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Review: The Edge of Evolution

Reports of the National Center for Science Education
Volume: 
27
Year: 
2007
Issue: 
1–2
Date: 
January–April
Page(s): 
38–40
Reviewer: 
David E Levin
This version might differ slightly from the print publication.
Work under Review
Title: 
The Edge of Evolution
Author(s): 
Michael J Behe
New York: Free Press, 2007. 320 pages
The same mistakes in the same [pseudo]gene in the same positions of both human and chimp DNA. If a common ancestor first sustained the mutational mistakes and subsequently gave rise to those two modern species, that would very readily account for why both species have them now. It’s hard to imagine how there could be stronger evidence for common ancestry of chimps and humans.
One could be forgiven for assuming this to be a quote from a prominent evolutionary biologist. Rather, they are the words of "intelligent design" (ID) advocate Michael J Behe in his new book The Edge of Evolution: The Search for the Limits of Darwinism (p 71–2). Oddly enough, Behe regards the notion of common ancestry as "trivial" - a characterization that will ruffle more than a few feathers among his creationist followers. The real issue, he argues, is the role of the designer in the evolutionary process.

This embrace of evolution is a divergence from Behe’s 1996 book, Darwin’s Black Box (New York: Free Press), in which he presented a molecular-age version of the argument from design, most eloquently championed by 18th-century theologian William Paley, which states that conscious design can be inferred from the complexity of living things. Behe, a biochemist at Lehigh University, recast this theological argument in terms of the molecular complexity of living cells. In doing so, he brought to the ID movement a veneer of scientific respectability. Behe argued in Darwin’s Black Box that a biological structure or biochemical pathway that would fail to function if any one of its parts were removed could be thought of as "irreducibly complex". Such complexity, he asserted, could not possibly have evolved, as suggested by Darwin, through numerous stepwise improvements of a simpler system, because the structure or pathway would not function until fully assembled. "Irreducible complexity" of biological systems was denounced universally by the scientific community as an intellectually bankrupt notion because of the great plasticity of the evolutionary process. Components of a complex structure or pathway that are today essential to its function were not necessarily always essential. Components, when initially recruited, may have been merely helpful to the function of a simpler version. Evolution refines function of a complex system both by adding new components and by remodeling existing parts along the way. So it is illogical to look at the final product, with its many well-matched interacting components, and assert that, because removal of a part would destroy function, it must have been created as a complete unit.

Nevertheless, Darwin’s Black Box was well received by many creationists who believed naively that Behe had posed a serious scientific challenge to evolutionary theory. The book made him such a prominent figure within the ID movement that he served as an expert witness for the defense in the recent case against the Dover, Pennsylvania, school board, which made the fateful decision to incorporate ID into its high school science curriculum. In his landmark verdict for the plaintiffs, Judge John E Jones III ruled that "ID is a religious and not a scientific proposition" and that "it is unconstitutional to teach ID as an alternative to evolution in a public school science classroom."

What is perhaps most remarkable about The Edge of Evolution is how much Behe now concedes to the evidence that supports Darwinian evolution. He not only accepts that life has existed on earth for billions of years, but that it has evolved over time. He now agrees with the Darwinian notion that all life on the planet "descended with modification from one stage to another." He even acknowledges that natural selection is the obvious mechanism by which adaptive gene variants spread through a population. It is difficult to imagine his core audience being receptive to this revised position. But at this point, Behe is stuck between the need to establish a semblance of scientific credibility and the desire to forward his distinctly unscientific creationist ideas.

Behe’s new thesis is that there are limits to what Darwinian evolution can accomplish. Evolutionary theory holds that genetic variation within populations is caused by random changes in the DNA, called mutations, which arise each generation. It is this variation that natural selection uses to reshape a population one step at a time. However, Behe believes that random mutation, coupled with natural selection, is not a sufficiently powerful engine to drive the evolution of complex subcellular structures and molecular machines. Most of the really important mutations, he insists, must have been directed by an intelligent agent.

