For Further Reading
5
God and Evolution
Michael J. Behe
The earth is full of wonderful creatures with marvelous abilities. Huge whales swim the ocean’s depths; delicate butterflies flitter by on a summer’s day, sporting breathtaking colors. Majestic eagles soar through the skies, shy deer nibble foliage in the evening, bees dutifully gather nectar in the sunshine, fierce lions stalk their prey. And humans, in some ways the most dazzling of all creatures, build civilizations and cultures, accumulating wisdom through the ages, and reflecting on the world around them.
Even though humans are born into this world, it has struck very few of us as humdrum, as something to be taken for granted. Since antiquity poets and wise men have written paeans to the beauty and bounty of nature. The creatures that fill the earth have evoked a love of nature in many a breast. The apparent extraordinariness of the living world, the intuited contingency of nature, the felt knowledge that it didn’t have to be like this, led from the earliest times of humans inexorably to the question, where did it all come from?
In the Beginning
For most of written history, the overwhelming answer to that question has been that a preexisting intelligence somehow fashioned it. The beauty and functionality of nature needed an explanation; it did not arise from nothing. The orderliness behind nature and the craft behind nature’s creatures pointed strongly to a craftsman, a lawgiver, who could order something as vast as life. As the medieval philosopher Thomas Aquinas would say, by this we mean God.
There were a few naysayers among the ancients, who thought that the world and life had no intelligent cause. For example, the Greek Democritus speculated that perhaps matter sometimes, rarely, formed itself into heads, or arms, or other body parts, which quickly perished. But, he went on, if by chance matter arranged itself into a coherent animal or plant—one with all its parts in the right relationship to the whole—then that plant or animal might survive and prosper.
The ancients who first pondered these questions were at a distinct disadvantage to modern people in several respects. They knew very little about the animals they could see. In a sense, they didn’t know how they “worked.” For example, the great Roman physician Galen thought that blood was pumped out from the heart of an animal to feed and “irrigate” its tissues, sinking into the tissues as water from an irrigation ditch sinks into farmland. He had no conception of the circulation of the blood. Galen was held in such high regard that his ideas were taught for more than a thousand years after his death. Not until the Middle Ages did educated people escape from his mistaken notion and begin to learn the wonders of the workings of life.
In the early 1600s, in an extraordinary act of intellect that presaged the advent of modern science, an Englishman named William Harvey calculated that the great Galen must be wrong. Harvey reasoned that if each beat of the heart pumped two ounces of blood, and if there were 72 beats per minute, and 60 minutes in an hour, and 16 ounces in a pound, then in just one hour a normal man’s heart would have pumped 540 pounds of blood! Clearly that much blood could not be produced by the body in such a short time; Harvey deduced that the blood had to recirculate.
In the Middle
One major disadvantage that premodern people had to contend with was that, as we now know, many of the working parts of life are microscopic, invisible to the naked eye, simply too small to see. So when they tried to puzzle out how life worked, they did so with no knowledge of the nuts and bolts of life. That began to change in the 1600s, with the modern invention of the microscope by Anton van Leeuwenhoek. Even with the crude instruments that could be fashioned at the time, which used candles rather than bright electric lights to illuminate a specimen on a microscope stage, it was immediately apparent that life was much, much more complex than anyone had previously suspected.
Before the availability of the microscope, it was thought that insects had no internal organs. That’s not because the people of the age were stupid but simply because the naked eye could not see to the required resolution. With the aid of the microscope, however, internal organs were seen aplenty. And even the external parts of familiar insects were seen to have very much more detail than had been known.
The perceived simplicity of insects and small animals had led many to think that small forms of life could arise spontaneously. For example, farmers who saw mice among their stored grain reasonably concluded that the grain had given rise to the mice. Meat left out in the open soon had maggots squirming on it, so decaying meat was thought to spontaneously give rise to insects. When the much greater complexity of insects and small animals was uncovered by the microscope, however, these ideas faded: although it may be easy to believe that relatively featureless insects could pop into existence from decaying meat, the complex bodies revealed by microscopes clearly could not. The more complex and functional life was discovered to be, the less plausible was the notion that it arose spontaneously, without guidance.
As microscopists studied life in more and more detail, cells were seen for the first time in plants, but their significance was unrecognized. It was not until the early nineteenth century that Schleiden and Schwann proposed the “cell theory” of life: living organisms are composed of cells and their secretions; and to a certain extent a cell has a life of its own.
