Part 2: What's the matter with evolution?

In a chapter of More Than Myth: Seeking the Full Truth About Genesis, Creation and Evolution (The Chartwell Press, 2014), Casey Luskin points out 10 problems in evolutionary theory. We ran his writing about the first five last Saturday, and here is the second quintet (plus a bonus problem).

Luskin holds graduate degrees in both science and law. Before law school he conducted geological research at the Scripps Institution for Oceanography, and he is now a program officer with Discovery Institute’s Center for Science and Culture. —Marvin Olaksy

Problem 6: Molecular Biology has Failed to Yield a Grand “Tree of Life”

When fossils failed to demonstrate that animals evolved from a common ancestor, evolutionary scientists turned to another type of evidence—DNA sequence data—to demonstrate a tree of life. In the 1960s, around the time the genetic code was first understood, biochemists Émile Zuckerkandl and Linus Pauling hypothesized that if DNA sequences could be used to produce evolutionary trees—trees which matched those based upon morphological or anatomical characteristics—this would furnish “the best available single proof of the reality of macro-evolution.”[99] Thus began a decades-long effort to sequence the genes of many organisms and construct “molecular” based evolutionary (“phylogenetic”) trees. The ultimate goal has been to construct a grand “tree of life,” showing how all living organisms are related through universal common ancestry.

The Main Assumption

The basic logic behind building molecular trees is relatively simple. First, investigators choose a gene, or a suite of genes, found across multiple organisms. Next, those genes are analyzed to determine their nucleotide sequences, so the gene sequences of various organisms can then be compared. Finally, an evolutionary tree is constructed based upon the principle that the more similar the nucleotide sequence, the more closely related the species. A paper in the journal Biological Theory puts it this way:

[M]olecular systematics is (largely) based on the assumption, first clearly articulated by Zuckerkandl and Pauling (1962), that degree of overall similarity reflects degree of relatedness.[100]

This assumption is essentially an articulation of a major feature of the theory—the idea of universal common ancestry. Nonetheless, it’s important to realize that it is a mere assumption to claim that genetic similarities between different species necessarily result common ancestry.

Operating strictly within a Darwinian paradigm, these assumptions flow naturally. As the aforementioned Biological Theory paper explains, the main assumption underlying molecular trees “derives from interpreting molecular similarity (or dissimilarity) between taxa in the context of a Darwinian model of continual and gradual change.”[101] So the theory is assumed to be true to construct a tree. But also, if Darwinian evolution is true, construction of trees using different sequences should reveal a reasonably consistent pattern across different genes or sequences.

This makes it all the more significant that efforts to build a grand “tree of life” using DNA or other biological sequence data have not conformed to expectations. The basic problem is that one gene gives one version of the tree of life, while another gene gives a highly different, and conflicting, version of the tree. For example, as we’ll discuss further below, the standard mammalian tree places humans more closely related to rodents than to elephants. But studies of a certain type of DNA called microRNA genes have suggested the opposite—that humans were closer to elephants than rodents. Such conflicts between gene-based trees are extremely common.

The genetic data is thus not painting a consistent picture of common ancestry, showing the assumptions behind tree-building commonly fail. This leads to justifiable questions about whether universal common ancestry is correct.

Conflicts in the Base of the Tree of Life

Problems first arose when molecular biologists sequenced genes from the three basic domains of life—bacteria, archaea, and eukarya—but those genes did not allow these basic groups of life to be resolved into a treelike pattern. In 2009, the journal New Scientist published a cover story titled, “Why Darwin was wrong about the tree of life” which explained these quandaries:

The problems began in the early 1990s when it became possible to sequence actual bacterial and archaeal genes rather than just RNA. Everybody expected these DNA sequences to confirm the RNA tree, and sometimes they did but, crucially, sometimes they did not. RNA, for example, might suggest that species A was more closely related to species B than species C, but a tree made from DNA would suggest the reverse.[102]

This sort of data led biochemist W. Ford Doolittle to explain that “Molecular phylogenists will have failed to find the ‘true tree,’ not because their methods are inadequate or because they have chosen the wrong genes, but because the history of life cannot properly be represented as a tree.”[103] New Scientist put it this way: “For a long time the holy grail was to build a tree of life … But today the project lies in tatters, torn to pieces by an onslaught of negative evidence.”[104]

Many evolutionists sometimes reply that these problems arise only when studying microorganisms like bacteria—organisms which can swap genes through a process called “horizontal gene transfer,” thereby muddying the signal of evolutionary relationships. But this objection isn’t quite true, since the tree of life is challenged even among higher organisms where such gene-swapping is not prevalent. Carl Woese, a pioneer of evolutionary molecular systematics, explains:

Phylogenetic incongruities can be seen everywhere in the universal tree, from its root to the major branchings within and among the various taxa to the makeup of the primary groupings themselves.[105]

Likewise, the New Scientist article notes that “research suggests that the evolution of animals and plants isn't exactly tree-like either.”[106] The article explains what happened when microbiologist Michael Syvanen tried to create a tree showing evolutionary relationships using 2000 genes from a diverse group of animals:

He failed. The problem was that different genes told contradictory evolutionary stories. … the genes were sending mixed signals. … Roughly 50 per cent of its genes have one evolutionary history and 50 per cent another.[107]

The data were so difficult to resolve into a tree that Syvanen lamented, “We’ve just annihilated the tree of life.”[108] Many other papers in the technical literature recognize similar problems.

Conflicts Between Higher Branches

A 2009 paper in Trends in Ecology and Evolution notes that, “A major challenge for incorporating such large amounts of data into inference of species trees is that conflicting genealogical histories often exist in different genes throughout the genome.”[109] Similarly, a paper in Genome Research studied the DNA sequences in various animal groups and found that “different proteins generate different phylogenetic tree[s].”[110]

A June, 2012 article in Nature reported that short strands of RNA called microRNAs “are tearing apart traditional ideas about the animal family tree.” Dartmouth biologist Kevin Peterson who studies microRNAs lamented, “I've looked at thousands of microRNA genes, and I can't find a single example that would support the traditional tree.” According to the article, microRNAs yielded “a radically different diagram for mammals: one that aligns humans more closely with elephants than with rodents.” Peterson put it bluntly: “The microRNAs are totally unambiguous … they give a totally different tree from what everyone else wants.”[111]

Conflicts Between Molecules and Morphology

Not all phylogenetic trees are constructed by comparing molecules like DNA from different species. Many trees are based upon comparing the form, structure, and body plan of different organisms—also called “morphology.” But conflicts between molecule-based trees and morphology-based trees are also common. A 2012 paper studying bat relationships made this clear, stating: “Incongruence between phylogenies derived from morphological versus molecular analyses, and between trees based on different subsets of molecular sequences has become pervasive as datasets have expanded rapidly in both characters and species.”[112]

This is hardly the only study to encounter conflicts between DNA- based trees and trees based upon anatomical or morphological characteristics. Textbooks often claim common descent is supported using the example of a tree of animals based upon the enzyme cytochrome c which matches the traditional evolutionary tree based upon morphology.[113] However, textbooks rarely mention that the tree based upon a different enzyme, cytochrome b, sharply conflicts with the standard evolutionary tree. As one article in Trends in Ecology and Evolution observed:

