The Edge of Evolution by Michael Behe (2007)

edge-of-evolution-michael-behe Michael Behe’s Edge of Evolution is a decade-later (2007) follow-up to his 1996 book Darwin’s Black Box, which described the “irreducible complexity” of certain biological structures and argued that Darwinian evolution could not produce them. In this book, Behe looks at the limits of what natural selection and random mutation can do, trying to define what he calls “the edge” of evolution.

Behe makes a careful distinction between the theory of common ancestry, which he believes and shares some evidence for, and the mechanism of random mutations acted on by natural selection (or, “Darwinian evolution”), which he argues is nowhere near powerful enough to account for the diversity of the creatures that share a common ancestry. He critiques scientists who present evidence of common ancestry as evidence of the power of random mutation.

Arms Race or Trench Warfare?

Behe looks at the best-touted examples of what Darwinian evolution can accomplish through the natural selection of random mutations, focusing on human resistance to malaria and malarial resistance to antibiotics. He argues that these “beneficial” single- or double-point mutations are really destructive: malaria hijacks machinery in human red blood cells to do its dirty work, and human mutations essentially break that machinery, sacrificing it as a loss for a net gain of stopping the malaria. Similarly, antibiotics hijack machinery in malaria cells to do their work, and malarial resistance essentially breaks that machinery in a similar sacrifice.

Far from an “arms race” of creatures developing new and complex machinery, Behe says these examples are actually the destructive consequences of a “trench warfare” where each side sustains damage to their own structures to prevent the attacker from taking advantage of them – like “burning a bridge” to block an invading army.

The “beneficial” mutations in malaria have not created new protein bindings, developed any new structures, or come up with any way to counter sickle-cell resistance, cooler temperatures, or other limitations. This explains why malaria has overcome many antibiotics within a few years but has not bested sickle-cell in centuries. “Darwinian evolution can deal quickly and easily with some problems, but slowly if at all with others.”

Since malaria multiplies to a trillion cells in a human host, and the number of malarial cells that exist each year (10^20) is more than the number of mammals that have ever existed, Behe argues we can compare the limited performance of malaria in the last few decades to the total performance of mammals over a hundred million years.

He argues it is not reasonable to expect Darwinian evolution to come up with any benefit that requires more than two point mutations. Quoting Coyne and Orr, he says we have to consider not just what is theoretically possible but probable enough to be “biologically reasonable.”

Behe discusses the evolution of an anti-freeze protein in the notothenoid fish over a few million years, arguing that a possible step-by-step pathway to its development is simple and fundamentally different from developing more complex structures. It “underscores the limits of random mutation, rather than its potential.”

Rugged Fitness Landscape

Unlike an imaginary smooth hill that can be climbed, mutation by single mutation, he describes a “rugged fitness landscape” of mutation effects, with a chaotic mess of valleys and local maximums. He argues that evolution by random mutation is most likely to get stuck on local hills. “Random mutation and natural solution can’t solve the rugged landscape dilemma – they actually cause the dilemma.”

“The eminent geneticist Francois Jacob famously wrote that Darwinian evolution is a ‘tinkerer,’ not an engineer.”

Behe highlights recent biological discoveries to look not just at the final complex structures of living beings but at their marvelous ability to self-assemble their complex pieces. Proteins must have matching shapes and charges to bind together from a huge array of possible shape space, quoting biophysicist Sarah Woodson, “it is as though cars could be manufactured by merely tumbling their parts onto the factory floor.”

He discusses intraflagellar transport (IFT) and its role in cilia construction, how materials are gathered at the base of a cilium before construction, how a rotating filament cap guides flagellum pieces down a rod. Repressors and hox genes and pyramids of cascading circuit switches. Markers that identify different segments of a body for the other pieces to fill in the details.

Behe says the “likelihood of getting two new binding sites” requires “more cells than likely have existed on earth.” He looks at HIV, a virus with nine genes that has a much faster mutation rate than human or malaria cells. “Every possible single-point mutation occurs 10^4 [one thousand] times per day in an HIV-infected individual.” Every double-point mutation would occur in each person once each day. And yet HIV has produced no new protein bindings for the development of new machinery.

To the objection that we cannot extrapolate to billions of years from the performance of malaria or HIV in a short amount of time:

“Time is actually not the chief factor in evolution – population numbers are… Since for many kinds of organisms the mutation rate is pretty similar, the waiting time for the appearance of helpful mutations depends mostly on numbers of organisms… The numbers of malaria cells and HIV in just the past fifty years have probably greatly surpassed the number of mammals that have lived on the earth in the past several hundred million years… The fact that no new cellular protein-protein interactions were fashioned, that mutations were incoherent, that changes in only a few genes were able to help, and that those changes were only relatively (not absolutely) beneficial – all that gives us strong reason to expect the same for larger organisms over longer time.”

Thus Behe’s conclusion: “Most mutations that built the great structures of life must have been nonrandom.”

Natural genetic engineering

Behe briefly discusses other scientific theories of how “unintelligent forces may mimic intent,” such as James Shapiro’s “natural genetic engineering,” which focuses on how the cell contains “sophisticated tools” to manipulate its own genes, so “evolution doesn’t have to proceed in a Darwinian manner by tiny random changes.”

Behe says “in many ways Shapiro has a higher, more respectful view of the genome than Darwinists do… it’s like a computer that contains not only specific programs, but an entire operating system.” But since it doesn’t explain where those tools came from, “if anything, he is pointing the way to a possible mechanism for the unveiling of a designed process of common descent.”

On the other hand, “the fact that natural genetic engineering processes are indeed quite active… yet malaria and HIV have made no good use of them in 10^20 tries, strongly suggests they have very limited utility.”

Implications

Behe spends a few chapters of the latter half of the book exploring some of the implications of his ideas and their connections to areas from science to theology. Among other things, he makes some good philosophical rebuttals to multi-verse explanations for the fine-tuned universe.

On matters of public health: “Darwin counsels despair. A consistent Darwinist must think that random mutation will get around any antibiotic eventually – after all, look at all that magnificent molecular machinery it built.. But intelligent design says there’s always real hope. If we can find the right monkeywrench, just one degree more difficult to oppose than chloroquine, it could be a showstopper.”

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