In 1996, Michael Behe’s publication of Darwin’s Black Box started a major debate about irreducible complexity at the biochemical level. In his book, Behe had the audacity to point out that many scientists asserted the Fact of Evolution before anybody really understood the complexity involved in biochemical systems.[1] Needless to say, Behe’s promotion of an Intelligent Designer (ID) was not popular among Evolutionists.
Those who challenge the reigning scientific paradigm often become targets of abuse. Behe is no exception. Thomas Kuhn, a well-known Philosopher of Science, described how rejecting a reigning scientific paradigm is often equated with rejecting science itself.[2] Using an old-west analogy, scientists who support the reigning paradigm tend to “circle the wagons” to shield it from all challenges.
Paradigm protection is not restricted to Evolution. For example, it also applies to the Big Bang Theory. In The End of Physics, David Lindley described how concepts like “inflationary expansion” and “dark matter” lack empirical proof.[3] Scientists who are skeptical of blindly accepting these constructs believe that the supporters of the Big Bang limit dissent by controlling funding sources and peer-review committees:
The big bang today relies on a growing number of hypothetical entities, things that we have never observed – inflation, dark matter and dark energy are the most prominent examples. Without them, there would be a fatal contradiction between the observations made by astronomers and the predictions of the big bang theory. In no other field of physics would this continual recourse to new hypothetical objects be accepted as a way of bridging the gap between theory and observation. It would, at the least, raise serious questions about the validity of the underlying theory.
…
Today, virtually all financial and experimental resources in cosmology are devoted to big bang studies. Funding comes from only a few sources, and all the peer-review committees that control them are dominated by supporters of the big bang. As a result, the dominance of the big bang within the field has become self-sustaining, irrespective of the scientific validity of the theory.[4]
In an attempt to silence the ID-movement, the mainstream scientific community won a court case in Dover , Pennsylvania .[5] But court decisions are never the final word. In the Dred Scott case, a Supreme Court justice wrote an opinion stating: “because Scott was black, he was not a citizen and therefore had no right to sue.”[6] However, about 10 years later, the 14th amendment was passed, and the Dred Scott ruling was overturned.[7]
After the Dover Court Decision, Behe pointed out that winning a court case is not the same as supplying detailed evolutionary explanations for the origin of extremely complex molecular machines:
All of that is regrettable, but in the end does not impact the realities of biology, which are not amenable to adjudication [i.e., a judicial decision]. On December 21, 2005, as before, the cell is run by amazingly complex, functional machinery that in any other context would immediately be recognized as designed. On December 21, 2005, as before, there are no non-design explanations for the molecular machinery of life, only wishful speculations and Just-So stories.[8]
If the Theory of Evolution is to be compatible with the latest biochemical research, Behe asserts that Evolutionists need to supply detailed molecular-level explanations for how Evolution created such complicated cellular machinery.[9] Behe argued that many of these biochemical systems are irreducibly complex (according to this definition):
By irreducibly complex I mean a single system composed of several well-matched, interacting parts that contribute to the basic function, wherein the removal of any one of the parts causes the system to effectively cease functioning.[10]
The concept of an irreducibly complex system is relatively simple. One does not have to be a technical genius to understand it. Behe provided an everyday example that many people can easily understand – a common mousetrap.[11] Behe argued that a standard mousetrap meets that criterion of an irreducibly complex system – i.e., it will not function unless all five of its system components are placed in a coordinated arrangement.
Evolutionists allege that random mutations and natural selection are sufficient to explain how complex biochemical systems were produced through a trial and error process of optimization. Behe believes that step-by-step explanations for irreducibly complex biological systems don’t work, because there would be no functioning systems to optimize unless all the components were in place.
