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Evolution – Smevolution!

 

An In-depth Analysis of the Evolution Debate
 

Copyright 2005 Rick Harrison

 

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How to Sort the “Poop from the Polish” on Evolution
 
 

Introduction

It has been an exciting time in science following the meeting of the cadre of intelligent design (ID) scientists at the home of noted author and attorney Phillip Johnson on a California beach in 1993.[1] Scientists have since reported unmistakable signs of intelligent design in biology. As a result, we are able to review here a volume of evidence that poses a startling challenge to the neo-Darwinian theory of accidental evolution.

 

Where does God fit into this new development? While the designer of life doesn’t have to be God under intelligent design theory (he/she/it might be an advanced extraterrestrial civilization, ET, for example), ID theory does leave conceptual room for God in science at the origin of things—something the neo-Darwinian evolutionary theory currently being taught in our schools and universities does not do. ID theory allows that God can legitimately remain in the honored place of the creator where Charles Darwin first placed him in his classic work, The Origin of Species.[2]

 

With the advent of a new, fully concrete, and scientifically formulated intelligent design theory one of the great questions of all time, the relation between God and science, has been reopened, and in grand style. Let’s take a closer look.

 

The Case for Intelligent Design

The evidence for intelligent design or “cosmic purpose” in evolution is, thankfully, less ambiguous than many of the experts who have been tasked to interpret it. The scientific evidence now firmly points to predominantly non-random processes at the heart of the origin and evolution of life, processes clearly fine-tuned in life’s favor. This makes intelligent design or cosmic purpose a fully defensible hypothesis, and, I would argue, the hypothesis most deserving of favored theory status. It’s really that simple. If it isn’t random, if it is highly complex, and if it has a plausible purpose on the surface of things, intelligent design becomes a more probable explanation than dumb accident. This question of cosmic purpose is not, as they say, rocket science; it is more one of common sense.

 

Dr. Stephen C. Meyer, Director of Discovery Institute’s Center for Science and Culture in Seattle, has presented a comprehensive case against accidental processes having originated life and the sophisticated biological information in higher life forms. His recent groundbreaking article (one surrounded, of course, by political controversy) entitled “The Origin of Biological Information and the Higher Taxonomic Categories,”[3] cites a plethora of peer-reviewed scientific studies. Controversy or not, Meyer presents straightforward arguments that establish a magnitude of improbability for classic neo-Darwinian evolution that science can no longer ignore. His new book, Signature in the Cell, substantially updates and expands that argument, an argument I adjudge to be fully successful.

 

Professor Michael Behe’s irreducible complexity thesis, presented in his landmark book, Darwin’s Black Box, and the excellent follow-on Edge of Evolution,[4] goes far, particularly in conjunction with Meyer’s work and William Dembski’s probability analysis (given in The Design Inference, No Free Lunch, and The Design Revolution), towards presenting a case for nothing less than the physical impossibility of accidental evolution. Dembski’s work, especially, makes clear that an accidental evolutionary process could not have produced our complex tree of life within the time and physical resources available in the history of the universe.[5]

 

To a layman like myself, the most immediately visible problem with the neo-Darwinian version of evolution is mirrored in Michael Behe’s irreducible complexity objection. Cells and other biological machines are simply too intricate, too complex, and too delicate to have been formed by accident. Neither can they be accidentally modified without harm because each component is critical to function. Prior to achieving any substantial (progressive) functional change an accidental process will inevitably break the machine. Not every aspect of biology is this way, but a central and critical core of the functions and structures of life are irreducibly complex. Everything in biology is built around the cell and the typical cell is irreducibly complex.

 

Our present knowledge of microbiology and genetics shows the gradual accidental form change process that defines classic neo-Darwinian theory to be impossible. This is because all of the parts of many intricate biological machines have to be in place at the same time for the system to function, and they must all remain closely matched to each other. This, in essence, is what “irreducible complexity” means. Accident cannot produce even the most minimally complex increments of form change that we now know are necessary to get the job of evolution done. In most cases, multiple genes are involved, often many, and in some cases perhaps even all. Even so staunch an opponent of purposive evolution as Richard Dawkins concedes that alteration of one gene in the active genome can potentially create effects cascading through the entire system, potentially affecting all the other active genes. Human beings have 25,000 genes, and some species have many more.

 

Furthermore, any substantial change in body form requires, in addition to alterations to the active operational genome, closely coordinated changes to both the developmental genome and nongenetic microtubule structures inside the cell wall. Complex networks of microtubules are critical to assembling the structural plan of the species, and in fact determine which species will be constructed. Genes, in addition to certain regulatory functions, specify only the complex mix of proteins required to build the species; they do not specify which species is to be built. Although proteins are the building blocks of life, if changes in the genes are not closely coordination with corresponding changes in the microtubule systems, one gets a fatal mismatch analogous to building a skyscraper out of moist chewing gum. Every part specified in the blueprint has been filled, yes, but, as President Bush once said: “This will not stand!”

 

Many key biological machines and structures can only be successfully assembled and integrated into an organism’s larger design by coordinating changes to as many as ten or more genes and associated nongenetic processes. In many cases this must be done in a closely orchestrated and time-dependent process. John A. Davison, Professor Emeritus of Biology at the University of Vermont, thus says that the very notion of a gradual genetic form change is now meaningless, and that gradual change requiring millions of years to observe makes the neo-Darwinian theory untestable (and therefore not scientific).

 

The fossil record supports Davison’s thesis of nongradual change. Large gaps remain in the fossil sequence, and in all the wrong places. They consistently appear where they should least likely be in the gradualist accidental scenario. Many more changes (the gradual accidental steps) should have occurred between radically different body types where many more intermediates would be required to bridge the physiological “distance” than between closely related relatives of the same family.[6]

 

The thesis that neo-Darwinian theory is largely untestable within practical limitations is a thesis with which Henry Gee agrees. Gee is Senior Editor at Nature magazine, one of the nation’s two premier science journals. Dr. Gee is the modern champion of pure scientific method. He insists that, given the “deep time” of evolution, we have too few points of evidence compared to the vast span of evolutionary time over which they must be stretched to support any historical narrative of lifeform evolution with confidence.[7] According to Gee we should abandon any and all theories of the process dynamic of evolution and concentrate instead on first collecting and accurately describing the pertinent paleontological phylogenetic data. In this view, which is the pure (and proper) concept of scientific method, the data collection phase should remain free of any preconceptions about how it all happened so as not to prejudice the data. We should not be theorizing in advance of the data, and much of the relevant data is not yet in. Gee does not argue that the theory of evolution is false, rather, he says that we have affirmed it prematurely according to proper scientific method; we should not yet be saying that we know it to be either true or false. We should concentrate our efforts on pure description of organisms and improving the (hypothetical) phylogenetic trees, neither of which tasks can legitimately be expected to yield an answer to either the “why” or the “how” of evolution, but only the “what.” Though Gee’s position in Deep Time is silent on the question of intelligent design, his point about prematurity absolutely pulls the rug out from under neo-Darwinian theory’s frequently haughty presumption of an accidental world. Gee establishes that neo-Darwinian theory is not so much an unassailable icon, as a scientific prematurity.

 

Neo-Darwinian evolution is hardly unassailable. Most laymen would agree with Professor Michael Behe that irreducibly complex machines simply are a “sign of intelligence,” that biological machines, or machines of any kind, are evidence of design. Common sense remains the hallmark of intelligence even in the twenty-first century, though at times one might hardly know it. In Mathematics of Evolution, Sir Fred Hoyle further reminds us that the fossil lineages of the different orders of creatures neither lead to a definite common ancestor nor fully link up.[8] Physicist and theologian Gerald L. Schroeder does the public another service in restating this now well-established truth, one that many scientists in addition to Hoyle, such as Michael Denton, Stephen Meyer, and Duane Gish have been echoing for years: “Transitional forms are totally absent from the fossil record at the basic level of phylum and rare if present at all in class. Only after basic body plans are well established are fossil transitions observed.”[9] (emphasis added)

 

All these things call the classic neo-Darwinian concept seriously into question. But one can go much further, indeed, as we shall see, for, if there is a designer of life, shouldn’t we expect that natural systems would give some discernable indication of the one absolute greatest influence on those systems, that of their designer—some signs of intelligent authorship? Signs of intelligence are exactly what have been recently discovered in biochemistry, microbiology and genetics. These signs are nonrandom and sufficiently complex that if the equivalent were translated into graphic symbols, blueprints, natural language, computer language, or mathematics they would be acknowledged as originating in an intelligent source. After all the nonsensical hullabaloo about an accidental world that the atheist propaganda machine has cranked out these many years, it turns out that God has signed his work after all.

 

The simple fact of the matter is that the improbability that any one significantly complex feature of biological design could be achieved by accident is sufficiently staggering to imply intelligent design. The aggregate improbability of achieving all of them in sequence as manifested in the varied life forms of 100,000,000 species, with biological machines hierarchically embedded within larger machines to 8-10 levels deep, as famed evolutionist G. G. Simpson conceded, simply forbids belief in an accidental process.[10] It is now clear: there is, undeniably, purpose in nature.

 

Step 1: Life from Dust

As a result of recent research, the effects of accidental or random tinkering on basic biological machines is no longer an unknown. Proteins, specifically, have been scrutinized with scientific rigor. Dr. Stephen Meyer’s synopsis of the foundational work of D. D. Axe gives us the embarkation point for a review of intelligent design theory’s probability argument against the accidental origin of the tree of life. According to Dr. Meyer, who cites peer-reviewed research, the probability of getting even the most rudimentary biologically viable protein (just one) by chance from nonliving sources is no more than 1 chance in 10125.[11] If your math is rusty, that is a 1 followed by 125 zeroes!

 

To construct a living cell, a hundred complex proteins are required at a minimum (most involve thousands). They must interact in intricate ways with several hundred other cell components, each cell performing over two million actions per minute. The improbability of accidentally generating a living cell from nonliving chemicals is therefore thousands of times more difficult than generating a single protein. I will conservatively estimate it at 1 chance in 10128.[12]

 

The effort Dr. Meyer has made to exercise conservative rigor in his estimate can be seen in comparing his work to other estimates that have been offered for the probability of accidentally accomplishing this first step of life. As Dean Overman informs us in his excellent book, A Case Against Accident and Self-Organization, the improbabilities range from fully trillions of times larger to even greater super-immense improbabilities like Overman’s own 10-10(110).[13] My estimates here are more than safe underestimates based upon known information and logic. As indisputable underestimates, they conserve the rigor of the Meyer/Axe values from which they are derived (Meyer’s numbers are themselves primarily derived from the recent protein synthesis studies of D. D. Axe).[14] My goal in simplifying is to see that the numbers do not jump so far so fast as to escape the nontechnical reader’s ability to trace the unbroken logic of our argument to its end.    

 

One way to see how far I have underestimated the difficulty of this first step is to read Russell Grigg’s paper on the problem of accidental creation of life, which includes among its many cogent arguments a discussion of the reversible reactions inherent in protein synthesis in water. Grigg explains that in evolutionary theory the first proteins are believed to have been formed in solution in earth’s oceans. Spontaneously generated amino acids are assumed to have been mixed randomly until they accidentally formed some useful combinations, that is, functional proteins. However, proteins break down in water. Water dissolves the bonds between the amino acids and returns them back into solution. The lifespan of most proteins accidentally hit upon in this way would therefore be so short as to preclude anything useful being done with them. They would not exist long enough to permit their assemblage into complex biological structures.

 

The way evolutionists rescue the process from reversibility is by assuming a long, varied and somewhat turbulent shoreline where accidentally constructed proteins are immediately washed ashore onto a hospitable moist clay substrata that stays just moist enough to hold the proteins in place but not so moist as to dissolve them again, and where the waves that brought the proteins ashore don’t immediately wash them away. Thus, although the reversibility of protein synthesis in solution does not make the accidental achievement of some proteins fully impossible, it does greatly increase the difficulty and improbability of accumulating the complete set of proteins needed for the first organism.[15]

 

To achieve a protein, of course, is not to achieve life. Far from it. The accidental production of the first single-celled creature from non-living chemicals needed to get the evolutionary ball rolling remains an enormous obstacle for neo-Darwinian theory—one that has not been scientifically resolved. As we shall see, there are many other equally difficult steps along the way to generating the higher life forms. Some are arguably much more difficult than originating the first single-celled organism. Therefore, even to achieve a bacterium by accident is not to prove the accidental evolution of more complex life forms.

 

Step 2: Proteins for 100,000,000 Highly Varied Species[16]

Many new proteins will have to be generated and integrated into new systems or organs for each step up the evolutionary ladder. The problem of reversible reaction eliminates much of the useful protein production from the external environment, as does the fact that, once bacteria were present they would rapidly consume or biodegrade any accidentally produced proteins and other biotic components. This leaves us with internal generation of new proteins from living organisms as the primary source for evolutionary progress. Dr. Meyer estimates that the odds of getting a single new biologically viable standard sized protein from random genetic mutation of an existing organism are roughly 1077 to 1 against.[17]

 

A full inventory of all animal proteins has not been completed—or of all animals for that matter. However, the human body alone is estimated to use, at a minimum, 85,000 different proteins.[18] Total estimates for living creatures range to the hundreds of thousands. I am going to set the probability value for evolutionary protein generation conservatively at a clear minimum of 1 chance in 85,000 X 1077. To show how conservative my estimate is, physicist Paul Davies estimates this much higher (and more accurately) at 1040,000.[19] (If we were to theoretically assume true randomness, as an accidental worldview would suggest, the probabilities of generating each different protein of the full compliment of 85,000 would have to be multiplied, that is, 10-77 times 10-77 85,000 times over, for a super immense improbability of 1 chance in 106,545,000! )

 

These are the proper computations required by standard probability theory for achievement of random events in sequence. The probability of rolling three 6s in sequence using standard gaming dice, for example, is not computed by adding the difficulty level of rolling any one of them to that of the others, which would yield 1 chance in 18. Rather, it requires multiplication, yielding only 1 chance in 216. This is because there are 216 alternative configurations for a three die set. Compare this to the computations Fazale Rana and Hugh Ross have made in Table 12.2 of their fascinating book, Origins of Life.[20] Here the odds of achieving the 1,500 gene minimum requisite to independent life is given as 10-112,500, which is Hubert Yockey’s estimate of the odds for random production of the common protein cytochrome C, 10-75, multiplied by itself 1,500 times.[21]   

 

I am therefore beginning the refutation of accidental evolution with one hand intentionally tied behind my back. I have already given away 6,544,920 orders of magnitude of improbability just to prove a point: accidental evolution still couldn’t happen. My ultraconservative underestimate of the synthesis of a complete set of proteins for the tree of life is done for two reasons. First, visibility lends credibility. If one cannot mentally track the derivation of a value one cannot hold full confidence in it. I want the nontechnical reader to be able to see why each step we make is legitimate, that is, why it makes sense, in order to have greater confidence in the final conclusion that accidental evolution simply could not have occurred. Second, I am afraid working with super immense numbers will scare some readers away; therefore, I will simplify wherever possible. The occasional basic math sequence that does occur involving big numbers can be skipped over as desired or scanned without loss of meaning. Still, only basic multiplication and addition is used in this book, no calculus, no trigonometry and no funny symbols. Most of the math argument has been moved to Appendix 2 where it is demonstrated beyond doubt that there are insufficient resources in the universe to ground an accidental evolutionary process. Even there only basic math is used. Give it a try; it is quite easy.

 

Already in the first two steps of life’s construction we see indications of design by way of incremental increases in the bias for life. The improbability of generating the complete inventory of human proteins (the improbability of each multiplied by the other) has been reduced by as much as 4,080,000 orders of magnitude[22] simply by moving the process of protein construction from outside a living creature to inside. That is the difference between 85,000 multiplications of 1077 (biologically viable protein production inside an organism) and 85,000 multiplications of 10125 (biologically viable protein production outside an organism).

 

Proteins can be as large as 10,000 amino acid residues, with approximately 100 amino acids linked in an average protein. The enormous complexity of creating a precisely folded three dimensional protein structure of typically from 50 to 300 amino acids, each amino acid with many functionally relevant properties of its own, is one thing (between them the 20 biologically useful amino acids have 437 properties relevant to determining function).[23] However, the full complexity of protein interactions in the cell, termed “systems proteomics” by Gabriel Waksman, is so complex that even our most state of the art computer simulations cannot represent it without employing shortcuts and simplifying assumptions.[24]

 

As Waksman’s book, Proteomics and Protein-Protein Interactions, and the new volume, Protein Folding: New Research, edited by Tony R. Obalinsky, make abundantly clear, we know a lot about proteins, but only a fraction of what there is to know. Protein science is still in its infancy. The added complexity that will be revealed is certain to be immense. Even the electromagnetic properties of amino acids are involved in protein folding. The exact nature of the fold is what imparts viable biological function to proteins. The full determinants of protein folding characteristics of amino acids are traceable down to the atomic level![25]

 

Step 3: Constructing Cellular Machines--The Astounding Complexity of the Cell

Extreme biological complexity at the genetic level, which many readers will already be familiar with, is mirrored in visibly intricate cellular machinery.[26] The functional attributes of these machines are determined by factors not only at the cellular level, but at the nanoscale, molecular, atomic and potentially even at the subatomic levels. Acclaimed science writer, Boyce Rensberger (The Washington Post) gives a masterful account of some of the truly amazing things cells can do in his 1996 page turner, Life Itself.  Here we learn that “cells have the biological equivalent of a containerized cargo system.”[27] In Darwin’s Black Box, Professor Michael Behe presents examples of a handful of other biological systems that have been currently described by science to such an extent that we can confidently analyze them. Within these closely studied systems every component has been found not only to be essential to its function but very closely matched to each other in design. Behe calls these systems “irreducibly complex” because they can’t be reduced by even one component without destroying the function of the design. These systems are too complex to permit accidental assemblage of the design one piece at a time. Behe’s thesis is that irreducible complexity is typical of living systems, not the exception (though not necessarily universal), and that cells, the essential building blocks of all life, are irreducibly complex. Michael Denton claimed very much the same thing in his book, Evolution: A Theory in Crisis,  in 1986. [28]

 

With irreducibly complex designs, random changes (accidents) of a magnitude sufficient to produce a functional variation so seriously impair existing functions that the cell does not survive to pass on the change to future generations, or it is so seriously degraded that natural selection soon removes the mutated cell line from the evolutionary tree. Nor does destruction of a mutated cell result in its being reduced to smaller survivable functional units that can then reform in novel ways to support evolution as some have hypothesized because, as elementary biology texts have always proclaimed, cells are the smallest survivable units (other than destructive pathogens such a retroviruses and prions).

 

Beyond the complexity of proteins and the DNA code itself is the actual day-to-day operation of the cell, which involves a myriad of complex machines. Professor Scott Minnich of the University of Idaho says the assembly instructions for cellular machines are even more complex than the protein coding instructions contained in DNA.[29]

 

The ribosome is one such machine, a critical organelle that manages the protein assembly process. To construct a ribosome, in addition to the basic protein composition of its two-part structure (20-21 proteins, and 31-35 proteins for the respective parts), several copies of ribosomal RNA must be created and added to the structure. In neo-Darwinian theory, the RNA coding sequence must first be achieved by accident. That accident must precisely configure 1500 base pairs of nucleotides for the small unit and 3,000 for the large unit. It must also assemble 50 or more structural proteins into two functional subunits. To get a better idea of just how complex even these deceptively simple miniscule protein tunnels are known to be, see Kathleen L. Triman's article, "Mutational Analysis of the Ribosome." Note particularly the bibliography, and the text she recommends by Liljas, Structural Aspects of Protein Synthesis.[30] What seems so simple on the surface turns out to be enormously complex.

 

Because the rarity of functional proteins implies the corresponding rarity of the genes that code for them in the vast ocean of possible DNA sequences, the frequency of useful randomly configured genes can be estimated at about the same magnitude as useful randomly generated proteins: 1 in every 1077.[31] Since genes perform complex regulatory functions in addition to directing protein synthesis the probability of randomly hitting upon a useful gene is actually much smaller than for achieving a single protein. Estimating the improbability of accidentally creating only the smaller portion of ribosomal DNA, representing a sequence of 1500 base pairs, as the improbability of one functional protein is then quite conservative.[32]

 

Another biological machine is the cellulosome. The cellulosome is a two-component machine composed of a dockerin sequence and a cohesion module. Bacteria use it to degrade polysaccharides on the cell walls of plants. The dockerin sequence is composed of approximately 70 amino acid residues, while the cohesion module requires around 150 residues. The genetic information required to create a cellulosome is approximately 6,000,000 base pairs.[33] Again the 6,000,000 long nucleotide sequence must be configured by accident under neo-Darwinian theory. Accidentally achieving the functional DNA of a cellulosome, at 6,000,000 base pairs, equates to making roughly 6,000 proteins, yielding an intentionally underestimated probability of 6,000 X 10-77, or 6 X 10-80. (Again, more strictly done, this should be 10-77 multiplied by itself 6,000 times, which is 10-462,000!)

 

There are plenty of other machines involved in life. The famed biological clock, for example, perhaps thought by some (young persons) to be mythical, turns out to be quite real, and quite complex. The circadian clock is found in all complex creatures and some bacteria. It has been studied for 50 years and all of its mysteries and mechanics are still not fully understood. In a creature as simple as the fungus it involves 11 proteins and a very complex system of interactions with many auxiliary components. Christian Heintzen and Yi Liu describe the circadian clock in amazing technical detail in a fascinating article, "The Neurospora crassa Circadian Clock," revealing feedback loops and a variety of regulatory actions, data input and output channels, etc. These clearly mark the clock as an intricately designed machine. (Heintzen and Liu neither advance nor deny the inference to intelligent design; they simply describe the clock.)

