Friday, May 27, 2016

The Naked Ape: An Open Letter to BioLogos on the Genetic Evidence, Part II

Toward a Consensus

In my previous article I reviewed Dennis Venema’s articles (here and here) which claimed that the genomes of different species are what we would expect if they evolved. For instance, allied species have similar genomes, and genetic features fall into evolution’s common descent pattern. I argued that this claim is inaccurate and that the scientific evidence tells a very different message. In a later article Venema focused his claim on the specific case of human evolution, and the similarity between the human and chimpanzee genomes. As before, Venema finds this genetic evidence to be a compelling confirmation of evolution:

The first line of evidence in favor of humans sharing ancestry with other forms of life is straightforward – there are other species that have a genome that is nearly identical to our own – the genomes found in great apes such as chimpanzees, gorillas and orangutans. Compared to our “book,” the “books” of these species match at the chapter and paragraph level – all three species have DNA sequences that have the same genes in the same basic order as we do. There are subtle differences, of course – blocks of sequence that have been rearranged through breakage and rejoining of chromosomes, as expected – but the overall pattern is clear. […]

Taken together, what we observe when comparing the overall structure of the human genome to other primates is that (a) our genomes do indeed have the features one would predict them to have if they are copies of a shared ancestral genome, and (b) the differences we do observe are easily accounted for by well-known mechanisms. These observations strongly support the hypothesis that our species arose through an evolutionary process.

It does not seem that the evidence supports evolutionary theory as Venema concludes. In fact, there seem to be several significant problems with this claim, as I will explain.

First, as we saw in my previous article, the genetic data from the different species do not fall into the expected evolutionary pattern. Here Venema focuses on the high genetic similarity between the primates, claiming it confirms evolution. But if this is what is required to confirm evolutionary relationships, then the substantial genetic differences that are so often found between otherwise similar species must falsify evolutionary relationships in those cases.

But evolutionists have never entertained any such doubts. Those evolutionary relationships are intact, according to evolutionists, and this suggests that the high similarity between the primate genomes never was required for evolutionists to believe they evolved from a common ancestor.

So it appears that Venema’s claim, that the high genetic similarity between the primates confirms their evolutionary relationship, is more of an “after the fact” claim rather than a confirmation of a genuine evolutionary prediction. In fact, given the substantial morphological differences between humans and the other primates, evolutionists had indeed expected greater genetic differences:

The chimpanzee is our closest living relative. The morphological differences between the two species are so large that there is no problem in distinguishing between them. However, the nucleotide difference between the two species is surprisingly small.

But even given the high similarity between the chimp and human genomes, there are many inconsistencies with evolution.

The gorilla genome is strangely similar to both the chimp and human genomes

When the human and chimpanzee genomes were compared a few years ago, the human genes showed some surprising differences in a few places, such as in genes thought to be related to hearing. Evolutionists called it “accelerated” evolution and they said that it was due to the development of human language. However it turns out that the gorilla genome has a similar pattern. And that doesn’t make sense since gorillas don’t have our advanced verbal skills:

Much of the 15% is in sections of the genome that do not code for proteins. But the researchers also looked at functional gene changes. They found that certain genes—including some involved in hearing and brain development—had gone through more rapid changes than expected in both the gorilla and human lineage. Some of these rapid changes are puzzling: the gene LOXHD1 is involved in hearing in humans and was therefore thought to be involved in speech, but the gene shows just as much accelerated evolution in the gorilla. “But we know gorillas don’t talk to each other—if they do they’re managing to keep it secret,” says [lead author] Scally.

So now evolutionists are calling it “parallel accelerated” evolution, because the same accelerated evolution, by random mutation, must have happened independently, in the human and gorilla genomes. But why would the same “accelerated evolution” occur in the gorilla? It wasn’t developing human language. Perhaps there is some other reason, but why then wouldn’t that “accelerated evolution” occur in the chimpanzee? It doesn’t make sense with evolution, for we must say that random mutations just happened to create the same pattern twice.

The gorilla genome also shows similarities to the chimp genome, including duplications that are not present in the other primates. Evolutionists say these various chimp-gorilla similarities were coincidences, occurring repeatedly by chance in the two different species:

We show that both the gorilla and chimpanzee genomes have experienced independent yet convergent patterns of structural mutation that have not occurred in humans, including the formation of subtelomeric heterochromatic caps, the hyperexpansion of segmental duplications, and bursts of retroviral integrations.

These events must have occurred independently and in parallel.


Human uniqueness is expansive. Relative brain size, hairless sweaty skin, striding bipedal posture, long-distance running, ability to learn to swim, innate ability to learn languages in childhood, prolonged helplessness of the young, ability to imitate and learn, inter-generational transfer of complex cultures, awareness of self and of the past and future, theory of mind, increased longevity, provisioning by post-menopausal females, difficult childbirth, and cerebral cortical asymmetry are just a few from a long list of features that make humans exceptional.

Another such unique feature is at the genome level: the lack of endemic infectious retroviruses in humans. The problem is that these viruses are present in the other primates, and so according to evolution these viruses must be present in their common ancestor which, again according to evolution, would be an ancestor of humans as well. Therefore this lack of endemic infectious retroviruses in humans is inconsistent with evolution:

Other than the recent introductions of HIV and human T leukaemia virus (HTLV) into humans from other animals, humans seem to be devoid of species-wide endemic infectious retroviruses. By contrast, like most other mammals studied, other hominids and non-human primates (NHPs) do have such viruses. Indeed, given the remarkable corroboration between the phylogenetic trees of primates and their lineage-specific simian foamy viruses (SFVs) our common ancestors with other hominids almost certainly had SFVs. The same is probably true of the lineage-specific simian infectious retroviruses (SIVs) found in most NHPs. Assuming that the common ancestors of hominids carried multiple endemic infectious retroviruses, how did the human lineage eliminate them? Given that humans remain susceptible to re-infection with both SFVs and SIVs from other hominids, this seems unlikely to be explained solely on the basis of more efficient host restriction systems. Rather, there seems to have been an episode in which the ancestral human lineage was somehow ‘purged’ of these endemic viruses.

In other words, the endemic infectious retroviruses do not align with the expected evolutionary pattern. The human lineage must, somehow, have been purged of these endemic viruses. Perhaps such a purging occurred, and future research may be able to strengthen that hypothesis. But as it stands, this evidence is not consistent with evolution.

Chimp-human genome beneficial differences are few

As noted above, evolutionists were surprised by the high similarity between the chimp and human genomes. With so few differences, how could evolution construct such tremendous differences? But not only is evolution limited to a relatively few genetic modifications to create the human, but according to evolution the majority of even those modifications would likely have had little or no consequence or even would have been slightly harmful. Here is how a 2005 paper on the chimpanzee-human genome comparisons put it:

In particular, we find that the patterns of evolution in human and chimpanzee protein-coding genes are highly correlated and dominated by the fixation of neutral and slightly deleterious alleles.

The paper is written from an evolutionary perspective, assuming that humans and chimpanzees share a common ancestor. Given that a priori assumption, they were forced to conclude that most of the mutations affecting protein-coding genes led to “neutral and slightly deleterious alleles.” So not only are evolution’s random mutation resources meager, in terms of both quality and quantity as explained above, but even worse, those mutations mostly led to “neutral and slightly deleterious alleles.”

In fact the beneficial mutations in protein-coding genes, which presumably would be important in evolving the human from a small, primitive ape, literally number only in the hundreds. It would be astonishing if the human could be evolved from so few mutations.

Chimp-human genome differences have discrepancies

Furthermore, the chimp-human genome differences show some strange patterns, with unexplainable variation towards the ends of most chromosomes, and with the chromosomal banding patterns.

A common response from evolutionists is that these discrepancies are small in magnitude. That is true, they are small in magnitude. But that is not what counts. Molecular spectra that make magnetic resonance imaging (MRI) possible are also small in magnitude. That doesn’t mean they don’t count. What is important is that the chimp-human genome differences show patterns that evolutionary theory struggles to account for. The evidence is not consistent with the theory, by a wide margin.

