Dr. Michael J. Behe is an American biochemist currently serving as Professor of Biochemistry at Lehigh University. He is best known for his argument of Irreducible Complexity (IC) as evidence for intelligent design in the complexity we now find in biochemical systems. Dr. Behe also serves as Senior Fellow on the Discovery Institute’s Center for Science and Culture, and is one of the strongest proponents of Intelligent Design Theory.

The main thesis behind Irreducible Complexity is that biochemical systems are now being discovered which are too complex to be explained by Darwinian evolution, with the alternative, and superior, explanation being intelligent design.

In the book’s introduction, Dr. Behe explains his why his work in Intelligent Design demands a hearing: “Understanding how something works is not the same as understanding how it came to be. Understanding the origin of something is different from understanding its day-to-day workings. As a writer who wants people to read my work, I have a dilemma: people hate to read details, yet the story of the impact of biochemistry on evolutionary theory rests solely in the details!”

He then challenges the scientific community with the need to explain how complexity in biochemistry came to be: “It was once expected that the basis of life would be exceedingly simple. That expectation has been smashed. Vision, motion, and other biological functions have proven to be no less sophisticated than television cameras and automobiles. Science has made enormous progress in understanding how the chemistry of life works, but the elegance and complexity of biological systems at the molecular level have paralyzed science’s attempt to explain their origins. There has been virtually no attempt to account for the origin of specific, complex biomolecular systems, much less any progress.”

Dr. Behe then strengthens his challenge to the scientific community with this statement on page 179: “There has never been a meeting, or a book, or a paper on details of the evolution of complex biochemical systems.” He further makes this point on pages 185-186: “Molecular evolution is not based on scientific authority. There is no publication in the scientific literature – in prestigious journals, specialty journals, or books – that describes how molecular evolution of any real, complex biochemical system either did occur or even might have occurred. There are assertions that such evolution occurred, but absolutely none are supported by pertinent experiments or calculations. Since no one knows molecular evolution by direct experience, and since there is no authority on which to base claims of knowledge, it can truly be said that the assertion of Darwinian molecular evolution is merely bluster.”

Dr. Behe titles his book “Darwin’s Black Box” because he takes you on a journey through the major discoveries in recent biology and biochemistry which point to a miniature world of complex, purposefully designed “machines” that scream for an intelligent source to cause them to be. These discoveries were beyond Darwin’s reach at the time he wrote ‘The Origin of Species’ – the world of the cell and the workings of life processes were a ‘black box’. Behe takes us inside the box.

On page 193, Dr. Behe explains how design has been detected within biochemistry to such an extent that the only logical conclusion is intelligent activity: “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, then 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.”

Throughout the 11 chapters of his book, Dr. Behe asks us 113 questions that are detailed below, with their page reference, to make it easy for anyone with a desire to do what Dr. Behe had hoped when he wrote this book: to “dig into the details”.

CHAPTER 1: LILLIPUTIAN BIOLOGY

1. When sciences such as physics finally uncovered their foundations, old ways of understanding the world had to be tossed out, extensively revised, or restricted to a limited part of nature. Will this happen to the theory of evolution by natural selection (p. 3)?
2. Darwin’s idea might explain horse hoofs, but can it explain life’s foundations (p. 4)?
3. Imagine that a computer with a long-lasting battery was transported back in time a thousand years to King Arthur’s court. How would people of that era react to a computer in action (p. 6)?
4. Matthias Schleiden wrote that “the question as to the fundamental power of organized bodies resolves itself into that of individual cells.” As Schleiden added, “Thus the primary question is, what is the origin of this peculiar little organism, the cell” (p. 9)?
5. This level of discovery began to allow biologists to approach the greatest black box of all. The question of how life works was not one that Darwin or his contemporaries could answer. They knew that eyes were for seeing – but how, exactly, do they see (p. 10)?
6. How does blood clot (p. 10)?
7. How does the body fight disease (p. 10)?
8. The complex structures revealed by the electron microscope were themselves made of smaller components. What were those components (p. 10)?
9. What did those components look like (p. 10)?
10. How did those components work (p. 10)?
11. In 1958, after decades of work, J.C. Kendrew determined the structure of the protein myoglobin using X-ray crystallography; finally, a technique showed the detailed structure of one of the basic components of life. And what was seen? Again, more complexity (p. 12).
12. Darwin had an excellent reason for declining the question of how vision began: it was completely beyond 19th-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 (p. 18).