 

There are a variety of clock functions in humans and other creatures as a very informative online article by Loes Pihlajamaa-Glimmerveen describes at http://www.glimmerveen.nl/LE/biological_clock.html. There may even be a clock in each cell, which would amount to trillions in a single human body. These intricate timekeepers interact with the genome and the overall metabolism to keep everything in tune and in time. Hundreds of clock-controlled genes have been identified in a wide variety of creatures, and gene expression feedback circuits are involved in the generation of circadian rhythms.[34]

 

A fourth biological machine that has gotten a lot of attention is the bacterial flagellum. Professor Michael Behe describes this intricate machine in Darwin’s Black Box. To get a more detailed view of the complexity of the flagellum ion powered motor, see Robert M. Macnab’s Annual Review of Microbiology article entitled “How Bacteria Assemble Flagella.”[35] The bottom line is that these are complex machines with very closely matched parts. They are, in fact, outboard motors, having rotor, bushing, and bearings, very intricately powered and controlled by miniscule electronic impulses. (See Access Research Network’s animations of the flagellum  here  and  here.)  

 

The Tip of the Iceberg

There are thousands of other biological machines that must be constructed accidentally under neo-Darwinian theory.[36] The complexity of some, like the human brain, simply defy description. The cerebral cortex alone has 10 billion neurons and 60 trillion synaptic connections. How our own perceptual/cognitive functions actually work is still not clear primarily because they are more complex than we can imagine, let alone calculate. Dr. David Faust of Brown University Medical School has this to say on the subject, citing J. C. Eccles 1977 book, The Understanding of the Brain.

 

If anything, I believe the case for complexity has been understated. Anyone who wishes to glimpse the complexity of processes needed to manage the sensory world might find current studies of the human brain illuminating. Eccles (1977) a prominent researcher in this area, makes the following statement when discussing human perception:[37]

 

Before the cerebral cortex is involved in the necessary complex patterned reaction to the sensory input so that it gives a conscious perception, there will be activity of this immense, unimaginable complexity…it will be necessary to develop new forms of mathematics, as yet unimagined, in order to cope with such immense patterned complexities.[38]

 

The complexity of even the most basic biological machines clearly signals the larger difficulty of the evolutionary task. Some simple organisms have thousands of ribosomes in one cell (the bacterium E. coli has 15,000).[39] Nor do we know absolutely everything regarding their construction. Substantial questions remain unanswered, and current research reveals the construction process for even “simple” machines like the ribosome to be enormously complex.[40]

 

Uniquely Complex Systems

The complexity of the human immune system is often marveled at in both popular and technical writing. The adaptive immune system can recognize approximately a trillion threats, and can construct defenses against man-made antigens that are not yet known to nature. Professor Michael Behe gives us a glimpse of the hidden workings of the immune system in Chapter 6 of Darwin’s Black Box; Boyce Rensberger expands that in Chapter 11 of Life Itself; and the rest of the story is beautifully laid out in the new textbook The Immune Response, by Tak W. Mak and Mary E. Saunders, a glorious work of 1194 pages.[41] A surprisingly good nontechnical overview of the immune system is given in a free online pamphlet from the National Institutes of Health, Understanding the Immune System: How It Works.                     .

 

As impressive as the human immune system is, our central nervous system far exceeds it in complexity, performing operations of much greater sophistication. There are 100 billion neurons in the human brain and spinal cord that make up the central nervous system, each with thousands of connecting fibers.[42] In his recent article, “Duplicating Human Intelligence is a Mirage,” computer scientist Peter Kassan informs us that a program mimicking human intelligence would have to be 25 million times the size of the largest computer software program ever written. The glial cells in the brain were long thought to be only structural, but Kassan reveals that in 2004 researchers discovered they had other functions as well. There are  nine times as many glial cells as neurons.[43] Entire areas of functionality in human intelligence, emotion, and the capacity for abstract thought continue to defy the reductionist analysis of science. Many of them most likely always will. They imply astronomical complexity beyond our current ability to estimate, and beyond our computers’ ability to model.[44] Obviously, we cannot restrict our estimate of biological complexity to genes and proteins alone.

 

The Cambrian Explosion Reduces the Time Available

During the Cambrian Period, which began some 530 to 570 million years ago, the vast majority of the animal body plans that have ever existed evolved within only five to ten million years.[45] In other words the bulk of the evolutionary task does not have the full lifespan of the earth (4.45 billion years) available for its completion. These basic forms gave rise to at least nineteen and as many as thirty-five of the forty different animal phyla we have today.[46] Having practically all the animal body forms evolve in only ten million years as opposed to the 4.45 billion years of the earth’s total existence dramatically increases the odds against it happening by chance.

 

Interruptions to Evolutionary Progress

There have been at least seven major disruptive events, ice ages or mass extinctions that would have cost evolution a significant amount of time. These catastrophes would almost certainly have "vetoed" many of natural selection's choices, removing thousands of previously favored species, at times compelling a near full restart on an entire branch of the tree of life. For example, ninety-six percent of marine animals were lost during an extinction occurring toward the end of the Permian period.[47] Major extinction events occurred within the last eighty million years, extending all the way up to the last ice age less than two million years ago. A large portion of evolutionary development was certainly lost in these catastrophes. The lost progress further increases the workload and derivative improbability of an accidental evolutionary process.

 

Symmetry and Fine Art in Biological Machine Design

The presence of substantial, even near perfect symmetry, is a hallmark feature of living things. Symmetry is easy to achieve because the biological information that directs it need merely be placed at a very early point in the embryonic construction process. The code simply says that whatever is done for the left of the torso segment should also be done for the right, or for the top the same as the bottom, etc.[48] Symmetry is a striking characteristic of most biological machine designs, and, in my view, something randomness is incapable of producing with consistency initially, that is, prior to natural selection's preferring the symmetrical performance profile on the battlefield of life. Swimming creatures clearly would eventually move to symmetry for efficiency of movement, but they need not have begun that way in an accidental process. Where are the fossils of the failed attempts at asymmetrical design? Granted, they would rarely, if ever, be competitive, but an accidental process, even given natural selection, would not know this at the outset. Given the neo-Darwinian assumption of an accidental process, there should be a substantial record of asymmetry in the fossil record. The percentage of initial proposals that seem to have worked well in regards to where to have or not to have symmetry is exorbitantly high for an accidental process, well outside standard probability distributions.

 

One can say that the solution is simple: UCA, universal common ancestor. The UCA, probably a bacterium, had symmetry so all the others simply inherited it. Sounds good, so it must be true, right? No. It might be true, but there are no links between bacterium and complex creatures in the fossil record. So it may not be true. Plus, millions of years of random mutations necessary to build all sorts of different complex creatures under the accidental view must somehow “decide” to consistently avoid tinkering with the symmetry that is already there in the unicellular ancestor, and then actively duplicate it error free for each added structural component that requires symmetry for optimal function. It is possible in pure theory that accident would be so consistent, but it is not probable that it would be so consistent.

 

The first complex innovations out of the chute, as it were, for each level of advancement on the tree of life would in many cases have no direct competition; they would be at the top of the food chain for a while. Thus, selective pressures favoring symmetrical over asymmetrical forms of that creature would often not arise for some time. There should therefore be evidence that asymmetry was often tried before failing if the evolutionary process were truly accidental. Neo-Darwinists can say, “Well, it must of just happened that way. That was one of the possibilities in the deck and consistent symmetry was simply the hand we were dealt.” It is technically correct to say that it may have just happened that way; but it is not a scientific explanation to say it. It is not an explanation of any kind.

 

Do not be misled by the occasional examples of a tendency to symmetry in certain simple structures of basic chemistry.[49] The same natural laws that govern chemistry do not constrain random mutations of DNA to a symmetrical result. Any of the four possible values of a DNA nucleotide, C,G,T or A are equally acceptable to the chemical bonding requirements of the “backbone” of the DNA strand. They will all snap into place with ease. However, only a very few nucleotide sequence combinations will preserve symmetry of bodily form, while many millions will radically disrupt it.

 

Symmetry in body form is useful for balance, stability, agility, grasping with counter pressure, efficient swimming, flying etc. Clearly, natural selection would preserve symmetry in these applications, once achieved. But why did an accidental process so unanimously and quickly hit upon symmetry in all the right places throughout all of evolutionary history without first creating imbalanced designs that were temporarily survivable but not optimized? Conversely, why didn't symmetry appear too often—in the wrong places? Two heads are better than one! Two computers working together can outperform one. The answer is simple: evolution is visibly  a "smart" process, not accidental at all. This is the only alternative that can explain the evidence. 

 

The presence of fine art in nature has long been an argument for intelligent design. Art in nature perhaps reaches its peak in tropical birds, tropical fish and flowers. The argument for design from these glorious moving and growing works of art is simple: we just know art when we see it, or so we often claim. This remains true despite the fact that an accident could achieve substantial variations of color and pattern much more easily than it could achieve complex mechanisms.

 

In other words, scribbling and junk design can immediately be identified and distinguished from good human art, and when we are shown the magnificent colorful designs in living creatures they “blow away” most of the human competition. They are gloriously fine art; we just know it. If they weren’t why would bird watching be the world’s most popular hobby? There must be something positive in favor of the cute little feathery dickenses, beyond carrying lice and crapping all over the patio. And, there is. That something is fine art. There are even elements of dance involved in some cases.

 

Any doubts one may have about the artistic merits of nature are easily dispelled. Simply stop philosophizing for moment and observe. Look at the video documentaries, books and magazines. Films like Richard Attenborough’s magnificent video, Life on Earth,[50] come to mind, in addition to Science and Nature magazines, National Geographic and Discovery Channel. Look at the field guides to the tropical birds and flowers in the nature area of your bookstore, or better yet, go to the high-end pet stores or zoos; see the real thing. Best of all, buy a good pair of binoculars and get into the field. Color patterns obviously add functional advantage in brilliant mating displays, camouflage, attraction of pollinating birds and insects, etc. Selective advantage may, and apparently does, explain some aspects of color variation; but it does not explain the overall artistic quality.

 

Total Body Complexity of Hierarchical Systems

Genetic information is not the only kind of complex information in living creatures. In humans, complex interactions of trillions of cells have to be organized and regulated to ensure the proper function of systems, organs and tissues. The entire body plan of the organism must somehow make all these components work together to provide integrated body-wide functions.[51] The probability of accidentally hitting upon hierarchically integrated designs of this complexity that may embed systems within systems to 10 levels deep greatly exceeds our estimate for protein synthesis alone.[52]

 

Simultaneous Development of Complimentary Traits

An additional problem for neo-Darwinian evolution is the improbability of accidentally generating a set of features that must work together, features that would individually convey no obvious advantage. The set of characteristics in birds comes to mind: acute long distance vision, wings, a lightweight frame, rapid flight capable reflexes, and feathers. At a minimum these features would have had to appear in the right order, otherwise they would pose an explicit vulnerability to the organism. For example, moving to such a fragile frame would be a decided disadvantage if the bird could not first get off the ground to escape predators. It would need strength and weight to stand and fight and a rugged durable frame to withstand the occasional injury from combat. Agile flight at high speed would be accident prone without the improved vision and fast reflexes etc.

 

Despite the fact that traditional discussions have dispensed with this objection by citing imaginary routes to evolving a related set of complementary traits,[53] achievement of those complex imaginary routes via accidental processes does add substantial improbability and additional time requirements to the neo-Darwinian process. An accidental process is not likely to manage such a complex transition efficiently on the first attempt. Additional tries at transition are required, which consume more time and resources. A transition procedure that is not sequenced exactly right is going to fail due to making the creature temporarily vulnerable and noncompetitive. To avoid quickly losing the prototype organism's new gene line (and the evolutionary progress it carries) to extinction, a highly improbable path, one more near to the perfect route of transition must be taken. An accidental process could not conceivably have achieved such a phenomenal string of successes of this kind as shown in the historical record of evolution.

 

Convergence: Achieving the Same Design by Independent Routes

Simon Conway Morris, a popular modern evolutionary writer, is Professor of Evolutionary Paleobiology at Cambridge University. His book, Life’s Solution: Inevitable Humans in a Lonely Universe, gives a fascinating account of the many and varied cases of convergence in evolution.[54] For example, the camera type eye common to humans and the octopus has evolved separately in at least six different creatures. Other features that have evolved independently in multiple instances include olfaction (smell), hearing, the trachea, myoglobin, anti-freezing mechanisms, photosynthesis, social organization, and quite a few others, almost certainly to include hemoglobin and even intelligence. Morris goes so far as to say that convergence is practically ubiquitous in nature. In convergence extreme similarity cannot be explained by inheritance because the creatures having a feature in common do not share ancestors on the tree of life. They appear to only have bacteria or other single-celled organisms as a common ancestor, after which their own separate branches were begun and continued to diverge.

 

Neo-Darwinists may try to dismiss convergence-based objections to their theory because arriving at the same biological design solution by multiple independent routes, even thousands of times, does not rule out inheritance for the vast majority of other cases. That much is true, and convergent achievements would typically show more variation in genetic sequence than an inherited trait. But convergence does add additional improbability to the accidental thesis, which would have difficulty consistently proposing the same complex design solution over and over again through independent routes. Granted, natural selection could lock in a good proposal once offered, but how does an accidental process manage to generate a hugely complex design proposal again and again in nearly identical fashion? A bias in the systems of nature for the repeated design solution is indicated even where there are noticeable variations on the theme.

 

If instances of convergence are in fact to be found practically everywhere in nature as Morris suggests the increase in workload and improbability for an accidental evolutionary process is quite significant. Reaccomplishing complex designs in thousands of instances as opposed to reusing a previous design achievement would require a substantially increased rate of mutation. The rate of mutation required for accidental evolution with full inheritance is already well beyond the rate currently established by science. Convergence does not disprove inheritance, but it adds the significant obstacles of increased time, increased resources and increased improbability to the already lagging credibility of an accidental evolutionary process.

 

Dr. Gerald Schroeder, a noted physicist and applied theologian, author of Genesis and the Big Bang, The Science of God, and The Hidden Face of God, (properly) estimates the probability of convergence at a magnitude well beyond what could be achieved within the lifetime and resources of our universe. That rules out chance.[55] There are only two other alternatives that can explain convergence: a master DNA library present at the beginning of life within bacteria and algae, or a built in channeling process that drives evolution towards predesignated goals (not necessarily in a perfectly straight line). There is presently no concrete evidence for a master DNA library other than this explanatory logic itself, although the late Professor Susumu Ohno has offered the hypothesis. That leaves a purposive channeling process or funnel towards life as the currently leading explanation. The existence of a master library of DNA so early would, of course, itself be highly suggestive of purpose.

 

In addition, if we consider another of Schroeder’s salient points, that life in the form of the first single-celled organisms is known to have appeared immediately after the appearance of water on the earth, we see that there was no time for an accidental process to compose the organism in small gradual steps. If we now place the monumentally greater burden of a master DNA library for the entire tree of life upon that first step it becomes nothing short of miraculous, a sort of special creation via blueprint, with the building of the actual life forms awaiting the 5 million year period of the Cambrian explosion. Thus, when properly understood, the phenomenon of convergence is itself an independent and sufficient proof of intelligent design and purpose in evolution.

 

Nongenetic Control Structures and Species Determination

Dr. Jonathan Wells reports that scientists have discovered developmental control factors that act independently of DNA: microtubule arrays in animal cell membranes and, particularly relevant to our purpose here, in the cell membrane structures of egg cells.[56] These are three dimensional control structures, a sort of patterned network of plumbing for cell product distribution and cell component assembly. Much like Willy Wanka’s chocolate factory, if you put the right ingredients in at the front, a specific well-defined result comes out the other end.

 

According to Wells, recent research in developmental biology reveals that DNA does not control species determination in animals, at least not directly: the microtubule arrays in egg cell membranes control species determination. Placing the DNA of species ‘A’ into the egg of species ‘B’ does not change the species from that of the ‘B’ egg to species ‘A’, and the result will not likely survive due to its being supplied with improper protein production from the foreign DNA. Scientists have observed varied instances of nongenetic factors of this kind since 1964.[57]

 

Given this revelation, an accidental evolutionary process must closely coordinate physical mutations of cell membrane control structures with corresponding random DNA mutations for protein synthesis and regulatory functions. This complication greatly slows the evolutionary process to await such an unlikely coincidence. Even allowing that DNA in some sense is the ultimate source of the microtubule patterns, changes to the areas of the genome that specify these microtubule patterns constitute an additional factor that has to be coordinated in real time to achieve even a survivable form change, let alone a competitive advantage.

 

Other form determining factors have to be taken into account in the evolutionary process as well, such as DNA methylation and other kinds of gene activation marker systems. Gene activation markers can at times effect morphological change in organisms stable enough to be passed on to the next generation. Such factors complicate random management of the evolutionary process further by adding additional variables that must be synchronized in real time to ensure a viable result.

 

The Genome & Genetic Machinery

The genetic machinery itself is the paradigm of biological complexity. We have yet to fully understand and describe the workings of the genome, though there are already volumes of description on file. Dr. Robert Pollack, in his excellent and gracefully aging primer on genetics, Signs of Life, explains that the process of translating genetic information into functioning bodily systems is extremely complex, going well beyond the task of simple protein production and assembly.[58] A myriad of various and subtle contexts within bodily systems, many yet to be fully scrutinized by science, alter the way a given gene will finally be expressed. Multiple genes interact in governing each other in a complex system of rules. Simple models have been devised to illustrate the general concept of gene interactions.

 

Unfortunately, real systems are vastly more complicated. More than two genes may be involved in activating a single gene. In the case of three controlling genes, there are already 256 different rules. And in a system of 25 genes, the number of possibilities is greater than the number of atoms in the known universe.[59] (My emphasis)

 

“But,” one might object, “haven’t we mapped the genomes?” Yes, we have mapped a few of them. But it is important to note that mapping a genome is not the same thing as describing its functions. Basic mapping does not even cross reference a gene to the function or feature it governs, it only records the nucleotide sequences and gives a preliminary identification of gene locations in the chromosome. Mapping is merely a list of the sequence of nucleotides. It does not explain the complex machinery involved in translation, transposition, error correction, repair and duplication, protein synthesis and biological systems regulation. Therefore, the mere fact that we have “mapped” the genomes of a few creatures does not mean that we have fully described or understood their functions.

 

In addition to protein synthesis, the genetic machinery must perform complex system regulatory functions. The regulatory task for the human body is enormous, requiring precise regulation of trillions of cells each doing millions of tasks per minute, with many organs, systems, tissues and body parts all working together in near perfect concert to maintain the functions of life. The human genome contains 3 billion base pairs of nucleotides spanning some 25,000 genes. New, substantial, and even basic revelations about genetic mechanisms continue to be revealed with each passing decade. Only recently have we realized that the classic concept of the gene as being a contiguous string of nucleotides all consolidated in the same spot on the chromosome is quite wrong. The various sections of a gene are scattered all around the chromosome with hundreds or thousands of nucleotides intervening between them. Nor is the concept involved a simple one gene/one protein relationship. There are only 25,000 genes, but 85,000 proteins in the human body. One gene obviously codes for more than one protein. As recent research reveals one way this gap can be bridged is through alternate reading frames where the sequence of nucleotides can be read from more than one frame of reference. We currently (2008) understand only a fraction of the complex operations of the genome.

 

As the “DNA Surveillance and Repair” chapter of the National Library of Medicine’s online bioscience library reveals, the complexity of DNA repair systems alone is extreme.[60] A recent textbook devoted entirely to that subject goes over 800 pages, describing an astoundingly complex system, for which we still do not know the full details.[61] Many readers will already be familiar with basic DNA transcription and repair tasks, but more complex functions are being discovered as research proceeds.[62] Even the straightforward task of translating a gene into a protein has hidden complexities.[63]

 

In Processes of Organic Evolution, G. Ledyard Stebbins offers a simplified chart of the interactive complexity of biological systems based upon the concept that more than one gene and multiple gene expression tags are involved in regulating or directing protein synthesis for any one complex functional feature.[64] In Stebbins’ chart one can trace 10 different junction points on the road to gene expression resulting in a functional phenotypic feature. In light of more current research (Stebbin’s book is over 35 years old) this has become somewhat of an underestimate as Stebbins already acknowledged in 1971. The expression of a single gene can involve up to 100 gene expression markers scattered around neighboring sequences up to many thousands of nucleotides away. A single gene can generate up to several thousand instructional sequences directing cellular activity. Genes can also be read from more than one reading frame, further complicating the gene translation process.[65] 

 

D. D. Axe’s random protein synthesis estimate cited by Meyer captures the improbability values for the genetic system regarding protein production. However, only a few of the hundreds to thousands of expressed sequences generated by a gene are used for protein building, the rest have regulatory functions. Although enzymes, the key instrument of regulation, are proteins, the regulatory mechanisms of the genome are enormously complex, pushing the improbability estimate for accidental evolution far beyond the previous figures derived from protein synthesis alone. 

 

Beyond the sheer complexity of the genome lies another, perhaps, more important point: DNA is a language, and language is a sign of intelligence. As Professor Emeritus James W. Valentine tells us in chapter 3 of his very enjoyable textbook On the Origin of the Phyla, DNA qualifies under all the technical requirements to be a language: “letter” symbols, rules of syntax or organization, standard dictionary, consistent translation (meaning), punctuation, etc. Valentine does not infer intelligent design from this, but there are no known instances of a naturally occurring language originating outside of an animal intelligence. All known languages are the artifacts of human intelligence, of civilization. The nearest non-qualifying candidates are simpler behavior systems of lower creatures that only mimic language (pseudo-languages).

 

What’d Ya Say?

Why do all creatures use the same biological language of DNA? I don’t mean the same 4-letter code as such, but why do they use that code in the same way? As many readers will know by now, there are four letters of the language of DNA: C, G, T, and A. Any given combination of them could be used to stand for different things in the biological architecture. (A triplet of nucleotides specifies which amino acid is to be built.) In other words, different DNA dictionaries might be used that associate different three “letter” strings of nucleotides with different amino acids.  They would all work as long as the alternate method was consistent. Why then do all creatures speak the same physiological language when they don’t have to? Why do all use the same dictionary? Darwinists say this phenomenon proves inheritance from a common ancestor, and that is a plausible explanation. Having the same designer is an equally good explanation. Some of  both, perhaps, is best.