The chimp-human genome differences has also been described using sliding 1-Mb windows. Those results also showed nonrandom variations, but later research found that those variations correlate with the observed de novo human mutation rate patterns. The research paper concluded that the variation in chimp-human genome differences “is only partly explained” by the mutation rate patterns. But these results raise the specter that the variations in the chimp-human genome differences seen in 1-Mb windows may be explainable by a known phenomenon.

This suggests the possibility that future research may also explain the variation towards the ends of chromosomes, and with the chromosomal banding patterns. But that was not the claim. Evolutionists such as Venema claim that today’s evidences “strongly support the hypothesis that our species arose through an evolutionary process.”

Chimp-human alternate splicing differences

You may have learned in your high school biology class that genes are segments of DNA, but it is a bit more complicated than that. For starters, in the higher species a gene is often not a simple continuous segment of DNA but rather is interrupted several times by intervening segments. So there are the coding segments (called exons for expressed regions) and then there are the intervening segments (called introns for intervening regions).

When a gene is transcribed, the transcript contains both the exons and introns. It is then spliced by a complicated spliceosome machine that removes the introns from the gene copy and glues the exons together.

One of the features of the exon/intron genetic architecture is that it allows for alternative splicing schemes. In fact, incredibly, a given gene can have thousands of different forms depending on how the spliceosome machine edits the gene.

When it was discovered that the human genome contained about twenty five thousand genes it seemed too few. Are not more genes required for a human body? More recently it has been discovered that we make up for that small number of genes with alternative splicing schemes. Most of our genes may undergo such editing, and the result can be a completely different function for the resulting protein.

We have an enormous alternative splicing program in our cells, far more than chimps have. And this is another inconsistency with evolutionary theory.

Given the high similarity between the chimp and human genomes, and the relatively few beneficial mutations in protein-coding genes (discussed above), evolutionists have considered the possibility of evolution by splicing. In other words, our enormous alternative splicing program may have been an important factor in our evolving from a small, primitive ape.

But there are many thousands of these gene splicing changes that would have to evolve. And unlike bacteria whose populations are large and generation times are short, our gene splicing changes would have to evolve in smaller populations with longer generation times.

It is difficult to see how evolution would have the resources to make this happen. The problem quickly becomes astronomically improbable if groups of genes would need to implement their new splicing logic together. And how could that not be the case?

In fact, even if only the order of implementing splicing for a small number of genes is important, the problem quickly becomes astronomically improbable. And again, how could that not be the case?

But this is only the beginning. In addition to the fact that the evolution of our enormous gene splicing changes is unlikely, it also represents an enormous serendipity problem. We would have to say that random mutations constructed complicated genes, with exons and introns and splicing codes, and the incredible splicing machinery, which, it would just so happen, would luckily be just what was needed to evolve humans.

It is even worse than this when one considers the exons themselves. Those random mutations would have divided the genetic instructions into so many exons, and it just so happened that they would be the right building blocks that, when rearranged, would lead to humans. The serendipity is astronomical here.

Imagine if you were building a tricycle and your friend modified each part you had crafted (not adding anything), and now the parts fit together to construct the space shuttle rocket motor.

The kangaroo-human genomes

In my previous article I explained that, in addition to striking differences in otherwise allied species, striking similarities in otherwise distant species are also inconsistent with evolution. This problem arises also with the human genome. Consider the kangaroo genome, which turned out to be similar to the human genome. As one evolutionist explained:

There are a few differences, we have a few more of this, a few less of that, but they are the same genes and a lot of them are in the same order. Which really surprised us, we thought they’d be completely scrambled, but they’re not, there’s great chunks of the human genome which is sitting right there in the kangaroo genome.

It was a surprise because under evolution humans and kangaroos must be quite distant relatives. Evolutionists believe a small mouse-like species split into two lineages—the marsupials and the placentals—about 150 million years ago. And according to evolutionists that mouse-like species eventually evolved by random mutations into, among other things, a kangaroo in the one lineage and into a human in the other. With that much evolutionary distance the kangaroo and human genomes should have evolved substantial differences.


The genomes of primates do not support evolutionary theory. As we have discussed, there are always speculations for whatever evidence is discovered. Perhaps evolution did this, perhaps it did that. But that does not change the fact that the primate genomes do not “strongly support the hypothesis that our species arose through an evolutionary process,” as Venema and the evolutionists claim. There are a wide variety of substantial contradictions and problems with this theory.

Wednesday, May 25, 2016

The Naked Ape: An Open Letter to BioLogos on the Genetic Evidence

Toward a Consensus

Dennis Venema, professor of biology at Trinity Western University, has written a series of articles that have been noted by evolutionists for their clarity and persuasiveness. So as a collector of evidences and reasons why evolution is a fact, I was interested to see Venema’s articles. What does the professor have to say to help confirm what Samuel Wilberforce rhetorically called “a somewhat startling conclusion”?

One of Venema’s basic points (see here and here) is that the genomes of different species are what we would expect if they evolved. Allied species have similar genomes, and genetic features fall into evolution’s common descent pattern:

If indeed speciation events produced Species A – D from a common ancestral population, we would expect their genomes to exhibit certain features when compared to each other. First and foremost, their overall genome sequence and structure should be highly similar to each other – they should be versions of the same book, with chapters and paragraphs of shared text in the same order. Secondly, the differences between them would be expected to fall into a pattern.

Does the evidence confirm these evolutionary expectations? Venema answers with an emphatic “yes.”

Here Venema is appealing to the empirical evidence. He is comparing the evidence to the theory of evolution, and finding that the evidence confirms evolution’s predictions. This means the theory can be empirically evaluated. And if evolution can be genuinely evaluated empirically, then it is, at least theoretically, possible for evolution to fail. If the evidence can confirm evolution, then it also can disconfirm evolution.

This is important because focusing the attention on the evidence means the non scientific arguments go away and science is allowed to speak. What does it say? Here I will take the opposing view, for it seems that what the science shows is that Venema’s claim, that the genetic evidence confirms evolutionary predictions, is inaccurate.

This is not to say that evolutionary explanations cannot be offered. As philosophers well understand, another sub hypothesis is always possible. Such hypotheses raise more profound questions of parsimony, likelihood and so forth. But it seems that such philosophical questions ought to be addressed after there is a consensus on what the empirical evidence has to say. The goal here is to move toward that consensus. Venema, and evolutionists in general, make a straightforward claim about the evidence. We ought to be able to dispassionately evaluate that claim.

Of course I realize that reaching consensus is not as simple as reading an article. There will be differing interpretations by fair-minded critics. And the topic of origins is certainly not always dispassionate. If you argue against evolution you will be disparaged. My response to such attacks has and always will be to forgive.

One final preliminary is simply to point out that it is a challenge just to do justice to this story. A thorough treatment could easily require an entire volume. But a few, typical, examples will have to suffice. They can provide readers with an approximate understanding how the evidence bears on Venema’s claim.

What does the evidence say?

For starters, phylogenetic incongruence is rampant in evolutionary studies. Genetic sequence data do not fall into the expected evolutionary pattern. Conflicts exist at all levels of the evolutionary tree and throughout both morphological and molecular traits. This paper reports on incongruent gene trees in bats. That is one example of many.

MicroRNAs are short RNA molecules that regulate gene expression, for example, by binding to messenger RNA molecules which otherwise would code for a protein at a ribosome. Increasingly MicroRNAs are understood to be lineage-specific, appearing in a few species, or even in just a single species, and are nowhere else to be found. In fact one evolutionist, who has studied thousands of microRNA genes, explained that he has not found “a single example that would support the traditional [evolutionary] tree.” It is, another evolutionist admitted, “a very serious incongruence.”

Trichodesmium or “sea sawdust,” a genus of oceanic bacteria described by Captain Cook in the eighteenth century and so prolific it can be seen from space, has a unique, lineage-specific genome. Less than two-thirds of the genome of this crucial ammonium-producing bacteria codes for proteins. No other such bacteria has such a low value, and conversely such a large percentage of the genome that is non coding. This lineage-specific genome, as one report explains, “defies common evolutionary dogma.”

