, but the evolutionist retorted that landscapers don’t understand probability. The evolutionist explained to the judge that all outcomes are equally probable. Every outcome, whether it spells out “Evolution Is True” or nothing at all, have a probability of one divided by the total number of possible arrangements. He said that I was committing a mistake that is common with nonscientific and uneducated people. He explained that if you toss a coin 500 times the sequence of heads and tails will be astronomically unlikely. But it happened. All such sequences, even if they spell out a message in Morse code, are equiprobable.

The judge agreed. He fined me for bringing a frivolous lawsuit against the evolutionist and made me write “Evolution Is True” 500 times.

Finally, the Details of How Proteins Evolve

A Step-By-Step Description

How did proteins evolve? It is a difficult question because, setting aside many other problems, the very starting point—the protein-coding gene—is highly complex. A large number of random mutations would seem to be required before you have a functional protein that helps the organism. Too often such problems are solved with vague accounts of “adaptations” and “selection pressure” doing the job. But this week researchers at the University of Illinois announced ground-breaking research that provides a step-by-step, detailed, description of the evolution of a new protein-coding gene and associated regulatory DNA sequences. The protein in question is a so-called “antifreeze” protein that keeps the blood of Arctic codfish from freezing, and the new research provides the specific sequence of mutations, leading to the new gene. It would be difficult to underestimate the importance of this research. It finally provides scientific details answering the age-old question of how nature’s massive complexity could have arisen. As the paper triumphantly declares, “Here, we report clear evidence and a detailed molecular mechanism for the de novo formation of the northern gadid (codfish) antifreeze glycoprotein (AFGP) gene from a minimal noncoding sequence.” Or as lead researcher, professor Christina Cheng, explained, “This paper explains how the antifreeze protein in the northern codfish evolved.” This is a monumental finding. Having the scientific details, down to the level of specific mutations, of how a new protein-coding gene evolved—not from a related gene but from non-coding DNA—is something evolutionists could only dream of only a few short years ago. There’s only one problem: it is all junk science.

The first problem is that this new “research” is, in actuality, a just-so story:

In science and philosophy, a just-so story is an unverifiable narrative explanation for a cultural practice, a biological trait, or behavior of humans or other animals. The pejorative nature of the expression is an implicit criticism that reminds the hearer of the essentially fictional and unprovable nature of such an explanation. Such tales are common in folklore and mythology.

For example, the antifreeze protein is of relatively low complexity chiefly consisting a repeating sequence of three amino acids (threonine-alanine-alanine), and the evolutionists claim that these repeating sequences “strongly suggest” that the protein-coding gene “evolved from repeated duplications of an ancestral 9-nucleotide threonine-alanine-alanine-coding element.”

Why is that true?

Why does a repeating genetic sequence “strongly suggest” that it “evolved from repeated duplications?” What experiment revealed this truth? What evidence gives us this profound principle? The answer, of course, is that there is none. Nowhere do the evolutionists justify this claim because there is no empirical justification.

There is no scientific evidence for it. Zero.

The paper continues with yet more non-empirical claims. Those nine nucleotides “likely originated within a pair of conserved 27-nucleotide” segments that flank each side of the repetitive region. And these four 27-nucleotide segments are similar to each other, “indicating they resulted from the duplication of an initial copy.” As the paper concludes, “chance duplications” of an ancestral 27-nucleotide segment “produced four tandem copies.”

But why are those claims true? Why do such similarities imply an origin via evolutionary mechanisms? The problem is, they don’t. There is no empirical evidence for any of this. This is completely evidence-free.

The evolutionists next explain that the 9-nucleotide segment duplicated a large number of times because it worked well:

We hypothesize that, upon the onset of selective pressure from cold polar marine conditions, duplications of a 9-nt ancestral element in the midst of the four GCA-rich duplicates occurred.

The above quote is an example of the non-empirical, teleology that pervades evolutionary thought. It was upon the onset of cold conditions that the needed genetic duplications occurred. This is not empirical; this is story-telling.

The paper continues with a series of one-time, contingent events crucial to their story and non-empirical claims. The genetic sequence “was appropriately delimited by an existing in-frame termination codon.”

Appropriately delimited?

The presence of a region in two of the species “indicates that it existed in the gadid ancestor before the emergence of the AFGP.” The absence of a thymine nucleotide at a location in some of the species “very likely resulted from a deletion event,” causing a fortuitous frameshift which supplied the crucial signal peptide segment, telling cellular machinery that the protein should be secreted to the bloodstream. As the paper concludes, “the emerging AFGP gene was thus endowed with the necessary secretory signal.”

Endowed with the necessary signal?

There is no empirical evidence for any of this.

Another problem with this just-so account, is the substantial level of serendipity required. The new antifreeze protein did not arise from some random DNA sequence, but rather from crucial, preexisting segments of DNA that just happened to be lying around. In other words, the fish were facing a colder environment, they needed some antifreeze in their blood, and the pieces needed for such an antifreeze gene were fortuitously available.

The authors hint at this serendipity when they conclude that their story of how this protein evolved is an example of “evolutionary ingenuity.”

Evolutionary ingenuity?

The press release is even more revealing. Cheng admits that the evolution of this gene “occurred as a result of a series of seemingly improbable, serendipitous events.” For “not just any random DNA sequence can produce a viable protein.” Furthermore, in addition to the gene itself, “several other serendipitous events occurred.”

The DNA was “edited in just the right way,” and “somehow, the gene also obtained the proper control sequence that would allow the new gene to be transcribed into RNA.”

Even the evolutionists admit to the rampant serendipity. Nonetheless they are triumphant, for “the findings offer fresh insights into how a cell can invent ‘a new, functional gene from scratch.’”

Fresh insights?

In actuality the findings arose from a series of non-empirical claims.

Religion drives science, and it matters.