The nineteenth century, of course, was also the time of Charles Darwin, who was born in 1809 and died in 1882. It was an age of great intellectual ferment, not only in biology but in geology as well. Excavations in the earth to build canals and railroad tracks unearthed fossil evidence of creatures that no longer appeared on earth; they were extinct. What’s more, the creatures seemed in many cases to resemble modern animals, so that it seemed that the prehistoric creatures gave rise to the modern creatures over great spans of time.
Nonetheless, although much progress had been made since van Leeuwenhoek, Darwin’s day was still quite ignorant of the foundation of life. In fact, in the nineteenth century many scientists such as the German Ernst Haeckel thought that the cell, the foundation of life, was “a simple little lump of albuminous combination of carbon,”[1] pretty much a piece of microscopic Jell-O. And like people in the middle ages who thought mice and flies could arise spontaneously because they were perceived as simple, many scientists of the nineteenth century thought cells might arise spontaneously—because they were then thought to be simple. In fact, Haeckel and Thomas Huxley, another friend and admirer of Darwin, thought that under the microscope some sea mud dredged up by an English exploring ship resembled cells they had seen from living tissue. So they concluded that the sea bottom could spontaneously give rise to cells. From there it was a short imaginative leap to simple creatures arising from the cells, and more complex creatures arising from the simpler ones.
This is the intellectual milieu, then, in which Darwin developed his theory of evolution by random variation and natural selection. The cellular and molecular foundation of life was a black box—a system that did marvelous things but whose workings were substantially unknown. And since they were unknown, many scientists thought they were simple. Darwin therefore concentrated his theory on how animal and plant forms might change but had no choice but to neglect the question of what mechanisms really undergirded those changes.
Now
Since Darwin’s day, although many mysteries remain, science has advanced relentlessly in our understanding of how life works. The intuition of nineteenth-century scientists that the cell is a simple glob of protoplasm has turned out to be spectacularly wrong. Rather, modern science now realizes that the cell is akin to an automated, nanoscale factory, filled with literal machines of great complexity which perform the necessary chores of life. We have found out that, much as the work of a computer takes place in tiny circuits invisible to the eye, so does the work of the cell take place with nanomachinery that can’t be seen even with a microscope. And just as biology was stalled until the invention of the microscope, and then quickly advanced, a host of new techniques that were not available to earlier scientists have enabled modern science to advance in its understanding of life by leaps and bounds.
One technique called x-ray crystallography has advanced our modern understanding of life comparably to the microscope’s advancement of medieval understanding. With x-ray crystallography (and related techniques) an investigator can “see” (or at least mathematically reconstruct) the shape of single molecules of life. Before the first x-ray picture of one of the cell’s components (a protein called myoglobin), it was thought (again) that proteins—the workhorses of the cell—would turn out to be simple entities, perhaps little crystals that used magnetism or some simple force to do their jobs. The structure of myoglobin turned out to be anything but simple. Rather, its shape was as complex as the shape of any sophisticated machine, like, say, an air conditioner or fan. Other proteins whose shapes were discerned by crystallography were similarly shown to be complex, not simple. So the science of the 1950s and 1960s did away forever with the notion that life fundamentally is a simple phenomenon. Instead, we discovered that it’s complexity and elegance all the way down.
That should have been the end of Darwinism’s strong claim right there—to explain all of life as the product of random mutation and natural selection—but intellectual inertia and wishful thinking kept it going.
With a gathering head of steam, science marched on during the second half of the twentieth century. In the 1950s the elegant double-helical shape of DNA was discovered by James Watson and Francis Crick. Shortly thereafter the genetic code was deciphered, showing that DNA actually carried information in the form of a code to specify all the protein machinery that the cell contains. The discovery of the genetic code was the first instance where biologists found themselves unwittingly using the language of information and intelligence to describe life. After all, no chemist had found anything like a “code” in organic chemistry thus far. This was followed by discoveries that the information carried by the DNA code was “transcribed” into an intermediary language made up of RNA before it was “translated” into the language of protein.
In the late 1960s and early 1970s clever techniques were invented by several scientists to determine the exact sequence of “building blocks” (called nucleotides) in DNA. Initially just small pieces of longer DNA fragments had their sequences determined. But as techniques improved rapidly, we have reached the point where the entire genetic complement of hundreds of organisms is known exactly, including that of human, dog, chimp, fruit fly and many more. Our knowledge has allowed us to see at least some of the mysteries of DNA. It turns out that many genes are not contiguous pieces of DNA as was once thought. Rather, the genes occur in discrete pieces, interrupted by DNA fragments called introns that don’t code for protein. The exact reason for this arrangement is still disputed.