It is not unusual for similar species to have significant differences in their genome. These results have surprised evolutionists and there does not seem to be any let up as new genomes are deciphered.

The mouse and rat genomes are far more different than expected. Before the rat genome was determined, evolutionists predicted it would be highly similar to the mouse genome. As one paper explained:

Before the launch of the Rat Genome Sequencing Project (RGSP), there was much debate about the overall value of the rat genome sequence and its contribution to the utility of the rat as a model organism. The debate was fuelled by the naive belief that the rat and mouse were so similar morphologically and evolutionarily that the rat sequence would be redundant.

The prediction that the mouse and rat genomes would be highly similar made sense according to evolution. But it was dramatically wrong.

One phylogenetic study attempted to compute the evolutionary tree relating a couple dozen yeast species using 1,070 genes. The tree that uses all 1,070 genes is called the concatenation tree. They then repeated the computation 1,070 times, for each gene taken individually. Not only did none of the 1,070 trees match the concatenation tree, they also failed to show even a single match between themselves. In other words, out of the 1,071 trees, there were zero matches. It was “a bit shocking” for evolutionists, as one explained: “We are trying to figure out the phylogenetic relationships of 1.8 million species and can’t even sort out 20 yeast.”

What is interesting is how this false prediction was accommodated. The evolutionists tried to fix the problem with all kinds of strategies. They removed parts of genes from the analysis, they removed a few genes that might have been outliers, they removed a few of the yeast species, they restricted the analysis to certain genes that agreed on parts of the evolutionary tree, they restricted the analysis to only those genes thought to be slowly evolving, and they tried restricting the gene comparisons to only certain parts of the gene.

These various strategies each have their own rationale. That rationale may be dubious, but at least there is some underlying reasoning. Yet none of these strategies worked. In fact they sometimes exacerbated the incongruence problem. What the evolutionists finally had to do, simply put, was to select the subset of the genes that gave the right evolutionary answer. They described those genes as having “strong phylogenetic signal.”

And how do we know that these genes have strong phylogenetic signal. Because they gave the right answer. This raises the general problem of prefiltering of data. Prefiltering is often thought of merely as cleaning up the data. But prefiltering is more than that, for built-in to the prefiltering steps is the theory of evolution. Prefiltering massages the data to favor the theory. The data are, as philosophers explain, theory-laden.

But even prefiltering cannot always help the theory. For even cleansed data routinely lead to evolutionary trees that are incongruent (the opposite of consilience). As one study explained, the problem is so confusing that results “can lead to high confidence in incorrect hypotheses.” As one paper explained, data are routinely filtered in order to satisfy stringent criteria so as to eliminate the possibility of incongruence. And although evolutionists thought that more data would solve their problems, the opposite has occurred. With the ever increasing volumes of data (particularly molecular data), incongruence between trees “has become pervasive.”

What is needed now is less data. Specifically, less contradictory data. As one evolutionist explained, “if you take just the strongly supported genes, then you recover the correct tree.” And what are “strongly supported” genes? Those would be genes that cooperate with the theory. So now in addition to prefiltering we have postfiltering.

Another issue are the striking similarities in otherwise distant species. This so-called convergence is rampant in biology and it takes on several forms.

Consider a paper from the Royal Society on “The mystery of extreme non-coding conservation” that has been found across many genomes. As the paper explains, there is currently “no known mechanism or function that would account for this level of conservation at the observed evolutionary distances.” Here is how the paper summarizes these findings of extreme sequence conservation:

… despite 10 years of research, there has been virtually no progress towards answering the question of the origin of these patterns of extreme conservation. A number of hypotheses have been proposed, but most rely on modes of DNA : protein interactions that have never been observed and seem dubious at best. As a consequence, not only do we still lack a plausible mechanism for the conservation of CNEs—we lack even plausible speculations.

And these repeated designs, in otherwise different species, are rampant in biology. It is not merely a rare occurrence which perhaps evolution could explain as an outlier. That the species do not fall into an evolutionary tree pattern is well established by science.

Furthermore, these repeated designs do not merely occur twice, in two distant species. They often occur repeatedly in a variety of otherwise distant species. So now the evolutionist must not only believe that there are many of these repeating design events, but that in most cases, they repeat multiple times, in disparate species.

Evolutionists have labeled this evidence as recurrent evolution. As a recent paper explains:

The recent explosion of genome sequences from all major phylogenetic groups has unveiled an unexpected wealth of cases of recurrent evolution of strikingly similar genomic features in different lineages.

In addition, many instances of a third more puzzling phylogenetic pattern have been observed: traits whose distribution is “scattered” across the evolutionary tree, indicating repeated independent evolution of similar genomic features in different lineages.

Of course these puzzling, striking similarities cannot be explained by common evolutionary history. Instead, they are explained by common evolutionary forces:

As ancestrally shared features are the result of a common evolutionary history, shared features evolved by recurrent evolution are often the result of common evolutionary forces acting on different lineages.

If the pattern fits the evolutionary tree, then it is explained as common evolutionary history. If not, then it is explained as common evolutionary forces.

With all of this contradictory evidence, even evolutionists have realized in recent years that the traditional evolutionary tree model is failing. As one evolutionist explained, “The tree of life is being politely buried.”

There are many more fascinating examples of biological patterns that are not consistent with the expected evolutionary pattern. These are not anomalies or rare exceptions. Here we have focused on the genetic level since that was the theme of Venema’s article. It seems that the species and their genomes do not fall into a consistent evolutionary pattern as evolutionists such as Venema claim. This does not mean evolutionists cannot explain any of this. They have a wide spectrum of mechanisms to draw upon, of varying levels of speculation and likelihood. These explanatory mechanisms greatly increase the theory’s complexity. They raise questions of realism, and whether the theory is following the data, or the data is following the theory. But such questions are for another day.

The point here is that evolutionist’s claims that the genomic data broadly and consistently fall into the evolutionary pattern and expectations do not seem to reflect the empirical data. This is the first step in moving the discourse forward. We need to reach consensus on what the evidence reveals.

Next time I will continue with an examination of the next evidences Venema presents.

[Ed: Comments critical of any position are welcome below, but they should be in a constructive tone]

Saturday, May 21, 2016

New Study Reveals How the Shape of My Nose Arose

The Nose Knows

It is ironic that Charles Lyell, whose seminal, if flawed, work in geology—the barrister is sometimes known as the father of modern geology—positively influenced Charles Darwin’s development of evolutionary theory—the young Darwin read Lyell’s book as he sailed around the world in the H.M.S. Beagle—and who helped to arrange for Darwin’s first formal, if awkward, presentation of his theory—an event precipitated by Wallace’s Ternate letter—was one of the last of the intelligentsia to accept Darwin’s new formulation of Epicureanism, known as evolution.

At one point an exasperated Darwin asked Lyell—it always comes down to metaphysics—if he believed “the shape of my nose was designed?” If Lyell did think so then, Darwin added, “I have nothing more to say.” The infra-dignitatem, or infra-dig for the irreverent, argument, which insisted that it was beneath the dignity of the Creator to stoop so low as to dwell in the details of the world, had been promoted by no less than the father of natural theology John Ray and Platonist Ralph Cudworth, and in Darwin’s day was in full swing. Its influence on the young Darwin was clear in the naturalist’s early notebooks, and here in his appeal to Lyell. One look at one’s nose is all one needs to know about origins. Obviously we evolved. Now, a century and a half later, science finally has its say in the matter.

A new study out of, appropriately enough, England, now reveals the underlying genetic details that influence the shape of our noses. It seems there are four genes that influence the width and length of our olfactory device and, as the press release informs us, “The new information adds to our understanding of how the human face evolved.”

Glad to have that cleared up. Religion drives science, and it matters.

Thursday, May 19, 2016

Local Fitness Landscape Mapped Out For Green Fluorescent Protein

It’s Just Getting Worse

As we have discussed many times, proteins are a show-stopper for evolution. Proteins consist of dozens, hundreds and even thousands of amino acids and, like most machines, they don’t work very well until most of the parts (amino acids in this case) are in place. Half of the amino acids don’t give you half the function of a protein. You can read more about this here and here. Now, a new paper reinforces the problem of protein evolution.

