Editor's Note: This article presents an overview of the key ideas in biochemist Michael Behe's book Darwin's Black Box: The Biochemical Challenge to Evolution. A more detailed discussion of these ideas can be found in the book itself. Those interested in the debate over intelligent design in biology should also check out Michael Behe's extensive responses to various critics.
Within a short time after Charles Darwin published The Origin of Species the explanatory power of the theory of evolution was recognized by the great majority of biologists. The hypothesis readily resolved the problems of homologous resemblance, rudimentary organs, species abundance, extinction, and biogeography. The rival theory of the time, which posited creation of species by a supernatural being, appeared to most reasonable minds to be much less plausible, since it would have a putative Creator attending to details that seemed to be beneath His dignity.
As time went on the theory of evolution obliterated the rival theory of creation, and virtually all working scientists studied the biological world from a Darwinian perspective. Most educated people now lived in a world where the wonder and diversity of the biological kingdom were produced by the simple, elegant principle of natural selection.
However, in science a successful theory is not necessarily a correct theory. In the course of history there have also been other theories which achieved the triumph that Darwinism achieved, which brought many experimental and observational facts into a coherent framework, and which appealed to people's intuitions about how the world should work. Those theories also promised to explain much of the universe with a few simple principles. But, by and large, those other theories are now dead.
A good example of this is the replacement of Newton's mechanical view of the universe by Einstein's relativistic universe. Although Newton's model accounted for the results of many experiments in his time, it failed to explain aspects of gravitation. Einstein solved that problem and others by completely rethinking the structure of the universe.
Similarly, Darwin's theory of evolution prospered by explaining much of the data of his time and the first half of the 20th century, but my article will show that Darwinism has been unable to account for phenomena uncovered by the efforts of modern biochemistry during the second half of this century. I will do this by emphasizing the fact that life at its most fundamental level is irreducibly complex and that such complexity is incompatible with undirected evolution.
A Series of Eyes
How do we see?
In the 19th century the anatomy of the eye was known in great detail and the sophisticated mechanisms it employs to deliver an accurate picture of the outside world astounded everyone who was familiar with them. Scientists of the 19th century correctly observed that if a person were so unfortunate as to be missing one of the eye's many integrated features, such as the lens, or iris, or ocular muscles, the inevitable result would be a severe loss of vision or outright blindness. Thus it was concluded that the eye could only function if it were nearly intact.
As Charles Darwin was considering possible objections to his theory of evolution by natural selection in The Origin of Species he discussed the problem of the eye in a section of the book appropriately entitled "Organs of extreme perfection and complication." He realized that if in one generation an organ of the complexity of the eye suddenly appeared, the event would be tantamount to a miracle. Somehow, for Darwinian evolution to be believable, the difficulty that the public had in envisioning the gradual formation of complex organs had to be removed.
Darwin succeeded brilliantly, not by actually describing a real pathway that evolution might have used in constructing the eye, but rather by pointing to a variety of animals that were known to have eyes of various constructions, ranging from a simple light sensitive spot to the complex vertebrate camera eye, and suggesting that the evolution of the human eye might have involved similar organs as intermediates.
But the question remains, how do we see? Although Darwin was able to persuade much of the world that a modern eye could be produced gradually from a much simpler structure, he did not even attempt to explain how the simple light sensitive spot that was his starting point actually worked. When discussing the eye Darwin dismissed the question of its ultimate mechanism by stating: "How a nerve comes to be sensitive to light hardly concerns us more than how life itself originated."
He had an excellent reason for declining to answer the question: 19th century science had not progressed to the point where the matter could even be approached. The question of how the eye works-that is, what happens when a photon of light first impinges on the retina-simply could not be answered at that time. As a matter of fact, no question about the underlying mechanism of life could be answered at that time. How do animal muscles cause movement? How does photosynthesis work? How is energy extracted from food? How does the body fight infection? All such questions were unanswerable.
The Calvin and Hobbes Approach
Now, it appears to be a characteristic of the human mind that when it is lacks understanding of a process, then it seems easy to imagine simple steps leading from nonfunction to function. A happy example of this is seen in the popular comic strip Calvin and Hobbes. Little boy Calvin is always having adventures in the company of his tiger Hobbes by jumping in a box and traveling back in time, or grabbing a toy ray gun and "transmogrifying" himself into various animal shapes, or again using a box as a duplicator and making copies of himself to deal with worldly powers such as his mom and his teachers. A small child such as Calvin finds it easy to imagine that a box just might be able to fly like an airplane (or something), because Calvin doesn't know how airplanes work.
A good example from the biological world of complex changes appearing to be simple is the belief in spontaneous generation. One of the chief proponents of the theory of spontaneous generation during the middle of the 19th century was Ernst Haeckel, a great admirer of Darwin and an eager popularizer of Darwin's theory. From the limited view of cells that 19th century microscopes provided, Haeckel believed that a cell was a "simple little lump of albuminous combination of carbon", not much different from a piece of microscopic Jell-O. Thus it seemed to Haeckel that such simple life could easily be produced from inanimate material.
In 1859, the year of the publication of The Origin of Species, an exploratory vessel, the H.M.S. Cyclops, dredged up some curious-looking mud from the sea bottom. Eventually Haeckel came to observe the mud and thought that it closely resembled some cells he had seen under a microscope. Excitedly he brought this to the attention of no less a personage than Thomas Henry Huxley, Darwin's great friend and defender, who observed the mud for himself. Huxley, too, became convinced that it was Urschleim (that is, protoplasm), the progenitor of life itself, and Huxley named the mud Bathybius haeckelii after the eminent proponent of abiogenesis.
The mud failed to grow. In later years, with the development of new biochemical techniques and improved microscopes, the complexity of the cell was revealed. The "simple lumps" were shown to contain thousands of different types of organic molecules, proteins, and nucleic acids, many discrete subcellular structures, specialized compartments for specialized processes, and an extremely complicated architecture. Looking back from the perspective of our time, the episode of Bathybius haeckelii seems silly or downright embarrassing, but it shouldn't. Haeckel and Huxley were behaving naturally, like Calvin: since they were unaware of the complexity of cells, they found it easy to believe that cells could originate from simple mud.
Throughout history there have been many other examples, similar to that of Haeckel, Huxley, and the cell, where a key piece of a particular scientific puzzle was beyond the understanding of the age. In science there is even a whimsical term for a machine or structure or process that does something, but the actual mechanism by which it accomplishes its task is unknown: it is called a "black box." In Darwin's time all of biology was a black box: not only the cell, or the eye, or digestion, or immunity, but every biological structure and function because, ultimately, no one could explain how biological processes occurred.
Biology has progressed tremendously due to the model that Darwin put forth. But the black boxes Darwin accepted are now being opened, and our view of the world is again being shaken.
Take our modern understanding of proteins, for example.
In order to understand the molecular basis of life it is necessary to understand how things called "proteins" work. Proteins are the machinery of living tissue that builds the structures and carries out the chemical reactions necessary for life. For example, the first of many steps necessary for the conversion of sugar to biologically-usable forms of energy is carried out by a protein called hexokinase. Skin is made in large measure of a protein called collagen. When light impinges on your retina it interacts first with a protein called rhodopsin. A typical cell contains thousands and thousands of different types of proteins to perform the many tasks necessary for life, much like a carpenter's workshop might contain many different kinds of tools for various carpentry tasks.
What do these versatile tools look like? The basic structure of proteins is quite simple: they are formed by hooking together in a chain discrete subunits called amino acids. Although the protein chain can consist of anywhere from about 50 to about 1,000 amino acid links, each position can only contain one of 20 different amino acids. In this they are much like words: words can come in various lengths but they are made up from a discrete set of 26 letters.
Now, a protein in a cell does not float around like a floppy chain; rather, it folds up into a very precise structure which can be quite different for different types of proteins. Two different amino acid sequences-two different proteins-can be folded to structures as specific and different from each other as a three-eighths inch wrench and a jigsaw. And like the household tools, if the shape of the proteins is significantly warped then they fail to do their jobs.
The Eyesight of Man
In general, biological processes on the molecular level are performed by networks of proteins, each member of which carries out a particular task in a chain.
Let us return to the question, how do we see? Although to Darwin the primary event of vision was a black box, through the efforts of many biochemists an answer to the question of sight is at hand. The answer involves a long chain of steps that begin when light strikes the retina and a photon is absorbed by an organic molecule called 11-cis-retinal, causing it to rearrange itself within picoseconds. This causes a corresponding change to the protein, rhodopsin, which is tightly bound to it, so that it can react with another protein called transducin, which in turn causes a molecule called GDP to be exchanged with a molecule called GTP.
To make a long story short, this exchange begins a long series of further bindings between still more specialized molecular machinery, and scientists now understand a great deal about the system of gateways, pumps, ion channels, critical concentrations, and attenuated signals that result in a current to finally be transmitted down the optic nerve to the brain, interpreted as vision. Biochemists also understand the many chemical reactions involved in restoring all these changed or depleted parts to make a new cycle possible.
To Explain Life
Although space doesn't permit me to give the details of the biochemistry of vision here, I have given the steps in my talks. Biochemists know what it means to "explain" vision. They know the level of explanation that biological science eventually must aim for. In order to say that some function is understood, every relevant step in the process must be elucidated. The relevant steps in biological processes occur ultimately at the molecular level, so a satisfactory explanation of a biological phenomenon such as sight, or digestion, or immunity, must include a molecular explanation.
It is no longer sufficient, now that the black box of vision has been opened, for an "evolutionary explanation" of that power to invoke only the anatomical structures of whole eyes, as Darwin did in the 19th century and as most popularizers of evolution continue to do today. Anatomy is, quite simply, irrelevant. So is the fossil record. It does not matter whether or not the fossil record is consistent with evolutionary theory, any more than it mattered in physics that Newton's theory was consistent with everyday experience. The fossil record has nothing to tell us about, say, whether or how the interactions of 11-cis-retinal with rhodopsin, transducin, and phosphodiesterase could have developed, step by step.
"How a nerve comes to be sensitive to light hardly concerns us more than how life itself originated", said Darwin in the 19th century. But both phenomena have attracted the interest of modern biochemistry in the past few decades. The story of the slow paralysis of research on life's origin is quite interesting, but space precludes its retelling here. Suffice it to say that at present the field of origin-of-life studies has dissolved into a cacophony of conflicting models, each unconvincing, seriously incomplete, and incompatible with competing models. In private even most evolutionary biologists will admit that science has no explanation for the beginning of life.
The same problems which beset origin-of-life research also bedevil efforts to show how virtually any complex biochemical system came about. Biochemistry has revealed a molecular world which stoutly resists explanation by the same theory that has long been applied at the level of the whole organism. Neither of Darwin's black boxes—the origin of life or the origin of vision (or other complex biochemical systems)—has been accounted for by his theory.
In The Origin of Species Darwin stated: "If it could be demonstrated that any complex organ existed which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down."
A system which meets Darwin's criterion is one which exhibits irreducible complexity. By irreducible complexity I mean a single system which is composed of several interacting parts that contribute to the basic function, and where the removal of any one of the parts causes the system to effectively cease functioning. An irreducibly complex system cannot be produced directly by slight, successive modifications of a precursor system, since any precursor to an irreducibly complex system is by definition nonfunctional.
Since natural selection requires a function to select, an irreducibly complex biological system, if there is such a thing, would have to arise as an integrated unit for natural selection to have anything to act on. It is almost universally conceded that such a sudden event would be irreconcilable with the gradualism Darwin envisioned. At this point, however, "irreducibly complex" is just a term, whose power resides mostly in its definition. We must now ask if any real thing is in fact irreducibly complex, and, if so, then are any irreducibly complex things also biological systems?
Consider the humble mousetrap (Figure 1). The mousetraps that my family uses in our home to deal with unwelcome rodents consist of a number of parts. There are: 1) a flat wooden platform to act as a base; 2) a metal hammer, which does the actual job of crushing the little mouse; 3) a wire spring with extended ends to press against the platform and the hammer when the trap is charged; 4) a sensitive catch which releases when slight pressure is applied, and 5) a metal bar which holds the hammer back when the trap is charged and connects to the catch. There are also assorted staples and screws to hold the system together.
If any one of the components of the mousetrap (the base, hammer, spring, catch, or holding bar) is removed, then the trap does not function. In other words, the simple little mousetrap has no ability to trap a mouse until several separate parts are all assembled.
Because the mousetrap is necessarily composed of several parts, it is irreducibly complex. Thus, irreducibly complex systems exist.
Now, are any biochemical systems irreducibly complex? Yes, it turns out that many are.
Earlier we discussed proteins. In many biological structures proteins are simply components of larger molecular machines. Like the picture tube, wires, metal bolts and screws that comprise a television set, many proteins are part of structures that only function when virtually all of the components have been assembled.
A good example of this is a cilium. Cilia are hairlike organelles on the surfaces of many animal and lower plant cells that serve to move fluid over the cell's surface or to "row" single cells through a fluid. In humans, for example, epithelial cells lining the respiratory tract each have about 200 cilia that beat in synchrony to sweep mucus towards the throat for elimination.
A cilium consists of a membrane-coated bundle of fibers called an axoneme. An axoneme contains a ring of 9 double microtubules surrounding two central single microtubules. Each outer doublet consists of a ring of 13 filaments (subfiber A) fused to an assembly of 10 filaments (subfiber B). The filaments of the microtubules are composed of two proteins called alpha and beta tubulin. The 11 microtubules forming an axoneme are held together by three types of connectors: subfibers A are joined to the central microtubules by radial spokes; adjacent outer doublets are joined by linkers that consist of a highly elastic protein called nexin; and the central microtubules are joined by a connecting bridge. Finally, every subfiber A bears two arms, an inner arm and an outer arm, both containing the protein dynein.
But how does a cilium work? Experiments have indicated that ciliary motion results from the chemically-powered "walking" of the dynein arms on one microtubule up the neighboring subfiber B of a second microtubule so that the two microtubules slide past each other (Figure 2). However, the protein cross-links between microtubules in an intact cilium prevent neighboring microtubules from sliding past each other by more than a short distance. These cross-links, therefore, convert the dynein-induced sliding motion to a bending motion of the entire axoneme.
Now, let us sit back, review the workings of the cilium, and consider what it implies. Cilia are composed of at least a half dozen proteins: alpha-tubulin, beta-tubulin, dynein, nexin, spoke protein, and a central bridge protein. These combine to perform one task, ciliary motion, and all of these proteins must be present for the cilium to function. If the tubulins are absent, then there are no filaments to slide; if the dynein is missing, then the cilium remains rigid and motionless; if nexin or the other connecting proteins are missing, then the axoneme falls apart when the filaments slide.
What we see in the cilium, then, is not just profound complexity, but it is also irreducible complexity on the molecular scale. Recall that by "irreducible complexity" we mean an apparatus that requires several distinct components for the whole to work. My mousetrap must have a base, hammer, spring, catch, and holding bar, all working together, in order to function. Similarly, the cilium, as it is constituted, must have the sliding filaments, connecting proteins, and motor proteins for function to occur. In the absence of any one of those components, the apparatus is useless.
The components of cilia are single molecules. This means that there are no more black boxes to invoke; the complexity of the cilium is final, fundamental. And just as scientists, when they began to learn the complexities of the cell, realized how silly it was to think that life arose spontaneously in a single step or a few steps from ocean mud, so too we now realize that the complex cilium can not be reached in a single step or a few steps.
But since the complexity of the cilium is irreducible, then it can not have functional precursors. Since the irreducibly complex cilium can not have functional precursors it can not be produced by natural selection, which requires a continuum of function to work. Natural selection is powerless when there is no function to select. We can go further and say that, if the cilium can not be produced by natural selection, then the cilium was designed.
A Non-Mechanical Example
A non-mechanical example of irreducible complexity can be seen in the system that targets proteins for delivery to subcellular compartments. In order to find their way to the compartments where they are needed to perform specialized tasks, certain proteins contain a special amino acid sequence near the beginning called a "signal sequence."
As the proteins are being synthesized by ribosomes, a complex molecular assemblage called the signal recognition particle or SRP, binds to the signal sequence. This causes synthesis of the protein to halt temporarily. During the pause in protein synthesis the SRP is bound by the trans-membrane SRP receptor, which causes protein synthesis to resume and which allows passage of the protein into the interior of the endoplasmic reticulum (ER). As the protein passes into the ER the signal sequence is cut off.
For many proteins the ER is just a way station on their travels to their final destinations. Proteins which will end up in a lysosome are enzymatically "tagged" with a carbohydrate residue called mannose-6-phosphate while still in the ER. An area of the ER membrane then begins to concentrate several proteins; one protein, clathrin, forms a sort of geodesic dome called a coated vesicle which buds off from the ER. In the dome there is also a receptor protein which binds to both the clathrin and to the mannose-6-phosphate group of the protein which is being transported. The coated vesicle then leaves the ER, travels through the cytoplasm, and binds to the lysosome through another specific receptor protein. Finally, in a maneuver involving several more proteins, the vesicle fuses with the lysosome and the protein arrives at its destination.
During its travels our protein interacted with dozens of macromolecules to achieve one purpose: its arrival in the lysosome. Virtually all components of the transport system are necessary for the system to operate, and therefore the system is irreducible. And since all of the components of the system are comprised of single or several molecules, there are no black boxes to invoke. The consequences of even a single gap in the transport chain can be seen in the hereditary defect known as I-cell disease. It results from a deficiency of the enzyme that places the mannose-6-phosphate on proteins to be targeted to the lysosomes. I-cell disease is characterized by progressive retardation, skeletal deformities, and early death.
The Study of "Molecular Evolution"
Other examples of irreducible complexity abound, including aspects of protein transport, blood clotting, closed circular DNA, electron transport, the bacterial flagellum, telomeres, photosynthesis, transcription regulation, and much more. Examples of irreducible complexity can be found on virtually every page of a biochemistry textbook. But if these things cannot be explained by Darwinian evolution, how has the scientific community regarded these phenomena of the past forty years?
A good place to look for an answer to that question is in the Journal of Molecular Evolution. JME is a journal that was begun specifically to deal with the topic of how evolution occurs on the molecular level. It has high scientific standards, and is edited by prominent figures in the field. In a recent issue of JME there were published eleven articles; of these, all eleven were concerned simply with the analysis of protein or DNA sequences. None of the papers discussed detailed models for intermediates in the development of complex biomolecular structures.
In the past ten years JME has published 886 papers. Of these, 95 discussed the chemical synthesis of molecules thought to be necessary for the origin of life, 44 proposed mathematical models to improve sequence analysis, 20 concerned the evolutionary implications of current structures, and 719 were analyses of protein or polynucleotide sequences. However, there weren't any papers discussing detailed models for intermediates in the development of complex biomolecular structures. This is not a peculiarity of JME. No papers are to be found that discuss detailed models for intermediates in the development of complex biomolecular structures in the Proceedings of the National Academy of Science, Nature, Science, the Journal of Molecular Biology or, to my knowledge, any journal whatsoever.
Sequence comparisons overwhelmingly dominate the literature of molecular evolution. But sequence comparisons simply can't account for the development of complex biochemical systems any more than Darwin's comparison of simple and complex eyes told him how vision worked. Thus in this area science is mute.
Detection of Design
What's going on? Imagine a room in which a body lies crushed, flat as a pancake. A dozen detectives crawl around, examining the floor with magnifying glasses for any clue to the identity of the perpetrator. In the middle of the room next to the body stands a large, gray elephant. The detectives carefully avoid bumping into the pachyderm's legs as they crawl, and never even glance at it. Over time the detectives get frustrated with their lack of progress but resolutely press on, looking even more closely at the floor. You see, textbooks say detectives must "get their man," so they never consider elephants.
There is an elephant in the roomful of scientists who are trying to explain the development of life. The elephant is labeled "intelligent design." To a person who does not feel obliged to restrict his search to unintelligent causes, the straightforward conclusion is that many biochemical systems were designed. They were designed not by the laws of nature, not by chance and necessity. Rather, they were planned. The designer knew what the systems would look like when they were completed; the designer took steps to bring the systems about. Life on earth at its most fundamental level, in its most critical components, is the product of intelligent activity.
The conclusion of intelligent design flows naturally from the data itself-not from sacred books or sectarian beliefs. Inferring that biochemical systems were designed by an intelligent agent is a humdrum process that requires no new principles of logic or science. It comes simply from the hard work that biochemistry has done over the past forty years, combined with consideration of the way in which we reach conclusions of design every day.
What is "design"? Design is simply the purposeful arrangement of parts. The scientific question is how we detect design. This can be done in various ways, but design can most easily be inferred for mechanical objects.
Systems made entirely from natural components can also evince design. For example, suppose you are walking with a friend in the woods. All of a sudden your friend is pulled high in the air and left dangling by his foot from a vine attached to a tree branch.
After cutting him down you reconstruct the trap. You see that the vine was wrapped around the tree branch, and the end pulled tightly down to the ground. It was securely anchored to the ground by a forked branch. The branch was attached to another vine-hidden by leaves-so that, when the trigger-vine was disturbed, it would pull down the forked stick, releasing the spring-vine. The end of the vine formed a loop with a slipknot to grab an appendage and snap it up into the air. Even though the trap was made completely of natural materials you would quickly conclude that it was the product of intelligent design.
Intelligent design is a good explanation for a number of biochemical systems, but I should insert a word of caution. Intelligent design theory has to be seen in context: it does not try to explain everything. We live in a complex world where lots of different things can happen. When deciding how various rocks came to be shaped the way they are a geologist might consider a whole range of factors: rain, wind, the movement of glaciers, the activity of moss and lichens, volcanic action, nuclear explosions, asteroid impact, or the hand of a sculptor. The shape of one rock might have been determined primarily by one mechanism, the shape of another rock by another mechanism.
Similarly, evolutionary biologists have recognized that a number of factors might have affected the development of life: common descent, natural selection, migration, population size, founder effects (effects that may be due to the limited number of organisms that begin a new species), genetic drift (spread of "neutral," nonselective mutations), gene flow (the incorporation of genes into a population from a separate population), linkage (occurrence of two genes on the same chromosome), and much more. The fact that some biochemical systems were designed by an intelligent agent does not mean that any of the other factors are not operative, common, or important.
It is often said that science must avoid any conclusions which smack of the supernatural. But this seems to me to be both bad logic and bad science. Science is not a game in which arbitrary rules are used to decide what explanations are to be permitted. Rather, it is an effort to make true statements about physical reality. It was only about sixty years ago that the expansion of the universe was first observed. This fact immediately suggested a singular event-that at some time in the distant past the universe began expanding from an extremely small size.
To many people this inference was loaded with overtones of a supernatural event-the creation, the beginning of the universe. The prominent physicist A.S. Eddington probably spoke for many physicists in voicing his disgust with such a notion:
Philosophically, the notion of an abrupt beginning to the present order of Nature is repugnant to me, as I think it must be to most; and even those who would welcome a proof of the intervention of a Creator will probably consider that a single winding-up at some remote epoch is not really the kind of relation between God and his world that brings satisfaction to the mind.
Nonetheless, the big bang hypothesis was embraced by physics and over the years has proven to be a very fruitful paradigm. The point here is that physics followed the data where it seemed to lead, even though some thought the model gave aid and comfort to religion. In the present day, as biochemistry multiplies examples of fantastically complex molecular systems, systems which discourage even an attempt to explain how they may have arisen, we should take a lesson from physics. The conclusion of design flows naturally from the data; we should not shrink from it; we should embrace it and build on it.
In concluding, it is important to realize that we are not inferring design from what we do not know, but from what we do know. We are not inferring design to account for a black box, but to account for an open box. A man from a primitive culture who sees an automobile might guess that it was powered by the wind or by an antelope hidden under the car, but when he opens up the hood and sees the engine he immediately realizes that it was designed. In the same way biochemistry has opened up the cell to examine what makes it run and we see that it, too, was designed.
It was a shock to the people of the 19th century when they discovered, from observations science had made, that many features of the biological world could be ascribed to the elegant principle of natural selection. It is a shock to us in the twentieth century to discover, from observations science has made, that the fundamental mechanisms of life cannot be ascribed to natural selection, and therefore were designed. But we must deal with our shock as best we can and go on. The theory of undirected evolution is already dead, but the work of science continues.
What is Intelligent Design?
Intelligent design — often called “ID” — is a scientific theory that holds that the emergence of some features of the universe and living things is best explained by an intelligent cause rather than an undirected process such as natural selection. ID theorists argue that design can be inferred by studying the informational properties of natural objects to determine if they bear the type of information that in our experience arises from an intelligent cause.
Proponents of neo-Darwinian evolution contend that the information in life arose via purposeless, blind, and unguided processes. ID proponents argue that this information arose via purposeful, intelligently guided processes. Both claims are scientifically testable using the standard methods of science. But ID theorists say that when we use the scientific method to explore nature, the evidence points away from unguided material causes, and reveals intelligent design.
Intelligent Design in Everyday Reasoning
Whether we realize it or not, we detect design constantly in our everyday lives. In fact, our lives often depend on inferring intelligent design. Imagine you are driving along a road and come to a place where the asphalt is covered by a random splatter of paint. You would probably ignore the paint and keep driving onward.
But what if the paint is arranged in the form of a warning? In this case, you would probably make a design inference that could save your life. You would recognize that an intelligent agent was trying to communicate an important message.
Only an intelligent agent can use foresight to accomplish an end-goal — such as building a car or using written words to convey a message. Recognizing this unique ability of intelligent agents allows scientists in many fields to detect design.
Intelligent Design in Archaeology and Forensics
ID is in the business of trying to discriminate between strictly naturally/materially caused objects on the one hand, and intelligently caused objects on the other. A variety of scientific fields already use ID reasoning. For example, archaeologists find an object and they need to determine whether it arrived at its shape through natural processes, so it’s just another rock (let’s say), or whether it was carved for a purpose by an intelligence. Likewise forensic scientists distinguish between naturally caused deaths (by disease, for example), and intelligently caused deaths (murder). These are important distinctions for our legal system, drawing on science and logical inference. Using similar reasoning, intelligent design theorists go about their research. They ask: If we can use science to detect design in other fields, why should it be controversial when we detect it in biology or cosmology?
Here is how ID works. Scientists interested in detecting design start by observing how intelligent agents act when they design things. What we know about human agents provides a large dataset for this. One of the things we find is that when intelligent agents act, they generate a great deal of information. As ID theorist Stephen Meyer says: “Our experience-based knowledge of information-flow confirms that systems with large amounts of specified complexity (especially codes and languages) invariably originate from an intelligent source—from a mind or personal agent.”1
Thus ID seeks to find in nature reliable indications of the prior action of intelligence—specifically it seeks to find the types of information which are known to be produced by intelligent agents. Yet not all “information” is the same. What kind of information is known to be produced by intelligence? The type of information that indicates design is generally called “specified complexity” or “complex and specified information” or “CSI” for short. I will briefly explain what these terms mean.
Something is complex if it is unlikely. But complexity or unlikelihood alone is not enough to infer design. To see why, imagine that you are dealt a five-card hand of poker. Whatever hand you receive is going to be a very unlikely set of cards. Even if you get a good hand, like a straight or a royal flush, you’re not necessarily going to say, “Aha, the deck was stacked.” Why? Because unlikely things happen all the time. We don't infer design simply because of something's being unlikely. We need more: specification. Something is specified if it matches an independent pattern.
A Tale of Two Mountains
Imagine you are a tourist visiting the mountains of North America. You come across Mount Rainier, a huge dormant volcano not far from Seattle. There are features of this mountain that differentiate it from any other mountain on Earth. In fact, if all possible combinations of rocks, peaks, ridges, gullies, cracks, and crags are considered, this exact shape is extremely unlikely and complex. But you don't infer design simply because Mount Rainier has a complex shape. Why? Because you can easily explain its shape through the natural processes of erosion, uplift, heating, cooling, freezing, thawing, weathering, etc. There is no special, independent pattern to the shape of Mount Rainier. Complexity alone is not enough to infer design.
But now let's say you go to a different mountain—Mount Rushmore in South Dakota. This mountain also has a very unlikely shape, but its shape is special. It matches a pattern—the faces of four famous Presidents. With Mount Rushmore, you don’t just observe complexity, you also find specification. Thus, you would infer that its shape was designed.
ID theorists ask “How can we apply this kind of reasoning to biology?” One of the greatest scientific discoveries of the past fifty years is that life is fundamentally built upon information. It's all around us. As you read a book, your brain processes information stored in the shapes of ink on the page. When you talk to a friend, you communicate information using sound-based language, transmitted through vibrations in air molecules. Computers work because they receive information, process it, and then give useful output.
Everyday life as we know it would be nearly impossible without the ability to use information. But could life itself exist without it? Carl Sagan observed that the “information content of a simple cell” is “around 1012 bits, comparable to about a hundred million pages of the Encyclopedia Britannica.”2 Information forms the chemical blueprint for all living organisms, governing the assembly, structure, and function at essentially all levels of cells. But where does this information come from?
As I noted previously, ID begins with the observation that intelligent agents generate large quantities of CSI. Studies of the cell reveal vast quantities of information in our DNA, stored biochemically through the sequence of nucleotide bases. No physical or chemical law dictates the order of the nucleotide bases in our DNA, and the sequences are highly improbable and complex. Yet the coding regions of DNA exhibit very unlikely sequential arrangements of bases that match the precise pattern necessary to produce functional proteins. Experiments have found that the sequence of nucleotide bases in our DNA must be extremely precise in order to generate a functional protein. The odds of a random sequence of amino acids generating a functional protein is less than 1 in 10 to the 70th power.3In other words, our DNA contains high CSI.
Thus, as nearly all molecular biologists now recognize, the coding regions of DNA possess a high “information content”—where “information content” in a biological context means precisely “complexity and specificity.” Even the staunch Darwinian biologist Richard Dawkins concedes that “[b]iology is the study of complicated things that give the appearance of having been designed for a purpose.”4 Atheists like Dawkins believe that unguided natural processes did all the "designing" but intelligent design theorist Stephen C. Meyer notes, “in all cases where we know the causal origin of ‘high information content,’ experience has shown that intelligent design played a causal role.”5
A DVD in Search of a DVD Player
But just having the information in our DNA isn't enough. By itself, a DNA molecule is useless. You need some kind of machinery to read the information in the DNA and produce some useful output. A lone DNA molecule is like having a DVD—and nothing more. A DVD might carry information, but without a machine to read that information, it's all but useless (maybe you could use it as a Frisbee). To read the information in a DVD, we need a DVD player. In the same way, our cells are equipped with machinery to help process the information in our DNA.
That machinery reads the commands and codes in our DNA much as a computer processes commands in computer code. Many authorities have recognized the computer-like information processing of the cell and the computer-like information-rich properties of DNA's language-based code. Bill Gates observes, “Human DNA is like a computer program but far, far more advanced than any software we've ever created.”6 Biotech guru Craig Venter says that “life is a DNA software system,”7 containing “digital information” or “digital code,” and the cell is a “biological machine” full of “protein robots.”8 Richard Dawkins has written that “[t]he machine code of the genes is uncannily computer-like.”9 Francis Collins, the leading geneticist who headed the human genome project, notes, “DNA is something like the hard drive on your computer,” containing “programming.”10
Cells are thus constantly performing computer-like information processing. But what is the result of this process? Machinery. The more we discover about the cell, the more we learn that it functions like a miniature factory, replete with motors, powerhouses, garbage disposals, guarded gates, transportation corridors, CPUs, and much more. Bruce Alberts, former president of the U.S. National Academy of Sciences, has stated:
[T]he entire cell can be viewed as a factory that contains an elaborate network of interlocking assembly lines, each of which is composed of a set of large protein machines. ... Why do we call the large protein assemblies that underlie cell function protein machines? Precisely because, like machines invented by humans to deal efficiently with the macroscopic world, these protein assemblies contain highly coordinated moving parts.11
There are hundreds, if not thousands, of molecular machines in living cells. In discussions of ID, the most famous example of a molecular machine is the bacterial flagellum. The flagellum is a micro-molecular propeller assembly driven by a rotary engine that propels bacteria toward food or a hospitable living environment. There are various types of flagella, but all function like a rotary engine made by humans, as found in some car and boat motors. Flagella also contain many parts that are familiar to human engineers, including a rotor, a stator, a drive shaft, a U-joint, and a propeller. As one molecular biologist writes, “More so than other motors the flagellum resembles a machine designed by a human.”12 But there's something else that's special about the flagellum.
Introducing "Irreducible Complexity"
In applying ID to biology, ID theorists often discuss “irreducible complexity,” a concept developed and popularized by Lehigh University biochemist Michael Behe. Irreducible complexity is a form of specified complexity, which exists in systems composed of “several interacting parts that contribute to the basic function, and where the removal of any one of the parts causes the system to effectively cease functioning.”13 Because natural selection only preserves structures that confer a functional advantage to an organism, such systems would be unlikely to evolve through a Darwinian process. Why? Because there is no evolutionary pathway where they could remain functional during each small evolutionary step. According to ID theorists, irreducible complexity is an informational pattern that reliably indicates design, because in all irreducibly complex systems in which the cause of the system is known by experience or observation, intelligent design or engineering played a role in the origin of the system.
Microbiologist Scott Minnich has performed genetic knockout experiments where each gene encoding a flagellar part is mutated individually such that it no longer functions. His experiments show that the flagellum fails to assemble or function properly if any one of its approximately 35 different protein-components is removed.14 By definition, it is irreducibly complex. In this all-or-nothing game, mutations cannot produce the complexity needed to evolve a functional flagellum one step at a time. The odds are also too daunting for it to evolve in one great mutational leap.
The past fifty years of biological research have showed that life is fundamentally based upon:
- A vast amount of complex and specified information encoded in a biochemical language.
- A computer-like system of commands and codes that processes the information.
- Irreducibly complex molecular machines and multi-machine systems.
Where, in our experience, do language, complex and specified information, programming code, and machines come from? They have only one known source: intelligence.
Intelligent Design Extends Beyond Biology
But there's much more to ID. Contrary to what many people suppose, ID is much broader than the debate over Darwinian evolution. That's because much of the scientific evidence for intelligent design comes from areas that Darwin's theory doesn't even address. In fact, much evidence for intelligent design from physics and cosmology.
The fine-tuning of the laws of physics and chemistry to allow for advanced life is an example of extremely high levels of CSI in nature. The laws of the universe are complex because they are highly unlikely. Cosmologists have calculated the odds of a life-friendly universe appearing by chance are less than 1 in 1010^123. That's ten raised to a power of 10 with 123 zeros after it—a number far too long to write out! The laws of the universe are specified in that they match the narrow band of parameters required for the existence of advanced life. This high CSI indicates design. Even the atheist cosmologist Fred Hoyle observed, “A common sense interpretation of the facts suggests that a super intellect has monkeyed with physics, as well as with chemistry and biology.”15 From the tiniest atom, to living organisms, to the architecture of the entire cosmos, the fabric of nature shows strong evidence that it was intelligently designed.
Using Mathematics to Detect Design
Intelligent design has its roots in information theory, and design can be detected via statistical mathematical calculations.
As noted, ID theorists begin by observing the types of information produced by the action of intelligent agents vs. the types of information produced through purely natural processes. By making these observations, we can infer that intelligence is the best explanation for many information-rich features we see in nature. But can the inference to design be made rigorously using mathematics? ID theorists think we can, by mathematically quantifying the amount of information present and determining if it is the type of information which, in our experience, is only produced by intelligence.
The fact that information is a real entity is attested by scientists both inside and outside the ID movement. In his essay “Intelligent Design as a Theory of Information,” a pro-ID mathematician and philosopher William Dembski notes:
No one disputes that there is such a thing as information. As Keith Devlin remarks, “Our very lives depend upon it, upon its gathering, storage, manipulation, transmission, security, and so on. Huge amounts of money change hands in exchange for information. People talk about it all the time. Lives are lost in its pursuit. Vast commercial empires are created in order to manufacture equipment to handle it.”16
The fundamental intuition behind measuring information is a reduction in possibilities. The more possibilities you rule out, the more information present. Thus Dembski uses accepted definitions from the field of information theory that define information as the occurrence of one event, or scenario, while excluding other events, or scenarios. In other words, information is what you get when you narrow down what you're talking about.
The amount of information in a system or represented by some event can be calculating the probability of that scenario, and converting that probability into units of information, called “bits.” These are the same “bits” and “bytes” from the computer world. We can calculate bits according to the following equation:
Given a probability p of some event or scenario, Information content = I = - Log2 (p)
For example, in binary code, each character has two possibilities—0 or 1—meaning the probability of any character is 0.5. Using the formula above, this leads to an information content of 1 bit for each binary digit. Thus, a binary string like “00110” contains 5 bits. But saying “this string carries 5 bits of information” says nothing about the meaning of the string! It only describes the likelihood of the string occurring. Nobel Prize winning molecular biologist Jack Szostak explains that this classical method of measuring information via raw probabilities does not help us discern the functional meaning of an information-rich system:
[C]lassical information theory ... does not consider the meaning of a message, defining the information content of a string of symbols as simply that required to specify, store or transmit the string. ... A new measure of information—functional information—is required to account for all possible sequences that could potentially carry out an equivalent biochemical function, independent of the structure or mechanism used.17
Szostak suggests that we must look at more than just the likelihood (i.e., the probability or raw information content in bits) to understand the functional workings of natural systems. We must look at the meaning of the information as well. ID theorists feel the same way.