Consequently, Behe claims that irreducible complexity causes Darwinian explanations to fall apart. Behe has pointed out that Darwin himself suggested a collapse of his entire theory, if one could demonstrate that irreducibly complex systems exist.[12] Here are Darwin ’s own words regarding this possibility:
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.[13]
In Darwin’s Black Box, Behe cited five different biochemical systems that he believes meet the criteria for irreducible complexity:
- Cilium and Flagellum.[14]
- The blood-clotting cascade.[15]
- Protein Transport.[16]
- The Immune System.[17]
- A Multistep Metabolic Pathway (AMP).[18]
It is not easy to describe the complexity of biochemical systems at a level that the general public can understand. But as Behe has pointed out, you can’t appreciate biochemical complexity without delving into at least some details.[19] Even Biochemist David Ussery (a harsh critic of Behe) has acknowledged that, “Behe does a good job describing Biochemical systems and making them interesting to the reader.”[20]
Ussery acknowledged that even though Behe’s descriptions were very detailed, they understated the complexity of a cell’s Protein Transport system:
The third example of irreducible complexity has to do with how proteins are transported within a cell. Believe it or not, I think Behe even UNDERSTATES the level of complexity here![21]
Behe’s credentials as a biochemist have been acknowledged by fellow scientists. For example, in a critical review of Darwin’s Black Box, Evolutionary Geneticist H. Allen Orr[22] provided this description of Behe and his book:
Michael J. Behe, a biochemist at Lehigh University , has published a (seemingly) sophisticated insider's attack on Darwinism. His book, Darwin's Black Box, is well-written, cleverly argued, and biologically informed. No one can deny Behe's grasp of biochemistry. Unlike a few previous "biologists" who have taken aim at Darwin , Behe is the real thing: a research scientist, someone who does experiments, gets grants, and publishes papers.[23]
Behe does not deny that Evolutionists have invoked imaginative stories to describe the origin of many complex biological systems. However, he argues that such descriptions often lack any details about step-by-step molecular-level changes. For example, here is a quote from Darwin’s Black Box:
Some Evolutionary Biologists – like Richard Dawkins – have fertile imaginations. Given a starting point, they almost always can spin a story to get to any biological structure you wish. The talent can be valuable, but it is a two-edged sword. Although they might think of possible evolutionary routes that other people overlook, they also tend to ignore roadblocks that would trip up their scenarios. Science, however, cannot ultimately ignore details, and at the molecular level all “details” become critical.[24]
Some members of the scientific community are very reluctant to admit that molecular-level details for the evolution of complex biochemical systems are not available. For example, Ussery criticized Behe’s assertion that the scientific literature was lacking in this regard.[25] However, in an article posted on the ARN website, Behe cites several harsh critics who have acknowledged the lack of detailed Darwinian accounts:
For example, microbiologist James Shapiro of the University of Chicago declared in National Review that "There are no detailed Darwinian accounts for the evolution of any fundamental biochemical or cellular system, only a variety of wishful speculations." … In Nature University of Chicago evolutionary biologist Jerry Coyne stated, "There is no doubt that the pathways described by Behe are dauntingly complex, and their evolution will be hard to unravel. ... [W]e may forever be unable to envisage the first proto-pathways." … (Coyne 1996)
In a particularly scathing review in Trends in Ecology and Evolution Tom Cavalier-Smith, an evolutionary biologist at the University of British Columbia , nonetheless wrote, "For none of the cases mentioned by Behe is there yet a comprehensive and detailed explanation of the probable steps in the evolution of the observed complexity. The problems have indeed been sorely neglected – though Behe repeatedly exaggerates this neglect with such hyperboles as 'an eerie and complete silence.'" (Cavalier-Smith 1997)
…
Yes, there are a lot of papers published on "molecular evolution," as I had clearly acknowledged in Darwin ’s Black Box. But very few of them concern Darwinian details of irreducibly complex systems, which is exactly the point I was making.[26]
Instead of conceding Behe’s allegation that biochemical systems are irreducibly complex, some Evolutionists have opted to attack the concept of irreducible complexity itself. For example, Kenneth Miller (a professor of Biology at Brown University ) has attacked Behe’s claim that his mousetrap example is irreducibly complex. Behe has responded to such challenges and defended his mousetrap.[27]
One such attack was made by Evolutionist Michael Ruse, who suggested that the platform component of a common mousetrap could be replaced by the floor.[28] However, imagine a relatively small room that is 10 feet long by 10 feet wide. One could easily fit very many common mousetraps in a room of that size. If the baiting area isn’t placed correctly with respect to the spring and hammer, the trap will not catch very many mice!
The size and relative location for the parts of a mousetrap have to be coordinated or the mousetrap will not be able to perform its function. The same principle holds true for systems built from biochemical parts. The proper arrangement of components is part of a systems irreducible complexity. Behe’s key issue is not about mousetraps. Rather, it is about missing molecular-level details for the origin of complex molecular machines.[29]
Although the technical details of Behe’s molecular machines are highly complicated, it is not hard to grasp the principle behind his claim, as this quote from an ARN article describes:
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.[30]
A cilium contains over 200 different kinds of proteins.[31] How could genetic mutations that alter a single protein at a time explain the origin of biochemical systems that require so many interacting proteins in order to function? Behe has argued that Evolutionists offer no in-depth explanations to explain that paradox. However, as this quote from Ussery illustrates, Evolutionists put forth some generic explanations:
How could this complex system have evolved? Often nature will simply take what's handy and use it. Take for example the substance that forms the crystal for the lens of the eye – this is nothing but a common enzyme that happens to have very nice crystallization properties – not necessarily a "tailor made" protein specifically (and ONLY) for this particular use. ... There are MANY examples of complicated systems which are constructed from components that themselves have perfectly viable roles as units in a completely different context.[32]
How plausible is such an explanation? As the last chapter pointed out, each protein has a unique 3-D structure that enables it to perform a unique function. In order to function as enzymes, proteins need a very specific shape. This is commonly referred to as the “lock and key” model.[33] So arbitrarily finding an existing enzyme with a shape that accurately matches the other proteins in a complex “protein machine” seems far from a sure thing.
The concept that Evolution uses already existing proteins to perform new functions is similar to the way Punctuated Equilibrium attempts to explain gaps in the fossil record. Both explanations place the tiny-steps attributed to Evolution behind a curtain where they can’t be observed and where no detailed evolutionary transitions need to be supplied. But ultimately the magical protein shapes had to have come from somewhere.
