From a speech delivered at Discovery Institute’s God & Culture Conference
Michael J. Behe
August 10, 1996
A Series of Eyes
How do we see? In the 19th century the anatomy of the eye was known in great detail, and its sophisticated features astounded everyone who was familiar with them. Scientists of the time 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. So it was concluded that the eye could only function if it were nearly intact.
Charles Darwin knew about the eye too. In the Origin of Species, Darwin dealt with many objections to his theory of evolution by natural selection. He discussed the problem of the eye in a section of the book appropriately entitled "Organs of extreme perfection and complication." Somehow, for evolution to be believable, Darwin had to convince the public that complex organs could be formed gradually, in a step-by-step process.
He succeeded brilliantly. Cleverly, Darwin didn’t try to discover a real pathway that evolution might have used to make the eye. Instead, he pointed to modern animals with different kinds of eyes, ranging from the simple to the complex, and suggested that the evolution of the human eye might have involved similar organs as intermediates.
Here is a paraphrase of Darwin’s argument. Although humans have complex camera-type eyes, many animals get by with less. Some tiny creatures have just a simple group of pigmented cells, or not much more than a light sensitive spot. That simple arrangement can hardly be said to confer vision, but it can sense light and dark, and so it meets the creature’s needs. The light-sensing organ of some starfishes is somewhat more sophisticated. Their eye is located in a depressed region. This allows the animal to sense which direction the light is coming from, since the curvature of the depression blocks off light from some directions. If the curvature becomes more pronounced, the directional sense of the eye improves. But more curvature lessens the amount of light that enters the eye, decreasing its sensitivity. The sensitivity can be increased by placement of gelatinous material in the cavity to act as a lens. Some modern animals have eyes with such crude lenses. Gradual improvements in the lens could then provide an image of increasing sharpness, as the requirements of the animal’s environment dictated.
Using reasoning like this, Darwin convinced many of his readers that an evolutionary pathway leads from the simplest light sensitive spot to the sophisticated camera-eye of man. But the question remains, how did vision begin? Darwin persuaded much of the world that a modern eye evolved gradually from a simpler structure, but he did not even try to explain where his starting point for the simple light sensitive spot came from. On the contrary, Darwin dismissed the question of the eye’s ultimate origin:
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 the question: it was completely beyond nineteenth century science. How the eye works; that is, what happens when a photon of light first hits the retina simply could not be answered at that time. As a matter of fact, no question about the underlying mechanisms of life could be answered. How did animal muscles cause movement? How did photosynthesis work? How was energy extracted from food? How did the body fight infection? No one knew.
To Darwin vision was a black box, but today, after the hard, cumulative work of many biochemists, we are approaching answers to the question of sight. Here is a brief overview of the biochemistry of vision. When light first strikes the retina, a photon interacts with a molecule called 11-cis-retinal, which rearranges within picoseconds to trans-retinal. The change in the shape of retinal forces a change in the shape of the protein, rhodopsin, to which the retinal is tightly bound. The protein’s metamorphosis alters its behavior, making it stick to another protein called transducin. Before bumping into activated rhodopsin, transducin had tightly bound a small molecule called GDP. But when transducin interacts with activated rhodopsin, the GDP falls off and a molecule called GTP binds to transducin. (GTP is closely related to, but critically different from, GDP.)
GTP-transducin-activated rhodopsin now binds to a protein called phosphodiesterase, located in the inner membrane of the cell. When attached to activated rhodopsin and its entourage, the phosphodiesterase acquires the ability to chemically cut a molecule called cGMP (a chemical relative of both GDP and GTP). Initially there are a lot of cGMP molecules in the cell, but the phosphodiesterase lowers its concentration, like a pulled plug lowers the water level in a bathtub.