His case for a designer who engineers mutations rests in this book on two arguments drawn largely from the evolutionary battle between humans and the single-celled parasite that causes malaria. To understand these arguments, it is necessary to know something about the interaction between the two species. The parasite lives within the red blood cells of infected people and uses hemoglobin, the protein that carries oxygen to our tissues, as its food source. A variety of human mutations that affect red blood cells have spread through malarious regions of the world because they confer some degree of resistance to infection by the often-lethal parasite, one of the species of Plasmodium. The best known of these is the sickle-cell mutation, which arose within a hemoglobin-encoding gene of an individual in Africa. The sickle hemoglobin mutation, when present in only one copy, prevents the parasite from establishing an infection. But when both copies of the hemoglobin gene carry the sickle mutation, the result is the devastating disorder known as sickle cell disease.

Behe first argues that sickle hemoglobin, as well as most of the other genetic alterations that have arisen in humans in the battle against malaria, are fundamentally destructive mutations. That is, they typically break or damage existing genes, rather than construct some new, protective system. By contrast, the author is most interested in how complex molecular machines came into existence. He insists that because humans have not evolved any complex structures to combat malaria, random mutation is not capable of such constructive adaptation. But evolutionary theory does not predict how a population will adapt to a selective pressure - only that it will, or that failure to do so will result in extinction. That we have not evolved complex defenses against malaria is no argument that it cannot happen, or that such complexity has not evolved through natural mechanisms in response to other selective pressures across vast geologic time spans.

The author’s second argument is one of large numbers. He correctly asserts that in cases where at least two mutations are required before any benefit arises, evolution is impaired. This is because, in the absence of an adaptive advantage conferred by the first mutation, natural selection cannot work to spread it through the population. In such a case, for evolution to proceed, both mutations would have to arise simultaneously - an exceedingly rare event. The example he provides is the evolution of drug resistance in malaria. Resistance to chloroquine, a widely used antimalarial drug, has evolved independently only a handful of times around the world because, according to Behe, resistance requires two specific mutations in the parasite’s protein, which have to arise together to confer any adaptive advantage. The parasite, he argues, has been able to solve this problem only because of the vast numbers of these organisms and their short generation time. In animal populations, such as vertebrates, with many fewer numbers and much longer generation times, an adaptive change that requires at least two simultaneous mutations would be so improbable as to be evolutionarily insignificant. Here, he claims to have found the "edge of evolution," jumping to the conclusion that "No mutation that is of the same complexity as chloroquine resistance in malaria arose by Darwinian evolution in the line leading to humans in the past ten million years" (p 61, emphasis in original) Throughout the remainder of the book, Behe uses the evolution of chloroquine resistance as a theoretical boundary beyond which random mutation coupled with natural selection cannot extend.

Behe’s thesis of evolutionary limits hangs on the assumption that important evolutionary steps require multiple simultaneous mutations without the benefit of cumulative selection. However, there is no evidence to support this claim. His error is evident even in his example of chloroquine resistance, which, by his logic, should not have involved evolutionary intermediates. But the scientific data say otherwise. The existence of natural isolates of malarial strains that possess one or the other of the supposedly critical mutations suggests not only that evolution of chloroquine resistance is a stepwise process, as has been argued by others, but that there are multiple mutational paths to resistance.