Randomly generating the DNA-code for the specific amino-acid sequence of a typical protein is a virtual impossibility (see Chapter 11 for details). For a similar reason, it is unlikely that a set of random proteins optimized for other uses could somehow be pieced together to build a crude cilium. But even if this hypothetical set of random proteins existed, there would still be many other issues to resolve.
Although Ussery doesn’t mention this, Behe actually does discuss the possibility of adapting pre-existing proteins to try and build a cilium.[34] For example, Behe describes how microtubule-proteins (a cilium component) are used for many structural purposes in cells. If somebody is looking for a quick evolutionary explanation, nothing more would be needed. But as Behe pointed out, there are real world problems with this explanation.
The unique properties of the Tubulin protein cause it to bind together with other Tubulin molecules in a specific way to form the microtubules of a cilium.[35] However, Behe points out the disastrous consequences of having random proteins sticking together inside a cell.[36] As Stuart Ira Fox describes in Human Physiology, cells have elaborate mechanisms to control protein (enzyme) production and prevent such disasters:
The many thousands of different types of enzymatic reactions within a cell do not occur independently of each other. They are, rather, all linked together by intricate webs of interrelationships, the total pattern of which constitutes cellular metabolism. …
The enzymes in a metabolic pathway cooperate in a manner analogous to workers on an assembly line where each contributes a small part to the final product.[37]
Various diagrams of metabolic pathways clearly show the complexity involved in cellular metabolism.[38] This quote from Molecular Biology of the Cell (Alberts et al.) describes why complex regulation schemes are required to avoid cellular disasters:
A living cell contains thousands of enzymes, many of which operate at the same time and in the same small volume … . By their catalytic action, these enzymes generate a complex web of metabolic pathways, each composed of chains of chemical reactions in which the product of one enzyme becomes the substrate of the next. In this maze of pathways, there are many branch points where different enzymes compete for the same substrate. The system is so complex (…) that elaborate controls are required to regulate when and how rapidly each reaction occurs.[39]
In order to prevent disastrous interactions, cells must tightly regulate the timing and quantity of production for each protein. Therefore, suggesting that extra copies of over 200 pre-existing cilium proteins might inadvertently come together in the same time and place seems very unrealistic. Thus, attempting to explain the evolution of a cilium through a dual-usage of random proteins is rather unbelievable.
It is certainly true that many proteins can have multiple uses (as Ussery suggests). It is also true that many proteins share similar sequences of amino acids with other proteins. But these two facts don’t add up to prove that evolutionary mechanisms created a cilium. It takes more than the presence of some common segments in a cell’s DNA code to cause a self-assembling cilium to appear in the right place and with the right timing.
Hypothetical stories of the evolutionary origin of protein building blocks can never fully explain the origin of biochemical complexity. This is because vastly different structures can be built with similar building materials. The set of building materials needed for a construction project are not the only important thing. A detailed plan for putting the materials together in a particular arrangement is also vitally important.
This is especially true in complex biochemical systems. For example, this quote from Geoffrey Simmons’ What Darwin Didn’t Know describes how the development of a human brain follows a specific plan that connects trillions of neuron building blocks:
During the early fetal period of brain development the body adds more than 250,000 nerve cells per minute. Every neuron knows where to go, how to get there, and where to connect. A newborn has close to a trillion nerve cells, each with as many as 10,000 specific connections.[40]
As a computer engineer with 25 years of experience, I think there are very good reasons to believe that a complex network of trillions of neurons can’t be built one blind step at a time. Adding new features to a computer often requires adding matching modifications in more than one place. This is analogous to not being able to change the shape/color of a piece in the middle of a jigsaw puzzle without changing multiple pieces.
Evolutionists can tell stories of how random mutations and natural selection created biological structures like a human brain one blind step at a time. But as an engineer, I am highly skeptical. Even simple human actions demonstrate a complexity beyond what modern engineers can produce. For example, consider watching a music video, reading lyrics on the screen, singing along, and clapping your hands in rhythm to the music.
This is not a hard task for most people. If singing out of tune is allowed, I could even do it. But a human-designed system that performed this task would need to input complex video and audio streams in real-time, compute their information content, and coordinate voice and hand clapping to the rhythm of the music. Even with modern technological advances, I would rate that an engineering impossibility.
As a real-world engineer, I have about 25-years of experience in designed complex interlocking networks. Thus, I have a far different view of biological complexity than an evolutionary biologist whose career focuses on telling hypothetical stories. If nothing else, Behe’s challenge is pushing biologists to leave behind hypothetical stories and focus more on the technical details of complex biochemical systems.
In order to survive, multicellular organisms require complicated control networks that use negative feedback systems to produce a stable operating environment. A normal thermostat provides a simple example of the principle behind a typical negative feedback system. The thermostat senses the temperature of the house, and turns the furnace on and off to keep the temperature in a stable range around the thermostat set point.