[T]he mitochondrial cytochrome b gene implied … an absurd phylogeny of mammals, regardless of the method of tree construction. Cats and whales fell within primates, grouping with simians (monkeys and apes) and strepsirhines (lemurs, bush-babies and lorises) to the exclusion of tarsiers. Cytochrome b is probably the most commonly sequenced gene in vertebrates, making this surprising result even more disconcerting.[114]

Strikingly, a different article in Trends in Ecology and Evolution concluded, “the wealth of competing morphological, as well as molecular proposals [of] the prevailing phylogenies of the mammalian orders would reduce [the mammalian tree] to an unresolved bush, the only consistent [evolutionary relationship] probably being the grouping of elephants and sea cows.”[115] Because of such conflicts, a major review article in Nature reported, “disparities between molecular and morphological trees” lead to “evolution wars” because “[e]volutionary trees constructed by studying biological molecules often don’t resemble those drawn up from morphology.”[116]

Finally, a study published in Science in 2005 tried to use genes to reconstruct the relationships of the animal phyla, but concluded that “[d]espite the amount of data and breadth of taxa analyzed, relationships among most [animal] phyla remained unresolved.” The following year, the same authors published a scientific paper titled, “Bushes in the Tree of Life,” which offered striking conclusions. The authors acknowledge that “a large fraction of single genes produce phylogenies of poor quality,” observing that one study “omitted 35% of single genes from their data matrix, because those genes produced phylogenies at odds with conventional wisdom.” The paper suggests that “certain critical parts of the [tree of life] may be difficult to resolve, regardless of the quantity of conventional data available.” The paper even contends that “[t]he recurring discovery of persistently unresolved clades (bushes) should force a re-evaluation of several widely held assumptions of molecular systematics.”[117]

Unfortunately, one assumption that these evolutionary biologists aren’t willing to re-evaluate is the assumption that universal common ancestry is correct. They appeal to a myriad of ad hoc arguments—horizontal gene transfer, long branch attraction, rapid evolution, different rates of evolution, coalescent theory, incomplete sampling, flawed methodology, and convergent evolution—to explain away inconvenient data which doesn’t fit the coveted treelike pattern. As a 2012 paper stated, “phylogenetic conflict is common, and frequently the norm rather than the exception.”[118] At the end of the day, the dream that DNA sequence data would fit into a nice-neat tree of life has failed, and with it a key prediction of neo-Darwinian theory.

Problem 7: Convergent Evolution Challenges Darwinism and Destroys the Logic Behind Common Ancestry

In Problem 6, we saw that the main assumption underlying all phylogenetic trees is that biological similarity is the result of inheritance from a common ancestor. The problem for evolutionary biologists faced with conflicting evolutionary trees is that biological similarity often appears in places not predicted by common descent. In other words, everyone recognizes that biological similarities often appear among species in cases where they cannot be explained as the result of inheritance from a common ancestor. This means the main assumption fails.

We also saw at the end of Problem 6 that when biologists are unable to construct phylogenetic trees, they often make ad hoc appeals to other processes to explain away data that won’t fit a treelike pattern. One of these explanations is convergent evolution, where evolutionary biologists postulate that organisms acquire the same traits independently, in separate lineages, and not through inheritance from a common ancestor. Whenever evolutionary biologists are forced to appeal to convergent evolution, it reflects a breakdown in the main assumption, and an inability to fit the data to a treelike pattern. Examples of this abound in the literature, but a few will suffice.

Genetic Convergent Evolution

A paper in the Journal of Molecular Evolution found that molecule-based phylogenies conflicted sharply with previously established phylogenies of major mammal groups, concluding that this anomalous tree “is not due to a stochastic error, but is due to convergent or parallel evolution.”[119]

A study in Proceedings of the U.S. National Academy of Sciences explains that when biologists tried to construct a phylogenetic tree for the major groups of birds using mitochondrial DNA (mtDNA), their results conflicted sharply with traditional notions of bird relationships. They even found “convergent” similarity between some bird mtDNA and the mtDNA of distant species such as snakes and lizards. The article suggests bird mtDNA underwent “multiple independent originations,” with their study proposing “multiple independent origins for a particular mtDNA gene order among diverse birds.”[120]

A 2005 paper in Nature Immunology observed that plants and animals have a highly similar biochemical organization of their respective innate immune systems, but their common ancestor didn’t have such an immune system:

Although it seems to be generally accepted that the innate immune responses of plants and animals share at least some common evolutionary origins, examination of the available data fails to support that conclusion, despite similarities in the overall ‘logic’ of the innate immune response in diverse multicellular [organisms].[121]

According to the paper, common descent cannot explain these "unexpectedly similar” systems, “suggesting independent evolutionary origins in plants and animals.” The paper is forced to conclude that such complex similarities make for a “compelling case for convergent evolution of innate immune pathways.”[122]

Another famous example of convergent evolution is the ability of bats and whales to use echolocation, even though their distant common ancestor did not have this trait. Evolutionary biologists long-believed this was a case of morphological convergence, but an article in Current Biology explains the “surprising” finding that echolocation in bats and whales also involves genetic convergence:

Only microbats and toothed whales have acquired sophisticated echolocation, indispensable for their orientation and foraging. Although the bat and whale biosonars originated independently and differ substantially in many aspects, we here report the surprising finding that the bottlenose dolphin, a toothed whale, is clustered with microbats in the gene tree constructed using protein sequences encoded by the hearing gene Prestin.[123]

One paper called this data, “one of the best examples of convergent molecular evolution discovered to date.”[124] But again, these are hardly isolated examples. In 2010, a paper in Trends in Genetics explained:

The recent wide use of genetic and/or phylogenetic approaches has uncovered diverse examples of repeated evolution of adaptive traits including the multiple appearances of eyes, echolocation in bats and dolphins, pigmentation modifications in vertebrates, mimicry in butterflies for mutualistic interactions, convergence of some flower traits in plants, and multiple independent evolution of particular protein properties.[125]

Biochemist and Darwin-skeptic Fazale Rana reviewed the technical literature and documented over 100 reported cases of convergent genetic evolution.[126] Each case shows an example where biological similarity—even at the genetic level—is not the result of inheritance from a common ancestor. So what does this do to the main assumption of tree-building that biological similarity implies inheritance from a common ancestor? With so many exceptions to the rule, one has to wonder if the rule itself holds merit.

The Earth Is Round, but Is Common Ancestry True?

One evolutionary scientist tried to pressure his readers into accepting Darwinism by claiming “biologists today consider the common ancestry of all life a fact on par with the sphericity of the earth.”[127] But are such categorical statements even helpful, much less true?

Proponents of neo-Darwinian evolution are forced into reasoning that biological similarity implies common ancestry, except for when it doesn’t. And in the many cases where it doesn’t, they appeal to all sorts of ad hoc rationalizations to save common ancestry.

Tellingly, the one assumption rarely questioned is the overall assumption of common ancestry itself. But perhaps the reason why different genes are telling different evolutionary stories is because the genes have wholly different stories to tell, namely stories that indicate that all organisms are not genetically related. There is some hope for a different story more attuned to the data, as Michael Syvanen dared to suggest in Annual Review of Genetics in 2012, that “life might indeed have multiple origins.”[128] In other words, universal common ancestry may in fact, not be true.