Another membrane protein that binds cGMP is called an ion channel. It acts as a gateway that regulates the number of sodium ions in the cell. Normally the ion channel allows sodium ions to flow into the cell, while a separate protein actively pumps them out again. The dual action of the ion channel and pump keeps the level of sodium ions in the cell within a narrow range. When the amount of cGMP is reduced because of cleavage by the phosphodiesterase, the ion channel closes, causing the cellular concentration of positively charged sodium ions to be reduced. This causes an imbalance of charge across the cell membrane which, finally, causes a current to be transmitted down the optic nerve to the brain. The result, when interpreted by the brain, is vision.
My explanation is just a sketchy overview of the biochemistry of vision. Ultimately, though, this is what it means to "explain" vision. This is the level of explanation for which biological science must aim. In order to truly understand a function, one must understand in detail every relevant step in the process. The relevant steps in biological processes occur ultimately at the molecular level, so a satisfactory explanation of a biological phenomenon such as vision, or digestion, or immunity must include its molecular explanation.
Now that the black box of vision has been opened it is no longer enough for an "evolutionary explanation" of that power to consider only the anatomical structures of whole eyes, as Darwin did in the nineteenth century, and as popularizers of evolution continue to do today. Each of the anatomical steps and structures that Darwin thought were so simple actually involves staggeringly complicated biochemical processes that cannot be papered over with rhetoric. Darwin’s simple steps are now revealed to be huge leaps between carefully tailored machines. Thus biochemistry offers a Lilliputian challenge to Darwin. Now the black box of the cell has been opened and a Lilliputian world of staggering complexity stands revealed. It must be explained.
How can we decide if Darwin’s theory can account for the complexity of molecular life? It turns out that Darwin himself set the standard. He acknowledged that:
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. But what type of biological system could not be formed by "numerous, successive, slight modifications"?
Well, for starters, a system that is irreducibly complex. Irreducible complexity is just a fancy phrase I use to mean a single system which is composed of several interacting parts, and where the removal of any one of the parts causes the system to cease functioning.
Let’s consider an everyday example of irreducible complexity: the humble mousetrap. The mousetraps that my family uses 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 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 connects to the catch and holds the hammer back when the trap is charged. Now you can’t catch a few mice with just a platform, add a spring and catch a few more mice, add a holding bar and catch a few more. All the pieces of the mousetrap have to be in place before you catch any mice. Therefore the mousetrap is irreducibly complex.
An irreducibly complex system cannot be produced directly by numerous, successive, slight modifications of a precursor system, because any precursor to an irreducibly complex system that is missing a part is by definition nonfunctional. An irreducibly complex biological system, if there is such a thing, would be a powerful challenge to Darwinian evolution. Since natural selection can only choose systems that are already working, then if a biological system cannot be produced gradually it would have to arise as an integrated unit, in one fell swoop, for natural selection to have anything to act on.
Demonstration that a system is irreducibly complex is not a proof that there is absolutely no gradual route to its production. Although an irreducibly complex system can’t be produced directly, one can’t definitively rule out the possibility of an indirect, circuitous route. However, as the complexity of an interacting system increases, the likelihood of such an indirect route drops precipitously. And as the number of unexplained, irreducibly complex biological systems increases, our confidence that Darwin’s criterion of failure has been met skyrockets toward the maximum that science allows.
Now, are any biochemical systems irreducibly complex? Yes, it turns out that many are. A good example is the cilium. Cilia are hairlike structures on the surfaces of many animal and lower plant cells that can move fluid over the cell’s surface or "row" single cells through a fluid. Inhumans, for example, cells lining the respiratory tract each have about 200 cilia that beat in synchrony to sweep mucus towards the throat for elimination. What is the structure of a cilium? A cilium consists of 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 composedof 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 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 a protein called dynein.
But how does a cilium work? Experiments have shown that ciliary motion results from the chemically-powered "walking" of the dynein arms on one microtubule up a second microtubule so that the two microtubules slide past each other. The protein cross-links between microtubules in a 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 consider what this implies. What components are needed for a cilium to work? Ciliary motion certainly requires microtubules; otherwise, there would be no strands to slide. Additionally we require a motor, or else the microtubules of the cilium would lie stiff and motionless. Furthermore, we require linkers to tug on neighboring strands, converting the sliding motion into a bending motion, and preventing the structure from falling apart. All of these parts are required to perform one function: ciliary motion. Just as a mousetrap does not work unless all of its constituent parts are present, ciliary motion simply does not exist in the absence of microtubules, connectors, and motors. Therefore, we can conclude that the cilium is irreducibly complex; an enormous monkey wrench thrown into its presumed gradual, Darwinian evolution.