One approach to studying how evolution could create new protein designs is to start with some sort of random sequence of amino acids, see how well it works, and try to evolve it to obtain a protein. This is difficult because the protein design space is astronomically huge and proteins are sparse within that space. Any random sequence of amino acids will merely give you junk. Furthermore, the fitness landscape is flat and doesn’t provide the guidance evolution needs to move toward functional proteins.

Another approach is to start at the end and work backwards. In other words, start with the finished product—a functional protein—and see what the fitness landscape looks like as you swap in different amino acids. This is difficult because, unfortunately for evolution, the fitness landscape drops off precipitously as you move away from the native protein design. Modifying only a few percent of the amino acids leads to a rapid loss of function.

The new paper takes this second approach. It uses a bioluminescent protein known as the green fluorescent protein, taken from the jellyfish, Aequorea victoria. It is a wonderful study that systematically mapped out the protein’s function (as measured by the protein’s fluorescence) for a total of 51,715 different protein sequences that are nearby the native sequence.

The results confirmed what earlier studies had indicated: the protein function drops off dramatically with only a relatively small number of substitutions. But the study also explored the effect of multiple substitutions. It is well known that the effect of two substitutions, for example, are not always simply the sum of their individual effects. They can interact with each other in either positive or negative ways. This is referred to as epistasis.

The new study found that negative epistasis was strong and prevalent. As one of the researchers explained:

We were really surprised when we finally had a chance to look at exactly how the interactions between mutations occur. We also did not expect that almost all the mutations that are only slightly damaging on their own can destroy fluorescence completely when combined together.

It was well understood that evolving a protein is an astronomically unlikely event, and these results indicate it is even more difficult. Those negative results, however, were not reported in the paper. Instead, the paper discussed possible ways that one green fluorescent protein, found in one particular species, may have evolved into other green fluorescent proteins, found in other species. The implications for the initial evolution of a protein were ignored.

Monday, May 16, 2016

We Can Say It, But You Can’t

Highly, Intricately, and Precisely Integrated Networks of Entities and Interactions

As Carl Woese explained in 2004:

The cells we know are not just loosely coupled arrangements of quasi-independent modules. They are highly, intricately, and precisely integrated networks of entities and interactions. … To think that a new cell design can be created more or less haphazardly from chunks of other modern cell designs is just another fallacy born of a mechanistic, reductionist view of the organism.

Mechanistic, reductionist view? It appears Woese put his finger on precisely what he believed in: evolution. Replace “cell” with just about any biological structure and Woese has, in a nutshell, summarized evolutionary theory, what little there is of it. As Richard Dawkins once explained:

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

Religion drives science, and it matters.

h/t: El hombre

Thursday, May 12, 2016

A Response to VJ Torley

One Long Argument

To read VJ Torley’s analysis of my criticism of S. Joshua Swamidass’ recent article, Evidence and Evolution, one would think that I mercilessly berated a poor fellow who was merely attempting to “extend an olive branch to creationists.” After all, nowhere did Swamidass belittle or ridicule his opponents, and nowhere was there so much as a trace of the smug superiority. And the guy is a Christian, not some atheistic reductionist. In fact, Swamidass does not even draw any conclusions in his article.

This is how Torley begins his article and unfortunately this gives those who have not read the two articles the wrong impression. I gave a lengthy, fact-based, scientific criticism of Swamidass’ claims which was not dismissive or sarcastic. I did not accuse of Swamidass of belittling or ridiculing anyone, nor did I accuse him of smugness, academic or otherwise. And I did not question his religious beliefs. All of this was injected by Torley.

As for drawing conclusions, yes contrary to Torley, Swamidass draws conclusions. He states in no uncertain terms that the evolutionary story “is by far the best scientific explanation of our origins.” In fact, the evidence is stunning:

What is the evidence for human common ancestry with apes? The strongest evidence is a series of stunningly accurate predictions about human genomes that have been confirmed in recent decades as the human and ape genomes have been sequenced.

The idea that Swamidass does not draw conclusions is inaccurate. Swamidass goes on to suggest that microevolution is sufficient to explain the evolution of humans from a small, ape-like creature.

Throughout his piece, Swamidass uses a scientist versus theologian, Warfare Thesis perspective. Scientists simply refer to the data whereas theologians must adjust their sights, drop their denial, and grapple with the undeniable truths of evolution. To object is futile and attempts to explain humans as a product of design are “lawyerly”:

A common lawyerly objection to this evidence is that these similarities are “equally” explained by common “design.” As scientists, our response to this objection is data.

Perhaps the theologian “could look for errors in the scientific analyses,” but even that would be futile:

Still, even if he [the theologian] found standing for quibbles here and there, the overall picture would remain the same and the evidence against common ancestry, at best, would be subtle and debatable.

Swamidass presents a story in order to “reduce the fear some feel when encountering evidence that might contradict their understanding of the Bible.”

This is all Warfare Thesis, and Torley finds it to be “irenic in tone, easy to follow, deeply learned, and absolutely right.”

On the other hand Torley throws occasional ad hominems my way and finds that my critique of Swamidass’ piece was “polemical and curtly dismissive in tone.” In fact, my criticism was about Swamidass’ arguments. I pointed out that his scientific claims were erroneous and that ultimately his arguments relied on metaphysical claims.

This is not to say there cannot be improvements in my article. It is, after all, a blog post. I’m thankful for feedback and corrections to my errors. But Torley’s casting of the two articles is simply a misrepresentation. It seems that his criticism of my post is, in fact, more applicable to his article.

What about the science?

Torley next castigates me for ignoring the main scientific evidence Swamidass presents. And what is Torley referring to? A series of references Swamidass made. So instead of addressing the key scientific claims made by Swamidass (which I did), I am supposed to do an expansive analysis on several references Swamidass provided as backup.

In fact I was planning on getting to those references at some point, time permitting, as they are yet more examples of failed science. But Torley’s requirements and criticisms are unrealistic.

Torley next quotes from one of Swamidass’ references, imagines what my response would be, and argues with it. This is getting silly. Normally I would not respond to this type of article, but this is different since it appears so close to my article.

Torley finishes with a series of erroneous rebuttals, ad hominems, and strawmen arguments. To be sure, Torley makes some good tangential points, but they are unfortunately the minority in a series of failed arguments.

Not surprisingly Torley shares Swamidass’ theological convictions which underwrite their claims. Their contrastive reasoning, if correct, proves their case. As Torley writes:

On a special creationist account of human origins, there is absolutely no reason to expect that humans would have what appear to be the remains of genes used for making egg yolks in their DNA – just as there is no particular reason to expect that humans would be more genetically similar to chimps than rats are to mice – or for that matter, than foxes are to wolves, or horses are to donkeys. [emphasis in original]

No reason. If Torley is correct here then, yes, we can safely conclude for evolution. Likewise:

Reasoning on Bayesian grounds, these striking and singular facts have a high probability on the hypothesis of common descent, but are surprising (and hence improbable) on a hypothesis of separate creation. One can only conclude that these facts lend scientific support to the hypothesis of common descent.

True enough. Such reasoning is perfectly valid, but it hinges on metaphysical premises. From a scientific perspective, evolution and common descent are unlikely to say the least, but from a metaphysical perspective, they are compelling.

Religion drives science, and it matters.

Wednesday, May 11, 2016

What Are They Teaching at Washington University? S. Joshua Swamidass and the Chimp-Human Divergence

Stunning Evidence For Common Ancestry

I once had a rare and valuable baseball card I wanted to sell. I placed an ad and was shortly contacted by a collector. But to my dismay he wasn’t interested. He had probably looked at hundreds of baseball cards and it only required one look for him to know that my treasured card held no value for him. He did not attempt any negotiating tricks, just a polite “thank you” and off he went. I would have felt better about the encounter if he had tried to haggle down the price. For I would have had the comfort of knowing my card held at least some value. Instead, there was no price discovery—apparently the card was worthless.