 

But what about the accidental question? A truly accidental process would have tended to try other possibilities, though they may not have survived long due to predation and/or extreme competition. Nobel laureate Francis Crick uses this same logic to defend his theory that life came here (on purpose) from outer space, expanding it to include not only the DNA dictionary but the structure of DNA:

 

Coming full circle to his groundbreaking discovery of DNA's structure, Crick wondered, if life began in the great "primeval soup" suggested by the Miller/Urey experiment, why there wouldn't be a multitude of genetic materials among the different life forms. Instead, all life on Earth shares the same basic DNA structure.[66]

 

If Crick’s theory is correct, it remains possible that other DNA structures and dictionaries were in fact tried on other planets. However, there is substantial evidence that life in fact arose on Earth.

 

Obviously the creatures using the first system that gets a good start would have a competitive advantage anywhere competition was relevant. The increased efficiency gained through years of being polished by natural selection could easily be a decisive. But all creatures do not compete with all others. The competitive constraint would apply only within competitive groups. Even then the fossil record should show traces of failed attempts to use an alternative system that later proved noncompetitive. 

 

All of these themes are potentially validated in the recent discovery of a few exceptions to the universal DNA dictionary. After decades of Darwinists flaunting the universality of the DNA dictionary as indisputable proof of inheritance, it turns out that the DNA dictionary is not quite universal after all. Back when the argument about the universality of DNA was first originated there were no fossilized DNA records of alternative DNA dictionaries available, and no known instances in creatures currently living. However, the universality argument has now been overcome by events and must be updated. Professor Geoffrey Zubay, professor of prebiotic chemistry at Columbia University, tells us in his book Origins of Life on the Earth and in the Cosmos, that exceptions to the standard DNA dictionary have now been found. What remains to be determined is whether the type and quantity of the exceptions imply anything significant for the evolutionary debate.

 

Considering that the newly discovered variations of the DNA dictionary occur predominantly in very primitive organelles like chloroplasts and mitochondria, the question of independent origination remains open. The variations may be a case of a few alterations occurring after inheritance of the otherwise universal system, or they may be the remnants of true alternative systems that never quite got off the ground. The fact that the variations occur exclusively in organelles that were originated at the very beginning of the tree of life but remained constrained to those limited applications is very suggestive. The harder question is what exactly does it suggest? The discovery of these exceptions to the DNA dictionary is one of the very few pieces of evidence that does fit an accidental scenario. However, in being restricted to only very simple systems in very simple creatures it also fits the intelligent design thesis that accident can only do very simple things.

 

We know only this much for certain, the DNA dictionary is not, in fact, fully universal.[67] Common sense and biological fact both suggest that regardless of how the DNA system was first originated, once bacteria were achieved they would literally eat much of the competition that originated outside of a living organism. Alternative systems in the external environment would stand little chance of getting a good start in any location where previously achieved bacterial forms could thrive once they had been introduced. Since bacteria can be transported in the wind and water, there are few places out of reach of their voracious appetites.

 

Thus, the only variations on the DNA dictionary likely to survive would be the ones that were internalized in early bacteria/algae level creatures. Changing the dictionary within a living creature would seem to be impossible unless the different translation systems could be physically segregated. The event of a step by step evolution of such parallel systems in living creatures would probably make them noncompetitive with creatures having a viable unitary system that evolution was not tinkering with because the intermediate steps to design completion via an accidental process would often be harmful or wasteful of resources. It is therefore unlikely that we will find many more variations of the DNA dictionary than have been found, and those that are found are likely to be of the same type, resident in the simple organelles that could have been components of early bacteria and algae.

 

So, what does all of this have to say on the question of intelligent design? Not much, beyond restricting the reach of an accidental process to the very simple. The discussion of the DNA dictionary is also somewhat interesting from the point of view of one of the traditional Darwinian arguments for a common ancestor. Darwinists used to assert the thesis of inheritance from a common ancestor based upon the huge improbability of a presumed to be accidental evolutionary process achieving multiple independent origins of life. That, according to the Darwinists would be too improbable. (Note the Darwinists’ acceptance of the probability argument here.) Thus, with this line of reasoning we are left with inheritance from a common ancestor as the only explanation of the tree of life. However, there is a self-contradiction built into this Darwinian argument. The accidental achievement of the entire tree of complex life forms is hundreds of orders of magnitudes more improbable than the event of originating the simplest creatures at the beginning in multiple independent origins. One can see this at a glance in comparing the genome of a bacterium at about 3 million with that of a human being, which is 3 billion. Although the complexity is only a thousand times greater, achieving it by accident adds exponential increases in improbability with each step due to the rules for computing sequential achievement of events by a random process (standard probability theory). Therefore, if a second event of life’s origination by accident is so improbable as to be ruled out, so is an accidental origination of the tree of life as a whole.

 

We see here that Darwinists and scientists generally are quite comfortable using probability arguments as valid scientific evidence. Therefore, when evolutionists such as W. Ford Doolittle or Richard Dawkins dismiss the probability argument for intelligent design as of no consequence they are both contradicting themselves and the standard practice of science. (See “Stacking the Deck” below.)

 

No Explanation for the Origin of the (Sets of) New Genes Required for Macroevolution

The late Ernst Mayr  (1904-2005) is one of the best writers and thinkers on their side of the debate, one who candidly admits that lack of intermediate fossils poses a serious challenge to Darwinian theory. He is admittedly one of the best writers and thinkers world literature has to offer on any subject. Nonetheless, in What Evolution Is, we find Mayr offering a single unevidenced phrase to address what is the only real point of contention between intelligent design and neo-Darwinist theories: how to originate complex biological information in the first place. “Even though all new genes are produced by mutation…”[68] That’s it. That is the entire neo-Darwinian explanation of the origin of meaningful information repositories comparable to whole libraries of books: it happens by mutation. Surely you exaggerate, you may challenge.

 

Am I glossing over the true depth of expertise of Darwinian scientists concerning the explanation of the origin of genes and biological information? You be the judge. Here is the entire section of Ernst Mayr’s discussion on the subject excerpted from What Evolution Is.

 

The Origin of New Genes

A bacterium has about 1,000 genes. A human has perhaps 30,000 functional genes. Where did all these new genes come from? They originate by duplication, with the duplicated gene inserted in tandem in the genome next to the sister gene. Such a new gene is called a paralogous gene. At first it will have the same function as its sister gene. However, it will usually evolve by having its own mutations and in due time it may acquire functions that differ from those of its sister gene. The original gene, however, will also evolve, and such direct descendants of the original gene are called arthologous genes.

 

Additions to the genome come not only by the duplication of single genes, but sometimes through the duplication of groups of genes, whole chromosomes, and entire chromosome sets. For instance, a special mechanism, involving kinetochores, can lead to a duplication of chromosome sets in certain orders of mammals, leading to highly variable chromosome numbers in these orders. Lateral transfer is another way for addition to the genome.[69]

 

We need to note several things about this “explanation.” First it doesn’t explain, it merely asserts, and no evidence is given to support the assertion. It doesn’t say how accidental mutations can create a radically different gene from an original one, it simply assumes that it happens. It does not address how to originate the first set of genes at a time when there were none to duplicate. Granted, this kind of process saves evolution from having to duplicate a lot of work in reinventing the entire “library system” all over again, leaving the library in place as it is expanded by duplicating a book and changing the material between its cover. But this explanation once again, skips the hard part, it doesn’t say how the new book is authored, how the complex information inside the books is achieved. Copying an existing book does not equate to authoring one. There is an obvious difference in difficulty level between copying an existing book and authoring a new one. The hard part here is simply assumed by Mayr, not explained. His explanation, though transparently deficient, is typical of evolutionists across the board. They don’t know how new meaningful genes are created, they simply assume that an unguided process can do it.

 

The explanation Darwinists have for the origin of new genes is “they just do—they just mutate and evolve.” However, they cite no direct evidence of genes having done so from observed to be random mutations, particularly not in a context that can be shown to have led to macroevolutionary change. The evolution between different genes has not been seen, it is merely inferred from the existence of closely similar genes in different creatures, and the fact that additional genes appear in creatures as the tree of life unfolds. To infer that one gene evolves from another because of similarity is one thing, and not unreasonable (though less than conclusive). However, to say the process of that evolution was accidental is a totally unevidenced assumption that flies in the face of logic, scientific fact, and common sense.

 

OK, OK. In fairness, the neo-Darwinists do say a little more than this, but not much. The genes of complex creatures come in pairs, called alleles. For simple traits only one pair is involved, for more complex traits several pairs. For each pair, one copy is active, the other is not. Thus the inactive gene of any given pair can be tinkered with, incur random change, and then be pulled into play in future generations by future processes of reproduction, accident or error. Thus little or no risk is incurred to the current generation by accidental mutations tinkering with an inactive allele. Two things must be considered in regards to an allele-based process of variation offering anything of substance to explain life. First complex life has already been achieved before such allele-based genetic processes even come into existence. Thus, this process cannot be used to explain the origination of complex life. It is itself dependent upon the preexistence of complex life. Second, evolution is not about the current generation so much as it is future generations. This explanation only postpones the problem of integration of a new feature into the complex organism until the next generation; it does not solve the problem of integration or even partially mitigate it. Yet this is the “fully satisfactory explanation” proposed by acknowledged experts like Ernst May and Richard Dawkins: genes mutate and split, or split and mutate, and thus we need only wait a few million years and its all done. Walla Booby! Abra cadabra! Presto chango! Accidental evolution proved! Obviously, had we been around at the beginning and able to wait millions of years, evolution would have occurred, but it would not have occurred in such a simple manner or without substantial direction beyond what an accident can provide. “What do you want to do tonight, Dear?” “Oh, let’s just wait around another few millenniums and see what evolution does by accident.” “Uh, well, you go ahead, Honey, I think I’ll watch the design channel.”

 

We may have seen a handful of simple degradations of existing genes that can still do something useful, altered genes that are created by removing a segment of DNA already present, or a few very simple changes in bacterial genes, but that’s it. We have never seen the origination of a new gene with complex functions in a complex organism, nor can we randomly create or substantially progress a gene or set of genes in the lab to produce an evolutionary advancement.

 

To see just how little evidence there is for the accidental generation of new beneficial genes go to the Wikipedia Web site and review the entries for “genetics” and “mutation.” Look for “beneficial mutations.” The sparseness of evidence will amaze you. Ask yourself “Is this enough to explain the entire tree of life?” If that doesn’t convince you, go to a biosciences library and ask for information on beneficial mutations and the origin of new genes, the genetics of evolution etc. You will be very disappointed, probably frustrated, and perhaps even angry at the politicized exaggeration of the evidence. The evidence for accidental origination of new genes sufficient to explain evolution is simply not out there. For 150 years science has merely assumed that the creation of the tree of life happened by random mutation. They have never demonstrated this assumption, nor have they even substantially evidenced it. All the while massive evidence has accumulated against the possibility of truly random (accidental) mutations producing complex new genes.

 

Richard Dawkins gives us another version of this, what I would call the “trust me” explanation, in his “The ‘Information Challenge’ ” article.[70] He confidently informs us that new genes have arisen quite unproblematically from gene duplication and splitting. This, to him, is obvious because of the branching of the tree of life, which requires a corresponding duplication/splitting of the genes (in addition to new gene creation, a requirement he ignores). Dawkins’ logic, which he does not make clear, seems to be: We can see that evolution happened—the historical fossil record says so—and multiplication and diversification of genes is necessary for it to happen. They had to come from somewhere. Therefore we can be confident that, following duplication and splitting, mutation got the job done. Michael Behe and D. W. Snoke, writing in Protein Science, provide ample reason to dispute this assumption in their article “Simulating Evolution by Gene Duplication of Protein Features That Require Multiple Amino Acid Residues.”[71] Obviously the job was done—somehow. But why should we assume with Dawkins and the neo-Darwinists that the multiplication and diversification of biologically meaningful genes could occur by accident?

 

Dawkins’ article defines information in so general a way that it is not necessary for data to be biologically meaningful to qualify as information. This fallacy cannot be overemphasized. Dawkins triumphantly announces the solution to the problem of creating new biologically meaningful “information” while only having addressed trivia. Dawkins’ use of the term “information’ is not the sense of biological information that the evolutionary debate over accident vs. intelligent design centers around. Dawkins here commits the logical fallacy of equivocation, switching the meaning of an important term from its proper connotation, in this case astronomically complex and meaningful genomes billions of nucleotides long to binary trivia.

 

For Dawkins, information is simply a yes or no answer to a question, any question. By restricting the alternatives that follow on a path of inquiry, or a physical event path, entering a yes or no at a given point reduces the possibilities. Therefore, in some sense, it is “useful” information because it reduces the alternatives, and in so doing drives the process forward. It is like a flow chart with decision steps, anything that provides a decision is meaningful or useful information, in the sense of propelling the process forward through the chart. However, merely advancing in the sense of choosing a path, any path whatsoever, is insufficient to explain the achievement of the astronomically improbable path of the evolution of complex life, or any other complex design. It has to be the right path, and the ability to achieve something so improbable has to be explained.

 

With Dawkins’ sense of information one can be guided around in a circle as easily as to a definite result. The decision to turn left is legitimate information to Dawkins regardless of the context in which the decision occurs. Turn left, turn left, turn left…this is all an informed process to Dawkins, but it is a useless waste of resources for evolution or complex design construction because it only goes in a circle. Such “information” accomplishes nothing useful for biology (it may occasionally work for dumb physical systems like propellers and windmills).

 

For Dawkins, a simple yes or no is always meaningful because it conveys a reduction in alternatives. Information in this simple theoretical sense is not meaningful in the sense used in evolutionary debates because it is vastly insufficient information. It is information that can lead in circles or nowhere at all. The fallacy is in implying that a little information will ultimately yield a lot. Such is not a fact of information theory, particularly as applied to biological systems. It is only a veiled restatement of the unevidenced neo-Darwinian assumption of gradualism, that by accumulation of many small changes complex machines can be built by accident. There is no evidence for such a belief, and much that argues against it.

 

Gradual changes, information decision points if you will, that just so happen to fall into the right place in the right manner, are meaningful to biology, yes. But Dawkins’ theory of “information” does not require the right decisions, only any decision. His theory of information does not tie the decision points to a specified end product. Therefore the genomes are not explained at all, except as an accident. A process “guided” by Dawkins’ type of information is not guided at all, it is not controlled to any definite end or in any consistent direction. A process informed by Dawkins’ “information” is free to wander all around the globe and back without doing anything useful for biology and much that is destructive to it. Richard Dawkins has therefore not explained the origin of biological information as he implies in his article “The ‘Information Challenge’;” he has only explained a useless and potentially destructive form of binary trivia.

 

The debate over accidental evolution/intelligent design centers around the ability of the evolutionary process to create information that promotes the advancement of efficiency, fitness, or complexity in living systems, not trivia. The rarity of useful genes in the pool of all possible combinations of nucleotides of approximate gene length (1,000 bp) is something of the order of 1077 to 1. To create a new biological feature sufficient to advance the tree of life is more rare yet. All of the binary decisions that could potentially be made along the route to exploring the 1077 possibilities are legitimate information to Dawkins, yet only the most infinitesimally small subset of those is useful to life. The mere reduction of purely theoretical alternatives minus a specification for biological fitness does not accomplish anything of use to evolution. Dawkins has not explained biological information. Information in Dawkins’ sense is not meaning, and biological information consists of only meaningful units. Nor does binary trivia require an explanation for it only states the obvious, that a decision point alters the course of the route once a decision has been made.

 

The question “Left or right?” to the direction that a single quantum particle may take is meaningful in Dawkins’s sense of information, but has no effect on anything in the physical world whatsoever because a single quantum particle passes through solid matter without causing any effect. Except perhaps in the rarest of cases, only groups of quantum particles acting in concert in ordered patterns have significant effects on the visible world. Thus, simply giving a yes or no answer at a trivial point in the process does not guarantee a meaningful effect.

 

The whole question at issue here is “Are single point mutations of nucleotides in the genome always meaningful or are they predominantly irrelevant to the outcome of the macroevolutionary process?” For much of the past 150 years Darwinian evolution has been hailed as an established fact, yet this question was never satisfactorily answered. It has yet to be shown that accidental point mutations or the gradual accumulation of other small accidental changes have had or could have a genuine effect on the evolutionary process.

 

Environmental mutagens, thought during the heyday of evolutionary theorizing of Morgan and De Vries et al.. to be the cause of all mutations have now been dismissed as of no significance to evolution. All we can show about point mutations is that they tend to harm the organism. Natural selection later takes out these mistakes, or most of them. Point mutations can only be demonstrated to be either trivial, having no effect on evolution, or somewhat obstructive of the process. For all science can demonstrate, the yes or no answers given by point mutations appear as irrelevant to the composition of viable genomes by evolution as individual quantum particle trajectory is to events in the history of the physical systems of the universe.

 

Nor is Dawkins’ theory of information fully immune to criticism even in the abstract. One can encounter trivial and meaningless “information” in Dawkins’s sense of information even in asking directions at a fork in the road. Let’s say a traveler encounters options to either London or Lisbon. A “yes” or a “no” to the question of “Take the left fork?” will have an effect. But a “yes” or a “no”  to the question “Does the option you want contain an ‘L’?” produces no visible effect at all.  Quite a number of such pointless questions can be asked. “Does your option contain an ‘O’ and a ‘N’?” etc.

 

If the fork in the road is not merely between Lisbon and London but rather is followed by trillions upon trillions of alternatives, as in evolution, with the one location the traveler desires to reach having 3,000,000,000 letter occurrences of a four letter alphabet (the human genome) in its name, is an unguided series of yes or no answers ever going to bring you to your destination? Adding more realistic conditions as in an accidental evolutionary process where the traveler must go a ways down the road with each guess only to be vetoed by natural selection before returning for another try, does Dawkins’ definition of information really resolve the dilemma of how to achieve the genomes within the realities of the time and resources available on the historical timeline of evolution? The answer is no, as Appendix 2 clearly demonstrates.

 

What then if the known realities of biology posited by Professor Michael Behe are added to the scenario? Whole sets of 3-10 genes, each gene 1-5 thousand nucleotides in length, must be proposed at or near the same time in a closely orchestrated manner to construct a new biological feature. Here the traveler is required to guess from 3,000 to 50,000 letter occurrences in the correct combinations at each branch in the road before proceeding! In Dawkins’ oversimplified view where binary information is mistakenly identified with biological information only one letter need be guessed at any given point, and it needn't be a letter of relevance to any specific goal at all. Dawkins’ theory of information is completely useless to the explanation of life, and really everything else. It merely says a turn is a turn; it is trivial.

 

There are three questions central to the debate over accidental evolution/intelligent design: 1) “What is the minimum number of genetic and physical changes that must be posed in conjunction or in a closely orchestrated sequence to generate each of the biologically viable changes in function or structure that match the historical record of evolution?" 2) “Which of these complex sets of alterations is achievable by accident, if any?” And, 3) "Could accident get the total job done within the time and physical resources available in the history of our universe?" Dawkins’ concept of information simply assumes that the answer to the first question is “one,” that the answer to the second is “all,” and that the answer to the last is "Why not? All information is created equal. It could all have just popped out of the hat as one big freak accident." Dawkins' position assumes that changing one nucleotide at a time can generate progressive evolution, all of it, and that accident can generate all the needed point mutations in the available time without aborting the process and without producing a haphazard trail of guesswork very much different from what is seen in the actual fossil record. Neither of these assumptions is warranted in view of the fossil evidence, modern microbiology and genetics.

 

Creation/alteration of 10 or more genes may have to be synchronized to achieve substantial phenotypic change. D. D. Axe’s protein synthesis values demonstrate that the ratio of trivia to meaning to be expected from random mutation is 1077 to 1! The improbability of achieving a biologically meaningful result from accidental mutation of 10 genes in sequence as is required to effect a macroevolutionary change is therefore less than one chance in 10770. Simply asserting that yes and no answers are given by random mutations does not prove that the universe has sufficient resources to randomly try such an astronomical number of alternatives. Nor does it establish a known physical process that could explore those alternatives in the complex combinations required with sufficient speed to achieve the tree of life in the time available. Arguing that purely abstract concepts of information can be shown to be satisfied by point mutations does not satisfy the requirements for real-time real-world achievement of the tree of life.

 

Random drift theorists posit that a few hundred neutral point mutations can accumulate in the right places and add up to a beneficial change over vast amounts of time, but this has not been demonstrated to be possible without first harming the organism. What has been demonstrated is that a single nucleotide change alters the triplet that specifies an amino acid, and that three or fewer random amino acid substitutions destroys the viability of a protein.[72] Therefore it is vastly unlikely that accumulations of initially neutral point mutations will survive the cut of natural selection long enough to construct a new advanced feature. 

 

Because thousands of mutagenesis studies demonstrate that only destructive changes come from accidental point mutations, or that they are neutral and have no effect, and because we now know that whole sets of complex genes are needed to make a viable change to biological function, a more realistic analogy is to say that a traveler enroute to Genome City will not have any navigable turns available for single letter (single nucleotide) guesses (mutations) at all, but if he insists on doing it that way he will be led off into the countryside, dangerous alleys, or side roads, from which he will never regain his path.

 

Despite the strong experimental case against the capabilities of random mutations, the perceived relationships between some modern genes and those in ancestral organisms makes the whole question of genome evolution an open and shut case for Dawkins. The genes are similar therefore they are inherited. New additions were simply achieved by splitting and later diversification via random mutation. Here again, Dawkins simply assumes accident can do this; he does not give evidence for the assumption. However, to the unwary reader, Dawkins’ tone and modality of language certainly suggests that he is giving evidence.

 

When all is said and done, Dawkins assumption that accidents can make machines is simply unwarranted. No matter how many times you split a volume of the poetry of Sir Alfred Lord Tennyson, no collection of subsequent typos is going to turn it into Shakespeare, and, in neo-Darwinian theory, the creation of the original volume remains unexplained. Such an unlikely accidental scenario as Dawkins posits has to be demonstrated to be believed. No such demonstration of random origination of new substantially more complex biological information adequate to ground a macroevolutionary advancement has ever been achieved by science.

 

Inheritance is the smaller part of the explanation of life, after all. The genomes of complex creatures are a thousand times the size of the hypothesized universal common ancestor (UCA) that began the tree of life. It is mathematically and physically impossible to inherit more from less. Complex creatures do entirely new kinds of things that Dawkins’ simple gene splitting operation simply cannot account for.

