Does Intelligent Design Rule Out Evolution?

In the next series of blog posts we are going to look at Christian questions about evolution. In my last post we saw that two of the Christian views of creation, Young Earth Creationism and Old Earth Creationism, disagree with the scientific account of the mechanism of creation. Because of this we need to ask, is evolution true? Perhaps the strongest recent challenge to evolution has been the Intelligent Design movement. For the rest of this post we are going to look at Intelligent Design and ask if it is a better explanation than the scientific view of evolution by natural selection.

What is Intelligent Design? Intelligent Design supporters make three claims.

1. Certain features of the universe and of living things are best explained by an intelligent cause, not an undirected process such as natural selection.
2. Intelligent design is detectable based on empirical observations using objective criteria.
3. Reference to intelligent design is legitimate within a scientific explanation of events in natural history.

How might we detect God’s supernatural intervention during the course of natural history? If God has intervened supernaturally during the course of natural history, one would expect to find gaps in the chain of natural explanations. And in fact there are gaps. Some examples are the origin of life, the origin of biological information, the origin of complex biological structures, the origin of the universe, and the fine-tuning of the laws of nature for life. So those gaps could represent places where  God has intervened supernaturally. However, all scientific explanations are underdetermined by the data so it is not surprising to find gaps. Furthermore, science has a history of filling in the gaps. Therefore the presence of gaps alone doesn’t prove that the gaps are due to direct action by God.

So how do we decide between these two options? Enter a man named William Dembski. In his book, Intelligent Design: The Bridge Between Science and Theology  (InterVarsity Press, 2002),  he outlined a design filter to help decide whether gaps have a natural explanation or whether they are due to the actions of an intelligent designer. The filter is basically a decision tree. Beginning with some event in natural history the first decision is whether the event was a necessity or whether it was contingent. An event is necessary if it is required by natural law. For example, if I drop a pencil it will fall until it hits a solid object such as a table or the floor. The fall of the pencil is necessary because of Newton’s law of gravitation. On the other hand the decision to drop the pencil was a contingent event since I didn’t have to drop the pencil.

If an event is contingent the next choice is between chance and design. In my pencil example, the initial event of dropping the pencil could have resulted from my conscious choice (design) or it could have been an accident (chance). In Dembski’s filter the decision between choice and design is based on probability, with the choice of design requiring that the event has a very low probability of occurring by chance. The choice of design requires that the event have two features: complexity and specification. Consider a random selection of 8 letters: axlmqyrz. If we allow the same letter to be selected more than once, then there are 26 possibilities at each position in the sequence of letters or 209 billion combinations of the eight letters. So the first requirement of complexity is met but there is no specificity, in other words the sequence of letters have no meaning. We would then conclude that the set of letters were drawn by chance. On the other hand if we selected the following eight letters: decision. This sequence of letters spells a word and thus does have meaning or specification. The probability of this sequence of letters occurring by chance is very low (one in 208 billion). Based on his decision tree we would conclude that drawing letters spelling the word decision occurred by design rather than by chance. Dembski refers to this situation as specified complexity.

Mount Rushmore is another example of specified complexity. The faces of the presidents carved into the mountainside clearly exhibit design because they are complex and they also have meaning or specification. On the other hand, the surrounding mountainside displays complexity due to variations in composition and effects of erosion but there is not specification or meaning. Using Dembski’s filter we could then conclude that the faces of the presidents are there by design not by chance.

There are two types of intelligent design: biological and cosmological. Biological intelligent design asserts that some biological structures are too complex to have been produced by natural selection. Cosmological intelligent design asserts that science is not able to answer certain basic questions about the origin of the universe and its basic properties. In this post I’m going to focus on biological intelligent design because it represents a challenge to the dominant scientific paradigm of evolution by natural selection. I will talk about cosmological intelligent design in a later post.

Biological Intelligent Design. In 1996, Michael Behe, a Biochemistry professor at Lehigh University, published a book called Darwin’s Black Box. He argued that cells were full of complex molecular machines and that natural selection was not able to explain the origin of these machines. Behe defined a parameter called irreducible complexity as an important feature of these complex systems. An irreducibly complex system displays two main features:

1. It is complex with many interacting parts.
2. All of the parts are necessary for function. The removal of any one part causes the system to stop working.

Behe goes on to argue that an irreducibly complex system can’t be created by natural selection because all of the parts must be present before the system starts to function. Natural selection works through a stair step process in which each step represents a small improvement or a movement towards a new function that can be selected for. In the case of an irreducibly complex structure there seems to be no way to select for intermediate steps because they are non-functional. Therefore Behe argues that intelligent design is a better explanation than natural selection.