Problem 8: Differences Between Vertebrate Embryos Contradict the Predictions of Common Ancestry

Another area where evolutionary biologists claim powerful evidence for common ancestry is the patterns of development of vertebrate embryos. Biology textbooks typically portray the embryos of different groups of vertebrate as starting off development in a highly similar fashion, reflecting their common ancestry.[129] However, such claims overstate the degree of similarity between the early stages of vertebrate embryos.

Biologists who investigate these questions have found considerable variability among vertebrate embryos from their earliest stages onward, contradicting what we are told to expect from common ancestry.[130] As a paper in Nature stated, “Counter to the expectations of early embryonic conservation, many studies have shown that there is often remarkable divergence between related species both early and late in development.”[131] Or, as another article in Trends in Ecology and Evolution stated, “despite repeated assertions of the uniformity of early embryos within members of a phylum, development before the phylotypic stage is very varied.”[132]

But most embryologists who acknowledge that vertebrate embyros start development differently will still claim embryos pass through a highly similar stage midway through development, called the “phylotypic” or “pharyngula” stage. These theorists propose an “hourglass model” of development, where it is claimed that similarities between embryos during this midpoint stage provide evidence for common ancestry. One critical biologist explains how this concept is viewed: “It is almost as though the phylotypic stage is regarded as a biological concept for which no proof is needed.”[133]

But when biologists have looked for evidence supporting the existence of a phylotypic or pharyngula stage, they found the data points in the opposite direction. One comprehensive study in Anatomy and Embryology surveyed the characteristics of many vertebrates during this purportedly similar stage, and found that embryos show differences in major traits, including:

• body size,
• body plan,
• growth patterns, and
• timing of development.[134]

The researchers conclude that the evidence is “[c]ontrary to the evolutionary hourglass model” and “difficult to reconcile” with the existence of a pharyngula stage.[135] Likewise, a paper in Proceedings of the Royal Society of London found the data was “counter to the predictions of the [phylotypic stage]: phenotypic variation between species was highest in the middle of the developmental sequence.” It concluded that a “surprising degree of developmental character independence argues against the existence of a phylotypic stage in vertebrates.”[136]

While vertebrate development shows wide variation, evolutionary embryologists seek to force-fit evolutionary interpretations to the data. When every rule is stymied by exceptions, a better way is to simply let the data speak for itself. A non-evolutionary approach to embryology would more easily acknowledge that differences exist between vertebrate embryos at all stages of development, and that vertebrate embryos show some similarities—but also significant differences—during the purported phylotypic stage.

Problem 9: Neo-Darwinism Struggles to Explain the Biogeographical Distribution of Many Species

Biogeography is the study of the distribution of organisms in time and space both in the present and past on Earth. It is often contended that biogeography strongly supports neo-Darwinian theory. For example, the National Center for Science Education (NCSE), a pro-Darwin advocacy group, claims that “consistency between biogeographic and evolutionary patterns provides important evidence about the continuity of the processes driving the evolution and diversification of all life,” and “[t]his continuity is what would be expected of a pattern of common descent.” However, the NCSE dramatically overstates its case and ignores the many instances where biogeography does not show the sort of “continuity” that would be expected under a pattern of common descent.

Evolutionary explanations of biogeography fail when terrestrial (or freshwater) organisms appear in a location (such as an island or a continent) where there is no standard migratory mechanism for them to have arrived there from some ancestral population. In other words, when we find two populations of organisms, Darwinian evolution claims that if we go back far enough, they must be linked by common descent. But sometimes it’s virtually impossible to explain how these populations could have arrived at their respective geographical locations on the globe from some ancestral population.

For example, one of the most severe biogeographical puzzles for Darwinian theory is the origin of South American monkeys, called “platyrrhines.” Based upon molecular and morphological evidence, New World platyrrhine monkeys are thought to be descended from African “Old World" or “catarrhine” monkeys. The fossil record shows that monkeys have lived in South America for about the past 30 million years.[137] But plate tectonic history shows that Africa and South America split off from one another between 100 and 120 million years ago (mya), and that South America was an isolated island continent from about 80 - 3.5 mya.[138] If South American monkeys split off from African monkeys around 30 mya, proponents of neo-Darwinism must somehow account for how they crossed hundreds, if not thousands, of kilometers of open ocean to end up in South America.

This problem for evolutionary biologists has been recognized by numerous experts. A Harper Collins textbook on human evolution states: “The origin of platyrrhine monkeys puzzled paleontologists for decades. … When and how did the monkeys get to South America?”[139]

Primatologists John G. Fleagle and Christopher C. Gilbert put it this way in a scientific volume on primate origins:

The most biogeographically challenging aspect of platyrrhine evolution concerns the origin of the entire clade. South America was an island continent throughout most of the Tertiary … and paleontologists have debated for much of this century how and where primates reached South America.[140]

Primate specialist Walter Carl Hartwig is similarly blunt: “The platyrrhine origins issue incorporates several different questions. How did platyrrhines get to South America?”[141] Such basic, vexing questions certainly don’t lend credence to the NCSE’s claims of “consistency between biogeographic and evolutionary patterns.”

For those unfamiliar with the sort of arguments made by neo- Darwinian biogeographers, responses to these puzzles can be almost too incredible to believe. A Harper Collins textbook explains: “The ‘rafting hypothesis’ argues that monkeys evolved from prosimians once and only once in Africa, and … made the water-logged trip to South America.”[142] And of course, there can't be just one seafaring monkey, or the monkey will soon die leaving no offspring. Thus, at least two monkeys (or perhaps a single pregnant monkey) must have made the rafting voyage.

Fleagle and Gilbert observe that the rafting hypothesis “raises a difficult biogeographical issue” because “South America is separated from Africa by a distance of at least 2600 km, making a phylogenetic and biogeographic link between the primate faunas of the two continents seem very unlikely.”[143] But they are wedded to an evolutionary paradigm, meaning that they are obligated to find such a “link” whether it is likely or not. They argue that in light of “[t]he absence of any anthropoids from North America, combined with the considerable morphological evidence of a South American-African connection with the rodent and primate faunas” that therefore “the rafting hypothesis is the most likely scenario for the biogeographic origin of platyrrines.”[144]

In other words, the “unlikely” rafting hypothesis is made “likely” only because we know common descent must be true.

