Many presume that because science is able to explain how nature works, it is also able to explain its origins. However, as Michael Behe explains, “ . . . understanding how something works is not the same as understanding how it came to be.” What modern science has learned is that biological systems at the molecular level are so complex that all attempts to explain their origins have been futile. Although Darwin’s mechanisms might explain many things, they do not explain molecular life. By diving into the details of modern scientific research, Behe tells the story of how biochemistry is challenging evolutionary theory.

A black box is an enigma—something with mysterious inner workings. In ancient times, all of biology was a black box. The ancients believed that all matter was made up of earth, air, fire and water. The human body was believed to be made of blood, yellow bile, black bile and phlegm; all disease was thought to arise from an imbalance of these four elements.

Aristotle systematically observed nature and was the first to group animals into two categories—those with and those without blood. Galen, a second-century physician, was one of only a few biological investigators to live in the millennium to follow. He used dissection to understand animal organs, and although he knew the heart pumped blood, he mistakenly concluded that blood was continuously made and then pumped out to irrigate the tissues. This misunderstanding would be taught for nearly fifteen hundred years.

In the seventeenth century, an Englishman, William Harvey, calculated that if the heart pumps out just two ounces of blood per beat, at 72 beats per minute, in one hour it would pump 540 pounds of blood. He concluded that since making that much blood in such a short time span would be impossible, it must be recirculated.

Although advances came more rapidly in the seventeenth and eighteenth centuries, they were hampered by being limited to what was visible to the naked eye. The human eye can resolve objects as small as one-tenth of a millimeter, but so much remained to be discovered on a minuscule, or Lilliputian scale. One black box had been opened only to reveal another. In order to proceed, biology needed a breakthrough.

Galileo was one of the first to use a crude microscope to observe the compound eyes of insects. Leeuwenhoek was the first person to see a bacterial cell. The discovery of a Lilliputian world had begun. Schleiden and Schwann introduced the cell theory of life in the early nineteenth century. The primary question for Schleiden had become, “What is the origin of this peculiar little organism, the cell?” The cell was a black box.

Since a microscope cannot resolve two points that are closer than one-half the wavelength of the light that is illuminating them, many of the critical details of cell structure could not be seen with a light microscope. The invention of the electron microscope followed several decades later, and since the wavelength of an electron is shorter than that of visible light, much smaller objects could be seen and studied. Suddenly, the same cell that looked so simple under a light microscope now revealed a whole new world of complex structures made of smaller components. These discoveries were taking us out of the realm of biology and into chemistry.

By the 1950s, science began to determine the properties of a few of the molecules that made up living organisms. It was soon discovered that life is run by machines made of molecules. Molecule machines operating within cells transport cargo along “highways” of molecules, and act as cables, ropes and pulleys. Finely calibrated machines are hard at work making other molecular machines, as well as themselves, and controlling every cellular process.

The last black box—Darwin’s black box—is the cell, which was opened to reveal molecules. We cannot go any deeper. No doubt, many surprises remain. But modern scientists are satisfied that what we now know of the actions of proteins and other molecules is enough for us to understand the basis of life. 

Since its inception, Darwinism has been met with a steady stream of opposition both from within and without the scientific community. In the 1940s, geneticist Richard Goldschmidt proposed the “hopeful monster” theory out of frustration over Darwin’s inadequate explanation for the formation of new structures. “Perhaps,” he mused, “a reptile laid an egg and from it hatched a bird.”

Several decades later, paleontologist Niles Eldredge described a similar frustration when he wrote, “When we do see the introduction of evolutionary novelty, it usually shows up with a bang, and often with no firm evidence that the fossils did not evolve elsewhere! Evolution cannot forever be going on somewhere else. Yet that’s how the fossil record has struck many a forlorn paleontologist looking to learn something about evolution.”

In the 1970s, in an attempt to address this issue, Eldredge and Gould proposed a theory they called “Punctuated Equilibrium.” This theory postulated that for long periods of time most species experience very little observable change, but when it does occur it does so rapidly. This, they suggested, would explain why fossil intermediates are hard to find. While reaffirming common descent, they proposed that a mechanism other than natural selection was needed to explain rapid, large-scale changes.

