I'm looking forward to Michael Behe's third book, which is due to be published in February. As most of you probably know, Michael Behe is a biochemist and a former professor at Lehigh University in Scranton, Pennsylvania, USA. He's also a senior fellow at the Discovery Institute’s Center for Science & Culture—the most prominent organization pushing Intelligent Design Creationism.
This will be Behe's third book. The first one was Darwin's Black Box (1996) where he argued against evolution by suggesting that some cellular complexes (e.g. bacterial flagella) are irreducibly complex and could not possibly have evolved by natural means. His second book was The Edge of Evolution (2007) where the theme was that there are limits to evolution preventing it from accomplishing significant beneficial changes.
I haven't read his third book but it looks like it will continue the pattern of trying to show that evolution is flawed rather than trying to show evidence of intelligent design. David Klinhoffer has posted a quotation from the new book indicating that the main approach is to argue that evolution can break things but not construct things [For #GivingTuesday, Help Michael Behe Demonstrate that Darwin Devolves].
This book…concentrates on completely unexpected, devastating new problems that could only have come to light after major recent advances in technical methods for probing the molecular level of life. With surpassing irony it turns out that, as with the polar bear, Darwinian evolution proceeds mainly by damaging or breaking genes, which, counter-intuitively, sometimes helps survival. In other words, the mechanism is powerfully de-volutionary.
Behe is one of the few ID proponents worth engaging because his arguments are much better than those of his colleagues at the Discovery Institute. Behe accepts common descent and limited examples of evolution and he rejects Young Earth Creationism.
You might imagine that Behe would take on his YEC colleagues as fiercely as he fights evolutionary biologists, but he doesn't. I find it very strange that ID proponents who still believe in a young Earth are fans of Michael Behe but I suppose they are happy because Behe is attacking evolution and as long as he keeps the focus on attacking a common enemy they are happy.1
Those of you who read the first two books will recall that they were also about "devastating problems" with evolution that only came to light with new research revealed in 1996 and 2007. For some strange reason the textbooks have not been re-written and the churches have not filled up with new converts. What happened?
Refuting his first book was pretty straightforward because Behe based his argument on his inability to imagine how an irreducibly complex system could have evolved by natural means. All we had to do was show that irreducibly complex systems could evolve without the help of a designer and this turned out to be relatively easy.2
Refuting his second book was much harder—not because he was making a valid scientific argument but because showing where he goes wrong requires a fairly deep understanding of modern evolution. Behe was arguing that many presumed examples of evolution required three or more mutations in order to produce a beneficial effect. He claims that in many cases none of the individual steps are beneficial and some of them might even be detrimental. Thus, three mutations have to occur simultaneously and that's not possible—it's beyond the edge of evolution.
Behe would be correct if the only way to fix mutations was by positive natural selection. That's the old-fashioned, adaptationist view of evolution from the 1960s and it's the view that dominates the thinking of ID proponents. But with the development of Neutral Theory and it's off-shoot, Nearly-Neutral Theory, we now know that neutral and detrimental alleles can be maintained in a population for a long time because random genetic drift is often as potent a mechanism as natural selection.3
Thus, it's relatively simple to imagine how a new system requiring several mutations can evolve under modern evolutionary theory and this extends the edge of evolution far beyond the limits postulated by Michael Behe.4 In fact, it's easy to show that this is exactly how Behe's favorite example, chloroquine resistance to malaria, evolved. But, while such ideas are easy for most of us, they are still very difficult for most creationists, including Behe. You can see for yourself how he resists any explanation involving random genetic drift [Revisiting Michael Behe's challenge and revealing a closed mind].
It's kinda cute to see that the Discovery Institute is still under the illusion that they can discredit evolution and convince the world that a creator god exists. It's been more than 20 years since Intelligent Design became a popular creationist idea and the predictions from back then were that by now we would all be creationists. Instead, evolution is as strong as ever and people all over the world are abandoning religion.
I'm 100% certain that I can refute Behe's latest claim because I've seen it all before. Nevertheless, I will wait until I've read the book so the creationists can enjoy their yearly round of gloating and premature celebration. It's just about the only thing they have going for them these days.