Now let’s talk about a different biochemical system of blood clotting. Amusingly, the way in which the blood clotting system works is reminiscent of a Rube Goldberg machine.
The name of Rube Goldberg; the great cartoonist who entertained America with his silly machines, lives on in our culture, but the man himself has pretty much faded from view. Here’s a typical example of his humor. In this cartoon Goldberg imagined a system where water from a drain-pipe fills a flask, causing a cork with attached needle to rise and puncture a paper cup containing beer, which sprinkles on a bird. The intoxicated bird falls onto a spring, bounces up to a platform, and pulls a string thinking it’s a worm. The string triggers a cannon which frightens a dog. The dog flips over, and his rapid breathing raises and lowers a scratcher over a mosquito bite, causing no embarrassment while talking to a lady.
When you think about it for a moment you realize that the Rube Goldberg machine is irreducibly complex. It is a single system which is composed of several interacting parts, and where the removal of any one of the parts causes the system to break down. If the dog is missing the machine doesn’t work; if the needle hasn’t been put on the cork, the whole system is useless.
It turns out that we all have Rube Goldberg in our blood. Here’s a picture of a cell trapped in a clot. The meshwork is formed from a protein called fibrin. But what controls blood clotting? Why does blood clot when you cut yourself, but not at other times when a clot would cause a stroke or heart attack? Here’s a diagram of what’s called the blood clotting cascade. Let’s go through just some of the reactions of clotting.
When an animal is cut a protein called Hageman factor sticks to the surface of cells near the wound. Bound Hageman factor is then cleaved by a protein called HMK to yield activated Hageman factor. Immediately the activated Hageman factor converts another protein, called prekallikrein, to its active form, kallikrein. Kallikrein helps HMK speed up the conversion of more Hageman factor to its active form. Activated Hageman factor and HMK then together transform another protein, called PTA, to its active form. Activated PTA in turn, together with the activated form of another protein (discussed below) called convertin, switch a protein called Christmas factor to its active form. Activated Christmas factor, together with antihemophilic factor (which is itself activated by thrombin in a manner similar to that of proaccelerin) changes Stuart factor to its active form. Stuart factor,working with accelerin, converts prothrombin to thrombin. Finally thrombin cuts fibrinogen to give fibrin, which aggregates with other fibrin molecules to form the meshwork clot you saw in the last picture.
Blood clotting requires extreme precision. When a pressurized blood circulation system is punctured, a clot must form quickly or the animal will bleed to death. On the other hand, if blood congeals at the wrong time or place, then the clot may block circulation as it does in heart attacks and strokes. Furthermore, a clot has to stop bleeding all along the length of the cut, sealing it completely. Yet blood clotting must be confined to the cut or the entire blood system of the animal might solidify, killing it. Consequently, clotting requires this enormously complex system so that the clot forms only when and only where it is required. Blood clotting is the ultimate Rube Goldberg machine.
The Professional Literature
Other examples of irreducible complexity abound in the cell, including aspects of protein transport, the bacterial flagellum, electron transport, 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 comparison of protein or DNA sequences. A sequence comparison is an amino acid-by-amino acid comparison of two different proteins, or a nucleotide-by-nucleotide comparison of two different pieces of DNA, noting the positions at which they are identical or similar, and the places where they are not. Although useful for determining possible lines of descent, which is an interesting question in its own right, comparing sequences cannot show how a complex biochemical system achieved its function; the question that most concerns us here. By way of analogy, the instruction manuals for two different models of computer putout by the same company might have many identical words, sentences, and even paragraphs, suggesting a common ancestry (perhaps the same author wrote both manuals), but comparing the sequences of letters in the instruction manuals will never tell us if a computer can be produced step by step starting from a typewriter.