Notably, it’s not just paleontologists complaining about a lack of bones in the fossil record. Biologists Mae-Wan Ho and Peter Saunders have complained that “ . . . the successes of the theory are limited to the minutiae of evolution, such as the adaptive change in coloration of moths; while it has remarkably little to say on the questions which interest us most, such as how there came to be moths in the first place.”

Charles Darwin wrote, “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.” Such an organ would be irreducibly complex, in the sense that if you took away one of its parts, it would cease to function.

Most of the skepticism of Darwin’s theory has centered on this problem. From Mirvart’s concern over the initial stages of new structures to Margulis’ objection of gradual evolution, critics have felt that the criterion for questioning Darwin’s theory has been met. 

It’s tempting to think that irreducible complexity can be overcome by multiple simultaneous mutations—while highly improbable, it might still be possible. Yet, this is a vain hope. A scientific explanation for the origin of an irreducibly complex system must appeal to a sufficient cause. Besides, sudden leaps forward run contrary to the gradualism of Darwinism. As Richard Dawkins concedes, “Without gradualness in these cases, we are back to miracle.”

The reason gradualism can’t be compromised is due to the nature of mutation. Generally, a mutation can only make a small change. Think of a step-by-step instruction manual. A mutation would effect a change on one of the lines of instructions. So instead of “Attach the seat to the seatpost,” we might get “Attach the seat to the handlebars.” What a mutation can’t do is change all of the instructions at once.

A cell with a cilium is enabled by an oar-like function to move about in liquid. Sperm use cilia to swim. Also, stationary cells lining the respiratory tract have cilia that beat in synchrony and push mucus up to the throat for expulsion. 

Just as a mousetrap must have all of its component parts in order to work, ciliary motion requires the presence of microtubules, connectors, and motors. Any biological system composed of numerous, well-matched, interacting parts, wherein the removal of any one of its parts would cause the system to fail, is irreducibly complex. The cilium is irreducibly complex, which means that all of its parts must have come together simultaneously in order for it to perform its function. This can’t be explained by a succession of gradual, slight modifications.

Biochemistry has discovered many irreducibly complex systems on the molecular level. One example is the formation of the blood clot. Although we take this phenomenon for granted, blood clotting is very complex, involving numerous interdependent proteins that must all function properly in order for blood to clot at the right time and place.

We begin with a protein called fibrinogen, which compromises about 2 to 3 percent of the protein found in blood plasma. Fibrinogen provides the “fibers” that form a clot. The other proteins involved in blood clotting control the timing and placement of the clot. Fibrinogen circulates in the blood stream unnoticed until an injury causes bleeding. Then another protein called thrombin slices off pieces of fibrinogen, exposing sticky ends, which find each other, forming a web of meshwork that entraps blood cells.

However, if these two proteins were the only ones involved, the process would go on unchecked, forming a massive blood clot throughout the circulatory system, solidifying it and causing death. This is why thrombin exists safely in an inactive form called prothrombin until it’s needed, at which point a protein called Stuart factor comes into the picture. At the right time, it cuts prothrombin, turning it into active thrombin so it can cut fibrinogen, turning it into sticky fibrin to form blood clots. But we still have the same problem of control, which is why Stuart factor also exists in an inactive state, waiting to be activated. What activates it?

There are two different route: one is called intrinsic and the other is extrinsic. With the intrinsic pathway, the remaining proteins involved are found in the blood plasma. With the extrinsic pathway, certain proteins are found on the cells. Each of these pathways initiates an even longer chain reaction of proteins acting as the catalyst for one another until finally, with the intrinsic pathway, the proteins Christmas factor and antihemophilic factor activate the Stuart factor. 

With the extrinsic pathway, the protein convertin activates Stuart factor. But convertin can only be activated in the presence of another protein called tissue factor, which is only found on the outside of cells that normally have no contact with blood. Therefore, only injuries that bring this tissue into contact with blood will initiate the extrinsic pathway to clotting.  