I too am a collector of sorts. And like that baseball card collector I have looked at hundreds of specimens. No matter how unlikely the source or the venue, I will go there and have a look. And in short order, I will know exactly what I am looking at, and if there is any value there. But unlike the baseball card collector, my subject is not something you can touch. What I am interested in are the arguments and evidences for evolution. Ever since Darwin, evolutionists have insisted that their idea is undeniable—beyond all reasonable doubt. I find that complete certainty to be fascinating. So I search, find, analyze and categorize every justification and explanation for that conclusion that I can find.

My goal is to find the strongest, most powerful, such arguments and evidences, and to understand how we can have such certainty. This brings us to S. Joshua Swamidass’s recent article, Evidence and Evolution where Swamidass explains, in typical fashion, that the evidence for evolution is powerful and compelling. Swamidass describes the evidence as stunning. As a professor in the Genomic Medicine Division at Washington University, Swamidass deserves to be listened to. This is definitely a specimen I want to have a look at.

In his article, Swamidass’ focus is human evolution. Evolutionists believe that we humans evolved from a small ape-like creature and that our closest relative on the evolutionary tree is the chimpanzee. The chimpanzee must be our closest relative, they reason, because the chimp’s genome is closest to ours, and according to evolution, genetic mutations are the fuel behind evolutionary change.

The problem with this reasoning is that the chimpanzee is not very similar to humans according to many other measures. There are enormous differences between the two species. Simply put, from an evolutionary perspective the genetic data are not congruent with the other data. Swamidass’ evidence will need to overcome this obvious problem.

But that’s not all.

The basic idea of humans arising via a long series of genetic mutations is, itself, not indicated by the science and unlikely to say the least. Remember, the mutations have to be random. According to evolution, you can’t have mutations occurring for some purpose, such as creating a design. And natural selection doesn’t help—it cannot induce or coax the right mutations to occur. This makes the evolution of even a single protein, let alone humans, statistically impossible. So this is another enormous problem Swamidass’ evidence will need to overcome.

But that’s not all.

The incredible designs in the human body are not the only thing those random mutations have to create—they will also have to create human consciousness. Evolutionists may try to explain consciousness as an “emergent” property that just luckily arose when our brain somehow evolved. Or they may try to explain that consciousness is really no more than an illusion. But these are just more demonstrations of anti realism in evolutionary thought. Evolutionary theory constructs mechanisms and explanations that do not correspond to the real world. So this is another problem Swamidass will need to overcome.

But that’s not all.

In recent decades the genomes of humans and chimps have been determined, and they make no sense on evolution. One of the main problems is that the genes of the two species are almost identical. They are only about 1-2% different and, if you’re an evolutionist, this means you have to believe that the evolution of humans from a small, primitive, ape-like creature was caused by only a tiny modification of the genome.

This goes against everything we have learned about genetics. You can insert far greater genetic changes with far less change arising as a consequence. It makes little sense that tiny genetic changes could cause such enormous design changes to occur. This is yet another problem for Swamidass to overcome.

But that’s not all.

Not only is evolution limited to tiny genetic modifications to create the human, but the majority of those modifications would have had to be of little or no consequence. Here is how a 2005 paper on the chimpanzee-human genome comparisons put it:

In particular, we find that the patterns of evolution in human and chimpanzee protein-coding genes are highly correlated and dominated by the fixation of neutral and slightly deleterious alleles.

The paper is written from an evolutionary perspective, assuming that humans and chimpanzees share a common ancestor. Given that a priori assumption, they were forced to conclude that most of the mutations affecting protein-coding genes led to “neutral and slightly deleterious alleles.” So not only are evolution’s random mutation resources meager, in terms of both quality and quantity as explained above, but even worse, those mutations mostly led to “neutral and slightly deleterious alleles.” This is no way to evolve the most complex designs in the world and it is yet another problem for Swamidass to overcome.

But that’s not all.

The supposed divergence rate between chimps and humans also has an unexplainable variation towards the ends of most chromosomes. This is another problem that seems to make no sense on evolution, which Swamidass must explain.

But that’s not all.

This supposed divergence rate between chimps and humans also has an unexplainable variation that correlates with chromosomal banding. Again, this makes no sense on evolution. Why should the chimp-human divergence vary with the banding pattern? Evolutionists have only just-so stories to imagine why this would have happened, and it is another problem for Swamidass to address.

But that’s not all.

This supposed divergence rate between chimps and humans is not consistent with the supposed divergence rate between the mouse and rat. The mouse-rat divergence is about an order of magnitude greater than the chimp-human divergence. And yet the mouse and rat are much more similar than the chimp and human. It makes no sense on evolution. In fact, before the rat genome was determined, evolutionists predicted it would be highly similar to the mouse genome. As one paper explained:

Before the launch of the Rat Genome Sequencing Project (RGSP), there was much debate about the overall value of the rat genome sequence and its contribution to the utility of the rat as a model organism. The debate was fuelled by the naive belief that the rat and mouse were so similar morphologically and evolutionarily that the rat sequence would be redundant.

The prediction that the mouse and rat genomes would be highly similar made sense according to evolution. But it was dramatically wrong.

Another approach is to ignore the morphological similarities and reason from the number of generations available to produce the genomic differences between the mouse and rat. The mouse-rat divergence date is estimated by evolutionists to be older than the chimp-human divergence date. Furthermore, the lifespan and generation time for mice and rats are much shorter than for chimps and humans. From this perspective, and given these two effects, one would conclude that the mouse-rat genetic divergence should be much greater—at least two orders of magnitude greater—than the chimp-human genetic divergence. But it isn’t. It is only about one order of magnitude greater.

So either way the mouse-rat comparison does not help to explain things and is another problem for Swamidass to explain.

Swamidass arguments and evidences

The science makes no sense on evolution. If we begin by assuming chimps and humans share a common ancestor, we end up with all kinds of contradictions and failures. So what exactly are Swamidass’ arguments and evidences? How is it that he is so certain? What is it in the data that he finds to be so stunning? And most importantly, how does he resolve the above problems?

Well, he doesn’t.

Astonishingly, Swamidass doesn’t even mention the above problems. It is as though they don’t exist. After some stories and high claims of certainty, here is what Swamidass says:

As predicted by common ancestry, human and chimpanzee genomes are extremely similar (greater than 98% similarity in coding regions), much more similar than we would expect without common descent. Remarkably, just as predicted by the fossil record, humans are about 10 times more genetically similar to chimpanzees than mice are to rats.

First, the high chimp-human genomic similarity was not predicted by common ancestry. No such prediction was made and no such prediction is required by common ancestry. Common ancestry would be just fine with very different levels of similarity than 98-99%. In fact, this high similarity makes no sense on evolution, for several of the reasons given above.

Swamidass’ claim that this evidence is a stunning confirmation of common ancestry is utterly at odds with the science. It is in stark contrast to the scientific facts.

Second, Swamidass’ claim that mouse-rat divergence, compared with the chimp-human divergence, is “just as predicted by the fossil record” is also blatantly false. While evolutionists can always combine various explanatory mechanisms to rationalize just about any comparison, that does not make for stunning evidence that is “just as predicted.”

Finally, the real strength of Swamidass’ argument lies in its metaphysics. The professor states that the chimp-human genome comparison is “much more similar than we would expect without common descent.”

Without common descent?

The evolutionist has just made an unbeatable (and unfalsifiable) argument.

This is not science. Swamidass’ claim about what is and isn’t likely “without common descent” is not open to scientific scrutiny.

Scientists, qua scientists, do not have knowledge of all possible explanations for the origin of life. This is why scientists, qua scientists, make statements about theories, not about the complement of a theory. A scientist cannot know that something is unlikely “without” his theory. That implies knowledge of all other possible theories. And that knowledge does not come from science.

This is the strength of Swamidass’ argument. Notice that with this metaphysical knowledge, all of the scientific problems melt away. No wonder he does not address them. They are inconsequential. At worst, they are simply interesting puzzles. The truth of the matter is already known.

If Swamidass is correct then, yes, of course, the genomic data must be strong evidence for common ancestry. But it all hinges on his metaphysics. This is not about science. It never was.

[Ed; Removed sentence about the orangutan, 1-Mb segments section, and the gene functionality section. Please see the followup article here.]