In more recent years parts of the genome that were thought to have no function (and derided with the epithet “junk DNA”) have been found to contain tiny regions that are transcribed into RNA but not translated into proteins. These have been dubbed micro-RNAs and are thought to regulate the activity of other parts of the genome, switching on and off other genes at the proper time and place. In the 1950s and early 1960s it was discovered that pieces of DNA that were near to genes could exert an effect on whether the genes were turned on or off. These are called regulatory elements, emphasizing the fact that DNA not only has to code for the proteins that make up the machinery of life; the construction program has to be regulated to an exquisite level of detail. In recent years, regulatory elements for genes have been discovered in sequences of DNA that are physically far removed from the genes they are supposed to regulate. The system has turned out to be so intricate that a writer for the journal Nature gushed that “the picture these studies paint is one of mind-boggling complexity.”[2]
Where Darwinism Stands Now
Darwin knew that his theory of gradual evolution by natural selection carried a heavy burden. “If it could be demonstrated,” he wrote, “that any complex organ existed which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down,” adding “but I can find out no such case.”[3] In this passage Darwin was emphasizing that evolution had to improve an organism slowly, in tiny steps, over long periods of time. He realized that if organisms improved rapidly, in large leaps, then it would look suspiciously as if something other than random variation and selection were driving the unfolding of life.
Yet, if we concentrate on the “complex organs” that fill the cell—the molecular machinery of life—then the prerequisite for his theory is destroyed. Almost none of the molecular machines discovered in the cell lend themselves easily to being built by a slow, gradual process of improvement. Rather, like the comparatively simple machines of our everyday lives—mousetraps, ballpoint pens, electric lights and so forth—the machines of the cell contain separate components needed for them to work. I have termed this property “irreducible complexity,” and it is a severe practical barrier to Darwinian explanations of life. The problem is that such systems don’t work as the modern systems we have discovered do until they are pretty much all put together. So natural selection has little to select, or is stuck selecting a property that has little or nothing to do with the final system.
In response to my argument, Darwinists have offered more speculative scenarios where random mutation might get around the problem of irreducible complexity. However, I find the scenarios quite unconvincing, and I think anyone with a modicum of skepticism will too.
So has the argument reached an impasse, with the majority of biologists content to imagine what has never been seen and the legions of skeptics mired in their skepticism? For a while it seemed that way, but new data has become available, showing with some precision the limits of Darwin’s theory. This new data has the power to settle the argument for anyone willing to consider it.
The Critical Role of Random Mutation
Darwin’s theory is not a simple one. It contains several different, independent ideas, some of which may be right, while others are wrong or are quite limited. The three most important ideas that are wrapped together under the name of “Darwin’s theory of evolution” are (1) random variation, or mutation, (2) natural selection, and (3) common descent.
The idea of common descent usually gets the most attention. It is the contention that modern day organisms are descended from creatures that lived in the distant past, and that therefore all living creatures share a common ancestor. So, for example, dogs and ducks share an ancestor that lived in the misty past. From that ancestor, the theory goes, different lines of organisms arose which led to the two quite different modern organisms. More contentiously, humans are postulated to share a common ancestor with other animals too; our most recent ancestor with other animals is thought to have given rise to us and to chimpanzees.
While that’s an interesting and publicly controversial contention about natural history, I take the position that, even if true (which I think it is) it is in a profound sense trivial. The reason I think common descent is trivial is because the bare fact of descent does not tell us what is driving this extraordinary process. It simply says that the ancestors lived in the past and gave rise to modern creatures. But the “how” of the process is missing.
Like common descent, I think Darwin’s idea of natural selection is interesting but not that surprising. After all, who would dispute the contention that on average creatures who are more fit than their siblings would stand a better chance of survival in nature?
While common descent and natural selection are interesting but unsurprising ideas, the role of random mutation is different. Every important scientific and philosophical claim of Darwin’s theory is packed into the too-neglected role of random mutation. In Darwin’s theory, random mutation is the fuel that allows natural selection to operate, giving rise to different creatures in the process of common descent. Random mutation supplies the raw material, the theory goes, that when winnowed by selection gives rise to all of the intricate, elegant, complex machinery of the cell, which in turn gives rise to the more visible features of life—flight in birds, the strength of tigers and so on—that we so admire.