The irony meter was a running joke on the newsgroup talk.origins back in the last century. Our irony meters were supposed to protect us from the craziness of creationists but as soon as we built a really good irony meter a new bit of creationist crazy came along and fried it. Apparently Jesus and Mo have the same problem.
This is the second post discussing creationist1 papers on pseudogenes. The first post addressed a paper by Jeffrey Tomkins on the β-globin pseudogene [Creationists questioning pseudogenes: the beta-globin pseudogene]. This post covers another paper by Tomkins claiming that the GULO pseudogenes in various primate species are not derived from a common ancestor but instead have been deactivated independently in each lineage.
The Tomkins' article was published in 2014 in Answers Research Journal, a publication that describes itself like this:
ARJ is a professional, peer-reviewed technical journal for the publication of interdisciplinary scientific and other relevant research from the perspective of the recent Creation and the global Flood within a biblical framework.
Tomkins explains two fundamental axioms of Young Earth Creationism.
"An emerging theme from the continuing progression of genomics research across the spectrum of eukaryotic life is the widespread decay of pathways for vitamin-synthesis (Helliwell, Wheeler, and Smith 2013). This paradigm is of great importance to the creationist model of genetic entropy which postulates that genomes are in a continual state of degradation over time, not forward progressing evolution (Sanford 2010)."
"Another important component of the creationist model of origins is the idea of molecular discontinuity between unrelated taxon (Tomkins and Bergman 2013). As will be demonstrated in this report, the enigma of the GULO pseudogene analyzed in the light of new genomic evidence most closely aligns with a creationist model incorporating both of these paradigms."
The idea here is that the loss of a gene for synthesizing vitamin C (GULO gene)2 is consistent with the YEC view of increasing loss and degradation of the genome. Such degradation must occur within species since the YEC model doesn't allow for shared ancestry. The main question Tomkins addresses is whether the pattern of GULO pseudogenes in various species is consistent with gene loss in an ancestral species and subsequent inheritance of a pseudogene in different lineages or whether the pattern is consistent with separate and independent loss in related species.
As you might have guessed, Tomkins argues that that the pattern is inconsistent with common ancestry and lends support to Young Earth Creationism. Here's the article ...
The Human GULO Pseudogene—Evidence for Evolutionary Discontinuity and Genetic Entropy Jeffrey P. Tomkins, Institute for Creation research, Dallas, TX, USA Answers in Genesis
Abstract: Modern genomics provides the ability to screen the DNA of a wide variety of organisms to scrutinize broken metabolic pathways. This wealth of data has revealed wide-spread genetic entropy in human and other genomes. Loss of the vitamin C pathway due to deletions in the GULO (L-gulonolactone oxidase) gene has been detected in humans, apes, guinea pigs, bats, mice, rats, pigs, and passerine birds. Contrary to the popularized claims of some evolutionists and neo-creationists, patterns of GULO degradation are taxonomically restricted and fail to support macroevolution. Current research and data reported here show that multiple GULO exon losses in human, chimpanzee, and gorilla occurred independently in each taxon and are associated with regions containing a wide variety of transposable element fragments. Thus, they are another example of sequence deletions occurring via unequal recombination associated with transposable element repeats. The 28,800 base human GULO region is only 84% and 87% identical compared to chimpanzee and gorilla, respectively. The 13,000 bases preceding the human GULO gene, which corresponds to the putative area of loss for at least two major exons, is only 68% and 73% identical to chimpanzee and gorilla, respectively. These DNA similarities are inconsistent with predictions of the common ancestry paradigm. Further, gorilla is considerably more similar to human in this region than chimpanzee—negating the inferred order of phylogeny. Taxonomically restricted gene degradation events are emerging as a common theme associated with genetic entropy and systematic discontinuity, not macroevolution.
The GULO gene encodes the enzyme L-glucono-γ-lactone oxidase, the terminal enzyme in the synthesis of ascorbic acid. Ascorbic acid is required in the synthesis of collagen and a few other processes in mammals. Mutations in the GULO gene can lead to loss of function but this is not lethal in many species because they get enough ascorbic acid in their diet.