To measure both the information content and the meaning of some event, Dembski developed the concept of complex and specified information (CSI), which was discussed earlier. To review, this method of detecting design can not only determine if an event unlikely (i.e., high information content), but also whether it matches a pre-existing pattern or “specification” (i.e., it has some functional meaning). This is seen in the diagram below:
In the figure above, Point A, which bears low CSI, represents something best explained by natural processes. Point B, which has high CSI, represents something best explained by design. Curve C represents the upper limit to what natural processes can produce-the "universal probability bound." Anything far beyond Curve C is best explained by design; anything far within Curve C is best explained by natural processes.
As seen in figure at above, there is a limit to the amount of CSI which can be produced by natural processes (represented by Curve C). When we see a specified event that is highly unlikely—high CSI—we know that natural processes were not involved, and that intelligent design is the best explanation. When low information content is involved, natural causes can produce the feature in question, and the best explanation is some natural cause.
To help us discriminate between systems that could arise naturally and those that are best explained by design, ID proponents have developed the “universal probability bound,” a measure of the maximum amount of CSI that could be produced during the entire history of the universe. In essence, if the CSI content of a system exceeds the universal probability bound, then natural causes cannot explain that feature and it can only be explained by intelligent design. Dembski and Jonathan Witt explain it this way:
Scientists have learned that within the known physical universe there are about 1080 elementary particles ... Scientists also have learned that a change from one state of matter to another can’t happen faster than what physicists call the Planck time. ... The Planck time is 1 second divided by 1045 (1 followed by forty-five zeroes). ... Finally, scientists estimate that the universe is about fourteen billion years old, meaning the universe is itself millions of times younger than 1025 seconds. If we now assume that any physical event in the universe requires the transition of at least one elementary particle (most events require far more, of course), then these limits on the universe suggest that the total number of events throughout cosmic history could not have exceeded 1080 x 1045 x 1025 = 10150.
This means that any specified event whose probability is less than 1 chance in 10150 will remain improbable even if we let every corner and every moment of the universe roll the proverbial dice. The universe isn’t big enough, fast enough or old enough to roll the dice enough times to have a realistic chance of randomly generating specified events that are this improbable.18
Using our equation for calculating bits, an event whose probability is 1 in 10150 carries about 500 bits of information. This means that if the CSI content of a system is greater than 500 bits, then we can rule out blind material causes and infer intelligent design. Dembski has applied this method to bacterial flagellum, an irreducibly complex molecular machine which contains high CSI, and calculated that it contains a few thousand bits of information—far greater than what can be produced by natural causes according to the universal probability bound.
But ID theorists have developed other ways to research the limits of what can be produced by natural processes, especially in the context of Darwinian evolution.
Intelligent Design and the Limits of Natural Selection
Intelligent design does not reject all aspects of evolution. Evolution can mean something as benign as (1) “life has changed over time,” or it can entail more controversial ideas, like (2) “all living things share common ancestry,” or (3) “natural selection acting upon random mutations produced life’s diversity.”
ID does not conflict with the observation that natural selection causes small-scale changes over time (meaning 1), or the view that all organisms are related by common ancestry (meaning 2). However, the dominant evolutionary viewpoint today is neo-Darwinism (meaning 3), which contends that life’s entire history was driven by unguided natural selection acting on random mutations (as well as other forces like genetic drift)—a collection of blind, purposeless process with no directions or goals. It is this specific neo-Darwinian claim that ID directly challenges.
Darwinian evolution can work fine when one small step (e.g., a single point mutation) along an evolutionary pathway gives an advantage that helps an organisms survive and reproduce. The theory of ID has no problem with this, and acknowledges that there are many small-scale changes that Darwinian mechanisms can produce.
But what about cases where many steps, or multiple mutations, are necessary to gain some advantage? Here, Darwinian evolution faces limits on what it can accomplish. Evolutionary biologist Jerry Coyne affirms this when he states: “natural selection cannot build any feature in which intermediate steps do not confer a net benefit on the organism.”19 Likewise, Darwin wrote in The Origin of Species:
If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down.
As Darwin’s quote suggests, natural selection gets stuck when a feature cannot be built through “numerous, successive, slight modifications”—that is, when a structure requires multiple mutations to be present before providing any advantage for natural selection to select. Proponents of intelligent design have done research showing that many such biological structures exist which would require multiple mutations before providing some advantage.
In 2004, biochemist Michael Behe co-published a study in Protein Science with physicist David Snoke demonstrating that if multiple mutations were required to produce a functional bond between two proteins, then “the mechanism of gene duplication and point mutation alone would be ineffective because few multicellular species reach the required population sizes.”20
Writing in 2008 in the journal Genetics, Behe and Snoke's critics tried to refute them, but failed. The critics found that, in a human population, to obtain a feature via Darwinian evolution that required only two mutations before providing an advantage “would take > 100 million years,” which they admitted was “very unlikely to occur on a reasonable timescale.”21 Such “multi-mutation features” are thus unlikely to evolve in humans, which have small population sizes and long generation times, reducing the efficiency of the Darwinian mechanism.
But can Darwinian processes produce complex multimutation features in bacteria which have larger population sizes and reproduce rapidly? Even here, Darwinian evolution faces limits.
In a 2010 peer-reviewed study, molecular biologist Douglas Axe calculated that when a “multi-mutation feature” requires more than six mutations before giving any benefit, it is unlikely to arise even in the whole history of the Earth—even in the case of bacteria.22 He provided empirical backing for this conclusion from experimental research he earlier published in the Journal of Molecular Biology. There, he found there that only one in 1074 amino-acid sequences yields a functional protein fold.23 That implies that protein folds in general are multimutation features, requiring many amino acids to be present before there is any functional advantage.
Another study by Axe and biologist Ann Gauger found that merely converting one enzyme to perform the function of a closely related enzyme—the kind of conversion that evolutionists claim can happen easily—would require a minimum of seven mutations.24 This exceeds the limits of what Darwinian can produce over the Earth’s entire history, as calculated by Axe’s 2010 paper.
A later study published in 2014 by Gauger, Axe and biologist Mariclair Reeves bolstered this finding. They examined additional proteins to determine whether they could be converted via mutation to perform the function of a closely related protein.25 After inducing all possible single mutations in the enzymes, and many other combinations of mutations, they found that evolving a protein, via Darwinian evolution, to perform the function of a closely related protein would take over 1015 years—over 100,000 times longer than the age of the earth!
Collectively, these research results indicate that many biochemical features would require many mutations before providing any advantage to an organism, and would thus be beyond the limit of what Darwinian evolution can do. If blind evolution cannot build these CSI-rich features, what can? Some non-random process is necessary that can “look ahead” and find the complex combinations of mutations to generate these high-CSI features. That process is intelligent design.
A Positive Argument or God of the Gaps?
When arguing against ID, some critics will contend that ID is merely a negative argument against evolution, what some will call a “God-of-the-gaps” argument. A “God-of-the-gaps” argument, critics observe, argues for God based upon gaps in our knowledge, rather than presenting a positive argument. Moreover, it is said that “God-of-the-gaps” arguments are dangerous to faith, because as our knowledge increases, our basis for believing in God is squeezed into smaller and smaller “gaps” in our knowledge. Eventually, the argument goes, there is no reason for believing in God at all. Does ID present a God-of-the-gaps argument? It does not, for many reasons.
First, ID refers to an intelligent cause and does not identify the designer as “God.” All ID scientifically detects is the prior action of an intelligent cause. ID respects the limits of scientific inquiry and does not attempt to address religious questions about the identity of the designer. Indeed, the ID movement includes people of many worldviews, including Christians, Jews, Muslims, people of Eastern religious views, and even agnostics. What unites them is not some religious view about the identity of the designer, but a conviction that there is scientific evidence for intelligent design in nature.
More to the point, the argument for design is not based on what we don’t know (i.e., gaps in our knowledge), but is rather based entirely on what we do know (evidence) about the known causes of information-rich systems. For example, irreducibly complex molecular machines contain high CSI, and we know from experience that high-CSI systems arise from the action of an intelligent agent. To elaborate on a quote given earlier from Stephen Meyer:
[W]e have repeated experience of rational and conscious agents—in particular ourselves—generating or causing increases in complex specified information, both in the form of sequence-specific lines of code and in the form of hierarchically arranged systems of parts. ... Our experience-based knowledge of information-flow confirms that systems with large amounts of specified complexity (especially codes and languages) invariably originate from an intelligent source—from a mind or personal agent.26
Similarly, Meyer and biochemist Scott Minnich explain that irreducibly complex systems in particular are always known to derive from an intelligent cause:
Molecular machines display a key signature or hallmark of design, namely, irreducible complexity. In all irreducibly complex systems in which the cause of the system is known by experience or observation, intelligent design or engineering played a role the origin of the system. ... Indeed, in any other context we would immediately recognize such systems as the product of very intelligent engineering. Although some may argue this is a merely an argument from ignorance, we regard it as an inference to the best explanation, given what we know about the powers of intelligent as opposed to strictly natural or material causes.27
It’s important to understand that when ID theorists argue that we can find in nature the kind of information and complexity that comes from intelligence, they are not making a mere argument from analogy. When one reduces natural systems to their raw informational properties, they are mathematically identical to those of designed systems. Though not an ID proponent, molecular biologist Hubert Yockey explains that form of information in DNA is identical to what we find in language:
It is important to understand that we are not reasoning by analogy. The sequence hypothesis [that the exact order of symbols records the information] applies directly to the protein and the genetic text as well as to written language and therefore the treatment is mathematically identical.28
Though Yockey is no ID proponent, he rightly observes that the informational properties of DNA are mathematically identical to language. Thus, the argument for design is much stronger than a mere appeal to analogy, and we don't infer design based upon merely finding and exploiting alleged “gaps” in our knowledge. Rather, ID is based upon the positive argument that nature contains the kind of information and complexity which, in our positive experience, comes only from the action of intelligence. Accordingly, intelligent design is, by standard scientific methods, the best explanation for high CSI in nature.
Using the Scientific Method to Positively Detect Design
As a final demonstration of how ID uses a positive scientific argument, consider how the scientific method can be used to detect design. The scientific method is commonly described as a four-step process involving observation, hypothesis, experiment, and conclusion. ID uses this precise scientific method to make a positive cases for design in various scientific fields, including biochemistry, paleontology, systematics, and genetics:
Example 1—Using the Scientific Method to Detect Design in Biochemistry:
- Observation: Intelligent agents solve complex problems by acting with an end goal in mind, producing high levels of CSI. In our experience, systems with large amounts of CSI—such as codes and languages—invariably originate from an intelligent source. Likewise, in our experience, intelligence is the cause of irreducibly complex machines.
- Hypothesis (Prediction): Natural structures will be found that contain many parts arranged in intricate patterns that perform a specific function—indicating high levels of CSI, including irreducible complexity.
- Experiment: Experimental investigations of DNA indicate that it is full of a CSI-rich, language-based code. Cells use computer-like information processing systems to translate the genetic information in DNA into proteins. Biologists have performed mutational sensitivity tests on proteins and determined that their amino acid sequences are highly specified. The end-result of cellular information processing system are protein-based micromolecular machines. Genetic knockout experiments and other studies show that some molecular machines, like the bacterial flagellum, are irreducibly complex.
- Conclusion: The high levels of CSI—including irreducible complexity—in biochemical systems are best explained by the action of an intelligent agent.
Example 2—Using the Scientific Method to Detect Design in Paleontology:
- Observation: Intelligent agents rapidly infuse large amounts of information into systems. As four ID theorists write: "intelligent design provides a sufficient causal explanation for the origin of large amounts of information… the intelligent design of a blueprint often precedes the assembly of parts in accord with a blueprint or preconceived design plan.”
- Hypothesis (Prediction): Forms containing large amounts of novel information will appear in the fossil record suddenly and without similar precursors.
- Experiment: Studies of the fossil record show that species typically appear abruptly without similar precursors. The Cambrian explosion is a prime example, although there are other examples of explosions in life’s history. Large amounts of CSI had to arise rapidly to explain the abrupt appearance of these forms.
- Conclusion: The abrupt appearance of new fully formed body plans in the fossil record is best explained by intelligent design.
Example 3—Using the Scientific Method to Detect Design in Systematics:
- Observation: Intelligent agents often reuse functional components in different designs. As Paul Nelson and Jonathan Wells explain: “An intelligent cause may reuse or redeploy the same module in different systems… [and] generate identical patterns independently.”
- Hypothesis (Prediction): Genes and other functional parts will be commonly reused in different organisms.
- Experiment: Studies of comparative anatomy and genetics have uncovered similar parts commonly existing in widely different organisms. Examples of extreme convergent evolution show reusage of functional genes and structures in a manner not predicted by common ancestry.
- Conclusion: The reusage of highly similar and complex parts in widely different organisms in non-treelike patterns is best explained by the action of an intelligent agent.
Example 4— Using the Scientific Method to Detect Design in Genetics:
- Observation: Observation: Intelligent agents construct structures with purpose and function. As William Dembski argues: “Consider the term ‘junk DNA.’… [O]n an evolutionary view we expect a lot of useless DNA. If, on the other hand, organisms are designed, we expect DNA, as much as possible, to exhibit function.”
- Hypothesis (Prediction): Much so-called “ junk DNA” will turn out to perform valuable functions.
- Experiment: Numerous studies have discovered functions for “junk DNA.” Examples include functions for pseudogenes, introns, and repetitive DNA.
- Conclusion: The discovery of function for numerous types of “junk DNA” was successfully predicted by intelligent design.
One might disagree with the conclusions of ID, but one cannot reasonably claim that these arguments for design are based upon religion, faith, or divine revelation. They are based upon science.
Follow the Evidence Where It Leads
There will, of course, always be gaps in scientific knowledge. But when critics accuse ID of being a “gaps-based” argument, they essentially insist that all gaps may only be filled with naturalistic explanations, and promote “materialism-of-the-gaps” thinking. This precludes scientists from fully seeking the truth and finding evidence for design in nature. ID rejects gaps-based reasoning of all kinds, and follows the motto that we should “follow the evidence wherever it leads.”
Adding ID to our explanatory toolkit leads to many advances in different scientific fields. In biochemistry, ID allows us to better understand the workings and origin of molecular machines. In paleontology, ID helps resolve long-standing questions about patterns of abrupt appearance—and disappearance—of species. In systematics, ID explains why studies of biomolecules and anatomy are failing to yield a grand “tree of life.” In genetics, ID leads biology into a new paradigm where life is full of functional, information rich molecules containing new layers of code and regulation. In this way, ID is best poised to lead biology into an information age that uncovers the complex, information-based genetic and epigenetic workings of life.
ID has scientific merit because it uses well-accepted methods of historical sciences in order to detect in nature the types of complexity that we understand, from present-day observations, are derived from intelligent causes. From top to bottom, when we study nature through science, we find evidence of fine-tuning and planning—intelligent design—from the macro-architecture of the entire universe to the tiniest submicroscopic biomolecular machines. The more we understand nature, the more clearly we see it is filled with evidence for design.
Good ID Websites for More Information:
- ID Portal: www.intelligentdesign.org
- IDEA Student Clubs: www.ideacenter.org
- ID News Site: www.evolutionnews.org
- ID Podcast: www.idthefuture.com
- Resources for Faith Leaders: www.faithandevolution.org
- Discovery Institute’s ID Program: www.discovery.org/ID
[1.] Stephen C. Meyer, “The origin of biological information and the higher taxonomic categories,” Proceedings of the Biological Society of Washington, 117(2):213-239 (2004).
[2.] Carl Sagan, “Life,” in Encyclopedia Britannica: Macropaedia Vol. 10 (Encyclopedia Britannica, Inc., 1984), 894.
[3.] Douglas D. Axe, “Extreme Functional Sensitivity to Conservative Amino Acid Changes on Enzyme Exteriors,” Journal of Molecular Biology, 301:585-595 (2000); Douglas D. Axe, “Estimating the Prevalence of Protein Sequences Adopting Functional Enzyme Folds,” Journal of Molecular Biology, 341: 1295–1315 (2004).
[4.] Richard Dawkins, The Blind Watchmaker (New York: W. W. Norton, 1986), 1.
[5.] Stephen C. Meyer et. al., “The Cambrian Explosion: Biology's Big Bang,” in Darwinism, Design, and Public Education, J. A. Campbell and S. C. Meyer eds. (Michigan State University Press, 2003).
[6.] Bill Gates, N. Myhrvold, and P. Rinearson, The Road Ahead: Completely Revised and Up-To-Date (Penguin Books, 1996), 228.
[7.] J. Craig Venter, “The Big Idea: Craig Venter On the Future of Life,” The Daily Beast (October 25, 2013), accessed October 25, 2013, www.thedailybeast.com/articles/2013/10/25/the-big-idea-craig-venter-the-future-of-life.html.
[8.] J. Craig Venter, quoted in Casey Luskin, “Craig Venter in Seattle: ‘Life Is a DNA Software System’,” (October 24, 2013), www.evolutionnews.org/2013/10/craig_venter_in078301.html.
[9.] Richard Dawkins, River Out of Eden: A Darwinian View of Life (New York: Basic Books, 1995), 17.
[10.] Francis Collins, The Language of God: A Scientist Presents Evidence for Belief (New York: Free Press, 2006), 91.
[11.] Bruce Alberts, “The Cell as a Collection of Protein Machines: Preparing the Next Generation of Molecular Biologists,” Cell, 92: 291-294 (Feb. 6, 1998).
[12.] David J. DeRosier, “The Turn of the Screw: The Bacterial Flagellar Motor,” Cell, 93: 17-20 (April 3, 1998).
[13.] Michael J. Behe, Darwin's Black Box: The Biochemical Challenge to Darwinism (Free Press 1996), 39.
[14.] Transcript of testimony of Scott Minnich, Kitzmiller et al. v. Dover Area School Board (M.D. Pa., PM Testimony, November 3, 2005), 103-112. See also Table 1 in R. M. Macnab, “Flagella,” in Escherichia Coli and Salmonella Typhimurium: Cellular and Molecular Biology Vol. 1, eds. F. C. Neidhardt, J. L. Ingraham, K. B. Low, B. Magasanik, M. Schaechter, and H. E. Umbarger (Washington D.C.: American Society for Microbiology, 1987), 73-74.
[15.] Fred Hoyle, “The Universe: Past and Present Reflections,” Engineering and Science, pp. 8-12 (November, 1981).
[16.] William Dembski, “Intelligent Design as a Theory of Information,” Naturalism, Theism and the Scientific Enterprise: An Interdisciplinary Conference at the University of Texas, Feb. 20-23, 1997, http://www.discovery.org/a/118 (citations omitted).
[17.] Jack W. Szostak, “Molecular messages,” Nature, 423: 689 (June 12, 2003).
[18.] William Dembski and Jonathan Witt, Intelligent Design Uncensored, pp. 68-69 (InterVarsity Press, 2010).
[19.] Jerry Coyne, “The Great Mutator,” The New Republic (June 14, 2007).
[20.] Michael Behe and David Snoke, “Simulating Evolution by Gene Duplication of Protein Features That Require Multiple Amino Acid Residues,” Protein Science, 13: 2651-2664 (2004).
[21.] Rick Durrett and Deena Schmidt, “Waiting for Two Mutations: With Applications to Regulatory Sequence Evolution and the Limits of Darwinian Evolution,” Genetics, 180:1501-1509 (2008).
[22.] Douglas Axe, “The Limits of Complex Adaptation: An Analysis Based on a Simple Model of Structured Bacterial Populations,” BIO-Complexity, 2010 (4): 1-10.
[23.] Axe, “Estimating the Prevalence of Protein Sequences Adopting Functional Enzyme Folds”; Axe, “Extreme Functional Sensitivity to Conservative Amino Acid Changes on Enzyme Exteriors.”
[24.] Ann Gauger and Douglas Axe, "The Evolutionary Accessibility of New Enzyme Functions: A Case Study from the Biotin Pathway," BIO-Complexity, 2011 (1): 1-17.
[25.] Mariclair A. Reeves, Ann K. Gauger, Douglas D. Axe, “Enzyme Families—Shared Evolutionary History or Shared Design? A Study of the GABA-Aminotransferase Family,” BIO-Complexity, 2014 (4): 1-16.
[26.] Meyer, “The origin of biological information and the higher taxonomic categories.”
[27.] Scott A. Minnich & Stephen C. Meyer, “Genetic analysis of coordinate flagellar and type III regulatory circuits in pathogenic bacteria," in Proceedings of the Second International Conference on Design & Nature, Rhodes Greece, p. 8 (M.W. Collins & C.A. Brebbia eds., 2004).
[28.] Hubert P. Yockey, “Self Organization Origin of Life Scenarios and Information Theory," Journal of Theoretical Biology, 91:13-31 (1981).
Copyright © 2016. Version 1.0 Permission Granted to Reproduce for Educational Purposes.
Abstract: "DNA and the Origin of Life" appears in the peer-reviewed* volume Darwinism, Design, and Public Education published with Michigan State University Press. Stephen C. Meyer contends that intelligent design provides a better explanation than competing chemical evolutionary models for the origin of the information present in large biomacromolecules such as DNA, RNA, and proteins. Meyer shows that the term information as applied to DNA connotes not only improbability or complexity but also specificity of function. He then argues that neither chance nor necessity, nor the combination of the two, can explain the origin of information starting from purely physical-chemical antecedents. Instead, he argues that our knowledge of the causal powers of both natural entities and intelligent agency suggests intelligent design as the best explanation for the origin of the information necessary to build a cell in the first place. Click here to download the article.
*Darwinism, Design, and Public Education is an interdisciplinary volume that was peer-reviewed by a professor of biological sciences, a professor of philosophy of science and a professor of rhetoric of science.
Editor’s note: The online journal Sapientia recently posed a good question to several participants in a forum: “Is Intelligent Design Detectable by Science?” This is one key issue on which proponents of ID and of theistic evolution differ. Stephen Meyer, philosopher of science and director of Discovery Institute's Center for Science & Culture, gave the following reply.
Biologists have long recognized that many organized structures in living organisms — the elegant form and protective covering of the coiled nautilus; the interdependent parts of the vertebrate eye; the interlocking bones, muscles, and feathers of a bird wing — “give the appearance of having been designed for a purpose.”1
Before Darwin, biologists attributed the beauty, integrated complexity, and adaptation of organisms to their environments to a powerful designing intelligence. Consequently, they also thought the study of life rendered the activity of a designing intelligence detectable in the natural world.
Yet Darwin argued that this appearance of design could be more simply explained as the product of a purely undirected mechanism, namely, natural selection and random variation. Modern neo-Darwinists have similarly asserted that the undirected process of natural selection and random mutation produced the intricate designed-like structures in living systems. They affirm that natural selection can mimic the powers of a designing intelligence without itself being guided by an intelligent agent. Thus, living organisms may look designed, but on this view, that appearance is illusory and, consequently, the study of life does not render the activity of a designing intelligence detectable in the natural world. As Darwin himself insisted, “There seems to be no more design in the variability of organic beings and in the action of natural selection, than in the course in which the wind blows.”2 Or as the eminent evolutionary biologist Francisco Ayala has argued, Darwin accounted for “design without a designer” and showed “that the directive organization of living beings can be explained as the result of a natural process, natural selection, without any need to resort to a Creator or other external agent.”3
But did Darwin explain away all evidence of apparent design in biology? Darwin attempted to explain the origin of new living forms starting from simpler pre-existing forms of life, but his theory of evolution by natural selection did not even attempt to explain the origin of life — the simplest living cell — in the first place. Yet there is now compelling evidence of intelligent design in the inner recesses of even the simplest living one-celled organisms. Moreover, there is a key feature of living cells — one that makes the intelligent design of life detectable — that Darwin didn’t know about and that contemporary evolutionary theorists have not explained away.
The Information Enigma
In 1953 when Watson and Crick elucidated the structure of the DNA molecule, they made a startling discovery. The structure of DNA allows it to store information in the form of a four-character digital code. Strings of precisely sequenced chemicals called nucleotide bases store and transmit the assembly instructions — the information — for building the crucial protein molecules and machines the cell needs to survive.
Francis Crick later developed this idea with his famous “sequence hypothesis” according to which the chemical constituents in DNA function like letters in a written language or symbols in a computer code. Just as English letters may convey a particular message depending on their arrangement, so too do certain sequences of chemical bases along the spine of a DNA molecule convey precise instructions for building proteins. The arrangement of the chemical characters determines the function of the sequence as a whole. Thus, the DNA molecule has the same property of “sequence specificity” that characterizes codes and language.
Moreover, DNA sequences do not just possess “information” in the strictly mathematical sense described by pioneering information theorist Claude Shannon. Shannon related the amount of information in a sequence of symbols to the improbability of the sequence (and the reduction of uncertainty associated with it). But DNA base sequences do not just exhibit a mathematically measurable degree of improbability. Instead, DNA contains information in the richer and more ordinary dictionary sense of “alternative sequences or arrangements of characters that produce a specific effect.” DNA base sequences convey instructions. They perform functions and produce specific effects. Thus, they not only possess “Shannon information,” but also what has been called “specified” or “functional information.”
Like the precisely arranged zeros and ones in a computer program, the chemical bases in DNA convey instructions by virtue of their specific arrangement — and in accord with an independent symbol convention known as the “genetic code.” Thus, biologist Richard Dawkins notes that “the machine code of the genes is uncannily computer-like.”4 Similarly, Bill Gates observes that “DNA is like a computer program, but far, far more advanced than any software we’ve ever created.”5 Similarly, biotechnologist Leroy Hood describes the information in DNA as “digital code.”6
After the early 1960s, further discoveries revealed that the digital information in DNA and RNA is only part of a complex information processing system — an advanced form of nanotechnology that both mirrors and exceeds our own in its complexity, design logic, and information storage density.
Where did the information in the cell come from? And how did the cell’s complex information processing system arise? These questions lie at the heart of contemporary origin-of-life research. Clearly, the informational features of the cell at least appear designed. And, as I show in extensive detail in my book Signature in the Cell, no theory of undirected chemical evolution explains the origin of the information needed to build the first living cell.7
Why? There is simply too much information in the cell to be explained by chance alone. And attempts to explain the origin of information as the consequence of pre-biotic natural selection acting on random changes inevitably presuppose precisely what needs explaining, namely, reams of pre-existing genetic information. The information in DNA also defies explanation by reference to the laws of chemistry. Saying otherwise is like saying a newspaper headline might arise from the chemical attraction between ink and paper. Clearly something more is at work.
Yet, the scientists who infer intelligent design do not do so merely because natural processes — chance, laws, or their combination — have failed to explain the origin of the information and information processing systems in cells. Instead, we think intelligent design is detectable in living systems because we know from experience that systems possessing large amounts of such information invariably arise from intelligent causes. The information on a computer screen can be traced back to a user or programmer. The information in a newspaper ultimately came from a writer — from a mind. As the pioneering information theorist Henry Quastler observed, “Information habitually arises from conscious activity.”8
This connection between information and prior intelligence enables us to detect or infer intelligent activity even from unobservable sources in the distant past. Archeologists infer ancient scribes from hieroglyphic inscriptions. SETI’s search for extraterrestrial intelligence presupposes that information imbedded in electromagnetic signals from space would indicate an intelligent source. Radio astronomers have not found any such signal from distant star systems; but closer to home, molecular biologists have discovered information in the cell, suggesting — by the same logic that underwrites the SETI program and ordinary scientific reasoning about other informational artifacts — an intelligent source.
DNA functions like a software program and contains specified information just as software does. We know from experience that software comes from programmers. We know generally that specified information — whether inscribed in hieroglyphics, written in a book, or encoded in a radio signal — always arises from an intelligent source. So the discovery of such information in the DNA molecule provides strong grounds for inferring (or detecting) that intelligence played a role in the origin of DNA, even if we weren’t there to observe the system coming into existence.
The Logic of Design Detection
In The Design Inference, mathematician William Dembski explicates the logic of design detection. His work reinforces the conclusion that the specified information present in DNA points to a designing mind.
Dembski shows that rational agents often detect the prior activity of other designing minds by the character of the effects they leave behind. Archaeologists assume that rational agents produced the inscriptions on the Rosetta Stone. Insurance fraud investigators detect certain “cheating patterns” that suggest intentional manipulation of circumstances rather than a natural disaster. Cryptographers distinguish between random signals and those carrying encoded messages, the latter indicating an intelligent source. Recognizing the activity of intelligent agents constitutes a common and fully rational mode of inference.
More importantly, Dembski explicates criteria by which rational agents recognize or detect the effects of other rational agents, and distinguish them from the effects of natural causes. He demonstrates that systems or sequences with the joint properties of “high complexity” (or small probability) and “specification” invariably result from intelligent causes, not chance or physical-chemical laws.9 Dembski noted that complex sequences exhibit an irregular and improbable arrangement that defies expression by a simple rule or algorithm, whereas specification involves a match or correspondence between a physical system or sequence and an independently recognizable pattern or set of functional requirements.
By way of illustration, consider the following three sets of symbols:
TIME AND TIDE WAIT FOR NO MAN
The first two sequences are complex because both defy reduction to a simple rule. Each represents a highly irregular, aperiodic, improbable sequence. The third sequence is not complex, but is instead highly ordered and repetitive. Of the two complex sequences, only the second, however, exemplifies a set of independent functional requirements — i.e., is specified.
English has many such functional requirements. For example, to convey meaning in English one must employ existing conventions of vocabulary (associations of symbol sequences with particular objects, concepts, or ideas) and existing conventions of syntax and grammar. When symbol arrangements “match” existing vocabulary and grammatical conventions (i.e., functional requirements), communication can occur. Such arrangements exhibit “specification.” The sequence “Time and tide waits for no man” clearly exhibits such a match, and thus performs a communication function.
Thus, of the three sequences only the second manifests both necessary indicators of a designed system. The third sequence lacks complexity, though it does exhibit a simple periodic pattern, a specification of sorts. The first sequence is complex, but not specified. Only the second sequence exhibits both complexity and specification. Thus, according to Dembski’s theory of design detection, only the second sequence implicates an intelligent cause — as our uniform experience affirms.
In my book Signature in the Cell, I show that Dembski’s joint criteria of complexity and specification are equivalent to “functional” or “specified information.” I also show that the coding regions of DNA exemplify both high complexity and specification and, thus not surprisingly, also contain “specified information.” Consequently, Dembski’s scientific method of design detection reinforces the conclusion that the digital information in DNA indicates prior intelligent activity.
So, contrary to media reports, the theory of intelligent design is not based upon ignorance or “gaps” in our knowledge, but on scientific discoveries about DNA and on established scientific methods of reasoning in which our uniform experience of cause and effect guides our inferences about the kinds of causes that produce (or best explain) different types of events or sequences.
Anthropic Fine Tuning
The evidence of design in living cells is not the only such evidence in nature. Modern physics now reveals evidence of intelligent design in the very fabric of the universe. Since the 1960s physicists have recognized that the initial conditions and the laws and constants of physics are finely tuned, against all odds, to make life possible. Even extremely slight alterations in the values of many independent factors — such as the expansion rate of the universe, the speed of light, and the precise strength of gravitational or electromagnetic attraction — would render life impossible. Physicists refer to these factors as “anthropic coincidences” and to the fortunate convergence of all these coincidences as the “fine-tuning of the universe.”
Many have noted that this fine-tuning strongly suggests design by a pre-existent intelligence. Physicist Paul Davies has said that “the impression of design is overwhelming.”10 Fred Hoyle argued that, “A common sense interpretation of the facts suggests that a superintellect has monkeyed with physics, as well as chemistry and biology.”11 Many physicists now concur. They would argue that — in effect — the dials in the cosmic control room appear finely-tuned because someone carefully fine-tuned them.
To explain the vast improbabilities associated with these fine-tuning parameters, some physicists have postulated not a “fine-tuner” or intelligent designer, but the existence of a vast number of other parallel universes. This “multiverse” concept also necessarily posits various mechanisms for producing these universes. On this view, having some mechanism for generating new universes would increase the number of opportunities for a life-friendly universe such as our own to arise — making ours something like a lucky winner of a cosmic lottery.
But advocates of these multiverse proposals have overlooked an obvious problem. The speculative cosmologies (such as inflationary cosmology and string theory) they propose for generating alternative universes invariably invoke mechanisms that themselves require fine-tuning, thus begging the question as to the origin of that prior fine-tuning. Indeed, all the various materialistic explanations for the origin of the fine-tuning — i.e., the explanations that attempt to explain the fine-tuning without invoking intelligent design — invariably invoke prior unexplained fine-tuning.
Moreover, as Jay Richards has shown,12 the fine-tuning of the universe exhibits precisely those features — extreme improbability and functional specification — that invariably trigger an awareness of, and justify an inference to, intelligent design. Since the multiverse theory cannot explain fine-tuning without invoking prior fine-tuning, and since the fine-tuning of a physical system to accomplish a propitious end is exactly the kind of thing we know intelligent agents do, it follows that intelligent design stands as the best explanation for the fine-tuning of the universe.
And that makes intelligent design detectable in both the physical parameters of the universe and the information-bearing properties of life.
Unless you've been hiding in a cave, you've heard of "intelligent design" (ID) and some of its leading proponents-Phillip Johnson, Michael Behe, William Dembski. Unfortunately, you probably got the mainstream media's spin. It's so predictable, I sometimes wonder if reporters aren't using computer macros.
The reporter types control-alt "CE" and out pops the witty headline: "Creationism Evolves." Control-alt "Scopes Trope" and out pops a lead referencing the old Spencer Tracy film "Inherit the Wind," a cartoon-like caricature of the 1925 Scopes Monkey Trial over evolution in the classroom.
Control-alt "Conspiracy" and, presto, a paragraph about the religious right and its scheme to smuggle Bibles into the science class as the first step toward establishing a theocracy. Next comes a quotation supposedly representing the view of all "serious scientists," with the phrase "overwhelming evidence" thrown in for good measure. The story practically writes itself, and it possesses this virtue: it saves the reporter the bother of actually investigating what design theory really is.
So what is ID, really? ID is not a deduction from religious dogma or scripture. It's simply the argument that certain features of the natural world — from miniature machines and digital information found in living cells, to the fine-tuning of physical constants — are best explained as the result of an intelligent cause. ID is thus a tacit rebuke of an idea inherited from the 19th century, called scientific materialism.
Natural science in the Victorian Age, or rather, its materialistic gloss, offered a radically different view of the universe: (1) The universe has always existed, so we need not explain its origin; (2) Everything in the universe submits to deterministic laws. (3) Life is the love child of luck and chemistry. (4) Cells, the basic units of life, are essentially blobs of Jell-O.
Onto this dubious edifice Charles Darwin added a fifth conjecture: All the sophisticated organisms around us grew from a process called natural selection: this process seizes and passes along those minor, random variations in a population that provide a survival advantage. With this, Darwin explained away the apparent design in the biological world as just that-only apparent.
Each of these 19th-century assumptions has been undermined or discredited in the 20th century, but the materialist gloss remains: There is one god, matter, and science is its prophet. It hides behind its more modest cousin, methodological naturalism. According to this tidy dictum, scientists can believe whatever they want in their personal lives, but they must appeal only to impersonal causes when explaining nature. Accordingly, any who discuss purpose or design within science (the founders of modern science generously excepted) cease to be scientists.
The Universe Strikes Back
There was one problem with this tidy rule. Nature forgot to cooperate. The trouble started in the 1920s when astronomer Edwin Hubble discovered that the light from distant galaxies was "red-shifted." It had stretched during the course of its travels. This suggested the universe is expanding. Reversing the process in their minds, scientists were suddenly confronted with a universe that had come into existence in the finite past. Who knew! Hubble's discovery, confirmed by later evidence, flatly contradicted the earlier picture of an eternal and self-existing cosmos. The universe itself had re-introduced the question of its origin to a community bent on avoiding the question altogether.
This was just the beginning. In the 1960s and '70s, physicists found that the universal constants of physics (e.g., gravity, electromagnetism) appeared finely tuned for complex life. To astrophysicist and atheist Fred Hoyle, this fine-tuning suggested the work of a "superintellect."
Still more recently, growing evidence in astronomy has revealed that even in a finely tuned universe, dozens of local conditions have to go just right to build a single habitable planet. This growing list of unlikely requirements is only half the story. In "The Privileged Planet," astronomer Guillermo Gonzalez and I argue that those conditions for habitability also provide the best overall conditions for doing science. The very places where observers can exist are the same places that provide the best overall conditions for observing. For instance, the most life-friendly region of the galaxy is also the best place to be an astronomer and cosmologist. You might expect this if the universe were designed for discovery, but not if, as astronomer Carl Sagan put it, "The universe is all there is, ever was, or ever will be."
Of course, even with a suitable environment, you don't automatically get man or even amoebas. Before the Darwinian mechanism can even get started, it needs a wealth of biological information as part of the first self-reproducing organism. For instance, there's the information encoded along the DNA molecule, often described as a sophisticated computer code for producing proteins, the three-dimensional building blocks of all life. These, in turn, need the right cellular hardware to function.
In recent years, philosophers William Dembski and Stephen Meyer have turned this evidence into a formidable argument for intelligent design. Dembski, also a mathematician, applies information and probability theory to the subject. Meyer argues that the usual aimless processes of chance and chemistry simply can't explain biological information and that, moreover, our everyday experience shows us where such information comes from-intelligent agents.
Moving up a level, we find complex and functionally integrated machines that are out of reach to the Darwinian mechanism. Biochemist Michael Behe immortalized some of these in his bestselling 1996 book, "Darwin's Black Box."