Indeed, the rafting hypothesis faces serious problems, as mammals like monkeys have high metabolisms and require large amounts of food and water.[145] Fleagle and Gilbert thus admit that “over-water dispersal during primate evolution seems truly amazing for a mammalian order,” and conclude, “[t]he reasons for the prevalence of rafting during the course of primate evolution remain to be explained.”[146] Or, as Hartwig puts it, “The overwhelming evidence for the late Cretaceous-Pliocene isolation of South America renders the mechanical aspect of platyrrhine dispersal virtually irresolvable” for "any late Eocene origins model must invoke a transoceanic crossing mechanism that is implausible (rafting) or suspect … at best.”[147]

And there are deeper problems: monkeys apparently made the journey from Africa to South America, but other smaller African primates never colonized the New World. If it was so easy for monkeys to raft across the proto-Atlantic ocean, why didn't these lower primates also make the voyage? The reason we’re given by Fleagle and Gilbert is that there is no reason, and it all comes down to sheer chance. In their own words, rafting is “clearly a chance event” and “[o]ne can only speculate that by a stroke of good luck anthropoids where able to ‘win’ the sweepstakes while lorises and galagos did not.”[148]

This is not the only case that appeals to rafting or other speculative mechanisms of “oceanic dispersal” to explain away biogeographical conundrums that challenge neo-Darwinism. Examples include the presence of lizards and large caviomorph rodents in South America,[149] the arrival of bees, lemurs, and other mammals in Madagascar,[150] the appearance of elephant fossils on “many islands,”[151] the appearance of freshwater frogs across isolated oceanic island chains,[152] and numerous similar examples.[153] This problem also exists for extinct species, as a paper in Annals of Geophysics notes the “still unresolved problem of disjointed distribution of fossils on the opposite coasts of the Pacific.”[154] A 2005 review in Trends in Ecology and Evolution explains the problem:

A classic problem in biogeography is to explain why particular terrestrial and freshwater taxa have geographical distributions that are broken up by oceans. Why are southern beeches (Nothofagus spp.) found in Australia, New Zealand, New Guinea and southern South America? Why are there iguanas on the Fiji Islands, whereas all their close relatives are in the New World?[155]

After reviewing a number of “unexpected” biogeographical examples that require oceanic dispersal, the review concludes: “these cases reinforce a general message of the great evolutionist [Darwin]: given enough time, many things that seem unlikely can happen.”[156]

Thus, neo-Darwinian evolutionists are forced to appeal to “unlikely” or “unexpected” migration of organisms, in some cases requiring the crossing of oceans to account for the biogeographical data. This kind of data may not necessarily absolutely falsify Darwinism, but at the least it challenges the simplistic argument that biogeography supports universal common descent through congruence between migration pathways and evolutionary history. In many cases, the congruence is simply not there.

Problem 10: Neo-Darwinism Has a Long History of Inaccurate Darwinian Predictions about Vestigial Organs and “Junk DNA”

For decades, evolutionists have claimed that our bodies and genomes are full of useless parts and genetic material—“vestigial” organs—showing life is the result of eons of unguided evolution. During the Scopes trial in 1925, evolutionary biologist Horatio Hackett Newman contended that there are over 180 vestigial organs and structures in the human body, “sufficient to make of a man a veritable walking museum of antiquitiea.”[157]

Over time, however, these predictions of vestigial body parts and useless DNA have not held true. As scientists have learned more and more about the workings of biology, important functions and purpose have been discovered for these so-called vestigial structures. Indeed, in 2008 the journal New Scientist reported that, since the days of Professor Newman, the list of vestigial organs “grew, then shrank again” to the point that today “biologists are extremely wary of talking about vestigial organs at all.”[158] Structures that were previously—and incorrectly—considered to be vestigial include:

• The tonsils: Atone time, they were routinely removed. Now it’s known they serve a purpose in the lymph system to help fight infection.[159]
• The coccyx (tailbone): Many evolutionsists still claim this is a hold-over from the tails of our supposed primate ancestors,[160] but it’s actually a vital part of our skeleton, used for attaching muscles, tendons, and ligaments that support the bones in our pelvis.
• The thyroid: This gland in the neck was once believed to have no purpose, and was ignored or even destroyed by medical doctors operating under false Darwinian assumptions. Now scientists know that it is vital for regulating metabolism.
• The appendix: Darwinian scientists have claimed the appendix is a “vestige of our herbivorous ancestry,”[161] and over eons of evolution its function in humans has been diminished, or lost. But it’s now known that the appendix performs important functions, such as providing a storehouse for beneficial bacteria, producing white blood cells, and playing important roles during fetal development.[162] In light of this evidence, Duke University immunologist William Parker observed that “Many biology texts today still refer to the appendix as a ‘vestigial organ’” but “it’s time to correct the textbooks.”[163]

Despite the poor track record of claiming organs were vestigial, evolutionary biologists have applied this same kind of thinking to our genomes. Many have postulated that the random nature of mutations would fill our genomes with useless genetic garbage, dubbed “junk DNA.” This hypothesis was seemingly confirmed when it was discovered that only 2% of the human genome coded for proteins, leaving the other 98% unexplained. Many scientists who serve as spokespersons for evolutionary biology have claimed this evidence provides case-closed evidence for Darwinian evolution:

• Brown University evolutionary biologist Kenneth Miller argues that “the human genome is littered with pseudogenes, gene fragments, ‘orphaned’ genes, ‘junk’ DNA, and so many repeated copies of pointless DNA sequences that it cannot be attributed to anything that resembles intelligent design.”[164]
• Richard Dawkins likewise writes that “creationists might spend some earnest time speculating on why the Creator should bother to litter genomes with untranslated pseudogenes and junk tandem repeat DNA.”[165]
• In his 2006 book The Language of God, Francis Collins claimed that some “45 percent of the human genome” is made up of “genetic flotsam and jetsam.”[166] (Flotsam and jetsam, of course, is useless trash floating in the ocean.) Sounding much like Dawkins, he makes the implications clear: “Unless one is willing to take the position that God has placed [shared functionless repetitive DNA] in these precise positions to confuse and mislead us, the conclusion of a common ancestor for humans and mice is virtually inescapable.”[167]

The problem with these arguments isn’t so much theological as it is scientific: Numerous examples of function have been discovered for so- called junk DNA.

Biologist Richard Sternberg surveyed the literature and found extensive evidence of function for repetitive DNA. Writing in the Annals of the New York Academy of Sciences, he found that functions for repeats include forming higher-order nuclear structures, centromeres, telomeres, and nucleation centers for DNA methylation. Repetitive DNA was found to be involved in cell proliferation, cellular stress responses; gene translation, and DNA repair.[168] Sternberg concluded that “the selfish [junk] DNA narrative and allied frameworks must join the other ‘icons’ of neo-Darwinian evolutionary theory that, despite their variance with empirical evidence, nevertheless persist in the literature.”[169]

Other research has continued to uncover functions for various types of repetitive DNA, including SINE,[170] LINE,[171] and Alu elements.[172] One paper even suggested that repetitive Alu sequences might be involved in “the development of higher brain function” in humans.[173] Numerous other functions have been discovered for various types of non-protein-coding DNA, including:

• repairing DNA[174]
• assisting in DNA replication[175]
• regulating DNA transcription[176]
• aiding in folding and maintenance of chromosome[177]
• controlling RNA editing and splicing[178]
• helping to fight disease[179]
• regulating embryological development[180]

Sternberg, along with University of Chicago geneticist James Shapiro, predicted in 2005 in the journal Cytogenetic and Genome Research that “one day, we will think of what used to be called ‘junk DNA’ as a critical component of truly ‘expert’ cellular control regimes.”[181]

The day foreseen by Sternberg and Shapiro may have come sooner than they expected. In September, 2012, the journal Nature reported the results of a years-long research project, involving over 400 international scientists studying the functions of non-coding DNA in humans. Called the ENCODE Project, its set of 30 groundbreaking papers reported that the “vast majority” of the genome has function. The lead paper reporting ENCODEs’ results stated:

These data enabled us to assign biochemical functions for 80% of the genome, in particular outside of the well-studied protein-coding regions.[182]

Ewan Birney, ENCODE’s lead analysis coordinator commented in Discover Magazine that since ENCODE looked at only 147 types of cells, and the human body has a few thousand, “It’s likely that 80 percent will go to 100 percent.”[183] The same article quoted Tom Gingeras, a senior scientist with ENCODE, noting that, “Almost every nucleotide is associated with a function of some sort or another, and we now know where they are, what binds to them, what their associations are, and more.”[184] Another Nature commentary noted that “80% of the genome contains elements linked to biochemical functions, dispatching the widely held view that the human genome is mostly ‘junk DNA.’”[185] Discover Magazine put it this way: “The key point is: It’s not ‘junk.’”[186]

While there’s still much we don’t know about the genome, the trendline of the research is clearly pointing in one direction: the more we study the genome, the more we detect function for non-coding DNA. Yet the now-dubious “junk-DNA” paradigm was born and bred inside the evolutionary paradigm based upon the idea that our genome was built through random mutations. Yes, a few rogue biologists dared to seek function for non-coding DNA, but the Darwinian “junk DNA” view of genetics has generally hindered the progress of science, as was admitted by a 2003 article in Science:

Although catchy, the term ‘junk DNA’ for many years repelled mainstream researchers from studying noncoding DNA. Who, except a small number of genomic clochards, would like to dig through genomic garbage? However, in science as in normal life, there are some clochards who, at the risk of being ridiculed, explore unpopular territories. Because of them, the view of junk DNA, especially repetitive elements, began to change in the early 1990s. Now, more and more biologists regard repetitive elements as a genomic treasure.[187]

Despite widespread Darwinian assumptions to the contrary, the paper concluded that “repetitive elements are not useless junk DNA but rather are important, integral components”[188] of animal genomes. Studies suggest that these long stretches of non-coding DNA between genes “constitute an important layer of genome regulation across a wide spectrum of species.”[189]

Like repetitive elements, another kind of “junk” DNA for which function is being discovered is pseudogenes. Pseudogenes are thought to be copies of once-functional genes that have been inactivated through mutations. One paper in Science Signaling observes that “pseudogenes have long been dismissed as junk DNA,”[190] but notes:

Recent advances have established that the DNA of a pseudogene, the RNA transcribed from a pseudogene, or the protein translated from a pseudogene can have multiple, diverse functions and that these functions can affect not only their parental genes but also unrelated genes. Therefore, pseudogenes have emerged as a previously unappreciated class of sophisticated modulators of gene expression, with a multifaceted involvement in the pathogenesis of human cancer.[191]

Indeed, functions for many pseudogenes have already been discovered;[192] the ENCODE project alone found over 850 pseudogenes that are “transcribed and associated with active chromatin.”[193] But what exactly are these pseudogenes doing? A 2011 paper in the journal RNA again argues they can regulate the expression of genes:

Pseudogenes have long been labeled as ‘junk’ DNA, failed copies of genes that arise during the evolution of genomes. However, recent results are challenging this moniker; indeed, some pseudogenes appear to harbor the potential to regulate their protein-coding cousins.[194]

Likewise, a 2012 paper in the journal RNA Biology similarly stated that “Pseudogenes were long considered as junk genomic DNA” but “pseudogene regulation is widespread”[195] in complex multicellular organisms. The paper proposed that “[t]he high abundance and conservation of the pseudogenes in a variety of species indicate that selective pressures preserve these genetic elements, and suggest that they may indeed perform important biological functions.[196]

Pseudogenes serve as another good example of how Darwinian biologists have assumed that a type of non-coding DNA they didn’t understand was functionless genetic junk, and thus ignored their functions. Indeed, the aforementioned paper in RNA Biology explains that one reason why evolutionists have been so slow to abandon the assumption that pseudogenes are junk is because their functions are difficult to detect. The authors observe that “almost all pseudogenes that exhibit significant biological activity are expressed in specific tissue or cell lines,” meaning only specific tissues or cell lines may use a given pseudogene for some function. Additionally, it's difficult to detect function for pseudogenes because we have lacked the research tools to understand how they influence gene expression. The paper predicts that “more and more functional pseudogenes will be discovered as novel biological technologies are developed in the future,” and concludes “The study of functional pseudogenes is just at the beginning.”[197] Indeed, two leading biologists writing in Annual Review of Genetics reported that “pseudogenes that have been suitably investigated often exhibit functional roles.”[198]

Many evolutionary biologists are wedded to the view that our genomes are full of junk, and resist the interpretation that virtually all DNA has function. Indeed, a 2012 evolution textbook teaches that “Over half of the genome is composed of neither genes, nor vestiges of human genes, nor regulatory regions. Instead, it is made up of parasite- like segments of DNA …”[199] Meanwhile, the evidence continues to point in the opposite direction. While much remains to be learned about the workings of our genome, the research trendline is unambiguous: the more we study non-coding DNA, the more we are finding evidence of widespread function.

Bonus Problem: Humans Display Many Behavioral and Cognitive Abilities That Offer No Apparent Survival Advantage

In recent years, evolutionary biologists have tried to explain the origin of human moral, intellectual, and religious abilities in terms of Darwinian evolution. Harvard University evolutionary psychologist Marc Hauser has promoted the increasingly common hypothesis that “people are born with a moral grammar wired into their neural circuits by evolution.”[200]

Humans do appear hard-wired for morality, but were we programmed by unguided evolutionary processes? Natural selection cannot explain extreme acts of human kindness. Regardless of background or beliefs, upon finding strangers trapped inside a burning vehicle, people will risk their own lives to help them escape—with no evolutionary benefit to themselves. For example, evolutionary biologist Jeffrey Schloss explains that Holocaust rescuers took great risks which offered no personal biological benefits:

The rescuer’s family, extended family and friends were all in jeopardy, and they were recognized to be in jeopardy by the rescuer. Moreover, even if the family escaped death, they often experienced deprivation of food, space and social commerce; extreme emotional distress; and forfeiture of the rescuer’s attention.[201]

Francis Collins gives the example of Oskar Schindler, the German businessman who risked his life “to save more than a thousand Jews from the gas chambers.”[202] As Collins points out, “That’s the opposite of saving his genes.”[203] Schloss adds other examples of “radically sacrificial” behavior that “reduces reproductive success” and offers no evolutionary benefit, such as voluntary poverty, celibacy, and martyrdom.[204]

In spite of the claims of evolutionary psychologists, many of humanity’s most impressive charitable, artistic, and intellectual abilities outstrip the basic requirements of natural selection. If life is simply about survival and reproduction, why do humans compose symphonies, investigate quantum mechanics, and build cathedrals?