Centrobin Found to be Important in Sperm Development

Numerous, Successive, Slight Modifications

Proteins are a problem for theories of spontaneous origins for many reasons. They consist of dozens, or often hundreds, or even thousands of amino acids in a linear sequence, and while many different sequences will do the job, that number is tiny compared to the total number of sequences that are possible. It is a proverbial needle-in-the-haystack problem, far beyond the reach of blind searches. To make matters worse, many proteins are overlapping, with portions of their genes occupying the same region of DNA. The same set of mutations would have to result in not one, but two proteins, making the search problem that much more tricky. Furthermore, many proteins perform multiple functions. Random mutations somehow would have to find those very special proteins that can perform double duty in the cell. And finally, many proteins perform crucial roles within a complex environment. Without these proteins the cell sustains a significant fitness degradation. One protein that fits this description is centrobin, and now a new study shows it to be even more important than previously understood.

Centrobin is a massive protein of almost a thousand amino acids. Its importance in the division of animal cells has been known for more than ten years. An important player in animal cell division is the centrosome organelle which organizes the many microtubules—long tubes which are part of the cell’s cytoskeleton. Centrobin is one of the many proteins that helps the centrosome do its job. Centrobin depletion causes “strong disorganization of the microtubule network,” and impaired cell division.

Now, a new study shows just how important centrobin is in the development of the sperm tail. Without centrobin, the tail, or flagellum, development is “severely compromised.” And once the sperm is formed, centrobin is important for its structural integrity. As the paper concludes:

Our results underpin the multifunctional nature of [centrobin] that plays different roles in different cell types in Drosophila, and they identify [centrobin] as an essential component for C-tubule assembly and flagellum development in Drosophila spermatogenesis.

Clearly centrobin is an important protein. Without it such fundamental functions as cell division and organism reproduction are severely impaired.

And yet how did centrobin evolve?

Not only is centrobin a massive protein, but there are no obvious candidate intermediate structures. It is not as though we have that “long series of gradations in complexity” that Darwin called for:

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.

Unfortunately, in the case of centrobin, we do not know of such a series. In fact, centrobin would seem to be a perfectly good example of precisely how Darwin said his theory could be falsified:

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.  

Darwin could “find out no such case,” but he didn’t know about centrobin. Darwin required “a long series of gradations,” formed by “numerous, successive, slight modifications.”

With centrobin we are nowhere close to fulfilling these requirements. In other words, today’s science falsifies evolution. This, according to Darwin’s own words.

Religion drives science, and it matters.

New 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.

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.

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.

Here is How Evolutionists Respond to the Evidence

Unresponsive

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.

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.

Protein Mutations Are Highly Coupled

A Rugged Fitness Landscape

A new study from Michael Harms’ laboratory at the University of Oregon finds that potential amino acid substitutions in protein sequences are highly coupled. That is, if one residue mutates to a new amino acid, the swap impacts the other possible substitutions—they now have a different impact on the protein tertiary structure. As the paper explains:

Proteins exist as ensembles of similar conformations. The effect of a mutation depends on the relative probabilities of conformations in the ensemble, which in turn, depend on the exact amino acid sequence of the protein. Accumulating substitutions alter the relative probabilities of conformations, thereby changing the effects of future mutations. This manifests itself as subtle but pervasive high-order epistasis. Uncertainty in the effect of each mutation accumulates and undermines prediction. Because conformational ensembles are an inevitable feature of proteins, this is likely universal.

This coupling leads to a “profound unpredictability in evolution,” and the authors conclude that “detailed evolutionary predictions are not possible given the chemistry of macromolecules.”

This finding seems to confirm what many evolutionists have said for decades—that evolution is a contingent, not law-like, process:

These [macro]evolutionary happenings are unique, unrepeatable, and irreversible.” – Theodosius Dobzhansky, 1957.

Laws and experiments are inappropriate techniques” for explaining evolutionary events and processes. – Ernst Mayr

What science needs are “plausible scenarios for a fully material universe, even if those scenarios cannot be currently tested.” – Victor Stenger, 2004

any replay of the tape would lead evolution down a pathway radically different from the road actually taken. – Stephen Jay Gould

All of this is in direct contradiction to the science, which reveals undeniable patterns in biology that have been repeated over and over. From the pervasive instances of convergence, recurrence, and all kinds of other “ence’s”, to the non adaptive patterns discussed by Michael Denton, the biological is anything but haphazard or random. Clearly, the same solution, for whatever reason, is used repeatedly across a wide range of species, in various patterns.

This is a clear falsification of an evolutionary expectation expressed across many years, and widely held by a consensus of experts.

But there is another problem with these protein findings. In addition to confirming the complexity and coupling of protein folding, the findings also seem to corroborate what theoretical and experimental studies have shown for years, that the fitness landscape of macromolecules in general, and proteins in particular, is rugged.

The problem of evolving a protein is difficult for several reasons. First, protein function drops off rapidly with only a few mutations. Very quickly a protein loses its function as you move away from the native sequence.

Second, random or starting sequences are stuck in a flat and rugged fitness landscape. There is little sign of a the kind of smooth and gradually increasing fitness landscape that would aid evolution’s enormous task of figuring out how proteins could evolve.

These problems are just getting worse, and this new finding a good example of that trend.

Religion drives science, and it matters.

Blindness in Cave Fish is Due to Epigenetics

Evolutionists Say “We See”

A recent paper out of Brant Weinstein’s and William Jeffery’s laboratories on eye development, or the lack thereof, in blind cave fish has important implications for evolutionary theory (paper discussed here). The study finds that the loss of eyes in fish living in dark Mexican caves is not due to genetic mutations, as evolutionists have vigorously argued for many years, but due to genetic regulation. Specifically, methylation of key development genes represses their expression and with it eye development in this venerable icon of evolution. But the finding is causing yet more problems for evolutionary theory.