Behe argues that molecular machines like the bacterial flagellum are "irreducibly complex." They're like a mousetrap. Without all of their basic parts, they don't work. Natural selection can only build systems one small step at a time, where each step provides an immediate survival advantage for the organism. It can't select for a future function. To do that requires foresight-the exclusive jurisdiction of intelligent agents. That's the positive evidence for design: Such structures are the sort produced by intelligent agents, who can foresee a future function. If you get this point, you've already comprehended more than most journalists writing on the subject.
The New Zoo Review
Moving to the macroscopic world, we see the three-dimensional complexity of many diverse animal body plans (phyla). In the fossil record, these show up suddenly. The problem for Darwinism is not that there are "gaps." Of course there are. Rather, it's the entire fossil record's pattern of sudden appearance of new phyla and persistent morphological isolation between them. This is not the gradually branching tree of life the Darwinian story leads us to expect.
Nor is this an argument from ignorance. In our experience, sudden innovations and massive infusions of information come from intelligent agents. The primary innovations come first (e.g., car, airplane, a new Cambrian phylum) followed by variations on the original form. This is the story the fossil record tells.
The Definition or the Evidence?
At the beginning of the 21st century, we have new evidence and new intellectual tools at our disposal. Standing in the way is the materialistic definition of science inherited from the Victorian Age. If a definition of science conflicts with the scientific evidence, should we go with the definition or the evidence?
To ask the question is to answer it. "Scientia" means knowledge. If we are properly scientific, then we should be open to the natural world, not decide beforehand what it's allowed to reveal. Either the universe provides evidence for purpose and design or it doesn't. The way to resolve the question isn't to play definitional games but to look.
Recently, Nobel-prize winning physicist Charles Townes asked, "What is the purpose or meaning of life? Or of our universe? These are questions which should concern us all.... If the universe has a purpose, then its structure, and how it works, must reflect this purpose."
Townes continues: "Serious intellectual discussion of the possible meaning of our universe, or the nature of religion and philosophical views of religion and science, needs to be openly and carefully discussed."
Unfortunately, few are willing to follow Townes' advice. If we talk about ID, we're warned, someone, somewhere, will start talking about God.
But certain ideas in science will always have theological implications. As arch-Darwinist Richard Dawkins so memorably said, "Darwin made it possible to be an intellectually fulfilled atheist." Right.
Both Dawkins and Townes agree that ideas in science can have theological implications. Isn't that obvious? Yet in our current climate, even the bare rumor of God causes some to reach for their stash of derisive terms-"theocrat," "fundamentalist," "creationist"-they don't require much imagination.
But that response rings increasingly hollow. The genie is out of the bottle, and name-calling and misinformation won't put him back. The mandarins can no longer control the flow of information to those who seek it. The implications can take care of themselves. It's time to discuss the evidence.
- Beckwith, Francis J. Law, Darwinism, and Public Education: The Establishment Clause and the Challenge of Intelligent Design. Lanham, Md., 2003.
- Behe, Michael J. Darwin’s Black Box: The Biochemical Challenge to Evolution. New York, 1996.
- Dawkins, Richard. The Blind Watchmaker: Why the Evidence of Evolution Reveals a Universe without Design. New York, 1986.
- Dembski, William A. No Free Lunch: Why Specified Complexity Cannot Be Purchased without Intelligence. Lanham, Md., 2002.
- Forrest, Barbara. “The Wedge at Work: How Intelligent Design Creationism Is Wedging Its Way into the Cultural and Academic Mainstream.” In Intelligent Design Creationism and Its Critics: Philosophical, Theological, and Scientific Perspectives, edited by Robert T. Pennock, pp. 5–53, Cambridge, Mass., 2001.
- Giberson, Karl W. and Donald A. Yerxa. Species of Origins: America’s Search for a Creation Story. Lanham, Md., 2002.
- Hunter, Cornelius G. Darwin’s God: Evolution and the Problem of Evil. Grand Rapids, Mich., 2002.
- Manson, Neil A., ed. God and Design: The Teleological Argument and Modern Science. London, 2003.
- Miller, Kenneth R. Finding Darwin’s God: A Scientist’s Search for Common Ground between God and Evolution. San Francisco, 1999.
- Rea, Michael C. World without Design: The Ontological Consequences of Naturalism. Oxford, 2002.
- Witham, Larry. By Design: Science and the Search for God. San Francisco, 2003.
- Woodward, Thomas. Doubts about Darwin: A History of Intelligent Design. Grand Rapids, Mich., 2003.
Bibliographic EssayLarry Witham provides the best overview of intelligent design, even-handedly treating its scientific, cultural, and religious dimensions. As a journalist, Witham has personally interviewed all the main players in the debate over intelligent design and allows them to tell their story. For intelligent design’s place in the science and religion dialogue, see Giberson and Yerxa. For histories of the intelligent design movement, see Woodward (a supporter) and Forrest (a critic). See Behe and Dembski to overview intelligent design’s scientific research program. For a critique of that program, see Miller. For an impassioned defense of Darwinism against any form of teleology or design, see Dawkins. Manson’s anthology situates intelligent design within broader discussions about teleology. Rea probes intelligent design’s metaphysical underpinnings. Hunter provides an interesting analysis of how intelligent design and Darwinism play off the problem of evil. Beckwith examines whether intelligent design is inherently religious and thus, on account of church-state separation, must be barred from public school science curricula.
In 2009, I discussed a paper in BioEssays titled “MicroRNAs and metazoan macroevolution: insights into canalization, complexity, and the Cambrian explosion” which stated that “elucidating the materialistic basis of the Cambrian explosion has become more elusive, not less, the more we know about the event itself, and cannot be explained away by coupling extinction of intermediates with long stretches of geologic time, despite the contrary claims of some modern neo-Darwinists.”(more…)
On this page you can download an annotated bibliography of peer-reviewed and peer-edited scientific articles supporting, applying, or arising from the theory of intelligent design. You also can read a description of the intelligent design research community and its aims.(more…)
The Current Landscape
In December of 2004, the renowned British philosopher Antony Flew made worldwide news when he repudiated a lifelong commitment to atheism, citing, among other factors, evidence of intelligent design in the DNA molecule. In that same month, the American Civil Liberties Union filed suit to prevent a Dover, Pennsylvania school district from informing its students that they could learn about the theory of intelligent design from a supplementary science textbook in their school library. The following February, The Wall Street Journal (Klinghoffer 2005) reported that an evolutionary biologist at the Smithsonian Institution with two doctorates had been punished for publishing a peer-reviewed scientific article making a case for intelligent design.
Since 2005, the theory of intelligent design has been the focus of a frenzy of international media coverage, with prominent stories appearing in The New York Times, Nature, The London Times, The Independent (London), Sekai Nippo (Tokyo), The Times of India, Der Spiegel, The Jerusalem Post and Time magazine, to name just a few. And recently, a major conference about intelligent design was held in Prague (attended by some 700 scientists, students and scholars from Europe, Africa and the United States), further signaling that the theory of intelligent design has generated worldwide interest.
But what is this theory of intelligent design, and where did it come from? And why does it arouse such passion and inspire such apparently determined efforts to suppress it?
According to a spate of recent media reports, intelligent design is a new “faith-based” alternative to evolution – one based on religion rather than scientific evidence. As the story goes, intelligent design is just biblical creationism repackaged by religious fundamentalists in order to circumvent a 1987 United States Supreme Court prohibition against teaching creationism in the U.S. public schools. Over the past two years, major newspapers, magazines and broadcast outlets in the United States and around the world have repeated this trope.
But is it accurate? As one of the architects of the theory of intelligent design and the director of a research center that supports the work of scientists developing the theory, I know that it isn't.
The modern theory of intelligent design was not developed in response to a legal setback for creationists in 1987. Instead, it was first proposed in the late 1970s and early 1980s by a group of scientists – Charles Thaxton, Walter Bradley and Roger Olson – who were trying to account for an enduring mystery of modern biology: the origin of the digital information encoded along the spine of the DNA molecule. Thaxton and his colleagues came to the conclusion that the information-bearing properties of DNA provided strong evidence of a prior but unspecified designing intelligence. They wrote a book proposing this idea in 1984, three years before the U.S. Supreme Court decision (in Edwards v. Aguillard) that outlawed the teaching of creationism.
Earlier in the 1960s and 1970s, physicists had already begun to reconsider the design hypothesis. Many were impressed by the discovery that the laws and constants of physics are improbably “finely-tuned” to make life possible. As British astrophysicist Fred Hoyle put it, the fine-tuning of the laws and constants of physics suggested that a designing intelligence “had monkeyed with physics” for our benefit.
Contemporary scientific interest in the design hypothesis not only predates the U.S. Supreme Court ruling against creationism, but the formal theory of intelligent design is clearly different than creationism in both its method and content. The theory of intelligent design, unlike creationism, is not based upon the Bible. Instead, it is based on observations of nature which the theory attempts to explain based on what we know about the cause and effect structure of the world and the patterns that generally indicate intelligent causes. Intelligent design is an inference from empirical evidence, not a deduction from religious authority.
The propositional content of the theory of intelligent design also differs from that of creationism. Creationism or Creation Science, as defined by the U.S. Supreme Court, defends a particular reading of the book of Genesis in the Bible, typically one that asserts that the God of the Bible created the earth in six literal twenty-four hour periods a few thousand years ago. The theory of intelligent design does not offer an interpretation of the book of Genesis, nor does it posit a theory about the length of the Biblical days of creation or even the age of the earth. Instead, it posits a causal explanation for the observed complexity of life.
But if the theory of intelligent design is not creationism, what is it? Intelligent design is an evidence-based scientific theory about life's origins that challenges strictly materialistic views of evolution. According to Darwinian biologists such as Oxford's Richard Dawkins (1986: 1), livings systems “give the appearance of having been designed for a purpose.” But, for modern Darwinists, that appearance of design is entirely illusory. Why? According to neo-Darwinism, wholly undirected processes such as natural selection and random mutations are fully capable of producing the intricate designed-like structures in living systems. In their view, natural selection can mimic the powers of a designing intelligence without itself being directed by an intelligence of any kind.
In contrast, the theory of intelligent design holds that there are tell-tale features of living systems and the universe – for example, the information-bearing properties of DNA, the miniature circuits and machines in cells and the fine tuning of the laws and constants of physics – that are best explained by an intelligent cause rather than an undirected material process. The theory does not challenge the idea of “evolution” defined as either change over time or common ancestry, but it does dispute Darwin's idea that the cause of biological change is wholly blind and undirected. Either life arose as the result of purely undirected material processes or a guiding intelligence played a role. Design theorists affirm the latter option and argue that living organisms look designed because they really were designed.
A Brief History of the Design Argument
By making a case for design based on observations of natural phenomena, advocates of the contemporary theory of intelligent design have resuscitated the classical design argument. Prior to the publication of The Origin of Species by Charles Darwin in 1859, many Western thinkers, for over two thousand years, had answered the question “how did life arise?” by invoking the activity of a purposeful designer. Design arguments based on observations of the natural world were made by Greek and Roman philosophers such as Plato (1960: 279) and Cicero (1933: 217), by Jewish philosophers such as Maimonides and by Christian thinkers such as Thomas Aquinas1 (see Hick 1970: 1).
The idea of design also figured centrally in the modern scientific revolution (1500-1700). As historians of science (see Gillespie 1987: 1-49) have often pointed out, many of the founders of early modern science assumed that the natural world was intelligible precisely because they also assumed that it had been designed by a rational mind. In addition, many individual scientists – Johannes Kepler in astronomy (see Kepler 1981: 93-103; Kepler 1995: 170, 240),2 John Ray in biology (see Ray 1701) and Robert Boyle in chemistry (see Boyle 1979: 172) – made specific design arguments based upon empirical discoveries in their respective fields. This tradition attained an almost majestic rhetorical quality in the writing of Sir Isaac Newton, who made both elegant and sophisticated design arguments based upon biological, physical and astronomical discoveries. Writing in the General Scholium to the Principia, Newton (1934: 543-44) suggested that the stability of the planetary system depended not only upon the regular action of universal gravitation, but also upon the very precise initial positioning of the planets and comets in relation to the sun. As he explained:
[T]hough these bodies may, indeed, continue in their orbits by the mere laws of gravity, yet they could by no means have at first derived the regular position of the orbits themselves from those laws [...] [Thus] [t]his most beautiful system of the sun, planets and comets, could only proceed from the counsel and dominion of an intelligent and powerful Being.
Or as he wrote in the Opticks:
How came the Bodies of Animals to be contrived with so much Art, and for what ends were their several parts? Was the Eye contrived without Skill in Opticks, and the Ear without Knowledge of Sounds? [...] And these things being rightly dispatch’d, does it not appear from Phænomena that there is a Being incorporeal, living, intelligent, omnipresent [...]. (Newton 1952: 369-70.)
Scientists continued to make such design arguments well into the early nineteenth century, especially in biology. By the later part of the 18th century, however, some enlightenment philosophers began to express skepticism about the design argument. In particular, David Hume, in his Dialogues Concerning Natural Religion (1779), argued that the design argument depended upon a flawed analogy with human artifacts. He admitted that artifacts derive from intelligent artificers, and that biological organisms have certain similarities to complex human artifacts. Eyes and pocket watches both depend upon the functional integration of many separate and specifically configured parts. Nevertheless, he argued, biological organisms also differ from human artifacts – they reproduce themselves, for example – and the advocates of the design argument fail to take these dissimilarities into account. Since experience teaches that organisms always come from other organisms, Hume argued that analogical argument really ought to suggest that organisms ultimately come from some primeval organism (perhaps a giant spider or vegetable), not a transcendent mind or spirit.
Despite this and other objections, Hume’s categorical rejection of the design argument did not prove entirely decisive with either theistic or secular philosophers. Thinkers as diverse as the Scottish Presbyterian Thomas Reid (1981: 59), the Enlightenment deist Thomas Paine (1925: 6) and the rationalist philosopher Immanuel Kant, continued to affirm3 various versions of the design argument after the publication of Hume’s Dialogues. Moreover, with the publication of William Paley’s Natural Theology, science-based design arguments would achieve new popularity, both in Britain and on the continent. Paley (1852: 8-9) catalogued a host of biological systems that suggested the work of a superintending intelligence. Paley argued that the astonishing complexity and superb adaptation of means to ends in such systems could not originate strictly through the blind forces of nature, any more than could a complex machine such as a pocket watch. Paley also responded directly to Hume’s claim that the design inference rested upon a faulty analogy. A watch that could reproduce itself, he argued, would constitute an even more marvelous effect than one that could not. Thus, for Paley, the differences between artifacts and organisms only seemed to strengthen the conclusion of design. And indeed, despite the widespread currency of Hume’s objections, many scientists continued to find Paley’s watch-to-watchmaker reasoning compelling well into 19th century.
Darwin and the Eclipse of Design
Acceptance of the design argument began to abate during the late 19th century with the emergence of increasingly powerful materialistic explanations of apparent design in biology, particularly Charles Darwin’s theory of evolution by natural selection. Darwin argued in 1859 that living organisms only appeared to be designed. To make this case, he proposed a concrete mechanism, natural selection acting on random variations, that could explain the adaptation of organisms to their environment (and other evidences of apparent design) without actually invoking an intelligent or directing agency. Darwin saw that natural forces would accomplish the work of a human breeder and thus that blind nature could come to mimic, over time, the action of a selecting intelligence – a designer. If the origin of biological organisms could be explained naturalistically,4 as Darwin (1964: 481-82) argued, then explanations invoking an intelligent designer were unnecessary and even vacuous.
Thus, it was not ultimately the arguments of the philosophers that destroyed the popularity of the design argument, but a scientific theory of biological origins. This trend was reinforced by the emergence of other fully naturalistic origins scenarios in astronomy, cosmology and geology. It was also reinforced (and enabled) by an emerging positivistic tradition in science that increasingly sought to exclude appeals to supernatural or intelligent causes from science by definition (see Gillespie 1979: 41-66, 82-108 for a discussion of this methodological shift). Natural theologians such as Robert Chambers, Richard Owen and Asa Gray, writing just prior to Darwin, tended to oblige this convention by locating design in the workings of natural law rather than in the complex structure or function of particular objects. While this move certainly made the natural theological tradition more acceptable to shifting methodological canons in science, it also gradually emptied it of any distinctive empirical content, leaving it vulnerable to charges of subjectivism and vacuousness. By locating design more in natural law and less in complex contrivances that could be understood by direct comparison to human creativity, later British natural theologians ultimately made their research program indistinguishable from the positivistic and fully naturalistic science of the Darwinians (Dembski 1996). As a result, the notion of design, to the extent it maintained any intellectual currency, soon became relegated to a matter of subjective belief. One could still believe that a mind superintended over the regular law-like workings of nature, but one might just as well assert that nature and its laws existed on their own. Thus, by the end of the nineteenth century, natural theologians could no longer point to any specific artifact of nature that required intelligence as a necessary explanation. As a result, intelligent design became undetectable except “through the eyes of faith.”
Though the design argument in biology went into retreat after the publication of The Origin, it never quite disappeared. Darwin was challenged by several leading scientists of his day, most forcefully by the great Harvard naturalist Louis Agassiz, who argued that the sudden appearance of the first complex animal forms in the Cambrian fossil record pointed to “an intellectual power” and attested to “acts of mind.” Similarly, the co-founder of the theory of evolution by natural selection, Alfred Russel Wallace (1991: 33-34), argued that some things in biology were better explained by reference to the work of a “Higher intelligence” than by reference to Darwinian evolution. There seemed to him “to be evidence of a Power” guiding the laws of organic development “in definite directions and for special ends.” As he put it, “[S]o far from this view being out of harmony with the teachings of science, it has a striking analogy with what is now taking place in the world.” And in 1897, Oxford scholar F.C.S. Schiller argued that “it will not be possible to rule out the supposition that the process of Evolution may be guided by an intelligent design” (Schiller 1903: 141).
This continued interest in the design hypothesis was made possible in part because the mechanism of natural selection had a mixed reception in the immediate post-Darwinian period. As the historian of biology Peter Bowler (1986: 44-50) has noted, classical Darwinism entered a period of eclipse during the late 19th and early 20th centuries mainly because Darwin lacked an adequate theory for the origin and transmission of new heritable variation. Natural selection, as Darwin well understood, could accomplish nothing without a steady supply of genetic variation, the ultimate source of new biological structure. Nevertheless, both the blending theory of inheritance that Darwin had assumed and the classical Mendelian genetics that soon replaced it, implied limitations on the amount of genetic variability available to natural selection. This in turn implied limits on the amount of novel structure that natural selection could produce.
By the late 1930s and 1940s, however, natural selection was revived as the main engine of evolutionary change as developments in a number of fields helped to clarify the nature of genetic variation. The resuscitation of the variation / natural selection mechanism by modern genetics and population genetics became known as the neo-Darwinian synthesis. According to the new synthetic theory of evolution, the mechanism of natural selection acting upon random variations (especially including small-scale mutations) sufficed to account for the origin of novel biological forms and structures. Small-scale “microevolutionary” changes could be extrapolated indefinitely to account for large-scale “macroevolutionary” development. With the revival of natural selection, the neo-Darwinists would assert, like Darwinists before them, that they had found a “designer substitute” that could explain the appearance of design in biology as the result of an entirely undirected natural process.5 As Harvard evolutionary biologist Ernst Mayr (1982: xi-xii) has explained, “[T]he real core of Darwinism [...] is the theory of natural selection. This theory is so important for the Darwinian because it permits the explanation of adaptation, the ‘design’ of the natural theologian, by natural means.” By the centennial celebration of Darwin’s Origin of Species in 1959, it was assumed by many scientists that natural selection could fully explain the appearance of design and that, consequently, the design argument in biology was dead.
Problems with the Neo-Darwinian Synthesis
Since the late 1960s, however, the modern synthesis that emerged during the 1930s, 1940s and 1950s has begun to unravel in the face of new developments in paleontology, systematics, molecular biology, genetics and developmental biology. Since then a series of technical articles and books – including such recent titles as Evolution: a Theory in Crisis (1986) by Michael Denton, Darwinism: The Refutation of a Myth (1987) by Soren Lovtrup, The Origins of Order (1993) by Stuart A. Kauffman, How The Leopard Changed Its Spots (1994) by Brian C. Goodwin, Reinventing Darwin (1995) by Niles Eldredge, The Shape of Life (1996) by Rudolf A. Raff, Darwin’s Black Box (1996) by Michael Behe, The Origin of Animal Body Plans (1997) by Wallace Arthur, Sudden Origins: Fossils, Genes, and the Emergence of Species (1999) by Jeffrey H. Schwartz – have cast doubt on the creative power of neo-Darwinism’s mutation/selection mechanism. As a result, a search for alternative naturalistic mechanisms of innovation has ensued with, as yet, no apparent success or consensus. So common are doubts about the creative capacity of the selection / mutation mechanism, neo-Darwinism’s “designer substitute,” that prominent spokesmen for evolutionary theory must now periodically assure the public that “just because we don’t know how evolution occurred, does not justify doubt about whether it occurred.”6 As Niles Eldredge (1982: 508-9) wrote, “Most observers see the current situation in evolutionary theory – where the object is to explain how, not if, life evolves – as bordering on total chaos.” Or as Stephen Gould (1980: 119-20) wrote, “The neoDarwinism synthesis is effectively dead, despite its continued presence as textbook orthodoxy.” (See also Müller and Newman 2003: 3-12.)
Soon after Gould and Eldredge acknowledged these difficulties, the first important books (Thaxton, et al. 1984; Denton 1985) advocating the idea of intelligent design as an alternative to neo-Darwinism began to appear in the United States and Britain.7 But the scientific antecedents of the modern theory of intelligent design can be traced back to the beginning of the molecular biological revolution. In 1953 when Watson and Crick elucidated the structure of the DNA molecule, they made a startling discovery. The structure of DNA allows it to store information in the form of a four-character digital code. (See Figure 1). Strings of precisely sequenced chemicals called nucleotide bases store and transmit the assembly instructions – the information – for building the crucial protein molecules and machines the cell needs to survive.
Francis Crick later developed this idea with his famous "sequence hypothesis" according to which the chemical constituents in DNA function like letters in a written language or symbols in a computer code. Just as English letters may convey a particular message depending on their arrangement, so too do certain sequences of chemical bases along the spine of a DNA molecule convey precise instructions for building proteins. The arrangement of the chemical characters determines the function of the sequence as a whole. Thus, the DNA molecule has the same property of “sequence specificity” or “specified complexity” that characterizes codes and language. As Richard Dawkins has acknowledged, “the machine code of the genes is uncannily computer-like” (Dawkins 1995: 11). As Bill Gates has noted, “DNA is like a computer program but far, far more advanced than any software ever created” (Gates 1995:188). After the early 1960s, further discoveries made clear that the digital information in DNA and RNA is only part of a complex information processing system – an advanced form of nanotechnology that both mirrors and exceeds our own in its complexity, design logic and information storage density.
Thus, even as the design argument was being declared dead at the Darwinian centennial at the close of the 1950s, evidence that many scientists would later see as pointing to design was being uncovered in the nascent discipline of molecular biology. In any case, discoveries in this field would soon generate a growing rumble of voices dissenting from neo-Darwinism. In By Design, a history of the current design controversy, journalist Larry Witham (2003) traces the immediate roots of the theory of intelligent design in biology to the 1960s, at which time developments in molecular biology were generating new problems for the neo-Darwinian synthesis. At this time, mathematicians, engineers and physicists were beginning to express doubts that random mutations could generate the genetic information needed to produce crucial evolutionary transitions in the time available to the evolutionary process. Among the most prominent of these skeptical scientists were several from the Massachusetts Institute of Technology.
These researchers might have gone on talking among themselves about their doubts but for an informal gathering of mathematicians and biologists in Geneva in the mid-1960s at the home of MIT physicist Victor Weisskopf. During a picnic lunch the discussion turned to evolution, and the mathematicians expressed surprise at the biologists’ confidence in the power of mutations to assemble the genetic information necessary to evolutionary innovation. Nothing was resolved during the argument that ensued, but those present found the discussion stimulating enough that they set about organizing a conference to probe the issue further. This gathering occurred at the Wistar Institute in Philadelphia in the spring of 1966 and was chaired by Sir Peter Medawar, Nobel Laureate and director of North London’s Medical Research Council's laboratories. In his opening remarks at the meeting, he said that the “immediate cause of this conference is a pretty widespread sense of dissatisfaction about what has come to be thought of as the accepted evolutionary theory in the English-speaking world, the so-called neo-Darwinian theory” (Taylor 1983: 4).
The mathematicians were now in the spotlight and they took the opportunity to argue that neo-Darwinism faced a formidable combinatorial problem (see Moorhead and Kaplan 1967 for the seminar proceedings).8 In their view, the ratio of the number of functional genes and proteins, on the one hand, to the enormous number of possible sequences corresponding to a gene or protein of a given length, on the other, seemed so small as to preclude the origin of genetic information by a random mutational search. A protein one hundred amino acids in length represents an extremely unlikely occurrence. There are roughly 10130 possible amino acid sequences of this length, if one considers only the 20 protein-forming acids as possibilities. The vast majority of these sequences – it was (correctly) assumed – perform no biological function (see Axe 2004: 1295-1314 for a rigorous experimental evaluation of the rarity of functional proteins within the “sequence space” of possible combinations). Would an undirected search through this enormous space of possible sequences have a realistic chance of finding a functional sequence in the time allotted for crucial evolutionary transitions? To many of the Wistar mathematicians and physicists, the answer seemed clearly ‘no.’ Distinguished French mathematician M. P. Schützenberger (1967: 73-5) noted that in human codes, randomness is never the friend of function, much less of progress. When we make changes randomly to computer programs, “we find that we have no chance (i.e. less than 1/101000) even to see what the modified program would compute: it just jams.” MIT’s Murray Eden illustrated with reference to an imaginary library evolving by random changes to a single phrase: “Begin with a meaningful phrase, retype it with a few mistakes, make it longer by adding letters, and rearrange subsequences in the string of letters; then examine the result to see if the new phrase is meaningful. Repeat until the library is complete” (Eden 1967: 110). Would such an exercise have a realistic chance of succeeding, even granting it billions of years? At Wistar, the mathematicians, physicists and engineers argued that it would not. And they insisted that a similar problem confronts any mechanism that relies on random mutations to search large combinatorial spaces for sequences capable of performing novel function – even if, as is the case in biology, some mechanism of selection can act after the fact to preserve functional sequences once they have arisen.
Just as the mathematicians at Wistar were casting doubt on the idea that chance (i.e., random mutations) could generate genetic information, another leading scientist was raising questions about the role of law-like necessity. In 1967 and 1968, the Hungarian chemist and philosopher of science Michael Polanyi published two articles suggesting that the information in DNA was “irreducible” to the laws of physics and chemistry (Polanyi 1967: 21; Polanyi 1968: 1308-12). In these papers, Polanyi noted that the DNA conveys information in virtue of very specific arrangements of the nucleotide bases (that is, the chemicals that function as alphabetic or digital characters) in the genetic text. Yet, Polanyi also noted the laws of physics and chemistry allow for a vast number of other possible arrangements of these same chemical constituents. Since chemical laws allow a vast number of possible arrangements of nucleotide bases, Polanyi reasoned that no specific arrangement was dictated or determined by those laws. Indeed, the chemical properties of the nucleotide bases allow them to attach themselves interchangeably at any site on the (sugar-phosphate) backbone of the DNA molecule. (See Figure 1). Thus, as Polanyi (1968: 1309) noted, “As the arrangement of a printed page is extraneous to the chemistry of the printed page, so is the base sequence in a DNA molecule extraneous to the chemical forces at work in the DNA molecule.” Polanyi argued that it is precisely this chemical indeterminacy that allows DNA to store information and which also shows the irreducibility of that information to physical-chemical laws or forces. As he explained:
Suppose that the actual structure of a DNA molecule were due to the fact that the bindings of its bases were much stronger than the bindings would be for any other distribution of bases, then such a DNA molecule would have no information content. Its code-like character would be effaced by an overwhelming redundancy. [...] Whatever may be the origin of a DNA configuration, it can function as a code only if its order is not due to the forces of potential energy. It must be as physically indeterminate as the sequence of words is on a printed page (Polanyi 1968:1309).
The Mystery of Life’s Origin
As more scientists began to express doubts about the ability of undirected processes to produce the genetic information necessary to living systems, some began to consider an alternative approach to the problem of the origin of biological form and information. In 1984, after seven years of writing and research, chemist Charles Thaxton, polymer scientist Walter Bradley and geochemist Roger Olsen published a book proposing “an intelligent cause” as an explanation for the origin of biological information. The book was titled The Mystery of Life’s Origin and was published by The Philosophical Library, then a prestigious New York scientific publisher that had previously published more than twenty Nobel laureates.
Thaxton, Bradley and Olsen’s work directly challenged reigning chemical evolutionary explanations of the origin-of-life, and old scientific paradigms do not, to borrow from a Dylan Thomas poem, “go gently into that good night.” Aware of the potential opposition to their ideas, Thaxton flew to California to meet with one of the world’s top chemical evolutionary theorists, San Francisco State University biophysicist Dean Kenyon, co-author of a leading monograph on the subject, Biochemical Predestination. Thaxton wanted to talk with Kenyon to ensure that Mystery’s critiques of leading origin-of-life theories (including Kenyon’s), were fair and accurate. But Thaxton also had a second and more audacious motive: he planned to ask Kenyon to write the foreword to the book, even though Mystery critiqued the very originof-life theory that had made Kenyon famous in his field.
One can imagine how such a meeting might have unfolded, with Thaxton’s bold plan quietly dying in a corner of Kenyon’s office as the two men came to loggerheads over their competing theories. But fortunately for Thaxton, things went better than expected. Before he had worked his way around to making his request, Kenyon volunteered for the job, explaining that he had been moving toward Thaxton’s position for some time (Charles Thaxton, interview by Jonathan Witt, August 16, 2005; Jon Buell, interview by Jonathan Witt, September 21, 2005).
Kenyon’s bestselling origin-of-life text, Biochemical Predestination, had outlined what was then arguably the most plausible evolutionary account of how a living cell might have organized itself from chemicals in the “primordial soup.” Already by the 1970s, however, Kenyon was questioning his own hypothesis. Experiments (some performed by Kenyon himself) increasingly suggested that simple chemicals do not arrange themselves into complex information-bearing molecules such as proteins and DNA without guidance from human investigators. Thaxton, Bradley and Olsen appealed to this fact in constructing their argument, and Kenyon found their case both well-reasoned and well-researched. In the foreword he went on to pen, he described The Mystery of Life’s Origin as “an extraordinary new analysis of an age-old question” (Kenyon 1984: v).
The book eventually became the best-selling advanced college-level work on chemical evolution, with sales fueled by endorsements from leading scientists such as Kenyon, Robert Shapiro and Robert Jastrow and by favorable reviews in prestigious journals such as the Yale Journal of Biology and Medicine.9 Others dismissed the work as going beyond science.
What was their idea, and why did it generate interest among leading scientists? First, Mystery critiqued all of the current, purely materialistic explanations for the origin of life. In the process, they showed that the famous Miller-Urey experiment did not simulate early Earth conditions, that the existence of an early Earth pre-biotic soup was a myth, that important chemical evolutionary transitions were subject to destructive interfering cross-reactions, and that neither chance nor energy-flow could account for the information in biopolymers such as proteins and DNA. But it was in the book’s epilogue that the three scientists proposed a radically new hypothesis. There they suggested that the information-bearing properties of DNA might point to an intelligent cause. Drawing on the work of Polanyi and others, they argued that chemistry and physics alone couldn’t produce information any more than ink and paper could produce the information in a book. Instead, they argued that our uniform experience suggests that information is the product of an intelligent cause:
We have observational evidence in the present that intelligent investigators can (and do) build contrivances to channel energy down nonrandom chemical pathways to bring about some complex chemical synthesis, even gene building. May not the principle of uniformity then be used in a broader frame of consideration to suggest that DNA had an intelligent cause at the beginning? (Thaxton et al. 1984: 211.)
Mystery also made the radical claim that intelligent causes could be legitimately considered as scientific hypotheses within the historical sciences, a mode of inquiry they called origins science.
Their book marked the beginning of interest in the theory of intelligent design in the United States, inspiring a generation of younger scholars (see Denton 1985; Denton 1986; Kenyon and Mills 1996: 9-16; Behe 2004: 352-370; Dembski 2002; Dembski 2004: 311-330; Morris 2000: 1-11; Morris 2003a: 13-32; Morris 2003b: 505-515; Lönnig 2001; Lönnig and Saedler 2002: 389-410; Nelson and Wells 2003: 303-322; Meyer 2003a: 223-285; Meyer 2003b: 371391; Bradley 2004: 331-351) to investigate the question of whether there is actual design in living organisms rather than, as neo-Darwinian biologists and chemical evolutionary theorists had long claimed, the mere appearance of design. At the time the book appeared, I was working as a geophysicist for the Atlantic Richfield Company in Dallas where Charles Thaxton happened to live. I later met him at a scientific conference and became intrigued with the radical idea he was developing about DNA. I began dropping by his office after work to discuss the arguments made in his book. Intrigued, but not yet fully convinced, the next year I left my job as a geophysicist to pursue a Ph.D. at The University of Cambridge in the history and philosophy of science. During my Ph.D. research, I investigated several questions that had emerged in my discussions with Thaxton. What methods do scientists use to study biological origins? Is there a distinctive method of historical scientific inquiry? After completing my Ph.D., I would take up another question: Could the argument from DNA to design be formulated as a rigorous historical scientific argument?
Of Clues and Causes
During my Ph.D. research at Cambridge, I found that historical sciences (such as geology, paleontology and archeology) do employ a distinctive method of inquiry. Whereas many scientific fields involve an attempt to discover universal laws, historical scientists attempt to infer past causes from present effects. As Stephen Gould (1986: 61) put it, historical scientists are trying to “infer history from its results.” Visit the Royal Tyrrell Museum in Alberta, Canada and you will find there a beautiful reconstruction of the Cambrian seafloor with its stunning assemblage of phyla. Or read the fourth chapter of Simon Conway Morris’s book on the Burgess Shale and you will be taken on a vivid guided tour of that long-ago place. But what Morris (1998: 63-115) and the museum scientists did in both cases was to imaginatively reconstruct the ancient Cambrian site from an assemblage of present-day fossils. In other words, paleontologists infer a past situation or cause from present clues.
A key figure in elucidating the special nature of this mode of reasoning was a contemporary of Darwin, polymath William Whewell, master of Trinity College, Cambridge and best known for two books about the nature of science, History of the Inductive Sciences (1837) and The Philosophy of the Inductive Sciences (1840). Whewell distinguished inductive sciences like mechanics (physics) from what he called palaetiology – historical sciences that are defined by three distinguishing features. First, the palaetiological or historical sciences have a distinctive object: to determine “ancient condition[s]” (Whewell 1857, vol. 3: 397) or past causal events. Second, palaetiological sciences explain present events (“manifest effects”) by reference to past (causal) events rather than by reference to general laws (though laws sometimes play a subsidiary role). And third, in identifying a “more ancient condition,” Whewell believed palaetiology utilized a distinctive mode of reasoning in which past conditions were inferred from "manifest effects" using generalizations linking present clues with past causes (Whewell 1840, vol. 2: 121-22, 101-103).
Inference to the Best Explanation
This type of inference is called abductive reasoning. It was first described by the American philosopher and logician C.S. Peirce. He noted that, unlike inductive reasoning, in which a universal law or principle is established from repeated observations of the same phenomena, and unlike deductive reasoning, in which a particular fact is deduced by applying a general law or rule to another particular fact or case, abductive reasoning infers unseen facts, events or causes in the past from clues or facts in the present.
As Peirce himself showed, however, there is a problem with abductive reasoning. Consider the following syllogism:
If it rains, the streets will get wet.
The streets are wet.
Therefore, it rained.
This syllogism infers a past condition (i.e., that it rained) but it commits a logical fallacy known as affirming the consequent. Given that the street is wet (and without additional evidence to decide the matter), one can only conclude that perhaps it rained. Why? Because there are many other possible ways by which the street may have gotten wet. Rain may have caused the streets to get wet; a street cleaning machine might have caused them to get wet; or an uncapped fire hydrant might have done so. It can be difficult to infer the past from the present because there are many possible causes of a given effect.
Peirce’s question was this: how is it that, despite the logical problem of affirming the consequent, we nevertheless frequently make reliable abductive inferences about the past? He noted, for example, that no one doubts the existence of Napoleon. Yet we use abductive reasoning to infer Napoleon’s existence. That is, we must infer his past existence from present effects. But despite our dependence on abductive reasoning to make this inference, no sane or educated person would doubt that Napoleon Bonaparte actually lived. How could this be if the problem of affirming the consequent bedevils our attempts to reason abductively? Peirce’s answer was revealing: "Though we have not seen the man [Napoleon], yet we cannot explain what we have seen without" the hypothesis of his existence (Peirce, 1932, vol. 2: 375). Peirce's words imply that a particular abductive hypothesis can be strengthened if it can be shown to explain a result in a way that other hypotheses do not, and that it can be reasonably believed (in practice) if it explains in a way that no other hypotheses do. In other words, an abductive inference can be enhanced if it can be shown that it represents the best or the only adequate explanation of the "manifest effects" (to use Whewell's term).