CHAPTER 2: NUTS & BOLTS

13. What then does this all-encompassing theory of evolution predict? Given a handful of postulates, such as random mutations, and selection coefficients, it will predict changes in gene frequencies over time. Is this what a grand theory of evolution ought to be (p. 28)?
14. The bombardier beetle is an insect of unassuming appearance, measuring about ½-inch in length. When it is threatened by another bug, however, the beetle has a special method of defending itself, squirting a boiling-hot solution at the enemy out of an aperture in its hind section. The heated liquid scalds its target, which then usually makes other plans for dinner. How is this trick done (p. 31)?
15. The key question is: How could complex biochemical systems be gradually produced (p. 34)?
16. What exactly are the stages of bombardier beetle evolution, in all their complex glory (p. 34)?
17. Given these stages, how does Darwinism get us from one to the next (p. 34)?
18. Hydroquinone alone, then, has the defensive function that we ascribed to the whole system. Can the other components be added to the bombardier’s system in such a way that the function continuously improves (p. 35)?
19. Has the development of the defensive apparatus of the bombardier beetle truly been explained (p. 36)?
20. Although we seem to have a continuously changing system, the components that control its operation are not known. For example, the collection vesicle is a complex, multicelled structure. What does it contain? Why does it have its particular shape (p. 36)?
21. What causes a collection vesicle to develop, hydrogen peroxide to be excreted, or a sphincter muscle to wrap around (p. 36)?
22. The eye either functions as a whole or not at all. So how did it come to evolve by slow, steady, infinitesimally Darwinian improvements (p. 37)?
23. Is it really plausible that thousands upon thousands of lucky chance mutations happened coincidentally so that the lens and the retina, which cannot work without each other, evolved in synchrony (p. 37)?
24. What survival value can there be in an eye that doesn’t see (p. 37)?
25. We are invited by Dawkins and Darwin to believe that the evolution of the eye proceeded step-by-step through a series of plausible intermediates in infinitesimal increments. But are they infinitesimal (p. 38)?
26. Remember that the “light-sensitive spot” that Darwin takes as his starting point requires a cascade of factors, including 11-CIS-retinal and rhodopsin, to function. Dawkins doesn’t mention them. And where did the “little cup” come from (p. 38)?
27. Explaining the functioning of the eye can be compared to answering the question “How is a stereo system made?” with the words “By plugging a set of speakers into an amplifier, and adding a CD player, radio receiver, and tape deck.” Either Darwinian theory can account for the assembly of the speakers and amplifier, or it can’t (p. 39).
28. What type of biological system could not be formed by “numerous, successive, slight modifications” (p. 39)?
29. Given the nature of mutation, when can we be sure that a biological system is irreducibly complex (p. 42)?
30. Which part of a mousetrap could be missing and still allow you to catch a mouse (p. 42)?
31. Is a bicycle a physical (and potentially Darwinian) precursor of a motorcycle? No. It is only a conceptual precursor (p. 43).
32. Can we evolve a bicycle into a motorcycle (p. 44)?
33. What part of a bicycle could be duplicated to begin building a motor (p. 44)?
34. Even if a lucky accident brought a lawnmower engine from a neighboring factory into the bicycle factory, the motor would have to be mounted on the bike and be connected in the right way to the drive chain. How could this be done step-by-step from bicycle parts (p. 44)?
35. Unlike irreducible complexity (where we can enumerate discrete parts), minimal function is hard to define. If one revolution per hour is sufficient for an outboard motor, how about a hundred? Or a thousand (p. 46)?
36. What is the minimum amount of hydroquinone that a predator can taste (p. 46)?
37. How much of a rise in temperature of the hydroquinone solution will a predator notice (p. 46)?