Leaving aside issues of the control and timing of clot formation, it’s difficult to imagine how this system might have evolved in small steps. If, for example, the Stuart factor, after being activated by the rest of the cascade, cut the fibrinogen directly, bypassing the thrombin, it would either turn the system on, resulting in death, or it would do nothing. The nature of a cascade demands that each protein, from the beginning, is able to be turned on and off at the right time and place. So, not only is the entire blood-clotting system irreducibly complex, so is each step in the chain.

Natural selection can only operate where there is something functional at each step in the evolutionary process; it cannot work with potential function that may occur sometime in the future. The fact is, no one knows how the coagulation cascade could have evolved. Faced with such complexity, Darwinian theory is silent.

There are twenty separate sections in a cell, counting the membranes’ interior spaces. Because compartments are closed off, receiving new material is a problem. Although some compartments produce some of their own material, most proteins are made elsewhere and shipped to them. The transportation of these proteins is an intricate process.

There are three methods employed to move proteins into cellular compartments. In the first, a gate opens and closes to control which proteins are allowed through the membrane. This is known as gated transport. The second method is called transmembrane transport, which involves the threading of a single protein through a channel. The third means is vesicular transport, where proteins are loaded into containers and shipped to the lysosome (the waste management unit).

Imagine a parking garage that is reserved for people with special diplomatic license plates. This garage is equipped with a barcode scanner that reads the code on the license plates and opens the door if the code is correct. Such a system has three components: an identification tag, a scanner, and a gate that is activated by the scanner. If any of these components is missing, the system fails. This is, by definition, an irreducibly complex system. 

Irreducibly complex systems cannot slowly evolve in the step-by-step process demanded by Darwinism. A mouse trap, for example, isn’t built one piece at a time. The wood platform on its own would never catch any mice. Add a spring, and it still wouldn’t catch any mice. It isn’t until you have the platform, spring and hammer all working together that a mouse trap becomes functional. In the same way, proteins cannot be transported to their cellular compartments unless every part of the transportation process is in place all at once. If you have only part of the process in place, the proteins would only make it part of the way to their destination. The system is either all there or nothing happens. 

In 1971, a specialty journal was established, the Journal of Molecular Evolution (JME), for the exclusive purpose of studying how life at the molecular level had evolved. Led by an impressive staff of editors, JME began publishing over a thousand papers a decade. The resulting research has fallen into three categories: chemical synthesis of vital molecules, protein sequences, and abstract mathematical models. But the majority of the research has focused on protein sequences, accounting for more than 80 percent of all the papers published in the journal.

While most of the research published by JME has focused on the analysis of sequences, no research paper has ever asked, “How did the photosynthetic reaction center develop? How did intramolecular transport start? How did phosphoprotein signaling pathways originate?” 

JME is not alone in choosing to avoid these kinds of questions. A review of all of the research published, either in a book, textbook, or any of the scientific journals, will not produce a single detailed explanation for how a complex biochemical system might have been developed by a gradual, step-by-step process. The fact that research scientists have not addressed the origin of complex biological systems strongly suggests that Darwinism does not offer a sufficient frame of reference to make this kind of research possible.

Confronted with the tremendous complexity of the cell, the scientific community has suffered paralysis. No one at Harvard, or the National Institutes of Health, or the National Academy of Sciences can give an account of how cilium, or vision, or blood clotting, or any other complex biochemical system might have evolved in a gradual, step-by-step process. 

Obviously, if a system could not be put together gradually, it must have come together suddenly. If adding individual pieces could not have improved a system, then multiple pieces must have been added at the same time. But by what mechanism?

Imagine a dozen detectives working a crime scene of a person who has been crushed to death. As they search the room looking for clues through their magnifying glasses, a large elephant stands in the middle of the room next to the victim! But they ignore the elephant because the detective textbook says they must “get their man.”

There is an elephant in the room and his name is “Intelligent Design.” If we restrict our search to non-intelligent causes, we will miss him. Biochemical systems were not designed by the laws of nature, or by chance, or by necessity, but by an intelligent designer who knew what the systems would become before they were made.