As Peirce pointed out, the problem with abductive reasoning is that there is often more than one cause that can explain the same effect. To address this problem, pioneering geologist Thomas Chamberlain (1965: 754-59) delineated a method of reasoning that he called “the method of multiple working hypotheses.” Geologists and other historical scientists use this method when there is more than one possible cause or hypothesis to explain the same evidence. In such cases, historical scientists carefully weigh the evidence and what they know about various possible causes to determine which best explains the clues before them. In modern times, contemporary philosophers of science have called this the method of inference to the best explanation. That is, when trying to explain the origin of an event or structure in the past, historical scientists compare various hypotheses to see which would, if true, best explain it. They then provisionally affirm that hypothesis that best explains the data as the most likely to be true.
Causes Now in Operation
But what constitutes the best explanation for the historical scientist? My research showed that among historical scientists it’s generally agreed that best doesn’t mean ideologically satisfying or mainstream; instead, best generally has been taken to mean, first and foremost, most causally adequate. In other words, historical scientists try to identify causes that are known to produce the effect in question. In making such determinations, historical scientists evaluate hypotheses against their present knowledge of cause and effect; causes that are known to produce the effect in question are judged to be better causes than those that are not. For instance, a volcanic eruption is a better explanation for an ash layer in the earth than an earthquake because eruptions have been observed to produce ash layers, whereas earthquakes have not.
This brings us to the great geologist Charles Lyell, a figure who exerted a tremendous influence on 19th century historical science generally and on Charles Darwin specifically. Darwin read Lyell’s magnum opus, The Principles of Geology, on the voyage of the Beagle and later appealed to its uniformitarian principles to argue that observed micro-evolutionary processes of change could be used to explain the origin of new forms of life. The subtitle of Lyell’s Principles summarized the geologist’s central methodological principle: “Being an Attempt to Explain the Former Changes of the Earth's Surface, by Reference to Causes now in Operation.” Lyell argued that when historical scientists are seeking to explain events in the past, they should not invoke unknown or exotic causes, the effects of which we do not know, but instead they should cite causes that are known from our uniform experience to have the power to produce the effect in question (i.e., “causes now in operation”).
Darwin subscribed to this methodological principle. His term for a “presently acting cause” was a vera causa, that is, a true or actual cause. In other words, when explaining the past, historical scientists should seek to identify established causes – causes known to produce the effect in question. For example, Darwin tried to show that the process of descent with modification was the vera causa of certain kinds of patterns found among living organisms. He noted that diverse organisms share many common features. He called these homologies and noted that we know from experience that descendents, although they differ from their ancestors, also resemble them in many ways, usually more closely than others who are more distantly related. So he proposed descent with modification as a vera causa for homologous structures. That is, he argued that our uniform experience shows that the process of descent with modification from a common ancestor is “causally adequate” or capable of producing homologous features.
And Then There Was One
Contemporary philosophers agree that causal adequacy is the key criteria by which competing hypotheses are adjudicated, but they also show that this process leads to secure inferences only where it can be shown that there is just one known cause for the evidence in question. Philosophers of science Michael Scriven and Elliot Sober, for example, point out that historical scientists can make inferences about the past with confidence when they discover evidence or artifacts for which there is only one cause known to be capable of producing them. When historical scientists infer to a uniquely plausible cause, they avoid the fallacy of affirming the consequent and the error of ignoring other possible causes with the power to produce the same effect. It follows that the process of determining the best explanation often involves generating a list of possible hypotheses, comparing their known or theoretically plausible causal powers with respect to the relevant data, and then like a detective attempting to identify the murderer, progressively eliminating potential but inadequate explanations until, finally, one remaining causally adequate explanation can be identified as the best. As Scriven (1966: 250) explains, such abductive reasoning (or what he calls “Reconstructive causal analysis”) “proceeds by the elimination of possible causes,” a process that is essential if historical scientists are to overcome the logical limitations of abductive reasoning.
The matter can be framed in terms of formal logic. As C.S. Peirce noted, arguments of the form:
if X, then Y
commit the fallacy of affirming the consequent. Nevertheless, as Michael Scriven (1959: 480), Elliot Sober (1988: 1-5), W.P. Alston (1971: 23) and W.B. Gallie (1959: 392) have observed, such arguments can be restated in a logically acceptable form if it can be shown that Y has only one known cause (i.e., X) or that X is a necessary condition (or cause) of Y. Thus, arguments of the form:
X is antecedently necessary to Y,
Therefore, X existed
are accepted as logically valid by philosophers and persuasive by historical and forensic scientists. Scriven especially emphasized this point: if scientists can discover an effect for which there is only one plausible cause, they can infer the presence or action of that cause in the past with great confidence. For instance, the archaeologist who knows that human scribes are the only known cause of linguistic inscriptions will infer scribal activity upon discovering tablets containing ancient writing.
In many cases, of course, the investigator will have to work his way to a unique cause one painstaking step at a time. For instance, both wind shear and compressor blade failure could explain an airline crash, but the forensic investigator will want to know which one did, or if the true cause lies elsewhere. Ideally, the investigator will be able to discover some crucial piece of evidence or suite of evidences for which there is only one known cause, allowing him to distinguish between competing explanations and eliminate every explanation but the correct one.
In my study of the methods of the historical sciences, I found that historical scientists, like detectives and forensic experts, routinely employ this type of abductive and eliminative reasoning in their attempts to infer the best explanation.10 In fact, Darwin himself employed this method in The Origin of Species. There he argued for his theory of Universal Common Descent, not because it could predict future outcomes under controlled experimental conditions, but because it could explain already known facts better than rival hypotheses. As he explained in a letter to Asa Gray:
I [...] test this hypothesis [Universal Common Descent] by comparison with as many general and pretty well-established propositions as I can find – in geographical distribution, geological history, affinities &c., &c. And it seems to me that, supposing that such a hypothesis were to explain such general propositions, we ought, in accordance with the common way of following all sciences, to admit it till some better hypothesis be found out. (Darwin 1896, vol. 1: 437.)
DNA by Design: Developing the Argument from Information
What does this investigation into the nature of historical scientific reasoning have to do with intelligent design, the origin of biological information and the mystery of life’s origin? For me, it was critically important to deciding whether the design hypothesis could be formulated as a rigorous scientific explanation as opposed to just an intriguing intuition. I knew from my study of origin-of-life research that the central question facing scientists trying to explain the origin of the first life was this: how did the sequence-specific digital information (stored in DNA and RNA) necessary to building the first cell arise? As Bernd-Olaf Küppers (1990: 170-172) put it, “the problem of the origin of life is clearly basically the equivalent to the problem of the origin of biological information.” My study of the methodology of the historical sciences then led me to ask a series of questions: What is the presently acting cause of the origin of digital information? What is the vera causa of such information? Or: what is the “only known cause” of this effect? Whether I used Lyell’s, Darwin’s or Scriven’s terminology, the question was the same: what type of cause has demonstrated the power to generate information? Based upon both common experience and my knowledge of the many failed attempts to solve the problem with “unguided” pre-biotic simulation experiments and computer simulations, I concluded that there is only one sufficient or “presently acting” cause of the origin of such functionally-specified information. And that cause is intelligence. In other words, I concluded, based on our experience-based understanding of the cause-and-effect structure of the world, that intelligent design is the best explanation for the origin of the information necessary to build the first cell. Ironically, I discovered that if one applies Lyell’s uniformitarian method – a practice much maligned by young earth creationists – to the question of the origin of biological information, the evidence from molecular biology supports a new and rigorous scientific argument to design.
What is Information?
In order to develop this argument and avoid equivocation, it was necessary to carefully define what type of information was present in the cell (and what type of information might, based upon our uniform experience, indicate the prior action of a designing intelligence). Indeed, part of the historical scientific method of reasoning involves first defining what philosophers of science call the explanandum – the entity that needs to be explained. As the historian of biology Harmke Kamminga (1986: 1) has observed, “At the heart of the problem of the origin of life lies a fundamental question: What is it exactly that we are trying to explain the origin of?” Contemporary biology had shown that the cell was, among other things, a repository of information. For this reason, origin-of-life studies had focused increasingly on trying to explain the origin of that information. But what kind of information is present in the cell? This was an important question to answer because the term “information” can be used to denote several theoretically distinct concepts.
In developing a case for design from the information-bearing properties of DNA, it was necessary to distinguish two key notions of information from one another: mere information carrying capacity, on the one hand, and functionally-specified information, on the other. It was important to make this distinction because the kind of information that is present in DNA (like the information present in machine code or written language) has a feature that the wellknown Shannon theory of information does not encompass or describe.
During the 1940s, Claude Shannon at Bell Laboratories developed a mathematical theory of information (1948: 379–423, 623–56) that equated the amount of information transmitted with the amount of uncertainty reduced or eliminated by a series of symbols or characters (Dretske, 1981: 6–10). In Shannon’s theory, the more improbable an event the more uncertainty it eliminates, and thus, the more information it conveys. Shannon generalized this relationship by stating that the amount of information conveyed by an event is inversely proportional to the prior probability of its occurrence. The greater the number of possibilities, the greater the improbability of any one being actualized, and thus the more information is transmitted when a particular possibility occurs.11
Shannon’s theory applies easily to sequences of alphabetic symbols or characters that function as such. Within a given alphabet of x possible characters, the occurrence or placement of a specific character eliminates x-1 other possibilities and thus a corresponding amount of uncertainty. Or put differently, within any given alphabet or ensemble of x possible characters (where each character has an equi-probable chance of occurring), the probability of any one character occurring is 1/x. In systems where the value of x can be known (or estimated), as in a code or language, mathematicians can easily generate quantitative estimates of informationcarrying capacity. The greater the number of possible characters at each site, and the longer the sequence of characters, the greater is the information-carrying capacity – or Shannon information – associated with the sequence.
The way that nucleotide bases in DNA function as alphabetic or digital characters enabled molecular biologists to calculate the information-carrying capacity of those molecules using the new formalism of Shannon’s theory. Since at any given site along the DNA backbone any one of four nucleotide bases may occur with equal probability (Küppers, 1987: 355-369), the probability of the occurrence of a specific nucleotide at that site equals 1/4 or .25. The information-carrying capacity of a sequence of a specific length n can then be calculated using
Shannon’s familiar expression (I = –log2p) once one computes a probability value (p) for the occurrence of a particular sequence n nucleotides long where p = (1/4)n. The probability value thus yields a corresponding measure of information-carrying capacity for a sequence of n nucleotide bases (Schneider 1997: 427-441; Yockey 1992: 246-258).
Though Shannon’s theory and equations provided a powerful way to measure the amount of information that could be transmitted across a communication channel, it had important limits. In particular, it did not and could not distinguish merely improbable (or complex) sequences of symbols from those that conveyed a message or performed a function. As Warren Weaver made clear in 1949, “The word information in this theory is used in a special mathematical sense that must not be confused with its ordinary usage. In particular, information must not be confused with meaning.” (Shannon and Weaver 1949: 8.) Information theory could measure the information-carrying capacity of a given sequence of symbols, but it could not distinguish the presence of a meaningful or functional arrangement of symbols from a random sequence.
As scientists applied Shannon information theory to biology it enabled them to render rough quantitative measures of the information-carrying capacity (or brute complexity or improbability) of DNA sequences and their corresponding proteins. As such, information theory did help to refine biologists’ understanding of one important feature of the crucial biomolecular components on which life depends: DNA and proteins are highly complex, and quantifiably so. Nevertheless, the ease with which information theory applied to molecular biology (to measure information-carrying capacity) created confusion about the sense in which DNA and proteins contain “information.”
Information theory strongly suggested that DNA and proteins possess vast informationcarrying capacities, as defined by Shannon’s theory. When molecular biologists have described DNA as the carrier of hereditary information, however, they have meant much more than that technically limited term information. Instead, leading molecular biologists defined biological information so as to incorporate the notion of specificity of function (as well as complexity) as early as 1958 (Crick, 1958: 144, 153). Molecular biologists such as Monod and Crick understood biological information – the information stored in DNA and proteins – as something more than mere complexity (or improbability). Crick and Monod also recognized that sequences of nucleotides and amino acids in functioning bio-macromolecules possessed a high degree of specificity relative to the maintenance of cellular function. As Crick explained in 1958, “By information I mean the specification of the amino acid sequence in protein [...] Information means here the precise determination of sequence, either of bases in the nucleic acid or on amino acid residues in the protein (1958: 144, 153).”
Since the late 1950s, biologists have equated the “precise determination of sequence” with the extra-information-theoretic property of “specificity” or “specification.” Biologists have defined specificity tacitly as ‘necessary to achieving or maintaining function.’ They have determined that DNA base sequences are specified, not by applying information theory, but by making experimental assessments of the function of those sequences within the overall apparatus of gene expression (Judson,1979: 470-487). Similar experimental considerations established the functional specificity of proteins.
In developing an argument for intelligent design based upon the information present in DNA and other bio-macromolecules, I emphasized that the information in these molecules was functionally-specified and complex, not just complex. Indeed, to avoid equivocation, it was necessary to distinguish:
“information content” from mere “information carrying capacity,”
“specified information” from mere “Shannon information”
“specified complexity” from mere “complexity.”
The first of the two terms in each of these couplets refer to sequences in which the function of the sequence depends upon the precise sequential arrangements of the constituent characters or parts, whereas second terms refer to sequences that do not necessarily perform functions or convey meaning at all. The second terms refer to sequences that may be merely improbable or complex; the first terms refer to sequences that are both complex and functionallyspecified.
In developing an argument for intelligent design from the information-bearing properties of DNA, I acknowledged that merely complex or improbable phenomena or sequences might arise by undirected natural processes. Nevertheless, I argued – based upon our uniform experience – that sequences that are both complex and functionally-specified (rich in information content or specified information) invariably arise only from the activity of intelligent agents. Thus, I argued that the presence of specified information provides a hallmark or signature of a designing intelligence. In making these analytical distinctions in order to apply them to an analysis of biological systems, I was greatly assisted in my conversations and collaboration with William Dembski who was at the same time (1992-1997) developing a general theory of design detection which I discuss in detail below.
In the years that followed, I published a series of papers (see Meyer 1998a: 519-56; Meyer 1998b, 117-143; Meyer 2000a: 30-38; Meyer 2003a: 225-285) arguing that intelligent design provides a better explanation than competing chemical evolutionary models for the origin of the biological information. To make this argument, I followed the standard method of historical scientific reasoning that I had studied in doctoral work. In particular, I evaluated the causal adequacy of various naturalistic explanations for the origin of biological information including those based on chance, law-like necessities and the combination of the two. In each case, I showed (or the scientific literature showed) that such naturalistic models failed to explain the origin of specified information (or specified complexity or information content) starting from purely physical / chemical antecedents. Instead, I argued, based on our experience, that there is a cause – namely, intelligence – that is known to be capable of producing such information. As the pioneering information theorist Henry Quastler (1964: 16) pointed out, “Information habitually arises from conscious activity.” Moreover, based upon our experience (and the findings of contemporary origin-of-life research) it is clear that intelligent design or agency is the only type of cause known to produce large amounts of specified information. Therefore, I argued that the theory of intelligent design provides the best explanation for the information necessary to build the first life.12
Darwin on Trial and Philip Johnson
While I was still studying historical scientific reasoning in Cambridge in 1987, I had a fateful meeting with a prominent University of California, Berkeley law professor named Phillip Johnson, whose growing interest in the subject of biological origins would transform the contours of the debate over evolution. Johnson and I met at a small Greek restaurant on Free School Lane next to the Old Cavendish Laboratory in Cambridge. The meeting had been arranged by a fellow graduate student who knew Johnson from Berkeley. My friend had told me only that Johnson was “a quirky but brilliant law professor” who “was on sabbatical studying torts,” and he “had become obsessed with evolution.” “Would you talk to him?” he asked. His description and the tone of his request led me to expect a very different figure than the one I encountered. Though my own skepticism about Darwinism had been well cemented by this time, I knew enough of the stereotypical evolution-basher to be skeptical that a late-in-career nonscientist could have stumbled onto an original critique of contemporary Darwinian theory.
Only later did I learn of Johnson’s intellectual pedigree: Harvard B.A., top of his class University of Chicago law-school graduate, law clerk for Supreme Court Chief Justice Earl Warren, leading constitutional scholar, occupant of a distinguished chair at University of California, Berkeley. In Johnson, I encountered a man of supple and prodigious intellect who seemed in short order to have found the pulse of the origins issue. Johnson told me that his doubts about Darwinism had started with a visit to the British Natural History Museum, where he learned about the controversy that had raged there earlier in the 1980s. At that time, the museum paleontologists presented a display describing Darwin’s theory as “one possible explanation” of origins. A furor ensued, resulting in the removal of the display when the editors of the prestigious journal Nature and others in the scientific establishment denounced the museum for its ambivalence about accepted fact. Intrigued by the response to such an apparently innocuous exhibit, Johnson decided to investigate further.
Soon thereafter, as Johnson was still casting about for a research topic early in his sabbatical year in London, he stepped off the bus and followed his usual route to his visiting faculty office. Along the way, he passed by a large science bookstore and, glancing in, noticed a pair of books about evolution, The Blind Watchmaker by Richard Dawkins and Evolution: A Theory in Crisis by Michael Denton. Historian of science Thomas Woodward recounts the episode:
His curiosity aroused, he entered the store, picked up copies of both books from a table near the door, and studied the dust jacket blurbs. The two biologists were apparently driving toward diametrically opposite conclusions. Sensing a delicious scientific dialectic, he bought both books and tucked them under his arm as he continued on to his office. (Woodward 2003: 69.)
The rest, as they say, is history. Johnson began to read whatever he could find on the issue: Gould, Ruse, Ridley, Dawkins, Denton and many others. What he read made him even more suspicious of evolutionary orthodoxy. “Something about the Darwinists’ rhetorical style,” he told me later, “made me think they had something to hide.”
An extensive examination of evolutionary literature confirmed this suspicion. Darwinist polemic revealed a surprising reliance upon arguments that seemed to assume rather than demonstrate the central claim of neo-Darwinism, namely, that life had evolved via a strictly undirected natural process. Johnson also observed an interesting contrast between biologists' technical papers and their popular defenses of evolutionary theory. He discovered that biologists acknowledged many significant difficulties with both standard and newer evolutionary models when writing in scientific journals. Yet, when defending basic Darwinist commitments (such as the common ancestry of all life and the creative power of the natural selection / mutation mechanism) in popular books or textbooks, Darwinists employed an evasive and moralizing rhetorical style to minimize problems and belittle critics. Johnson began to wonder why, given mounting difficulties, Darwinists remained so confident that all organisms had evolved naturally from simpler forms.
In the book Darwin on Trial, Johnson (1991) argued that evolutionary biologists remain confident about neo-Darwinism, not because empirical evidence generally supports the theory, but instead because their perception of the rules of scientific procedure virtually prevent them from considering any alternative view. Johnson cited, among other things, a communiqué from the National Academy of Sciences (NAS) issued to the Supreme Court during the Louisiana “creation science” trial. The NAS insisted that “the most basic characteristic of science” is a “reliance upon naturalistic explanations.”
While Johnson accepted this convention, called “methodological naturalism,” as an accurate description of how much of science operates, he argued that treating it as a normative rule when seeking to establish that natural processes alone produced life assumes the very point that neo-Darwinists are trying to establish. Johnson reminded readers that Darwinism does not just claim that evolution (in the sense of change over time) has occurred. Instead, it purports to establish that the major innovations in the history of life arose by purely natural mechanisms – that is, without any intelligent direction or design. Thus, Johnson distinguished the various meanings of the term “evolution” (such as change over time or common ancestry) from the central claim of Darwinism, namely, the claim that a purely undirected and unguided process had produced the appearance of design in living organisms. Following Richards Dawkins, the staunch modern defender of Darwinism, Johnson called this latter idea “the Blind Watchmaker thesis” to make clear that Darwinism as a theory is incompatible with the design hypothesis. In any case, he argued, modern Darwinists refuse to consider the possibility of design because they think the rules of science forbid it.
Yet if the design hypothesis must be denied consideration from the outset, and if, as the U.S. National Academy of Sciences also asserted, exclusively negative argumentation against evolutionary theory is “unscientific,” then Johnson (1991: 8) observed that “the rules of argument. [...] make it impossible to question whether what we are being told about evolution is really true.” Defining opposing positions out of existence “may be one way to win an argument,” but, said Johnson, it scarcely suffices to demonstrate the superiority of a protected theory.
When I first met Johnson at the aforementioned Greek restaurant it was not long after he had started his investigation of Darwinism. Nevertheless, we came to an immediate meeting of minds, albeit from different starting points. Johnson saw that, as matter of logic, the convention of methodological naturalism forced scientists into a question-begging affirmation of the proposition that life and humankind had arisen “by a purposeless and natural process that did not have him in mind,” as the neo-Darwinist George Gaylord Simpson (1967: 45) had phrased it. For my part, I had come to question methodological naturalism because it seemed to prevent historical scientists from considering all the possible hypotheses that might explain the evidence – despite a clear methodological desideratum to do otherwise. How could an historical scientist claim that he or she had inferred the best explanation if the causal adequacy of some hypotheses were arbitrarily excluded from consideration? For the method of multiple competing hypotheses to work, hypotheses must be allowed to compete without artificial restrictions on the competition.
In any case, when Darwin on Trial was published in 1991 it created a minor media sensation with magazines and newspapers all over America either reviewing the book or profiling the eccentric Berkeley professor who had dared to take on Darwin. Major science journals including Nature, Science and Scientific American also reviewed Darwin on Trial. The reviews, including one by Stephen J. Gould, were uniformly critical and even hostile. Yet these reviews helped publicize Johnson’s critique and attracted many scientists who shared Johnson’s skepticism about neo-Darwinism. This allowed Johnson to do something that, until that time, hadn’t been done: to bring together dissenting scientists from around the world.
Darwin’s Black Box and Michael Behe
One of those scientists, a tenured biochemist at Lehigh University, Michael Behe, had come to doubt Darwinian evolution in the same way that Johnson had – by reading Denton’s Evolution: A Theory in Crisis. Behe was a Roman Catholic and had been raised to accept Darwinism as the way God chose to create life. Thus, he had no theological objections to Darwinian evolution. For years he had accepted it without questioning. When he finished Denton’s book, he still had no theological objections to evolution, but he did have serious scientific doubts. He soon began to investigate what the evidence from his own field of biochemistry had to say about the plausibility of the neo-Darwinian mechanism. Although he saw no reason to doubt that natural selection could produce relatively minor biological changes, he became extremely skeptical that the Darwinian mechanism could produce the kind of functionally integrated complexity that characterizes the inner workings of the cell. Intelligent design, he concluded, must also have played a role.
As his interest grew, he began teaching a freshman course on the evolution controversy. Later in 1992, he wrote a letter to Science defending Johnson’s new book after it had been panned in the review that appeared there. When Johnson saw the letter in Science, he contacted Behe and eventually invited him to a symposium at Southern Methodist University in Texas, where Johnson debated the Darwinist philosopher of science Michael Ruse. The meeting was significant for two reasons. First, as Behe (2006: 37-47) explained, the scientists skeptical of Darwin who were present at the debate were able to experience what they already believed intellectually – they had strong arguments that could withstand high-level scrutiny from their peers. Second, at SMU, many of the leaders of the intelligent design research community would meet together for the first time in one place. Before, we had each been solitary skeptics, unsure of how to proceed against an entrenched scientific paradigm. Now we understood that we were part of an interdisciplinary intellectual community. After the symposium, Johnson arranged a larger meeting the following year for a core group of dissidents at Pajaro Dunes, California (shown in the film Unlocking the Mystery of Life). There we talked science and strategy and, at Johnson’s prompting, joined an e-mail listserv so that we would remain in contact and hone our ideas. At Pajaro Dunes, “the movement” congealed.
Behe, in particular, used the new listserv to test and refine the various arguments for a book he was working on. Within three years, Darwin’s Black Box appeared with The Free Press, a major New York trade publisher. The book went on to sell a quarter million copies.
In Darwin’s Black Box, Behe pointed out that over the last 30 years, biologists have discovered an exquisite world of nanotechnology within living cells – complex circuits, molecular motors and other miniature machines. For example, bacterial cells are propelled by tiny rotary engines called flagellar motors that rotate at speeds up to 100,000 rpm. These engines look as if they were designed by the Mazda corporation, with many distinct mechanical parts (made of proteins) including rotors, stators, O-rings, bushings, U-joints and drive shafts. (See Figure 2). Behe noted that the flagellar motor depends on the coordinated function of 30 protein parts. Remove one of these necessary proteins and the rotary motor simply doesn't work. The motor is, in Behe's terminology, “irreducibly complex.”
This, he argued, creates a problem for the Darwinian mechanism. Natural selection preserves or “selects” functional advantages. If a random mutation helps an organism survive, it can be preserved and passed on to the next generation. Yet the flagellar motor does not function unless all of its thirty parts are present. Thus, natural selection can “select” or preserve the motor once it has arisen as a functioning whole, but it can't produce the motor in a step-bystep Darwinian fashion.
Natural selection purportedly builds complex systems from simpler structures by preserving a series of intermediate structures, each of which must perform some function. In the case of the flagellar motor, most of the critical intermediate stages – like the 29 or 28-part version of the flagellar motor – perform no function for natural selection to preserve. This leaves the origin of the flagellar motor, and many complex cellular machines, unexplained by the mechanism – natural selection – that Darwin specifically proposed to replace the design hypothesis.
Is there a better explanation? Based upon our uniform experience, we know of only one type of cause that produces irreducibly complex systems – namely, intelligence. Indeed, whenever we encounter such complex systems – whether integrated circuits or internal combustion engines – and we know how they arose, invariably a designing intelligence played a role.
The strength of Behe's argument can be judged in part by the responses of his critics. The neo-Darwinists have had ten years to respond and have so far mustered only vague stories about natural selection building irreducibly complex systems (like the flagellar motor) by “coopting” simpler functional parts from other systems. For example, some of Behe’s critics, such as Kenneth Miller of Brown University, have suggested that the flagellar motor might have arisen from the functional parts of other simpler systems or from simpler subsystems of the motor. He and others have pointed to a tiny molecular syringe called a type III secretory system (or TTSS) – that is sometimes found in bacteria without the other parts of the flagellar motor present – to illustrate this possibility. Since the type III secretory system is made of ten or so proteins that are also found in the thirty-protein motor, and since this tiny pump does perform a function, Professor Miller (2004: 81-97) has intimated13 that the bacterial flagellar motor might have arisen from this smaller pump.
While it’s true that the type III secretory system can function separately from the other parts of the flagellar motor, attempts to explain the origin of the flagellar motor by co-option of the TTSS face at least three key difficulties. First, the other twenty or so proteins in the flagellar motor are unique to it and are not found in any other bacterium. This raises the question: from where were these other protein parts co-opted? Second, as microbiologist Scott Minnich (Minnich and Meyer 2004: 295-304) of the University of Idaho points out, even if all the genes and protein parts were somehow available to make a flagellar motor during the evolution of life, the parts would need to be assembled in a specific temporal sequence similar to the way an automobile is assembled in factory. Yet, in order to choreograph the assembly of the flagellar motor, present-day bacteria need an elaborate system of genetic instructions as well as many other protein machines to regulate the timing of the expression of these assembly instructions. Arguably, this system is itself irreducibly complex. Thus, advocates of cooption tacitly presuppose the need for the very thing that the co-option hypotheses seek to explain: a functionally interdependent system of proteins (and genes). Co-option only explains irreducible complexity by presupposing irreducible complexity. Third, analyses of the gene sequences of the two systems (Saier 2004: 113-115) suggest that the flagellar motor arose first and the pump came later. In other words, if anything, the syringe evolved from the motor, not the motor from the syringe. (See Behe 2006b: 255-272 for Behe’s response to his critics.)
An Institutional Home
In the same year, 1996, that Behe’s book appeared, the Center for Science and Culture was launched as part of the Seattle-based Discovery Institute. The Center began with a research fellowship program to support the research of scientists and scholars such as Michael Behe, Jonathan Wells and David Berlinski who were challenging neo-Darwinism or developing the alternative theory of intelligent design. The Center has now become the institutional hub for an international groups of scientists and scholars who are challenging scientific materialism or developing the theory of intelligent design.
William Dembski and The Design Inference
One of the first Center-supported research projects was completed two years later when mathematician and probability theorist William Dembski (1998) completed a monograph for Cambridge University Press titled The Design Inference. In this book, Dembski argued that rational agents often infer or detect the prior activity of other designing minds by the character of the effects they leave behind. Archaeologists assume, for example, that rational agents produced the inscriptions on the Rosetta Stone. Insurance fraud investigators detect certain “cheating patterns” that suggest intentional manipulation of circumstances rather than natural disasters. Cryptographers distinguish between random signals and those that carry encoded messages. Dembski’s work showed that recognizing the activity of intelligent agents constitutes a common and fully rational mode of inference.
More importantly, Dembski’s work explicated criteria by which rational agents recognize the effects of other rational agents, and distinguish them from the effects of natural causes. He argued that systems or sequences that have the joint properties of “high complexity” (or low probability) and “specification” invariably result from intelligent causes, not chance or physical-chemical laws (see Dembski 1998: 36-66). Dembski noted that complex sequences are those that exhibit an irregular and improbable arrangement that defies expression by a simple rule or algorithm. According to Dembski, a specification, on the other hand, is a match or correspondence between a physical system or sequence and a set of independent functional requirements or constraints. To illustrate these concepts (of complexity and specification), consider the following three sets of symbols:
“Time and tide waits for no man.”
Both the first and second sequences shown above are complex because both defy reduction to a simple rule. Each represents a highly irregular, aperiodic and improbable sequence of symbols. The third sequence is not complex, but is instead highly ordered and repetitive. Of the two complex sequences, only one exemplifies a set of independent functional requirements – i.e., is specified. English has a number of such functional requirements. For example, to convey meaning in English one must employ existing conventions of vocabulary (associations of symbol sequences with particular objects, concepts or ideas) and existing conventions of syntax and grammar (such as “every sentence requires a subject and a verb”). When arrangements of symbols “match” or utilize existing vocabulary and grammatical conventions (i.e., functional requirements), communication can occur. Such arrangements exhibit “specification.” The second sequence (“Time and tide waits for no man”) clearly exhibits such a match between itself and the preexisting requirements of vocabulary and grammar. It has employed these conventions to express a meaningful idea.
Of the three sequences above only the second (“Time and tide waits for no man”) manifests both the jointly necessary indicators of a designed system. The third sequence lacks complexity, though it does exhibit a simple periodic pattern, a specification of sorts. The first sequence is complex, but not specified as we have seen. Only the second sequence exhibits both complexity and specification. Thus, according to Dembski’s theory, only the second sequence, but not the first and third, implicates an intelligent cause – as indeed our intuition tells us. (See Dembski 1998).
As it turns out, these criteria are equivalent (or “isomorphic”) to the notion of specified complexity or information content. Thus, Dembski’s work suggested that “high information content” or “specified information” or “specified complexity” indicates prior intelligent activity. This theoretical insight comported with common, as well as scientific, experience. Few rational people would, for example, attribute hieroglyphic inscriptions to natural forces such as wind or erosion; instead, they would immediately recognize the activity of intelligent agents. Dembski’s work shows why: Our reasoning involves a comparative evaluation process that he represents with a device he calls “the explanatory filter.” The filter outlines a formal method by which scientists (as well as ordinary people) decide among three different types of explanations: chance, necessity and design. (See Figure 3). His “explanatory filter” constituted, in effect, a scientific method for detecting the effects of intelligence.
Dembski’s academic credentials were impeccable, and since the book had been published after a rigorous peer review process as part of the prestigious Cambridge University Press monograph series, his argument was difficult to ignore. Dembski’s formal method also reinforced the argument that I was making simultaneously, namely, that the specified information in DNA is best explained by reference to an intelligent cause rather than by reference to chance, necessity or a combination of the two (Meyer 1998a; Meyer 1998b; Meyer 2003a; Meyer et al., 2003.) Indeed, the coding regions of the nucleotide base sequences in DNA manifest both complexity and specification just as does the second of the three symbol strings in the preceding illustration.
Design Beyond Biology
Meanwhile, the fledgling Center for Science and Culture was working with scientists and scholars around the world to develop the case for intelligent design not only in biology but also in the physical sciences. Since then, its fellows have written more than sixty books and hundreds of articles (including many peer-reviewed scientific articles challenging Darwinian evolution or, in some cases, explicitly arguing for intelligent design [see Meyer 2004: 213239; see http://www.discovery.org/csc for other peer-reviewed books and articles supporting intelligent design]), and have appeared on hundreds of television and radio broadcasts, many of them national or international. In addition, the center co-produced four science documentaries and helped improve science education policy in seven states and in the U.S. Congress. As a result of these efforts, the work of the center has generated an international discussion about the growing evidence for design in nature.
Since so much of the intelligent design debate concerns biology, many journalists covering the debate – particularly those guided by boilerplate of the 1925 Scopes Monkey Trial and its Hollywood embodiment, Inherit the Wind – fail to mention that the theory of intelligent design is larger than biology. In recent decades, molecular and cell biology have provided powerful evidence of design, but so too have chemistry, astronomy and physics.
Consider, for example, the role that physics has played in reviving the case for intelligent design. Since Fred Hoyle’s prediction and discovery of the resonance levels of Carbon in 1954 (Hoyle 1954: 121-146), physicists have discovered that the existence of life in the universe depends upon a number of precisely balanced physical factors (see Giberson 1997: 63-90; Yates, 1997: 91-104). The constants of physics, the initial conditions of the universe and many other of its contingent features appear delicately balanced to allow for the possibility of life. Even very slight alterations in the values of many independent factors such as the expansion rate of the universe, the speed of light, the precise strength of gravitational or electromagnetic attraction, would render life impossible. Physicists now refer to these factors as “anthropic coincidences” and to the fortunate convergence of all these coincidences as the “fine-tuning of the universe.” Many have noted that this fine-tuning strongly suggests design by a pre-existent intelligence. As physicist Paul Davies (1988: 203) has put it, “The impression of design is overwhelming.”
To see why, consider the following illustration. Imagine a cosmic explorer has just stumbled into the control room for the whole universe. There he discovers an elaborate “universe creating machine,” with rows and rows of dials each with many possible settings. As he investigates, he learns that each dial represents some particular parameter that has to be calibrated with a precise value in order to create a universe in which life can survive. One dial represents the possible settings for the strong nuclear force, one for the gravitational constant, one for Planck’s constant, one for the speed of light, one for the ratio of the neutron mass to the proton mass, one for the strength of electromagnetic attraction and so on. As our cosmic explorer examines the dials, he finds that the dials can be easily spun to different settings – that they could have been set otherwise. Moreover, he determines by careful calculation (he is a physicist) that even slight alterations in any of the dial settings would alter the architecture of the universe such that life would cease to exist. Yet for some reason each dial sits with just the exact value necessary to keep the universe running – like an already-opened bank safe with multiple dials in which every dial is found with just the just the right value. What should one infer about how these dial settings came to be set?
Not surprisingly, many physicists have been asking the same question about the anthropic coincidences. And for many,14 the design hypothesis seems the most obvious and intuitively plausible answer to this question. As George Greenstein (1988: 26-27) muses, “the thought insistently arises that some supernatural agency, or rather Agency, must be involved.” As Fred Hoyle (1982: 16) commented, “a commonsense interpretation of the facts suggests that a superintellect has monkeyed with physics, as well as chemistry and biology, and that there are no blind forces worth speaking about in nature.” Or as he put it in his book The Intelligent Universe, “A component has evidently been missing from cosmological studies. The origin of the Universe, like the solution of the Rubik cube, requires an intelligence” (Hoyle 1983: 189). Many physicists now concur. They would argue that – in effect – the dials in the cosmic control room appear finely-tuned because someone carefully set them that way.
In the 2004 book The Privileged Planet, astronomer Guillermo Gonzalez and philosopher Jay Richards extended this fine-tuning argument to planet earth (Gonzalez and Richards 2004). They showed first that the Earth’s suitability as a habitable planet depends on a host of very improbable conditions – conditions so improbable in fact as to call into question the widespread assumption that habitable planets are common in our galaxy or even the universe. Further, by drawing on a host of recent astronomical discoveries, Gonzalez and Richards also showed that the set of improbable conditions that render the earth habitable also make it an optimal place for observing the cosmos and making various scientific discoveries. As they put it, habitability correlates with discoverability. They argued that the best explanation for this correlation is that the earth was intelligently designed to be a habitable planet and a platform for making scientific discovery. The Privileged Planet makes a nuanced and cumulative argument15 – one that resists easy summation, but their groundbreaking advance of the finetuning argument for design was persuasive enough that such scientists as Cambridge’s Simon Conway Morris and Harvard’s Owen Gingerich endorsed the book, and David Hughes (2005: 113), a vice-president of the Royal Astronomical Society, gave it an enthusiastic review in the pages of The Observatory.
Three Philosophical Objections
On this and other fronts, advocates of the theory of intelligent design have stirred up debate at the highest levels of the scientific community. In response opponents have often responded with philosophical rather than evidential objections. The three of the most common are: (1) that the theory of intelligent design is an argument from ignorance, (2) that it represents the same kind of fallacious argument from analogy that David Hume criticized in the 18th century and (3) that the theory of intelligent design is not “scientific.” Let us examine each of these arguments in turn.
An Argument from Knowledge
Opponents of intelligent design frequently characterize the theory as an argument from ignorance. According to this criticism anyone who makes a design inference from the presence of information or irreducible complexity in the biological world uses our present ignorance of an adequate materialistic cause of these phenomena as the sole basis for inferring an intelligent cause. Since, the objection goes, ‘design advocates can’t imagine a natural process that can produce biological information or irreducibly complex systems, they resort to invoking the mysterious notion of intelligent design.’ In this view, intelligent design functions not as an explanation, but as a placeholder for ignorance.