The human gene is nonfunctional giving rise to a unitary pseudogene located on chromosome 8 at p21. As a result, ascorbic acid is now an essential component of the human diet. Because it has become essential, it is now called a vitamin (vitamin C) (see Helliwell et al., 2013) [Human GULOP Pseudogene].
The standard explanation for the origin of this pseudogene—and all other unitary pseudogenes—is that the original gene became inactivated by mutation at some time in the past. That null allele then became fixed in the population by random genetic drift. All descendants of that population inherited the pseudogene.
Tomkins takes a scattergun approach to the problem by bringing up all kinds of objections to the standard explanation. I don't have time to discuss all of his objections and I don't have enough knowledge of some of the issues to respond to his points. For example, I don't know enough about bird evolution to say whether the pattern of GULO gene loss is compatible with common ancestry or not.
Let's just look at the pseudogenes in primates to see which explanation is more reasonable. Lapachapelle and Drouin (2011) looked at the pattern of neutral substitutions in the primate lineages. All Haplorrhini3 primates (e.g. humans, chimpanzees, macaque, gibbon etc) have a pseudogene with certain shared characteristics, including a number of identical substitutions. This suggests that the ancestor of all Haplorrhini primates contained the pseudogene, which must have arisen shortly after the the split between Haplorrhini and Strepsirrhini (lemurs, galagos, etc.). According to the fossil record, the split occurred about 63 million years ago.
Lapachapelle and Drouin calculated that the pseudogene must have arisen about 61 Mya based on the neutral substitution rate. The fact that these values are so close lends support to the idea that all Haplorrhini species are derived from a common ancestor that lost the GULO gene.
The authors also looked at specific deletions to see if the results are consistent with common ancestry. All of the primate pseudogenes are missing exons 1 and 2 of the intact, functional, gene.4 They compared the sequences of the human, chimpanzee, and macaque genes to that of the galago gene. The result is shown in Figure 4 of their paper (see below).
Note that the large deletion of the two exons ("deletion") occurs at the same position in the human, chimpanzee, and macaque genomes. All three genomes also have two identical seven base pair indels in the upstream region preceding exon 1. This is evidence of common ancestry.
Lachapelle and Drouin were testing the hypothesis that large deletions in the GULO pseudogene were due to aberrant recombination between flanking transposable elements (TE). They mapped all surrounding transposons in the primate genes and concluded that TE's did not play a role in the deletion.
Tomkins discusses this paper in his creationist journal article. He ignores the evidence of common descent and focuses instead on the transposable elements. He points out that Lachapelle and Drouin failed to find evidence that TE's were responsible for the deletions. Here's what he wants his readers to conclude from a paper that strongly supports common descent ....
Despite the fact that TEs are apparently one of the main genomic drivers of deletion events in the genome, the researchers (Lachapelle and Drouin 2011) concluded that the lineage specific TE insertion patterns, which defied the standard inferred evolutionary model for primates, did not contribute to the loss of exons in the GULO gene. Thus, their evolutionary presuppositions caused the rejection of otherwise strong genomic data that implicated TE related unequal recombination at the GULO locus (resulting in exon deletion) that occurred in taxonomically restricted events.
I think it's disingenuous of Tomkins to focus on that aspect of the study while ignoring all the evidence for common descent.
The GULO pseudogene locus on human chromosome 8 is in a gene-rich region. Orthologous genes are present at the same site in all vertebrate species although the order of the surrounding genes has been repeatedly shuffled by microrearrangements (Yang, 2013).
The presence and order of the exons within the GULO gene/pseudogene in diverse vertebrates is consistent with several independent inactivations and descent from a common ancestor (Yang, 2013). One of them occurred in the primate lineage. All of the primate pseudogenes are missing exons 1 & 2 as well as exons 5, 7, and 10 as shown in the figure below.
The data is consistent with an ancestral pseudogene gene that was missing exons 1, 2, 5, 7, and 10. Exons 3 & 4 were subsequently lost in a separate events in the gibbon lineage. The orangutan and human pseudogenes are similar with respect to exon loss and the chimpanzee pseudogene is probably the same. (The 5′ region of the GULO pseudogene was not present in the chimp genome sequence.)