Behe discussed several examples of irreducibly complex systems including: the bacterial flagellum, the human blood clotting apparatus, the machinery for transporting materials within cells, the immune system, and the biochemical pathway for the synthesis of ATP the energy currency in cells. Behe argued that these biological machines were too complex to have been created through natural selection and thus required the intervention of an intelligent designer.

Human blood clotting apparatus. Let’s look at the human blood clotting apparatus as a well-characterized example of an irreducibly complex system. When you cut your finger it begins to bleed but after a while it stops. What makes it stop? The answer is that a protein in blood called fibrin aggregates and forms a clot that plugs the leak.

How does a clot form? There is a precursor form of fibrin in blood called fibrinogen. This protein accounts for about 3% of the protein in the liquid part of blood. In response to injury fibrinogen is converted to fibrin through the action of a protease called thrombin. A protease is an enzyme which acts like a kind of scissors to clip off pieces of a protein molecule. In this case the pieces that are clipped off mask a sticky part of the fibrin molecule that allows individual fibrin molecules to stick together and form the blood clot.

How does clot formation get started? There are two ways called the extrinsic and the intrinsic pathways. Both involve the conversion of prothrombin which is inactive as a protease to active thrombin. The extrinsic pathway (Fig. 5, left) begins when injury to tissue exposes a protein on the surface of cells called Tissue Factor (TF). This sets off a chain of events in which Tissue Factor combines with and activates Factor VII which in turn activates Factor X which then converts prothrombin to thrombin. Factors VII and X are both proteases which activate their targets by clipping off parts of the inactive molecule. In the diagram, the letter “a” after the factor indicates the active form. Factor V is a protein helper in the activation of Factor X.

The intrinsic pathway (Fig. 5, right) also sets off a chain reaction but there are more components in the pathway. The pathway is initiated when blood comes in contact with a foreign surface due to injury. This results in the activation of a protease called Kallikrien which sets off the chain of events. Factors XII, XI, and IX are proteases whereas factor VIII is protein that acts as a helper in the activation of Factor X.

Why are the two pathways complex with so many steps? Let’s first consider the extrinsic pathway. The major components in the pathway (Factor VII, Factor X and Thrombin) are all enzymes. Because of this one Factor VII molecule is able to activate many molecules of Factor X. Once activated Factor X is able to convert many molecules of prothrombin to thrombin which then converts many fibrinogen molecules to fibrin which then aggregates to form the clot. This creates a snowball effect in which a small beginning leads to a large ending. So the purpose of the cascade of events in the extrinsic pathway is to amplify the signal from the tissue damage and to speed up the response to the injury. Similarly the multiple steps in the intrinsic pathway also amplify the response to contact activation. Amplification of the response to injury is important for the human circulatory system because it is under high pressure and thus a lead needs to be plugged quickly to prevent excess bleeding.

Both of the blood clotting pathways meets Behe’s criteria for an irreducibly complex system.

1. Each pathway has multiple interacting parts that participate in the blood clotting process
2. Each pathway fails with the removal of any one clotting factor. As an example, deficiencies in Factors VIII and X in the intrinsic pathway are responsible for the two most common types of Hemophilia.

Could the human blood clotting system have arisen through evolution by natural selection? Russell Doolittle has devoted his career to studying the evolution of the blood clotting cascade in humans and other vertebrate animals (animals that have a backbone). He has studied the appearance of clotting factors during the course of vertebrate evolution. His work has been greatly aided by the development of DNA sequencing technologies that have provided detailed information about the genes present in modern members of fish, amphibians, reptiles and mammals. The complete extrinsic clotting system is present in fish but the intrinsic clotting system is absent. During the transitions from fish to amphibians to reptiles to mammals there is a gradual appearance of the clotting factors needed for the intrinsic pathway. The intrinsic pathway is complete in mammals but not in amphibians and reptiles. During the intermediate stages of evolution (amphibians and reptiles) the clotting factors of the intrinsic pathway are used to enhance the function of the extrinsic pathway.

Doolittle’s work provides solid evidence for the evolution of the intrinsic pathway by natural selection. But what about the origin and evolution of the extrinsic pathway. We don’t yet know how the pathway developed during the transition from non-vertebrates to vertebrate animals. But here is a plausible mechanism. The large scale sequencing of genomes has revealed that most genes and the proteins that they code for can be grouped into families that are related in structure. These families have arisen through a well-known process called gene duplication. Gene duplication occurs occasionally during cell division when part of the DNA in a chromosome gets copied twice. Once gene duplication has occurred, the original gene continues with its normal function but the duplicate gene is free to undergo mutations.