On the contrary, the arguments for intelligent design described in this essay do not constitute fallacious arguments from ignorance. Arguments from ignorance occur when evidence against a proposition is offered as the sole grounds for accepting another, alternative proposition. The inferences and arguments to design made by contemporary design theorists don’t commit this fallacy. True, the design arguments employed by contemporary advocates of intelligent design do depend in part upon negative assessments of the causal adequacy of competing materialistic hypotheses. And clearly, the lack of an adequate materialistic cause does provide part of the grounds for inferring design from information or irreducibly complex structures in the cell. Nevertheless, this lack is only part of the basis for inferring design. Advocates of the theory of intelligent design also infer design because we know that intelligent agents can and do produce information-rich and irreducibly complex systems. In other words, we have positive experience-based knowledge of an alternative cause that is sufficient to have produced such effects. That cause is intelligence. Thus, design theorists infer design not just because natural processes do not or cannot explain the origin of specified information or irreducible complexity in biological systems, but also because we know based upon our uniform experience that only intelligent agents produce these effects. In other words, biological systems manifest distinctive and positive hallmarks of intelligent design – ones that in any other realm of experience would trigger the recognition of an intelligent cause.
Thus, Michael Behe has inferred design not only because the mechanism of natural selection cannot (in his judgment) produce “irreducibly complex” systems, but also because in our experience “irreducible complexity” is a feature of systems known always to result from intelligent design. That is, whenever we see systems that have the feature of irreducible complexity and we know the causal story about how such systems originated, invariably “intelligent design” played a role in the origin of such systems. Thus, Behe infers intelligent design as the best explanation for the origin of irreducible complexity in cellular molecular motors and circuits based upon what we know, not what we do not know, about the causal powers of intelligent agents and natural processes, respectively.
Similarly, the “specified complexity” or “specified information” of DNA implicates a prior intelligent cause, not only because (as I have argued) materialistic scenarios based upon chance, necessity and the combination of the two fail to explain the origin of such information, but also because we know that intelligent agents can and do produce information of this kind. In other words, we have positive experience-based knowledge of an alternative cause that is sufficient to have produced such effects, namely, intelligence. To quote Henry Quastler again, “Information habitually arises from conscious activity” (Quastler 1964: 16). For this reason, specified information also constitutes a distinctive hallmark (or signature) of intelligence. Indeed, in all cases where we know the causal origin of such information, experience has shown that intelligent design played a causal role. Thus, when we encounter such information in the bio-macromolecules necessary to life, we may infer – based upon our knowledge of established cause-effect relationships (i.e., “presently acting causes”) – that an intelligent cause operated in the past to produce the information necessary to the origin of life.
Thus, contemporary design advocates employ the standard uniformitarian method of reasoning used in all historical sciences. That contemporary arguments for design necessarily include critical evaluations of the causal adequacy of competing hypotheses is entirely appropriate. All historical scientists must compare causal adequacy of competing hypotheses in order to make a judgment as to which hypothesis is best. We would not say, for example, that an archeologist had committed a “scribe of the gaps” fallacy simply because – after rejecting the hypothesis that an ancient hieroglyphic inscription was caused by a sand storm – he went on to conclude that the inscription had been produced by a human scribe. Instead, we recognize that the archeologist has made an inference based upon his experience-based knowledge that information-rich inscriptions invariably arise from intelligent causes, not solely upon his judgment that there are no suitably efficacious natural causes that could explain the inscription.
Not Analogy but Identity
Nor does the design argument from biological information depend on the analogical reasoning that Hume critiqued since it does not depend upon assessments of degree of similarity. The argument does not depend upon the similarity of DNA to a computer program or human language but upon the presence of an identical feature (“information” defined as “complexity and specification”) in both DNA and all other designed systems, languages or artifacts. For this reason, the design argument from biological information does not represent an argument from analogy of the sort that Hume criticized, but an “inference to the best explanation.” Such arguments turn not on assessments of the degree of similarity between effects, but instead on an assessment of the adequacy of competing possible causes for the same effect. Because we know intelligent agents can (and do) produce complex and functionally specified sequences of symbols and arrangements of matter (information so defined), intelligent agency qualifies as a sufficient causal explanation for the origin of this effect. In addition, since naturalistic scenarios have proven universally inadequate for explaining the origin of such information, mind or creative intelligence now stands as the best explanation for the origin of this feature of living systems.
But Is It Science?
Of course, many simply refuse to consider the design hypothesis on grounds that it does not qualify as “scientific.” Such critics (see Ruse 1988: 103) affirm the extra-evidential principle mentioned above known as methodological naturalism or methodological materialism. Methodological naturalism asserts that, as a matter of definition, for a hypothesis, theory or explanation to qualify as “scientific,” it must invoke only materialistic entities. Thus, critics say, the theory of intelligent design does not qualify. Yet, even if one grants this definition, it does not follow that some nonscientific (as defined by methodological naturalism) or metaphysical hypothesis couldn’t constitute a better, more causally adequate, explanation of some phenomena than competing materialistic hypotheses. Design theorists argue that, whatever its classification, the design hypothesis does constitute a better explanation than its materialistic rivals for the origin of biological information, irreducibly complex systems and the fine-tuning of the constants of physics. Surely, simply classifying an argument as “not scientific” does not refute it.
In any case, methodological materialism now lacks justification as a normative definition of science. First, attempts to justify methodological materialism by reference to metaphysically neutral (that is, non-question begging) demarcation criteria have failed (see Meyer 2000b; Meyer 2000c; Laudan 2000a: 337-50; Laudan 2000b: 351-355; Plantinga 1986a: 1826; Plantinga 1986b: 22-34). Second, to assert methodological naturalism as a normative principle for all of science has a negative effect on the practice of certain scientific disciplines, especially those in the historical sciences. In origin-of-life research, for example, methodological materialism artificially restricts inquiry and prevents scientists from considering some hypotheses that might provide the best, most causally adequate explanations. To be a truthseeking endeavor, the question that origin-of-life researchers must address is not “Which materialistic scenario seems most adequate?” but rather “What actually caused life to arise on Earth?” Clearly, it’s at least logically possibly that the answer to the latter question is this: “Life was designed by an intelligent agent that existed before the advent of humans.” If one accepts methodological naturalism as normative, however, scientists may never consider the design hypothesis as possibly true. Such an exclusionary logic diminishes the significance of any claim of theoretical superiority for any remaining hypothesis and raises the possibility that the best “scientific” explanation (as defined by methodological naturalism) may not be the best in fact.
As many historians and philosophers of science now recognize, scientific theory-evaluation is an inherently comparative enterprise. Theories that gain acceptance in artificially constrained competitions can claim to be neither ‘most probably true’ nor ‘most empirically adequate.’ At best, such theories can be considered the ‘most probably true or adequate among an artificially limited set of options.’ Thus, an openness to the design hypothesis would seem necessary to any fully rational historical science – that is, to one that seeks the truth, “no holds barred” (Bridgman 1955: 535). An historical science committed to following the evidence wherever it leads will not exclude hypotheses a priori on metaphysical grounds. Instead, it will employ only metaphysically neutral criteria – such as explanatory power and causal adequacy – to evaluate competing hypotheses. This more open (and seemingly rational) approach to scientific theory evaluation suggests the theory of intelligent design as the best, most causally adequate explanation for the origin of certain features of the natural world, especially including the origin of the specified information necessary to build the first living organism.
Of course, many continue to dismiss intelligent design as nothing but “religion masquerading as science.” They point to the theory’s obviously friendly implications for theistic belief as a justification for classifying and dismissing the theory as “religion.” But such critics confuse the implications of the theory of intelligent design with its evidential basis. The theory of intelligent design may well have theistic implications. But that is not grounds for dismissing it. Scientific theories must be judged by their ability to explain evidence, not by whether they have undesirable implications. Those who say otherwise flout logic and overlook the clear testimony of the history of science. For example, many scientists initially rejected the Big Bang theory because it seemed to challenge the idea of an eternally self-existent universe and pointed to the need for a transcendent cause of matter, space and time. But scientists eventually accepted the theory despite such apparently unpleasant implications because the evidence strongly supported it. Today a similar metaphysical prejudice confronts the theory of intelligent design. Nevertheless, it too must be evaluated on the basis of the evidence, not our philosophical preferences or concerns about its possible religious implications. As Professor Flew, the long-time atheistic philosopher who has come to accept the case for design, advises: we must “follow the evidence wherever it leads.”
Acknowledgement: The author would like to acknowledge the assistance of Dr. Jonathan Witt in the preparation of parts of this article.
- Alston, W. P. (1971): The place of the explanation of particular facts in science, in: Philosophy of science 38, 13-34.
- Axe, D. (2004): Estimating the prevalence of protein sequences adopting functional enzyme folds, in: Journal of Molecular Biology, 341, 1295-1315.
- Behe, M. (2004): Irreducible complexity: Obstacle to Darwinian evolution, in: W. A. Dembski/M. Ruse (eds.), Debating design: from Darwin to DNA, Cambridge, 352-370.
- – (2006a): From muttering to mayhem: How Phillip Johnson got me moving, in: W. A. Dembski (ed.), Darwin’s nemesis: Phillip Johnson and the intelligent design movement, Downers Grove, IL, 37-47.
- – (2006b): Darwin’s black box: The biochemical challenge to evolution. Afterword, New York, 255-272.
- Berlinski, D. (1996): The deniable Darwin, in: Commentary 101.6, 19-29.
- Bowler, P. J. (1986): Theories of human evolution: A century of debate, 1844-1944, Baltimore, 44-50.
- Boyle, R. (1979): Selected philosophical papers of Robert Boyle, edited by M. A. Stewart, Manchester, 172.
- Bradley, W. (2004): Information, entropy and the origin of life, in: W. A. Dembski / M. Ruse (eds.), Debating design: from Darwin to DNA, Cambridge, 331-351.
- Bridgman, P. W. (1955): Reflections of a physicist, 2nd edition, New York, 535.
- Capretti, G. (1983): Peirce, Holmes, Popper, in: U. Eco and T. Sebeok (eds.), The sign of three, Bloom
- ington, IN, 135-153.
- Chamberlain, T. C. (1965): The method of multiple working hypotheses, in: Science 148, 754-59.
- Cicero (1933): De natura deorum, translated by Harris Rackham, Cambridge, MA, 217.
- Crick, F. (1958): On Protein Synthesis, in: Symposium for the Society of Experimental Biology, 12,138– 63, esp. 138-63.
- Darwin, C. (1896): Life and letters of Charles Darwin, 2 volumes, edited by Francis Darwin, London, vol. 1, 437.
- – (1964): On the origin of species, Cambridge, MA, 481-82.
- Dawkins, R. (1986): The blind watchmaker, London, 1.
- – (1995): River out of Eden, New York, 11.
- Davies, P. (1988): The cosmic blueprint, New York, 203.
- Dembski, W. A. (1996): Demise of British natural theology. Unpublished paper presented to Philosophy of Religion seminar, University of Notre Dame, fall.
- – (1998): The design inference: Eliminating chance through small probabilities. Cambridge.
- – (2002): No free lunch: why specified complexity cannot be purchased without intelligence. Lanham, Maryland.
- – (2004): The logical underpinnings of intelligent design, in: W. A. Dembski / M. Ruse (eds.), Debating design: from Darwin to DNA, Cambridge, 311-440.
- Denton, M. (1985): Evolution: a theory in crisis, London.
- – (1986): Nature’s destiny, New York.
- Dretske, F. (1981): Knowledge and the flow of information, Cambridge, MA, 6-10.
- Eden, M. (1967): Inadequacies of neo-Darwinian evolution as a scientific theory, in: P. S. Moorhead / M.M. Kaplan (eds.), Mathematical challenges to the neo-Darwinian interpretation of evolution, Philadelphia, 109-111.
- Eldredge, N. (1982): An ode to adaptive transformation, in: Nature 296, 508-9.
- Futuyama, D. (1985): Evolution as fact and theory, in: Bios 56, 3-13.
- Gallie, W. B. (1959): Explanations in history and the genetic sciences, in: P. Gardiner (ed.), Theories of history: Readings from classical and contemporary sources, Glencoe, IL, 386-402.
- Gates, B. (1995): The road ahead, New York, 188.
- Giberson, K. (1997): The anthropic principle, in: Journal of interdisciplinary studies 9, 63-90.
- Gillespie, N. (1979): Charles Darwin and the problem of creation, Chicago, 41-66, 82-108.
- – (1987): Natural history, natural theology, and social order: John Ray and the “Newtonian Ideology”, in: Journal of the History of Biology 20, 1-49.
- Gonzalez, G. and Richards, J. W. (2004): The privileged planet: How our place in the cosmos was designed for discovery. Washington, D.C.
- Gould, S. J. (1986): Evolution and the triumph of homology: Or, why history matters, in: American scientist 74, 61.
- – (2003): Is a new and general theory of evolution emerging? In: Paleobiology 119, 119-20.
- Greenstein, G. (1988): The symbiotic universe: Life and mind in the cosmos, New York, 26-27; 223.
- Hick, J. (1970): Arguments for the existence of God, London, 1.
- Hoyle, F. (1954): On nuclear reactions occurring in very hot stars. I. The synthesis of elements from carbon to nickel, in: Astrophysical journal supplement 1, 121-146.
- – (1982): The universe: Past and present reflections, in: Annual Review of Astronomy and Astrophysics 20, 16.
- – (1983): The intelligent universe, New York, 189.
- Hughes, D. (2005): The observatory, 125.1185, 113.
- Judson, H. (1979): Eighth day of creation, New York.
- Johnson, P. E. (1991): Darwin on trial, Washington, D.C., 8.
- Kamminga, H. (1986): Protoplasm and the Gene, in: A. G. Cairns-Smith / H. Hartman (eds.), Clay Minerals and the Origin of Life, Cambridge, 1-10.
- Kant, I. (1963): Critique of pure reason, translated by Norman Kemp Smith, London, 523.
- Kenyon, D. (1984): Foreword to The mystery of life’s origin, New York, v-viii.
- Kenyon, D. / Gordon, M. (1996): The RNA world: A critique, in: Origins & Design 17 (1), 9-16.
- Kepler, J. (1981): Mysterium cosmographicum [The secret of the universe], translated by A. M. Duncan, New York, 93-103.
- Kepler, J. (1995): Harmonies of the world, translated by Charles Glen Wallis, Amherst, NY, 170, 240.
- Kline, M. (1980): Mathematics: The loss of certainty, New York, 39.
- Klinghoffer, D. (2005): The Branding of a Heretic, in: The Wall Street Journal, 28 January, W11.
- Küppers, B.-O. (1987): On the Prior Probability of the Existence of Life, in: L. Krüger et al. (eds.), The Probabilistic revolution, Cambridge, MA, 355–69.
- – (1990): Information and the origin of life, Cambridge, MA, 170-172.
- Laudan, L. (2000a): The demise of the demarcation problem, in: M. Ruse (ed.), But is it science?, Amherst, NY, 337-350.
- – (2000b): Science at the bar – causes for concern, in: M. Ruse (ed.), But is it science?, Amherst, NY, 351-355.
- Lönnig, W.-E. (2001): Natural selection, in: W. E. Craighead / C. B. Nemeroff (eds.), The Corsini encyclopedia of psychology and behavioral sciences, 3rd edition, New York, vol. 3, 1008-1016.
- Lönnig, W.-E. / Saedler, H. (2002): Chromosome rearrangements and transposable elements, in: Annual review of genetics 36, 389-410.
- Mayr, E. (1982): Foreword to Darwinism defended, by Michael Ruse, Reading, MA, xi-xii.
- Meyer, S. C. (1998): DNA by design: An inference to the best explanation for the origin of biological information, in: Journal of rhetoric and public affairs 4.1, 519-556.
- – (1998b): The Explanatory power of design: DNA and the origin of information, in: W. A. Dembski (ed.), Mere creation: science, faith and intelligent design, Downers Grove, IL, 114-147.
- – (2000a): DNA & other designs, in: First things 102 (April 2000), 30-38.
- – (2000b): The scientific status of intelligent design: The methodological equivalence of naturalistic and non-naturalistic origins theories, in: M. J. Behe / W. A. Dembski / S. C. Meyer (eds.), Science and evidence for design in the universe, San Francisco, 151-211.
- – (2000c): The demarcation of science and religion, in: G. B. Ferngren et al. (eds.), The history of science and religion in the western tradition, New York, 12-23.
- – (2003a): DNA and the origin of life: information, specification and explanation, in: J. A. Campbell / S. C. Meyer (eds.), Darwinism, design and public education, Lansing, MI, 223-285.
- – (2004): The Cambrian information explosion: evidence for intelligent design, in: W. A. Dembski / M. Ruse (eds.), Debating design, Cambridge, 371-391.
- – (2004): The origin of biological information and the higher taxonomic categories, in: Proceedings of the Biological Society of Washington 117, 213-239.
- Meyer, S. C. / Ross, M. / Nelson, P. / Chien, P. (2003): The Cambrian explosion: Biology’s big bang, in: J. A. Campbell / S. C. Meyer (eds.), Darwinism, design and public education, Lansing, MI, 323-402.
- Miller, K. (2004): The bacterial flagellum unspun, in: W. A. Dembski / M. Ruse (eds.), Debating design: from Darwin to DNA, Cambridge, 81-97.
- Minnich, S. A. / Meyer, S. C. (2004): Genetic analysis of coordinate flagellar and type III regulatory circuits in pathogenic bacteria, in: M. W. Collins / C. A. Brebbia (eds.), Design and nature II: Comparing design in nature with science and engineering, Southampton, 295-304.
- Moorhead, P. S. / Kaplan, M. M. (eds.) (1967): Mathematical challenges to the neo-Darwinian interpretation of evolution, Philadelphia.
- Morris, S. C. (1998): The crucible of creation: The Burgess Shale and the rise of animals, Oxford, 63115.
- – (2000): Evolution: bringing molecules into the fold, in: Cell 100, 1-11.
- – (2003a): The Cambrian “explosion” of metazoans, in: Origination of organismal form, 13-32.
- – (2003b): Cambrian “explosions” of metazoans and molecular biology: would Darwin be satisfied?, in: International journal of developmental biology 47 (7-8), 505-515.
- Müller, G. B. / Newman, S. A. (2003): Origination of organismal form: The forgotten cause in evolutionary theory, in: G. B. Müller / S. A. Newman (eds.), Origination of organismal form: Beyond the gene in developmental and evolutionary biology, Cambridge, MA, 3-12.
- Nelson, P. / Wells, J. (2003): Homology in biology: problem for naturalistic science and prospect for intelligent design, in: J. A. Campbell / S. C. Meyer (eds.), Darwinism, design and public education, Lansing, MI, 303-322.
- Newton, I. (1934): Newton’s Principia: Motte’s translation revised (1686), translated by A. Motte, revised by F. Cajori, Berkeley, 543-44.
- – (1952): Opticks, New York, 369-70.
- Paine, T. (1925): The life and works of Thomas Paine, vol. 8: The age of reason, New Rochelle, NY, 6.
- Paley, W. (1852): Natural theology, Boston, 8-9.
- Peirce, C. S. (1932): Collected papers, Vols. 1-6, edited by C. Hartshorne and P. Weiss, Cambridge, MA, vol. 2, 375.
- Plantinga, A. (1986a): Methodological naturalism?, in: Origins and design 18.1, 18-26.
- – (1986b): Methodological naturalism?, in: Origins and design 18.2, 22-34.
- Plato (1960): The laws, translated by A. E. Taylor, London, 279.
- Polanyi, M. (1967): Life transcending physics and chemistry, in: Chemical and engineering news 45(35), 21.
- – (1968): Life’s irreducible structure, in: Science 160, 1308-12.
- Ray, J. (1701): The wisdom of God manifested in the works of the creation, 3rd edition, London.
- Quastler, H. (1964): The emergence of biological organization, 16. New Haven, Connecticut.
- Reid, T. (1981): Lectures on natural theology (1780), edited by E. Duncan and W. R. Eakin, Washington, D.C., 59.
- Ruse, M. (1988): McLean v. Arkansas: Witness testimony sheet, in: M. Ruse (ed.), But is it science?, Amherst, NY, 103.
- Saier, M. H. (2004): Evolution of bacterial type III protein secretion systems, in: Trends in microbiology 12, 113-115.
- Shannon, C. E. (1948): A Mathematical theory of communication, in: Bell System Technical Journal, 27, 379–423; 623–56.
- Shannon, C. E. / Weaver, W. (1949): The Mathematical theory of communication. Urbana, IL.
- Schiller, F. C. S. (1903): Darwinism and design argument, in: Humanism: Philosophical essays, New York, 141.
- Schneider, T. D. (1997): Information content of individual genetic sequences, in: Journal of Theoretical Biology, 189, 427–41.
- Schützenberger, M. (1967): Algorithms and neo-Darwinian theory, in: P. S. Moorhead / M. M. Kaplan (eds.), Mathematical challenges to the neo-Darwinian interpretation of evolution, Philadelphia, 73-5.
- Scriven, M. (1959): Explanation and prediction in evolutionary theory, in: Science 130, 477-82.
- – (1966): Causes, connections and conditions in history, in: W. H. Dray (ed.), Philosophical analysis and history, New York, 238-64.
- Simpson, G. G. (1978): The meaning of evolution, Cambridge, MA, 45.
- Smith, J. M. (1975): The theory of evolution, 3rd edition, London, 30.
- Sober, E. (1988): Reconstructing the past: parsimony, evolution, and inference, Cambridge, MA, 1-5.
- Taylor, G. R. (1983): The great evolution mystery, New York, 4.
- Thaxton, C. / Bradley, W. / Olsen, R. L. (1984): The mystery of life’s origin, New York.
- Wallace, A. R. (1991): Sir Charles Lyell on geological climates the origin of species, in: C. H. Smith (ed.), An anthology of his shorter writings, Oxford, 33-34.
- Whewell, W. (1840): The philosophy of the inductive sciences, 2 vols., London, vol. 2, 121-22; 101-03.
- – (1857): History of the inductive sciences, 3 vols., London, vol. 3, 397.
- Witham, L. (2003): By design, San Francisco, chapter 2.
- Woodward, T. (2003): Doubts about Darwin: A history of intelligent design, Grand Rapids, Michigan, 69.
- Yates, S. (1997): Postmodern creation myth? A response, in: Journal of interdisciplinary studies 9, 91104.
- Yockey, H. P. (1992): Information theory and molecular biology, Cambridge.
For those who are studying aspects of the origin of life, the question no longer seems to be whether life could have originated by chemical processes involving non-biological components but, rather, what pathway might have been followed.— National Academy of Sciences (1996)
It is 1828, a year that encompassed the death of Shaka, the Zulu king, the passage in the United States of the Tariff of Abominations, and the battle of Las Piedras in South America. It is, as well, the year in which the German chemist Friedrich Wöhler announced the synthesis of urea from cyanic acid and ammonia.
Discovered by H.M. Roulle in 1773, urea is the chief constituent of urine. Until 1828, chemists had assumed that urea could be produced only by a living organism. Wöhler provided the most convincing refutation imaginable of this thesis. His synthesis of urea was noteworthy, he observed with some understatement, because "it furnishes an example of the artificial production of an organic, indeed a so-called animal substance, from inorganic materials."
Wöhler's work initiated a revolution in chemistry; but it also initiated a revolution in thought. To the extent that living systems are chemical in their nature, it became possible to imagine that they might be chemical in their origin; and if chemical in their origin, then plainly physical in their nature, and hence a part of the universe that can be explained in terms of "the model for what science should be."*
In a letter written to his friend, Sir Joseph Hooker, several decades after Wöhler's announcement, Charles Darwin allowed himself to speculate. Invoking "a warm little pond" bubbling up in the dim inaccessible past, Darwin imagined that given "ammonia and phosphoric salts, light, heat, electricity, etc. present," the spontaneous generation of a "protein compound" might follow, with this compound "ready to undergo still more complex changes" and so begin Darwinian evolution itself.
Time must now be allowed to pass. Shall we say 60 years or so? Working independently, J.B.S. Haldane in England and A.I. Oparin in the Soviet Union published influential studies concerning the origin of life. Before the era of biological evolution, they conjectured, there must have been an era of chemical evolution taking place in something like a pre-biotic soup. A reducing atmosphere prevailed, dominated by methane and ammonia, in which hydrogen atoms, by donating their electrons (and so "reducing" their number), promoted various chemical reactions. Energy was at hand in the form of electrical discharges, and thereafter complex hydrocarbons appeared on the surface of the sea.
The publication of Stanley Miller's paper, "A Production of Amino Acids Under Possible Primitive Earth Conditions," in the May 1953 issue of Science completed the inferential arc initiated by Friedrich Wöhler 125 years earlier. Miller, a graduate student, did his work at the instruction of Harold Urey. Because he did not contribute directly to the experiment, Urey insisted that his name not be listed on the paper itself. But their work is now universally known as the Miller-Urey experiment, providing evidence that a good deed can be its own reward.
By drawing inferences about pre-biotic evolution from ordinary chemistry, Haldane and Oparin had opened an imaginary door. Miller and Urey barged right through. Within the confines of two beakers, they re-created a simple pre-biotic environment. One beaker held water; the other, connected to the first by a closed system of glass tubes, held hydrogen cyanide, water, methane, and ammonia. The two beakers were thus assumed to simulate the pre-biotic ocean and its atmosphere. Water in the first could pass by evaporation to the gases in the second, with vapor returning to the original alembic by means of condensation.
Then Miller and Urey allowed an electrical spark to pass continually through the mixture of gases in the second beaker, the gods of chemistry controlling the reactions that followed with very little or no human help. A week after they had begun their experiment, Miller and Urey discovered that in addition to a tarry residue "its most notable product" their potent little planet had yielded a number of the amino acids found in living systems.
The effect among biologists (and the public) was electrifying, all the more so because of the experiment's methodological genius. Miller and Urey had done nothing. Nature had done everything. The experiment alone had parted the cloud of unknowing.
The Double Helix
In April 1953, just four weeks before Miller and Urey would report their results in Science, James Watson and Francis Crick published a short letter in Nature entitled "A Structure for Deoxyribose Nucleic Acid." The letter is now famous, if only because the exuberant Crick, at least, was persuaded that he and Watson had discovered the secret of life. In this he was mistaken: the secret of life, along with its meaning, remains hidden. But in deducing the structure of deoxyribose nucleic acid (DNA) from X-ray diffraction patterns and various chemical details, Watson and Crick had discovered the way in which life at the molecular level replicates itself.
Formed as a double helix, DNA, Watson and Crick argued, consists of two twisted strings facing each other and bound together by struts. Each string comprises a series of four nitrogenous bases: adenine (A), guanine (G), thymine (T), and cytosine (C). The bases are nitrogenous because their chemical activity is determined by the electrons of the nitrogen atom, and they are bases because they are one of two great chemical clans - the other being the acids, with which they combine to form salts.
Within each strand of DNA, the nitrogenous bases are bound to a sugar, deoxyribose. Sugar molecules are in turn linked to each other by a phosphate group. When nucleotides (A, G, T, or C) are connected in a sugar-phosphate chain, they form a polynucleotide. In living DNA, two such chains face each other, their bases touching fingers, A matched to T and C to G. The coincidence between bases is known now as Watson-Crick base pairing.
"It has not escaped our notice," Watson and Crick observed, "that the specific pairings we have postulated immediately suggests a possible copying mechanism for the genetic material"(emphasis added). Replication proceeds, that is, when a molecule of DNA is unzipped along its internal axis, dividing the hydrogen bonds between the bases. Base pairing then works to prompt both strands of a separated double helix to form a double helix anew.
So Watson and Crick conjectured, and so it has proved.
The Synthesis of Protein
Together with Francis Crick and Maurice Wilkins, James Watson received the Nobel Prize for medicine in 1962. In his acceptance speech in Stockholm before the king of Sweden, Watson had occasion to explain his original research goals. The first was to account for genetic replication. This, he and Crick had done. The second was to describe the "way in which genes control protein synthesis." This, he was in the course of doing.
DNA is a large, long, and stable molecule. As molecules go, it is relatively inert. It is the proteins, rather, that handle the day-to-day affairs of the cell. Acting as enzymes, and so as agents of change, proteins make possible the rapid metabolism characteristic of modern organisms.
Proteins are formed from the alpha-amino acids, of which there are twenty in living systems. The prefix "alpha" designates the position of the crucial carbon atom in the amino acid, indicating that it lies adjacent to (and is bound up with) a carboxyl group comprising carbon, oxygen, again oxygen, and hydrogen. And the proteins are polymers: like DNA, their amino-acid constituents are formed into molecular chains.
But just how does the cell manage to link amino acids to form specific proteins? This was the problem to which Watson alluded as the king of Sweden, lost in a fog of admiration, nodded amiably.
The success of Watson-Crick base pairing had persuaded a number of molecular biologists that DNA undertook protein synthesis by the same process, the formation of symmetrical patterns or "templates" that governed its replication. After all, molecular replication proceeded by the divinely simple separation-and-recombination of matching (or symmetrical) molecules, with each strand of DNA serving as the template for another. So it seemed altogether plausible that DNA would likewise serve a template function for the amino acids.
It was Francis Crick who in 1957 first observed that this was most unlikely. In a note circulated privately, Crick wrote that "if one considers the physico-chemical nature of the amino-acid side chains, we do not find complementary features on the nucleic acids. Where are the knobby hydrophobic . . . surfaces to distinguish valine from leucine and isoleucine? Where are the charged groups, in specific positions, to go with acidic and basic amino acids?"
Should anyone have missed his point, Crick made it again: "I don't think that anyone looking at DNA or RNA [ribonucleic acid] would think of them as templates for amino acids."
Had these observations been made by anyone but Francis Crick, they might have been regarded as the work of a lunatic; but in looking at any textbook in molecular biology today, it is clear that Crick was simply noticing what was under his nose. Just where are those "knobby hydrophobic surfaces"? To imagine that the nucleic acids form a template or pattern for the amino acids is a little like trying to imagine a glove fitting over a centipede. But if the nucleic acids did not form a template for the amino acids, then the information they contained - all of the ancient wisdom of the species, after all - could only be expressed by an indirect form of transmission: a code of some sort.
The idea was hardly new. The physicist Erwin Schrödinger had predicted in 1945 that living systems would contain what he called a "code script"; and his short, elegant book, What Is Life?, had exerted a compelling influence on every molecular biologist who read it. Ten years later, the ubiquitous Crick invoked the phrase "sequence hypothesis" to characterize the double idea that DNA sequences spell a message and that a code is required to express it. What remained obscure was both the spelling of the message and the mechanism by which it was conveyed.
The mechanism emerged first. During the late 1950's, Franςois Jacob and Jacques Monod advanced the thesis that RNA acts as the first in a chain of intermediates leading from DNA to the amino acids.
Single- rather than double-stranded, RNA is a nucleic acid: a chip from the original DNA block. Instead of thymine (T), it contains the base uracil (U), and the sugar that it employs along its backbone features an atom of oxygen missing from deoxyribose. But RNA, Jacob and Monod argued, was more than a mere molecule: it was a messenger, an instrument of conveyance, "transcribing" in one medium a message first expressed in another. Among the many forms of RNA loitering in the modern cell, the RNA bound for duties of transcription became known, for obvious reasons, as "messenger" RNA.
In transcription, molecular biologists had discovered a second fundamental process, a companion in arms to replication. Almost immediately thereafter, details of the code employed by the messenger appeared. In 1961, Marshall Nirenberg and J. Heinrich Matthaei announced that they had discovered a specific point of contact between RNA and the amino acids. And then, in short order, the full genetic code emerged. RNA (like DNA) is organized into triplets, so that adjacent sequences of three bases are mapped to a single amino acid. Sixty-four triplets (or codons) govern twenty amino acids. The scheme is universal, or almost so.
The elaboration of the genetic code made possible a remarkably elegant model of the modern cell as a system in which sequences of codons within the nucleic acids act at a distance to determine sequences of amino acids within the proteins: commands issued, responses undertaken. A third fundamental biological process thus acquired molecular incarnation. If replication served to divide and then to duplicate the cell's ancestral message, and transcription to re-express it in messenger RNA, "translation" acted to convey that message from messenger RNA to the amino acids.
For all the boldness and power of this thesis, the details remained on the level of what bookkeepers call general accounting procedures. No one had established a direct, a physical, connection between RNA and the amino acids.
Having noted the problem, Crick also indicated the shape of its solution. "I therefore proposed a theory," he would write retrospectively, "in which there were twenty adaptors (one for each amino acid), together with twenty special enzymes. Each enzyme would join one particular amino acid to its own special adaptor."
In early 1969, at roughly the same time that a somber Lyndon Johnson was departing the White House to return to the Pedernales, the adaptors whose existence Crick had predicted came into view. There were twenty, just as he had suggested. They were short in length; they were specific in their action; and they were nucleic acids. Collectively, they are now designated "transfer" RNA (tRNA).
Folded like a cloverleaf, transfer RNA serves physically as a bridge between messenger RNA and an amino acid. One arm of the cloverleaf is called the anti-coding region. The three nucleotide bases that it contains are curved around the arm's bulb-end; they are matched by Watson-Crick base pairing to bases on the messenger RNA. The other end of the cloverleaf is an acceptor region. It is here that an amino acid must go, with the structure of tRNA suggesting a complicated female socket waiting to be charged by an appropriate male amino acid.
The adaptors whose existence Crick had predicted served dramatically to confirm his hypothesis that such adaptors were needed. But although they brought about a physical connection between the nucleic and the amino acids, the fact that they were themselves nucleic acids raised a question: in the unfolding molecular chain, just what acted to adapt the adaptors to the amino acids? And this, too, was a problem Crick both envisaged and solved: his original suggestion mentioned both adaptors (nucleic acids) and their enzymes (proteins).
And so again it proved. The act of matching adaptors to amino acids is carried out by a family of enzymes, and thus by a family of proteins: the aminoacyl-tRNA synthetases. There are as many such enzymes as there are adaptors. The prefix "aminoacyl" indicates a class of chemical reactions, and it is in aminoacylation that the cargo of a carboxyl group is bonded to a molecule of transfer RNA.
Collectively, the enzymes known as synthetases have the power both to recognize specific codons and to select their appropriate amino acid under the universal genetic code. Recognition and selection are ordinarily thought to be cognitive acts. In psychology, they are poorly understood, but within the cell they have been accounted for in chemical terms and so in terms of "the model for what science should be."
With tRNA appropriately charged, the molecule is conveyed to the ribosome, where the task of assembling sequences of amino acids is then undertaken by still another nucleic acid, ribosomal RNA (rRNA). By these means, the modern cell is at last subordinated to a rich narrative drama. To repeat:
- Replication duplicates the genetic message in DNA.
- Transcription copies the genetic message from DNA to RNA.
- Translation conveys the genetic message from RNA to the amino acids - whereupon, in a fourth and final step, the amino acids are assembled into proteins.
The Central Dogma
It was once again Francis Crick, with his remarkable gift for impressing his authority over an entire discipline, who elaborated these facts into what he called the central dogma of molecular biology. The cell, Crick affirmed, is a divided kingdom. Acting as the cell's administrators, the nucleic acids embody all of the requisite wisdom - where to go, what to do, how to manage - in the specific sequence of their nucleotide bases. Administration then proceeds by the transmission of information from the nucleic acids to the proteins.
The central dogma thus depicts an arrow moving one way, from the nucleic acids to the proteins, and never the other way around. But is anything ever routinely returned, arrow-like, from its target? This is not a question that Crick considered, although in one sense the answer is plainly no. Given the modern genetic code, which maps four nucleotides onto twenty amino acids, there can be no inverse code going in the opposite direction; an inverse mapping is mathematically impossible.
But there is another sense in which Crick's central dogma does engender its own reversal. If the nucleic acids are the cell's administrators, the proteins are its chemical executives: both the staff and the stuff of life. The molecular arrow goes one way with respect to information, but it goes the other way with respect to chemistry.
Replication, transcription, and translation represent the grand unfolding of the central dogma as it proceeds in one direction. The chemical activities initiated by the enzymes represent the grand unfolding of the central dogma as it goes in the other. Within the cell, the two halves of the central dogma combine to reveal a system of coded chemistry, an exquisitely intricate but remarkably coherent temporal tableau suggesting a great army in action.
From these considerations a familiar figure now emerges: the figure of a chicken and its egg. Replication, transcription, and translation are all under the control of various enzymes. But enzymes are proteins, and these particular proteins are specified by the cell's nucleic acids. DNA requires the enzymes in order to undertake the work of replication, transcription, and translation; the enzymes require DNA in order to initiate it. The nucleic acids and the proteins are thus profoundly coordinated, each depending upon the other. Without amino-acyl-tRNA synthetase, there is no translation from RNA; but without DNA, there is no synthesis of aminoacyl-tRNA synthetase.
If the nucleic acids and their enzymes simply chased each other forever around the same cell, the result would be a vicious circle. But life has elegantly resolved the circle in the form of a spiral. The aminoacyl-tRNA synthetase that is required to complete molecular translation enters a given cell from its progenitor or "maternal" cell, where it is specified by that cell's DNA. The enzymes required to make the maternal cell's DNA do its work enter that cell from its maternal line. And so forth.