Human beings have a similar control network that keeps our bodies regulated at around 98 degrees Fahrenheit.[41] If our bodies depart from a stable temperature range, we will die. Thus, when we become too hot, sweat cools us down. And when we become too cold, shivering warms us up. These mechanisms are simple to understand. However, very many complex factors combine to maintain our bodies at a stable temperature.[42]
The complex process of keeping our internal environment in a stable state is known as homeostasis.[43] As this quote from a Cambridge University Press article by Wilfrid Janig indicates, the importance of maintaining homeostasis cannot be overstressed:
The body’s motor activity and behavior are only possible when its internal milieu is controlled to keep the component cells, tissues and organs (including the brain and skeletal muscles) maintained in an optimal environment for their function.[44]
Which came first, a set of interacting body parts, or the control systems required to maintain a stable environment for these body parts? This is one example of the numerous chicken or egg problems that exist at the macroscopic level of multicellular organisms. Evolutionists often attempt to cover over these paradoxes with hypothetical stories that are far removed from specific technical details.
However, empirical research at the level of cellular logic is uncovering the technical details driving these complex biochemical systems. This development has led Behe to point out that we need more than hypothetical explanations to explain these technical details. This quote from a technical article (Peter Satir et al.) describes how difficult it is to explain the origin of a cilium (one of Behe’s examples of irreducible complexity):
The origin of cilia, a fundamental eukaryotic organelle, not present in prokaryotes, poses many problems including the origins of motility and sensory function, the origins of nine-fold symmetry, of basal bodies, and of transport and selective mechanisms involved in ciliogenesis.[45]
Satir is a leading microbiologist who has spent his career studying cilia.[46] Satir’s article describes how current theories “do not readily account for” certain features of cilia.[47] Thus, Satir’s article proposes another competing theory. Satir’s article was published ten years after Darwin’s Black Box. But it indicates that a detailed explanation for the evolution of cilia is still lacking. This is exactly what Behe claimed.[48]
There is no doubt that scientists are actively seeking detailed explanations for the evolution of the biochemical systems that Behe classified as irreducibly complex. But whether such explanations supply enough details to qualify Evolution as a Fact is a very debatable question. The abstract of Satir’s article makes it clear that explaining the evolutionary origin of cilia poses many difficult problems.
Many evolutionary explanations attempt to invoke the “proteins were already there” argument that was suggested by Ussery in his critique of Behe. Satir’s article adds the “proteins came from somewhere else” argument. For example, Satir’s theory invokes a hypothetical self-assembling “RNA enveloped virus” to carry the vital Tubulin protein to a hypothetical host cell that has no gene for a Tubulin protein in its DNA stream.
Satir theory assumes that his hypothetical cell already has “transport machinery and molecular motors.”[49] Thus, when the Tubulin protein arrives, Satir’s hypothetical cell will have a set of fundamental cilium components in place. Satir’s proposal is analogous to a prefab form of construction, in which building components are partially assembled before being brought together at the construction site.
However, Satir’s hypothetical theory of cilium construction doesn’t fully explain how cilia evolved. It simply moves several critical issues behind a curtain where no one can look:
- What detailed evolutionary processes created the “transport machinery,” “molecular motors,” and a “self-assembling RNA virus containing the vital Tubulin protein”?
- How likely is it that these highly complex sub-assemblies would simply come together in a hypothetical cell to construct a functional cilium, keeping in mind that natural selection can’t tune a cilium that has no functionality?
Prefab construction doesn’t make complicated structures less complex. It simply moves the complexity to a different time and place. Sub-assemblies need to conform to a design plan so that they will fit together properly. Prefab construction also requires an assembly process that can be very complicated. For example, even if you have all the parts available, assembling a modern automobile would not be a simple task.
There is much more involved in assembling a house than accumulating a stockpile of prefab building materials. For a similar reason, stockpiling the biochemical materials needed to make the neurons of a human brain or the proteins of a cilium represents the tip of a complexity iceberg. Complex structures require more than a stockpile of building materials. They also require a complex assembly process.
Behe cites the flagellum as another example of an irreducibly complex system. In The Edge of Evolution, he describes how the proteins for each layer of the flagellum are not manufactured until the construction of the preceding layer completes.[50] An article published in Science (S. Kalir et al.) has described the complex ordering used to manufacture flagellum proteins in the sequence that they are needed:
The observed temporal program of transcription was much more detailed than was previously thought and was associated with multiple steps of flagella assembly.[51]
…
The observed order corresponds to the spatial position of the gene products during flagellar motor assembly.[52]
This empirical study of flagellum construction demonstrates an optimized control mechanism for producing flagellum. However, the blind hill-climbing algorithm of an evolutionary process will tend to get stuck on low-level peaks rather than climbing to optimal heights. In The Edge of Evolution, Michael Behe provides a good explanation of why blind hill-climbing algorithms have this problem.[53]
Imagine you are attempting to climb to the top of the highest building in a major city while blindfolded (elevators allowed and safety constraints ignored). This attempt at blind-hill climbing has only one restriction. If you start to go downhill, you must abort this path and try again from the last point where you gained elevation. This restriction corresponds to the guidance of natural selection, which only seeks to climb uphill.
With such an algorithm, you are probably not going to end up on top of a huge building like the Sears Tower . In fact, you may not even end up on top of an average-size building. For example, you could get stuck at the top of a staircase with a locked door that prevents access to higher levels. At this point, you will have nowhere to go but downhill. And the rule that you can never go downhill prevents this.