Natural Academy of Sciences member Philip Skell explained why evolutionary psychology does not adequately predict human behavior:

Darwinian explanations for such things are often too supple: Natural selection makes humans self-centered and aggressive—except when it makes them altruistic and peaceable. Or natural selection produces virile men who eagerly spread their seed—except when it prefers men who are faithful protectors and providers. When an explanation is so supple that it can explain any behavior, it is difficult to test it experimentally, much less use it as a catalyst for scientific discovery.[205]

Contrary to Darwinism, the evidence indicates that human life isn’t about mere survival and reproduction. But in addition to our moral uniqueness, humans are also distinguished by their use of complex language. As MIT professor and linguist Noam Chomsky observes:

Human language appears to be a unique phenomenon, without significant analogue in the animal world. If this is so, it is quite senseless to raise the problem of explaining the evolution of human language from more primitive systems of communication that appear at lower levels of intellectual capacity. … There is no reason to suppose that the “gaps” are bridgeable.[206]

Finally, humans are also the only species that seeks to investigate the natural world through science. In fact, the next time someone tries to break down the differences between humans and apes, remind them that it’s humans who write scientific papers studying apes, not the other way around.

Science vs. Religion

This chapter has cited dozens of papers from the technical scientific literature and by credible scientists which, taken together, pose strong scientific challenges to modern evolutionary theory. Yet defenders of neo-Darwinism commonly assert that legitimate scientific objections to their viewpoint do not exist, and that the only criticisms which remain are based upon religion. Clearly, this is not true. In fact, the attempt to re-label criticisms of neo-Darwinian evolution as religion is typically a ploy to dismiss scientific criticisms without addressing them.

The balance of this book, of course, raises both religious and scientific arguments supporting the progressive creation view that God created life on earth over the course of millions of years. This viewpoint has both religious and scientific dimensions, and for that reason is different from the strictly scientific approach taken in this chapter.

The fact that some arguments in this book may be based upon religion, in no way changes the fact that there are strong scientific challenges to neo-Darwinian theory. Likewise, the fact that there are important religious dimensions to this debate does not mean that materialists can ignore the scientific weaknesses in their own arguments. Until those scientific problems are addressed, scientists will continue to grow skeptical of evolutionary theory.

Reprinted by permission from the website of the Discovery Institute's Center for Science and Culture.

FOOTNOTES

99. Zuckerkandl and Pauling, "Evolutionary Divergence and Convergence in Proteins," 101.

100. Jeffrey H. Schwartz, Bruno Maresca, “Do Molecular Clocks Run at All? A Critique of Molecular Systematics,” Biological Theory, 1(4):357-371, (2006).

101. Ibid.

102. Graham Lawton, "Why Darwin was wrong about the tree of life," New Scientist (January 21, 2009).

103. W. Ford Doolittle, "Phylogenetic Classification and the Universal Tree," Science, 284:2124-2128 (June 25, 1999).

104. Partly quoting Eric Bapteste, in Lawton, “Why Darwin was wrong about the tree of life,” (internal quotations omitted).

105. Carl Woese "The Universal Ancestor," Proceedings of the National Academy of Sciences USA, 95:6854-9859 (June, 1998) (emphasis added).

106. Graham Lawton, "Why Darwin was wrong about the tree of life," New Scientist (January 21, 2009).

107. Partly quoting Michael Syvanen, in Lawton, “Why Darwin was wrong about the tree of life,” (internal quotations omitted).

108. Michael Syvanen, quoted in Lawton, “Why Darwin was wrong about the tree of life.”

109. James H. Degnan and Noah A. Rosenberg, “Gene tree discordance, phylogenetic inference and the multispecies coalescent,” Trends in Ecology and Evolution, 24 (2009): 332-340.

110. Arcady R. Mushegian, James R. Garey, Jason Martin and Leo X. Liu, “Large-Scale Taxonomic Profiling of Eukaryotic Model Organisms: A Comparison of Orthologous Proteins Encoded by the Human, Fly, Nematode, and Yeast Genomes,” Genome Research, 8 (1998): 590-598.

111. Elie Dolgin, “Rewriting Evolution,” Nature, 486: 460-462 (June 28, 2012).

112. Liliana M. Dávalos, Andrea L. Cirranello, Jonathan H. Geisler, and Nancy B. Simmons, “Understanding phylogenetic incongruence: lessons from phyllostomid bats,” Biological Reviews of the Cambridge Philosophical Society, 87:991–1024 (2012).

113. For example, see BSCS Biology: A Molecular Approach (Glencoe/McGraw Hill, 2006), 227; Sylvia S. Mader, Jeffrey A. Isaacson, Kimberly G. Lyle-Ippolito, Andrew T. Storfer, Inquiry Into Life, 13th ed. (McGraw Hill, 2011), 550.

114. See Michael S. Y. Lee, “Molecular Phylogenies Become Functional,” Trends in Ecology and Evolution, 14: 177 (1999).

115. W. W. De Jong, “Molecules remodel the mammalian tree,” Trends in Ecology and Evolution, 13(7), pp. 270-274 (July 7, 1998).

116. Trisha Gura, “Bones, Molecules or Both?,” Nature, 406 (July 20, 2000): 230-233.

117. Antonis Rokas & Sean B. Carroll, “Bushes in the Tree of Life,” PLoS Biology, 4(11): 1899-1904 (Nov., 2006) (internal citations and figures omitted).

118. Liliana M. Dávalos, Andrea L. Cirranello, Jonathan H. Geisler, and Nancy B. Simmons, “Understanding phylogenetic incongruence: lessons from phyllostomid bats,” Biological Reviews of the Cambridge Philosophical Society, 87:991–1024 (2012).

119. Ying Cao, Axel Janke, Peter J. Waddell, Michael Westerman, Osamu Takenaka, Shigenori Murata, Norihiro Okada, Svante Pääbo, Masami Hasegawa, “Conflict Among Individual Mitochondrial Proteins in Resolving the Phylogeny of Eutherian Orders,” Journal of Molecular Evolution, 47 (1998): 307-322.

120. David P. Mindell, Michael D. Sorenson, and Derek E. Dimcheff, “Multiple independent origins of mitochondrial gene order in birds,” Proceedings of the National Academy of Sciences USA, 95 (September, 1998): 10693-10697.

121. Frederick M Ausubel, “Are innate immune signaling pathways in plants and animals conserved?,” Nature Immunology, 6 (10): 973-979 (October, 2005).

122. Ibid.

123. Ying Li, Zhen Liu, Peng Shi, and Jianzhi Zhang, “The hearing gene Prestin unites echolocating bats and whales,” Current Biology, 20(2):R55-R56 (January, 2010) (internal citations removed);

124. Gareth Jones, “Molecular Evolution: Gene Convergence in Echolocating Mammals,” Current Biology, 20(2):R62-R64 (January, 2010); Yong-Yi Shen, Lu Liang, Gui-Sheng Li, Robert W. Murphy, Ya-Ping Zhang, “Parallel Evolution of Auditory Genes for Echolocation in Bats and Toothed Whales,” PLoS Genetics, 8 (6): e1002788 (June, 2012).

125. Pascal-Antoine Christin, Daniel M. Weinreich, and Guillaume Besnard, “Causes and evolutionary significance of genetic convergence,” Trends in Genetics, 26(9):400-405 (2010) (internal citations omitted).

126. See Fazale Rana, The Cell's Design: How Chemistry Reveals the Creator's Artistry, pp. 207-214 (Baker Books, 2008).

127. Karl W. Giberson, Saving Darwin: How to be a Christian and Believe in Evolution, p. 53 (HarperOne, 2008).

128. Michael Syvanen, "Evolutionary Implications of Horizontal Gene Transfer," Annual Review of Genetics, 46:339-356 (2012).