On the level of intuition and experience, these facts suggest nothing more mysterious than the longstanding truism that life comes only from life. Omnia viva ex vivo, as Latin writers said. It is only when they are embedded in various theories about the origins of life that the facts engender a paradox, or at least a question: in the receding molecular spiral, which came first - the chicken in the form of DNA, or its egg in the form of various proteins? And if neither came first, how could life have begun?
The RNA World
It is 1967, the year of the Six-Day war in the Middle East, the discovery of the electroweak forces in particle physics, and the completion of a twenty-year research program devoted to the effects of fluoridation on dental caries in Evanston, Illinois. It is also the year in which Carl Woese, Leslie Orgel, and Francis Crick introduced the hypothesis that "evolution based on RNA replication preceded the appearance of protein synthesis" (emphasis added).
By this time, it had become abundantly clear that the structure of the modern cell was not only more complex than other physical structures but complex in poorly understood ways. And yet no matter how far back biologists traveled into the tunnel of time, certain features of the modern cell were still there, a message sent into the future by the last universal common ancestor. Summarizing his own perplexity in retrospect, Crick would later observe that "an honest man, armed with all the knowledge available to us now, could only state that, in some sense, the origin of life appears at the moment to be almost a miracle." Very wisely, Crick would thereupon determine never to write another paper on the subject, although he did affirm his commitment to the theory of "directed panspermia," according to which life originated in some other portion of the universe and, for reasons that Crick could never specify, was simply sent here.
But that was later. In 1967, the argument presented by Woesel, Orgel, and Crick was simple. Given those chickens and their eggs, something must have come first. Two possibilities were struck off by a process of elimination. DNA? Too stable and, in some odd sense, too perfect. The proteins? Incapable of dividing themselves, and so, like molecular eunuchs, useful without being fecund. That left RNA. While it was not obviously the right choice for a primordial molecule, it was not obviously the wrong choice, either.
The hypothesis having been advanced, if with no very great sense of intellectual confidence, biologists differed in its interpretation. But they did concur on three general principles. First: that at some time in the distant past, RNA rather than DNA controlled genetic replication. Second: that Watson-Crick base pairing governed ancestral RNA. And third: that RNA once carried on chemical activities of the sort that are now entrusted to the proteins. The paradox of the chicken and the egg was thus resolved by the hypothesis that the chicken was the egg.
The independent discovery in 1981 of the ribozyme, a ribonucleic enzyme, by Thomas Cech and Sidney Altman endowed the RNA hypothesis with the force of a scientific conjecture. Studying the ciliated protozoan Tetrahymena thermophila, Cech discovered to his astonishment a form of RNA capable of inducing cleavage. Where an enzyme might have been busy pulling a strand of RNA apart, there was a ribozyme doing the work instead. That busy little molecule served not only to give instructions: apparently it took them as well, and in any case it did what biochemists had since the 1920's assumed could only be done by an enzyme and hence by a protein.
In 1986, the biochemist Walter Gilbert was moved to assert the existence of an entire RNA "world," an ancestral state promoted by the magic of this designation to what a great many biologists would affirm as fact. Thus, when the molecular biologist Harry Noller discovered that protein synthesis within the contemporary ribosome is catalyzed by ribosomal RNA (rRNA), and not by any of the familiar, old-fashioned enzymes, it appeared "almost certain" to Leslie Orgel that "there once was an RNA world" (emphasis added).
From Molecular Biology to the Origins of Life
It is perfectly true that every part of the modern cell carries some faint traces of the past. But these molecular traces are only hints. By contrast, to everyone who has studied it, the ribozyme has appeared to be an authentic relic, a solid and palpable souvenir from the pre-biotic past. Its discovery prompted even Francis Crick to the admission that he, too, wished he had been clever enough to look for such relics before they became known.
Thanks to the ribozyme, a great many scientists have become convinced that the "model for what science should be" is achingly close to encompassing the origins of life itself. "My expectation," remarks David Liu, professor of chemistry and chemical biology at Harvard, "is that we will be able to reduce this to a very simple series of logical events." Although often overstated, this optimism is by no means irrational. Looking at the modern cell, biologists propose to reconstruct in time the structures that are now plainly there in space.
Research into the origins of life has thus been subordinated to a rational three-part sequence, beginning in the very distant past. First, the constituents of the cell were formed and assembled. These included the nucleotide bases, the amino acids, and the sugars. There followed next the emergence of the ribozyme, endowed somehow with powers of self-replication. With the stage set, a system of coded chemistry then emerged, making possible what the molecular biologist Paul Schimmel has called "the theater of the proteins." Thus did matters proceed from the pre-biotic past to the very threshold of the last universal common ancestor, whereupon, with inimitable gusto, life began to diversify itself by means of Darwinian principles.
This account is no longer fantasy. But it is not yet fact. That is one reason why retracing its steps is such an interesting exercise, to which we now turn.
It is perhaps four billion years ago. The first of the great eras in the formation of life has commenced. The laws of chemistry are completely in control of things - what else is there? It is Miller Time, the period marking the transition from inorganic to organic chemistry.
According to the impression generally conveyed in both the popular and the scientific literature, the success of the original Miller-Urey experiment was both absolute and unqualified. This, however, is something of an exaggeration. Shortly after Miller and Urey published their results, a number of experienced geochemists expressed reservations. Miller and Urey had assumed that the pre-biotic atmosphere was one in which hydrogen atoms gave up (reduced) their electrons in order to promote chemical activity. Not so, the geochemists contended. The pre-biotic atmosphere was far more nearly neutral than reductive, with little or no methane and a good deal of carbon dioxide.
Nothing in the intervening years has suggested that these sour geochemists were far wrong. Writing in the 1999 issue of Peptides, B.M. Rode observed blandly that "modern geochemistry assumes that the secondary atmosphere of the primitive earth (i.e., after diffusion of hydrogen and helium into space) . . . consisted mainly of carbon dioxide, nitrogen, water, sulfur dioxide, and even small amounts of oxygen." This is not an environment calculated to induce excitement.
Until recently, the chemically unforthcoming nature of the early atmosphere remained an embarrassing secret among evolutionary biologists, like an uncle known privately to dress in women's underwear; if biologists were disposed in public to acknowledge the facts, they did so by remarking that every family has one. This has now changed. The issue has come to seem troubling. A recent paper in Science has suggested that previous conjectures about the pre-biotic atmosphere were seriously in error. A few researchers have argued that a reducing atmosphere is not, after all, quite so important to pre-biotic synthesis as previously imagined.
In all this, Miller himself has maintained a far more unyielding and honest perspective. "Either you have a reducing atmosphere," he has written bluntly, "or you're not going to have the organic compounds required for life."
If the composition of the pre-biotic atmosphere remains a matter of controversy, this can hardly be considered surprising: geochemists are attempting to revisit an era that lies four billion years in the past. The synthesis of pre-biotic chemicals is another matter. Questions about them come under the discipline of laboratory experiments.
Among the questions is one concerning the nitrogenous base cytosine (C). Not a trace of the stuff has been found in any meteor. Nothing in comets, either, so far as anyone can tell. It is not buried in the Antarctic. Nor can it be produced by any of the common experiments in pre-biotic chemistry. Beyond the living cell, it has not been found at all.
When, therefore, M.P. Robertson and Stanley Miller announced in Nature in 1995 that they had specified a plausible route for the pre-biotic synthesis of cytosine from cyanoacetaldehyde and urea, the feeling of gratification was very considerable. But it has also been short-lived. In a lengthy and influential review published in the 1999 Proceedings of the National Academy of Science, the New York University chemist Robert Shapiro observed that the reaction on which Robertson and Miller had pinned their hopes, although active enough, ultimately went nowhere. All too quickly, the cytosine that they had synthesized transformed itself into the RNA base uracil (U) by a chemical reaction known as deamination, which is nothing more mysterious than the process of getting rid of one molecule by sending it somewhere else.
The difficulty, as Shapiro wrote, was that "the formation of cytosine and the subsequent deamination of the product to uracil occur[ed] at about the same rate." Robertson and Miller had themselves reported that after 120 hours, half of their precious cytosine was gone-and it went faster when their reactions took place in saturated urea. In Shapiro's words, "It is clear that the yield of cytosine would fall to 0 percent if the reaction were extended."
If the central chemical reaction favored by Robertson and Miller was self-defeating, it was also contingent on circumstances that were unlikely. Concentrated urea was needed to prompt their reaction; an outhouse whiff would not do. For this same reason, however, the pre-biotic sea, where concentrates disappear too quickly, was hardly the place to begin - as anyone who has safely relieved himself in a swimming pool might confirm with guilty satisfaction. Aware of this, Robertson and Miller posited a different set of circumstances: in place of the pre-biotic soup, drying lagoons. In a fine polemical passage, their critic Shapiro stipulated what would thereby be required:
An isolated lagoon or other body of seawater would have to undergo extreme concentration. . . .
- It would further be necessary that the residual liquid be held in an impermeable vessel [in order to prevent cross-reactions].
- The concentration process would have to be interrupted for some decades . . . to allow the reaction to occur.
- At this point, the reaction would require quenching (perhaps by evaporation to dryness) to prevent loss by deamination.
At the end, one would have a batch of urea in solid form, containing some cytosine (and urea).
Such a scenario, Shapiro remarked, "cannot be excluded as a rare event on early earth, but it cannot be termed plausible."
Like cytosine, sugar must also make an appearance in Miller Time, and, like cytosine, it too is difficult to synthesize under plausible pre-biotic conditions.
In 1861, the German chemist Alexander Bulterow created a sugar-like substance from a mixture of formaldehyde and lime. Subsequently refined by a long line of organic chemists, Bulterow's so-called formose reaction has been an inspiration to origins-of-life researchers ever since.
The reaction is today initiated by an alkalizing agent, such as thallium or lead hydroxide. There follows a long induction period, with a number of intermediates bubbling up. The formose reaction is auto-catalytic in the sense that it keeps on going: the carbohydrates that it generates serve to prime the reaction in an exponentially growing feedback loop until the initial stock of formaldehyde is exhausted. With the induction over, the formose reaction yields a number of complex sugars.
Nonetheless, it is not sugars in general that are wanted from Miller Time but a particular form of sugar, namely, ribose, and not simply ribose but dextro ribose. Compounds of carbon are naturally right-handed or left-handed, depending on how they polarize light. The ribose in living systems is right-handed, hence the prefix "dextro." But the sugars exiting the formose reaction are racemic, that is, both left- and right-handed, and the yield of usable ribose is negligible.
While nothing has as yet changed the fundamental fact that it is very hard to get the right kind of sugar from any sort of experiment, in 1990 the Swiss chemist Albert Eschenmoser was able to change substantially the way in which the sugars appeared. Reaching with the hand of a master into the formose reaction itself, Eschenmoser altered two molecules by adding a phosphate group to them. This slight change prevented the formation of the alien sugars that cluttered the classical formose reaction. The products, Eschenmoser reported, included among other things a mixture of ribose-2,4,-diphosphate. Although the mixture was racemic, it did contain a molecule close to the ribose needed by living systems. With a few chemical adjustments, Eschenmoser could plausibly claim, the pre-biotic route to the synthesis of sugar would lie open.
It remained for skeptics to observe that Eschenmoser's ribose reactions were critically contingent on Eschenmoser himself, and at two points: the first when he attached phosphate groups to a number of intermediates in the formose reaction, and the second when he removed them.
What had given the original Miller-Urey experiment its power to excite the imagination was the sense that, having set the stage, Miller and Urey exited the theater. By contrast, Eschenmoser remained at center stage, giving directions and in general proving himself indispensable to the whole scene.
Events occurring in Miller Time would thus appear to depend on the large assumption, still unproved, that the early atmosphere was reductive, while two of the era's chemical triumphs, cytosine and sugar, remain for the moment beyond the powers of contemporary pre-biotic chemistry.
From Miller Time to Self-Replicating RNA
In the grand progression by which life arose from inorganic matter, Miller Time has been concluded. It is now 3.8 billion years ago. The chemical precursors to life have been formed. A limpid pool of nucleotides is somewhere in existence. A new era is about to commence.
The historical task assigned to this era is a double one: forming chains of nucleic acids from nucleotides, and discovering among them those capable of reproducing themselves. Without the first, there is no RNA; and without the second, there is no life.
In living systems, polymerization or chain-formation proceeds by means of the cell's invaluable enzymes. But in the grim inhospitable pre-biotic, no enzymes were available. And so chemists have assigned their task to various inorganic catalysts. J.P. Ferris and G. Ertem, for instance, have reported that activated nucleotides bond covalently when embedded on the surface of montmorillonite, a kind of clay. This example, combining technical complexity with general inconclusiveness, may stand for many others.
In any event, polymerization having been concluded, by whatever means, the result was (in the words of Gerald Joyce and Leslie Orgel) "a random ensemble of polynucleotide sequences": long molecules emerging from short ones, like fronds on the surface of a pond. Among these fronds, nature is said to have discovered a self-replicating molecule. But how?
Darwinian evolution is plainly unavailing in this exercise or that era, since Darwinian evolution begins with self-replication, and self-replication is precisely what needs to be explained. But if Darwinian evolution is unavailing, so, too, is chemistry. The fronds comprise "a random ensemble of polynucleotide sequences" (emphasis added); but no principle of organic chemistry suggests that aimless encounters among nucleic acids must lead to a chain capable of self-replication.
If chemistry is unavailing and Darwin indisposed, what is left as a mechanism? The evolutionary biologist's finest friend: sheer dumb luck.
Was nature lucky? It depends on the payoff and the odds. The payoff is clear: an ancestral form of RNA capable of replication. Without that payoff, there is no life, and obviously, at some point, the payoff paid off. The question is the odds.
For the moment, no one knows how precisely to compute those odds, if only because within the laboratory, no one has conducted an experiment leading to a self-replicating ribozyme. But the minimum length or "sequence" that is needed for a contemporary ribozyme to undertake what the distinguished geochemist Gustaf Arrhenius calls "demonstrated ligase activity" is known. It is roughly 100 nucleotides.
Whereupon, just as one might expect, things blow up very quickly. As Arrhenius notes, there are 4100 or roughly 1060 nucleotide sequences that are 100 nucleotides in length. This is an unfathomably large number. It exceeds the number of atoms contained in the universe, as well as the age of the universe in seconds. If the odds in favor of self-replication are 1 in 1060, no betting man would take them, no matter how attractive the payoff, and neither presumably would nature.
"Solace from the tyranny of nucleotide combinatorials," Arrhenius remarks in discussing this very point, "is sought in the feeling that strict sequence specificity may not be required through all the domains of a functional oligmer, thus making a large number of library items eligible for participation in the construction of the ultimate functional entity." Allow me to translate: why assume that self-replicating sequences are apt to be rare just because they are long? They might have been quite common.
They might well have been. And yet all experience is against it. Why should self-replicating RNA molecules have been common 3.6 billion years ago when they are impossible to discern under laboratory conditions today? No one, for that matter, has ever seen a ribozyme capable of any form of catalytic action that is not very specific in its sequence and thus unlike even closely related sequences. No one has ever seen a ribozyme able to undertake chemical action without a suite of enzymes in attendance. No one has ever seen anything like it.
The odds, then, are daunting; and when considered realistically, they are even worse than this already alarming account might suggest. The discovery of a single molecule with the power to initiate replication would hardly be sufficient to establish replication. What template would it replicate against? We need, in other words, at least two, causing the odds of their joint discovery to increase from 1 in 1060 to 1 in 10120. Those two sequences would have been needed in roughly the same place. And at the same time. And organized in such a way as to favor base pairing. And somehow held in place. And buffered against competing reactions. And productive enough so that their duplicates would not at once vanish in the soundless sea.
In contemplating the discovery by chance of two RNA sequences a mere 40 nucleotides in length, Joyce and Orgel concluded that the requisite "library" would require 1048 possible sequences. Given the weight of RNA, they observed gloomily, the relevant sample space would exceed the mass of the earth. And this is the same Leslie Orgel, it will be remembered, who observed that "it was almost certain that there once was an RNA world."
To the accumulating agenda of assumptions, then, let us add two more: that without enzymes, nucleotides were somehow formed into chains, and that by means we cannot duplicate in the laboratory, a pre-biotic molecule discovered how to reproduce itself.
From Self-Replicating RNA to Coded Chemistry
A new era is now in prospect, one that begins with a self-replicating form of RNA and ends with the system of coded chemistry characteristic of the modern cell. The modern cell, meaning one that divides its labors by assigning to the nucleic acids the management of information and to the proteins the execution of chemical activity. It is 3.6 billion years ago.
It is with the advent of this era that distinctively conceptual problems emerge. The gods of chemistry may now be seen receding into the distance. The cell's system of coded chemistry is determined by two discrete combinatorial objects: the nucleic acids and the amino acids. These objects are discrete because, just as there are no fractional sentences containing three-and-a-half words, there are no fractional nucleotide sequences containing three-and-a-half nucleotides, or fractional proteins containing three-and-a-half amino acids. They are combinatorial because both the nucleic acids and the amino acids are combined by the cell into larger structures.
But if information management and its administration within the modern cell are determined by a discrete combinatorial system, the work of the cell is part of a markedly different enterprise. The periodic table notwithstanding, chemical reactions are not combinatorial, and they are not discrete. The chemical bond, as Linus Pauling demonstrated in the 1930's, is based squarely on quantum mechanics. And to the extent that chemistry is explained in terms of physics, it is encompassed not only by "the model for what science should be" but by the system of differential equations that play so conspicuous a role in every one of the great theories of mathematical physics.
What serves to coordinate the cell's two big shots of information management and chemical activity, and so to coordinate two fundamentally different structures, is the universal genetic code. To capture the remarkable nature of the facts in play here, it is useful to stress the word code.
By itself, a code is familiar enough: an arbitrary mapping or a system of linkages between two discrete combinatorial objects. The Morse code, to take a familiar example, coordinates dashes and dots with letters of the alphabet. To note that codes are arbitrary is to note the distinction between a code and a purely physical connection between two objects. To note that codes embody mappings is to embed the concept of a code in mathematical language. To note that codes reflect a linkage of some sort is to return the concept of a code to its human uses.
In every normal circumstance, the linkage comes first and represents a human achievement, something arising from a point beyond the coding system. (The coordination of dot-dot-dot-dash-dash-dash-dot-dot-dot with the distress signal S-O-S is again a familiar example.) Just as no word explains its own meaning, no code establishes its own nature.
The conceptual question now follows. Can the origins of a system of coded chemistry be explained in a way that makes no appeal whatsoever to the kinds of facts that we otherwise invoke to explain codes and languages, systems of communication, the impress of ordinary words on the world of matter?
In this regard, it is worth recalling that, as Hubert Yockey observes in Information Theory, Evolution, and the Origin of Life (2005), "there is no trace in physics or chemistry of the control of chemical reactions by a sequence of any sort or of a code between sequences."
Writing in the 2001 issue of the journal RNA, the microbiologist Carl Woese referred ominously to the "dark side of molecular biology." DNA replication, Woese wrote, is the extraordinarily elegant expression of the structural properties of a single molecule: zip down, divide, zip up. The transcription into RNA follows suit: copy and conserve. In each of these two cases, structure leads to function. But where is the coordinating link between the chemical structure of DNA and the third step, namely, translation? When it comes to translation, the apparatus is baroque: it is incredibly elaborate, and it does not reflect the structure of any molecule.
These reflections prompted Woese to a somber conclusion: if "the nucleic acids cannot in any way recognize the amino acids," then there is no "fundamental physical principle" at work in translation (emphasis added).
But Woese's diagnosis of disorder is far too partial; the symptoms he regards as singular are in fact widespread. What holds for translation holds as well for replication and transcription. The nucleic acids cannot directly recognize the amino acids (and vice versa), but they cannot directly replicate or transcribe themselves, either. Both replication and translation are enzymatically driven, and without those enzymes, a molecule of DNA or RNA would do nothing whatsoever. Contrary to what Woese imagines, no fundamental physical principles appear directly at work anywhere in the modern cell.
The most difficult and challenging problem associated with the origins of life is now in view. One half of the modern system of coded chemistry, the genetic code and the sequences it conveys, is, from a chemical perspective, arbitrary. The other half of the system of coded chemistry, the activity of the proteins, is, from a chemical perspective, necessary. In life, the two halves are coordinated. The problem follows: how did that, the whole system, get here?
The prevailing opinion among molecular biologists is that questions about molecular-biological systems can only be answered by molecular-biological experiments. The distinguished molecular biologist Horoaki Suga has recently demonstrated the strengths and the limitations of the experimental method when confronted by difficult conceptual questions like the one I have just posed.
The goal of Suga's experiment was to show that a set of RNA catalysts (or ribozymes) could well have played the role now played in the modern cell by the protein family of aminoacyl synthetases. Until his work, Suga reports, there had been no convincing demonstration that a ribozyme was able to perform the double function of a synthetase - that is, recognizing both a form of transfer RNA and an amino acid. But in Suga's laboratory, just such a molecule made a now-celebrated appearance. With an amino acid attached to its tail, the ribozyme managed to cleave itself and, like a snake, affix its amino-acid cargo onto its head. What is more, it could conduct this exercise backward, shifting the amino acid from its head to its tail again. The chemical reactions involved acylation: precisely the reactions undertaken by synthetases in the modern cell.
Horoaki Suga's experiment was both interesting and ingenious, prompting a reaction perhaps best expressed as, "Well, would you look at that!" It has altered the terms of debate by placing a number of new facts on the table. And yet, as so often happens in experimental pre-biotic chemistry, it is by no means clear what interpretation the facts will sustain.
Do Suga's results really establish the existence of a primitive form of coded chemistry? Although unexpected in context, the coordination he achieved between an amino acid and a form of transfer RNA was never at issue in principle. The question is whether what was accomplished in establishing a chemical connection between these two molecules was anything like establishing the existence of a code. If so, then organic chemistry itself could properly be described as the study of codes, thereby erasing the meaning of a code as an arbitrary mapping between discrete combinatorial objects.
Suga, in summarizing the results of his research, captures rhetorically the inconclusiveness of his achievement. "Our demonstration indicates," he writes, "that catalytic precursor tRNA's could have provided the foundation of the genetic coding system." But if the association at issue is not a code, however primitive, it could no more be the "foundation" of a code than a feather could be the foundation of a building. And if it is the foundation of a code, then what has been accomplished has been accomplished by the wrong agent.
In Suga's experiment, there was no sign that the execution of chemical routines fell under the control of a molecular administration, and no sign, either, that the missing molecular administration had anything to do with executive chemical routines. The missing molecular administrator was, in fact, Suga himself, as his own account reveals. The relevant features of the experiment, he writes, "allow[ed] us to select active RNA molecules with selectivity toward a desired amino acid" (emphasis added). Thereafter, it was Suga and his collaborators who "applied stringent conditions" to the experiment, undertook "selective amplification of the self-modifying RNA molecules," and "screened" vigorously for "self-aminoacylation activity"(emphasis added throughout).
If nothing else, the advent of a system of coded chemistry satisfied the most urgent of imperatives: it was needed and it was found. It was needed because once a system of chemical reactions reaches a certain threshold of complexity, nothing less than a system of coded chemistry can possibly master the ensuing chaos. It was found because, after all, we are here.
Precisely these circumstances have persuaded many molecular biologists that the explanation for the emergence of a system of coded chemistry must in the end lie with Darwin's theory of evolution. As one critic has observed in commenting on Suga's experiments, "If a certain result can be achieved by direction in a laboratory by a Suga, surely it can also be achieved by chance in a vast universe."
A self-replicating ribozyme meets the first condition required for Darwinian evolution to gain purchase. It is by definition capable of replication. And it meets the second condition as well, for, by means of mistakes in replication, it introduces the possibility of variety into the biological world. On the assumption that subsequent changes to the system follow a law of increasing marginal utility, one can then envisage the eventual emergence of a system of coded chemistry - a system that can be explained in terms of "the model for what science should be."
It was no doubt out of considerations like these that, in coming up against what he called the "dark side of molecular biology," Carl Woese was concerned to urge upon the biological community the benefits of "an all-out Darwinian perspective." But the difficulty with "an all-out Darwinian perspective" is that it entails an all-out Darwinian impediment: notably, the assignment of a degree of foresight to a Darwinian process that the process could not possibly possess.
The hypothesis of an RNA world trades brilliantly on the idea that a divided modern system had its roots in some form of molecular symmetry that was then broken by the contingencies of life. At some point in the transition to the modern system, an ancestral form of RNA must have assigned some of its catalytic properties to an emerging family of proteins. This would have taken place at a given historical moment; it is not an artifact of the imagination. Similarly, at some point in the transition to a modern system, an ancestral form of RNA must have acquired the ability to code for the catalytic powers it was discarding. And this, too, must have taken place at a particular historical moment.
The question, of course, is which of the two steps came first. Without life acquiring some degree of foresight, neither step can be plausibly fixed in place by means of any schedule of selective advantages. How could an ancestral form of RNA have acquired the ability to code for various amino acids before coding was useful? But then again, why should "ribozymes in an RNA world," as the molecular biologists Paul Schimmel and Shana O. Kelley ask, "have expedited their own obsolescence?"
Could the two steps have taken place simultaneously? If so, there would appear to be very little difference between a Darwinian explanation and the frank admission that a miracle was at work. If no miracles are at work, we are returned to the place from which we started, with the chicken-and-egg pattern that is visible when life is traced backward now appearing when it is traced forward.
It is thus unsurprising that writings embodying Woese's "all-out Darwinian perspective" are dominated by references to a number of unspecified but mysteriously potent forces and obscure conditional circumstances. I quote without attribution because the citations are almost generic (emphasis added throughout):
- The aminoacylation of RNA initially must have provided some selective advantage.
- The products of this reaction must have conferred some selective advantage.
- However, the development of a crude mechanism for controlling the diversity of possible peptides would have been advantageous.
- [P]rogressive refinement of that mechanism would have provided further selective advantage.
And so forth - ending, one imagines, in reduction to the all-purpose imperative of Darwinian theory, which is simply that what was must have been.
Now It Is Now
At the conclusion of a long essay, it is customary to summarize what has been learned. In the present case, I suspect it would be more prudent to recall how much has been assumed:
First, that the pre-biotic atmosphere was chemically reductive; second, that nature found a way to synthesize cytosine; third, that nature also found a way to synthesize ribose; fourth, that nature found the means to assemble nucleotides into polynucleotides; fifth, that nature discovered a self-replicating molecule; and sixth, that having done all that, nature promoted a self-replicating molecule into a full system of coded chemistry.
These assumptions are not only vexing but progressively so, ending in a serious impediment to thought. That, indeed, may be why a number of biologists have lately reported a weakening of their commitment to the RNA world altogether, and a desire to look elsewhere for an explanation of the emergence of life on earth. "It's part of a quiet paradigm revolution going on in biology," the biophysicist Harold Morowitz put it in an interview in New Scientist, "in which the radical randomness of Darwinism is being replaced by a much more scientific law-regulated emergence of life."
Morowitz is not a man inclined to wait for the details to accumulate before reorganizing the vista of modern biology. In a series of articles, he has argued for a global vision based on the biochemistry of living systems rather than on their molecular biology or on Darwinian adaptations. His vision treats the living system as more fundamental than its particular species, claiming to represent the "universal and deterministic features of any system of chemical interactions based on a water-covered but rocky planet such as ours."
This view of things - metabolism first, as it is often called - is not only intriguing in itself but is enhanced by a firm commitment to chemistry and to "the model for what science should be." It has been argued with great vigor by Morowitz and others. It represents an alternative to the RNA world. It is a work in progress, and it may well be right. Nonetheless, it suffers from one outstanding defect. There is as yet no evidence that it is true.
It is now more than 175 years since Friedrich Wöhler announced the synthesis of urea. It would be the height of folly to doubt that our understanding of life's origins has been immeasurably improved. But whether it has been immeasurably improved in a way that vigorously confirms the daring idea that living systems are chemical in their origin and so physical in their nature, that is another question entirely.
In "On the Origins of the Mind," I tried to show that much can be learned by studying the issue from a computational perspective. Analogously, in contemplating the origins of life, much - in fact, more - can be learned by studying the issue from the perspective of coded chemistry. In both cases, however, what seems to lie beyond the reach of "the model for what science should be" is any success beyond the local. All questions about the global origins of these strange and baffling systems seem to demand answers that the model itself cannot by its nature provide.
It goes without saying that this is a tentative judgment, perhaps only a hunch. But let us suppose that questions about the origins of the mind and the origins of life do lie beyond the grasp of "the model for what science should be." In that case, we must either content ourselves with its limitations or revise the model. If a revision also lies beyond our powers, then we may well have to say that the mind and life have appeared in the universe for no very good reason that we can discern.
Worse things have happened. In the end, these are matters that can only be resolved in the way that all such questions are resolved. We must wait and see.
On August 4th, 2004 an extensive review essay by Dr. Stephen C. Meyer, Director of Discovery Institute's Center for Science & Culture appeared in the Proceedings of the Biological Society of Washington (volume 117, no. 2, pp. 213-239). The Proceedings is a peer-reviewed biology journal published at the National Museum of Natural History at the Smithsonian Institution in Washington D.C.
In the article, entitled "The Origin of Biological Information and the Higher Taxonomic Categories", Dr. Meyer argues that no current materialistic theory of evolution can account for the origin of the information necessary to build novel animal forms. He proposes intelligent design as an alternative explanation for the origin of biological information and the higher taxa.
Due to an unusual number of inquiries about the article, Dr. Meyer, the copyright holder, has decided to make the article available now in HTML format on this website. (Off prints are also available from Discovery Institute by writing to Rob Crowther at: firstname.lastname@example.org. Please provide your mailing address and we will dispatch a copy).
In a recent volume of the Vienna Series in a Theoretical Biology (2003), Gerd B. Muller and Stuart Newman argue that what they call the "origination of organismal form" remains an unsolved problem. In making this claim, Muller and Newman (2003:3-10) distinguish two distinct issues, namely, (1) the causes of form generation in the individual organism during embryological development and (2) the causes responsible for the production of novel organismal forms in the first place during the history of life. To distinguish the latter case (phylogeny) from the former (ontogeny), Muller and Newman use the term "origination" to designate the causal processes by which biological form first arose during the evolution of life. They insist that "the molecular mechanisms that bring about biological form in modern day embryos should not be confused" with the causes responsible for the origin (or "origination") of novel biological forms during the history of life (p.3). They further argue that we know more about the causes of ontogenesis, due to advances in molecular biology, molecular genetics and developmental biology, than we do about the causes of phylogenesis--the ultimate origination of new biological forms during the remote past.
In making this claim, Muller and Newman are careful to affirm that evolutionary biology has succeeded in explaining how preexisting forms diversify under the twin influences of natural selection and variation of genetic traits. Sophisticated mathematically-based models of population genetics have proven adequate for mapping and understanding quantitative variability and populational changes in organisms. Yet Muller and Newman insist that population genetics, and thus evolutionary biology, has not identified a specifically causal explanation for the origin of true morphological novelty during the history of life. Central to their concern is what they see as the inadequacy of the variation of genetic traits as a source of new form and structure. They note, following Darwin himself, that the sources of new form and structure must precede the action of natural selection (2003:3)--that selection must act on what already exists. Yet, in their view, the "genocentricity" and "incrementalism" of the neo-Darwinian mechanism has meant that an adequate source of new form and structure has yet to be identified by theoretical biologists. Instead, Muller and Newman see the need to identify epigenetic sources of morphological innovation during the evolution of life. In the meantime, however, they insist neo-Darwinism lacks any "theory of the generative" (p. 7).
As it happens, Muller and Newman are not alone in this judgment. In the last decade or so a host of scientific essays and books have questioned the efficacy of selection and mutation as a mechanism for generating morphological novelty, as even a brief literature survey will establish. Thomson (1992:107) expressed doubt that large-scale morphological changes could accumulate via minor phenotypic changes at the population genetic level. Miklos (1993:29) argued that neo-Darwinism fails to provide a mechanism that can produce large-scale innovations in form and complexity. Gilbert et al. (1996) attempted to develop a new theory of evolutionary mechanisms to supplement classical neo-Darwinism, which, they argued, could not adequately explain macroevolution. As they put it in a memorable summary of the situation: "starting in the 1970s, many biologists began questioning its (neo-Darwinism's) adequacy in explaining evolution. Genetics might be adequate for explaining microevolution, but microevolutionary changes in gene frequency were not seen as able to turn a reptile into a mammal or to convert a fish into an amphibian. Microevolution looks at adaptations that concern the survival of the fittest, not the arrival of the fittest. As Goodwin (1995) points out, 'the origin of species--Darwin's problem--remains unsolved'" (p. 361). Though Gilbert et al. (1996) attempted to solve the problem of the origin of form by proposing a greater role for developmental genetics within an otherwise neo-Darwinian framework,1 numerous recent authors have continued to raise questions about the adequacy of that framework itself or about the problem of the origination of form generally (Webster & Goodwin 1996; Shubin & Marshall 2000; Erwin 2000; Conway Morris 2000, 2003b; Carroll 2000; Wagner 2001; Becker & Lonnig 2001; Stadler et al. 2001; Lonnig & Saedler 2002; Wagner & Stadler 2003; Valentine 2004:189-194).
What lies behind this skepticism? Is it warranted? Is a new and specifically causal theory needed to explain the origination of biological form?
This review will address these questions. It will do so by analyzing the problem of the origination of organismal form (and the corresponding emergence of higher taxa) from a particular theoretical standpoint. Specifically, it will treat the problem of the origination of the higher taxonomic groups as a manifestation of a deeper problem, namely, the problem of the origin of the information (whether genetic or epigenetic) that, as it will be argued, is necessary to generate morphological novelty.
In order to perform this analysis, and to make it relevant and tractable to systematists and paleontologists, this paper will examine a paradigmatic example of the origin of biological form and information during the history of life: the Cambrian explosion. During the Cambrian, many novel animal forms and body plans (representing new phyla, subphyla and classes) arose in a geologically brief period of time. The following information-based analysis of the Cambrian explosion will support the claim of recent authors such as Muller and Newman that the mechanism of selection and genetic mutation does not constitute an adequate causal explanation of the origination of biological form in the higher taxonomic groups. It will also suggest the need to explore other possible causal factors for the origin of form and information during the evolution of life and will examine some other possibilities that have been proposed.
The Cambrian Explosion
The "Cambrian explosion" refers to the geologically sudden appearance of many new animal body plans about 530 million years ago. At this time, at least nineteen, and perhaps as many as thirty-five phyla of forty total (Meyer et al. 2003), made their first appearance on earth within a narrow five- to ten-million-year window of geologic time (Bowring et al. 1993, 1998a:1, 1998b:40; Kerr 1993; Monastersky 1993; Aris-Brosou & Yang 2003). Many new subphyla, between 32 and 48 of 56 total (Meyer et al. 2003), and classes of animals also arose at this time with representatives of these new higher taxa manifesting significant morphological innovations. The Cambrian explosion thus marked a major episode of morphogenesis in which many new and disparate organismal forms arose in a geologically brief period of time.
To say that the fauna of the Cambrian period appeared in a geologically sudden manner also implies the absence of clear transitional intermediate forms connecting Cambrian animals with simpler pre-Cambrian forms. And, indeed, in almost all cases, the Cambrian animals have no clear morphological antecedents in earlier Vendian or Precambrian fauna (Miklos 1993, Erwin et al. 1997:132, Steiner & Reitner 2001, Conway Morris 2003b:510, Valentine et al. 2003:519-520). Further, several recent discoveries and analyses suggest that these morphological gaps may not be merely an artifact of incomplete sampling of the fossil record (Foote 1997, Foote et al. 1999, Benton & Ayala 2003, Meyer et al. 2003), suggesting that the fossil record is at least approximately reliable (Conway Morris 2003b:505).
As a result, debate now exists about the extent to which this pattern of evidence comports with a strictly monophyletic view of evolution (Conway Morris 1998a, 2003a, 2003b:510; Willmer 1990, 2003). Further, among those who accept a monophyletic view of the history of life, debate exists about whether to privilege fossil or molecular data and analyses. Those who think the fossil data provide a more reliable picture of the origin of the Metazoan tend to think these animals arose relatively quickly--that the Cambrian explosion had a "short fuse." (Conway Morris 2003b:505-506, Valentine & Jablonski 2003). Some (Wray et al. 1996), but not all (Ayala et al. 1998), who think that molecular phylogenies establish reliable divergence times from pre-Cambrian ancestors think that the Cambrian animals evolved over a very long period of time--that the Cambrian explosion had a "long fuse." This review will not address these questions of historical pattern. Instead, it will analyze whether the neo-Darwinian process of mutation and selection, or other processes of evolutionary change, can generate the form and information necessary to produce the animals that arise in the Cambrian. This analysis will, for the most part, 2 therefore, not depend upon assumptions of either a long or short fuse for the Cambrian explosion, or upon a monophyletic or polyphyletic view of the early history of life.
Defining Biological Form and Information
Form, like life itself, is easy to recognize but often hard to define precisely. Yet, a reasonable working definition of form will suffice for our present purposes. Form can be defined as the four-dimensional topological relations of anatomical parts. This means that one can understand form as a unified arrangement of body parts or material components in a distinct shape or pattern (topology)--one that exists in three spatial dimensions and which arises in time during ontogeny.
Insofar as any particular biological form constitutes something like a distinct arrangement of constituent body parts, form can be seen as arising from constraints that limit the possible arrangements of matter. Specifically, organismal form arises (both in phylogeny and ontogeny) as possible arrangements of material parts are constrained to establish a specific or particular arrangement with an identifiable three dimensional topography--one that we would recognize as a particular protein, cell type, organ, body plan or organism. A particular "form," therefore, represents a highly specific and constrained arrangement of material components (among a much larger set of possible arrangements).