 

The problem of how to create new complex genetic information at many points along the development of the tree of life is simply ignored by neo-Darwinists despite the fact that it is the hardest thing to explain in the entire evolutionary process. It is perhaps the only thing that really warrants an explanation. From the point of view of intellectual integrity and objective science neo-Darwinists are therefore fully cheating in this regard, ignoring the hard parts while touting their theory as fully explanatory. The sheer presumption in lieu of evidence that marks the neo-Darwinian case at all the difficult points of explanation is nothing less than a scandal in science. 

 

In saying that genes must have split, duplicated and mutated for the simple reason that the visible branching of the tree of life requires it Dawkins is not explaining how it happened but merely restating that it happened. He certainly does not establish an accidental process. Nor has Dawkins given us an explanation of the initial achievement of specific genomes in higher animals. He only offers a very abstract and general account of how versions of essentially the same gene (hemoglobin) might have achieved minor variations as it descended among various ancestral lineages. Are these small changes meaningful? Yes. Are they surprising or explanatory? No. Are they macroevolution? No. Can Dawkins (or anyone else) produce a set of these smaller changes that are known to have occurred and add up to macroevolution? No. Known microevolutions such as changes in a finch’s beak size, the body shape of a minnow, and the coloring of a moth do not combine to make a human being.

 

The occasional small change may occur by accident and preserve meaning, assuming the number of nucleotide alterations needed are not many and the effects of the intermediate steps for some reason are not fatally destructive to system performance. But using limited, rare, atypical and imaginary cases does not constitute scientific evidence for the capabilities of the larger process of macroevolution. Minor variations of the same gene are not the core issue of macroevolution at all. Many thousands of such changes could occur either by accident or design and there be no major evolutionary consequence. The real question is how to originate radically new features never before seen on the tree of life. This requires many absolutely new and radically different genes working in concert. Randomly achieving this greater feat prior to “breaking” the existing design functions of the host creature is not a thesis we are entitled to believe without proof. It can be demonstrated to be more improbable than the standard scientific threshold for falsification.

 

Dawkins gives no proof for his, what one might call the “easy as pie,” explanation of new genes. He offers no coherent argument against purpose. He merely says that the historical record shows that the expansion of the genome occurred. One wants to say “Well, we knew that much, didn’t we?” Even pie is not that easy.

 

On the one hand there is information in Dawkins’ trivial sense, and on the other there is information in the sense meaningful to a given practical application, in the case before us, the macroevolutionary change of one type of creature into another. Answering a series of yes or no questions concerning the type, quantity, and location of every atom and molecule on one’s plate at dinner, for example, explains the structure of the material, yes, but only in the sense of a description; it does not reveal the chain of causation in real time and limited space. How could those molecules accidentally appear in a configuration that is (almost always) hot, aromatic, and delicious in time for dinner? Dawkins’ concept of information does not answer that question; only the presence of the cook answers it.

 

Don’t get me wrong. Although Dawkins’ attempt to explain the genome completely fails, there are some excellent texts on the subject of genome evolution out there. The Evolution of the Genome, edited by Dr. T. Ryan Gregory (published in 2005) is a superb example. It portrays many of the concrete mechanics of how the genome might evolve and grow. These mechanics do not argue for an accidental process, however.

 

Gregory comments, without supporting argument, that the fact that the transpositional systems of the genome are nonrandom does not obligate us to infer intelligent design. Nor does he argue against intelligent design. This is less than helpful. Despite the unquestionable value of his book, this single innocuous statement may mislead some readers. How so?

 

One of the points intelligent design theorists like William Dembski and Stephen Meyer have been trying to bring to the public awareness is that science has yet to formally establish a means, that is, an objective criterion, to use to answer the question of when the conclusion of intelligent design (called the “design inference”) is warranted. Professor Dembski has gone to great lengths to propose some preliminary models of how this could be done, but until these models are confirmed/ refined and incorporated into mainstream science, science has no criterion to use. Until science does establish a design inference criterion, statements regarding the absence of an obligation to make a design inference, such as Gregory innocently proposes, are trivial and unhelpful because there is absolutely no basis upon which to evaluate them. It is like saying, “I don’t do mathematics myself, but I see absolutely no reason to accept Einstein’s equations.”

 

Such perfunctory dismissals are less than helpful for an intricate debate and scientific/philosophical inquiry spanning 150 years, one that has ranged far beyond paleontology and comparative anatomy to complex arguments in quantum physics, cosmology, microbiology and genetics. There may be defensible logical grounds for a given scientist to withhold his or her judgment on the question of intelligent design, but those grounds must be made explicit in order to add merit to any recommendation for or against the ID thesis. Other than William Dembski’s recent proposals, there is no criterion for ID, and therefore no previous application of a criterion. There is therefore no default position for science to assume. Gregory’s book clearly adds to our understanding of the process of genome growth. It contains a wealth of the latest research and is much appreciated. But his failure to commit to ID is not sufficient justification to casually dismiss the intelligent design hypothesis when there is so much that argues for it.

 

The bottom line is that the creation of highly complex sets of new biologically meaningful genes is necessary to enable a creature to perform any radically new function, to accomplish the vast macroevolutionary leaps shown in the fossil record. It is now clear that evolution is not merely a matter of a bunch of small accidental mutations as Darwin believed 150 years ago, himself and his peers having no knowledge of either microbiology or genetics. In light of what we now know, it is no more reasonable to expect large jumps in design evolution by accident, than for a bachelor to postpone sleep and work in anticipation of duck ala orange magically appearing on his dining room table before bedtime. He must first hire a cook. Richard Dawkins, on the other hand, would say “Just hold tight, the information is available.” I, myself, would opt (as I often do) to simply get up and drive to Burger King.

 

Does the Immune System Reveal a Short-cut to Gene Production?

Professor Maxim D. Frank-Kamenetskii (Boston University’s Department of Biomedical Engineering) has acknowledged the lack of a current scientific explanation for the origination of new genes. To remedy this lack, he has proposed a new hypothesis for novel gene formation. He speculates that a process similar to our immune system antibody construction mechanism may have assisted evolution in the past, perhaps involving a hyper-mutation rate similar to what the human immune system generates in rapidly finding an antibody match to the protein coat of a new pathogen that has invaded the body.[73] Given this identifying signature, immune cells can then hunt and destroy the invader.

 

However, Frank-Kamenetskii does not explain how this new information finds its way back from the somatic (non-reproductive) cells of the immune system into the reproductive cells, the germ line, of the host genome. This is the same problem that defeated the Lamarckian theory of inheritance of acquired characteristics. Unless the acquired change can be passed on to a creature’s progeny, it does evolution no good to generate the change in the structural cells of a sole individual. Frank-Kamenetskii’s hyper-mutation is similarly restricted to the somatic cells of the immune system. Until research can demonstrate a plausible route from the immune system into the reproductive cells it can do the evolutionary explanation no good.

 

But if the evolutionary process is as capable as neo-Darwinists say it is, it would have found a way, as Kirk says in Star Trek III; it would have found a way, a way to reroute the new dramatically useful advancements generated by the immune system into the genome—but it hasn’t! That must surely be telling us something. I suggest that Frank-Kamenetskii’s immune system analogy reveals the integration problem. In a sense, complex designs are cursed; their complexity prevents the successful implementation of random changes. Here we have a truly astoundingly rapid genetic information producing mechanism already present in our bodies;  yet it has only been used to match the most primitive and earliest genes on the tree of life, the genes of bacteria, instead of generating amazing beneficial advances. Why? There must be a reason for natural selection would favor nothing so strongly or so rapidly as a rapid genetic change mechanism—other things being equal.

 

One might say, well we (humans) have survived as a species, so we apparently didn’t need rapid gene substitution after all. But we are only entitled to say that we have survived so far. And what about the thousands of other creatures that haven’t survived extinction? Why didn’t they inherit such an astounding advantage that was available in their ancestors? They cannot benefit from the same argument because the are extinct. The obvious answer is that rapid gene substitution doesn’t work in complex systems

 

The sequence changes for a beneficial new gene could be produced; the problem does not lie in production. In fact our immune systems almost certainly have produced many such useful new genetic sequences, only to cavalierly toss them away again because they don’t match the prehistorically simple characteristics of an invading germ! The human body has the basic genetic machinery that, with not too substantial a modification, could reroute the gene sequences produced by the immune system into the DNA of a reproductive cell. So what’s the problem? The problem is apparently integration. The system wouldn’t be able to install the new information after it is produced because so many other complex changes would have to be accomplished at the same time to prevent serious disruption to existing biological functions—too many other parts of the system have to interact with the new genetic string.

 

Once again, Professor Behe’s irreducible complexity thesis rears its theoretically formidable head. Living machines have passed certain threshold levels of complexity; they are too complex to tolerate accidental tinkering. So, even if an accidental process could get so far as to reroute the immune antibody sequence generator into the genome, it could not successfully integrate the new gene sequence into the total system without breaking the system prior to accomplishing a rework of the entire network of components that interact with the area changed—or else the new gene would just sit there watching evolution by other means pass it by. A random mechanism for rapid generation of new genes therefore cannot lead to a rapid macroevolutionary advancement due to the integration barrier. The Oxford Journal, Molecular Biology and Evolution, recently published the first study analyzing the mechanisms for and speed of integration of lateral gene transfers. Researchers Martin J. Lercher and Casaba Pal report in a 2008 article “Integration of Horizontally Transferred Genes into Regulatory Interaction Networks Takes Many Million Years,” that the process of integration is not simple and must take place in incremental steps over vast amounts of time. This reveals that rapid generation of new sequences is not a time saving solution for evolution because integration cannot keep up. 

 

Far from making accidental evolution more plausible, Frank-Kamenetskii’s revelation of the immensely useful potential in the immune system antibody production routine merely argues that large genetic transfers affecting the more complex functions cannot be successfully integrated into living organisms in real evolutionary time by a random process, for if it were possible, nature would have found a way to reap such a great advantage..

 

The integration barrier similarly negates the entire gamut of potential time-saving devices that accidental evolution needs to overcome the limitations of the basic mutation rate: large genetic transfers, across the board symbiotic mergers (some may work because the merger brings an integrated subsystem as opposed to a fractional component of a larger system), across the board acquisition of foreign genomes. These kinds of large random genetic transfers cannot be integrated any better than a redirection of Frank-Kamenetskii’s immune antibody genetic sequence generator. Thus we are left to face the music: the basic mutation rate is far too slow to support the historical record of the advancement of the tree of life.

 

Lateral Transfers and Acquisition of Genomes

One might easily ask, what if errors in the transcription and repair of DNA could cause the cutting and pasting of very large segments of DNA, to include whole genes? This might be accomplished in either one or several transactions, combining progress of the genetic lines of thousands of individual creatures into one through a series of diploid reproductions, bacteria plasmid transfers, conjugations, symbiotic mergers etc. Wouldn’t that solve the time problem?

 

If it could happen in the right places, in the right sequence, in the right manner, at the right frequency such that the vast time required for normal integration was skipped, yes, it would, in theory, solve the time problem. Even then the time problem would be solved only in part. To solve the time problem in full, the information has to be new to the tree of life. This means not a transfer but an origination event. In any case, transfer phenomena are too limited in scope and frequency in their actual occurrence to have accomplished the enormous total workload of evolution. Current data indicate that gene transfers account for no more than 2% of bacterial genomes.[74] Because of complexity barriers, they are probably far less frequent among vertebrates.

 

The probabilities derivable from biological design complexity tell us that only the nonrandom integration of large genetic transfers within the more complex areas of a organism’s design could ever succeed in real evolutionary time. Beyond that, recent research indicates that it has taken 8-22 million years to integrate lateral single gene transfers into genomic regulatory networks.[75] Thus, lateral transfer is clearly not a time-saving device. The Cambrian explosion generated most of the animal body types in only 5 million years. Obviously, if lateral gene transfers take 8-22 million years to achieve integration, lateral gene transfer has not been the primary mechanism of evolution.

 

There apparently have been frequent transfers among bacterial species, according to recent statistical analyses of genomes, but two important discoveries have come out of such studies that indicate that neither bacteria nor lateral gene transfers can save accidental evolution. First of all, in bacteria, which are extremely simple creatures, the operational genes seem to have no difficulty being transferred, but the informational genes that govern the more complex functions of genome management are not being transferred.[76] Thus, a complexity barrier is indicated that limits the types of transfers that can succeed to the simple ones. Next, analysis of genomes reveals that relatively few gene transfers have occurred between bacteria and vertebrates.[77] Thus bacteria have not served, as was once hypothesized, as rapid gene production factories that fueled all of evolution.

 

There is one known instance where lateral transfers have apparently been key to the success of a major evolutionary jump. That is at the mysterious evolutionary leap from simple prokaryotic celled creatures such as bacteria and the more advanced eukaryotic cell lines of complex creatures.    “Analyses of complete genomes indicate that a massive prokaryotic gene transfer (or transfers) preceded the formation of the eukaryotic cell.”[78] Lateral transfers are not useless to evolution, but neither are they a magic wand that allows an accident to make a sophisticated machine.

 

We must also consider the possibility of symbiotic genome mergers as a genuine contributing factor to evolution. As Professor Lynn Margulis explains in Acquiring Genomes, the merging of the genomes of symbiotic host and parasite remains more than an open question; it is a likely hypothesis. But the process of symbiotic genome merger is neither fully understood nor demonstrably random. Margulis herself vigorously disavows the traditional neo-Darwinian line that asserts accidental mutations as the primary source of evolutionary form change.[79] In any case, while symbiosis may provide the opportunity for some genome mergers that have influenced evolution, the phenomenon of symbiosis is not widespread enough to explain the foundational dynamics of macroevolutionary events across the entire tree of life.

 

Our experience in successfully transplanting genes, organs, cells and tissues from one species into another may suggest accidental evolution is not so ineffective, but the process being used to install and integrate those transfers is not accidental. Human doctors and scientists are the intelligent designers in those cases. Those situations actually suggest that intelligent design is what is needed to make viable biological form changes of any substance.

 

Chimerical experiments (transferring genes between species) tell us that successful transplantation of a gene requires that the affected subsystem of the recipient must have a set of features that fall within a compatible range of functional capacity and a general similarity of biomechanics to the donor, otherwise the gene will not be successfully integrated. Absent the preexistence of these prerequisites in design compatibility successful integration of a genetic transfer will not occur. In these cases, evolution is not being advanced so much as acknowledged because the requisite preexistent similarity means that evolution must have already “been there and done that,” as it were, at least in general terms. Gene transfers cannot, therefore, produce radical form change but only relatively minor modifications, and modifications that are, with very high probability, less beneficial to the recipient than the finely tuned interrelated system already in place. This limitation is very much confirmed in what we have seen in genetic science to date in chimerical operations and in horizontal gene transfer studies. Speculations to the contrary abound in fiction and popular media, but observations to the contrary are unheard of in real science.

 

Bacteria may seem to be the exception to this rule, but bacteria are extremely simple designs. Bacterial genes seem to have unique characteristics that make plug and play gene transfers among bacteria occasionally possible. They can only receive genes already custom made to fit certain narrow parameters (antibiotic resistance and so on). Nothing radically new is going to come out of the bacterial gene transfer process for the purpose of evolution, and complex creatures simply do not have the ability to do this kind of gene transfer in most areas of their physiology due to the integration barrier. Unless it is a simple change routed to the exterior of the organism, or otherwise bypasses the complex interrelated functions of critical systems, it cant’ be done.

 

We can place a human gene to produce insulin into bacteria and they will mass produce this very valuable medical substance for us. But this is an ultra simple function compared to the complex interrelated systems that would have to be generated to produce, say, mammals from reptiles, and it does not benefit bacteria in terms of physiological evolution, but only indirectly, making them a pseudo-symbiotic, pseudo-domesticated creature that humans have chosen to preserve for their own use. Nothing complex and truly evolutionary can be done with gene transfers.

 

We cannot put the genes for wings from a chicken in a rat and give him flight. Extensive integration work is required and many complex changes must be accomplished at the same time to maintain a match between closely interrelated parts. It is reasonable to conclude that, if we can’t do this on purpose after much study by our most expert scientists, nature can’t do it by accident. But, in a sense nature has done something very much like it with the bat, which is a flying mouse. Therefore, one may conclude that evolution did not happen by accident. Once again the prevailing rules of accidental biological change are confirmed: the simple can be, rarely, done by accident, the complex cannot be done at all. If it turns out that the way bats evolved has been preserved in the developmental and/transpositional genomes, we might, at some future time, be able to transfer a large, complex, set of genes that would turn a mouse into a bat, but it wouldn’t have chicken wings; it would have bat wings.

 

There would be nothing accidental or simple about doing such a thing for we would be, as intelligent designers ourselves, transferring large complex modules of preexistent design. We would merely be painstakingly and intelligently copying a design achievement rather than showing it to have been produced by accident in the first instance. Even if we could go the further step to identify just which gene segments determined the nature of the materials used for the wings, and then substitute feathers for leather, it would not establish the process to be accidental anymore than substituting the wings of a stealth fighter onto a B-1 bomber would demonstrate that the planes were constructed by accident. Intelligently guided chimerical gene substitutions are not evolution, and they are not beneficial to the recipient except to remedy a genetic illness.

 

Treatment of genetic illnesses does not represent a situation where a more primitive design is advanced by gene therapy, rather, a dysfunctional individual who deviates from the design of the species, having a malformation or pathology, is returned to the original design of the species. Such a procedure does not advance the species design as is required for evolution. In theory, where, for example, the human organism is so complex that geneticists cannot identify the totality of the gene complex that is involved, or it is fragmented in complex ways that forbid reliable gene therapy using a healthy human version of the same system to substitute into a dysfunctional recipient, a simpler version from another species may be used instead to ameliorate the illness. In such a case, this would be a regression to a more primitive system, not a progressive evolution, and intelligent design (medical science) would be required to make the change.

 

Darwin was right about one thing: If random evolution can work, it must work through slight gradual modifications. Anything else translates to a large wrench in a delicate machine. But what modern research has revealed is that large and varied sets of modifications have to occur in close coordination across substantial sections of the genome to integrate a functional design change. Therefore, when all is said and done, large random genetic transfers do more harm than good, and the small ones do nothing until the aggregate of many of them grows to the equivalent of a large transfer, at which point it causes the same disruptive effect as a large accidental transfer. An intelligently managed genetic marker system that chooses to activate or silence selected segments of large transfers until they are further modified to preclude damage to the system could ameliorate this damage; but such a system is not accidental.

 

Thus, the single linear incremental nucleotide change model (LINC) is the most efficient, that is, less self-destructive, route accidental evolution could take. But even LINC, that is, evolution by a series of individual point mutations, will fail minus an intelligently guided system that orchestrates complex sets of related changes in real time.

 

For computational purposes, then, it is legitimate (and conservative) to assume that the neo-Darwinian process has to do evolutionary advancement the slow way if it does it at all, that is, it has to individually configure each nucleotide of the non-“junk” portion (about half) of the 3,000,000,000 base pairs of the human genome over time to move from amoeba to man. Larger transfers create destructive results too severe to be absorbed by the recipient organism, degrading design and causing the gene line to fail the test of natural selection. Therefore, no matter how the accidental process approaches the evolutionary task, the magnitude of improbability and amount of time required are never reduced below that applicable to the LINC model and the standard mutation rate of 1% every 10 million years. But there is simply not enough time for the LINC model to work.

 

Starting with a 3,000,000 bp genome of a primitive organism and giving evolution 3.5 billion years to work, which are reasonably liberal assumptions for the beginning genome size and the first appearance of a simple bacterium, we then assume the standard mutation rate and that only 1 out of a thousand mutations will be beneficial (this is exorbitantly generous for an accidental process). This only advances the 3,000,000 bp bacterial genome to a fraction of that required (well under 3,200,000) by the time homo sapiens appears with its genome of 3,000,000,000.

 

Can Mythical Chimeras Come to Life? (Aloe Dolly!)

Scientists have successfully transplanted genes from one creature into another, achieving some simple mixing of characteristics between species.[80] They have not thereby created new body forms, however. They have only added a feature or two to an existing body plan without radically changing the plan or imparting major new functions. The scientists function as intelligent designers in these situations, so chimeric transfers cannot be construed as either random, or representative of an accidental process.

 

The chimera experiments lend force to our argument against neo-Darwinian evolution in that the limitations on what is possible in these interspecies gene transfers imply that preexisting complex interfaces are needed to assimilate foreign genes and that the integration problem still forbids macroevolutionary success. This is true because the only successful transfers have been between creatures having substantially similar donating and receiving subsystems. This establishes them as already relatives on the tree of life. Such plug and play opportunities are the exception, not the rule for gene transfers. They require evolution but cannot produce it. Using such examples to prove the viability of gene transfers as a mechanism of accidental evolution is invalid. It is circular in requiring a previous event of evolution from an unknown mechanism to prepare the way for the new gene to be assimilated, and it cheats in skipping the otherwise standard requirement to closely integrate a new gene into the larger system.

 

In “chimerical” gene transfers we are really only repeating what evolution has already cleared a path for, we are not demonstrating how the evolutionary process initially achieved the larger complex design that serves to receive the already created gene. The larger picture of chimerical gene transfers suggests that the interphyla barrier to random genetic change is real, not that a chain of accidents can produce a human being from a germ.

 

The chimera discussion raises another question, one about evolution generally: Why didn’t evolution find some of the obviously beneficial chimerical variations, like Aloe vera cactus leaves on a sheep? Would that benefit all the sheep, or only those with dry skin? It would benefit all by keeping their primary predator, wolves, from eating them. The long thick and sturdy leaves have strong cactus needles along two edges which, though possibly tasty, would be nearly impossible and immensely painful to eat.

 

How could a plant animal hybrid be possible? Its all in the genetics, you know. The Darwinists explain greater mysteries this way. In this case, however, it appears to be truly possible. A second layer of skin could contain the plant system, water could be routed to that layer from internal supplies without much trouble and the animal could have a scooped nose and flexible neck to give itself dust baths daily to keep the plant in mineral nutrients. What could be simpler?