Saturday, May 7, 2016

How Did Birds Get Their Wings? Bacteria May Provide a Clue to the Genomic Basis of Evolutionary Innovation, Say Evolutionists

30 Days of Evolution

That evolution occurred is known to be a fact but how evolution occurred is not known. In particular we are ignorant of how evolutionary innovations arose. Of course biological novelties and innovations arose from a series of random chance events, but it is less than reassuring that we cannot provide more detail. How exactly did the most complex designs spontaneously arise? What mechanisms overcame, over and over, the astronomical entropy barriers, by sheer luck of the draw? As Craig MacLean’s and Andreas Wagner’s, and coworker’s, new PLOS Genetics paper begins, “Novel traits play a key role in evolution, but their origins remain poorly understood.” Could it be that evolution is not actually a fact? No, not according to evolutionists. And this new paper claims to provide the basis for how the seemingly impossible became the mundane.

The paper begins by summarizing the many proposed genetic mechanisms for the evolution of biological innovations:

An evolutionary innovation is a new trait that allows organisms to exploit new ecological opportunities. Some popular examples of innovations include flight, flowers or tetrapod limbs [1,2]. Innovation has been proposed to arise through a wide variety of genetic mechanisms, including: domain shuffling [3], changes in regulation of gene expression [4], gene duplication and subsequent neofunctionalization [5,6], horizontal gene transfer [7,8] or gene fusion [9]. Although innovation is usually phenotypically conspicuous, the underlying genetic basis of innovation is often difficult to discern, because the genetic signature of evolutionary innovation erodes as populations and species diverge through time.

1. Mayr E. Animal Species and Evolution. Cambridge: MA: Harvard University Press; 1963.

2. Pigliucci M. What, if anything, is an evolutionary novelty? Philos Sci. 2008;75: 887–898. Available:

3. Patthy L. Genome evolution and the evolution of exon-shuffling—a review. Gene. 1999;238: 103–14. Available: pmid:10570989

4. True JR, Carroll SB. Gene co-option in physiological and morphological evolution. Annu Rev Cell Dev Biol. 2002;18: 53–80. doi: 10.1146/annurev.cellbio.18.020402.140619. pmid:12142278

5. Zhang J. Evolution by gene duplication: An update. Trends Ecol Evol. 2003;18: 292–298. doi: 10.1016/S0169-5347(03)00033-8.

6. Bergthorsson U, Andersson DI, Roth JR. Ohno’s dilemma: evolution of new genes under continuous selection. Proc Natl Acad Sci U S A. 2007;104: 17004–9. doi: 10.1073/pnas.0707158104. pmid:17942681

7. Boucher Y, Douady CJ, Papke RT, Walsh DA, Boudreau MER, Nesbø CL, et al. Lateral gene transfer and the origins of prokaryotic groups. Annu Rev Genet. 2003;37: 283–328. doi: 10.1146/annurev.genet.37.050503.084247. pmid:14616063

8. Wiedenbeck J, Cohan FM. Origins of bacterial diversity through horizontal genetic transfer and adaptation to new ecological niches. FEMS Microbiol Rev. 2011;35: 957–976. doi: 10.1111/j.1574-6976.2011.00292.x. pmid:21711367

9. Thomson TM, Lozano JJ, Loukili N, Carrió R, Serras F, Cormand B, et al. Fusion of the human gene for the polyubiquitination coeffector UEV1 with Kua, a newly identified gene. Genome Res. 2000;10: 1743–56. pmid:11076860 doi: 10.1101/

The unspoken problem here is, as usual, serendipity. The various proposed genetic mechanisms for the evolution of biological innovations all suggest an amazing bit of fortuitous luck. For random chance events just happened to create these various complicated structures and mechanisms (such as horizontal gene transfer and protein domains their shuffling) which then produced new evolutionary breakthroughs.

Evolution didn’t know what was coming. Evolution did not plan this out, it did not realize that horizontal gene transfer would lead the way to new biological worlds. The evolution of horizontal gene transfer would require a long sequence of random mutations, many of which would not provide any fitness advantage. And when the construction project was completed, and the first horizontal gene transfer capability was possible, there would be no immediate advantage.

This is because there would have been no genes to transfer. The mechanism works only when it is present in more than one, neighboring, cells. One cell gives, and another cells receives. By definition the mechanism involves multiple cells.

But it doesn’t stop there. Even if the first horizontal gene transfer capability was able to spread across a population, and even if it did provide a fitness advantage to the fortunate citizens, there would not be even a hint of the enormous world of biological innovations that had just been opened.

In other words, what this evolutionary narrative entails is monumental serendipity. Biological structures and mechanisms (horizontal gene transfer in this case, but it is the same story with the other hypotheses listed above) are supposed to have evolved as a consequence of a local, proximate, fitness advantage: a bacteria could now have a gene it didn’t have before.

But it just so happened that the new structures and mechanisms would also, as a free bonus, be just what was needed to produce all manner of biological innovations, far beyond assisting a lowly bacteria increase its fecundity.

This is monumental serendipity.

The science contradicts the theory

Undaunted, the new paper finds that one of the other mechanisms, gene duplication and subsequent neofunctionalization, is a key enabler and pathway to biological innovations.

That conclusion resulted from what otherwise was a fine piece of research work. The experimenters exposed different populations of Pseudomonas aeruginosa, a dangerous infectious bacteria, to 95 new sources of its favorite food: carbon.

The bacteria had to adjust to the new flavors of carbon and they did so with various genetic modifications, including various genetic mutations. In the most challenging cases (where the new carbon sources were most difficult for the bacteria to adjust to), the bacteria often produced mutations in genes involved in transcription and metabolism. And these mutations often occurred in genes where there were multiple copies, so the mutations occurred in one copy while the other copy could continue in its normal duties.

The problem is, these genetic duplicates were preexisting in the P. aeruginosa genome. This is yet another instance of serendipity.

Why? Because preexisting duplicates are not common. Only about 10% of the genes have duplicates lying around, and fortunately, the genes needed for adaptation (involving transcription and metabolism) just happened to have such duplicates.

Now there were a few instances of de novo gene duplication. That is, once the experiment began, and after the P. aeruginosa populations were exposed to the challenging diets, a total of six genes underwent duplication events. But in each and every case, the duplication events occurred repeatedly and independently, in different populations (for each of the 95 different carbon sources, the experimenters ran four parallel trials with independent populations).

This result indicates directed gene duplication. This is because it is highly unlikely that random, chance, gene duplication events just happened hit on the same gene in different populations. Here is an example calculation.

Let’s assume that in the course of the experiment, which ran for 30 days and about 140 generations of P. aeruginosa, some genes may undergo duplication events by chance. Next assume there is a particular gene that needs to be duplicated and modified in order to for P. aeruginosa to adapt to the new food source. (Note that there may be several such genes, but as we shall see that will not affect the conclusion). Given that there are four separate, independent trials, what is the probability that the gene will be duplicated in two or more of those trials?

Let P_dup be the probability that any gene is duplicated in the course of the experiment. For our gene of interest, it may be duplicated in 0, 1, 2, 3, or all 4 of the trials. The binomial distribution describes the probability, P, of each of these outcomes. To answer our question (i.e., What is the probability that the gene will be duplicated in two or more of those trials?) we sum the binomial distribution’s value for N = 2, 3 and 4. In other words, we calculate P(2) + P(3) + P(4).

This will give us the probability of observing what was observed in the experiment (i.e., the duplication events occurred repeatedly and independently, in different populations, in all 6 cases where duplication events were observed).

Well for a reasonable value of P_dup, the probability that any gene is duplicated in the course of the experiment, such as 0.0001, the probability of observing multiple duplications events for any given food source (i.e., P(2) + P(3) + P(4)) is about 60 in one billion, or 6  times 10^-8. Even worse, the probability of observing this in all 6 cases where duplication events were observed is about 5 times 10^-44.

It isn’t going to happen.

Exceptionally high rates of gene duplication, in particular genomic regions of Salmonella typhimurium, in a high growth rate medium, were observed to be about 0.001 and even slightly above 0.01 in rare cases.