Darwin appealed to the blind cave fish in his one long argument for evolution. It is a curious argument in many ways, and the first sign of problems was in Darwin’s presentation where he flipped between two different explanations. At one point he explained the loss of vision in the cave fish as an example of evolutionary change not due to his key mechanism, natural selection. Instead, the Sage of Kent resorted to using the Lamarckian mechanism or law of “use and disuse.” Privately Darwin despised and harshly criticized Lamarck, but when needed he occasionally employed his French forerunner’s ideas.

Elsewhere Darwin hit upon a natural selection-based mechanism for the blind cave fish, explaining that elimination of the costly and unneeded vision system would surely raise the fitness of the hapless creatures.

This latter explanation would become a staple amongst latter day evolutionary apologists, convinced that it mandates the fact of evolution. Anyone who has discussed or debated evolutionary theory with today’s Epicureans has likely encountered this curious argument that because blind cave fish lost their eyes, therefore the world must have arisen by itself.

Huh?

To understand the evolutionary logic, or lack thereof, one must understand the history of ideas, and in particular the idea of fixity, or immutability, of species. According to evolutionists, species are either absolutely fixed in their designs, or otherwise there are no limits to their evolutionary changes and the biological world, and everything else for that matter, spontaneously originated.

Any evidence, for any kind of change, no matter how minor, is immediately yet another proof text for evolution, in all that the word implies.

Of course, from a scientific perspective, the evidence provides precisely zero evidence for evolution. Evolution requires the spontaneous (i.e., by natural processes without external input) creation of an unending parade of profound designs. The cave fish evidence shows the removal, not creation, of such a design.

The celebration of such evidence and argument by Darwin and his disciples reveals more about evolutionists than evolution. That they would find this argument persuasive reveals their underlying metaphysics and the heavy lifting it performs. It is all about religion.

We are reminded of all this with the news of Weinstein’s new study. But we also see something new: The insertion, yet again, of Lamarck into the story. The irony is that the epigenetics, now revealed as the cause of repressed eye development in the cave fish, hearkens back to Lamarck.

Darwin despised Lamarck and later evolutionists made him the third rail in biology. Likewise they have pushed back hard against the scientific findings of epigenetics and their implications.

The environment must not drive biological change.

False.

Well such biological change must not be transgenerational.

False.

Well such inheritance must not be long lasting, or otherwise robust.

False again.

This last failure is revealed yet again in the new blind cave fish findings.

False predictions count. A theory that is repeatedly wrong, over and over, in all of its fundamental expectations, will eventually be seen for what it is.

The rise of epigenetics is yet another such major failure. Evolutionists pushed back against it because it makes no sense on the theory, and that means it cannot now be easily accommodated.

One problem is that epigenetics is complex. The levels of coordination and intricacy of mechanism are far beyond evolution’s meager resources.

It’s not going to happen.

Another problem is the implied serendipity. For instance, one epigenetic mechanism involves the molecular tags places on the tails of the DNA packing proteins called histones. While barcoding often seems to be an apt metaphor for epigenetics, the tagging of histone tails can influence the histone three dimensional structures. It is not merely an information-bearing barcode. Like the tiny rudder causing the huge ship to change course, the tiny molecular tag can cause the much larger packing proteins to undergo conformational change, resulting in important changes in gene accessibility and expression.

This is all possible because of the special, peculiar, structure and properties of the histone protein and its interaction with DNA. With evolution we must believe this just happened to evolve for no reason, and thus fortuitously enabled the rise of epigenetics.

Another problem with epigenetics is that it is worthless, in evolutionary terms that is. The various mechanisms that sense environmental shifts and challenges, attach or remove one of the many different molecular tags to one of the many different DNA or histone locations, propagate these messages across generations, and so forth, do not produce the much needed fitness gain upon which natural selection operates.

The incredible epigenetics mechanisms are helpful only at some yet to be announced future epoch when the associated environmental challenge presents itself. In the meantime, selection is powerless and according to evolution the incredible system of epigenetics, that somehow just happened to arise from a long, long series or random mutations, would wither away with evolution none the wiser.

These are the general problems with epigenetics. In the case of the blind cave fish, however, there is possible explanation. It is a longshot, but since this case specifically involves the loss of a stage of the embryonic development, evolutionists can say that genetic mutations caused changes in the methylating proteins, causing them to be overactive.

This explanation relies on the preexistence of the various epigenetic mechanisms, so does not help to resolve the question of how they could have evolved. What the explanation does provide is a way for evolutionists to dodge the bullet presented by the specter of the cave fish intelligently responding to an environmental shift.

Such teleology in the natural world is not allowed.

So the evolutionary prediction is that these proteins will be found to have particular random changes causing an increase in their methylation function, in particular at key locations in key genes (i.e., the genes associated eye development).

That’s a long shot, and an incredible violation of Occam’s Razor.

My predictions are that (i) this evolutionary prediction will fail just as the hundreds that came before, and (ii) as with those earlier failures, this failure will do nothing to open the evolutionist’s eyes.

Religion drives science, and it matters.

World’s Oldest Tree is World’s Most Complex Tree

Makes Perfect Sense

We have often discussed the problem of “early complexity,” and how as we peer back in time—whether in the geographic strata or by phylogenetic reconstruct—things don’t get simpler. This makes no sense on evolution and this week’s news of a fossil specimen in northwest China, revealing and ancient, and highly complex, tree, just makes it worse. As one of the authors admitted:

This raises a provoking question: why are the very oldest trees the most complicated?

Fortunately evolution is a fact.