129. For example, see Colleen Belk and Virginia Borden Maier, Biology: Science for Life, p. 234 (Benjamin Cummings, 2010) (“Similarity among chordate embryos. These diverse organisms appear very similar in the first stages of development (shown in the top row), evidence that they share a common ancestor that developed along the same pathway”); Neil. A. Campbell and Jane B. Reece, Biology, p. 449 (Benjamin Cummings, 7th ed., 2005) (“Anatomical similarities in vertebrate embryos. At some stage in their embryonic development, all vertebrates have a tail located posterior to the anus, as well as pharyngeal (throat) pouches. Descent from a common ancestor can explain such similarities”); Holt Science & Technology, Life Science, p. 183 (Holt, Rinehart, and Winston, 2001) (“Early in development, the human embryos and the embryos of all other vertebrates are similar. These early similarities are evidence that all vertebrates share a common ancestor. … They embryos of different vertebrates are very similar during the earliest stages of development”).

130. For example, one paper states “Recent workers have shown that early development can vary quite extensively, even within closely related species, such as sea urchins, amphibians, and vertebrates in general. By early development, I refer to those stages from fertilization through neurolation (gastrulation for such taxa as sea urchins, which do not undergo neurulation). Elinson (1987) has shown how such early stages as initial cleavages and gastrula can vary quite extensively across vertebrates.” Andres Collazo, “Developmental Variation, Homology, and the Pharyngula Stage,” Systematic Biology, 49 (2000): 3 (internal citations omitted). Another paper states, “According to recent models, not only is the putative conserved stage followed by divergence, but it is preceded by variation at earlier stages, including gastrulation and neurulation. This is seen for example in squamata, where variations in patterns of gastrulation and neurulation may be followed by a rather similar somite stage. Thus the relationship between evolution and development has come to be modelled as an ‘evolutionary hourglass.’” Michael K. Richardson et al., "There is no highly conserved embryonic stage in the vertebrates: implications for current theories of evolution and development," Anatomy and Embryology, 196:91-106 (1997) (internal citations omitted).

131. Kalinka et al., “Gene expression divergence recapitulates the developmental hourglass model,” Nature, 468:811 (December 9, 2010) (internal citations removed).

132. Brian K. Hall, “Phylotypic stage or phantom: is there a highly conserved embryonic stage in vertebrates?," Trends in Ecology and Evolution,” 12(12): 461-463 (December, 1997).

133. Michael K. Richardson et al., “There is no highly conserved embryonic stage in the vertebrates: implications for current theories of evolution and development,” Anatomy and Embryology, 196:91-106 (1997).

134. Michael K. Richardson et al., “There is no highly conserved embryonic stage in the vertebrates: implications for current theories of evolution and development,” Anatomy and Embryology, 196:91-106 (1997). See also Steven Poe and Marvalee H. Wake, “Quantitative Tests of General Models for the Evolution of Development,” The American Naturalist, 164 (September, 2004): 415-422; Michael K. Richardson, “Heterochrony and the Phylotypic Period,” Developmental Biology, 172 (1995): 412-421; Olaf R. P. Bininda-Emonds, Jonathan E. Jeffery, and Michael K. Richardson, “Inverting the hourglass: quantitative evidence against the phylotypic stage in vertebrate development,” Proceedings of the Royal Society of London, B, 270 (2003): 341-346;

135. Michael K. Richardson et al., “There is no highly conserved embryonic stage in the vertebrates: implications for current theories of evolution and development,” Anatomy and Embryology, 196:91-106 (1997).

136. Olaf R. P. Bininda-Emonds, Jonathan E. Jeffery, and Michael K. Richardson, “Inverting the hourglass: quantitative evidence against the phylotypic stage in vertebrate development,” Proceedings of the Royal Society of London, B, 270:341-346 (2003) (emphases added). See also Steven Poe and Marvalee H. Wake, “Quantitative Tests of General Models for the Evolution of Development,” The American Naturalist, 164 (3):415-422 (September 2004).

137. Alfred L Rosenberger and Walter Carl Hartwig, “New World Monkeys,” Encyclopedia of Life Sciences (Nature Publishing Group, 2001).

138. Carlos G. Schrago and Claudia A. M. Russo, “Timing the origin of New World monkeys,” Molecular Biology and Evolution, 20(10):1620–1625 (2003); John J. Flynn and A.R. Wyss, “Recent advances in South American mammalian paleontology,” Trends in Ecology and Evolution, 13(11):449-454 (November, 1998); C. Barry Cox & Peter D. Moore, Biogeography: An Ecological and Evolutionary Approach, p. 185 (Blackwell Science, 1993).

139. Adrienne L. Zihlman, The Human Evolution Coloring Book, pp. 4-11 (Harper Collins, 2000).

140. John G. Fleagle and Christopher C. Gilbert, “The Biogeography of Primate Evolution: The Role of Plate Tectonics, Climate and Chance,” in Primate Biogeography: Progress and Prospects, pp. 393-394 (Shawn M. Lehman and John G. Fleagle, eds., Springer, 2006) (emphasis added).

141. Walter Carl Hartwig, “Patterns, Puzzles and Perspectives on Platyrrhine Origins,” in Integrative Paths to the Past: Paleoanthropological Advances in Honor of F. Clark Howell, p. 69 (Edited by Robert S. Corruccini and Russell L. Ciochon, Prentice Hall, 1994).

142. Adrienne L. Zihlman, The Human Evolution Coloring Book, pp. 4-11 (Harper Collins, 2000).

143. John G. Fleagle and Christopher C. Gilbert, “The Biogeography of Primate Evolution: The Role of Plate Tectonics, Climate and Chance,” in Primate Biogeography: Progress and Prospects, p. 394 (Shawn M. Lehman and John G. Fleagle, eds., Springer, 2006) (emphasis added).

144. Ibid. at 394-395 (emphasis added).

145. Ibid. at 404.

146. Ibid. at 403-404.

147. Walter Carl Hartwig, “Patterns, Puzzles and Perspectives on Platyrrhine Origins,” in Integrative Paths to the Past: Paleoanthropological Advances in Honor of F. Clark Howell, pp. 76, 84 (Edited by Robert S. Corruccini and Russell L. Ciochon, Prentice Hall, 1994).

148. John G. Fleagle and Christopher C. Gilbert, “The Biogeography of Primate Evolution: The Role of Plate Tectonics, Climate and Chance,” in Primate Biogeography: Progress and Prospects, p. 395 (Shawn M. Lehman and John G. Fleagle, eds., Springer, 2006).

149. John C. Briggs, Global Biogeography, p. 93 (Elsevier Science, 1995).

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151. Richard John Huggett, Fundamentals of Biogeography, p. 60 (Routledge, 1998).

152. G. John Measey, Miguel Vences, Robert C. Drewes, Ylenia Chiari, Martim Melo, and Bernard Bourles, “Freshwater paths across the ocean: molecular phylogeny of the frog Ptychadena newtoni gives insights into amphibian colonization of oceanic islands,” Journal of Biogeography, 34: 7-20 (2007).