 

Darwinists will say that it is precisely because the process of evolution is accidental that this didn’t happen. In other words evolution was fortunate to stumble upon those beneficial combinations it did find, and natural selection preserved those, but evolution took a haphazard hit and miss kind of a course, producing results that did not exhaust the possibilities. That’s all fine and good so long as we don’t foul up our imagination with any inconvenient facts. In this case it is the math that is the problem. Any random biological search routine thorough enough to achieve improbabilities so vast as we here demonstrate as applicable to the origin and evolution of complex life would have had to have been so potent as to literally exhaust the alternatives.

 

If an undirected search routine could develop an eye and a brain from scratch it could arrange to patch simple plant extremities onto the exterior of a grazing animal that spends its time immersed in the sun in an otherwise plant hospitable environment. A nonrandom or directed search need not have done it, something like Dr. Michael Denton has recently suggested in his articles on natural law restricting the outcomes of natural event processes to a set of predetermined forms.[81] But, in that case, evolution is no longer accidental. In contrast, a random search routine that must run so long and reach so far and wide among the possibilities to achieve the ultra complex mechanisms of life, should always find the easy combinations first, before moving on to the complex. The Darwinists own arguments imply this by suggesting evolution used a modular or building block approach and that none of the modules individually were super complex. For them, complexity simply “emerges” by tacking a large number of simple components together. It is all nonsense of course, but that’s what they say.

 

The Destructive Nature of Random Mutations

During the first (and primary) evolutionary synthesis of the fifties just prior to the discovery of the double stranded DNA molecule in 1959 scientists modified Darwin’s original theory in an attempt to incorporate the basic concepts of the primitive Mendelian genetic science of the day. They knew, or hypothesized, that there were genes, but had no clue how they functioned. From Darwin’s time it had been claimed that accidental changes in the vital substance of life (protoplasm), and later this genetic material (as yet unanalyzed) that the Catholic monk, Gregor Mendel, discovered, and finally that accidental or “random” point mutations of single nucleotides, were the source of the variations that natural selection chooses from to evolve new forms of life. This, as opposed to the much more complex transpositions of whole sets of genes and gene segments that now appears necessary for biological form change, and which is nonrandomly governed by the genetic machinery. Here, in a 1941 Time magazine article reviewing Columbia University Assistant Professor of History Jacques Martin Barzun’s book, Darwin, Marx, Wagner, you see that the godless accidental worldview was in fact built into neo-Darwinian theory. To be clear, Darwin did not do this, his successors did.

 

Darwin's discovery was "evolution by natural selection from accidental variations." The dynamite, says Author Barzun, was in the phrase "from accidental variations." Reason: it denied the role of God in the universe, ruled out a purpose in existence, made men mere puppets of mechanical forces.[82]

 

This was merely a theory, of course, not a “discovery” at all. Neither Darwin nor any scientist who came after him knew or could prove that accidental changes or single point mutations could do this, produce major life form evolution; they had not seen it; they could not demonstrate it; they merely assumed it. The whole enterprise that sprung up during the 1920’s to 1960’s of quantum physicists and neo-Darwinian evolutionists asserting an accidental worldview was vastly premature. To redirect all of science towards a radically different worldview based upon nothing more than an unevidenced assumption, not once observed to have occurred, never tested, and never reproduced under scientific scrutiny, is not to do science at all, but merely antireligious politics. Nonetheless, many of the scientists, writers and commentators of the fifties and sixties forward threw the entire weight and confidence of science behind this unevidenced and outrageously implausible assumption of an accidental process in biological evolution and in quantum physics.

 

In those days our knowledge of the genome was only the merest fraction of what we now have and the view of the genome unavoidably overly simplistic. What we have since discovered is that truly accidental mutations cannot generate complex life form evolution because they fail to preserve the basic mechanical integrity of the organism. While the design of living systems has turned out to be vastly more complex than anyone ever imagined, to believe that an accident can build a complex living machine or a sophisticated machine of any kind has always been inane.

 

One can say, well, a consistently recurring string of events that mimic the set of natural laws required to provide the needed cohesion is itself such a chance combination. While this is true in a sense, it is a vastly more expensive combination in terms of probability because it not only has to arrive at the correct chance combination but repeat it in an endless sequence over and over again requiring the initial incomprehensibly large magnitude of improbability to be multiplied by itself trillions upon trillions upon trillions of times.

 

One need merely note the enormous improbability figures arrived at by famous mathematical physicist Roger Penrose for the odds against our life-hospitable universe being produced, 10 raised to the power of 10123,  to see that the assumption that accident could achieve it within the time and physical resources available in the history of our universe is beyond the threshold of scientific credibility. For the nonmathematician, the difference between 10123 and 10 raised to the power of 10123 is that 10123 is 1 followed by 123 zeroes, whereas 10 raised to the power of 10123 is 1 followed by enough zeroes to fill trillions upon trillions of books. Science has never affirmed and cannot rationally affirm anything so vastly improbable, therefore an accidental origin of our universe is ruled out as a scientifically credible hypothesis.

 

In the mid twentieth century, when neo-Darwinism came into vogue, positing randomness in the strong, truly accidental sense, as the source of variation seemed to offer a powerful explanation because we had not as yet observed its destructive effects in practice. We were experimentally (though not theoretically) free to ignore the subtle but unavoidable implications of thermodynamics for the accidental worldview, that is, we were free to ignore the fact that the accidental worldview is self-contradictory. Thousands of mutagenesis experiments later the accidental hypothesis has turned out to be a problem even in the experimental lab because random mutations (in the strong, truly accidental, sense) have proved themselves, with only the rarest and insignificant exceptions, exclusively destructive or neutral.[83]

 

We knew this as far back as 1977 when G. L. Stebbins, writing with Theodosius Dobzhansky and others, in the seminal tome, Evolution, acknowledged that “…mutations having conspicuous effects on the phenotype usually reduce fitness and tend to be rejected by natural selection.” Modern evolutionary biologists agree. “Undoubtedly many mutations are neutral or nearly so, having very slight effects on fitness…However, many do affect fitness, and their average, or net, effect is deleterious.”[84] 

 

Professor Michael Behe, author of Darwin’s Black Box and Edge of Evolution, points out that the designs of living systems involve so many critical interrelationships that many changes must be made at the same time for the system to advance. What this means is that, contrary to the undemonstrated beliefs of random drift theorists, small changes that do not have conspicuous effects are not comprehensive enough to accomplish any progressive evolutionary change; they can only produce an occasional triviality, color change or something fully irrelevant to the complex internal mechanics of an organism, such as scaling up or down the overall size of the creature. When such small changes do finally accumulate sufficiently to cause a change in internal functions, the effect is destructive due to the inevitable occurrence of a conflict among closely matched interrelated parts.

 

Dr. Jonathan Wells confirms that in the developmental genes that govern embryonic development random mutations never produce beneficial changes, and typically lead to death or deformity.[85] But the developmental genes are where major body type evolution must occur, else it cannot occur at all. Enter yet another impassable barrier for neo-Darwinian theory: developmental sensitivity. Dr. Robert Pollack who worked with James Watson, co-discoverer of DNA’s structure, at Cold Spring Harbor Laboratory, also says that major alterations to the DNA of embryonic cells caused by environmentally induced mutations are normally tragic.[86] This poses a sort of catch-22 for the accidental mutation theory of evolution. Mutations occurring outside of reproductive cells do not get passed on to the next generation and those that do alter reproductive cells are invariably harmful or have no effect. Therefore, the only evolutionary result accidental mutations appear capable of producing is a destructive result, though many are neutral in their effect.

 

It is not surprising that random mutations show no beneficial effect. Remember, there is an enormous amount of DNA for random mutation to have to sort through (the rough equivalent of 600 round trips to the Sun).[87] Reports of modern genetic research reveal that the available options for new biologically viable DNA sequences are so rare within the vast library of DNA sequence options, the distance between them so great, that the odds are overwhelmingly against random search ever finding an alteration that works to advance the organism.[88] Contrary to the approximate rule of thumb that seems to be casually implied in some of the neo-Darwinian literature, that one could expect roughly one in a thousand mutations to be beneficial, the protein synthesis research of D. D. Axe cited by Stephen Meyer indicates the true ratio to be closer to 1 out of 1077. This assumes the minimum number of multiple point mutations that must occur in concert to generate one new biologically viable protein. Trillions of trillions of trillions of trillions of trillions of trillions of useless or harmful mutations must occur to get one beneficial change at the simplest level of biological construction, the protein. How many would be needed to produce the sets of multiple genes that must work in concert to construct a new biological function or structural feature? The increase would be exponential due to the rules of probability theory, in other words,  something on the order of 1077 X 1077 X 1077 X 1077, or 1 mutation event out of 10308 might be of use to macroevolution. But, as we discuss in Appendix 2, Professor William Dembski has informed us that there are only enough resources in the history of the universe to generate the smallest fraction of that number of mutations.

 

A Mickey Mouse Operation

Neo-Darwinian theory makes the outrageous claim that nature has, while blindfolded, and with no blueprint in mind, successfully tinkered with the Mickey Mouse watch (a bacterium) without stopping the watch or malforming it beyond natural selection’s standards more than 1,500,000,000 times (the non-“junk” portion of the human genome). It claims that an accident has inconceivably succeeding in advancing the Mickey Mouse watch design to the Space Shuttle (a human being). However, the historical fossil record, in fact, now reveals that the larger part of the work of evolution was done in the brief 5-10 million years of the Cambrian explosion. Billions of years of working time have been lost to the imagined accidental process at the same time that the known complexity of biological systems has skyrocketed. Simply put, such a thing seems both fully impossible and contrary to the historical evidence.

 

Darwinists respond to this objection with an oversimplified and, therefore, fallacious, logic. They note that bacteria can, and clearly do, generate “useful” mutations each year, for there are trillions of them and they mutate all the time. Granted, bacteria do come up with some useful changes every day, but they are only useful for bacteria. There is no evidence that these changes ever exceed a very simple threshold of form change. In the larger evolutionary event process, as soon as complex designs arrive on the scene, the ability for accidental mutations to do anything useful to advance life disappears. This loss of ability to tolerate random design change proposals occurs at the same point on the evolutionary tree that creatures lose two other features unique to bacteria: enormous population size and a life span so short as to make the generational input to the rate of genetic change astronomical. Thus, what little credibility the Darwinian dynamic has ever had relies fully upon the fallacy of using a creature that is atypical of nature (the bacterium) to model what is claimed to be the typical evolutionary process for the entire tree of life.

 

In point of fact, the neo-Darwinian hypothesis implies the exact reverse of the observed history of life. Bacteria appeared almost instantaneously once water formed on the Earth. There was no time for accident to work up their design. The same bacteria, which neo-Darwinists say are hyper-mutative, have taken 2 billion years to go practically nowhere, while in the Cambrian explosion most of the complex animal body plans developed in 5-10 million years under some still unknown dynamic. Once again, no time for accident to work up the designs (if one assumes it ever could, which I do not).

 

Can we now in the laboratory, while simulating the Cambrian and post-Cambrian environments of earth regarding mutagen prevalence and delivery, and with true random targeting of nucleotide base pairs, generate two or three ultimately progressive mutations per year?[89] No. We cannot produce any. We can only demonstrate that under limited conditions creatures with genetic features quite unique in nature, bacteria, can produce varied changes of the simplest form and function within a definite and very limited set of options, useful only to themselves, at no time yielding a new type of organism outside the family of bacteria.

 

After thousands of laboratory studies, all we know for certain is that accidental mutations are almost always harmful. A mechanism (accidental mutation) that cannot be conclusively demonstrated to account for any new increments of viable biological information sufficient to generate one substantial evolutionary advancement certainly cannot be rationally held to account for all of them.

 

The Phylogenetic Tree from Hell

Darwinists are fond of holding up tree diagrams as proof of evolution. One wants to ask, specifically, “Where is the tree full of documented viable progressive results from random mutations?” “Where is the tree of the requisite steps that must be accomplished to move between the known species?” For every newly evolved animal type there must have been thousands of mutative steps along the way. Where are the examples from nature and the lab that such frequently needed occurrences do in fact occur and that they link up in real time to form cumulatively progressive results? There is, of course the unfortunate fruit fly with a leg on its head, a poor dog turned into a cyclops, and the fly with broken wings that replace its flight stabilizers, thus fouling up flight dynamics. Aberrant deformities, genetic illnesses, regressive changes, and malfunctions are practically the only documented form changing mutations we have on record![90]

 

The only exceptions are simple changes that don’t require complex integration with the rest of the organism’s design and which do not evidence a change in form and function significant enough to be a step towards macroevolution. Therefore they are not exceptions to the intelligent design claim that accident cannot do what is required for evolution. Professor Douglas Futuyma notes two of these kinds of simple changes as proof of evolution: a bacterium that gains the ability to metabolize new organic chemicals and the fruit fly becoming more efficient in the use of their food. He also notes that hair color and height vary continuously across a very complete spectrum in humans. While this is true, such things are the simplest, least problematic, alterations to make. They pose no integration challenges to the complex internal machinery of the body.[91] Science still has no idea how any of the hard parts of evolutionary development were achieved! Despite this glaring limitation neo-Darwinian evolutionists have been insisting that accidental evolution is an established fact for decades.

 

The known results of accidental mutations would indeed fill a tree, but it would be a horrible thing to behold, with monstrous deformities and birth defects hanging from every limb. I challenge any scientist or team of scientists to construct an evolutionary tree from the known results of accidental mutations, anything that has produced a beneficial progressive macroevolution vice a chamber of horrors. It can’t be done. The practice of good objective science requires us to hypothesize not that accidental evolution can produce large changes in complex biological functions resulting in the entire tree of life, but, that accident can, at best, produce only the small simple changes that we have actually seen. We should stick to the evidence.

 

“Show Me the Money!”

Neo-Darwinists cite minor changes to the already completed genomes, so called “random mutations,” as convincing evidence for accidental evolution. However, they can’t give even one example of a mutation that can be demonstrated to be both truly random and that can be shown to have lead to a significant step in progressive evolution. In fact, they can’t give a definite concrete causal explanation of any kind, random or otherwise, for even one major step in evolution.

 

Neither Darwin, nor any Darwinian, has so far given an actual causal explanation of the adaptive evolution of any single organism or any single organ. All that has been shown…is that such explanations might exist (that is to say, they are not logically impossible). [92]

 

In scientific writing the allusion is often made to “beneficial mutations.” Typically, studies documenting the referenced mutations are not cited, nor is it even made clear what the term “mutation” in that context fully implies. Are the referenced mutations confirmed by observation, or are they, rather, merely theoretical assumptions? Are we speaking of mutations beneficial in some minor way to one species, or mutations that can be demonstrated to link with others to advance the creature towards a more complex organism on the tree of life? Are they truly accidental point mutations caused by toxic exposure or replicative error, accidental chromosome relocations caused by physical or chemical injury, or are they not so accidental allele substitutions, reproductive mixing of genes, genetic transpositional element induced changes, or genetic marker changes closely managed and shepherded by the governing mechanisms of the genome? The answer makes all the difference in the world to the question before us: accident or purpose? Yet no effort is made to give the reader the information they need to properly evaluate the neo-Darwinian claim of an accidental process.

 

One can find the biomechanical aspects of each of these types of mutations discussed in genetics texts in general terms, but documented and observed examples of instances of truly accidental mutations leading to evolutionary advancement are not to be found. Demonstrably accidental mutations known to have led to a major evolutionary advancement are the unicorns of biology. They are believed in, they are imagined, they are hypothesized, but they have never been seen. Recently Dr. Jerry Bergman accomplished an exhaustive search of the scientific literature and did not find any genuine examples of information gaining gene mutations at all. The few examples that did anything useful for an organism generally required an unusual circumstance to be beneficial and were otherwise injurious. Dr. Bergman’s paper recounting that search entitled “Darwinism and the Deterioration of the Genome” is available online at True Origin and also at the Creation Research Society Quarterly journal online.

                                  

In order to locate all alleged examples of beneficial mutations, I carried out a computer search of the literature.  My review covered all published scientific studies that dealt with beneficial mutations.  The definition of beneficial mutation used was a mutation that was regarded as beneficial by the authors surveyed.  Key words used in the computer search included synonyms of beneficial, such as “favorable, helpful, usable, valuable, adaptive, good, advantageous, supportive, positive,” etc.  The search of two data bases totaling 18.8 million records found that, of all articles discussing mutations, only 0.04 percent, or 4 in 10,000 articles on mutations, were located that discussed beneficial or favorable mutations.  Some overlap exists in the data bases searched, consequently the actual total number of records searched was less than 18.8 million.  The overlap in the search was estimated by extrapolating from the records found.  Assuming that the same level of overlap exists in the entire database, a total of approximately 16 million records was searched.  These searches may have missed some relevant articles but are useful to indicate trends.

 

All of the 126 examples located were then reviewed, focusing on evidence for information-gaining beneficial mutations.  It was found that none of them contained clear, empirically supported examples of information-gaining, beneficial mutations.  Most “examples” of actual, beneficial mutations were loss mutations in which a gene was disabled or damaged, all of which were beneficial only in a limited situation.[93]

 

I have myself made a much less exhaustive search through two of the electronic academic journal services by obtaining a user account at the local university and could find nothing reflecting any viable mutations that might lead to evolutionary advancement. There is apparently no central databank of beneficial mutations leading to progressive evolution maintained for the common use of researchers and the public. But why not? There is a databank for absolutely everything else. If beneficial mutations exist in such abundance and neo-Darwinian theory so critically depends upon them, why haven’t they been traced and recorded with the greatest of care? Why don’t pro-Darwinian articles wave this alleged multitude of progressive evolutionary mutations around in public view as a great victory for their theory? Certainly they have tried to do more with less. The obvious conclusion is that they don’t have anything beyond the trivial to present, or worse, nothing that is not demonstrably fallacious.

 

Evolutionists explain the process of evolution to students and the public in the simplest of terms as if the process were child’s play, easy as pie, implying that any fool can see how it happens. But when pressed to demonstrate real examples of specific mutations that have led to evolution they protest that it is an unfair demand because of the enormous size and complexity of the event process, and the trillions of small gradual changes involved. However, when one looks at the fossil record one sees that the changes were neither small nor gradual.

 

“OK fine,” we respond. “We can agree on this much. It is not simple. Which complex set, then, of accidental changes must occur in sequence or conjunction in order to create a specific recognizable step in macroevolution? Just give us one complete set of accidental mutations for just one substantial step in macroevolution as an example. Then we can test that hypothesis in accordance with proper scientific method. We can go try to randomly replicate those steps in the lab. This is how science works, after all.”

 

The Darwinists protest again. “We can’t do that. We don’t know a complete set of mutations sufficient to accomplish any specific macroevolutionary step, and, even if we did, attempting to randomly generate enough useful mutations to produce a new complex feature in biology would exceed the budget of all of science for millenniums! (They don’t add, as they should, “If it could be done at all.”) The entire process is too big.” What they fail to recognize, though their objection is in other ways well grounded (the process is enormous), is that implicit in their own objection is the truth that accomplishing all of the needed complex new features and function changes required for the evolution of the tree of life by accident exceeds more than the budget of science, it exceeds the total budget of the universe in time and materiel. (See Appendix 2)

 

“Well, how about this?” they may say. “Let us break something for you. We can do that easy enough. No trouble at all. We can make a fly that doesn’t fly; oh, and a one-eyed dog. How about that?” “No, thanks,” we politely demure. “Any fool can break something; but evolution is the process of building more and more complex forms of life well fit to survive in their environment. To demonstrate evolution you have to demonstrate forward progress, not major malfunctions and regressions.” Yet, this is all that science can do in the genetics lab to this day, break things (or produce trivia).

 

This demonstrates that progressive evolution is not a simple matter of a few accidental point mutations, but an enormous closely guided process involving multitudes of time-coordinated changes affecting the many interrelated parts of highly complex integrated systems (irreducible complexity). If life is not irreducibly complex as Professor Michael Behe claims, if it is all simple and easily thrown together as the neo-Darwinists say, why can’t we reproduce these easy steps in the lab?

 

Some Darwinists, of course, claim that new genes are created by the bushel every single day, and that beneficial mutations are everywhere. But they are not everywhere documented. They are not everywhere in the textbooks and science journals. They are only everywhere hypothesized without proof. The next time you confront a Darwinist say “Show me the money! Where are the documented mutations that have generated the difficult steps of evolution toward the complex forms of life?” They will only produce a few bacterial changes that go nowhere beyond bacteria, regressions of genes that go backward in functional capacity, genetic illnesses, horrific defects, and trivial changes requiring no substantial integration with the complex internal design functions of the organism.

 

Beware the word game. Consider the following quote from Douglas Futuyma:

 

So is it true, as the creationists claim, that good mutations are vanishingly rare? Certainly it is true that many, many mutations are harmful. But if even only one hundredth of 1 percent of all mutations are beneficial, 20,000 of them should crop up in the gypsy moths of Long Island just this year. Moreover, the early geneticists significantly underestimated the proportion of beneficial mutations, because they studied a biased sample of possible mutations, the ones that drastically change an organism instead of modifying it only slightly.[94]

 

The wording here is very misleading in several ways. “if even only one hundredth of 1 percent of all mutations are beneficial”—is this a generous figure as Futuyma clearly suggests? Hardly. Do we have any hard research indicating such a figure is in fact generous? No. The only concrete research we have is quite to the contrary. D. D. Axe’s protein synthesis research, which, in fairness, was completed after Futuyma’s statement was published, has revealed that the proportion of useful mutations in the sense of being able to produce at least one biologically viable protein (the minimum change to have a significant effect on the organism’s design structure) is not 1 one hundredth of 1 percent but only a trillionth of a trillionth of a trillionth of a trillionth of a trillionth of a trillionth of that, or one part in every 1077! Thus we should expect, not 20,000 (simple) beneficial evolutionary changes in the gypsy moths of Long Island each year, but only one change every 10,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000 years. But the universe is only 20,000,000,000 years old! Thus, the truth is not what Futuyma implies, that there are more than sufficient numbers of beneficial mutations to ground accidental evolution. Rather, we should expect no beneficial random macroevolutionary change whatsoever.