The National Association of Biology Teachers Versus the Ribosome

A Fascinating Dissonance

Theodosius Dobzhansky famously wrote in 1973 that “Nothing in Biology Makes Sense Except in the Light of Evolution.” That phrase has since become a staple amongst evolutionists. It appears throughout the literature, from popular works to journal papers, and it motivates the view that evolution is fundamental. Students must learn biology through the lens of evolution. Researchers must formulate experiments from a Darwinian perspective. Medical students must understand the human body as the result of evolution, and so forth. As the National Association of Biology Teachers explains:

The frequently-quoted declaration of Theodosius Dobzhansky that “Nothing in biology makes sense except in the light of evolution” accurately reflects the central, unifying role of evolution in the science of biology. … Just as nothing in biology makes sense except in the light of evolution, nothing in biology education makes sense without reference to and thorough coverage of the principle and mechanisms provided by the science of evolution. Therefore, teaching biology in an effective, detailed, and scientifically and pedagogically honest manner requires that evolution be a major theme throughout the life science curriculum both in classroom discussions and in laboratory investigations. … Biology educators at all levels must work to encourage the development of and support for standards, curricula, textbooks, and other instructional frameworks that prominently include evolution and its mechanisms

Clearly the NABT thinks highly of Dobzhansky’s phrase and it draws some fairly important conclusions from it. But there is one slight problem: Dobzhansky’s phrase is unequivocally false.

Is it really true that nothing in biology makes sense except with evolution? No it is not as I have discussed many times (here, here, here, here, here, here, here, here, and here). Dobzhansky’s phrase is equivalent to: “Everything in biology only makes sense in light of evolution,” or “If-and-only-if evolution is true, then will we find what we find in biology.” In its logical form, Dobzhansky’s phrase is clearly not even scientific. Indeed, the phrase comes from the title of a paper which appeared in the American Biology Teacher, the official journal of the National Association of Biology Teachers, and in that paper Dobzhansky gave a litany of theological arguments that mandated evolution.

But it gets worse. Not only is this famous phrase a theological claim, it also fails the test of comparative anatomy. For example, consider the various types of echolocation found in different species of bats. As I have discussed (here, here, and here), the echolocation designs do not fit the expected evolutionary pattern. In other words, here we have something in biology that does not make sense with evolution. Evolution does not help to explain what we observe, instead with evolution we must resort to ad hoc stories. As one paper concluded:

the animal’s habitat is often more important in shaping its [echolocation] call design than is its evolutionary history

If you want to understand a bat’s echolocation design, look to its habitat, not its supposed evolutionary history. The scientific evidence makes no sense on the theory of evolution.

Or again, consider how glycan molecules compare across the different species. Again, it isn’t according to the evolutionary model (see here). As one paper explained, glycans show “remarkably discontinuous distribution across evolutionary lineages,” for they “occur in a discontinuous and puzzling distribution across evolutionary lineages.” This dizzying array of glycans can be (i) specific to a particular lineage, (i) similar in very distant lineages, (iii) and conspicuously absent from very restricted taxa only. The patterns contradict what evolution expected. As another paper admitted:

There is also no clear explanation for the extreme complexity and diversity of glycans that can be found on a given glycoconjugate or cell type. Based on the limited information available about the scope and distribution of this diversity among taxonomic groups, it is difficult to see clear trends or patterns consistent with different evolutionary lineages.

In other words, the glycans make no sense on evolution.

Echolocation and the glycans are but two examples. There are many, many more examples where they came from. The biological world is full of patterns of comparative anatomy across different species which make no sense on evolution.

But it gets worse.

It is not just comparative anatomy where the evidence fails to make sense on evolution. In design after design, what we observe in biology does not reflect contingency, as Darwin and later evolutionists predicted, but functional need. In fact, the designs we find are highly efficient and optimal in various ways. To cite just one example of a great many, consider the work of William Bialek.

Bialek discusses compound eyes of insects such as the fly. These compound eyes have a large number of small lenses packed into an array. A large number of small lenses gives high resolution, just as does a digital camera with a large number of pixels.

But when the lens becomes too small its optics become distorted due to diffraction. So in determining the best lens size there is a tradeoff between resolution and diffraction. In the optimum solution the lens size is roughly proportional to the square root of the radius of the head. And indeed, Bialek shows an old paper surveying the compound eye designs in more than two dozen different insects. That paper shows that for the different size insects, the lens size is proportional, as predicted, to the square root of the head size.

This is one of Bialek’s half a dozen or so examples showing the optimization of biological designs and, as Bialek assures us that there are many, many more. Here is how one science writer explained it:

Yet for all these apparent flaws, the basic building blocks of human eyesight turn out to be practically perfect. Scientists have learned that the fundamental units of vision, the photoreceptor cells that carpet the retinal tissue of the eye and respond to light, are not just good or great or fabulous at their job. They are not merely exceptionally impressive by the standards of biology, with whatever slop and wiggle room the animate category implies. Photoreceptors operate at the outermost boundary allowed by the laws of physics, which means they are as good as they can be, period. Each one is designed to detect and respond to single photons of light — the smallest possible packages in which light comes wrapped.

And where did those “apparent flaws” come from? Evolutionists of course. From an evolutionary perspective, vision systems were full of “flaws.” But in fact those systems were optimized—we just had to stop looking at biology in terms of evolution.

This brings us to the protein synthesis machine—the ribosome. A paper from last month out of Johan Paulsson’s laboratory elaborates on several of the ribosome’s highly efficient, or optimal, design features. Ribosomes are comprised of both protein and RNA molecules, and their proteins make up a sizable fraction of the total protein content of many cells. Cells contain many ribosomes, and naturally in order for the cell to duplicate, the ribosomes must be duplicated. This means a lot of protein synthesis must take place, in order to create all the proteins in all the ribosomes.

One way to help alleviate this production problem would be to have yet more ribosomes in the cell. But that would, in turn, create an even greater protein synthesis burden, since even more proteins would be needed for those additional ribosomes. One way to solve this conundrum is to use RNAs in ribosomes rather than proteins, where possible.

It is a fascinating problem, and the paper concludes that we can understand the solution not as the result of evolutionary contingencies, but as a solution to a functional need:

Rather than being relics of an evolutionary past, the unusual features of ribosomes may reflect an additional layer of functional optimization that acts on the collective properties of their parts.