Understanding form in this way suggests a connection to the notion of information in its most theoretically general sense. When Shannon (1948) first developed a mathematical theory of information he equated the amount of information transmitted with the amount of uncertainty reduced or eliminated in a series of symbols or characters. Information, in Shannon's theory, is thus imparted as some options are excluded and others are actualized. The greater the number of options excluded, the greater the amount of information conveyed. Further, constraining a set of possible material arrangements by whatever process or means involves excluding some options and actualizing others. Thus, to constrain a set of possible material states is to generate information in Shannon's sense. It follows that the constraints that produce biological form also imparted information. Or conversely, one might say that producing organismal form by definition requires the generation of information.
In classical Shannon information theory, the amount of information in a system is also inversely related to the probability of the arrangement of constituents in a system or the characters along a communication channel (Shannon 1948). The more improbable (or complex) the arrangement, the more Shannon information, or information-carrying capacity, a string or system possesses.
Since the 1960s, mathematical biologists have realized that Shannon's theory could be applied to the analysis of DNA and proteins to measure the information-carrying capacity of these macromolecules. Since DNA contains the assembly instructions for building proteins, the information-processing system in the cell represents a kind of communication channel (Yockey 1992:110). Further, DNA conveys information via specifically arranged sequences of nucleotide bases. Since each of the four bases has a roughly equal chance of occurring at each site along the spine of the DNA molecule, biologists can calculate the probability, and thus the information-carrying capacity, of any particular sequence n bases long.
The ease with which information theory applies to molecular biology has created confusion about the type of information that DNA and proteins possess. Sequences of nucleotide bases in DNA, or amino acids in a protein, are highly improbable and thus have large information-carrying capacities. But, like meaningful sentences or lines of computer code, genes and proteins are also specified with respect to function. Just as the meaning of a sentence depends upon the specific arrangement of the letters in a sentence, so too does the function of a gene sequence depend upon the specific arrangement of the nucleotide bases in a gene. Thus, molecular biologists beginning with Crick equated information not only with complexity but also with "specificity," where "specificity" or "specified" has meant "necessary to function" (Crick 1958:144, 153; Sarkar, 1996:191).3 Molecular biologists such as Monod and Crick understood biological information--the information stored in DNA and proteins--as something more than mere complexity (or improbability). Their notion of information associated both biochemical contingency and combinatorial complexity with DNA sequences (allowing DNA's carrying capacity to be calculated), but it also affirmed that sequences of nucleotides and amino acids in functioning macromolecules possessed a high degree of specificity relative to the maintenance of cellular function.
The ease with which information theory applies to molecular biology has also created confusion about the location of information in organisms. Perhaps because the information carrying capacity of the gene could be so easily measured, it has been easy to treat DNA, RNA and proteins as the sole repositories of biological information. Neo-Darwinists in particular have assumed that the origination of biological form could be explained by recourse to processes of genetic variation and mutation alone (Levinton 1988:485). Yet if one understands organismal form as resulting from constraints on the possible arrangements of matter at many levels in the biological hierarchy--from genes and proteins to cell types and tissues to organs and body plans--then clearly biological organisms exhibit many levels of information-rich structure.
Thus, we can pose a question, not only about the origin of genetic information, but also about the origin of the information necessary to generate form and structure at levels higher than that present in individual proteins. We must also ask about the origin of the "specified complexity," as opposed to mere complexity, that characterizes the new genes, proteins, cell types and body plans that arose in the Cambrian explosion. Dembski (2002) has used the term "complex specified information" (CSI) as a synonym for "specified complexity" to help distinguish functional biological information from mere Shannon information--that is, specified complexity from mere complexity. This review will use this term as well.
The Cambrian Information Explosion
The Cambrian explosion represents a remarkable jump in the specified complexity or "complex specified information" (CSI) of the biological world. For over three billions years, the biological realm included little more than bacteria and algae (Brocks et al. 1999). Then, beginning about 570-565 million years ago (mya), the first complex multicellular organisms appeared in the rock strata, including sponges, cnidarians, and the peculiar Ediacaran biota (Grotzinger et al. 1995). Forty million years later, the Cambrian explosion occurred (Bowring et al. 1993). The emergence of the Ediacaran biota (570 mya), and then to a much greater extent the Cambrian explosion (530 mya), represented steep climbs up the biological complexity gradient.
One way to estimate the amount of new CSI that appeared with the Cambrian animals is to count the number of new cell types that emerged with them (Valentine 1995:91-93). Studies of modern animals suggest that the sponges that appeared in the late Precambrian, for example, would have required five cell types, whereas the more complex animals that appeared in the Cambrian (e.g., arthropods) would have required fifty or more cell types. Functionally more complex animals require more cell types to perform their more diverse functions. New cell types require many new and specialized proteins. New proteins, in turn, require new genetic information. Thus an increase in the number of cell types implies (at a minimum) a considerable increase in the amount of specified genetic information. Molecular biologists have recently estimated that a minimally complex single-celled organism would require between 318 and 562 kilobase pairs of DNA to produce the proteins necessary to maintain life (Koonin 2000). More complex single cells might require upward of a million base pairs. Yet to build the proteins necessary to sustain a complex arthropod such as a trilobite would require orders of magnitude more coding instructions. The genome size of a modern arthropod, the fruitfly Drosophila melanogaster, is approximately 180 million base pairs (Gerhart & Kirschner 1997:121, Adams et al. 2000). Transitions from a single cell to colonies of cells to complex animals represent significant (and, in principle, measurable) increases in CSI.
Building a new animal from a single-celled organism requires a vast amount of new genetic information. It also requires a way of arranging gene products--proteins--into higher levels of organization. New proteins are required to service new cell types. But new proteins must be organized into new systems within the cell; new cell types must be organized into new tissues, organs, and body parts. These, in turn, must be organized to form body plans. New animals, therefore, embody hierarchically organized systems of lower-level parts within a functional whole. Such hierarchical organization itself represents a type of information, since body plans comprise both highly improbable and functionally specified arrangements of lower-level parts. The specified complexity of new body plans requires explanation in any account of the Cambrian explosion.
Can neo-Darwinism explain the discontinuous increase in CSI that appears in the Cambrian explosion--either in the form of new genetic information or in the form of hierarchically organized systems of parts? We will now examine the two parts of this question.
Novel Genes and Proteins
Many scientists and mathematicians have questioned the ability of mutation and selection to generate information in the form of novel genes and proteins. Such skepticism often derives from consideration of the extreme improbability (and specificity) of functional genes and proteins.
A typical gene contains over one thousand precisely arranged bases. For any specific arrangement of four nucleotide bases of length n, there is a corresponding number of possible arrangements of bases, 4n. For any protein, there are 20n possible arrangements of protein-forming amino acids. A gene 999 bases in length represents one of 4999 possible nucleotide sequences; a protein of 333 amino acids is one of 20333 possibilities.
Since the 1960s, some biologists have thought functional proteins to be rare among the set of possible amino acid sequences. Some have used an analogy with human language to illustrate why this should be the case. Denton (1986, 309-311), for example, has shown that meaningful words and sentences are extremely rare among the set of possible combinations of English letters, especially as sequence length grows. (The ratio of meaningful 12-letter words to 12-letter sequences is 1/1014, the ratio of 100-letter sentences to possible 100-letter strings is 1/10100.) Further, Denton shows that most meaningful sentences are highly isolated from one another in the space of possible combinations, so that random substitutions of letters will, after a very few changes, inevitably degrade meaning. Apart from a few closely clustered sentences accessible by random substitution, the overwhelming majority of meaningful sentences lie, probabilistically speaking, beyond the reach of random search.
Denton (1986:301-324) and others have argued that similar constraints apply to genes and proteins. They have questioned whether an undirected search via mutation and selection would have a reasonable chance of locating new islands of function--representing fundamentally new genes or proteins--within the time available (Eden 1967, Shutzenberger 1967, Lovtrup 1979). Some have also argued that alterations in sequencing would likely result in loss of protein function before fundamentally new function could arise (Eden 1967, Denton 1986). Nevertheless, neither the extent to which genes and proteins are sensitive to functional loss as a result of sequence change, nor the extent to which functional proteins are isolated within sequence space, has been fully known.
Recently, experiments in molecular biology have shed light on these questions. A variety of mutagenesis techniques have shown that proteins (and thus the genes that produce them) are indeed highly specified relative to biological function (Bowie & Sauer 1989, Reidhaar-Olson & Sauer 1990, Taylor et al. 2001). Mutagenesis research tests the sensitivity of proteins (and, by implication, DNA) to functional loss as a result of alterations in sequencing. Studies of proteins have long shown that amino acid residues at many active positions cannot vary without functional loss (Perutz & Lehmann 1968). More recent protein studies (often using mutagenesis experiments) have shown that functional requirements place significant constraints on sequencing even at non-active site positions (Bowie & Sauer 1989, Reidhaar-Olson & Sauer 1990, Chothia et al. 1998, Axe 2000, Taylor et al. 2001). In particular, Axe (2000) has shown that multiple as opposed to single position amino acid substitutions inevitably result in loss of protein function, even when these changes occur at sites that allow variation when altered in isolation. Cumulatively, these constraints imply that proteins are highly sensitive to functional loss as a result of alterations in sequencing, and that functional proteins represent highly isolated and improbable arrangements of amino acids -arrangements that are far more improbable, in fact, than would be likely to arise by chance alone in the time available (Reidhaar-Olson & Sauer 1990; Behe 1992; Kauffman 1995:44; Dembski 1998:175-223; Axe 2000, 2004). (See below the discussion of the neutral theory of evolution for a precise quantitative assessment.)
Of course, neo-Darwinists do not envision a completely random search through the set of all possible nucleotide sequences--so-called "sequence space." They envision natural selection acting to preserve small advantageous variations in genetic sequences and their corresponding protein products. Dawkins (1996), for example, likens an organism to a high mountain peak. He compares climbing the sheer precipice up the front side of the mountain to building a new organism by chance. He acknowledges that his approach up "Mount Improbable" will not succeed. Nevertheless, he suggests that there is a gradual slope up the backside of the mountain that could be climbed in small incremental steps. In his analogy, the backside climb up "Mount Improbable" corresponds to the process of natural selection acting on random changes in the genetic text. What chance alone cannot accomplish blindly or in one leap, selection (acting on mutations) can accomplish through the cumulative effect of many slight successive steps.
Yet the extreme specificity and complexity of proteins presents a difficulty, not only for the chance origin of specified biological information (i.e., for random mutations acting alone), but also for selection and mutation acting in concert. Indeed, mutagenesis experiments cast doubt on each of the two scenarios by which neo-Darwinists envisioned new information arising from the mutation/selection mechanism (for review, see Lonnig 2001). For neo-Darwinism, new functional genes either arise from non-coding sections in the genome or from preexisting genes. Both scenarios are problematic.
In the first scenario, neo-Darwinists envision new genetic information arising from those sections of the genetic text that can presumably vary freely without consequence to the organism. According to this scenario, non-coding sections of the genome, or duplicated sections of coding regions, can experience a protracted period of "neutral evolution" (Kimura 1983) during which alterations in nucleotide sequences have no discernible effect on the function of the organism. Eventually, however, a new gene sequence will arise that can code for a novel protein. At that point, natural selection can favor the new gene and its functional protein product, thus securing the preservation and heritability of both.
This scenario has the advantage of allowing the genome to vary through many generations, as mutations "search" the space of possible base sequences. The scenario has an overriding problem, however: the size of the combinatorial space (i.e., the number of possible amino acid sequences) and the extreme rarity and isolation of the functional sequences within that space of possibilities. Since natural selection can do nothing to help generate new functional sequences, but rather can only preserve such sequences once they have arisen, chance alone--random variation--must do the work of information generation--that is, of finding the exceedingly rare functional sequences within the set of combinatorial possibilities. Yet the probability of randomly assembling (or "finding," in the previous sense) a functional sequence is extremely small.
Cassette mutagenesis experiments performed during the early 1990s suggest that the probability of attaining (at random) the correct sequencing for a short protein 100 amino acids long is about 1 in 1065 (Reidhaar-Olson & Sauer 1990, Behe 1992:65-69). This result agreed closely with earlier calculations that Yockey (1978) had performed based upon the known sequence variability of cytochrome c in different species and other theoretical considerations. More recent mutagenesis research has provided additional support for the conclusion that functional proteins are exceedingly rare among possible amino acid sequences (Axe 2000, 2004). Axe (2004) has performed site directed mutagenesis experiments on a 150-residue protein-folding domain within a B-lactamase enzyme. His experimental method improves upon earlier mutagenesis techniques and corrects for several sources of possible estimation error inherent in them. On the basis of these experiments, Axe has estimated the ratio of (a) proteins of typical size (150 residues) that perform a specified function via any folded structure to (b) the whole set of possible amino acids sequences of that size. Based on his experiments, Axe has estimated his ratio to be 1 to 1077. Thus, the probability of finding a functional protein among the possible amino acid sequences corresponding to a 150-residue protein is similarly 1 in 1077.
Other considerations imply additional improbabilities. First, new Cambrian animals would require proteins much longer than 100 residues to perform many necessary specialized functions. Ohno (1996) has noted that Cambrian animals would have required complex proteins such as lysyl oxidase in order to support their stout body structures. Lysyl oxidase molecules in extant organisms comprise over 400 amino acids. These molecules are both highly complex (non-repetitive) and functionally specified. Reasonable extrapolation from mutagenesis experiments done on shorter protein molecules suggests that the probability of producing functionally sequenced proteins of this length at random is so small as to make appeals to chance absurd, even granting the duration of the entire universe. (See Dembski 1998:175-223 for a rigorous calculation of this "Universal Probability Bound"; See also Axe 2004.) Yet, second, fossil data (Bowring et al. 1993, 1998a:1, 1998b:40; Kerr 1993; Monatersky 1993), and even molecular analyses supporting deep divergence (Wray et al. 1996), suggest that the duration of the Cambrian explosion (between 5-10 x 106 and, at most, 7 x 107 years) is far smaller than that of the entire universe (1.3-2 x 1010 years). Third, DNA mutation rates are far too low to generate the novel genes and proteins necessary to building the Cambrian animals, given the most probable duration of the explosion as determined by fossil studies (Conway Morris 1998b). As Ohno (1996:8475) notes, even a mutation rate of 10-9 per base pair per year results in only a 1% change in the sequence of a given section of DNA in 10 million years. Thus, he argues that mutational divergence of preexisting genes cannot explain the origin of the Cambrian forms in that time.4
The selection/mutation mechanism faces another probabilistic obstacle. The animals that arise in the Cambrian exhibit structures that would have required many new types of cells, each of which would have required many novel proteins to perform their specialized functions. Further, new cell types require Asystems of proteins that must, as a condition of functioning, act in close coordination with one another. The unit of selection in such systems ascends to the system as a whole. Natural selection selects for functional advantage. But new cell types require whole systems of proteins to perform their distinctive functions. In such cases, natural selection cannot contribute to the process of information generation until after the information necessary to build the requisite system of proteins has arisen. Thus random variations must, again, do the work of information generation--and now not simply for one protein, but for many proteins arising at nearly the same time. Yet the odds of this occurring by chance alone are, of course, far smaller than the odds of the chance origin of a single gene or protein--so small in fact as to render the chance origin of the genetic information necessary to build a new cell type (a necessary but not sufficient condition of building a new body plan) problematic given even the most optimistic estimates for the duration of the Cambrian explosion.
Dawkins (1986:139) has noted that scientific theories can rely on only so much "luck" before they cease to be credible. The neutral theory of evolution, which, by its own logic, prevents natural selection from playing a role in generating genetic information until after the fact, relies on entirely too much luck. The sensitivity of proteins to functional loss, the need for long proteins to build new cell types and animals, the need for whole new systems of proteins to service new cell types, the probable brevity of the Cambrian explosion relative to mutation rates--all suggest the immense improbability (and implausibility) of any scenario for the origination of Cambrian genetic information that relies upon random variation alone unassisted by natural selection.
Yet the neutral theory requires novel genes and proteins to arise--essentially--by random mutation alone. Adaptive advantage accrues after the generation of new functional genes and proteins. Thus, natural selection cannot play a role until new information-bearing molecules have independently arisen. Thus neutral theorists envisioned the need to scale the steep face of a Dawkins-style precipice of which there is no gradually sloping backside--a situation that, by Dawkins' own logic, is probabilistically untenable.
In the second scenario, neo-Darwinists envisioned novel genes and proteins arising by numerous successive mutations in the preexisting genetic text that codes for proteins. To adapt Dawkins's metaphor, this scenario envisions gradually climbing down one functional peak and then ascending another. Yet mutagenesis experiments again suggest a difficulty. Recent experiments show that, even when exploring a region of sequence space populated by proteins of a single fold and function, most multiple-position changes quickly lead to loss of function (Axe 2000). Yet to turn one protein into another with a completely novel structure and function requires specified changes at many sites. Indeed, the number of changes necessary to produce a new protein greatly exceeds the number of changes that will typically produce functional losses. Given this, the probability of escaping total functional loss during a random search for the changes needed to produce a new function is extremely small--and this probability diminishes exponentially with each additional requisite change (Axe 2000). Thus, Axe's results imply that, in all probability, random searches for novel proteins (through sequence space) will result in functional loss long before any novel functional protein will emerge.
Blanco et al. have come to a similar conclusion. Using directed mutagenesis, they have determined that residues in both the hydrophobic core and on the surface of the protein play essential roles in determining protein structure. By sampling intermediate sequences between two naturally occurring sequences that adopt different folds, they found that the intermediate sequences "lack a well defined three-dimensional structure." Thus, they conclude that it is unlikely that a new protein fold via a series of folded intermediates sequences (Blanco et al. 1999:741).
Thus, although this second neo-Darwinian scenario has the advantage of starting with functional genes and proteins, it also has a lethal disadvantage: any process of random mutation or rearrangement in the genome would in all probability generate nonfunctional intermediate sequences before fundamentally new functional genes or proteins would arise. Clearly, nonfunctional intermediate sequences confer no survival advantage on their host organisms. Natural selection favors only functional advantage. It cannot select or favor nucleotide sequences or polypeptide chains that do not yet perform biological functions, and still less will it favor sequences that efface or destroy preexisting function.
Evolving genes and proteins will range through a series of nonfunctional intermediate sequences that natural selection will not favor or preserve but will, in all probability, eliminate (Blanco et al. 1999, Axe 2000). When this happens, selection-driven evolution will cease. At this point, neutral evolution of the genome (unhinged from selective pressure) may ensue, but, as we have seen, such a process must overcome immense probabilistic hurdles, even granting cosmic time.
Thus, whether one envisions the evolutionary process beginning with a noncoding region of the genome or a preexisting functional gene, the functional specificity and complexity of proteins impose very stringent limitations on the efficacy of mutation and selection. In the first case, function must arise first, before natural selection can act to favor a novel variation. In the second case, function must be continuously maintained in order to prevent deleterious (or lethal) consequences to the organism and to allow further evolution. Yet the complexity and functional specificity of proteins implies that both these conditions will be extremely difficult to meet. Therefore, the neo-Darwinian mechanism appears to be inadequate to generate the new information present in the novel genes and proteins that arise with the Cambrian animals.
Novel Body Plans
The problems with the neo-Darwinian mechanism run deeper still. In order to explain the origin of the Cambrian animals, one must account not only for new proteins and cell types, but also for the origin of new body plans. Within the past decade, developmental biology has dramatically advanced our understanding of how body plans are built during ontogeny. In the process, it has also uncovered a profound difficulty for neo-Darwinism.
Significant morphological change in organisms requires attention to timing. Mutations in genes that are expressed late in the development of an organism will not affect the body plan. Mutations expressed early in development, however, could conceivably produce significant morphological change (Arthur 1997:21). Thus, events expressed early in the development of organisms have the only realistic chance of producing large-scale macroevolutionary change (Thomson 1992). As John and Miklos (1988:309) explain, macroevolutionary change requires alterations in the very early stages of ontogenesis.
Yet recent studies in developmental biology make clear that mutations expressed early in development typically have deleterious effects (Arthur 1997:21). For example, when early-acting body plan molecules, or morphogens such as bicoid (which helps to set up the anterior-posterior head-to-tail axis in Drosophila), are perturbed, development shuts down (Nusslein-Volhard & Wieschaus 1980, Lawrence & Struhl 1996, Muller & Newman 2003).5 The resulting embryos die. Moreover, there is a good reason for this. If an engineer modifies the length of the piston rods in an internal combustion engine without modifying the crankshaft accordingly, the engine won't start. Similarly, processes of development are tightly integrated spatially and temporally such that changes early in development will require a host of other coordinated changes in separate but functionally interrelated developmental processes downstream. For this reason, mutations will be much more likely to be deadly if they disrupt a functionally deeply-embedded structure such as a spinal column than if they affect more isolated anatomical features such as fingers (Kauffman 1995:200).
This problem has led to what McDonald (1983) has called "a great Darwinian paradox" (p. 93). McDonald notes that genes that are observed to vary within natural populations do not lead to major adaptive changes, while genes that could cause major changes--the very stuff of macroevolution--apparently do not vary. In other words, mutations of the kind that macroevolution doesn't need (namely, viable genetic mutations in DNA expressed late in development) do occur, but those that it does need (namely, beneficial body plan mutations expressed early in development) apparently don't occur.6 According to Darwin (1859:108) natural selection cannot act until favorable variations arise in a population. Yet there is no evidence from developmental genetics that the kind of variations required by neo-Darwinism--namely, favorable body plan mutations--ever occur.
Developmental biology has raised another formidable problem for the mutation/selection mechanism. Embryological evidence has long shown that DNA does not wholly determine morphological form (Goodwin 1985, Nijhout 1990, Sapp 1987, Muller & Newman 2003), suggesting that mutations in DNA alone cannot account for the morphological changes required to build a new body plan.
DNA helps direct protein synthesis.7 It also helps to regulate the timing and expression of the synthesis of various proteins within cells. Yet, DNA alone does not determine how individual proteins assemble themselves into larger systems of proteins; still less does it solely determine how cell types, tissue types, and organs arrange themselves into body plans (Harold 1995:2774, Moss 2004). Instead, other factors--such as the three-dimensional structure and organization of the cell membrane and cytoskeleton and the spatial architecture of the fertilized egg--play important roles in determining body plan formation during embryogenesis.
For example, the structure and location of the cytoskeleton influence the patterning of embryos. Arrays of microtubules help to distribute the essential proteins used during development to their correct locations in the cell. Of course, microtubules themselves are made of many protein subunits. Nevertheless, like bricks that can be used to assemble many different structures, the tubulin subunits in the cell's microtubules are identical to one another. Thus, neither the tubulin subunits nor the genes that produce them account for the different shape of microtubule arrays that distinguish different kinds of embryos and developmental pathways. Instead, the structure of the microtubule array itself is determined by the location and arrangement of its subunits, not the properties of the subunits themselves. For this reason, it is not possible to predict the structure of the cytoskeleton of the cell from the characteristics of the protein constituents that form that structure (Harold 2001:125).
Two analogies may help further clarify the point. At a building site, builders will make use of many materials: lumber, wires, nails, drywall, piping, and windows. Yet building materials do not determine the floor plan of the house, or the arrangement of houses in a neighborhood. Similarly, electronic circuits are composed of many components, such as resistors, capacitors, and transistors. But such lower-level components do not determine their own arrangement in an integrated circuit. Biological symptoms also depend on hierarchical arrangements of parts. Genes and proteins are made from simple building blocks--nucleotide bases and amino acids--arranged in specific ways. Cell types are made of, among other things, systems of specialized proteins. Organs are made of specialized arrangements of cell types and tissues. And body plans comprise specific arrangements of specialized organs. Yet, clearly, the properties of individual proteins (or, indeed, the lower-level parts in the hierarchy generally) do not fully determine the organization of the higher-level structures and organizational patterns (Harold 2001:125). It follows that the genetic information that codes for proteins does not determine these higher-level structures either.
These considerations pose another challenge to the sufficiency of the neo-Darwinian mechanism. Neo-Darwinism seeks to explain the origin of new information, form, and structure as a result of selection acting on randomly arising variation at a very low level within the biological hierarchy, namely, within the genetic text. Yet major morphological innovations depend on a specificity of arrangement at a much higher level of the organizational hierarchy, a level that DNA alone does not determine. Yet if DNA is not wholly responsible for body plan morphogenesis, then DNA sequences can mutate indefinitely, without regard to realistic probabilistic limits, and still not produce a new body plan. Thus, the mechanism of natural selection acting on random mutations in DNA cannot in principle generate novel body plans, including those that first arose in the Cambrian explosion.
Of course, it could be argued that, while many single proteins do not by themselves determine cellular structures and/or body plans, proteins acting in concert with other proteins or suites of proteins could determine such higher-level form. For example, it might be pointed out that the tubulin subunits (cited above) are assembled by other helper proteins--gene products--called Microtubule Associated Proteins (MAPS). This might seem to suggest that genes and gene products alone do suffice to determine the development of the three-dimensional structure of the cytoskeleton.
Yet MAPS, and indeed many other necessary proteins, are only part of the story. The location of specified target sites on the interior of the cell membrane also helps to determine the shape of the cytoskeleton. Similarly, so does the position and structure of the centrosome which nucleates the microtubules that form the cytoskeleton. While both the membrane targets and the centrosomes are made of proteins, the location and form of these structures is not wholly determined by the proteins that form them. Indeed, centrosome structure and membrane patterns as a whole convey three-dimensional structural information that helps determine the structure of the cytoskeleton and the location of its subunits (McNiven & Porter 1992:313-329). Moreover, the centrioles that compose the centrosomes replicate independently of DNA replication (Lange et al. 2000:235-249, Marshall & Rosenbaum 2000:187-205). The daughter centriole receives its form from the overall structure of the mother centriole, not from the individual gene products that constitute it (Lange et al. 2000). In ciliates, microsurgery on cell membranes can produce heritable changes in membrane patterns, even though the DNA of the ciliates has not been altered (Sonneborn 1970:1-13, Frankel 1980:607-623; Nanney 1983:163-170). This suggests that membrane patterns (as opposed to membrane constituents) are impressed directly on daughter cells. In both cases, form is transmitted from parent three-dimensional structures to daughter three-dimensional structures directly and is not wholly contained in constituent proteins or genetic information (Moss 2004).
Thus, in each new generation, the form and structure of the cell arises as the result of both gene products and preexisting three-dimensional structure and organization. Cellular structures are built from proteins, but proteins find their way to correct locations in part because of preexisting three-dimensional patterns and organization inherent in cellular structures. Preexisting three-dimensional form present in the preceding generation (whether inherent in the cell membrane, the centrosomes, the cytoskeleton or other features of the fertilized egg) contributes to the production of form in the next generation. Neither structural proteins alone, nor the genes that code for them, are sufficient to determine the three-dimensional shape and structure of the entities they form. Gene products provide necessary, but not sufficient conditions, for the development of three-dimensional structure within cells, organs and body plans (Harold 1995:2767). But if this is so, then natural selection acting on genetic variation alone cannot produce the new forms that arise in history of life.
Of course, neo-Darwinism is not the only evolutionary theory for explaining the origin of novel biological form. Kauffman (1995) doubts the efficacy of the mutation/selection mechanism. Nevertheless, he has advanced a self-organizational theory to account for the emergence of new form, and presumably the information necessary to generate it. Whereas neo-Darwinism attempts to explain new form as the consequence of selection acting on random mutation, Kauffman suggests that selection acts, not mainly on random variations, but on emergent patterns of order that self-organize via the laws of nature.
Kauffman (1995:47-92) illustrates how this might work with various model systems in a computer environment. In one, he conceives a system of buttons connected by strings. Buttons represent novel genes or gene products; strings represent the law-like forces of interaction that obtain between gene products-i.e., proteins. Kauffman suggests that when the complexity of the system (as represented by the number of buttons and strings) reaches a critical threshold, new modes of organization can arise in the system "for free"--that is, naturally and spontaneously--after the manner of a phase transition in chemistry.
Another model that Kauffman develops is a system of interconnected lights. Each light can flash in a variety of states--on, off, twinkling, etc. Since there is more than one possible state for each light, and many lights, there are a vast number of possible states that the system can adopt. Further, in his system, rules determine how past states will influence future states. Kauffman asserts that, as a result of these rules, the system will, if properly tuned, eventually produce a kind of order in which a few basic patterns of light activity recur with greater-than-random frequency. Since these actual patterns of light activity represent a small portion of the total number of possible states in which the system can reside, Kauffman seems to imply that self-organizational laws might similarly result in highly improbable biological outcomes--perhaps even sequences (of bases or amino acids) within a much larger sequence space of possibilities.
Do these simulations of self-organizational processes accurately model the origin of novel genetic information? It is hard to think so.
First, in both examples, Kauffman presupposes but does not explain significant sources of preexisting information. In his buttons-and-strings system, the buttons represent proteins, themselves packets of CSI, and the result of preexisting genetic information. Where does this information come from? Kauffman (1995) doesn't say, but the origin of such information is an essential part of what needs to be explained in the history of life. Similarly, in his light system, the order that allegedly arises for "for free" actually arises only if the programmer of the model system "tunes" it in such a way as to keep it from either (a) generating an excessively rigid order or (b) developing into chaos (pp. 86-88). Yet this necessary tuning involves an intelligent programmer selecting certain parameters and excluding others--that is, inputting information.
Second, Kauffman's model systems are not constrained by functional considerations and thus are not analogous to biological systems. A system of interconnected lights governed by pre-programmed rules may well settle into a small number of patterns within a much larger space of possibilities. But because these patterns have no function, and need not meet any functional requirements, they have no specificity analogous to that present in actual organisms. Instead, examination of Kauffman's (1995) model systems shows that they do not produce sequences or systems characterized by specified complexity, but instead by large amounts of symmetrical order or internal redundancy interspersed with aperiodicity or (mere) complexity (pp. 53, 89, 102). Getting a law-governed system to generate repetitive patterns of flashing lights, even with a certain amount of variation, is clearly interesting, but not biologically relevant. On the other hand, a system of lights flashing the title of a Broadway play would model a biologically relevant self-organizational process, at least if such a meaningful or functionally specified sequence arose without intelligent agents previously programming the system with equivalent amounts of CSI. In any case, Kauffman's systems do not produce specified complexity, and thus do not offer promising models for explaining the new genes and proteins that arose in the Cambrian.
Even so, Kauffman suggests that his self-organizational models can specifically elucidate aspects of the Cambrian explosion. According to Kauffman (1995:199-201), new Cambrian animals emerged as the result of "long jump" mutations that established new body plans in a discrete rather than gradual fashion. He also recognizes that mutations affecting early development are almost inevitably harmful. Thus, he concludes that body plans, once established, will not change, and that any subsequent evolution must occur within an established body plan (Kauffman 1995:201). And indeed, the fossil record does show a curious (from a neo-Darwinian point of view) top-down pattern of appearance, in which higher taxa (and the body plans they represent) appear first, only later to be followed by the multiplication of lower taxa representing variations within those original body designs (Erwin et al. 1987, Lewin 1988, Valentine & Jablonski 2003:518). Further, as Kauffman expects, body plans appear suddenly and persist without significant modification over time.
But here, again, Kauffman begs the most important question, which is: what produces the new Cambrian body plans in the first place? Granted, he invokes "long jump mutations" to explain this, but he identifies no specific self-organizational process that can produce such mutations. Moreover, he concedes a principle that undermines the plausibility of his own proposal. Kauffman acknowledges that mutations that occur early in development are almost inevitably deleterious. Yet developmental biologists know that these are the only kind of mutations that have a realistic chance of producing large-scale evolutionary change--i.e., the big jumps that Kauffman invokes. Though Kauffman repudiates the neo-Darwinian reliance upon random mutations in favor of self-organizing order, in the end, he must invoke the most implausible kind of random mutation in order to provide a self-organizational account of the new Cambrian body plans. Clearly, his model is not sufficient.
Of course, still other causal explanations have been proposed. During the 1970s, the paleontologists Eldredge and Gould (1972) proposed the theory of evolution by punctuated equilibrium in order to account for a pervasive pattern of "sudden appearance" and "stasis" in the fossil record. Though advocates of punctuated equilibrium were mainly seeking to describe the fossil record more accurately than earlier gradualist neo-Darwinian models had done, they did also propose a mechanism--known as species selection--by which the large morphological jumps evident in fossil record might have been produced. According to punctuationalists, natural selection functions more as a mechanism for selecting the fittest species rather than the most-fit individual among a species. Accordingly, on this model, morphological change should occur in larger, more discrete intervals than it would given a traditional neo-Darwinian understanding.
Despite its virtues as a descriptive model of the history of life, punctuated equilibrium has been widely criticized for failing to provide a mechanism sufficient to produce the novel form characteristic of higher taxonomic groups. For one thing, critics have noted that the proposed mechanism of punctuated evolutionary change simply lacked the raw material upon which to work. As Valentine and Erwin (1987) note, the fossil record fails to document a large pool of species prior to the Cambrian. Yet the proposed mechanism of species selection requires just such a pool of species upon which to act. Thus, they conclude that the mechanism of species selection probably does not resolve the problem of the origin of the higher taxonomic groups (p. 96).8 Further, punctuated equilibrium has not addressed the more specific and fundamental problem of explaining the origin of the new biological information (whether genetic or epigenetic) necessary to produce novel biological form. Advocates of punctuated equilibrium might assume that the new species (upon which natural selection acts) arise by known microevolutionary processes of speciation (such as founder effect, genetic drift or bottleneck effect) that do not necessarily depend upon mutations to produce adaptive changes. But, in that case, the theory lacks an account of how the specifically higher taxa arise. Species selection will only produce more fit species. On the other hand, if punctuationalists assume that processes of genetic mutation can produce more fundamental morphological changes and variations, then their model becomes subject to the same problems as neo-Darwinism (see above). This dilemma is evident in Gould (2002:710) insofar as his attempts to explain adaptive complexity inevitably employ classical neo-Darwinian modes of explanation.9
Another attempt to explain the origin of form has been proposed by the structuralists such as Gerry Webster and Brian Goodwin (1984, 1996). These biologists, drawing on the earlier work of D'Arcy Thompson (1942), view biological form as the result of structural constraints imposed upon matter by morphogenetic rules or laws. For reasons similar to those discussed above, the structuralists have insisted that these generative or morphogenetic rules do not reside in the lower level building materials of organisms, whether in genes or proteins. Webster and Goodwin (1984:510-511) further envisioned morphogenetic rules or laws operating ahistorically, similar to the way in which gravitational or electromagnetic laws operate. For this reason, structuralists see phylogeny as of secondary importance in understanding the origin of the higher taxa, though they think that transformations of form can occur. For structuralists, constraints on the arrangement of matter arise not mainly as the result of historical contingencies--such as environmental changes or genetic mutations--but instead because of the continuous ahistorical operation of fundamental laws of form--laws that organize or inform matter.
While this approach avoids many of the difficulties currently afflicting neo-Darwinism (in particular those associated with its "genocentricity"), critics (such as Maynard Smith 1986) of structuralism have argued that the structuralist explanation of form lacks specificity. They note that structuralists have been unable to say just where laws of form reside--whether in the universe, or in every possible world, or in organisms as a whole, or in just some part of organisms. Further, according to structuralists, morphogenetic laws are mathematical in character. Yet, structuralists have yet to specify the mathematical formulae that determine biological forms.
Others (Yockey 1992; Polanyi 1967, 1968; Meyer 2003) have questioned whether physical laws could in principle generate the kind of complexity that characterizes biological systems. Structuralists envision the existence of biological laws that produce form in much the same way that physical laws produce form. Yet the forms that physicists regard as manifestations of underlying laws are characterized by large amounts of symmetric or redundant order, by relatively simple patterns such as vortices or gravitational fields or magnetic lines of force. Indeed, physical laws are typically expressed as differential equations (or algorithms) that almost by definition describe recurring phenomena--patterns of compressible "order" not "complexity" as defined by algorithmic information theory (Yockey 1992:77-83). Biological forms, by contrast, manifest greater complexity and derive in ontogeny from highly complex initial conditions--i.e., non-redundant sequences of nucleotide bases in the genome and other forms of information expressed in the complex and irregular three-dimensional topography of the organism or the fertilized egg. Thus, the kind of form that physical laws produce is not analogous to biological form--at least not when compared from the standpoint of (algorithmic) complexity. Further, physical laws lack the information content to specify biology systems. As Polyanyi (1967, 1968) and Yockey (1992:290) have shown, the laws of physics and chemistry allow, but do not determine, distinctively biological modes of organization. In other words, living systems are consistent with, but not deducible, from physical-chemical laws (1992:290).
Of course, biological systems do manifest some reoccurring patterns, processes and behaviors. The same type of organism develops repeatedly from similar ontogenetic processes in the same species. Similar processes of cell division reoccur in many organisms. Thus, one might describe certain biological processes as law-governed. Even so, the existence of such biological regularities does not solve the problem of the origin of form and information, since the recurring processes described by such biological laws (if there be such laws) only occur as the result of preexisting stores of (genetic and/or epigenetic) information and these information-rich initial conditions impose the constraints that produce the recurring behavior in biological systems. (For example, processes of cell division recur with great frequency in organisms, but depend upon information-rich DNA and proteins molecules.) In other words, distinctively biological regularities depend upon preexisting biological information. Thus, appeals to higher-level biological laws presuppose, but do not explain, the origination of the information necessary to morphogenesis.