Tomkins doesn't discuss the evidence for the common ancestry of the primate pseudogenes and he doesn't try to explain the pattern according to a Young Earth Creationist worldview. Instead, he draws attention to another part of Yang's paper—the part where he documents the rearrangements of the genes surrounding the GULO locus. There's nothing unusual about such rearrangements. They are common between closely related species and even within a species. Over time, blocks of genes are shuffled and re-ordered so that distantly related vertebrates show very little synteny.
Tomkins thinks this is a serious problem for evolution ...
The GULO gene lies within a gene-dense region in all vertebrate genomes studied thus far (Yang 2013). Related to this fact is the evolutionary anomaly that the gene neighborhood surrounding the GULO locus is rearranged across the vertebrate spectrum of life, and the patterns cannot be readily resolved into the standard inferred evolutionary lineages (Yang 2013).
Once again, Tomkins is cherry-picking the data to focus on minor anomalies that don't fit with his strawman version of evolution. Once, again, he ignores the much more important data in the same paper that supports an ancient origin of an ancesral GULO pseudogene.
Let me close by mentioning one other "anomaly" that Tomkins raises. He questions whether the functional rat gene is an appropriate standard of comparison. You might be amused by his logic ...
Traditionally, the human GULO pseudogene has been compared to the functional rat GULO gene (Nishikimi, Kawai, and Yagi 1992; Nishikimi et al. 1994; Ohta and Nishikimi 1999). According to the UCSC genome browser (genome.ucsc.edu) and the Rat Genome Database (rgd.mcw.edu), the rat GULO gene (chr15, region p12) is oriented and transcribed on the minus strand. Interestingly, the human and ape GULO pseudogenes are oriented in the plus strand configuration (chr8, region p21.2 in human). While the rat GULO gene may serve as a general guide to exon presence and absence in degraded GULO genes in other mammals, the rat GULO is clearly in a different chromosomal configuration (compared to humans and apes) and represents a unique design pattern specific to rodents (mouse GULO is on chr15, minus strand).
Jonathan Kane recently (Oct. 6, 2017) posted an article on The Panda's Thumb where he claimed that Young Earth Creationists often don't get enough credit for raising serious issues about evolution [Five principles for arguing against creationism].
He mentioned some articles about pseudogenes as prime examples. I asked him for references and he responded with two articles by Jeffrey Tomkins that were published on the Answers in Genesis website. The first was on the β-globin pseudogene and the second was on the GULO pseudogene. Both articles claim that these DNA sequences aren't really pseudogenes because they have functions.
I'll deal with the β-globin pseudogene in this post and the GULO pseudogene in a subsequent post.
Here's the article ....
The Human Beta-Globin Pseudogene is Non-Variable and Functional. Jeffrey P. Tomkins, Institute for Creation research, Dallas, TX, USA Answers Research Journal
Abstract: One of the iconic (yet enigmatic) arguments for human-ape common ancestry has been the β-globin pseudogene (HBBP1). Evolutionists originally speculated that apparent mutations in HBBP1 were shared mutational mistakes derived from a human-chimpanzee common ancestor. However, others noted that if the gene was indeed non-functional, then it should have mutated markedly in the past 3 to 6 million years of human evolution due to a lack of selective constraint on the region. Recent research confirms that the HBBP1 region of the 6-gene β-globulin cluster is highly non-variable compared to the other β-globin genes based on large-scale DNA diversity assessment within both humans and chimpanzees. Highlighting the lack of HBBP1 sequence variability is genetic data from three different reports that link point mutations in the HBBP1 gene with β-thalassemia disease pathologies. Biochemical evidence for functionality is indicated by multiple categories of functional genomics data showing that the HBBP1 gene is transcriptionally active and a key interactive component of the β-globin gene network. In brief, the HBBP1 gene encodes two consensus regulatory RNAs that are alternatively transcribed and/or post-transcriptionally spliced. This functional complexity produces at least 16 different exon variant transcripts and 42 different intron variant transcripts. Two major regulatory regions in the HBBP1 locus contain active transcription factor binding sites that overlap multiple categorical regions of epigenetic data for functionally active chromatin. The HBBP1 gene also has the most regulatory associations with active and open chromatin within the entire β-globin cluster and its transcripts are expressed in at least 251 different human cell and/or tissue types. Instead of being a useless genomic fossil according to evolutionary predictions, the HBBP1 gene appears to be a highly functional and cleverly integrated feature of the human genome that is intolerant of mutation.