These are but a few examples and there are many more showing that evolution is by no means required to understand biology. Indeed, evolution is usually redundant—a “multiplied entity” in the language of Ockam’s Razor.

There is no question that Dobzhansky famous phrase has failed. It simply is not true that “Nothing in Biology Makes Sense Except in the Light of Evolution.” Indeed, it would be difficult to imagine a perspective more at odds with the science of biology. But while a few rare voices, such as Massimo Pigliucci, admit that the phrase is “patently wrong,” evolutionists for the most part continue to rehearse the famous phrase in robotic fashion, revealing an underlying agenda that has strayed badly from the science.

Evolutionists are so heavily invested in Dobzhansky’s phrase they will never admit it has failed. Even Pigliucci soft-pedaled the problem, explaining that “Dobzhansky was writing for an audience of science high school teachers,” as though it is OK to misrepresent science to high school teachers. Also, Pigliucci’s admission was limited to the fact that spectacular progress has occurred in the life sciences while ignoring evolutionary theory. True enough, and that certainly demolishes Dobzhansky’s phrase, but it is only the tip of the iceberg. It is a safe criticism that avoids the more damning problems.

There simply is too much at stake here. It isn’t like admitting that a particular prediction went wrong. Dobzhansky’s phrase was not merely a prediction, it was meta-prediction—the rallying cry of the entire world view—and walking it back in any genuine way would be to reveal the man behind the curtain. Suddenly all those epistemological claims, such as that evolution is as much a fact as is gravity, heliocentrism and the round shape of the earth, would be left hanging, open to scrutiny and with a long, long way to fall.

The National Association of Biology Teachers’ holding up of Dobzhansky’s phrase reveals the underlying, nonscientific dogma at work. We are seeing a fascinating dissonance and hypocrisy, for the phrase is unequivocally false and yet it cannot be abandoned.

A demonstrably false claim is feverishly held up as true. Religion drives science, and it matters.

Subcellular Map of the Human Proteome Reveals “Highly Complex Architecture”

A High Degree of Regulation and Control

New research is using antibodies to map out the spatio-temporal locations of 12,003 different proteins in human cells. The results are another example of how, as Bruce Alberts put it in 1998: “We have always underestimated cells.” Alberts explained how cells were once naively viewed as something of a random affair, where molecules “were thought to diffuse freely, randomly colliding.” The new research reveals the “the highly complex architecture of the human cell” and adds more detail to the fact that the workings of the cell are far from random:

A total of 12,003 proteins targeted by 13,993 antibodies were classified into one or several of 30 cellular compartments and substructures, altogether defining the proteomes of 13 major organelles.

Although evolutionists “thought the cell was so simple,” this research is showing that the “cellular proteome is compartmentalized and spatiotemporally regulated to a high degree.” In fact “[m]ore than half of these 12,003 proteins localize in more than one compartment at the same time.” This is consistent with the fact that most proteins are capable of performing multiple functions, and is another indicator of high complexity:

Moreover, proteins that localize to more than one compartment may have context-specific functions, increasing the functionality of the proteome. The fact that proteins “moonlight” in different parts of the cell is now well accepted. … The more complex a system is, the greater the number of parts that must be sustained in their proper place, and the lesser the tolerance for errors; therefore, a high degree of regulation and control is required.

Indeed, the degree of regulation and control required for this system is not only enormous, but contrary to evolutionary expectations.

New Book: Olfactory Receptor Genes Prove Common Descent

The “Shared Error” Argument

We have seen that a new evolution book co-authored by evolutionist Dennis Venema and Scot McKnight is influenced by the mythical Warfare Thesis (here and here) and makes erroneous arguments that the fossils and echolocation support evolution (here and here). We now move on to another topic: broken genes, or pseudogenes. This is a popular argument amongst evolutionists and Venema uses as his example the olfactory receptor genes. The idea here is that, in different species (such as the human and chimpanzee), the same damaging mutation can be found in the same pseudogenes. When we find the same strange spelling mistake in the homework of different students we conclude that plagiarism occurred. It is more likely that the mistake had one source, rather than occurred twice, independently. Likewise, the same mutation in different species points to a single source in a common ancestor—common descent. Furthermore, we don’t see mutations that violate the expected pattern. Clearly common descent is the obvious, most parsimonious explanation. As Venema concludes, common descent is “overwhelmingly supported.” [36] This is a powerful argument for evolution that has influenced many people. There’s only one problem: It fails historically, philosophically, and scientifically.

First, the olfactory system is profoundly complex. Odors entering the nose interact with finely-tuned receptor proteins (created from the olfactory receptor genes), setting off an incredible cascade of events in the cell, resulting in an electrical signal sent to the brain. Studies have found that each cell expresses only a single olfactory receptor gene, and so is sensitive to a particular odor. At the brain, the signals are grouped and organized by odor. In other words, for all the cells in the nose expressing the same olfactory receptor gene (and thus sensitive to the same odor), their signals spatially converge as they feed into the brain area.

And of course, as with all the senses, These incoming signals are providing mere electrical information. There is no odor, or light, or sound entering the brain via these nerve cells. Instead, a bunch of electrical signals are entering the brain via these nerve cells. The brain, by itself, has no way of knowing what these electrical signals mean. It must somehow be given the source and meaning of these incoming signals. It then processes and interprets these signals and the end result is that we are conscious of images reported by our eyes, sounds reported by our ears, smells reported by our nose, and so forth. All of this defies evolution, and should give us pause.