If we go all out and set P_dup to an unrealistically high 0.1, our results are still unlikely. The P(2) + P(3) + P(4)) is .05, and the probability of observing this in all 6 cases where duplication events were observed is about 2 times 10^-8.

In order to raise these probabilities to reasonable levels, such that what was observed in the experiment is actually likely to have occurred, we need to raise P_dup to much higher values. For example, for a P_dup of .67 (two-thirds probability), P(2) + P(3) + P(4)) is .89, and the probability of observing this in all 6 cases where duplication events were observed is about .5.

But even this doesn’t work. For if we were to imagine unrealistically high P_dup values of 0.1 or higher, then massive numbers of duplication events would have been observed in the experiments.

But they weren’t.

Once again, the science contradicts the theory. Our a priori assumption that evolution is a fact, and that the P. aeruginosa adaptations to the new food sources were driven by random mutations, did not work. The theory led to astronomically low probabilities of the observed results.

What the observed gene duplications are consistent with is directed gene duplications. Just as mutations have been found to be directed in cases of environmental challenges, it appears that gene duplications may also be directed.

The paper’s premise, that biological innovations such as flowers and wings are analogous to bacteria adapting to new nutrient sources, is fallacious. But setting that aside, the experimental results do not make sense on evolution’s mechanism of random mutations and natural selection. Instead, the results indicate directed adaptation.

Thursday, May 5, 2016

Okeanos Explorer Searches The Deep Sea

What Will They Find Next?

There is a reason why explorers have always gone forth—they are rewarded. And so not surprisingly there have been many rewards for the National Oceanic and Atmospheric Administration’s Okeanos Explorer which is exploring the ocean floor, several miles beneath the surface, near the Marianas Trench. In this far away land the mission has found all manner of strange life forms never before seen. You can watch the video live and, as one report put it, “The video makes for strangely addicting viewing. There's a constant cliffhanger: What will they find next?”

What they have found is an array of incredible, and lowly (pun intended), creatures. Surely Ralph Cudworth and John Ray would have, by this point, doubled down on their infra-dignitatem argument that such creatures are beneath the Creator’s dignity. There must have been an intermediate creative force to account for the muck and its inhabitants, not to mention those bungles and errors we find in creation.

Isn't it amazing what those random mutations will come up with? (And no, natural selection doesn’t help).

Saturday, April 30, 2016

Life Begins With a Dramatic Burst of Light

The Light That Was Dark

Researchers studying the fertilization of human eggs are barred by federal law from using actual sperm. Federal law rightly imposes particularly strong restrictions on experiments on humans. Nonetheless, using sperm enzymes researchers have confirmed that at the moment of fertilization the human egg, as with other species, emits a dramatic burst of light. As one newspaper put it, “Bright flash of light marks incredible moment life begins when sperm meets egg.” And:

Human life begins in bright flash of light as a sperm meets an egg, scientists have shown for the first time, after capturing the astonishing “fireworks” on film.

One of the researchers described the burst of light as “breathtaking.”

All of this reminds us of something we already knew. In spite of evolutionist’s attempts to hide the science, the light shines through. Even federal law testifies to the fact—the scientific fact—that life begins, not at birth, not at some arbitrarily and conveniently selected point in development, but at conception. That is not a political argument or a religious belief. It simply is the science.

Friday, April 29, 2016

Evolution Arguments Are Not Holding Water

Absurd and Pathetic

Being an evolutionist means never having to say you’re sorry. Just look at Richard Dawkins who will say pretty much anything at any time, no matter how much it contradicts science or just plain logic. If he ever gets into trouble he can always lapse back into a rant about those creationist rascals and the audience will automatically erupt with applause. And so arguing evolution with an evolutionist is a lot like the Monty Python argument skit. They will pull out all manner of canards, misdirections, and fallacies, depending on their mood at the moment. One common example is the use of normal science as confirmatory evidence.

As Thomas Kuhn pointed out, science sometimes operates in paradigms. Scientific research on a particular problem can embrace a type of solution, or paradigm. The research tries to elaborate on and refine the paradigm, but otherwise does not question the paradigm. Paradigms provide a stable framework, within which concepts and terminology can be developed to support scientific thinking.

But because the paradigm is taken for granted and assumed from the start, the research conclusions do not generally confirm or prove the paradigm. The research work develops and critically examines concepts within the paradigm, but not the paradigm itself. Kuhn called the research work done with a paradigm normal science.

Evolutionary theory very much works this way. Normal science, within the evolution paradigm, takes it for granted that the world evolved—that everything arose from strictly naturalistic, chance events. That is, that the world arose spontaneously. Therefore in evolutionary research, the evidence is interpreted according to evolution. You could say the evidence is theory-laden.

A typical evolutionary research study goes as follows: Given that X evolved, here is how X probably evolved. All of this is at odds with the empirical evidence, and so the results inevitably lack all kinds of detail normally required in science, and include all kinds of improbable events normally unacceptable in science. It is a kind of storytelling underwritten by the paradigm.

This evolutionary normal science formula has produced a tremendous volume of literature, ranging from journal papers to popular works. And, one of the favorite lines of argumentation, when evolution is rightly questioned, is to point to this “mountain” of evidence. A simple internet search can usually be counted on to produce dozens of papers advertising “The Evolution of Echolocation in Bats” or whatever wonder the skeptic has in mind as problematic for evolution.

Of course, if anyone were ever actually to read the produced papers (and usually the evolutionist presenting the paper has not), that person would find a marked absence of any actual scientific description of how echolocation, or whatever, actually did, in fact, evolve.

Normal science is used inappropriately as confirmatory evidence. When we explained, for example, that epigenetics in plants contradicts evolution, an evolutionist caustically responded with a paper subtitled: “The Evolution of a Complex Epigenetic Pathway in Flowering Plants.”

And did that paper actually explain “The Evolution of a Complex Epigenetic Pathway in Flowering Plants”?

No. The paper presupposed “The Evolution of a Complex Epigenetic Pathway in Flowering Plants.” As we explained, the paper presents several dubious “findings” of how epigenetics evolved which, in fact, are not supported by the science and instead are completely beholden to the assumption that evolution is true.

The paper’s highly unlikely scenarios of how evolution occurred are underwritten and mandated by the a priori assumption that (drumroll), evolution occurred.

And when we pointed this out, the evolutionist next retorted:

In the same way NASA and ESA assume the Earth is a globe and not flat every time they launch a satellite into orbit. What were those dumb space scientists and engineers thinking using assumptions??

Which brings us back to Monte Python and the argument skit. There’s always another canard. After inappropriately using normal science as confirmatory evidence, and having the fallacy explained in no uncertain terms, the evolutionist effortlessly switches over to the next available fallacy: riding the coattails of science.

The analogy between the age-old Epicurean claims that the world spontaneously arose, and space flight, is of course absurd and pathetic. It reveals how silly is evolutionary thought. But like the Monte Python skit, evolutionists will always have another argument.

Religion drives science, and it matters.

Saturday, April 23, 2016

RNA-Directed DNA Methylation: The Evolution of a Complex Epigenetic Pathway in Flowering Plants


The problem with epigenetic mechanisms is that they respond to future, unforeseen, environmental challenges. They don’t work in the present, and so even if random mutations somehow created such mechanisms, they would not be selected for. In other words, epigenetic mechanisms contradict evolutionary theory—there is no fitness improvement at the time of origin by random mutations, so there is no selection. Nor do evolutionists have an explanation for this—they don’t even try. Consider a paper discussing a particular epigenetic mechanism subtitled: “The Evolution of a Complex Epigenetic Pathway in Flowering Plants.”

The paper discusses a complicated cellular process in which different segments of DNA are copied (creating RNA transcripts). The RNAs work together to methylate the DNA at a particular location. The methylation “mark” helps to regulate gene expression. But how did this epigenetic mechanism evolve?

This epigenetic mechanism involves a small army of molecular machines. For instance, the different RNAs are transcribed, from the DNA, by different copying machines. These copying machines consist of a dozen protein subunits. The paper states that two of the copying machines—which are central to the epigenetic mechanism—each evolved from a third copying machine. Why?