Thus, structuralism faces a difficult in principle dilemma. On the one hand, physical laws produce very simple redundant patterns that lack the complexity characteristic of biological systems. On the other hand, distinctively biological laws--if there are such laws--depend upon preexisting information-rich structures. In either case, laws are not good candidates for explaining the origination of biological form or the information necessary to produce it.
Cladism: An Artifact of Classification?
Some cladists have advanced another approach to the problem of the origin of form, specifically as it arises in the Cambrian. They have argued that the problem of the origin of the phyla is an artifact of the classification system, and therefore, does not require explanation. Budd and Jensen (2000), for example, argue that the problem of the Cambrian explosion resolves itself if one keeps in mind the cladistic distinction between "stem" and "crown" groups. Since crown groups arise whenever new characters are added to simpler more ancestral stem groups during the evolutionary process, new phyla will inevitably arise once a new stem group has arisen. Thus, for Budd and Jensen what requires explanation is not the crown groups corresponding to the new Cambrian phyla, but the earlier more primitive stem groups that presumably arose deep in the Proterozoic. Yet since these earlier stem groups are by definition less derived, explaining them will be considerably easier than explaining the origin of the Cambrian animals de novo. In any case, for Budd and Jensen the explosion of new phyla in the Cambrian does not require explanation. As they put it, "given that the early branching points of major clades is an inevitable result of clade diversification, the alleged phenomenon of the phyla appearing early and remaining morphologically static is not seen to require particular explanation" (Budd & Jensen 2000:253).
While superficially plausible, perhaps, Budd and Jensen's attempt to explain away the Cambrian explosion begs crucial questions. Granted, as new characters are added to existing forms, novels morphology and greater morphological disparity will likely result. But what causes new characters to arise? And how does the information necessary to produce new characters originate? Budd and Jensen do not specify. Nor can they say how derived the ancestral forms are likely to have been, and what processes, might have been sufficient to produce them. Instead, they simply assume the sufficiency of known neo-Darwinian mechanisms (Budd & Jensen 2000:288). Yet, as shown above, this assumption is now problematic. In any case, Budd and Jensen do not explain what causes the origination of biological form and information.
Convergence and Teleological Evolution
More recently, Conway Morris (2000, 2003c) has suggested another possible explanation based on the tendency for evolution to converge on the same structural forms during the history of life. Conway Morris cites numerous examples of organisms that possess very similar forms and structures, even though such structures are often built from different material substrates and arise (in ontogeny) by the expression of very different genes. Given the extreme improbability of the same structures arising by random mutation and selection in disparate phylogenies, Conway Morris argues that the pervasiveness of convergent structures suggests that evolution may be in some way "channeled" toward similar functional and/or structural endpoints. Such an end-directed understanding of evolution, he admits, raises the controversial prospect of a teleological or purposive element in the history of life. For this reason, he argues that the phenomenon of convergence has received less attention than it might have otherwise. Nevertheless, he argues that just as physicists have reopened the question of design in their discussions of anthropic fine-tuning, the ubiquity of convergent structures in the history of life has led some biologists (Denton 1998) to consider extending teleological thinking to biology. And, indeed, Conway Morris himself intimates that the evolutionary process might be "underpinned by a purpose" (2000:8, 2003b:511).
Conway Morris, of course, considers this possibility in relation to a very specific aspect of the problem of organismal form, namely, the problem of explaining why the same forms arise repeatedly in so many disparate lines of decent. But this raises a question. Could a similar approach shed explanatory light on the more general causal question that has been addressed in this review? Could the notion of purposive design help provide a more adequate explanation for the origin of organismal form generally? Are there reasons to consider design as an explanation for the origin of the biological information necessary to produce the higher taxa and their corresponding morphological novelty?
The remainder of this review will suggest that there are such reasons. In so doing, it may also help explain why the issue of teleology or design has reemerged within the scientific discussion of biological origins (Denton 1986, 1998; Thaxton et al. 1992; Kenyon & Mills 1996: Behe 1996, 2004; Dembski 1998, 2002, 2004; Conway Morris 2000, 2003a, 2003b, Lonnig 2001; Lonnig & Saedler 2002; Nelson & Wells 2003; Meyer 2003, 2004; Bradley 2004) and why some scientists and philosophers of science have considered teleological explanations for the origin of form and information despite strong methodological prohibitions against design as a scientific hypothesis (Gillespie 1979, Lenior 1982:4).
First, the possibility of design as an explanation follows logically from a consideration of the deficiencies of neo-Darwinism and other current theories as explanations for some of the more striking "appearances of design" in biological systems. Neo-Darwinists such as Ayala (1994:5), Dawkins (1986:1), Mayr (1982:xi-xii) and Lewontin (1978) have long acknowledged that organisms appear to have been designed. Of course, neo-Darwinists assert that what Ayala (1994:5) calls the "obvious design" of living things is only apparent since the selection/mutation mechanism can explain the origin of complex form and organization in living systems without an appeal to a designing agent. Indeed, neo-Darwinists affirm that mutation and selection--and perhaps other similarly undirected mechanisms--are fully sufficient to explain the appearance of design in biology. Self-organizational theorists and punctuationalists modify this claim, but affirm its essential tenet. Self-organization theorists argue that natural selection acting on self organizing order can explain the complexity of living things--again, without any appeal to design. Punctuationalists similarly envision natural selection acting on newly arising species with no actual design involved.
And clearly, the neo-Darwinian mechanism does explain many appearances of design, such as the adaptation of organisms to specialized environments that attracted the interest of 19th century biologists. More specifically, known microevolutionary processes appear quite sufficient to account for changes in the size of Galapagos finch beaks that have occurred in response to variations in annual rainfall and available food supplies (Weiner 1994, Grant 1999).
But does neo-Darwinism, or any other fully materialistic model, explain all appearances of design in biology, including the body plans and information that characterize living systems? Arguably, biological forms--such as the structure of a chambered nautilus, the organization of a trilobite, the functional integration of parts in an eye or molecular machine--attract our attention in part because the organized complexity of such systems seems reminiscent of our own designs. Yet, this review has argued that neo-Darwinism does not adequately account for the origin of all appearances of design, especially if one considers animal body plans, and the information necessary to construct them, as especially striking examples of the appearance of design in living systems. Indeed, Dawkins (1995:11) and Gates (1996:228) have noted that genetic information bears an uncanny resemblance to computer software or machine code. For this reason, the presence of CSI in living organisms, and the discontinuous increases of CSI that occurred during events such as the Cambrian explosion, appears at least suggestive of design.
Does neo-Darwinism or any other purely materialistic model of morphogenesis account for the origin of the genetic and other forms of CSI necessary to produce novel organismal form? If not, as this review has argued, could the emergence of novel information-rich genes, proteins, cell types and body plans have resulted from actual design, rather than a purposeless process that merely mimics the powers of a designing intelligence? The logic of neo-Darwinism, with its specific claim to have accounted for the appearance of design, would itself seem to open the door to this possibility. Indeed, the historical formulation of Darwinism in dialectical opposition to the design hypothesis (Gillespie 1979), coupled with the neo-Darwinism's inability to account for many salient appearances of design including the emergence of form and information, would seem logically to reopen the possibility of actual (as opposed to apparent) design in the history of life.
A second reason for considering design as an explanation for these phenomena follows from the importance of explanatory power to scientific theory evaluation and from a consideration of the potential explanatory power of the design hypothesis. Studies in the methodology and philosophy of science have shown that many scientific theories, particularly in the historical sciences, are formulated and justified as inferences to the best explanation (Lipton 1991:32-88, Brush 1989:1124-1129, Sober 2000:44). Historical scientists, in particular, assess or test competing hypotheses by evaluating which hypothesis would, if true, provide the best explanation for some set of relevant data (Meyer 1991, 2002; Cleland 2001:987-989, 2002:474-496).10 Those with greater explanatory power are typically judged to be better, more probably true, theories. Darwin (1896:437) used this method of reasoning in defending his theory of universal common descent. Moreover, contemporary studies on the method of "inference to the best explanation" have shown that determining which among a set of competing possible explanations constitutes the best depends upon judgments about the causal adequacy, or "causal powers," of competing explanatory entities (Lipton 1991:32-88). In the historical sciences, uniformitarian and/or actualistic (Gould 1965, Simpson 1970, Rutten 1971, Hooykaas 1975) canons of method suggest that judgments about causal adequacy should derive from our present knowledge of cause and effect relationships. For historical scientists, "the present is the key to the past" means that present experience-based knowledge of cause and effect relationships typically guides the assessment of the plausibility of proposed causes of past events.
Yet it is precisely for this reason that current advocates of the design hypothesis want to reconsider design as an explanation for the origin of biological form and information. This review, and much of the literature it has surveyed, suggests that four of the most prominent models for explaining the origin of biological form fail to provide adequate causal explanations for the discontinuous increases of CSI that are required to produce novel morphologies. Yet, we have repeated experience of rational and conscious agents--in particular ourselves--generating or causing increases in complex specified information, both in the form of sequence-specific lines of code and in the form of hierarchically arranged systems of parts.
In the first place, intelligent human agents--in virtue of their rationality and consciousness--have demonstrated the power to produce information in the form of linear sequence-specific arrangements of characters. Indeed, experience affirms that information of this type routinely arises from the activity of intelligent agents. A computer user who traces the information on a screen back to its source invariably comes to a mind--that of a software engineer or programmer. The information in a book or inscriptions ultimately derives from a writer or scribe--from a mental, rather than a strictly material, cause. Our experience-based knowledge of information-flow confirms that systems with large amounts of specified complexity (especially codes and languages) invariably originate from an intelligent source from a mind or personal agent. As Quastler (1964) put it, the "creation of new information is habitually associated with conscious activity" (p. 16). Experience teaches this obvious truth.
Further, the highly specified hierarchical arrangements of parts in animal body plans also suggest design, again because of our experience of the kinds of features and systems that designers can and do produce. At every level of the biological hierarchy, organisms require specified and highly improbable arrangements of lower-level constituents in order to maintain their form and function. Genes require specified arrangements of nucleotide bases; proteins require specified arrangements of amino acids; new cell types require specified arrangements of systems of proteins; body plans require specialized arrangements of cell types and organs. Organisms not only contain information-rich components (such as proteins and genes), but they comprise information-rich arrangements of those components and the systems that comprise them. Yet we know, based on our present experience of cause and effect relationships, that design engineers--possessing purposive intelligence and rationality--have the ability to produce information-rich hierarchies in which both individual modules and the arrangements of those modules exhibit complexity and specificity--information so defined. Individual transistors, resistors, and capacitors exhibit considerable complexity and specificity of design; at a higher level of organization, their specific arrangement within an integrated circuit represents additional information and reflects further design. Conscious and rational agents have, as part of their powers of purposive intelligence, the capacity to design information-rich parts and to organize those parts into functional information-rich systems and hierarchies. Further, we know of no other causal entity or process that has this capacity. Clearly, we have good reason to doubt that mutation and selection, self-organizational processes or laws of nature, can produce the information-rich components, systems, and body plans necessary to explain the origination of morphological novelty such as that which arises in the Cambrian period.
There is a third reason to consider purpose or design as an explanation for the origin of biological form and information: purposive agents have just those necessary powers that natural selection lacks as a condition of its causal adequacy. At several points in the previous analysis, we saw that natural selection lacked the ability to generate novel information precisely because it can only act after new functional CSI has arisen. Natural selection can favor new proteins, and genes, but only after they perform some function. The job of generating new functional genes, proteins and systems of proteins therefore falls entirely to random mutations. Yet without functional criteria to guide a search through the space of possible sequences, random variation is probabilistically doomed. What is needed is not just a source of variation (i.e., the freedom to search a space of possibilities) or a mode of selection that can operate after the fact of a successful search, but instead a means of selection that (a) operates during a search--before success--and that (b) is guided by information about, or knowledge of, a functional target.
Demonstration of this requirement has come from an unlikely quarter: genetic algorithms. Genetic algorithms are programs that allegedly simulate the creative power of mutation and selection. Dawkins and Kuppers, for example, have developed computer programs that putatively simulate the production of genetic information by mutation and natural selection (Dawkins 1986:47-49, Kuppers 1987:355-369). Nevertheless, as shown elsewhere (Meyer 1998:127-128, 2003:247-248), these programs only succeed by the illicit expedient of providing the computer with a "target sequence" and then treating relatively greater proximity to future function (i.e., the target sequence), not actual present function, as a selection criterion. As Berlinski (2000) has argued, genetic algorithms need something akin to a "forward looking memory" in order to succeed. Yet such foresighted selection has no analogue in nature. In biology, where differential survival depends upon maintaining function, selection cannot occur before new functional sequences arise. Natural selection lacks foresight.
What natural selection lacks, intelligent selection--purposive or goal-directed design--provides. Rational agents can arrange both matter and symbols with distant goals in mind. In using language, the human mind routinely "finds" or generates highly improbable linguistic sequences to convey an intended or preconceived idea. In the process of thought, functional objectives precede and constrain the selection of words, sounds and symbols to generate functional (and indeed meaningful) sequences from among a vast ensemble of meaningless alternative combinations of sound or symbol (Denton 1986:309-311). Similarly, the construction of complex technological objects and products, such as bridges, circuit boards, engines and software, result from the application of goal-directed constraints (Polanyi 1967, 1968). Indeed, in all functionally integrated complex systems where the cause is known by experience or observation, design engineers or other intelligent agents applied boundary constraints to limit possibilities in order to produce improbable forms, sequences or structures. Rational agents have repeatedly demonstrated the capacity to constrain the possible to actualize improbable but initially unrealized future functions. Repeated experience affirms that intelligent agents (minds) uniquely possess such causal powers.
Analysis of the problem of the origin of biological information, therefore, exposes a deficiency in the causal powers of natural selection that corresponds precisely to powers that agents are uniquely known to possess. Intelligent agents have foresight. Such agents can select functional goals before they exist. They can devise or select material means to accomplish those ends from among an array of possibilities and then actualize those goals in accord with a preconceived design plan or set of functional requirements. Rational agents can constrain combinatorial space with distant outcomes in mind. The causal powers that natural selection lacks--almost by definition--are associated with the attributes of consciousness and rationality--with purposive intelligence. Thus, by invoking design to explain the origin of new biological information, contemporary design theorists are not positing an arbitrary explanatory element unmotivated by a consideration of the evidence. Instead, they are positing an entity possessing precisely the attributes and causal powers that the phenomenon in question requires as a condition of its production and explanation.
An experience-based analysis of the causal powers of various explanatory hypotheses suggests purposive or intelligent design as a causally adequate--and perhaps the most causally adequate--explanation for the origin of the complex specified information required to build the Cambrian animals and the novel forms they represent. For this reason, recent scientific interest in the design hypothesis is unlikely to abate as biologists continue to wrestle with the problem of the origination of biological form and the higher taxa.
Adams, M. D. Et alia. 2000. The genome sequence of Drosophila melanogaster.--Science 287:2185-2195.
Aris-Brosou, S., & Z. Yang. 2003. Bayesian models of episodic evolution support a late Precambrian explosive diversification of the Metazoa.--Molecular Biology and Evolution 20:1947-1954.
Arthur, W. 1997. The origin of animal body plans. Cambridge University Press, Cambridge, United Kingdom.
Axe, D. D. 2000. Extreme functional sensitivity to conservative amino acid changes on enzyme exteriors.--Journal of Molecular Biology 301(3):585-596.
______. 2004. Estimating the prevalence of protein sequences adopting functional enzyme folds.--Journal of Molecular Biology (in press).
Ayala, F. 1994. Darwin's revolution. Pp. 1-17 in J. Campbell and J. Schopf, eds., Creative evolution?! Jones and Bartlett Publishers, Boston, Massachusetts.
______. A. Rzhetsky, & F. J. Ayala. 1998. Origin of the metazoan phyla: molecular clocks confirm paleontological estimates--Proceedings of the National Academy of Sciences USA. 95:606-611.
Becker, H., & W. Lonnig, 2001. Transposons: eukaryotic. Pp. 529-539 in Nature encyclopedia of life sciences, vol. 18. Nature Publishing Group, London, United Kingdom.
Behe, M. 1992. Experimental support for regarding functional classes of proteins to be highly isolated from each other. Pp. 60-71 in J. Buell and V. Hearn, eds., Darwinism: science or philosophy? Foundation for Thought and Ethics, Richardson, Texas.
______. 1996. Darwin's black box. The Free Press, New York.
______. 2004. Irreducible complexity: obstacle to Darwinian evolution. Pp. 352-370 in W. A. Dembski and M. Ruse, eds., Debating design: from Darwin to DNA. Cambridge University Press, Cambridge, United Kingdom.
Benton, M., & F. J. Ayala. 2003. Dating the tree of life--Science 300:1698-1700.
Berlinski, D. 2000. "On assessing genetic algorithms." Public lecture. Conference: Science and evidence of design in the universe. Yale University, November 4, 2000.
Blanco, F., I. Angrand, & L. Serrano. 1999. Exploring the confirmational properties of the sequence space between two proteins with different folds: an experimental study.--Journal of Molecular Biology 285:741-753.
Bowie, J., & R. Sauer. 1989. Identifying determinants of folding and activity for a protein of unknown sequences: tolerance to amino acid substitution.--Proceedings of the National Academy of Sciences, U.S.A. 86:2152-2156.
Bowring, S. A., J. P. Grotzinger, C. E. Isachsen, A. H. Knoll, S. M. Pelechaty, & P. Kolosov. 1993. Calibrating rates of early Cambrian evolution.--Science 261:1293-1298.
______. 1998a. A new look at evolutionary rates in deep time: Uniting paleontology and high-precision geochronology.--GSA Today 8:1-8.
______. 1998b. Geochronology comes of age.--Geotimes 43:36-40.
Bradley, W. 2004. Information, entropy and the origin of life. Pp. 331-351 in W. A. Dembski and M. Ruse, eds., Debating design: from Darwin to DNA. Cambridge University Press, Cambridge, United Kingdom.
Brocks, J. J., G. A. Logan, R. Buick, & R. E. Summons. 1999. Archean molecular fossils and the early rise of eukaryotes.--Science 285:1033-1036.
Brush, S. G. 1989. Prediction and theory evaluation: the case of light bending.--Science 246:1124-1129.
Budd, G. E. & S. E. Jensen. 2000. A critical reappraisal of the fossil record of the bilaterial phyla.--Biological Reviews of the Cambridge Philosophical Society 75:253-295.
Carroll, R. L. 2000. Towards a new evolutionary synthesis.--Trends in Ecology and Evolution 15:27-32.
Cleland, C. 2001. Historical science, experimental science, and the scientific method.--Geology 29:987-990.
______. 2002. Methodological and epistemic differences between historical science and experimental science.--Philosophy of Science 69:474-496.
Chothia, C., I. Gelfland, & A. Kister. 1998. Structural determinants in the sequences of immunoglobulin variable domain.--Journal of Molecular Biology 278:457-479.
Conway Morris, S. 1998a. The question of metazoan monophyly and the fossil record.--Progress in Molecular and Subcellular Biology 21:1-9.
______. 1998b. Early Metazoan evolution: Reconciling paleontology and molecular biology.--American Zoologist 38 (1998):867-877.
______. 2000. Evolution: bringing molecules into the fold.--Cell 100:1-11.
______. 2003a. The Cambrian "explosion" of metazoans. Pp. 13-32 in G. B. Muller and S. A. Newman, eds., Origination of organismal form: beyond the gene in developmental and evolutionary biology. The M.I.T. Press, Cambridge, Massachusetts.
______. 2003b. Cambrian "explosion" of metazoans and molecular biology: would Darwin be satisfied?--International Journal of Developmental Biology 47(7-8):505-515.
______. 2003c. Life's solution: inevitable humans in a lonely universe. Cambridge University Press, Cambridge, United Kingdom.
Crick, F. 1958. On protein synthesis.--Symposium for the Society of Experimental Biology. 12(1958):138-163.
Darwin, C. 1859. On the origin of species. John Murray, London, United Kingdom.
______. 1896. Letter to Asa Gray. P. 437 in F. Darwin, ed., Life and letters of Charles Darwin, vol. 1., D. Appleton, London, United Kingdom.
Davidson, E. 2001. Genomic regulatory systems: development and evolution. Academic Press, New York, New York.
Dawkins, R. 1986. The blind watchmaker. Penguin Books, London, United Kingdom.
______. 1995. River out of Eden. Basic Books, New York.
______. 1996. Climbing Mount Improbable. W. W. Norton & Company, New York.
Dembski, W. A. 1998. The design inference. Cambridge University Press, Cambridge, United Kingdom.
______. 2002. No free lunch: why specified complexity cannot be purchased without intelligence. Rowman & Littlefield, Lanham, Maryland.
______. 2004. The logical underpinnings of intelligent design. Pp. 311-330 in W. A. Dembski and M. Ruse, eds., Debating design: from Darwin to DNA. Cambridge University Press, Cambridge, United Kingdom.
Denton, M. 1986. Evolution: a theory in crisis. Adler & Adler, London, United Kingdom.
______. 1998. Nature's density. The Free Press, New York.
Eden, M. 1967. The inadequacies of neo-Darwinian evolution as a scientific theory. Pp. 5-12 in P. S. Morehead and M. M. Kaplan, eds., Mathematical challenges to the Darwinian interpretation of evolution. Wistar Institute Symposium Monograph, Allen R. Liss, New York.
Eldredge, N., & S. J. Gould. 1972. Punctuated equilibria: an alternative to phyletic gradualism. Pp. 82-115 in T. Schopf, ed., Models in paleobiology. W. H. Freeman, San Francisco.
Erwin, D. H. 1994. Early introduction of major morphological innovations.--Acta Palaeontologica Polonica 38:281-294.
______. 2000. Macroevolution is more than repeated rounds of microevolution.--Evolution & Development 2:78-84.
______. 2004. One very long argument.--Biology and Philosophy 19:17-28.
______, J. Valentine, & D. Jablonski. 1997. The origin of animal body plans.--American Scientist 85:126-137.
______, ______, & J. J. Sepkoski. 1987. A comparative study of diversification events: the early Paleozoic versus the Mesozoic.--Evolution 41:1177-1186.
Foote, M. 1997. Sampling, taxonomic description, and our evolving knowledge of morphological diversity.--Paleobiology 23:181-206.
______, J. P. Hunter, C. M. Janis, & J. J. Sepkoski. 1999. Evolutionary and preservational constraints on origins of biologic groups: Divergence times of eutherian mammals.--Science 283:1310-1314.
Frankel, J. 1980. Propagation of cortical differences in tetrahymena.--Genetics 94:607-623.
Gates, B. 1996. The road ahead. Blue Penguin, Boulder, Colorado.
Gerhart, J., & M. Kirschner. 1997. Cells, embryos, and evolution. Blackwell Science, London, United Kingdom.
Gibbs, W. W. 2003. The unseen genome: gems among the junk.--Scientific American. 289:46-53.
Gilbert, S. F., J. M. Opitz, & R. A. Raff. 1996. Resynthesizing evolutionary and developmental biology.--Developmental Biology 173:357-372.
Gillespie, N. C. 1979. Charles Darwin and the problem of creation. University of Chicago Press, Chicago.
Goodwin, B. C. 1985. What are the causes of morphogenesis?--BioEssays 3:32-36.
______. 1995. How the leopard changed its spots: the evolution of complexity. Scribner's, New York, New York.
Gould, S. J. 1965. Is uniformitarianism necessary?--American Journal of Science 263:223-228.
Gould, S. J. 2002. The structure of evolutionary theory. Harvard University Press, Cambridge, Massachusetts.
Grant, P. R. 1999. Ecology and evolution of Darwin's finches. Princeton University Press, Princeton, New Jersey.
Grimes, G. W., & K. J. Aufderheide. 1991. Cellular aspects of pattern formation: the problem of assembly. Monographs in Developmental Biology, vol. 22. Karger, Baseline, Switzerland.
Grotzinger, J. P., S. A. Bowring, B. Z. Saylor, & A. J. Kaufman. 1995. Biostratigraphic and geochronologic constraints on early animal evolution.--Science 270:598-604.
Harold, F. M. 1995. From morphogenes to morphogenesis.--Microbiology 141:2765-2778.
______. 2001. The way of the cell: molecules, organisms, and the order of life. Oxford University Press, New York.
Hodge, M. J. S. 1977. The structure and strategy of Darwin's long argument.--British Journal for the History of Science 10:237-245.
Hooykaas, R. 1975. Catastrophism in geology, its scientific character in relation to actualism and uniformitarianism. Pp. 270-316 in C. Albritton, ed., Philosophy of geohistory (1785-1970). Dowden, Hutchinson & Ross, Stroudsburg, Pennsylvania.
John, B., & G. Miklos. 1988. The eukaryote genome in development and evolution. Allen & Unwinding, London, United Kingdom.
Kauffman, S. 1995. At home in the universe. Oxford University Press, Oxford, United Kingdom.
Kenyon, D., & G. Mills. 1996. The RNA world: a critique.--Origins & Design 17(1):9-16.
Kerr, R. A. 1993. Evolution's Big Bang gets even more explosive.-- Science 261:1274-1275.
Kimura, M. 1983. The neutral theory of molecular evolution. Cambridge University Press, Cambridge, United Kingdom.
Koonin, E. 2000. How many genes can make a cell?: the minimal genome concept.--Annual Review of Genomics and Human Genetics 1:99-116.
Kuppers, B. O. 1987. On the prior probability of the existence of life. Pp. 355-369 in L. Kruger et al., eds., The probabilistic revolution. M.I.T. Press, Cambridge, Massachusetts.
Lange, B. M. H., A. J. Faragher, P. March, & K. Gull. 2000. Centriole duplication and maturation in animal cells. Pp. 235-249 in R. E. Palazzo and G. P. Schatten, eds., The centrosome in cell replication and early development. Current Topics in Developmental Biology, vol. 49. Academic Press, San Diego.
Lawrence, P. A., & G. Struhl. 1996. Morphogens, compartments and pattern: lessons from Drosophila?--Cell 85:951-961.
Lenior, T. 1982. The strategy of life. University of Chicago Press, Chicago.
Levinton, J. 1988. Genetics, paleontology, and macroevolution. Cambridge University Press, Cambridge, United Kingdom.
______. 1992. The big bang of animal evolution.--Scientific American 267:84-91.
Lewin, R. 1988. A lopsided look at evolution.--Science 241:292.
Lewontin, R. 1978. Adaptation. Pp. 113-125 in Evolution: a Scientific American book. W. H. Freeman & Company, San Francisco.
Lipton, P. 1991. Inference to the best explanation. Routledge, New York.
Lonnig, W. E. 2001. Natural selection. Pp. 1008-1016 in W. E. Craighead and C. B. Nemeroff, eds., The Corsini encyclopedia of psychology and behavioral sciences, 3rd edition, vol. 3. John Wiley & Sons, New York.
______, & H. Saedler. 2002. Chromosome rearrangements and transposable elements.--Annual Review of Genetics 36:389-410.
Lovtrup, S. 1979. Semantics, logic and vulgate neo-darwinism.--Evolutionary Theory 4:157-172.
Marshall, W. F. & J. L. Rosenbaum. 2000. Are there nucleic acids in the centrosome? Pp. 187-205 in R. E. Palazzo and G. P. Schatten, eds., The centrosome in cell replication and early development. Current Topics in Developmental Biology, vol. 49. San Diego, Academic Press.
Maynard Smith, J. 1986. Structuralism versus selection--is Darwinism enough? Pp. 39-46 in S. Rose and L. Appignanesi, eds., Science and Beyond. Basil Blackwell, London, United Kingdom.
Mayr, E. 1982. Foreword. Pp. xi-xii in M. Ruse, Darwinism defended. Pearson Addison Wesley, Boston, Massachusetts.
McDonald, J. F. 1983. The molecular basis of adaptation: a critical review of relevant ideas and observations.--Annual Review of Ecology and Systematics 14:77-102.
McNiven, M. A. & K. R. Porter. 1992. The centrosome: contributions to cell form. Pp. 313-329 in V. I. Kalnins, ed., The centrosome. Academic Press, San Diego.
Meyer, S. C. 1991. Of clues and causes: a methodological interpretation of origin of life studies. Unpublished doctoral dissertation, University of Cambridge, Cambridge, United Kingdom.
______. 1998. DNA by design: an inference to the best explanation for the origin of biological information.--Rhetoric & Public Affairs, 1(4):519-555.
______. The scientific status of intelligent design: The methodological equivalence of naturalistic and non-naturalistic origins theories. Pp. 151-211 in Science and evidence for design in the universe. Proceedings of the Wethersfield Institute. Ignatius Press, San Francisco.
______. 2003. DNA and the origin of life: information, specification and explanation. Pp. 223-285 in J. A. Campbell and S. C. Meyer, eds., Darwinism, design and public education. Michigan State University Press, Lansing, Michigan.
______. 2004. The Cambrian information explosion: evidence for intelligent design. Pp. 371-391 in W. A. Dembski and M. Ruse, eds., Debating design: from Darwin to DNA. Cambridge University Press, Cambridge, United Kingdom.
______, M. Ross, P. Nelson, & P. Chien. 2003. The Cambrian explosion: biology's big bang. Pp. 323-402 in J. A. Campbell & S. C. Meyer, eds., Darwinism, design and public education. Michigan State University Press, Lansing. See also Appendix C: Stratigraphic first appearance of phyla body plans, pp. 593-598.
Miklos, G. L. G. 1993. Emergence of organizational complexities during metazoan evolution: perspectives from molecular biology, palaeontology and neo-Darwinism.--Mem. Ass. Australas. Palaeontols, 15:7-41.
Monastersky, R. 1993. Siberian rocks clock biological big bang.--Science News 144:148.
Moss, L. 2004. What genes can't do. The M.I.T. Press, Cambridge, Massachusetts.
Muller, G. B. & S. A. Newman. 2003. Origination of organismal form: the forgotten cause in evolutionary theory. Pp. 3-12 in G. B. Muller and S. A. Newman, eds., Origination of organismal form: beyond the gene in developmental and evolutionary biology. The M.I.T. Press, Cambridge, Massachusetts.
Nanney, D. L. 1983. The ciliates and the cytoplasm.--Journal of Heredity, 74:163-170.
Nelson, P., & J. Wells. 2003. Homology in biology: problem for naturalistic science and prospect for intelligent design. Pp. 303-322 in J. A. Campbell and S. C. Meyer, eds., Darwinism, design and public education. Michigan State University Press, Lansing.
Nijhout, H. F. 1990. Metaphors and the role of genes in development.--BioEssays 12:441-446.
Nusslein-Volhard, C., & E. Wieschaus. 1980. Mutations affecting segment number and polarity in Drosophila.--Nature 287:795-801.
Ohno, S. 1996. The notion of the Cambrian pananimalia genome.--Proceedings of the National Academy of Sciences, U.S.A. 93:8475-8478.
Orgel, L. E., & F. H. Crick. 1980. Selfish DNA: the ultimate parasite.--Nature 284:604-607.
Perutz, M. F., & H. Lehmann. 1968. Molecular pathology of human hemoglobin.--Nature 219:902-909.
Polanyi, M. 1967. Life transcending physics and chemistry.--Chemical and Engineering News, 45(35):54-66.
______. 1968. Life's irreducible structure.--Science 160:1308-1312, especially p. 1309.
Pourquie, O. 2003. Vertebrate somitogenesis: a novel paradigm for animal segmentation?--International Journal of Developmental Biology 47(7-8):597-603.
Quastler, H. 1964. The emergence of biological organization. Yale University Press, New Haven, Connecticut.
Raff, R. 1999. Larval homologies and radical evolutionary changes in early development, Pp. 110-121 in Homology. Novartis Symposium, vol. 222. John Wiley & Sons, Chichester, United Kingdom.
Reidhaar-Olson, J., & R. Sauer. 1990. Functionally acceptable solutions in two alpha-helical regions of lambda repressor.--Proteins, Structure, Function, and Genetics, 7:306-316.
Rutten, M. G. 1971. The origin of life by natural causes. Elsevier, Amsterdam.
Sapp, J. 1987. Beyond the gene. Oxford University Press, New York.
Sarkar, S. 1996. Biological information: a skeptical look at some central dogmas of molecular biology. Pp. 187-233 in S. Sarkar, ed., The philosophy and history of molecular biology: new perspectives. Kluwer Academic Publishers, Dordrecht.
Schutzenberger, M. 1967. Algorithms and the neo-Darwinian theory of evolution. Pp. 73-75 in P. S. Morehead and M. M. Kaplan, eds., Mathematical challenges to the Darwinian interpretation of evolution. Wistar Institute Symposium Monograph. Allen R. Liss, New York.
Shannon, C. 1948. A mathematical theory of communication.--Bell System Technical Journal 27:379-423, 623-656.
Shu, D. G., H. L. Loud, S. Conway Morris, X. L. Zhang, S. X. Hu, L. Chen, J. Han, M. Zhu, Y. Li, & L. Z. Chen. 1999. Lower Cambrian vertebrates from south China.--Nature 402:42-46.
Shubin, N. H., & C. R. Marshall. 2000. Fossils, genes, and the origin of novelty. Pp. 324-340 in Deep time. The Paleontological Society.
Simpson, G. 1970. Uniformitarianism: an inquiry into principle, theory, and method in geohistory and biohistory. Pp. 43-96 in M. K. Hecht and W. C. Steered, eds., Essays in evolution and genetics in honor of Theodosius Dobzhansky. Appleton-Century-Crofts, New York.
Sober, E. 2000. The philosophy of biology, 2nd edition. Westview Press, San Francisco.
Sonneborn, T. M. 1970. Determination, development, and inheritance of the structure of the cell cortex. In Symposia of the International Society for Cell Biology 9:1-13.
Sole, R. V., P. Fernandez, & S. A. Kauffman. 2003. Adaptive walks in a gene network model of morphogenesis: insight into the Cambrian explosion.--International Journal of Developmental Biology 47(7-8):685-693.
Stadler, B. M. R., P. F. Stadler, G. P. Wagner, & W. Fontana. 2001. The topology of the possible: formal spaces underlying patterns of evolutionary change.--Journal of Theoretical Biology 213:241-274.
Steiner, M., & R. Reitner. 2001. Evidence of organic structures in Ediacara-type fossils and associated microbial mats.--Geology 29(12):1119-1122.
Taylor, S. V., K. U. Walter, P. Kast, & D. Hilvert. 2001. Searching sequence space for protein catalysts.--Proceedings of the National Academy of Sciences, U.S.A. 98:10596-10601.
Thaxton, C. B., W. L. Bradley, & R. L. Olsen. 1992. The mystery of life's origin: reassessing current theories. Lewis and Stanley, Dallas, Texas.
Thompson, D. W. 1942. On growth and form, 2nd edition. Cambridge University Press, Cambridge, United Kingdom.
Thomson, K. S. 1992. Macroevolution: The morphological problem.--American Zoologist 32:106-112.
Valentine, J. W. 1995. Late Precambrian bilaterians: grades and clades. Pp. 87-107 in W. M. Fitch and F. J. Ayala, eds., Temporal and mode in evolution: genetics and paleontology 50 years after Simpson. National Academy Press, Washington, D.C.
______. 2004. On the origin of phyla. University of Chicago Press, Chicago, Illinois.
______, & D. H. Erwin, 1987. Interpreting great developmental experiments: the fossil record. Pp. 71-107 in R. A. Raff and E. C. Raff, eds., Development as an evolutionary process. Alan R. Liss, New York.
______, & D. Jablonski. 2003. Morphological and developmental macroevolution: a paleontological perspective.--International Journal of Developmental Biology 47:517-522.
Wagner, G. P. 2001. What is the promise of developmental evolution? Part II: A causal explanation of evolutionary innovations may be impossible.--Journal of Experimental Zoology (Mol. Dev. Evol.) 291:305-309.
______, & P. F. Stadler. 2003. Quasi-independence, homology and the Unity-C of type: a topological theory of characters.--Journal of Theoretical Biology 220:505-527.
Webster, G., & B. Goodwin. 1984. A structuralist approach to morphology.--Rivista di Biologia 77:503-10.
______, & ______. 1996. Form and transformation: generative and relational principles in biology. Cambridge University Press, Cambridge, United Kingdom.
Weiner, J. 1994. The beak of the finch. Vintage Books, New York.
Willmer, P. 1990. Invertebrate relationships: patterns in animal evolution. Cambridge University Press, Cambridge, United Kingdom.
______. 2003. Convergence and homoplasy in the evolution of organismal form. Pp. 33-50 in G. B. Muller and S. A. Newman, eds., Origination of organismal form: beyond the gene in developmental and evolutionary biology. The M.I.T. Press, Cambridge, Massachusetts.
Woese, C. 1998. The universal ancestor.--Proceedings of the National Academy of Sciences, U.S.A. 95:6854-6859.
Wray, G. A., J. S. Levinton, & L. H. Shapiro. 1996. Molecular evidence for deep Precambrian divergences among metazoan phyla.--Science 274:568-573.
Yockey, H. P. 1978. A calculation of the probability of spontaneous biogenesis by information theory.--Journal of Theoretical Biology 67:377-398.
______, 1992. Information theory and molecular biology, Cambridge University Press, Cambridge, United Kingdom.
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PROCEEDINGS OF THE BIOLOGICAL SOCIETY OF WASHINGTON
The origin of biological information and the higher taxonomic categories
Stephen C. Meyer