Second, the evolutionist’s contention that common descent is needed to explain those shared mutations in different species contradicts the most basic biology. Simply put, similarities across species which cannot be explained by common descent, are rampant in biology. The olfactory system is no exception. Its several fundamental components, if evolution is true, must have evolved several times independently. The level of independent origin which evolutionists must admit to (variously referred to as convergent evolution, parallel evolution, recurrent evolution, cascades of convergence, and so forth depending on the pattern) is staggering and dwarfs the levels of similarities in the olfactory receptor genes. To cast those relatively few similarities as mandates for common descent, while ignoring the volumes of similarities that violate common descent constitutes the mother of all confirmation biases.

Third, the strength of this evolution argument is lack of function, but that renders it fallacious. As lawyers know, if you can’t convict the defendant on the facts, you decry how horrifying the crime is. In this case, the entire argument hinges on the utter uselessness of the broken genes. As Venema explains, they are “damaged,” “defective,” “mess[ed] up,” “wrong,” and “ruin[ed].” Clearly, according to Venema, these genes are useless—that’s why they are called pseudogenes. This is crucial because, for evolutionists, this means they would only arise by chance (what designer would implement useless designs?).

All of this means that evolutionists have a very simple formulation: Either those crippling mutations arose once in a common ancestor, or they just happened to arise by chance, coincidentally, multiple times. Clearly the former is much more likely, and this points to common descent. It is, as Venema concludes, “overwhelmingly supported.” [36]

But this powerful argument comes at a cost. There is no free lunch.

The conclusion that common descent is “overwhelmingly supported” utterly depends on our knowing the pseudogenes are useless. Disutility underwrites the assumption of chance as the only alternative to common descent. And chance as the only alternative is crucial. It is why the argument is so powerful, because the chance hypothesis is so unlikely.

Restricting the problem to a contest between evolution and chance makes evolution the obvious winner, but amidst the celebration we forget the weak link. We forget that the entire edifice resides on our certainty of disutility. This, it turns out, is a very weak link.

The history of evolutionary thought, going back to the Epicureans, is full of predictions of disutility gone wrong. It is, quite literally, a theory of gaps. When gaps in our scientific knowledge leave us with ignorance about function, evolutionists routinely assume there is no function. After all, if the world arose by chance, it should be a claptrap, full of aimless, useless designs, if they could even be called that.

But as those gaps close with the inexorable march of scientific progress, it seems we inevitably learn of function. Evolutionists are consistently claiming disutility at brand new findings, only to be proved wrong, again and again. Look no further than the seemingly endless parade of “We thought it was junk, but now …” stories.

Ultimately, the long history of disutility claims are informed by the theory rather than the evidence. This is a classic example of what philosophers refer to as theory-laden observations.

None of this means there are no truly useless structures in biology. There may well be plenty of them. But it has a terrible history.

Furthermore, regardless of the history, disutility is very difficult to know. As with the proverbial “proving a negative,” proving that a pseudogene, or anything else in biology for that matter, actually is useless, is a very difficult undertaking.

From introns to transposons, initial claims of uselessness have given way to a steady stream of findings of function. And, yes, the olfactory receptor “pseudo” genes are no exception. They are now being called pseudo-pseudogenes because all those evolutionary claims of uselessness are rapidly fading. As one recent paper concluded, “such ‘pseudo-pseudogenes’ could represent a widespread phenomenon.”

This is yet another example in a long history of failed disutility predictions. Clearly, the assumption that we know that olfactory receptor pseudogenes are useless is unfounded. Even the name (pseudogenes) will serve future generations of scientists as a constant reminder of this evolutionary foible. Venema’s powerful argument was demolished before the book was even published.

The story does not end here for even if something like pseudogenes could somehow be proven useless, this would not justify the evolutionary formulation of random chance origin as the only other alternative.

Evolution fails to explain how even a single gene could evolve, let alone the entire olfactory system. In fact the presence of supposedly useless structures, such as pseudogenes, is hardly a plus for evolution. As Elliott Sober has pointed out, there is nothing about this story that provides a positivistic argument for evolution.

The argument, and all its strength, hinges entirely on the refutation of the alternative. This is a proof by the process of elimination. Hence it becomes utterly crucial that the alternatives are carefully and exhaustively considered. In particular, all possible alternatives must be known, understood, evaluated, and disproved.

Do you see a pattern here?

This powerful evolutionary argument not only crucially depends on knowing that the pseudogenes are useless, it also crucially depends on knowing that a simple random chance model is the only alternative to evolution, for their origin.

Not only is this philosophically problematic (how do we know that the random chance model is the only alternative?), historically it has a terrible track record. As Kyle Stanford has shown, the history of science is full of theories that were advocated with this type of contrastive reasoning (by disproving a perceived alternative), only later to fail because the assumed alternative was wrong.

To summarize, this highly influential, popular, argument from similar structures that appear to be useless, lies in ruins. It is a disaster. It fails historically, philosophically, and scientifically. It should never have been used in the first place, for its scientific failure was entirely predictable from both the history and philosophy of science.

New Evolution Book: Echolocation Solved

Just Add Water

We have seen that a new evolution book co-authored by evolutionist Dennis Venema is influenced by the mythical Warfare Thesis (here and here) and makes erroneous arguments that the fossil evidence supports evolution (here). Regarding the Warfare Thesis the book propagates the false history that the basic issue of the seventeenth century Galileo Affair was “the veracity of the new science, and its perceived threat to biblical authority.” As we saw, this is the false, evolutionary rendition of history. The Warfare Thesis is a myth, and the Galileo Affair is perhaps the favorite example for evolutionists. Regarding the fossil evidence (which reveals species appearing abruptly in the strata), the book makes two erroneous arguments: that evolution is needed for science to work at all (the “intellectual necessity” philosophical argument) and the use of random design as the alternative to evolution (a theological argument). Now we move on to another topic: echolocation. This was of particular interest to me since I have used echolocation as an example of how evolution fails, and fails badly. When I saw that Venema appealed to echolocation to argue for evolution I was interested to see what he had to say. I am always looking for good arguments for evolution, but I did not find one here. Below I summarize the five different reasons why echolocation destroys evolution. Finally, I turn to Venema’s argument, if it can be called that. What we will see is that his argument utterly fails. Venema fails to address any of the problems with echolocation, and he fails to present any kind of a positive case that might be used to overcome the many problems. In short, it is a complete disaster.