The idea of the two copying machines evolving from the third copying machine is problematic because there are significant differences between them. The paper gives no justification for such an unlikely event. It gives no justification because there is none, save for the presupposition that evolution is true. Under evolutionary theory it must have occurred.

In other words, there is no empirical evidence that the two copying machines evolved from the third copying machine and there are enormous problems with the idea. But it is taken as a given because evolution is assumed to begin with.

The point here is that in attempting to explain the evolution of a complex epigenetic pathway the paper presupposed evolution a priori.

Similarly, the paper states that the two copying machines “are evolving rapidly.” Again, where did this come from? Does the science actually show this to be true? Does the science even merely provide any evidence at all for this astonishing claim?

Again, no and no.

Nowhere does the science demonstrate or prove that the two copying machines “are evolving rapidly.” In fact, the science doesn’t even provide any evidence at all for this.


What the science shows is that the proteins in the two copying machines have significant differences compared to the corresponding proteins in the third copying machine. The two copying machines are more different from the third copying machine, than would normally be expected if they had evolved from that third copying machine.

But since evolution is assumed to be true to begin with, then those two copying machines must be “evolving rapidly.”

Again, the claim is driven by the belief that evolution is true. There is no empirical evidence that the two copying machines are evolving rapidly, let alone that they even evolved at all.

This is all dogma. There is no science here.

The paper then spends considerable effort attempting to reckon with the various problems that arise when their evolutionary history is assumed. There are duplication events and introns are mysteriously inserted. There are fusion events to explain unexpected differences, and other cases are simply unknown. There must have been a complex series of evolutionary events the reasons for which “remain obscure,” and the evolutionary origin of one gene is “a mystery.”

It is a long sequence of just-so stories. A long sequence of special events just happened to happen, which luckily produced this new epigenetic mechanism.

And then, after all of this, it would not be selected for. All of these events, and the resulting epigenetic mechanism would not improve the evolutionary fitness.

This evolutionary tale is not supported by the empirical evidence. Instead, it is supported by the prior assumption that evolution occurred.

Friday, April 22, 2016

“Evolution” of Darwin’s Finches Tracked at Genetic Level

Fat, Drunk and Stupid

One thing we can all agree on is that the infamous finches on the Galápagos Islands are a classic icon of evolution. The difference is that evolutionists are playing the fool. Ever since Darwin wondered aloud that if the different types of finches he saw on the Galápagos Islands were not merely variants of a species, but in fact different species, then it “would undermine the stability of species,” and therefore the finches (and everything else) must have spontaneously arisen, evolutionists’ dullness has been embarrassing. Like the co-worker who reveals his ignorance as he rambles on about his pet peeve, evolutionists positivistic proclamations about the finches reveals an astonishing level of ignorance.

Darwin’s findings on the Galápagos Islands told him precisely nothing about how the finches, or anything else for that matter, could spontaneously arise as he would claim. Instead, it was all a silly, eighteenth century, non-scientific, religious argument. God would never create those finches, so they must have evolved.

To this day evolutionists continue to parrot this silly argument as though it has any relevance to modern science. And so not surprisingly, they import their centuries-old, religious views into today’s science, failing to comprehend what it actually means. Witness yesterday’s news item from the leading journal, Nature, which begins:

Researchers are pinpointing the genes that lie behind the varied beaks of Darwin’s finches – the iconic birds whose facial variations have become a classic example of Charles Darwin's theory of natural selection.

A classic example? It is a classic example of how utterly non scientific evolutionary “theory” is. The article discusses particular genes that have been identified as influencing the size and shape of the finch’s beak. And it rehearses the myth that changes that occurred in the finch populations over the course of recent drought years reveal “evolution in action”:

Shifts in this gene underlay an evolutionary change that researchers watched in 2004-05, during a drought that ravaged the Galápagos Islands, where the finches live. The beak sizes of one population of finches shrank, so as to avoid competing for food sources with a different kind of finch – and their genetics changed accordingly.

Of course there was no “evolution in action.” This is evolutionary mythology.

The finch’s beaks altered in response to the drought. The finches were still finches. No new finches arose, and no new beak designs arose.

This is not a story of random mutations luckily finding a new, improved, design that was then fixed in the population via natural selection. Preexisting genes influenced preexisting beak designs in preexisting finch species. And when the drought ceased the populations cycled back to their pre drought designs. New designs were not created.

But that is the science, and evolution never was about the science. Evolutionist’s on-going claims about the Galápagos finches are non scientific and, frankly, ridiculous. The finches truly are a classic icon of evolution. They don’t reveal a case of evolution in action, but rather evolutionary thought in action.

Tuesday, April 19, 2016

Name It / Claim It: Epigenetics Now Just Another Evolutionary Mechanism

In Spite of the Cognitive Dissonance

It is often said that all truth passes through three stages. First, it is ridiculed. Second, it is violently opposed. Third, it is accepted as being self-evident. And so it is with epigenetics which evolutionists opposed and blackballed for a century before finally appropriating it as just another mode of evolutionary change. (see here, here, and here for more discussion of this history of misdirections regarding Lamarckism and epigenetics). Here is an example of evolutionists, after a century of denial and rejection, claiming epigenetics as their own.

Our example comes from this 2011 review paper on epigenetics in plants. Since plants are sessile they cannot simply move away from environmental challenges that occur. Therefore they need adaptation mechanisms. And since seeds are dispersed not too far from the parent plant, the next generation is likely to face the same environmental challenge. Therefore the adaptation mechanisms should be transgenerational, or heritable. Finally, since environmental challenge may be relatively short lived, lasting only a few generations, there is insufficient time for evolution by random mutations and natural selection to act. Therefore the adaptation mechanisms need to be fast-acting and reversible. These various requirements make epigenetics an “attractive alternative”:

The heritability of reversible epigenetic modifications that regulate gene expression without changing DNA sequence makes them an attractive alternative mechanism.

Note the design language. Not only are evolutionists naming and claiming the once evil epigenetics as just another mode of evolution, they also identify it as “an attractive alternative mechanism,” which is precisely how engineers discuss their design options.

Note, as we have discussed, the notion that such epigenetic mechanisms are just another mode of evolution makes no sense for several reasons. Unlike evolutionary change which is slow, epigenetics is fast. Unlike evolutionary change which propagates through the population from a single mutation occurring in a single individual, epigenetics works in parallel, occurring in many individuals across the population. Unlike evolutionary change which must come about by the selection of changes that must not be induced by the environment, epigenetics is induced by the environment. Unlike evolutionary change which generally is not repeatable, epigenetics is repeatable.

Furthermore, epigenetic mechanisms are, themselves, sophisticated designs. Their origin is far beyond evolution’s meager resources. Random mutations are not going to produce such directed adaptation mechanisms. And even if such a miracle were to occur, it would not survive, because it would not be selected for. This is because such mechanisms provide a differential reproductive advantage, and therefore a fitness improvement, not under the current conditions, but under some future, unforeseen conditions. There is no fitness improvement at the time of origin by random mutations.

There is a reason why evolutionists have so vehemently opposed this Lamarckian idea—it contradicts evolutionary theory. But like saltationism which was once rejected (by Darwin) due to its obvious implications, only to be guardedly accepted years later when the coast was clear (though it makes no sense on evolution), so too epigenetics must be accepted while downplaying the cognitive dissonance it forces on evolution.

Saturday, April 16, 2016

Birds Developed Cognitive Adaptations to Beat the Ants

The Philosopher is Dead, Long Live the Philosopher

Think Aristotelianism went out with Galileo? Think again—teleological language is rampant in the evolution literature because that is how evolutionists think. A new paper in Nature Communications on dietary influences on bird evolution states that “birds that attend army ant raids have to deal with the unpredictability of those raids, and have developed cognitive and behavioural adaptations to surpass these challenges.” As usual, the infinitive form tells the tale. This isn’t a one-off slip of the pen. The underlying Aristotelianism in evolutionary thought has been noted repeatedly. Evolutionists have even scolded themselves for their malapropisms. But they can’t stop describing evolution as a target-driven, goal-oriented, design-like process. It just makes no sense otherwise.