He applies the same unfounded assumption to assert that the evolution of new protein-to-protein interactions, a critical step in the assembly of complex cellular machines, is not possible without the assistance of a designer. His reasoning is that five or six simultaneous mutations would be required to generate a new interaction site, and the likelihood of a protein’s acquiring so many random mutations at once is vanishingly small. This number is based on the requirements for tight associations that antibodies form with their targets - interactions that involve five or six protein parts called amino acids. However, Behe ignores volumes of experimental evidence that many classes of proteins can interact with other proteins through the recognition of fewer than five amino acids. For example, enzymes that add sugars to other proteins (often important to their function) typically recognize as few as two amino acids. Although such enzymes normally interact only transiently with their target proteins, weak interactions can evolve gradually into stable associations through the sequential accumulation of mutations if the association confers an adaptive advantage. Behe’s logical error here is identical to the one he committed in asserting that many biochemical pathways are irreducibly complex. He looks at the final product, incorrectly assumes that each part always existed as it does today, and cannot imagine how stepwise evolution could have generated such an integrated system.

Behe is likely aware of at least some of the existing evidence that new protein-to-protein interactions have evolved. One must look no further than one of his acknowledged examples of evolutionary prowess. Under the heading of "What Darwinism Can Do," he describes the stepwise evolution of an antifreeze protein from a digestive enzyme in Antarctic fish. This was an important evolutionary adaptation that allowed fish that possess this protein to survive in frigid Antarctic waters. However, he omits an interesting detail from his description - the antifreeze protein has sugars added to it (by an enzyme), whereas the protein from which it evolved does not. Therefore, a new protein-to-protein interaction must also have evolved to allow modification of the antifreeze protein. In fact, this beautiful example of evolution involves the construction of significant complexity.

The author next uses his unsupported claim that groups of simultaneous mutations are required for the evolution of complex cellular structures in a weakly argued attempt to define a demarcation between intelligently designed features and those that arise through Darwinian evolution. Behe allows that random mutation and selection are capable of driving the evolution of closely related species and perhaps even account for the divergence between humans and chimpanzees. But he asserts that design extends from the early construction of cellular machinery all the way into the animal kingdom at least through the separation of vertebrate classes - mammals, birds, reptiles, amphibians, and fish. This is because these classes possess unique cell types, the appearance of which he assumes to be beyond the "edge of evolution." With only his flawed logic to support his claims, Behe’s perceived "edge" reflects nothing more than the limits of his own conceptual horizon.

The final chapter is devoted to a philosophical discussion of the designer’s identity and motivations. Although Behe describes himself as a "pretty conventional Roman Catholic," he dissembles here in quoting philosopher Nick Bostrom, "The ‘agent’ doing the designing need not be a theistic God." Considering Behe’s testimonial concession at the Dover trial that "the plausibility of the argument for ID depends upon the extent to which one believes in the existence of God," this position seems disingenuous and intended to distance his ideas from their religious foundations. As for the goal of the designer, Behe claims that it was none other than the emergence of intelligent life. Here, he makes the classic creationist error of assuming the primacy of humans among all living things, a distinctly religious notion. Behe offers no evidence or arguments to support this presumed goal, yet remarkably clings to his insistence that ID is a scientific proposition.

In the end, the most irritating aspect of this book is Behe’s selective use of the ever-expanding base of scientific knowledge as a soapbox from which to shout his embrace of perpetual ignorance. The better our understanding of the intricate details of complex biological systems, the stronger is his belief that they must have been designed and that science will never unravel how they came to be. This is a trend for him. As Eric Rothschild, chief counsel for the plaintiffs at the Dover trial, observed of Behe’s claim that the immune system is irreducibly complex, "Thankfully, there are scientists who do search for answers to the question of the origin of the immune system … Their efforts help us combat and cure serious medical conditions. By contrast, Professor Behe and the entire "intelligent design" movement are doing nothing to advance scientific or medical knowledge and are telling future generations of scientists, don’t bother." Scientists have never listened to him. But with so many concessions to evolution mixed with his new message of God-as-mutagen, will anyone?

About the Author(s): 
David E Levin
Department of Biochemistry and Molecular Biology
The Johns Hopkins Bloomberg School of Public Health
Baltimore MD 21205
dlevin@jhsph.edu

David E Levin is Professor of Biochemistry and Molecular Biology at the Johns Hopkins Bloomberg School of Public Health.