The Edge of Evolution: The Search for the Limits of Darwinism

by Michael Behe
Reviewed date: 2007 Oct 30
276 pages
cover art

More than a decade ago, in 1996, Michael Behe published Darwin's Black Box. In it, Behe argued that Darwinian evolution is impossible: random mutation and natural selection cannot account for the intricate, irreducibly complex systems that make life possible. These systems--such as the way blood clots in mammals--are essential to life, and are made up of dozens--even hundreds--of parts. If even one part is missing, the system is useless and the creature dies. Behe argued that it is impossible for random mutations to build these irreducibly complex systems up piece by piece, step by step.

In 1996, Behe could offer no actual evidence for the impossibility of Darwinian evolution. All he offered was the idea of irreducible complexity. In the decade since Darwin's Black Box, studies of mutation rates have furnished Behe with real-world data to support his earlier conclusions. In a new book published earlier this year, The Edge of Evolution, Behe uses scientific data to reveal what Darwinism can and cannot accomplish.

Definition of terms
Behe begins The Edge of Evolution by defining some terms, which we shall do also. The word Darwinism encompasses three distinct ideas:

  • common descent
  • natural selection
  • random mutation

Common descent is the idea that all living creatures have similar features that were inherited from a common ancestor. For example, dolphins and whales are descended from a common ancestor, as are dogs and cats, and even elephants and mice. "Common descent is what most people think of when they hear the word 'evolution,'" says Behe. But common descent is not the full story.

Common descent tries to account only for the similarities between creatures. It merely says that certain shared features [e.g., complex cells with nuclei] were there from the beginning--the ancestor had them. But all by itself, it doesn't try to explain how either the features or the ancestor got there in the first place, or why the descendants differ.

This brings us to Darwin. Darwin's theory is that small random mutations, coupled with the mechanism of natural selection, can account for all the forms of life on earth. Natural selection means simply survival of the fittest: the creatures that have some natural advantage will produce more offspring, and thus pass on their natural advantages. Random mutations introduce small changes; natural selection weeds out the useless and harmful mutations; the beneficial mutations survive. Eventually, a lot of small changes add up to big changes--and thus life evolves into different forms and species.

So Darwinism means common descent, by means of random mutation and natural selection. If Darwinism is true, all three ideas must be true, and they must be sufficient to account for all the different forms of life on Earth. Behe considers the DNA evidence in support of common descent to be overwhelming, and he does not dispute its truth. Random mutation and natural selection have been studied, and they "can modify life in important ways." But not in ways sufficient to account for the origin of species. For proof, Behe turns to some real-world studies of mutation rates in the malaria parasite.

Throughout human history, malaria has remained a deadly killer. Even today, malaria kills approximately one million people each year. The epic battle between man and malaria offers us insight into evolution in action. We invent drugs which work for a time, and the malarial parasite develops immunities to the drugs. Curiously, malaria develops resistance to some kinds of drugs faster than to others. Some drugs are effective only a few years before malaria evolves a defense. Others, like chloroquine, are effective against malaria for many years until the inevitable resistant strains appeared. Inevitable resistance? Perhaps not. There is one mechanism against which malaria has evolved no resistance, even after thousands of years: sickle cell disease.

Sickle cell is a human genetic mutation that causes human hemoglobin to be subtly deformed. It is normally detrimental to one's health, so one would expect sickle cell to eventually die out. But it provides one great benefit: the malaria parasite cannot effectively infect the blood cells of a person with sickle hemoglobin. This mutation arose somewhere in Africa, thousands of years ago. In all those years, random mutation has not provided malaria with a defense against sickle cell. Why? Why can malaria develop resistance against drugs like chloroquine, but not against sickle hemoglobin?

Single and double mutations
The answer lies in DNA. Malaria develops resistance to most drugs by a single mutation. One copying error in the DNA results in a single, isolated point mutation. If the single mutation happens to give the malarial parasite an immunity to a drug, then the mutated parasite proliferates. But what if there is no single mutation that can confer resistance to the drug? What if resistance requires two simultaneous mutations, each of which is fatal on its own? Resistance to the drug would require the highly unlikely occurrence of just the right two mutations happening at the same time. In the case of chloroquine resistance, that's exactly what it takes: chloroquine-resistant malaria has two mutated gene nucleotides. That's why it took so long for chloroquine resistance to develop, compared to other drugs that required only a single point mutation to be rendered ineffective.

If chloroquine requires a double mutation, sickle hemoglobin might require three, four, or even more simultaneous mutations to result in a resistant organism. It's clear, from the experimental data, that such a mutation is wildly improbable. In fact, no mutation of such complexity has ever been discovered in any organism that science has studied. Sickle hemoglobin is an obstacle for malaria; an obstacle that random mutation cannot be expected to solve.

But what does this have to do with Darwinism? What can we learn from this data concerning malaria mutation rates? To answer that question, we must consider time.