In theory, the blind process of genetic mutations and natural selection provides access to the lofty peaks of biological complexity. However, Behe references a sophisticated mathematical model that indicates each gene is likely only to take several mutational steps before getting stuck on a local peak.[54] Consequently, finding a set of optimized peaks with blind walks is a very unlikely event.
This does not imply that blind-walks can never reach a lofty height. However, it does imply that blind walks are much more likely to get stuck on a local peak. This creates a paradox. If evolutionary processes were responsible for creating biological complexity, then we would expect to find very few systems with optimal peaks. However, biological life is full of highly optimized structures.
For example, the Blood Clotting Cascade is another one of the biochemical systems cited by Behe as being irreducibly complex.[55] Kenneth Miller is a Brown University Biologist, who has been a fierce opponent of Behe’s concept of irreducible complexity. In an article entitled The Evolution of Vertebrate Blood Clotting, Miller describes the complexities involved in blood clotting:
Michael Behe is in awe of the intricate complexity of this system, and so am I. And he is also correct in pointing out that if we take away part of this system, we're in trouble. Hemophiliacs, for example, are unable to synthesize the active form of Factor VIII. This means that they are unable to complete the final step of one of the pathways, and that's why hemophilia is sometimes known as the bleeder's disease. Defects or deficiencies in any of the other factors are equally serious. No doubt about it – clotting is an essential function and it's not something to be messed with.[56]
Evolutionist Russell Doolittle is also a harsh critic of Behe’s view that the blood-clotting cascade represents the work of an Intelligent Designer. While Behe has clearly acknowledged Doolittle’s factual knowledge of the blood-clotting cascade, he has argued that Doolittle’s explanations for the evolutionary history of blood clotting offer very little in the way of technical details.[57]
In Darwin’s Black Box, Behe included an extended paraphrase of an article Doolittle published in the journal Thrombosis and Haemostasis.[58] Behe points out that Doolittle’s article describes the origin of the vital blood-clotting proteins with very vague language:
Thus tissue factor “appears,” fibrinogen “is born,” anitplasmin “arises,” TPA “springs forth,” a cross-linking protein “is unleashed,” and so forth. What exactly, we might ask, is causing all this springing and unleashing?[59]
The major gripe that Behe has with Doolittle’s paper is that it supplied no technical details about what caused such magical actions. In a critique of Darwin’s Black Box (published in Boston Review), Doolittle responded to Behe’s charges:
The main point [of my paper] was to demonstrate that the delicate balance of forward and reverse reactions that regulate blood clotting came about in a step-by-step fashion.[60]
Behe does not dispute Doolittle’s assertion that the blood-clotting cascade requires a delicate balance of forward and reverse reactions. What Behe disputes is that Doolittle’s casual, yin-yang description provided adequate technical details for the origin of the blood-clotting cascade through a step-by-step process of Evolution. In response, Doolittle has downplayed Behe’s contention that his yin-yang paper was really “state of the art.”[61]
Doolittle has described his article as using casual language with a light and breezy tone. However, a 2003 article by William C. Aird published in the Journal of Thrombosis and Haemostasis continued to describe Doolittle’s paper as state of the art:
In 1993, Russell Doolittle from the University of California , San Diego , an authority on protein evolution wrote a state-of-the-art review about the evolution of blood clotting.[62]
In his article, Aird is very critical of the concept of Intelligent Design. Aird cites Richard Dawkins’ description of a slow climb up the back of Mount Improbable to explain how Evolution could produce systems that have the appearance of design.[63] However, Aird cites evidence from the original Doolittle paper that suggests the vertebrate blood-clotting cascade did not develop at a slow and regular pace:
[The blood-clotting cascade] was assembled over a period of only 50 million years and then remained relatively unchanged for the next 450 million years … [it] took a giant leap during [a relatively brief interval of] evolution and plateaued early. How do we explain this apparent departure from the rules of the mountain?[64]
Aird interprets evidence for the sudden-appearance and stability of the blood-clotting cascade as verification that Doolittle’s speculation is correct. For example, Aird argues that the sudden appearance of a functional cascade “speaks to the power and versatility of gene duplications and exon shuffling.”[65] However, the sudden appearance of the blood- clotting cascade might also be interpreted as evidence for an intelligent designer.