 

Second, by opting to include the slight changes that do not “drastically change the organism” Futuyma has excluded a demonstration of macroevolution by definition. Finally, nothing is said here as to whether the mutations are accidental in any real sense, but, since no delimiting characteristic is given, Futuyma is apparently considering all types of mutations taken together. Once again, when one takes the nonrandom mutations generated by the internal mechanisms of the genome out of this group to leave only the apparently accidental, there will not be thousands of beneficial mutations per species per year; there will be none, barring only the horror stories and trivialities previously discussed.

 

Why aren’t the examples of new randomly produced genes that effect evolutionary advancement in the textbooks if we get 20,000 beneficial mutations per species per region per year? One thousand roughly correlates to a gene totally rebuilt from scratch, which yields roughly 20 new genes per species per region per year. Where are they? This would be the best evidence neo-Darwinian theory could produce, rapid generation of new genes with beneficial results. All we see in the text books and science journals are deleterious mutations such as Sickle-cell Anemia, Downs syndrome, Cystic Fibrosis, Muscular Dystrophy,[95] wings that don’t work, a leg in place of an antennae, regression in the capability of a gene, etc. A collection of mistakes and regressions, no matter how elaborate, will never assemble themselves into an evolutionary advancement of a complex living machine.

 

It is time for the public to put the neo-Darwinists on the spot: show us the new genes, show us that they make substantial progressive change, and demonstrate that they were evolved by accident! Then link a set of them together to show a real step in macroevolution, one phyla evolved from another, one class evolved from another. Then replicate the process in the laboratory. This would be proof of accidental evolution, and only this—and accidental evolution will not be a fact, as neo-Darwinists have prematurely claimed, until this is done. The requirement to replicate a substantial step in evolution in the laboratory is fair for the neo-Darwinists who claim the process is accidental because, if the process is easy enough for an accident to achieve it, surely it can be replicated in the lab.

 

Let’s visibly catalog those alleged new gene evolutions and place the complete data before the public where it can be rigorously scrutinized to see if it adds up to an achievement of new, complex, and highly integrated biological systems. This would comport more with the presumed integrity and known method of science, as opposed to what is presently occurring, that is, casually referring to volumes of evidence that exist only in the interpretive imaginations of the neo-Darwinists. I guarantee you that, when produced, the so-called evidence will be a thin catalog indeed, consisting of front cover, back cover and a single insert saying TBD (to be determined by further research). If the quality of the evidence was as good as Darwinists have claimed, we wouldn’t have to publish in the nation’s leading science journal studies of regressive change as proof of progressive evolution.

 

A catalog of beneficial mutations would be the best, certainly the most direct, evidence neo-Darwinian theory could conceivably offer. Professor Futuyma says there are plenty of instances of beneficial mutations. Why not lay them out for inspection and see what they add up to? Frankly, I just don’t believe it. I think the neo-Darwinists’ extreme faith in evolutionary theory has blinded them to the truth. Their theory has explanatory power only in the abstract, that is, in the imagination. There is no genetic or biochemical evidence for accidental evolution. Accidental mutations that can be shown to lead to macroevolution simply do not exist—they are unknown to science.

 

Neo-Darwinists may reply that gradual random mutation-based changes that lead to macroevolution take too much time to be observed, and this may be true; but that makes their claim unobservable and their theory not scientific because it can’t be tested.[96] The implications of the mutations we can observe are very different from the assertions of neo-Darwinian theory, however. Truly random mutations are observed to consistently degrade the efficiency of the organism, or even destroy it—cancer and birth defects being cases in point. The neo-Darwinist objection then amounts to “The changes that support our theory are too big to be observed, the beneficial changes, but the destructive changes that argue against neo-Darwinian evolution are small enough to be seen all the time.” That is rather a dubious claim, and it is hard to see how it helps their case.

 

Granted, if random mutations could produce beneficial change, it would take them longer to make a sophisticated biological machine than to break it. But this does not further the neo-Darwinist case. Quite the opposite. It places the neo-Darwinists in a logical pin, or checkmate. It amounts to an implicit admission that biological machines should break long before they constructively evolve under the influence of random mutation. But this is exactly Michael Behe’s irreducible complexity thesis, one of the primary arguments against accidental evolution!

 

The Mutation Factor: Darwin Runs Out of Geologic Time

Could the beneficial mutagenic rate be high enough to make neo-Darwinian theory credible? Genetic science, unavailable to Darwin, now says no. According to Dr. Stephen Meyer, citing Dr. Susumu Ohno, the scientist who discovered the link between cancer and genetic mutation, a random mutation rate of 10-9 per nucleotide base pair per year is taken to be a reasonably liberal assumption. That is one mutation per billion base pairs per year and includes all types of point mutations: harmful, beneficial and neutral.

 

Other scholarly sources confirm the standard mutation rate and there is general agreement upon it.[97] As Dr. Ohno indicates, a standard mutation rate of 10-9 would correspond to only a 1% change in DNA over 10 million years, almost all of which would be destructive or neutral.[98] How then were 48%-87% of our elegantly functional body types evolved during the Cambrian period in the time that should have generated only a 1% predominantly destructive change to the genome as a whole, producing no new viable body types and wounding any already present?

 

Believing that even a 1% change useful to evolution could happen requires the unreasonable assumption that all mutations will be beneficial for 10 million years running when all the evidence to date says we should expect none to be beneficial—if they are truly accidental. The time available on the geologic timeline established by the fossil record to move from bacteria to man is approximately 550 million years. The standard mutation rate allows for a 55% change in that time, only the smallest fraction of which should be beneficial, and most of that trivial. The bacterial genome, however, is only in the neighborhood of 3,000,000 base pairs of nucleotides, whereas the human genome is 3,000,000,000. That equates to a 100% change, a thousand times over! Considering that hardly any mutations are ever beneficial, the discrepancy between the amount of change expected from the mutation rate and the actual observed rate of evolutionary change is 100,000,000 to 1.

 

How long does it take to achieve one beneficial mutation, and of those few that are beneficial, one that goes further to contribute to advancement of macroevolution of highly complex species? No one knows. We have never seen any randomly generated mutations that can be positively linked to the development of a significant new body form or a beneficial complex functional innovation—not one. That may be because we haven’t been looking long enough, because the process is simply too big and too complex for empirical science to ever complete the linkage, or it may be, as complexity analysis, probability theory, and mutational studies suggest, because there aren’t any accidental mutations that lead to macroevolution.

 

Where we do see phenotypic changes arise within a species in nature, they are minor microevolutions that do not lead to a significant change of body form—and these have not been linked to external/toxin-induced (accidental) mutations as their source.[99] Rather, nontrivial biological form change appears to be coming exclusively from the internal shuffling of highly configured genetic information. This information is already present in the organism and is being both randomly and nonrandomly rearranged by allele substitutions, modification of gene expression tags that turn on or off a complex design module already complete, transpositional mechanisms that move genetic components around based upon the built-in rules of the genome (in part still poorly understood but on the surface nonrandom), and the well known variations that result from reproductive combinations.[100] It is the recently discovered role of transpositional elements and mechanisms that I wish to highlight here. Retrotransposons are one such mechanism.

 

Retrotransposons are mobile genetic elements that transpose through reverse transcription of an RNA intermediate. Retrotransposons are ubiquitous in plants and play a major role in plant gene and genome evolution. In many cases, retrotransposons comprise over 50% of nuclear DNA content, a situation that can arise in just a few million years. Plant retrotransposons are structurally and functionally similar to the retrotransposons and retroviruses that are found in other eukaryotic organisms…Recent studies are providing valuable insights into the mechanisms involved in regulating the expression and transposition of retrotransposons.[101]

 

Mobile group II introns, found in bacterial and organellar genomes, are both catalytic RNAs and retrotransposable elements. They use an extraordinary mobility mechanism in which the excised intron RNA reverse splices directly into a DNA target site and is then reverse transcribed by the intron-encoded protein. After DNA insertion, the introns remove themselves by protein-assisted, autocatalytic RNA splicing, thereby minimizing host damage.[102]

 

The genetic shuffling required for macroevolutionary form change is often performed by a very sophisticated mechanism of transpositional elements that recent research suggests is significantly directed/nonrandom.[103] In sum, the problem of intelligent authorship of the books that govern the designs of living creatures remains unsolved, substantial parts of the juggling process are demonstrably not accidental, probably even directed, and the transpositions that have apparently done the bulk of the task of evolution are closely constrained by the machinery of the genome. In other words, there is nothing accidental about biological evolution.

 

Given the large number of genes and the tasks those genes perform across the entire spectrum of the tree of life, yes, there may arise an occasional opportunity for a single point mutation, or small set of them, to generate a “component” step of a larger evolutionary change. But there is no indication in the fossil record that the rest of the set of changes that must complement such small mutations has in fact occurred in close conjunction. The bottom line is that neo-Darwinian theory cannot explain how the first full compliment of genes and the genetic machinery could be originated by chance, and it has now become apparent that it is that machinery that is accomplishing the evolution of life, not accidental mutations.

 

The Bacterial Cavalry

But don’t’ panic yet, you die hard neo-Darwinians; here come billions upon billions of gene transferring hyper-reproductive bacteria and viruses to save the day. Hurray for germs! There are undeniably an astounding number of them (70,000,000,000,000 in your intestines alone[104]), and they reproduce at amazing rates. Bacteria do carry spare genetic information around with them in “sacks” called plasmids that spontaneously mutate the organism via recombinant DNA processes.[105] Walla Booby, accidental neo-Darwinian evolution proved this time for sure! Right? No.

 

Bacteria are visibly exceptional to all other creatures in nature in that they carry spare bags of genetic material around, material clearly designed to be periodically integrated into their (ultra-simple) genome in routine ways, and they are exceptional in being astronomically simple. Nor is bacteria’s extraordinary reproductive rate typical of nature. Therefore, what accidental genetic substitutions can do for bacteria they can do for no other creature on earth.

 

Although early Darwinian discussions often pointed to plasmid gene substitutions as if they were true random accidents, we now know that the plasmid is not just a patch of stray genetic sequences stuck onto the bacterium; it is a closley governed portion of the organisms overall machinery.  When the bacterial cell reproduces the plasmid also divides and the process is controlled by genes within the plasmid. The plasmid phenomena is therefore hardly an accident.

 

Bacterial plasmids encode partitioning (par) loci that ensure ordered plasmid segregation prior to cell division. par loci come in two types: those that encode actin-like ATPases and those that encode deviant Walker-type ATPases. ParM, the actin-like ATPase of plasmid R1, forms dynamic filaments that segregate plasmids paired at mid-cell to daughter cells. Like microtubules, ParM filaments exhibit dynamic instability (i.e., catastrophic decay) whose regulation is an important component of the DNA segregation process. The Walker box ParA ATPases are related to MinD and form highly dynamic, oscillating filaments that are required for the subcellular movement and positioning of plasmids.[106]

 

Ultimately, the unique success rate of bacteria in adaptive gene substitutions may derive from two very simple things: the rate at which bacteria try substitutions, which is astronomically high, and the fact that it is not hard to do what they do, that is, to decompose things, to tear things apart. It is always easier to break something (in this case to break it down) than to construct it. The bacterial enzyme based digestion/defense mechanism is unitary and functions on the exterior of the organism’s design. It requires neither close nor complex interaction with other components. Like a piece of a jigsaw puzzle with a single simple standard node that plugs into the exterior border, there is practically nothing to conflict. Genes of more complex animals that govern critical internal processes, on the other hand, have multiple functions and are additionally cross-referenced to a very sensitive developmental genome. They therefore correspond to a highly complex internal piece of the puzzle with multiple nodes. There is more to conflict. Necessary modifications might cascade in a chain reaction that extends to as many as ten vertical levels in the hierarchy of the organism’s design, and to untold instances laterally. A new genetic change, the effect of which is simple and routed solely to the exterior of the organism, however, as is the bacterial defense mechanism or digestive enzyme, avoids the necessity for a cascading series of modifications, and is thus much easier to implement.

 

Mutations of plasmid DNA have only demonstrated the capacity to do simple things like add antibiotic resistance or generate a new enzyme to breakdown an additional source of food. No plasmids are known to routinely transfer from bacteria to complex organisms and the cells of complex creatures are not able to pick up free DNA as bacteria do.[107] Once again, the problem of equating the process of microevolution in one “abnormal” species with the very different processes of macroevolution across the entire tree of life must be avoided. [108] The ability to generate a single type of useful change does not establish the ability to do anything more. To say that because bacteria can evolve and transfer simple enzyme affecting DNA segments that they can evolve and transfer absolutely everything else necessary to generate the entire tree of life is ungrounded speculation. Genetic transfers from bacteria to other species, if they happen at all, are not the norm, but the very rare exception. Therefore we do not have benefit of the enormous numbers of bacteria and their fantastic reproductive rate to create trillions upon trillions of mutations of all types that might solve Darwin’s lack of time problem.

 

Even if large numbers of bacterial gene transfers to other species could take place, transferring in many genes from simple creatures does not make a complex creature. As Peter Kassan tells us in his refreshingly candid discussion of the failed attempt to duplicate human intelligence by artificial means,[109] transferring in 3,000,000 cockroach genes doesn’t equate to the functionality of a human, it equates to the functionality of a colony of cockroaches.

 

Known genetic recombination systems are internalized mechanisms of genetic transfer, in highly simplified systems like bacteria, and they involve transfer within an optimized environment, that is, an environment where a supportive internal mechanism is in place to facilitate the transfer. Our previous discussion of evolution’s failure to adapt the immune system’s ability to rapidly generate new genetic strings of information into a system of genetic recombination in humans reveals that, if large transfers cannot occur the easy way within a supportive structure of a creature's internal mechanisms honed to optimization over millenniums of natural selection, they certainly cannot occur the hard way as a completely random proposal from outside the organism.

 

One constituent of the irreducible complexity that forms a barrier to accidental recombinant DNA substitutions in complex organisms is alternative splicing or alternative reading frames. Alternate splicing is used on as many as three quarters of the genes of complex creatures. Those genes are “read” or edited in several different ways in order to produce more than one protein from the same gene. In addition, in complex creatures, a single gene tends to be involved in regulating multiple processes, not the single process of biodegrading one substance as is the case with the simple bacterial genes. Gene substitutions that work for bacteria are no longer so simple for other creatures.

 

Instead of effecting a simple change in immunity to a standard threat, the substitution of a single gene in complex creatures can, hypothetically, alter the development of the embryo causing children to be stillborn, remove cancer protection, and flatten the arches all at the same time. Consequently, one cannot say with confidence that the ability of bacteria to spontaneously evolve new antibiotic resistance demonstrates any real potential for the larger process of evolution across the taxonomic inventory of life. For the substitution of a gene from bacteria to be less than catastrophic in the far more complex variably-read machinery of a mammal, the entire mammalian genetic system would have to be regressed to remove the developmental genome and the alternate reading frame mechanism. Thus, bacterial gene transfer may have played a minor part in evolving bacteria and primitive creatures, but would be of little or no use in promoting further advancement and differentiation of mammals.

 

The relative simplicity of bacterial design taken together with their closely circumscribed enzyme altering mechanism may explain our strong suspicion of successful horizontal DNA transfers among prokaryotes.[110] On the other hand, it simultaneously invalidates the larger evolutionary inference that the same thing could be routinely accomplished with higher organisms, too sophisticated to tolerate such a primitive tool. In short, bacteria are set up to handle such transfers, while other creatures are not. All that we can safely conclude is that some microevolution of bacteria may be promoted by DNA transfers. We may not safely conclude the ability to move from one type of creature to another via DNA transfers.[111]

 

Retroviruses, do, in a sense, routinely alter the DNA of the host, but it is normally nothing other than the simple genome of the virus that is added. Therefore, the transfer of viral DNA isn’t going to cause an advancement or a continuing series of advancements, it is simply going to make the host ill, as is commonly seen. Good evolutionary science like good police work should confine itself to the facts, and to valid logical inferences from those facts. All we truly know to have resulted from naturally occurring bacterial and viral exposures are infectious or genetic diseases and birth defects.

 

Nor can the use in the laboratory of germs as gene vectors, that is, delivery vehicles, be used to evidence an accidental evolutionary process. Here a genetic sequence is analytically chosen by scientists and then carefully edited. All the troublesome aspects are (hopefully, but not necessarily) cut out or cropped off. The carefully prepared gene segment is then placed by an expert scientist into a germ already known to be suitable for the delivery task. The germ is introduced into the recipient cell via an a substantially controlled procedure, not a random or accidental one. This tells us that, under artificial intelligently guided conditions, germs can effect a beneficial genetic change to an organism within certain limits. It does not demonstrate that an accident can do the same thing. It certainly does not demonstrate that an accident can do absolutely everything that macroevolution requires. To date it has not been possible to achieve the radical biological form changes needed for macroevolution (any of them) even with intelligently guided laboratory procedures.

 

The amazing adaptations of germs and the adaptive capacity of bugs to pesticides, when compared to the dramatically smaller adaptive capacity of higher life forms suggest that there is an inverse relationship between complexity and the ability to rapidly evolve viable biological form change. It also suggests that the adaptive options are primarily/exclusively limited to those options predetermined by the overall design of the organism viz the generation of antibiotic and pesticide resistance and the creation of new biodegrading enzymes. This is a good example of a random generator program built into a larger highly ordered and constrained design that does not have unlimited capacity to generate novel change. Rather it can only run through a list of predetermined options, many of which are “preflighted” to work but cannot, as it were, step outside of their programming to do anything truly novel in terms of macroevolutionary form change.

 

Even where such gene substitutions have occurred in bacteria they are substitutions of a precomposed gene from a preexistent set of such genes containing at least some genes that convey an advantage.  It is not a case of visible evolution in real time.

 

It is almost certainly not a coincidence that the only thing the human body does comparable to the bacterial ability to rapidly generate new genetic information, that is, antibody production by our immune system, also routes the results to the “exterior” dead end of an event chain, a point in the process architecture where an ensuing cascade of design changes is not required. After the human antibody is produced, like the bacterial enzyme, it then confronts an exterior threat, an invader. It attacks the external enemy with a chemical attack that destroys design, which is much easier than interacting with it. Such examples seem to me to more precisely describe the limitations of accidental genetic substitutions than to demonstrate their unevidenced hypothetical capability to generate the evolution of complex life forms.

 

While almost always destructive to living systems, it is (in theory) possible that an accidental process might (rarely) achieve a simple system, such as a bacterium, from nonliving components, given sufficient time and a highly improbable and complex set of conditions. It may seem odd to allow that an accidental process might achieve a bacterium but go no further, but bacteria are both uniquely simple and, in many ways, simply unique. As such, they may be a genuine dead end for accidental evolution. Bacteria may represent the upward delimiting boundary of the capabilities of an accidental process in biology. It is possible that accident can do that much but no more.

 

Whole gene or large DNA segment substitution events, such as occur with bacterial plasmid substitutions, as opposed to single or multiple nucleotide change events, don’t qualify as true examples of novel design origination because is these cases the existing design merely rotates preexisting design modules within a common interface. New complex design modules are not originated; they are already present. It is like turning a multi-lens microscope to a higher magnification or moving between slides during a slide show on your home computer. The high power lens is not created on the spot; nor is the next slide, its design is already present, made available by a prior process. A feature of the microscope’s design permits alternation between optional preexisting components but it does not generate those components in real time. So it is with bacterial plasmid gene transfers. This is not a case of visible evolution in real time, but a case of an existing design performing a preexistent function, in this case rotating genes much as a shooter rotates the cylinders in a gun.

 

Point mutations of nucleotides are a different matter than gene substitutions, however. Something new is added in the rare event of a point mutation. But point mutations are normally destructive and they are too rare to drive the enormous mechanism of evolution. Evolutionists now admit that the point mutations caused by environmental mutagens do not play a significant role in evolution.[112] That leaves replicative errors or transpositions within the genome. These latter two events are so closely shepherded by error correction and repair, transpositional and reproductive mechanisms that it is far from clear that any viable change can be traced to true randomness (accident).

 

A Precambrian Master Genome?

But neo-Darwinists never say die. Here’s another proposed solution to Darwin’s lack of time problem. It is a truly ingenious one belonging to the late, much loved, and highly respected Professor Susumu Ohno. Ohno proposed that at some time in the distant past, probably during the Precambrian period, a creature or creatures somehow spawned a genome containing a large set of genes sufficient to quickly generate the advanced features of the more complex organisms that so quickly followed on the tree of life during the 5 million year surge of development that is called the Cambrian Explosion.[113]

 

Most of the creatures of the early Cambrian or Precambrian, in Ohno’s view, came to possess this same master genome. Later variations in biological form, including most of the major body types of the animal kingdom, were produced from the master genome by altering the gene expression and silencing tags. Thus we have a plausible explanation, though not an accidental one, of the rapid explosion of life form variation in the Cambrian period. Ohno calls this master genome the “pananimalia.” His theory allows for a more reasonable period of time to develop the first comprehensive set of genes: three billion years leading up to the first bacteria, as opposed to the mere ten million years of the Cambrian explosion.

 

The pananimalia genome can explain things otherwise fully inexplicable. How to accomplish the jump from bacteria to the first complex invertebrates. How to rapidly develop thousands of radically divergent vertebrate and nonvertebrate forms without leaving fossil traces of intermediate transitionary stages. How to accomplish so much in so little time without making a complete mess of the attempt. The pananimalia hypothesis suggests that these near miracles were accomplished by shifting a large number of gene silencing and expression markers within only one or a very few generations instead of many.

 

Ohno’s proposal makes perfect sense as a solution to the time problem, though it remains to be corroborated by direct evidence. But when employed as a neo-Darwinian argument, it only goes so far before encountering insurmountable obstacles. Ohno did not so state it, that is, he doesn’t explicitly invoke accidental processes as the exclusive or primary mechanism involved.

 

In the pananimalia scenario the new genes must either originate inactive or quickly become inactive. We know this because, if the widely varied genes of the pananimalia were all actively expressed, the pananimalian creatures would be bizarre mixed genre chimeras of which the fossil record gives no evidence. Inactive genes are good from one perspective. Partially developed new parts proposed by evolution, and some of the associated integration work for use in a later design, could, in theory (though not by accident), be perfected in inactive DNA prior to implementation. With inactive DNA, modifications to a developing inactive genetic sequence place no wrenches into the working machinery of the organism.