CHAPTER 3: ROW, ROW, ROW YOUR BOAT

38. Do any cells swim? If so, what swimming systems do they use? Are they, like a Mississippi steamboat, irreducibly complex? Could they have evolved gradually (p. 58)?
39. Proteases allowed biochemists to see how a cilium would work without nexin linkers. What would removal of linkers do (p. 63)?
40. How did the cilium arise (p. 65)?
41. Intriguing as this scenario may sound, though, critical details are overlooked. The question we must ask of this indirect scenario is one for which many evolutionary biologists have little patience: but how exactly (p. 66)?

CHAPTER 4: RUBE GOLDBERG IN THE BLOOD

42. Accelerin also initially exists in an inactive form, called proaccelerin. And what activates it? Thrombin (p. 83)!
43. Once clotting has begun, what stops it from continuing until all the blood in the animal has solidified (p. 87)?
44. Is it possible that this ultra-complex system could have evolved according to Darwinian theory (p. 89)?
45. Professor Russell Doolittle begins his article by asking a big question: “How in the world did this complex and delicately balanced process evolve (p. 91)?
46. The paradox was, if each protein depended on activation by another, how could the system ever have arisen (p. 91)?
47. Of what use would any part of the scheme be without the whole ensemble (P. 91)?
48. Professor Doolittle: Tissue factor “appears”, fibrinogen “is born”, antiplasmin “arises”, TPA “springs forth”, a cross-linked protein “is unleashed”, and so forth. What exactly, we might ask, is causing all this springing and unleashing (p. 93)?
49. The 2nd question to consider is the implicit assumption that a protein made from a duplicated gene would immediately have the new, necessary properties (p. 94).

CHAPTER 5: FROM HERE TO THERE

50. This is science fiction, isn’t it? Things this complex don’t exist in nature, do they? The cell is a “homogeneous globule of protoplasm,” isn’t it (p. 106)?
51. Perhaps the components of the cell’s intracellular transport system were originally performing other tasks in the cell, then switched to their present role. Could that happen (p. 111)?
52. Suppose further that it was beneficial for the protein to be there because it toughened the membrane, making it resistant to tears and holes. Could that protein somehow turn into a gated channel (p. 111)?
53. Suppose wooden beams were brought together, and the area between them was weakened so much that plaster cracked and a hole formed in the wall. Would that be an improvement (p. 111)?
54. Placing a folded protein on new, unfolded proteins would protect them until they were fully made and folded. Could such a protein develop into, say, the signal recognition particle SRP (p. 112)?
55. We might expect the evolutionary development of vesicular protein transport to be a busy area of research. How could such a system develop step-by-step (p. 114)?
56. What hurdles would the cell have to overcome as it moved from some other method of dealing with garbage to a coated vesicle specifically targeted to, and equipped for merger with, the lysosome. Once again, if we looked in the literature for an explanation of the evolution of vesicular transport, we would be crushingly disappointed. Nothing is there (p. 114).

CHAPTER 6: A DANGEROUS WORLD

57. Could this antibody system have evolved step-by-step (p. 124)?
58. Our analysis overlooked many complexities: how does the cell switch from putting the extra oily piece on the membrane to not putting it on (p. 126)?
59. When the protein carrying the synthetic molecules was injected into a rabbit, the scientists were astonished to find that, yes, the rabbit made antibodies that bound tightly to the synthetic molecule. How could this be (p. 126)?
60. Neither the rabbit nor its ancestors ever met the synthetic molecule, so how did it know how to make antibodies against it (p. 127)?
61. Why should the rabbit recognize a molecule it had never seen before (p. 127)?
62. The regions that code for contiguous protein segments are themselves in a contiguous arrangement on the RNA. How does this process explain antibody diversity (p. 128)?
63. Remember the difference between B-cell factories and plasma factories? That oily piece of Y that anchors the antibody in the B-cell membrane (p. 129)?
64. But if C3b is on the surface of a cell, then another protein (properdin) binds to and protects C3b from degradation so that it can do its job. How does C3b target foreign cells in the absence of antibodies (p. 134)?
65. When a bacterium invades, why does the body make antibodies against it but not against the red blood cells that are continually circulated in the bloodstream, or any of the other tissues that antibody cells constantly bump up against (p. 138)?