Aird acknowledged that Doolittle provided a critical review of his article.[66] However, does Doolittle’s stamp of approval on his own speculation certify it as fact? As Jonathan Marks pointed out, “it’s very easy to come up with results that you already believe”[67] Doolittle has implied that Behe’s assertions mean that his entire scientific career has been wasted.[68] But Behe actually applauds the value of Doolittle’s prestigious career:
Professor Doolittle is a prominent scientist, a member of the National Academy of Sciences who has worked hard on many aspects of protein structure over the course of a distinguished career. He knows more about the process of blood clotting, and more about the relationships among the protein members of the clotting cascade, then perhaps anyone else on earth.[69]
Behe doesn’t dispute the value of scientific work done by Doolittle. What Behe disputes is the concept that Doolittle’s speculation about the evolutionary origin of blood clotting is unchallengeable. For example, Doolittle states that no “Creator would have designed such a circuitous and contrived system.”[70] However, Miller has pointed out that complex multi-step cascades have a distinct design advantage over simpler pathways:
It sure does look pretty, but why a cascade? Why couldn't we have a simpler pathway … Well, we could, but a complex pathway … has advantages of its own. Clotting with fewer steps would still work, but it would take longer to produce a substantial clot, and would be much less responsive to smaller injuries.[71]
In his review of Darwin’s Black Box, Doolittle uses Behe’s analogy of a Rube-Goldberg system to ridicule the concept of an Intelligent Designer for the vertebrate blood-clotting cascade: But Aird describes its extreme durability and unchanged nature:
Finally, the cascade has weathered many storms and remained relatively unchanged for 450 million years. In other words, for all its complexity, the coagulation mechanism is extraordinarily durable.[72]
Any engineer whose design remained unchanged for 450 million years would be quite proud. Shouldn’t a similar standard apply to Doolittle’s hypothetical Creator? But instead of considering that possibility, Miller suggests that a smooth evolutionary path traces blood clotting back to in invertebrates.[73] However, this quote from Aird’s article implies that there is no smooth evolutionary path tracing back to invertebrates:
All living vertebrates have … a well-developed coagulation cascade; … In contrast, the invertebrates do not possess even a vestige of the vertebrate clotting cascade.[74]
The hard work of Russell Doolittle has helped to gather the empirical information supporting Aird’s statement. If Doolittle rated his career based on the importance of gathering such empirical facts, it would have tremendous value. But if Doolittle believes that his only important accomplishment has been to offer speculation supporting the Fact of Evolution, it would be hard to classify him as an independent judge.
Nobody disputes that the vertebrate blood-clotting system is complex and that its parts function together to serve a useful purpose. Evidence also indicates that it has appeared suddenly and has remained relatively unchanged for a very long period of time. Is this evidence consistent with a theory based on continuous random change in biological systems? Or is it more consistent with the work of an Intelligent Designer?
I believe it is not in the interest of science to jump to the first conclusion. Promoting genetic shuffling as a factual cause for the sudden appearance of blood clotting is far from certain. For example, Behe did some simple calculations that illustrate the extreme improbability of the genetic shuffling suggested by Doolittle.[75] In response, Doolittle’s challenged Behe’s “improbability argument” as being based on “absurd arithmetic.”[76]
Proponents of Evolution often denounce the probability calculations done by skeptics of the Fact of Evolution. However, Behe has pointed out that Doolittle has provided no alternate calculations to illustrate the likelihood of his suggested set of genetic shuffles:
At no step – not even one – does Doolittle give a model that includes numbers or quantities; without numbers there is no science. When a merely verbal picture is painted of the development of such a complex system, there is absolutely no way to know if it would actually work.[77]
There is evidence that suggests Doolittle is quick to leap to conclusions about the creative power of evolution. For example, Doolittle described how scientists removed genes for two of the vital proteins in the blood-clotting cascade of mice. Doolittle acknowledged that in both cases, the mice had the expected health issues.[78] But he then described how crossing the two genetic lines created completely normal mice:
And what do you think happened when these two lines of mice were crossed? For all practical purposes, the mice lacking both genes were normal! Contrary to claims about irreducible complexity, the entire ensemble of proteins is not needed. ... No one doubts that mice deprived of these two genes would be compromised in the wild, but the mere fact that they appear normal in the laboratory setting is a striking example of the point and counterpoint, step-by-step scenario in reverse![79]
While such evidence seems to prove that not all proteins in the blood-clotting cascade are necessary, it turns out that Doolittle had misinterpreted the scientific findings. Behe has acknowledged that anybody could misread a paper. But he pointed out that the result of the experimental work cited by Doolittle was not a set of normal mice, but a set of mice with fatal flaws:
The mice that have had both genes knocked out do not have a functioning clotting system: they can’t form clots; they hemorrhage; females die during pregnancy. They are certainly not candidates for evolutionary intermediates.[80]
Behe contends that Evolution is fatally flawed because step-by-step development algorithms cannot generate systems composed of interlocked components. Whether or not Behe’s assertion about irreducible complexity is true, his work has demonstrated that Evolutionary explanations lack many significant details. This calls into question the validity of the Fact of Evolution. In the words of Evolutionist Kenneth Miller:
Can we know for sure that this is how blood clotting (or any other biochemical system) evolved? The strict answer, of course, is we cannot.[81]
Acknowledgements
Endnotes are contained in the following section. The following shorthand notation connects the numbered endnotes to permission statements:
N(x, y, z, …) indicates endnotes numbered ‘x’, ‘y’, ‘z’.
I gratefully acknowledge permission to reproduce quotes from the following copyrighted material:
N(3): David Lindley, The End of Physics: The Myth of a Unified Theory (New York: Basic Books, 1993). Used with permission of the Perseus Books Group.
N(11, 26): The Access Research Network permits this document to be reproduced in its entirety for non-commercial use: Michael Behe, “A Mousetrap Defended: Response to Critics,” 31 July 2000, http://www.arn.org/docs/behe/mb_mousetrapdefended.htm.