Well, that has been the theory. However, as I wrote above, in Darwin’s day the underlying basis for the variation in creatures was unknown; the central role of DNA—even its structure—was unknown. In modern times we have unraveled those knotty problems, but it has still been a massive effort to track down which changes in which parts of DNA give rise to beneficial mutations.
It turns out that mutations in DNA can come in several “flavors.” Perhaps the simplest kind of mutation is called a substitution mutation, because one nucleotide in DNA is switched for another. A second kind of mutation is called a deletion which, as the name implies, results from a chunk of DNA being accidentally left out when the double helix is replicated. There are also mutations called insertions, gene duplications, transversions and others which I will not describe here.
Since organisms contain much DNA (even “simple” bacteria have millions of building block nucleotides; large animals and plants can have billions), until recently it was a very difficult, nearly impossible problem to track down the change in an organism’s DNA that gave it an advantage over its brother and sister organisms. Scientists could see that, for example, a bacterium could survive in the presence of an antibiotic where other bacteria died, but the difficulty of determining what change in the bacterium’s DNA conferred that ability was daunting. Similarly, some humans are resistant to malaria, but it was only comparatively recently that science determined the molecular changes in DNA that were responsible for this benefit. It turns out that, when the changes were finally tracked down, they told a rather different story than many Darwinists expected. Rather than mutations building up molecular machinery, improving an organism relentlessly, many mutations actually destroyed parts of a creature’s DNA, or rendered some of the molecular machinery it coded for ineffective. It turns out that mutations which break things can sometimes have a salutary effect.
Malaria and Random Mutation
To see the effect of random mutation on the human genome, how it can help and hurt, let’s look at what science has learned about the battle between humans and malaria over the past ten thousand years. Many people in the Western world forget, since malaria has been substantially eliminated here, but the disease remains a major cause of death and morbidity in the world. Each year a million people, mostly children under the age of five, die from the mosquito-borne disease. Hundreds of millions of people yearly are sickened by it. During the ten millennia in which the most lethal form of malaria has plagued humankind, a number of mutations have cropped up in the human genome which give their lucky bearers a measure of immunity to malaria. Since these human mutants can survive in malarious areas of the world where their unmutated relatives die, the mutation increases in the population when the resistant people have children.
The most well-known of such mutations is the sickle cell mutation, which is mentioned in almost every biology textbook that discusses evolution. In the sickle cell mutation one DNA nucleotide is changed from what it normally would be. This causes a single change in the protein hemoglobin, which the DNA gene codes for. The change is the replacement of one kind of amino acid (called glutamic acid), which enjoys being in water, with another kind of amino acid (called valine), which would much rather be shielded from water. Because of this single change in the hundreds of amino acids that comprise hemoglobin, under certain circumstances the hemoglobin aggregates to shield the valine and bury it away from water. While for technical reasons this behavior helps protect against malaria’s effects when a child has just one copy of the sickle gene from one parent (and a normal gene from the other parent), when a child inherits two copies of the mutated gene (one from each parent) the results are deadly. Two copies lead to sickle cell disease, which in underdeveloped areas of the world generally means death by the age of ten. So while the sickle mutation does help some people, it has a dark side, leading to the death of many others. Even more interesting, the sickle mutation is not a change in the body’s immune system, whose role it is to protect us from infection. The sickle mutation is a random change in another system that by happenstance did a bit of good.
Other mutations have been discovered in recent decades which give a measure of resistance to malaria. One class of mutations is called thalassemia. In this class an entire gene coding for a part of hemoglobin is either deleted or rendered less- or nonfunctional. Here random mutation breaks functioning genes, which again are not part of the immune system but which by serendipity help in the fight against malaria. The story is similar for a handful of other human genes whose mutation helps fight malaria. The breakage or diminution of certain genes coding for proteins (namely, glucose-6-phosphate dehydrogenase, Duffy factor, pyruvate kinase, Band 3 protein and more) aids the fight against malaria. So we see from our new knowledge of the mutations underlying malaria resistance in humans that the mutations are all reductive—that is, they reduce the number of functioning features coded for by the normal human genome.