CHAPTER 7: ROAD KILL

66. Much like a child’s snap-lock beads, amino acids or nucleotides can be strung to give an almost infinite variety of amino acids. But where do the beads come from (p. 142)?
67. The problem with Darwinian evolution is this: if only the end product of a complicated biosynthetic pathway is used in the cell, how did the pathway evolve in steps (p. 151)?
68. If A, B, and C have no use other than as precursors to D, what advantage is there to an organism to make just A (p. 151)?
69. If an organism makes A, what advantage is there to make B (p. 151)?
70. If a cell needs AMP, what good is it to just make intermediate III, or IV, or V? On their face, metabolic pathways where intermediates are not useful present severe challenges to a Darwinian scheme of evolution (p. 151).
71. Here is the source for the explanation of the development of biochemical pathways given by modern textbooks. But what was the state of science in Horowitz’s day (p. 154)?
72. In order to function at all, a metabolism must minimally be a connected series of catalyzed transformations leading from food to needed products. Conversely, however, without the connected web to maintain the flow of energy and products, how could there have been a living entity to evolve connected metabolic pathways (p. 155)?

CHAPTER 8: PUBLISH OR PERISH

73. If complex biochemical systems are unexplained, what type of biochemical work has been published under the heading of “evolution” (p. 165)?
74. What leads a professional in the field to such a bleak view, especially after the progress in the heady days following Miller’s trailblazing experiment (p. 168)?
75. The 3 general topics of papers published in Journal of Molecular Evolution (JME) – 1) the origin of life, 2) mathematical models of evolution, and 3) sequence analysis – have included many intricate, difficult, and erudite studies. Does such valuable and interesting work contradict this book’s message? NOT AT ALL (p. 175).
76. To say that Darwinian evolution cannot explain everything in nature is not to say that evolution, random mutation, and natural selection do not occur; they have been observed (at least in cases of microevolution) many different times. Like the sequence analysts, I believe the evidence strongly supports COMMON DESCENT. But the root question remains unanswered: What has caused complex systems to form? No one has explained in detailed, scientific fashion how mutation and natural selection could build the complex, intricate structures discussed in this book (p. 176).
77. Although many scientists ask how sequences can change or how chemicals necessary for life might be produced in the absence of cells, no one has ever asked in the pages of JME such questions as: 1) How did photosynthetic reaction center develop? 2) How did intramolecular transport start? 3) How did cholesterol biosynthesis begin? 4) How did retinal become involved in vision? 5) How did phosphoprotein signaling pathways develop (p. 176)?
78. An enthusiastic young scientist would first have to think of a precursor to the modern mousetrap, one that was simpler. Suppose he started with just a wooden platform? No, that won’t catch mice. Suppose he started with a modern mousetrap that had a shortened holding bar? No, if the bar is too short it wouldn’t reach the catch, and the trap would spring uselessly while he was holding it. Suppose he started with a smaller trap? No, that wouldn’t explain the complexity. Suppose the parts developed individually for other functions – such as a Popsicle stick for the platform, a clock spring for the trap spring, and so on – and then accidentally got together? No, their previous functions would leave them unfit for trapping mice, and he’d still have to explain how they gradually developed into a mousetrap (p. 176).
79. Since we have just seen that the professional biochemical literature contains no papers or books that explain in detail how complex systems might have arisen, why is Darwinism nonetheless credible with many biochemists (p. 179)?
80. How do we know what we say we know – not in some deep philosophical sense, but on a practical, everyday level (p. 183)?
81. Clearly these different assertions are based on different ways of knowing. What are they (p. 184)?