 

Once the inactive code was perfected, gene expression tags could be changed to active and the creatures could start to differentiate into the fifty different major body types of the animal kingdom and on to a myriad of diverse species. But how would an accidental process know when to switch which tags in which combinations? If gene expression markers were being moved around in a truly random manner, as neo-Darwinian theory requires, one would expect to see nearly all the intermediate variations that the DNA of the host creature could produce in the fossil record—if the creatures could survive the accidental tinkering at all. It is highly improbable that an accident could reset thousands of gene expression markers in very complex interrelationships with precision in one generation.

 

At least some of the randomly tagged gene combinations would produce inefficient, disabled and dysfunctional designs that could nonetheless survive for a time sufficient to make fossil imprints. However, there is no fossil evidence of an abnormal spate of aberrant, chimerical, or even intermediate functional forms in or around the Precambrian/Cambrian boundary! This is problem for the accidental theory of evolution. An accidental process would have tried to produce the intermediates. Their absence indicates either that the intermediates were not survivable, which defeats the gradualist view essential to classic accidental evolution, or that a built-in (nonrandom) filter of some kind ruled out most of the options being tried. The sensitivity of the developmental genome to mutation suggests there may be such a filter. Alternatively, the absence of intermediates suggests that the process was otherwise guided, directed, channeled or informed, not accidental at all.

 

Another serious objection to a neo-Darwinian pananimalia hypothesis is that random development of the new DNA sequences in inactive mode takes natural selection out of the lineup. Natural selection would be precluded from picking the intermediate modules of design variations or rejecting them because inactive genes have no effect on the survival of the organism. The developing pananimalia would, in effect, be invisible to natural selection. Without natural selection there would be nothing to give direction to the accidental development process, to tell it where to go or when to stop. In this scenario, new design development would have to be accomplished exclusively by random drift or other fully non-directed processes. This could not have been done in the time available, and arguably not in any amount of time at all.

 

Because a pananimalia genome would explain so much, one cannot, by any means, rule out its existence. On the other hand, it is clear that, minus aid from natural selection acting as a quality control mechanism, such a large genome could not have originated in inactive mode completely by accident. The lack of intermediates to the many large jumps in design advancement simply rules out the accidental neo-Darwinian model.

 

Ultimately, the deciding evidence for or against the pananimalia master genome hypothesis will have to come from the fossil record, including fossilized DNA from ancient creatures,[114] and comparative studies of the genomes of early life. Although the evidence currently presented by fossilized and comparative DNA studies of living organisms shows a lot of similar sequences going back to bacteria, thus hinting at common ancestry, it falls a long way short of demonstrating an early master genome—and it says nothing whatsoever in favor of accidental evolution.

 

The Fossil Record

As of 1985, 250,000 species of complex life forms (Cambrian forward) were represented in fossil records.[115] However, an insignificant number and range of transitional forms between major body types and between phyla were present in these fossil records to support neo-Darwinian theory.[116] Michael Denton an Australian medical doctor, research geneticist, and author of Evolution: A Theory in Crisis and Nature’s Destiny, points out that although the fossil record was not complete as of 1986 it had systematic problems in relation to Darwinian theory so extensive that the significance would remain at any rate of fossil sampling. What Denton is pointing to is the fact that there are consistently fewer intermediates between the large branches on the tree of life than between the smaller. For example, there are many intermediate forms between an ancient and a modern horse, but relatively few between land mammals and whales. [117]

 

D. M. Raup, writing in an official NASA publication on evolution says “…the basic evolutionary tree of life has been worked out and it is not likely to change very much as a result of further study.”[118] Other scientists have more recently suggested that now, more than twenty years later, our fossil record is substantially reliable. Nonetheless, Denton’s objection remains: the systematic problem of lack of sufficient intermediate species between major divisions on the evolutionary tree to support an accidental process.[119]  We have only 40 phyla and over 250,000 fossilized species. While granting that there are many legitimate unknowns that remain to be discovered in the evolutionary process, the one thing we are entitled to affirm is that the fossil record should reflect many more intermediate species between the phyla than between the species and genera if (accidental) neo-Darwinian theory is true.

 

The point Denton makes about systematic problems, though seemingly an elementary one, is formidable. Despite its simplicity, it is crucial to understanding the weight of the fossil evidence. There should be many more intermediates populating the larger distances between the major divisions of the tree of life than populate the shorter distances between species if the evolutionary process is undirected, random or accidental. Even Darwin acknowledged this, as noted evolutionary writer Dr. David Raup reports.[120] The exact opposite is seen however, clearly suggesting that minor changes, that is, microevolutions, are the only form changes that occurred via a random processes, if any truly did. The large number of variations of horses and humans, suggests that randomness, if it plays a part at all, contributes to variation after the hard part of primary design achievement has occurred. It can get away with modifying an existing machine in minor ways by moving preexisting design components around or making small changes to them, but it cannot build the total machine from scratch.

 

Given that there are as many as 100,000,000 species presumed to have existed through the history of life (estimates vary, ranging to 2,000,000,000 or higher),[121] having only 250,000 represented in fossil records raises a concern about incomplete or nonrepresentative sampling. It might be said that the missing links could all still be out there because we are missing 400 fossil species (possibly many more) for every one that we have. But it is scientifically invalid to presume the nature of the evidence prior to its discovery. Instead of filling in the gaps, future fossil and fossilized DNA discoveries could pose new problems for neo-Darwinian evolutionary theory or further corroborate the formidable problems already present.

 

Critics of the completeness of the fossil record rightly point out that soft shelled and invertebrate creatures are rarely preserved as useable fossils. Though this is true, fossil evidence of invertebrate history is not fully lacking. Invertebrates compose some 90% of the species on the planet. Given their enormous numbers, despite the comparative infrequency of fossil creation from soft bodied creatures, invertebrate fossils are still frequently found. The fossil database at The National Center for Ecological Analysis and Synthesis (NCEAS) in Santa Barbara, California has a substantial number of invertebrate fossils. Their fossil catalog consists of over 110,000 taxonomic occurrences, with an emphasis on marine invertebrates.[122] Although critics of the presumed inadequacy of the fossil record have made much of the slight representation of invertebrates, the marine invertebrates clearly have a substantial presence in the fossil record. The global marine invertebrate database either grounds or supplements more significant modern studies than any other, and much progress has been made in sampling reliability.[123]

 

With this in mind, it is not surprising that, in Problems of Phylogenetic Reconstruction, C.R.C. Paul tells us that the "fossil record is much less incomplete than is generally accepted. Its incompleteness is largely irrelevant to the sequence of preserved fossils and hence to phylogenetic reconstruction provided only that we confine our phylogenies to known organisms. We ignore the fossil record at our peril.” David Woodruff echoes the same belief in his May 1980 Science article, "Evolution: The Paleobiological View" in saying "Evolutionary biologists can no longer ignore the fossil record on the ground that it is imperfect." By far the strongest case that has been made of restraining the unbounded imagination of the Darwinists and sticking to a strict cladistic description of the fossil record is made by Henry Gee. Gee discloses in his recent paradigm shattering, In Search of Deep Time, that there are no grounds for evolutionists to presume to assert why creatures have emerged through history as they have, but only to describe the record of that emergence in an objective way. Over an extended and very convincing course of argument grounded in the concrete facts of the fossil record, Gee demonstrates that to say more is to move well beyond what rigorous science can in fact support. It is to arbitrarily import and impose sociological or philosophical preconceptions on the objective data.[124]

 

Ultimately, Denton's argument boils down to the fact that, whatever the level of sampling reliability may be (and we now see that it is really quite good), in at least the majority of cases (and probably all) we should have seen many more intermediate forms between the originating and terminating creatures of a presumed large evolutionary jump (i.e., between the phyla) than between the smaller jumps that separate the lower divisions, yet we have not seen this in any case—not once.

 

There is another problem with the fossils. Given the destructive nature of random mutations and the enormous mutation rate required to support neo-Darwinian theory (accidental evolution), there should be an extraordinary number of aberrant designs reflected in fossil records. When the predominantly deleterious accidental mutations posited by neo-Darwinian theory were less than lethal, partially disabled mutants should have survived long enough to leave trillions of imprints in the fossil record. Natural selection has often been proposed as the answer to this, that is, natural selection rapidly vetoes the continuance of defective designs, so little time is available for mutant fossil imprints to be made. But defective designs must survive long enough for natural selection to act upon them, thus making some fossil imprints. For natural selection to explain the absence of multitudes of mutant forms it would have to have magical powers, to be able to veto a mutant before it was born. Of course, natural selection can do no such thing; it must wait until the creature has competed in the natural environment and been found wanting. The developmental genome and the larger system of the living embryo often do filter out bad design, producing lethal birth defects in lieu of a viable mutant, but the developmental genome/embryonic organism is a highly complex machine itself whose functions are not random. The absence of mutant fossils, unexplained except for the influence of nonrandom systems, therefore implies a nonrandom evolutionary process.

 

Considering the horrid efficiency of an accidental design process there should have been, not merely individual defects, but millions of bad species designs. Defective species could have reproduced successfully for several generations (perhaps many) before natural selection culled them out. In the early millenniums of life these nonoptimized creatures would, at times, only have had to compete with designs equally horrid. I am assuming the accidental neo-Darwinian process here, not the actual event of evolution or the fossil record of it. In a truly accidental process, the early competitors would all be stumbling and fumbling around, having substantial design flaws for quite some time. One competitor would be more or less as equally inept as the other. A predatory act would be like comedian Tim Conway going to Harvey Korman as his dentist. The dentist would be as likely to lose a tooth as the patient. Early predators would have been more akin to Wily Coyote than T-Rex, with each attempt at a meal being a comedy of errors. In many cases then, at least in the early epochs, natural selection would have been in no great hurry to vote out an imperfect design because it was either living in a friendly niche or one with little or no superior competition. Thus many of the defective designs that should have vastly predominated in the proposal stage of an accidental process could have survived and reproduced sufficiently to make fossil imprints. But the fossil record does not reveal their presence.

 

Granted the fossil record would reveal to us only a small portion of failed designs. Some would be birth defects, and the creature would not live to reproduce. More minor defects, however, would impair the long term survivability of the species, but not its immediate reproduction. Certainly, we would be entitled to expect less occurrences in the fossil record than if the species had lived a fuller term, but we should still find myriads of malformed yet survivable designs in the fossil record. The sheer number of defective designs based upon standard probability computations would produce a number of defective species that in aggregate would equate to an enormous combined population.

 

If the false starts toward optimal design number into the trillions of trillions as probability data requires, the combination of all short-lived mutant populations taken in total should create a huge presence in the fossil record. Mutant fossil occurrence should also be relatively uniform across the geographic and ecological strata because the random process of neo-Darwinian theory is presumed to be ubiquitous. Paleontologists  and paleobiologists could not, then, easily miss the myriad of defective fossils that an accidental process would have created. A trillion trillion trillion trillion bacteria may fit in a few thimbles of solution and therefore be overlooked in fossil sampling, but a trillion trillion trillion trillion antelope with horns on their rump (or a variety of other disabilities and disfigurations) do not fit in a thimble. Where are the mutants in the fossil record?

 

When fossils are found, in most cases it is not a case of finding an individual occurrence of a single fossilized species, but rather whole communities of species are found entombed together. Helmut Mayr tell us in his nice little book, A Guide to Fossils, that, because of the hit and miss nature of the geophysical forces that produce fossils, we should only expect to see the most abundant species in the fossil record. While this is true, it is still a mistake to assume that the most abundant rule applies only to species; it applies to any characteristic whatsoever. This is a simple mathematical truth (a standard probability outcome) about statistical sampling: a large, assumed to be representative, sample will tend to give an approximately true representation of the relative proportions of different characteristics of any kind occurring in an ecosystem subject to fossilization. If microscopic creatures are more abundant, microscopic creatures will be most often found in the fossil community, vice macroscopic creatures. If swimming creatures are more abundant, vice crawlers, their fossils will appear the most etc., assuming only conditions where fossilization can in fact occur. Again, this rule holds for absolutely any characteristic or criteria one can devise to differentiate members of a population, including the presence or absence of a dysfunctional design feature.

 

The odds against achieving even a single functional protein by accident are 1077 to 1. It is reasonable to assume that the odds against accidentally achieving a complex functional design feature requiring several if not hundreds of proteins are at least as great. If only a single individual survived with each of the possible dysfunctional features that would have resulted from an accidental process, approximating the limit of  1077 defects for each success in design improvement, visibly dysfunctional aberrant designs would strongly predominate in the fossil record.

 

One can say that the quality control filter of the developmental genome or the irreducible complexity of living designs precludes any significant survival rate for functional and structural defects substantial enough to reflect in the fossil record, but having such a bias for optimized design in a quality control filter such as the developmental genome provides makes the process nonaccidental, as does affirming irreducible complexity. An accident cannot assemble an irreducibly complex machine, by definition.

 

One might object that there are only so many ways to foul up a living design such that it could continue to live long enough to make a fossil imprint, and that is true. There are not 1077 survivable options available for any given design. But if there are only a hundred survivable defective options per design, it is of no matter to our argument because the accidental process will continue to try those 100 over and over again with minor variations until the ratio of actual defects to good design achievements is extraordinarily high. Why? Because, although in a simple statistical probability analysis, one that assumes all options are equal, those 100 options should only appear with equal frequency to all the others in the total set options. However, the optimized design achievements are much more complex and thus much harder to achieve than the more simple defective ones. The options are therefore not equal and standard probability theory does not apply in the usual way. The complexity of optimized living systems, makes the optimized designs less probable for an accident to achieve. They will occur far less often than any of the 100 or so simpler defective options. In other words, all design options are not created equal in regards to the probability of their occurrence.

 

Current estimates indicate that at least 100,000,000 species have lived on earth. Originating a new species by accident will, presumably, require, at a minimum, several increments of viable design innovations affecting functional and structural modules and subsystems. Therefore, the number of successful design innovation events involving major systemic or body form changes (that is, the easily visible alterations that might be detectable in a fossil) can be conservatively estimated to be at least 300,000,000. The probability of achieving any one of these advancements must be at least that of achieving a single protein, for proteins are at the heart of every function in living systems, again, 1 chance in 1077.

 

The ratio of detectable mutant fossils to fully functional designs then is something of the order of >1077 X 300,000,000, or 3 X 1085. That constitutes an enormous aggregate population from which to generate fossil imprints, especially considering that the mutational process is ubiquitous occurring everywhere at all times, that is, across all ecological niches. This aggregate mutant population is in fact many trillions of times larger than the entire population of all creatures that have ever lived on Earth. There should, therefore, be trillions of disfigured/dysfunctional designs in the fossil record for each normal/optimized one.

 

There is simply no historical evidence for mass implementation of accidental form change proposals. To clinch the matter, the recent experimental evidence of thousands of mutation studies and the protein synthesis work of D. D. Axe reveals accidental mutations to be an impossible source of viable biological form change, producing for all intents and purposes only destructive effects, the rare useful achievement being statistically insignificant to the overall evolutionary process.

 

One may rationally object here: the developmental genomes and the embryonic development process would filter out most of the malformations prior to birth as abortive zygotes and embryos. Therefore, the number of survivable mutants would be practically nil. While this may be true, an accidental process would not initially develop such a developmental genome/embryonic system. Early accidental attempts at developmental systems would not filter out anything at all. Given an accidental process, the early embryonic system would itself be a fiasco. The fact that the developmental system seems to have always been good at filtering out birth defects argues strongly against the process having been accidental.

 

Darwinists may counter from the depths of their scientific expertise, that, “Well…shit happens.” It could simply be that the final polished versions of the developmental genomes for all 100,000,000 species were quickly hit upon by sheer luck and that is all there is to it. Nature got lucky and we will simply have to live with it. Two telling objections must be raised against them here. First, this is not science, for it forsakes the possibility of genuine explanation. Second, as G. G. Simpson points out, such a process as we see in evolution manifests an overwhelming bias for viable design. It can, therefore, in no way be classified as accidental.

 

One can only get lucky in the same direction and same manner with astounding consistency for a very brief period before rational analysis must cease to call it luck, that is, before one is rudely thrown out of the casino. A string of mathematics defying luck stretching over millions of years is too much to believe. Such a built in bias, present at the beginning of the evolutionary process, precluding dysfunctional proposals from getting past the embryonic stage, means that the model is not neo-Darwinian at all; it is not truly accidental.

 

Granted, as modern evolutionists insist, there is no bias that requires an evolutionary change to match the organism’s present environment. But there is another kind of bias, a bias for avoiding disabling mutations, structural inefficiencies, and serious systemic dysfunctions. An accidental process would not have such a bias. What the fossil record suggests, then, is that the evolutionary process, although occasionally marred by accident, does not have accident at its foundations. 

 

In The Fossils Still Say No! professor Duane Gish leaves little room for doubt that the intermediates needed by accidental evolution to be present between single celled organisms and complex invertebrates have not been found in the fossil record.”[125] Given the absence of demonstrable links to a common ancestor at the base of the evolutionary tree, the absence of intermediate links between the phyla (the main branches of the tree of life), and an approximately reliable fossil record, we are forced to conclude that if anything like Darwinian evolution occurred it accomplished approximately forty partial restarts: once at the beginning of each phylum. As Dr. Jonathan Wells tells us in Icons of Evolution, that is exactly what the evidence suggests. Many of the phyla appeared abruptly and fully formed. [126]

 

NASA scientists’ study of the fossil record echoes or at least suggests the theme of independent origins of the phyla in acknowledging that “…multicellularity appeared independently in many different lineages…Fossil records of the first evolutionary steps in the development of multicellular animals are lacking.”[127] The necessity of duplicating the jump between single-celled and multicellular organisms some forty times over increases the already enormous improbability of neo-Darwinian evolution. Furthermore, as Dr. Jonathan Wells points out, according to the fossil record, the phyla essentially did the equivalent of coming out of nowhere. Even Darwinists who hold the nonaccidental synthetic theory can’t explain it, let al.one neo-Darwinists who assert an accidental process.

 

Arguments have been made that the 3% representation of primate species in the fossil record is too small to ground a criticism of Darwinian theory because randomly placing 3% of the species on a tree diagram of primates doesn’t yield a single instance of the known fossils of even two creatures occurring in immediate proximity on the same branch.[128] The objection that there are too many missing links is, Darwinists say, therefore, shown to be premature; we should wait for the discovery of more fossils. But this same inadequacy in the fossil record argues just as strongly that we have far too little fossil evidence to solidly ground any hereditary theory of evolution, let al.one an accidental one. If one can’t establish at least two inheritance related relatives without question raising gaps between them on the tree, how does one know she has an inheritance-based family tree at all?

 

To be consistent, if we are to wait for more evidence from the fossil record to draw conclusions, then all of our conclusions should await that evidence, not just some of them. Otherwise we are violating the standards of scientific thinking by anticipating what the nature of new discoveries will be. “We don’t yet know” is an answer scientists are not reticent to give anywhere else in science where the evidence is inadequate or ambiguous, except where huge political stakes exist, such as in the struggle between materialism/atheism and  the religious worldview.

 

 

 

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[1] This seminal meeting is documented in a fascinating video entitled Unlocking the Mystery of Life, from, Illustra Media (DVD), http://www.illustramedia.com. Many of the primary intelligent design team members make significant appearances in this video, such as Scott Minnich, Michael Behe, Jonathan Wells, Phillip Johnson, Jed Macosko, and Dean Kenyon. Professor Phillip Johnson is the author of one of the early trailblazing works on intelligent design, Darwin on Trial (Downers Grove, IL: InterVarsity Press, 1991), as well as The Wedge of Truth: Splitting the Foundations of Naturalism (Downers Grove, IL: InterVarsity Press, 2000) and Defeating Darwinism (Downers Grove, IL: InterVarsity Press, 1997).

[2] Charles Darwin, The Origin of Species, 1st edition, (New York: Barnes & Noble Books, 2004), 525.

[3] Stephen C. Meyer, “The Origin of Biological Information and the Higher Taxonomic Categories,” Proceedings of the Biological Society of Washington 117, no. 2 (2004): 217.

   This article is available on the Web at http://www.discovery.org/; free offprints are available upon request. There is also a heavily politicized controversy concerning the unusual event of the peer review status of Meyer’s article being withdrawn after its publication, and the firing of the editor who approved it. All of this, of course, is highly nonstandard, but the Darwinists assure us no politics were involved whatsoever. In any case, the research Meyer cites in his article is peer-reviewed, and the logic of his argument stands on its own merits. Also see his new full length book on the subject: Meyer, Stephen C. Signature in the Cell: DNA and the Evidence for Intelligent Design. New York: HarperCollins, 2009.

[4] Michael J. Behe, The Edge of Evolution (New York: The Free Press, 2007).

[5] See Appendix 2 for a detailed presentation of this case, what has been called the resource exhaustion argument.

[6] If you have trouble remembering the taxonomic divisions, kingdom, phylum, class, order, family, genus, species see thefreedictionary.com for some mnemonic tricks.

[7] Henry Gee, In Search of Deep Time: Beyond the Fossil Record to a New History of Life (Ithaca, NY: Cornell University Press, 1999.)

[8] John A. Davison, “Instant Evolution” published to the Internet at http://www.iscid.org/papers/Davison_InstantEvolution_050204.pdf, 1; Fred Hoyle, Mathematics of Evolution (Memphis, TN: Acorn Enterprises, LLC, 1999), 107.

[9] Schroeder, The Science of God, 10.

[10] Simpson, View, 71, 202.

[11] Stephen C. Meyer, “Word Games,” in Dembski, Intelligence, 110; Axe, D. D., “Estimating the Prevalence of Protein Sequences Adopting Functional Enzyme Folds,” Journal of Molecular Biology, vol. 341 (2004): 1295-1315.

[12] This is a gross oversimplification and underestimate. The simplest living things we know for certain are alive, Mycoplasma, require, at an absolute minimum 300 genes. The actual improbability of achieving these genes by chance exceeds 10-77 (one gene not from scratch) times itself 300 times, or  10-23,100.  See the Astrobiology Magazine article, “Life from Scratch,” Nov 26, 2002, at http://www.astrobio.net/news/article319.html.

[13] Dean L. Overman, A Case Against Accident and Self-Organization (Lanham, Maryland: Rowman & Litllefield Publishers, Inc., 2001), 58-64.