153. Alan de Queiroz, “The resurrection of oceanic dispersal in historical biogeography,” Trends in Ecology and Evolution, 20(2): 68-73 (February 2005). For a more detailed discussion, see Casey Luskin, “The Constitutionality and Pedagogical Benefits of Teaching Evolution Scientifically,” University of St. Thomas Journal of Law & Public Policy, VI (1): 204-277 (Fall, 2009).

154. Giancarlo Scalera, "Fossils, frogs, floating islands and expanding Earth in changing-radius cartography – A comment to a discussion on Journal of Biogeography," Annals of Geophysics, 50(6):789-798 (December, 2007).

155. Alan de Queiroz, “The resurrection of oceanic dispersal in historical biogeography,” Trends in Ecology and Evolution, 20(2):68-73 (February 2005).

156. Ibid.

157. Horatio Hackett Newman, quoted in The World’s Most Famous Court Trial: Tennessee Evolution Case, 2nd ed. (Dayton, TN: Bryan College, 1990), 268. See also Robert Wiedersheim, The Structure of Man: An Index to His Past History (London: MacMillan and Co, 1895; reprinted by Kessinger, 2007).

158. Laura Spinney, “Vestigial organs: Remnants of evolution,” NewScientist, 2656 (May 14, 2008), at http://www.newscientist.com/article/mg19826562.100- vestigial-organs-remnants-of-evolution.html.

159. Sylvia S. Mader, Inquiry into Life, 10th ed. (McGraw Hill, 2003), 293.

160. Laura Spinney, “The Five things humans no longer need,” NewScientist (May 19, 2008), at http://www.newscientist.com/article/dn13927-five-things-humans-no- longer-need.html.

161. Douglas Theobald, “29+ Evidences for Macroevolution,” TalkOrigins.org, at http://www.talkorigins.org/faqs/comdesc/section2.html.

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163. William Parker quoted in Charles Q. Choi, “The Appendix: Useful and in Fact Promising,” LiveScience (August 24, 2009).

164. Miller, “Life’s Grand Design,” 24-32. Miller cites “orphaned genes” but these are not normally understood to be functionless genes. Rather, orphan genes are functional genes that have no known homology to any other gene. Such orphan genes provide evidence for intelligent design because there is no plausible source for their information.

165. Richard Dawkins, “The Information Challenge,” The Skeptic, 18 (December, 1998).

166. Francis Collins, The Language of God: A Scientist Presents Evidence for Belief (New York: Free Press, 2006), 136-37.

167. Francis Collins, The Language of God, pp. 134-137 Free Press, 2006).

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169. Ibid.

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183. Ewan Birney, quoted in Ed Yong, “ENCODE: the rough guide to the human genome,” Discover Magazine (September 5, 2012), at http://blogs.discovermagazine.com/notrocketscience/2012/09/05/encode-the- rough-guide-to-the-human-genome/.

184. Tom Gingeras, quoted in Ed Yong, “ENCODE: the rough guide to the human genome,” Discover Magazine (September 5, 2012), at http://blogs.discovermagazine.com/notrocketscience/2012/09/05/encode-the- rough-guide-to-the-human-genome/.

185. Joseph R. Ecker, "Serving up a genome feast," Nature, 489:52-55 (September 6, 2012).

186. Ed Yong, “ENCODE: the rough guide to the human genome,” Discover Magazine (September 5, 2012), at http://blogs.discovermagazine.com/notrocketscience/2012/09/05/encode-the- rough-guide-to-the-human-genome/.

187. Makalowski, “Not Junk After All,” 1246-47.

188. Ibid.

189. David R. Kelley and John L. Rinn, “Transposable elements reveal a stem cell specific class of long noncoding RNAs,” Genome Biology, 13:R107 (2012).

190. Laura Poliseno, “Pseudogenes: Newly Discovered Players in Human Cancer,” Science Signaling, 5 (242) (September 18, 2012).

191. Ibid.

192. See for example D. Zheng and M. B. Gerstein, “The ambiguous boundary between genes and pseudogenes: the dead rise up, or do they?,” Trends in Genetics, 23 (May, 2007): 219-24; S. Hirotsune et al., “An expressed pseudogene regulates the messenger-RNA stability of its homologous coding gene,” Nature, 423 (May 1, 2003): 91-96; O. H. Tam et al., “Pseudogene-derived small interfering RNAs regulate gene expression in mouse oocytes,” Nature, 453 (May 22, 2008): 534-38; D. Pain et al., “Multiple Retropseudogenes from Pluripotent Cell-specific Gene Expression Indicates a Potential Signature for Novel Gene Identification,” The Journal of Biological Chemistry, 280 (February 25, 2005):6265-68; J. Zhang et al., “NANOGP8 is a retrogene expressed in cancers,” FEBS Journal, 273 (2006): 1723-30.

193. The ENCODE Project Consortium, “An integrated encyclopedia of DNA elements in the human genome,” Nature, 489:57-74 (September 6, 2012).

194. Ryan Charles Pink, Kate Wicks, Daniel Paul Caley, Emma Kathleen Punch, Laura Jacobs, and David Paul Francisco Carter, “Pseudogenes: Pseudo-functional or key regulators in health and disease?,” RNA, 17 (2011): 792-98.

195. Yan-Zi Wen, Ling-Ling Zheng, Liang-Hu Qu, Francisco J. Ayala and Zhao-Rong Lun, “Pseudogenes are not pseudo any more,” RNA Biology, 9(1):27-32 (January, 2012).

196. Yan-Zi Wen, Ling-Ling Zheng, Liang-Hu Qu, Francisco J. Ayala and Zhao-Rong Lun, “Pseudogenes are not pseudo any more,” RNA Biology, 9(1):27-32 (January, 2012).

197. Ibid.

198. Evgeniy S. Balakirev and Francisco J. Ayala, “Pseudogenes, Are They ‘Junk’ or Functional DNA?,” Annual Review of Genetics, 37 (2003): 123-51.

199. Carl Zimmer and Douglas Emlen, Evolution: Making Sense of Life, p. 132 (Roberts and Company, 2012).

200. Nicholas Wade, “An Evolutionary Theory of Right and Wrong,” The New York Times (October 31, 2006), accessed April 28, 2012, http://www.nytimes.com/2006/10/31/health/psychology/31book.html.

201. Jeffrey P. Schloss, “Evolutionary Accounts of Altruism & the Problem of Goodness by Design,” in Mere Creation; Science, Faith & Intelligent Design, ed. William A. Dembski (Downers Grove, IL, Intervarsity Press, 1998), 251.

202. Francis Collins quoted in Dan Cray, “God vs. Science,” Time Magazine (November 5, 2006), accessed April 28, 2012, http://www.time.com/time/printout/0,8816,1555132,00.html.

203. Ibid.

204. Jeffrey P. Schloss, “Emerging Accounts of Altruism: ‘Love Creation's Final Law’?,” in Altruism and Altruistic Love: Science, Philosophy, & Religion in Dialogue, eds. Stephen G. Post, Lynn G. Underwood, Jeffrey P. Schloss, and William B. Hurlbut (Oxford: Oxford University Press, 2002), 221.

205. Philip S. Skell, “Why do we invoke Darwin?,” The Scientist, 19 (August 29, 2005): 10.

206. Noam Chomsky, Language and Mind, 3rd ed. (Cambridge: Cambridge University Press, 2006), 59.