CHAPTER 9: INTELLIGENT DESIGN

82. The complex systems are here. All these things got here somehow: if not Darwinian fashion, then how (p. 187)?
83. The important question for us biochemists is, can synthesis explain the origin of complex biochemical systems (p. 189)?
84. A biologist or biochemist would want to know, if you opened the computer clam, would you see a pearl inside (p. 191)?
85. A biologist or biochemist would want to know, if you enlarged the image sufficiently, would you see cilia and ribosomes and mitochondria and intracellular transport systems and all the other systems that real, live organisms need? To ask the question is to answer it (p. 191).
86. Granted its premises, can complexity theory explain the complex biochemical systems we have discussed in this book? I don’t believe so (p. 191).
87. Although there is no evidence for it, let us say that complexity theory has something to do with the switch that turns one cell into a red blood cell and another into a nerve cell. Can this explain the origin of complex biochemical systems? No (p. 192).
88. What is “design” (p. 193)?
89. The scientific problem then becomes, how do we confidently detect design (p. 194)?
90. When is it reasonable to conclude, in the absence of firsthand knowledge or eyewitness accounts, that something has been designed (p. 194)?
91. A sophisticated computer can be used as a paper weight; is that its function (p. 196)?
92. A complex automobile can be sued to help dam a stream; is that what we should consider (p. 196)?
93. As time marches and rains fall and winds gust, Mt. Rushmore will change its shape. Millennia in the future, people may pass the mountain and see just the barest hint of faces in the rocks. Could a person conclude that an eroded Mt. Rushmore had been designed (p. 198)?
94. Suppose the bacteria and mold on the refrigerator formed an image of Elvis that was well nigh identical to one of those velvet posters of him that you see in variety stores. Can we conclude that the image was designed? Yes, we can (p. 199).
95. Might there be an as-yet-undiscovered natural process that would explain biochemical complexity (p. 203)?
96. If we assume we already have an oxygen-building protein like myoglobin, can we infer intelligent design from the function of hemoglobin (p. 207)?

CHAPTER 10: QUESTIONS ABOUT DESIGN

97. Exactly where was Paley refuted (p. 213)?
98. Who has answered Paley’s argument (p. 213)?
99. How was Paley’s watch produced without an intelligent designer (p. 213)?
100. If Paley knows what to look for in his mechanical paradigm, why did he go downhill so quickly (p. 215)?
101. What is the chance now that the disks will display the message METHINKSITSAWEASEL after, say, 50 repetitions (p. 220)?
102. What is wrong with the Dawkins-Sober analogy (p. 221)?
103. What function is there in a lock combination that is wrong (p. 221)?
104. Evolution, we are told by proponents of the theory, is not goal directed. But then, if we start from a random string of letters, why do we end up with METHINKSITSAWEASEL instead of MYDARLINGCLEMENTINE or MEBETARZANYOUBEJANE? As the disk turns, who is deciding which letters to freeze and why (p. 221)?
105. Because intelligent design works from a clean sheet of paper, it should produce organisms that have been optimally designed for the tasks they perform. Conversely, because evolution is confined to modifying existing structures, it should not necessarily produce perfection. Which is it (p. 222)?
106. Why is Gould’s Panda scenario incompatible with intelligent-design theory (p. 229)?

CHAPTER 11: SCIENCE, PHILOSOPHY, RELIGION

107. Why does the scientific community not greedily embrace its startling discovery (p. 233)?
108. Why is the observation of design handled with intellectual gloves (p. 234)?
109. With all of this public affirmation, why should science find it difficult to accept a theory that supports what most people believe anyway (p. 233)?
110. Let’s focus on the 2nd question. Dickerson mentions just one rule, the one disbarring the supernatural. Where did he get it? Is it written in a textbook? Is it found in the by-laws of scientific societies? No, of course not (p. 240).
111. The anxiety is that if the supernatural were allowed as an explanation, then there would be no stopping it – it would be invoked frequently to explain many things that in reality have natural explanations. Is this a reasonable fear (p. 241)?
112. Hypothesis, careful testing, replicability – all these have served science well. But how can an intelligent designer be tested? Can a designed be put in a test tube? No, of course not (p. 242).
113. This scenario still leaves open the question of who designed the designer – how did life originally originate? Is a philosophical naturalist now trapped? Again, no (p. 249).