Time has always figured prominently in Darwinian explanations. Although few changes can be noticed in our own age, Darwinists say, over vast stretches of geological time imperceptible modifications of life can add up to profound ones. It's no wonder that we don't see much coherent variation going on in the biology of our everyday world--evolutionary processes are so slow that a human lifetime is like a moment.
Time is actually not the chief factor in evolution--population numbers are. In calculating how quickly a beneficial mutation might appear, evolutionary biologists multiply the mutation rate times the population size.
[Emphasis mine]

Malaria and mammals
The population size of malaria is enormous. Each year, approximately 1020 malaria cells live and die. Humans have been studying malaria for over fifty years. By way of comparison, there have been more malaria cells in the past fifty years than the number all the mammals that have ever existed on the earth--going back hundreds of millions of years. Since the population sizes are equal, our fifty-year-study of malaria gives us a good idea of what kinds of random mutations should naturally appear in the entire evolutionary history of mammals. And judging by what we see in malaria, the answer is clear: random mutation is not sufficient to account for the development and proliferation of mammal species on earth.

Behe goes into some detail about precisely why the malaria evidence shows that random mutation is insufficient. All the beneficial malaria mutations are destructive mutations. They are actually destructive--in other words, all of the beneficial mutations work by breaking some natural process in the malaria microbe--a process that a drug (chloroquine, atovaquone, etc.) uses to kill the microbe. So yes, it's a beneficial mutation, but the microbe is not really gaining any new abilities. It's just losing a natural ability, but an ability that the drug was targeting. Behe compares it to burning bridge to protect a city from an invading army. Malaria has never developed any new systems, new abilities, or anything novel. Behe sums it up: "despite huge population numbers and intense selective pressure, ... malaria [microbes] yield ... minor, evolutionary responses. ... We have genetic studies over thousands upon thousands of generations, of trillions upon trillions of organisms, and little of biochemical significance to show for it." Malaria burns bridges, but builds nothing new.

If malaria has not produced even one novel mutation--one new ability, one new protein binding site--in the last fifty years, we must make the obvious conclusion. Based on population sizes, we cannot expect any changes of equal significance to have randomly occurred in the entire history of mammals. It is beyond the edge of evolution.

But mammals are here nonetheless. In vast numbers and myriad forms. Behe is not the only one to have noticed this problem. A whole new field of science called evolutionary development biology (evo-devo) has arisen to deal with the thorny issue that Darwinism simply doesn't explain how evolution happens. Evo-devo scientists seek answers to explain the mechanisms of Darwinism, but Behe points out that their efforts "do more to undermine Darwin than to save his theory." For, consciously or not, evo-devo scientists admit that Darwinism does not answer the "profound, fundamental evolutionary questions."

While evo-devo is looking for ways to explain the unexplainable, Behe says we should accept the evidence: random mutation cannot account for life on Earth. That raises the question: if not random mutation, then what? Behe explores a number of possible answers, but the best answer is that evolution is driven by nonrandom mutations. That's where an unnamed, unknown Intelligent Designer comes into play. The Designer arranges for those nonrandom mutations to occur. Behe, as a Catholic, believes God is that Designer. But the identify of the Designer is beyond the realm of science, and Behe admits as much.

Response to Behe
The critical response to Behe has been almost universally negative. Those who disagreed with Darwin's Black Box view The Edge of Evolution as a disingenuous retreat. Behe's concept of irreducible complexity was shot down, they say, and so he's regrouped with a new book that simply ignores the critics.

If the critics feel ignored or slighted, perhaps that explains their viciousness. Renowned atheist Richard Dawkins wrote a 1300 word review of The Edge of Evolution that maligns Behe's character, ridicules his ideas, calls his intelligence into question, and fails to address any of the central arguments in Behe's book. Good show, Dawkins. Jerry Coyne at Powell's books examines Behe's claims in more detail, but again fails to consider the import of Behe's core arguments. Coyne dismisses Behe's malaria evidence by saying "Evolutionary theory predicts only that parasites will adapt, not how they will adapt. ... That is all evolution can do." Perhaps Coyne does not realize what he is saying: that is indeed "all evolution can do." Minor, insignificant changes. Not sweeping changes involving intricate new biochemical systems.

Credit to Darwin
In contrast to how Behe's critics give him no credit, Behe is decent enough to give Darwin--whose theory he criticizes--a great deal of credit. If you're looking for a complete rejection of evolution and Darwin, you won't find it in The Edge of Evolution. Behe accepts common descent wholeheartedly. Yes, that means man and ape are cousins. He accepts that natural selection and random mutation can explain a great deal, and that modern science owes a debt to Darwin.

Charles Darwin deserves a lot of credit. Although it had been proposed before him, he championed the idea of common descent and gathered a lot of evidence to support it. Despite some puzzles, much evidence from sequencing projects and other work points very strongly to common ancestry. Darwin also proposed the concept of random variation/natural selection. Selection does explain a number of important details of life--including the development of sickle hemoglobin, drug and insecticide resistance, and cold tolerance in fish--where progress can come in tiny steps.

But, although Darwin hoped otherwise, random variation doesn't explain the most basic features of biology. It doesn't explain the elegant, sophisticated molecular machinery that undergirds life. To account for that--and to account for the root and thick branches of common descent--multiple coherent genetic mutations are needed. Now that we know what sorts of mutations can happen to DNA, and what random changes can produce, we can begin to do the math to find the edge of evolution with some precision.

What we'll discover is something quite basic, yet heresy to Darwinists: Most mutations that build the great structures of life must have been nonrandom.

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