Before addressing the specific criticisms in this article it's important to not lose sight of the bigger issue. Creationists tend to focus on particular examples while ignoring the big picture. In this case, there is abundant evidence of gene duplications in all species and there's abundant evidence that the fate of one duplicated copy of a gene is often to become inactivated rendering it a pseudogene. This has given rise to a robust explanation of multigene families referred to as Birth-and-Death Evolution [The Evolution of Gene Families] [On the evolution of duplicated genes: subfunctionalization vs neofunctionalization]. In order for Young Earth Creationists to mount a serious challenge to evolution they need to provide a better explanation for all this data and they need to provide solid evidence that the Earth is less than 10,000 years old.
There are about 15,000 pseudogenes of various kinds in the human genome. You can't challenge the big picture of pseudogenes and junk DNA by picking out one example and trying to prove it has a function. This will not refute evolution even if it turns out to be true that one particular stretch of DNA looks like a pseudogene but actually has a function. And it certainly won't be evidence of a Young Earth.
Now let's deal with the Tomkins article. Here's a diagram showing the pseudogene in the β-globin gene cluster in humans and chimps.
There's a pseudogene at this locus in most of the great apes—an observation that's consistent with a duplication event tens of million of years ago followed by the loss of function of one of the copies. The pseudogene became fixed in the ancestral population and was passed down to all modern species. The rate at which most of the pseudogene sequence has accumulated base substitutions is consistent with the rate at which neutral mutations are fixed by random genetic drift. This indicates that most of the sequence is not under negative selection. As far as I know, creationists—especially Young Earth Creationists—haven't offered a reasonable explanation of this observation.
Tomkins' main point is that this stretch of DNA has a function so, presumably, the creator(s) copied this useful part of the genome and plugged it into one of the chromosomes as they were building each of the species. They didn't really care very much about the surrounding DNA so they didn't worry about copying it exactly. As it turns out, they introduced differences in the surrounding DNA so that the sequences of chimps and humans differ by about 2% and chimps and gorillas differ by about 4%. Humans and gorillas also differ by about 4%. The important point is that there are far fewer differences in the exons of the functional genes so they look "conserved" if you adopt an evolutionary perspective.
There's a stretch of DNA near the human β-globin pseudogene that has far fewer changes if you examine the chimp and human genomes. In evolutionary terms, it is "conserved." (It is reusable design if you are a Young Earth Creationist.) Tomkins quotes a paper by Moleirinho et al. (2013) documenting this conservation. The explanation is that the region between the γ-globin genes and the pseudogene is involved in regulating expression of the β-globin genes, probably because it contains a scaffold attachment site and associated sequences that regulate chromatin conformation. This role appears to have arisen shortly before the divergence of chimps and humans.
Here's what the sequence similarities look like on the UCSC Genome Browser. The degree of sequence similarity between the human genome and the genomes of chimps, gorillas, orangutans, and monkeys is shown as a histogram where the height of the bar indicates significant similarity. As you can see, the exons of the functional genes are conserved but the pseudogene sequence is not conserved. This is exactly what you expect if the pseudogene sequence is gradually drifting away from the ancestral gene that was functional right after the gene duplication event.
Much of the sequence surrounding the γ-globin genes is under selection, including a stretch that extend toward the pseudogene. This is the regulatory region that controls expression of the entire locus.
Thus, the evolutionary explanation is that a gene duplication occurred and one of the copies became a pseudogene. Subsequently, a region in the vicinity of the pseudogene acquired a new function involved in chromatin looping and regulation. That's why a large stretch of DNA near the γ-globin gene is conserved. I don't know how Tomkins explains the data other than just saying that the presence of function casts doubt on evolution.
Tomkins' other evidence for function relies on the ENCODE data. He notes that the pseudgogene region is transcribed as part of the pervasive transcription noted by ENCODE. It also contain numerous transcription factor binding sites, DNase I sensitive regions, and histone markers. Some of this might be remnants of the original gene but most are just spurious events that occur throughout the genome in junk DNA. Sandwalk readers will be familiar with the idea that ENCODE data does not prove function.