[14] Axe, “Estimating.”

[15] Russell Grigg, “Could monkeys type the 23rd Psalm?” published to the Answers in Genesis Internet site at http://www.answersingenesis.org/creation/v13/i1/monkeys.asp.

[16] See Paul Davies, The Fifth Miracle (New York: Simon & Schuster, 1999), 271. Paul Davies here cites a debate between Carl Sagan and Ernst Mayr published as "The Search for Extraterrestrial Intelligence: Scientific Quest or Hopeful Folly?" Planetary Report, vol. 16 (1996):4. Mayr indicates that the number of species in Earth's history may be as high as 50,000,000,000. Estimates of the number of species have varied widely over the past fifty years but appear to have been steadily declining. The only significance of the figure I use here is that it is a visible underestimate. There is no consensus on the best estimate of the number of species in the history of life, or even on the number of living species.

[17] Meyer, “Biological Information,” 220.

[18] D. B. Davison, “Brute Force Estimation of the Number of Human Genes Using EST Clustering as a Measure,” IBM Journal of Research and Development 45, no. 3/4 (2001): 439.

[19] Paul Davies, The Fifth Miracle, (New York: Simon & Schuster, 1999), 95.

[20] This book is highly recommended to those who wish to understand the origins of life question. See the following note for bibliographical data.

[21] Fazale Rana and Hugh Ross, Origins of Life: Biblical and Evolutionary Models Face Off (Colorado Springs, CO: NavPress, 2004), 164; Hubert P. Yockey, Information Theory and Molecular Biology. Cambridge: Cambridge University Press, 1992.

[22] An order of magnitude equates to a factor of 10. One order of magnitude reduction from 1,000 is 100, and from 100, is 10.

[23] Jacques Monod, Chance and Necessity (New York: Vintage Books), 1972, 47; Andre R. O. Cavalcanti, Elisa Soares Leite, Benicio B. Neto, and Ricardo Ferreira, “On the Classes of Aminoacyl-tRNA Synthetases, Amino Acids and the Genetic Code,” Origins of Life and the Evolution of the Biosphere, 34, no. 4 (2004), 409; Fox, Emergence, 13.

[24] Gabriel Waksman, ed., Proteomics and Protein-Protein Interactions: Biology, Chemistry, Bioinformatics, and Drug Design, Protein Reviews, vol. 3 (New York: Springer Science+Business Media, Inc., 2005), vi; Also see Joseph D. Puglisi, ed., Structure and Biophysics – New Technologies for Current Challenges in Biology and Beyond (Dordrecht, Netherlands: Springer, 2005) for a good indication of the astronomical complexity of protein shape prediction and related research.

[25] Tony R. Obalinsky, ed., Protein Folding: New Research (New York: Nova Science Publishers, Inc., 2006), viii-ix; Cathy H. Wu and Jerry W. McLarty. Neural Networks and Genome Informatics, Methods in Computational Biology and Biochemistry, vol. 1 (Amsterdam: Elsevier, 2000); Lev. A. Blumenfeld and Alexander N. Tikhonov, Biophysical Thermodynamics of Intracellular Processes: Molecular Machines of the Living Cell (New York: Springer-Verlag, 1994), 102-105. D. Bashford, “Macroscopic Electrostatics with Atomic Detail (MEAD): Applications to Biomacromolecules,” in Biomacromolecules: From 3-D Structure to Applications, edited by Rick L Ornstein (Columbus, OH: Battelle Press, 1995): 53-68.

[26] Michael J. Behe, Darwin’s Black Box (New York: The Free Press, 1996), 46.

[27] Boyce Rensberger, Life Itself: Exploring the Realm of the Living Cell (Oxford: Oxford University Press, 1996), chap. 2.

[28] Denton, Crisis, 223-225.

[29] William Dembski, et al., Unlocking the Mystery of Life, Illustra Media (DVD), http://www.illustramedia.com.

[30] Ada Yonath, "Ribosomal Crystallography: Peptide Bond Formation, Chaperone Assistance, and Antibiotics Inactiviation", in Joseph D. Puglisi, ed., Structure and Biophysics – New Technologies for Current Challenges in Biology and Beyond (Dordrecht, Netherlands: Springer, 2005); Kathleen L. Triman, "Mutational Analysis of the Ribosome," in Jeffrey C. Hall, Jay C. Dunlap, Theodore Friedmann, and Veronica van Heyningen. Advances in Genetics, vol. 58 (Amsterdam: Elsevier, 2007); A. Liljas, Structural Aspects of Protein Synthesis (Singapore: World Scientific, 2004); R. A. Garrett, S. R. Douthwaite, A. Liljas, A. T. Matheson, P. B. Moore, and H. Noller, eds. The Ribosome: Structure, Function, Antibiotics and Cellular Interactions (Washington D.C.: ASM Press, 2000). Ribosomal DNA sequence size is given at http://rdp.cme.msu.edu/, Michigan State University’s Ribosomal Database Project – II. Also see M.J. Farabee, An Online Biology Book published to the Internet at http://www.emc.maricopa.edu/faculty/farabee/BIOBK/BioBookCELL2.html.

[31] Meyer, "Biological Information," 220.

[32] A DNA sequence length for a standard size gene across the tree of life is approximately 1,000 base pairs; human genes average around 5,000 bp.

[33] Edward A. Bayer, Jean-Pierre Belaich, Yuval Shoham, and Raphael Lamed “The Cellulosomes: Multienzyme Machines for Degradation of Plant Cell Wall Polysaccharides,” Annual Review of Microbiology, 58 (2004): 521-54.

[34] H. Wijnen and M. W. Young, “Interplay of Circadian Clocks and Metabolic Rhythms,” Annual Review of Genetics, vol. 40 (2006): 409-448.

[35] Robert M. Macnab, “How Bacteria Assemble Flagella,” Annual Review of Microbiology, 57 (2003): 77-100; Christian Heintzen and Yi Liu, "The Neurospora crassa Circadian Clock," in Jeffrey C. Hall, Jay C. Dunlap, Theodore Friedmann, and Veronica van Heyningen. Advances in Genetics, vol. 58 (Amsterdam: Elsevier, 2007).

[36] For an overview of key selected systems within the human body see Discover magazine’s special issue, Discover Presents: The Body, Summer 2008, 26-35.

[37] David Faust, The Limitations of Scientific Reasoning (Minneapolis: University of Minnesota Press, 1984), 152.

[38] J. C. Eccles, The Understanding of the Brain (New York: McGraw-Hill Book Company, 1977), 204.

[39] Helena Curtis and N. Sue Barnes, Biology (New York: Worth Publishers, Inc., 1989), 115.

[40] Tiffany D. Miles, Jelena Jakovljevic, Edward W. Horsey, Piyanun Harnpicharnchai, Lan Tang, and John L. Woolford, Jr., “Ytm1, Nop7, and erb1 Form a Complex Necessary for Maturation of Yeast 66S Preribosomes,” Molecular and Cellular Biology, vol. 25, no. 23 (2005): 10419-10432.

[41] Behe, Black Box, chap. 6; Rensberger, Life Itself, chap. 11; Tak W. Mak and Mary E. Saunders, The Immune Response, (Burlington, MA: Elsevier Academic Press, 2006), 20.

[42] Barry J. Gibb, The Rough Guide to the Brain (London: Rough Guide, 2007), 31

[43] Peter Kassan, “Duplicating Human Intelligence is a Mirage” in Artificial Intelligence, edited by Sylvia Engdahl (Farmington Hills, MI: Greenhaven Press, 2008), 112-122.

[44] Enrico Cherubini, S. Gustincich, and H. Robinson, “The Mammalian Transcriptome and the Cellular Complexity of the Brain,” Journal of Physiology-London, vol. 575, no. 2 (2005): 319-320; Stefano Gustincich, Albin Sandelin, Charles Plessy, Shintaro Katayama, Roberto Simone, Dejan Lazarevici, Yoshihide Hayashizaki and Piero Carnici, "The Complexity of the Mammalian Transcriptome," Journal of Physiology-London, vol. 575, no. 2 (2005): 321-332; Anthony R. Ruffa, Darwinism and Determinism: The Role of Direction in Evolution (Brookline Village, MA: Branden Press, Inc., 1983).

[45] James W. Valentine , On the Origin of Phyla (Chicago: University of Chicago Press, 2004), chap. 5.

[46] Robert F. Dehaan and John L. Wiester “The Cambrian Explosion” in Dembski, Intelligence, 148; Meyer “Biological Information,” 214.

[47] Raup, “Life, Terrestrial Environments, and Events in Space,” in David Milne et al. eds., The Evolution of Complex and Higher Organisms -NASA Special Publication 478 (Washington, DC: NASA, 1985), 14; MacPhee, Ross D. E. Extinctions in Near Time (New York: Kluwer Academic, 1999).

[48] Valentine, Phyla, 66.

[49] John Gribbin, Q is for Quantum: An Encyclopedia of Particle Physics (New York: The Free Press, 1998), 77-79.

[50] Life on Earth is produced by BBC Natural History Unit in association with Warner Brothers and Reiner Moritz Productions, 1986. Distributed by Warner Home Video.

[51] Valentine, Phyla, 40-65.

[52] W. Ford Doolittle, “Evolutionary Creativity and Complex Adaptations: A Molecular Biologist’s Perspective,” in John H. Campbell and J. William Schopf ed., Creative Evolution (Boston: Jane and Bartlett Publishers, 1994), 50.

[53] Futuyma, Evolutionary Biology, 152-154.

[54] Simon Conway Morris, Life’s Solution: Inevitable Humans in a Lonely Universe (Cambridge: Cambridge University Press, 2003).

[55] Schroeder, The Science of God, chap. 6.

[56] Jonathan Wells, “Making Sense of Biology” in Dembski, Intelligence, 120-122.

[57] Eva Jablonka and Marion J. Lamb, Epigenetic Inheritance and Evolution: The Lamarckian Dimension (Oxford: Oxford University Press, 1995), 86-90.

[58] Pollack, Signs, chap. 1-5.

[59] “Ordering Genes,” Astrobiology Magazine, Dec 7, 2004.

[60] “DNA Surveillance and Repair,” spans multiple chapters in the Eurekah Bioscience Database published as open access documents to the Web at http://www.eurekah.com/chapters/category/78; Mark J. Schofield and Peggy Hsieh, “DNA Mismatch Repair: Molecular Mechanisms and Biological Function,” Annual Review of Microbiology, 57 (2003).

[61] Wolfram Seide, Yoke Wah Kow, and Paul W. Doetsch, DNA Damage Recognition (New York: Taylor & Francis Group, 2006).

[62] Paul Nelson, “Uncovering the Hidden Meanings of the Genome,” Access Research Network, Literature Survey 19:1, published to the Internet at  http://www.arn.org/docs/odesign/od191/ls191.htm, citing Chiou-Hwa Yuh, Hamid Bolouri, and Eric H. Davidson, “Genomic Cis-Regulatory Logic: Experimental and Computational Analysis of a Sea Urchin Gene,” Science 279 (20 March 1998):1896-1902.

[63] Gil Ast, “The Alternative Genome,” Scientific American, vol. 292, no. 4 (2005): 58-65.

[64] G. Ledyard Stebbins, Processes of Organic Evolution (Englewood Cliffs, NJ: Prentice-Hall, Inc, 1971), 15, Fig.1-6.

[65]Valentine, Phyla (Chicago: University of Chicago Press, 2004), 81-82; Anton Nekrutenko, “Reconciling the Numbers: ESTs Versus Protein-Coding Genes,” Molecular Biology and Evolution, 21, no. 7 (2204): 1278-1282. Published to the Internet at http://mbe.oxfordjournals.org/cgi/content/full/21/7/1278;  Anton Nekrutenko, “Functionality of unspliced XBP1 is required to explain evolution of overlapping reading frames,” Trends in Genetics,  9 Oct 2006, an advance Epub published to the Internet at   http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17034899&query_hl=1&itool=pubmed_docsum.

[66] “Francis Crick Remembered,” Astrobiology Magazine, Jul 30,2004. Also see Francis Crick and Leslie E. Orgel, “Directed Panspermia,” Icarus,  vol. 19 (1973): 341-346.

[67] Geoffrey Zubay, Origins of Life on the Earth and in the Cosmos (San Diego: Academic Press, 2000), 496.

[68] Mayr, What Evolution Is, 98.

[69] Mayr, What Evolution Is, 108-109.

[70] Richard Dawkins, “The ‘Information Challenge’ ”, in Robert T. Pennock, ed., Intelligent Design Creationism and Its Critics (Cambridge, MA: The MIT Press, 2002), 617-631.

[71] Michael J. Behe and D. W. Snoke, “Simulating Evolution by Gene Duplication of Protein Features That Require Multiple Amino Acid Residues,” Protein Science, vol. 13 (2004): 2651-2664.

[72] Meyer, “Biological Information.”

[73] Maxim D. Frank-Kamenetskii, Unraveling DNA the Most Important Molecule of Life (Cambridge, MA: Perseus Publishing, 1997), chap. 7; Male, David et al.., Immunology, 7th ed. (Burlington, MA: Elsevier Academic Press, 2006).

[74] I. G. Choi and S. H. Kim, “Global Extent of Horizontal Gene Transfer,” Proceedings of the National Academy of Sciences of the United States of America, vol. 104, no. 11 (2007): 4489-94; F. Ge, L. S. Wang, and J. Kim, “The Cobweb of Life Revealed by Genome-Scale Estimates of Horizontal Gene Transfer,” PloS Biology, vol.  3, no. 10 (2005): e316.

[75] Martin J. Lercher and Csaba Pal, “Integration of Horizontally Transferred Genes into Regulatory Interaction Networks Takes Many Million Years,” Molecular Biology and Evolution, vol. 25, no. 3 (2008): 559-567.

[76] Ravi Jain, Maria C. Rivera, and James A. Lake, “Horizontal Gene Transfer Among Genomes: The Complexity Hypothesis,” Proceedings of the National Academy of Sciences of the United States of America, vol. 96, no. 7 (1999): 3801-6.

[77] M. J. Stanhope, A. Lupas, M. J. Italia, K. K. Koretke, C. Volker, J. R. Brown, “Phylogenetic Analyses Do Not Support Horizontal Gene Transfers from Bacteria to Vertebrates,” Nature, vol. 411, no. 6840 (2001): 940-4.

[78] Maria C. Rivera, Ravi Jain, Jonathan E. Moore and James A. Lake, “Genomic Evidence for Two Functionally Distinct Gene Classes” Proceedings of the National Academy of Sciences of the United States of America, vol. 95, no. 11 (1998): 6239-44.

[79] Margulis, Acquiring Genomes, 12.

[80] Jamie Shreeve, “I, Chimera,” New Scientist, 186, no. 2505 (2005): 39-43.

[81] Michael J. Denton, “Physical Law Not Natural Selection as the Major Determinant of Biological Complexity in the Subcellular Realm: New Support for the Pre-Darwinian Conception of Evolution by Natural Law,” Bio Systems, vol. 71, no. 3 (2003): 297-303; Michael J. Denton,  “The Protein Folds as Platonic Forms: New Support for the Pre-Darwinian Conception of Evolution by Natural Law,” Journal of Theoretical Biology, vol. 219, no. 3 (2002): 325-342.

[82] “The Struggle of Ideas,” Time, 16 Jun 1941.

[83] James F. Crow and Carter Denniston, “Mutation in Human Populations,” Advances in Human Genetics 14 (1985): 61, 107.

[84] Robert Pollack, Signs of Life: The Language and Meanings of DNA (Boston: Houghton Mifflin Co., 1994), 32; Futuyma, Evolutionary Biology, 278; Lynn Margulis and Dorion Sagan. Acquiring Genomes: A Theory of the Origin of Species (New York: Basic Books, 2002), 11-12.

[85] Wells, “Making Sense” in Dembski, Intelligence, 120.

[86] Robert Pollack, Signs of Life: The Language and Meanings of DNA (Boston: Houghton Mifflin Co., 1994), 32.

[87] From the PBS Web site at http://www.pbs.org/wgbh/nova/genome/facts.html.

[88] Meyer, “Biological Information,” 218.

[89] Progressive is here defined to mean the organism survives the mutation moving towards an overall design improvement related to the journey toward humanity or any other advanced creature.

[90] Jonathan Wells, Icons of Evolution.(Washington, DC: Regnery Publishing, Inc., 2002).

[91] Douglas J. Futuyma, Science on Trial (Sunderland, MA: Sinauer Associates, Inc., 1995), 138-139.

[92] Karl Popper, Objective Knowledge: An Evolutionary Approach (Oxford: Oxford University Press, 1972), 267.

[93] Jerry Bergman, “Darwinism and the Deterioration of the Genome,” Creation Research Society Quarterly, vol. 42  no. 2 (2005).

[94] Ibid, 141.

[95] Steve Corbett, “Evolution” (Johnson County Community College, KS Anthropology 126 Syllabus, Evolution Segment) published to the Internet at http://staff.jccc.net/scorbett01/Physical/evolution.htm.

[96] Davison, “Instant Evolution” published to the Internet at http://www.iscid.org/papers/Davison_InstantEvolution_050204.pdf, 2.

[97] Futuyma, Evolutionary Biology, 294.

[98] Susumu Ohno, “The Notion of the Cambrian Pananimalia Genome,” Proceedings of the National Academy of Sciences of the United States of America 93, no. 16 (1996): 8475-8478.

[99] Ridley, Evolution, 76-78.

[100] Davison, “Instant Evolution” published to the Internet at http://www.iscid.org/papers/Davison_InstantEvolution_050204.pdf, 2; T. Ryan Gregory, ed., The Evolution of the Genome (Amsterdam: Elsevier Academic Press, 2005).

[101] A. Kumar and J. L. Bennetzen, “Plant Retrotransposons,” Annual Review of Genetics, vol. 33 (1999):  479-532.

[102] A. M. Lambowitz and S. Zimmerly, “Mobile Group II Introns,” Annual Review of Genetics, vol. 38 (2004):  1-35.

[103] W. E. Lonnig and H. Saedler, “Chromosome Rearrangements and Transposable Elements,” Annual Review of Genetics, vol. 36 (2002):  389-410.

[104] Michael Gleich, et al., Life Counts (New York: Atlantic Monthly Press, 2000), 28.

[105] L. Aravind, Kira S. Makarova and Eugene V. Koonin, “Holliday junction resolvases and related nucleases: identification of new families, phyletic distribution and evolutionary trajectories,” Nucleic Acids Research, 28, no. 18 (2000): 3417-3432.

[106] G. Ebersbach and K. Gerdes, “Plasmid Segregation Mechanisms,” Annual Review of Genetics, vol. 39 (2005):  453-479.

[107] Don B. Clewell and Cynthia Gawron-Burke, “Conjugative Transposons and the Dissemination of Antibiotic Resistance in Streptococci,” Annual Review of Microbiology, 40 (1986): 635-659; Gregory, Evolution of the Genome, 612.

[108] Gordon C. Mills, Malcolm Lancaster, and Walter L. Bradley “Origin of Life and Evolution in Biology Textbooks: A Critique,” in John Angus Campbell and Stephen C. Meyer ed., Darwinism, Design, and Public Education (East Lansing: Michigan State University Press, 2003), 214.

[109] Kassan, “Mirage,” 121

[110] Aravind, “Holliday,” 3417-3432.

[111] Mayr, What Evolution Is, 106

[112] Mark Ridley, Evolution (Boston: Blackwell Scientific Publications, 1993), 76-78.

[113] Ohno, “Pananimalia,” 8475-8478.

[114] Martin Jones, The Molecule Hunt: Archaeology and the Search for Ancient DNA (New York: Arcade Publishing, 2001).

[115] Raup, “Terrestrial Environments,” 11.

[116] Deehan, “Cambrian,” 147-154.

[117] Michael Denton, Evolution: A Theory in Crisis (Bethesda, Maryland: Adler & Adler, 1986), 191-2; In-Young Chang and Jennifer Curry ed., Evolution, The Reference Shelf, vol. 78, no. 5 (New York: The H. W. Wilson Company, 2006), chap. IV.

[118] Raup, “Terrestrial Environments,” 12; Chang, Evolution, chap.. IV; Meyer “Biological Information,” 215.

[119] Meyer “Biological Information,” 215.

[120] See Stephen Jones “Evolution Quotes” Web site at http://bevets.com/equotesr.htm.

[121] Richard C. Lewontin, “Adaptation” in The Fossil Record and Evolution (San Francisco: W. H. Freeman and Company, 1982).

[122] “The Pull of the Recent,” Astrobiology Magazine, May 19, 2003, Web Published at http://www.astrobio.net/news/modules.php?op=modload&name=News&file=article&sid=468.

[123] “A sampling-standardized analysis of Phanerozoic marine diversification and extinction,” A Working Group proposed by John Alroy Department of Paleobiology Smithsonian Institution MRC 121 Washington, DC 20560 & Charles R. Marshall Department of Earth and Space Sciences, Molecular Biology Institute, and Institute for Geophysics and Planetary Physics University of California Los Angeles, CA 90095-1567, Web published as an Adobe PDF document at

http://www.nceas.ucsb.edu/nceas-web/projects/98ALROY1/proposal.pdf.

[124] C. R. C. Paul “The Adequacy of the Fossil Record” in K. A. Joysey and A. E. Friday, eds, Problems of Phylogenetic Reconstruction, 75-117 (London: Academic, 1982); David S. Woodruff, "Evolution: A Paleobiological View," Science, 208 (1980): 717. Gee, Deep Time.

[125] Duane T. Gish, Evolution: The Fossils Still Say No! (El Cajon, Calif.: Institute for Creation Research, 1995), 53, 55, 59; Dehaan, “Cambrian,” 149-154.

[126] Jonathan Wells, Icons of Evolution (Washington, DC: Regnery Publishing, Inc., 2002), 35.

[127] R. K. Bamback, et al.  “Geologic History of Complex Organisms” in David Milne et al. eds, The Evolution of Complex and Higher Organisms (Washington, DC: NASA, 1985): 29-30.

[128] Charles R. Marshall, “Missing Links in the History of Life,” in J. William Schopf, ed., Evolution Facts and Fallacies (San Diego: Academic Press, 1999), 43.