None of the papers discussed detailed models for intermediates in the development of complex biomolecular structures. In the past ten years JME has published over a thousand papers. Of these, about one hundred discussed the chemical synthesis of molecules thought to be necessary for the origin of life, about 50 proposed mathematical models to improve sequence analysis, and about 800 were analyses of sequences. There were ZERO 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 science journal whatsoever.
"Publish or perish" is a proverb that academicians take seriously. If you do not publish your work for the rest of the community to evaluate, then you have no business in academia and, if you don’t already have tenure, you will be banished. But the saying can be applied to theories as well. If a theory claims to be able to explain some phenomenon but does not generate even an attempt at an explanation, then it should be banished. Despite comparing sequences, molecular evolution has never addressed the question of how complex structures came to be. In effect, the theory of Darwinian molecular evolution has not published, and so it should perish.
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. While walking through a junkyard you might observe separated bolts and screws and bits of plastic and glass, most scattered, some piled on top of each other, some wedged together. Suppose you saw a pile that seemed particularly compact, and when you picked up a bar sticking out of the pile, the whole pile came along with it. When you pushed on the bar it slid smoothly to one side of the pile and pulled an attached chain along with it. The chain in turn yanked a gear which turned three other gears which turned a red-and-white striped rod, spinning it like a barber pole. You quickly conclude that the pile was not a chance accumulation of junk, but was designed, was put together in that order by an intelligent agent, because you see that the components of the system interact with great specificity to do something.
It is not only artificial mechanical systems for which design can easily be concluded. 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.
A Complicated World
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. The possibility of a meteor’s impact does not mean that volcanos can be ignored; the existence of sculptors does not mean that many rocks are not shaped by weather. 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), meiotic drive (the preferential selection during sex cell production of one of the two copies of a gene inherited from an organism’s parents), transposition (the transfer of a gene between widely separated species by non-sexual means), 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.
Curiouser and Curiouser
So as this talk concludes we are left with what many people feel to be a strange conclusion: that life was designed by an intelligent agent. In a way, though, all of the progress of science over the last several hundred years has been a steady march toward the strange. People up until the middle ages lived in a natural world. The stable earth was at the center of things; the sun, moon, and stars circled endlessly to give light by day and night; the same plants and animals had been known since antiquity. Surprises were few.
Then it was proposed, absurdly, that the earth itself moved, spinning while it circled the sun. No one could feel the earth spinning; no one could see it. But spin it did. From our modern vantage it’s hard to realize what an assault on the senses was perpetrated by Copernicus and Galileo; they said in effect that people could no longer rely on even the evidence of their eyes.
Things got steadily worse over the years. With the discovery of fossils it became apparent that the familiar animals of field and forest had not always been on earth; the world had once been inhabited by huge, alien creatures who were now gone. Sometime later Darwin shook the world by arguing that the familiar biota was derived from the bizarre, vanished life over lengths of time incomprehensible to human minds. Einstein told us that space is curved and time is relative. Modern physics says that solid objects are mostly space, that sub atomic particles have no definite position, that the universe had a beginning.
Now it’s the turn of the fundamental science of life, modern biochemistry, to disturb. The simplicity that was once expected to be the foundation of life has proven to be a phantom. Instead, systems of horrendous, irreducible complexity inhabit the cell. The resulting realization that life was designed by an intelligence is a shock to us in the twentieth century who have gotten used to thinking of life as the result of simple natural laws. But other centuries have had their shocks and there is no reason to suppose that we should escape them. Humanity has endured as the center of the heavens moved from the earth to beyond the sun, as the history of life expanded to encompass long-dead reptiles, as the eternal universe proved mortal. We will endure the opening of Darwin’s black box.
Michael J. Behe is Associate Professor of Chemistry at Lehigh University in Pennsylvania and a Fellow of the Discovery Institute’s Center for Renewal of Science & Culture.