John Harshman send me his comparison of the β-globin region on the UCSC Genome Browser.
As you can see, the pseudogene region seems to be only slightly less conserved than the functional genes in this analysis. This isn't unexpected. The functional genes will drift apart over 100 million years by accumulating neutral mutations in the coding regions. The pseudogene arose about 65 million years ago in primate ancestors so it will have accumulated mutations at a faster rate since that time but not before. The difference in the primate lineage should amount to about 20% in that time.
When you compare the "conservation" of the various loci using an outgroup to the primate lineage, the pseudogene will only be about 20% less conserved than the functional genes. That's pretty much what you see in the figure.
When you do a binary comparison (e.g. chimp vs human), I'm assuming the algorithm subtracts the neutral mutation rate in order to calculate whether a sequence is conserved or not. Thus, in my figure, the pseudogene region only shows up as a small blip. This may be statistical error or a small bit of conserved sequence within the the second exon.
That's how I interpret the results. Any help will be appreciated. If you know how to get % sequence similarity comparisons on this browser then please post that information in the comments or email me.
Moleirinho, A., Seixas, S., Lopes, A.M., Bento, C., Prata, M.J., and Amorim, A. (2013) Evolutionary constraints in the β-globin cluster: the signature of purifying selection at the δ-globin (HBD) locus and its role in developmental gene regulation. Genome Biology and Evolution 5:559-571. [doi: 10.1093/gbe/evt029]
Before reading that review, let's make sure we understand Jerry's position. Here's what he says on page xx of his book.
My main thesis is narrower and, I think, more defensible: understanding reality, in the sense of being able to use what we know to predict what we don't, is best achieved using the tools of science, and is never achieved using the methods of faith. That is attested by the acknowledged success of science in telling us everything from the smallest bits of matter to the origin of the universe itself—compared with the abject failure of religion to tell us anything about gods, including whether they exist.
Jerry's position is that science is a way of knowing and it has been remarkably successful at discovering truths. There are no other ways of knowing that have found truths.
I'll argue that in fact science is the only way to find such truths—if you construe "science" broadly.
I agree with his broad definition of "science" and I agree that science is the only proven way of acquiring knowledge.1 I also agree with his view that science vs religion is a subset of the real conflict; namely, rationalism vs superstition.
Believers accept the existence of their god(s) without defensible evidence to support that belief. The science way of knowing rejects the idea that you would believe in anything without supporting evidence and logic. Thus, science and religion are not compatible.
Now, read Derrick's review to see how a "sophisticated theologian" deals with the main thesis of Jerry Coyne's book. What you'll see is the typical obfuscation and avoidance that characterizes such theologians.
Keep in mind what Jerry says about so-called "sophisticated" theologians, "... while theologians may know more about the history of religion—or the works of other theologians—than do regular believers, they have no special expertise in discerning the nature of God, what he wants, or how he interacts with the world." [my emphasis LAM]
1. We can quibble about whether mathematics is another way of knowing that falls outside of the broad definition of science. I don't think it does but that debate has nothing to do with the science vs religion conflict.
We all know that the purpose of education should be to teach students how to think critically. We're not doing a very good job. Take biochemistry, for example. We spend a lot of time transferring information from lecture notes to student notes and then examining students on whether the transfer has worked. We think that teaching students to read the primary literature will make them better scientists when, in fact, teaching them to be skeptical of the primary literature is what's really necessary.
The ENCODE fiasco is just one of many examples where the scientific literature got it wrong. We need to make sure that our students appreciate the important parts of science; namely, the necessity of repeating experiments and the value of scientific consensus. Our students, and many of my colleagues, are prone to hype and promotion just like every one else but that's exactly what critical thinking is supposed to avoid. And it's exactly what proper science—no matter how you define it—is designed to overcome.
If students and scientists are having trouble with these concepts, imagine how difficult it is for the general public. How are they supposed to know that not every "breakthrough" is a real breakthrough and not every new study is correct?