How might gene duplication help to explain the origin of the Extrinsic Pathway? The first thing to notice is that all of the components in the pathway are proteases (protein-cutting enzymes) with the exception of Tissue Factor and Factor VIII. In fact they belong to the serine-protease gene family. Figure 6 illustrates a plausible scenario for the evolution of this pathway through gene duplication. The parent system consists of just three components (Fig. 6, top), a Tissue Factor, Protease 1 and a Clotting Protein. Tissue factor would be exposed upon injury and then bind to and activate Protease 1 which in turn would activate the Clotting Protein leading to aggregation and clotting. Duplication of the protease 1 gene would lead first to an intermediate system (Fig. 6, middle) with two identical proteases acting on the Clotting Protein. Both would be activated by Tissue Factor. Modification of the active site of Protease 2 by mutation could lead to a new arrangement (Fig. 6, bottom) in which the specificity of Protease 2 was changed allowing it to act on Protease 1 rather than the Clotting Protein. This new arrangement would amplify and speed up the clotting process and thus provide a basis for natural selection.

The scenario outlined above represents a plausible, although not proven, scenario for the evolution of the extrinsic blood clotting pathway beginning with a simple three component system. The process of gene duplication followed by gene modification could be repeated to add additional proteases thus further accelerating the response and providing a basis for natural selection at each step.

A scenario similar to that in Fig. 5 would also explain the evolution of the clotting factors in the intrinsic pathway. Again most of the components of the pathway belong to the serine protease family and thus could have arisen through gene duplication and subsequent modification as illustrated in Fig. 5. The only exception is Factor VIII which is closely related to Factor V (extrinsic pathway) and presumably arose through duplication of Factor VIII.

Conclusions.

1. Irreducible complexity does not always rule out evolution by natural selection. We’ve seen that the blood clotting system meets Behe’s definition of an irreducibly complex system and yet there is good evidence that it arose through evolution by natural selection.
2. Dembski’s design filter works through the process of elimination. It considers only two possible explanations for a contingent event, chance and design. If chance is eliminated then design is inferred because it is the only choice left. But, what we’ve seen is that natural selection is another viable alternative for the origin of at least some irreducibly complex biological systems. Natural selection gives the appearance of design without actually being design. The filter doesn’t provide a way of distinguishing between natural selection and design as the explanation for the origin of irreducibly complex biological systems.
3. At the beginning of this post, I said that there were two explanations for gaps in the chain of natural explanations of events in natural history. They could be places where God has intervened supernaturally or they could be places where the natural explanation has yet to be discovered. What I’ve shown in this post is that neither Dembski’s design filter nor Behe’s notion of irreducible complexity produces a convincing argument for the supernatural action of God in these gaps.
4. As a Christian I deeply believe that God is the Designer and Creator of life and the universe! But it is difficult to prove this using science alone. In a later blog post, I’m going to suggest a different approach to seeing God as the designer that combines God’s revelations in scripture and in nature (i.e. science).

Looking ahead: In my next post (March 19), we are going to look at the question: Does science in general and evolution in particular rule out God? On April 2 we will explore: Is  evolution compatible with belief in God as the Creator?

Questions for further reflection:

1. What is your view of the Intelligent Design argument? Is it more convincing than evolution by natural selection?
2. Should Intelligent Design be taught in public schools as an alternative to evolution by natural selection?
3. The Intelligent Design movement is neutral about who the designer is, but Christians would see God as the designer. Is it important to prove that God is the Creator through science alone?

Suggestions for further reading:

1. Intelligent Design: The Bridge Between Science and Theology,  William Dembski.  InterVarsity Press, 2002.
2. Darwin’s Black Box: The Biochemical Challenge to Evolution, Michael J. Behe. Free Press, 1998.
3. Finding Darwin’s God: A Scientist’s Search for Common Ground between God and Evolution, Kenneth R. Miller. Harper Collins, 2007.
4. Much of the work on Intelligent Design is being supported by the Discovery Institute in their Center for Science and Culture. There you can access more information about the design argument.
5. Added by the editor:  PDF  with the titles and links to the posts in Tom Ingebritsen‘s Christianity and Science series. Yes, this was created to meet the requests of readers and will be updated. Your interest in and encouragement of this series is much appreciated.

Note: Originally titled  Is Evolution True? The Case of Intelligent Design. Figure 4 Updated. Changes made on 3/14/2014 (5:04 pm).