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Notes and References
[1]. Michael Behe, Darwin’s Black Box (New York: Free Press, 1996), 307 pages.
[2]. Phillip E. Johnson, Darwin on Trial, 2nd ed. (Downers Grove, IL: Intervarsity Press, 1993), pp. 120-124; Frank Pajeras, “Outline and Study Guide of ‘The Structure of Scientific Revolutions’ by Thomas S. Kuhn,” http://des.emory.edu/mfp/Kuhn.html.
[3]. David Lindley, The End of Physics: The Myth of a Unified Theory (New York: Basic Books, 1993), p. 205.
[4]. “An Open Letter to the Scientific Community,” http://www.cosmologystatement.org/. This letter was published in the May 22, 2004 edition of New Scientist.
[5]. “Judgment Day: Intelligent Design on Trial,” Nova, 13 November 2007, http://www.pbs.org/wgbh/nova/id/.
[6]. PBS, “Dred Scott Case: The Supreme Court Decision,” http://www.pbs.org/wgbh/aia/part4/4h2933.html.
[7]. See http://en.wikipedia.org/wiki/Fourteenth_Amendment_to_the_United_States_Constitution for background information.
[8]. Michael Behe, “Whether Intelligent Design Is Science: A Response to the Opinion of the Court in Kitzmiller vs
[11]. Michael Behe, Darwin’s Black Box (New York: Free Press, 1996), pp. 42-43. Also see: Michael Behe, “A Mousetrap Defended: Response to Critics,” 31 July 2000, http://www.arn.org/docs/behe/mb_mousetrapdefended.htm.
[13]. Charles Darwin, On the Origin of Species by Means of Natural Selection, 6th ed., Chapter 6, http://www.literature.org/authors/darwin-charles/the-origin-of-species-6th-edition/chapter-06.html.
[20]. David Ussery, “A Biochemist's Response to "The Biochemical Challenge to Evolution”, Bios 70, pp. 40-45, 1999, as quoted from the website: http://www.cbs.dtu.dk/staff/dave/Behe.html.
[21]. David Ussery, “A Biochemist's Response to "The Biochemical Challenge to Evolution”, Bios 70, pp. 40-45, 1999, as quoted from the website: http://www.cbs.dtu.dk/staff/dave/Behe.html.
[23]. H. Allen Orr, “Darwin v. Intelligent Design (Again),” Boston Review, December 1996 – January 1997, http://bostonreview.net/BR21.6/orr.html.
[25]. David Ussery, “A Biochemist's Response to "The Biochemical Challenge to Evolution”, Bios 70, pp. 40-45, 1999, as quoted from the website: http://www.cbs.dtu.dk/staff/dave/Behe.html
[26]. Michael Behe, "Irreducible Complexity and the Evolutionary Literature: Response to Critics,” 31 July 2000, http://www.arn.org/docs/behe/mb_evolutionaryliterature.htm.
[27]. Michael Behe, “A Mousetrap Defended: Response to Critics,” 31 July 2000, http://www.arn.org/docs/behe/mb_mousetrapdefended.htm.
[28]. Michael Ruse, "
[29]. Michael Behe, "Molecular Machines – Experimental Support for the Design Inference,” 1997, http://www.arn.org/docs/behe/mb_mm92496.htm.
[30]. Michael Behe, "Molecular Machines – Experimental Support for the Design Inference,” 1997, http://www.arn.org/docs/behe/mb_mm92496.htm.
[32]. David Ussery, “A Biochemist's Response to "The Biochemical Challenge to Evolution”, Bios 70, pp. 40-45, 1999, as quoted from the website: http://www.cbs.dtu.dk/staff/dave/Behe.html
[38]. “Metabolic Pathway,” Wikipedia, http://en.wikipedia.org/wiki/Metabolic_pathway; Bruce Alberts, Alexander Johnson, Julian Lewis, Martin Raff,
[39]. Bruce Alberts, Alexander Johnson, Julian Lewis, Martin Raff,
[43]. Stuart Ira Fox, Human Physiology, 2nd ed. (Dubuque, IA: Wm. C. Brown, 1987), pp. 16-18. See http://en.wikipedia.org/wiki/Human_homeostasis for more background information. Also see this website: Physiological Homeostasis,” Biology on Line, http://www.biology-online.org/4/1_physiological_homeostasis.htm.
[44]. Wilfrid Janig, “The Integrative Action of the Autonomic Nervous System: Neurobiology of Homeostasis,” Cambridge University Press, Excerpt, http://assets.cambridge.org/97805218/45182/excerpt/9780521845182_excerpt.pdf.
[45]. Peter Satir et al., “Evolution and persistence of the cilium, Cell Motility and the Cytoskeleton 64(12):906-13, December 2007, Abstract, http://www.ncbi.nlm.nih.gov/pubmed/17896340.
[47]. Peter Satir et al., “Evolution and persistence of the cilium, Cell Motility and the Cytoskeleton 64(12):906-13, December 2007, Abstract, http://www.ncbi.nlm.nih.gov/pubmed/17896340.