John Oliver did an excellent job of explaining the problem on a recent (May 8, 2016) episode of Last Week Tonight. Watch it. It's worth 20 minutes of your time. The last bit on "Todd Talks" is classic.
A large statue of Charles Darwin was installed in the main foyer of the London's Natural History Museum in 1885—just a few years after Darwin's death. It was removed in 1927 and replaced by a statue of Richard Owen who was no fan of Darwin.
The museum came to its senses in 2009 and put the statue back in it's original position. (It had been in the cafeteria in the basement.) Read the story at: Moving Darwin.
Owen was the man who founded the museum and he was also known for his support of structuralism—the idea that basic body plans cannot be easily explained by evolution. Structuralism is the new buzzword among Intelligent Design Creationists. They don't understand the concept but they're certain it refutes evolution and supports goddidit.
Watch Paul Nelson combine his lack of knowledge of evolution and evolutionary theory with misinformation (i.e. lies) and a little bit of false developmental biology then stir the pot with a large dose of god-of-the-gaps to produce a smooth argument that refutes evolution.
There's lots of other stuff going on in this talk. I was especially amused by the discussion of methodological naturalism at the end. Paul Nelson argues that science is blind to all the evidence of a creator because the "rule" of science is that it can't even consider that evidence.
I'll say one thing about this talk: it's very clever. It would take a book to show that Paul Nelson is wrong about everything and the explanations would be far too complicated for the average creationist. For them, it's easier to believe that Paul Nelson is telling them the truth and evolutionary biologists are too stupid to understand their own discipline.
Otangelo Grasso has posted a transcript of the talk. Thank-you Otangelo.
Antonin Gregory Scalia (March 11, 1936 – February 13, 2016), justice of the Supreme Court of the United States, died a few days ago. This creates a crisis in American politics because they have a strange set of Constitutional requirements guaranteed to maximize the probability of crises every time they need a new Supreme Court justice.
Scalia's death reminded me of the dissenting opinion in EDWARDS V. AGUILLARD (June 19, 1987). This was the case that invalidated Louisiana's "Balanced Treatment for Creation-Science and Evolution-Science Act." Stephen Jay Gould was puzzled by the dissenting opinion so he wrote a wonderful essay to explain Justice Scalia's Misunderstanding.
It's worth reading the entire essay but here's the conclusion,
Following this theme, Scalia presents his most confused statement in the written dissent:
Creation science, its proponents insist, no more must explain whence life came than evolution must explain whence came the inanimate materials from which it says life evolved. But even if that were not so, to posit a past creator is not to posit the eternal and personal God who is the object of religious veneration.
True indeed; one might be a creationist in some vernacular sense by maintaining a highly abstract and impersonal view of the creator. But Aristotle's unmoved mover is no more part of science than the Lord of Genesis. Science does not deal with questions of ultimate origins. We would object just as strongly if the Aristotelophiles of Delaware forced a law through the state legislature requiring that creation of each species ex nihilo by an unmoved mover be presented every time evolution is discussed in class. The difference is only historical circumstance, not the logic of argument The unmoved mover doesn't pack much political punch; fundamentalism ranks among our most potent irrationalisms.
Consider also, indeed especially, Scalia's false concept of science. He equates creation and evolution because creationists can't explain life's beginning, while evolutionists can't resolve the ultimate origin of the inorganic components that later aggregated to life. But this inability is the very heart of creationist logic and the central reason why their doctrine is not science, while science's inability to specify the ultimate origin of matter is irrelevant because we are not trying to do any such thing. We know that we can't, and we do not even consider such a question as part of science.
We understand Hutton's wisdom. We do not search for unattainable ultimates.
We define evolution, using Darwin's phrase, as "descent with modification" from prior living things. Our documentation of life's evolutionary tree records one of science's greatest triumphs, a profoundly liberating discovery on the oldest maxim that truth can make us free. We have made this discovery by recognizing what can be answered and what must be left alone. If Justice Scalia heeded our definitions and our practices, he would understand why creationism cannot qualify as science. He would also, by the way, sense the excitement of evolution and its evidence; no person of substance could be unmoved by something so interesting. Only Aristotle's creator may be so impassive.