Complexity: The original sonar technology

Most people are familiar with the concept of radar and sonar. Simply put, a reflected signal is used to track a target. But what most people are less familiar with are the many details and complications any radar or sonar system must reckon with. For example, the transmitted pulse must be very strong because it will weaken as the square of the distance it travels, and only a tiny fraction of it will be reflected. Ultimately, the return signal is very weak, so while the receiver is exposed to the very powerful transmitted signal, it must then detect a return signal many orders of magnitude weaker. Think of shouting as loud as you can, and then listening for the echo off of a mosquito.

This is just the beginning of the many sonar design issues. The pulse rate, duration, intensity, pitch are all design parameters that influence how small a target can be detected, how far away it can be detected, how accurately it can be tracked and resolved, and so forth. An advanced sonar design can vary these parameters to optimize the tracking.

Sonar design must also consider how to compensate for target motion and the resulting Doppler effect, erroneous reflections from clutter in the environment, and how to guide toward a moving target. There is also the possibility of imaging to determine what type of target it is.

Not surprisingly, there are many different sonar design strategies. Depending on the clutter environment, typical types of targets, and so forth, various design strategies might work better.

All of this is what we find in nature’s echolocation designs. Whales and bats have incredibly efficient and accurate tracking capabilities. We have developed sonar, but nature had it all along—the original sonar technology. In fact nature’s designs are better than our military equipment. Which is one reason why they are studied so closely.

Complexity at the molecular level

We have seen how complicated echolocation can be. Not surprisingly the molecular machines that help to make it happen are also highly complex. Prestin, a protein important in mammalian hearing, is a transmembrane protein in the outer hair cells of the cochlea. It serves as a frequency-selective amplifier in a sound system that works something like this.

As sound enters the ear, it deflects the outer hair causing tiny amounts of stretching or compression in the outer hair cells. There are channel proteins that sit in the membrane of these cells which are sensitive to such mechanical strain. These proteins provide a tunnel (or channel) across the membrane so that ions can easily cross, and the mechanical strain can cause the channels to open.

These channels are precisely designed to allow only certain types of ions to cross. For example, some channels allow the positively charged potassium ion to cross but not the positively charged sodium ion, and vice-versa.

When a channel opens, ions usually tend to cross through the membrane (either into the cell or out of the cell) because the ion concentration is not uniform, and because there is a voltage, across the membrane. Such differences in concentrations across the membrane, and the voltage, are actively maintained by the cell. They serve as a sort of battery whose energy can be tapped at any time by opening membrane channels.

When the incoming sound causes certain channels to open, the ions that cross cause a change in the membrane voltage. In the outer hair cells, this voltage change encourages negatively charged chlorine ions to exit the cell. They interact with the prestin protein, in the membrane, to cause a mechanical deformation resulting in the elongation of the cell.

In other words, the incoming sound, that caused the hair to move, ends up causing yet more hair movement, and this serves precisely to amplify the incoming sound. This amplification is greater at low sound levels, as it should be.

One of the interesting features of this system is the speed at which it operates. Obviously in order to amplify sound you need to respond as fast as the changes in sound occur. Protein motors often use chemical energy (such as the splitting of the ATP molecule) but that would be too slow for the ear's sound system. Instead, prestin uses the membrane's voltage. This electrical energy can be used much faster and prestin operates at microsecond rates. Here is how one paper summarized the system:

The exquisitely high sensitivity and frequency selectivity of the mammalian hearing organ originates from a mechanical amplification mechanism that resides in the organ of Corti, the sense organ of hearing in mammals. The gain provided by this amplification can reach as high as a thousandfold; it is highest at low sound levels and progressively diminishes with increasing sound energy.

Evolution has no explanation for the origin of this system beyond unfounded speculation, and this is only the beginning of the many molecular machines behind the echolocation systems found in nature.

Echolocation designs incongruent with evolutionary tree

It does not appear that random mutations are the cause of systems such as echolocation in bats and whales. Although this is an enormous problem for evolutionary theory, it is not the only one. As discussed above, there are many different types of echolocation designs. Evolution would predict that species that are thought to be close neighbors on the evolutionary tree would share similar echolocation designs. In other words, the echolocation designs should be congruent with the evolutionary tree. But they are not.

Whereas Darwin argued that the evolutionary tree explained nature’s designs rather than habitat, nature’s echolocation designs follow the exact opposite rule. Here is how one paper described it:

the animal’s habitat is often more important in shaping its call design than is its evolutionary history.

This is an enormous falsification of a key prediction of evolutionary theory.

Convergence at the morphological level

One consequence of this falsification is that evolutionists must construct highly complicated narratives for the origin of echolocation. For example, if evolution is true, then we must believe that the incredible echolocation ability found in some bats arose multiple times, by evolving independently. That’s not easy for evolutionists to explain. How could such uncanny design details repeat themselves via blind biological variation (no, natural selection doesn’t help)?

But this convergence problem goes far beyond the bats. Whales and bats share some uncanny similarities in how they track their prey. But if evolution is true, we would have to believe that their common ancestor had none of these capabilities. So in completely different parts of the world, in completely different environments, random mutations in these different species must have independently constructed the same ultra complex designs. As one report explained:

Though they evolved separately over millions of years in different worlds of darkness, bats and toothed whales use surprisingly similar acoustic behavior to locate, track, and capture prey using echolocation, the biological equivalent of sonar. Now a team of Danish researchers has shown that the acoustic behavior of these two types of animals while hunting is eerily similar.