[49]. Peter Satir et al., “Evolution and persistence of the cilium, Cell Motility and the Cytoskeleton 64(12):906-13, December 2007, Abstract, http://www.ncbi.nlm.nih.gov/pubmed/17896340.
[51]. S. Kalir et al., “Ordering Genes in a Flagella Pathway by Analysis of Expression Kinetics from Living Bacteria,” Science 292(2524):2080-2083, 15 June 2001, p. 280, http://www.weizmann.ac.il/mcb/UriAlon/Papers/flagella.pdf.
[52]. S. Kalir et al., “Ordering Genes in a Flagella Pathway by Analysis of Expression Kinetics from Living Bacteria,” Science 292(2524):2080-2083, 15 June 2001, p. 281, http://www.weizmann.ac.il/mcb/UriAlon/Papers/flagella.pdf.
[54]. H. Allen Orr, “A Minimum on the Mean Number of Steps Taken in Adaptive Walks,” Journal of Theoretical Biology 220(2):241-, 21 January 2003, http://www.ncbi.nlm.nih.gov/pubmed/12468295?dopt=Abstract, cited in the book: Michael Behe, The Edge of Evolution (
[56]. Kenneth R. Miller, “The Evolution of Vertebrate Blood Clotting,” http://www.millerandlevine.com/km/evol/DI/clot/Clotting.html.
[61]. Russell F. Doolittle, “A Delicate Balance,” Boston Review, February/March 1997, http://bostonreview.net/BR22.1/doolittle.html.
[62]. William C. Aird, “Hemostasis and irreducible complexity,” Journal of Thrombosis and Haemostasis 1(2):227-30, February 2003, p. 229, http://onlinelibrary.wiley.com/doi/10.1046/j.1538-7836.2003.00062.x/pdf.
[63]. William C. Aird, “Hemostasis and irreducible complexity,” Journal of Thrombosis and Haemostasis 1(2):227-30, February 2003, p. 227, http://onlinelibrary.wiley.com/doi/10.1046/j.1538-7836.2003.00062.x/pdf.
[64]. William C. Aird, “Hemostasis and irreducible complexity,” Journal of Thrombosis and Haemostasis 1(2):227-30, February 2003, p. 229, http://onlinelibrary.wiley.com/doi/10.1046/j.1538-7836.2003.00062.x/pdf.
[65]. William C. Aird, “Hemostasis and irreducible complexity,” Journal of Thrombosis and Haemostasis 1(2):227-30, February 2003, p. 227, http://onlinelibrary.wiley.com/doi/10.1046/j.1538-7836.2003.00062.x/pdf.
[66]. William C. Aird, “Hemostasis and irreducible complexity,” Journal of Thrombosis and Haemostasis 1(2):227-30, February 2003, p. 230, http://onlinelibrary.wiley.com/doi/10.1046/j.1538-7836.2003.00062.x/pdf.
[67]. Jonathan Marks, What it means to be 98% chimpanzee (
[68]. Russell F. Doolittle, “A Delicate Balance,” Boston Review, February/March 1997, http://bostonreview.net/BR22.1/doolittle.html.
[70]. Russell F. Doolittle, “A Delicate Balance,” Boston Review, February/March 1997, http://bostonreview.net/BR22.1/doolittle.html.
[71]. Kenneth R. Miller, “The Evolution of Vertebrate Blood Clotting,” http://www.millerandlevine.com/km/evol/DI/clot/Clotting.html.
[72]. William C. Aird, “Hemostasis and irreducible complexity,” Journal of Thrombosis and Haemostasis 1(2):227-30, February 2003, p. 230, http://onlinelibrary.wiley.com/doi/10.1046/j.1538-7836.2003.00062.x/pdf.
[73]. Kenneth R. Miller, “The Evolution of Vertebrate Blood Clotting,” http://www.millerandlevine.com/km/evol/DI/clot/Clotting.html.
[74]. William C. Aird, “Hemostasis and irreducible complexity,” Journal of Thrombosis and Haemostasis 1(2):227-30, February 2003, p. 229http://onlinelibrary.wiley.com/doi/10.1046/j.1538-7836.2003.00062.x/pdf.
[76]. Russell F. Doolittle, “A Delicate Balance,” Boston Review, February/March 1997, http://bostonreview.net/BR22.1/doolittle.html.
[78]. Bugge et al., "Loss of Fibrinogen Rescues Mice from the Pleiotropic Effects of Plasminogen Deficiency," Cell 87(14):709-19, 15 November 1996, cited by Russell Doolittle in: “A Delicate Balance,” Boston Review, February/March 1997, http://bostonreview.net/BR22.1/doolittle.html.
[79]. Russell F. Doolittle, “A Delicate Balance,” Boston Review, February/March 1997, http://bostonreview.net/BR22.1/doolittle.html.
[80]. Michael J. Behe, “Behe Responds to the Boston Review,” 1999, http://www.arn.org/docs/behe/mb_brrespbr.htm.
[81]. Kenneth R. Miller, “The Evolution of Vertebrate Blood Clotting,” http://www.millerandlevine.com/km/evol/DI/clot/Clotting.html.
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