Our knowledge of the evolutionary battle between humans and malaria has shown us, for the first time in history, that random mutation is incoherent; that is, it makes changes in any genes that help, no matter whether the changes add up to any “system” or not. Such incoherent changes are, to say the least, unlikely to be responsible for the profoundly coherent, integrated, complex systems that fill the cell. Rather, something that has the ability to look forward—to see what an integrated system should be like when it is completed—is required for cellular systems.
Our experience with malaria also shows us that random mutation much more easily breaks genes than makes them. Like a bull in a china shop, random changes of delicate structures are unlikely to help, and if they do help they are likely to be crude, quick fixes for an urgent problem.
E. Coli and Random Mutation
Is our experience with malaria backed up by experiments in other systems? Yes. I discuss several such systems in my recent book The Edge of Evolution: The Search for the Limits of Darwinism. Here I will discuss in a bit of detail just one other system, the common gut bacterium Eschericia coli. Almost all of the pertinent work that has been done on E. coli is from the laboratory of Richard Lenski of Michigan State University, who was recently honored with election to the National Academy of Sciences.
In the late 1980s Lenski began a long-term project to grow E. coli in his lab and watch how it evolved over time. The advantage of doing evolutionary experiments on bacteria is that they can be grown in enormous numbers and have very short generation times. Every day in his laboratory Lenski would grow six to seven generations of bacteria, in numbers approaching ten trillion. Over the decades his experiment has been in progress there have now been a total of over forty thousand generations of bacteria with a cumulative population size of one hundred trillion. The very large numbers of bacteria and many generations allow solid answers to many evolutionary questions.
Almost from the beginning of his experiment Lenski saw that the bacteria became better and better adapted to their environment, as beneficial mutations apparently accumulated. However, as discussed above, in the early days it was quite difficult to track down which mutations were responsible for the benefits. But over the past decade, as the result of laborious efforts, Lenski and colleagues have identified the mutations which have the greatest beneficial effects. The overarching pattern of the results is surprisingly similar to that seen in the human response to malaria—completely different organisms.
The first mutations to help were the breaking of genes. The bacteria rapidly lost the ability to make the sugar ribose (a component of RNA); for some reason that helped the mutant bacteria compete against non-mutants. A handful of other genes involved in metabolism were also deleted. Some bacteria had their ability to repair DNA badly damaged. Most bacteria lost the ability to metabolize the sugar maltose.
The mutations were incoherent, scattered in different genes, with no recognizable theme among them. They were not in the process of building any new system in the cell. They simply took advantage of opportunities that helped them grow faster in their current milieu. This is what random mutation does, even when it “helps.”
The Design of the Universe and Life
For most of written history, the overwhelming answer to the question of how life got here has been that a preexisting intelligence, God, somehow fashioned it. Yet for most of history humanity could see only the beauty and elegance of the external features of life. As science has advanced we now see that the hidden foundation of life is even more ingenious than its visible features. For a while, in our ignorance, we thought that chance might explain the overwhelming appearance of design in life, if it were filtered by natural selection. Now, after the hard work of many scientists, there is no longer any reason to think that. The complex and elegant molecular machinery of the cell strongly proclaims its design, and the incoherent breaking of genes by random mutation shows the pitiful limits of the ability of unguided processes to fashion life.
Our discovery of the design of life coincides with great progress in understanding the design of the universe as a whole. In the nineteenth century, not only was the cell thought to be relatively simple, so was the universe at large. It seemed to be eternal and largely unchanging, obeying a few simple rules. Now, through the work of many physicists and astronomers, we know the universe is balanced on a knife edge to allow for life. And not just the universe, but our solar system, our moon and our world are fashioned for life in ways that scientists of earlier centuries never recognized. With the help of science we reaffirm and extend the wisdom of antiquity in its affirmation of the purposeful design of life.
For Further Reading
Behe, Michael J. Darwin’s Black Box: The Biochemical Challenge to Evolution. New York: Free Press, 1996.
———. The Edge of Evolution: The Search for the Limits of Evolution. New York: Free Press, 2007.
Denton, Michael J. Nature’s Destiny: How the Laws of Biology Reveal Purpose in the Universe. New York: Free Press, 1998.
Gonzalez, Guillermo, and Jay Richards. The Privileged Planet: How Our Place in the Cosmos Is Designed for Discovery. Washington, D.C.: Regnery, 2004.
Witt, Jonathan, and Benjamin Wiker. A Meaningful World: How the Arts and Sciences Reveal the Genius of Nature. Downers Grove, Ill.: InterVarsity Press, 2006.