If evolution is true then bats and whales would have been evolving independently for millions of years. And yet they both constructed a sonar capability which involves transmitting loud signals while receiving incredibly weak signals, adjusting the signal parameters in real time, processing the received signals, and so forth. They even share the same range of ultrasonic frequencies:

Bats and toothed whales (which include dolphins and porpoises) had many opportunities to evolve echolocation techniques that differ from each other, since their nearest common ancestor was incapable of echolocation. Nevertheless – as scientists have known for years – bats and toothed whales rely on the same range of ultrasonic frequencies, between 15 to 200 kilohertz, to hunt their prey.

And that similarity is in spite of the different environments:

This overlap in frequencies is surprising because sound travels about five times faster in water than in air, giving toothed whales an order of magnitude more time than bats to make a choice about whether to intercept a potential meal.

But that is not all. The bat and whale also use similar strategies for adjusting their signals while homing in on prey:

Bats increase the number of calls per second (what researchers call a “buzz rate”) while in pursuit of prey. Whales were thought to maintain a steady rate of calls or clicks no matter how far they were from a target. But the new research shows that wild whales also increase their rate of calls or clicks during a kill – and that whales’ buzz rates are nearly identical to that of bats, at about 500 calls or clicks per second.

It is another example of a complex design evolution can only speculate about, and once again the evolutionary tree fails to predict its pattern.

Convergence at the molecular level

Not only is incredible echolocation convergence evident at the morphological level, it is also seen at the molecular level. For instance, the prestin proteins in certain bat and whale species are more similar than evolution would expect. The massive prestin protein has too many amino acids that match up between these species. If one were to construct an evolutionary tree on the basis of prestin comparisons alone, then the bat and whale would be grouped together, and that cannot be correct.

This fact alone need not be a problem for evolutionists. They simply say that prestin is under the influence of strong selection. In other words, there are strong functional constraints on prestin that require more similarity, even between distant species, than we typically find in proteins.

In particular, researchers identified nine amino acids in prestin that seem to be responsible for the overly-consistent whale-bat matchup. Those nine amino acids must be under very strong selection. If one of them mutated then the biosonar system would not work well. The bat or whale would not survive, and that is why we don’t observe such changes. That is how natural selection works.

But if all nine amino acids are required, how did evolution stumble onto the design in the first place? It would be highly unlikely for the right nine amino acids to arise via blind mutations, at the same time.

But the convergence of molecular machines behind echolocation goes far beyond prestin. As one paper explains, “convergence is not a rare process restricted to several loci but is instead widespread”.

As one evolutionist admitted, “These results imply that convergent molecular evolution is much more widespread than previously recognized”. And another admitted that the results are astonishing:

We had expected to find identical changes in maybe a dozen or so genes but to see nearly 200 is incredible. We know natural selection is a potent driver of gene sequence evolution, but identifying so many examples where it produces nearly identical results in the genetic sequences of totally unrelated animals is astonishing.

Astonishing.

Venema’s argument for why echolocation is not a problem

This brings us to Venema’s argument for why echolocation is not a problem. Given the enormous problems briefly reviewed above, how exactly does Venema find echolocation to be evolution-friendly? We have looked at the problem of complexity of echolocation, including at the molecular level, the problem that echolocation designs are incongruent with the evolutionary tree and, as an example, the problem of convergence at both the morphological and molecular levels. Surely no objective scientist would find evidence for evolution in nature’s echolocation designs.

Would they?

Believe it or not, here is what Venema writes:

If you’ve ever stumbled through a pitch-black room and pulled yourself up short just before colliding with a wall or other object, you have employed your (very rudimentary) sense of echolocation. What you detected (though you might not have even consciously perceived it) was that sound waves were reflecting off the object in your way. All mammals can do this, but most (like us) do it very poorly. We need to be very close to the object in question before it is even possible for us to notice reflected sound, and more likely than not we won’t, and we’ll stub our toe or worse.

As it turns out, cetacean echolocation is a specifically tuned sense of hearing that is based on the same genes used for hearing in other mammals. One key gene used for hearing in all mammals is called the “prestin” gene, a protein involved with the specialized structures in the mammalian ear that vibrate in response to sound waves. In whales, the prestin gene is tuned to the ultrasonic frequencies that are better suited to echolocation. This tuning required only a few amino acid changes within the protein—an amount of change easily within the reach of the sort of molecular tinkering we saw for the insulin gene in various mammals. This tinkering within the prestin gene to tune it for echolocation was so easy to achieve, it would seem, that nearly identical changes occurred independently in the lineage leading to modern bats, who also use a prestin tuned to ultrasonic frequencies for echolocation. So even echolocation is not “new”—it too is remodeled from a standard mammalian sense of hearing.

This is a complete disaster. Venema’s equating of echolocation with his imagined ability to avoid a wall in a dark room, his transforming convergence to a virtue, his casting of echolocation as “easy to achieve” and the result of mere “tinkering,” and nothing new but rather simply a remodel of “standard mammalian sense of hearing,” is all standard evolutionary pretzel logic.

This is the evolutionary “just add water” view of biology where you add a couple of mutations and, poof, you have echolocation. But as we saw above, echolocation is not at all comparable to “standard mammalian” hearing. It doesn’t fit the evolutionary tree, and the convergence is astonishing and utterly unexpected and unexplained.

Venema’s attempt to explain away echolocation as a standard result of evolution is not even wrong.

When I saw that this new book had a section on echolocation I was keen to read it over. I have followed the echolocation research for years. I write about it, and often include it in presentations. I discuss the various ways the echolocation evidence contradicts evolution. So why would there be a section on this subject in this book promoting evolution? Have I missed something? Is there some fundamental aspect of echolocation I have missed? Is there a new paper I have missed, overturning the large body of research?

But as I read the section, I quickly realized it was nothing more than the usual evolutionary just-so story. A wholesale ignoring of well-established science, an embracing of imagined thought experiments that make no sense, and an utterly unscientific conclusion.

It isn’t even wrong.