Meet Michael Behe
Michael Behe is no stranger to controversy. The Lehigh University Professor of Biochemistry first burst onto the world stage with his 1998 book Darwin’s Black Box. In it, he recounted Darwin’s famous challenge in the Origin of Species:
“If it could be demonstrated that any complex organ existed which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down.”
Behe went on to show that such complex organs abound in nature. There are countless cellular systems which need multiple interacting parts to achieve their essential function. To demonstrate this, Behe used the example of a mousetrap. Take just one of its components away, and a mousetrap won’t trap mice. Though there are many mousetraps in nature, biochemical mousetraps are immeasurably more complex. Many of these systems are termed molecular machines by biochemists, a name that betrays their complexity. One famous example is the bacterial flagellum.
This flagellum closely resembles the ‘outboard motor’ of speedboats, able to propel adrenaline-junkie bacteria at breakneck microbial speeds, with rotations reaching up to 300 turns per second. Another irreducibly complex biochemical system is the blood clotting cascade, involving a series of clotting factors which interact with each other in a highly specific sequence. A perennial bane of a medical student’s life, the blood clotting cascade has enormous implications in the field of medicine. If you lack one of those factors, like the famous haemophiliacs in the royal families of Europe, you either bleed too much or clot too much. Either can be deadly.
Such systems of integrated complexity abound in biology. As Behe recounted, they can’t be produced by Darwinian evolution in a step-by-step manner, one mutation at a time. They require multiple coordinated mutations in the DNA. It’s not a matter of tinkering, it’s a matter of wholesale re-engineering.
But as the number of coordinated mutations needed increases, the likelihood of this being achieved by an undirected evolutionary process falls precipitously. As Behe and many of his colleagues have long argued, there just isn’t time for enough random mutations to occur. Even 4 billion years since the origin of the Earth won’t cut it, because the odds are that low. A bacterial flagellum and the blood clotting cascade are just two examples, but the problem is multiplied across countless biological systems in life’s prodigious history. Behe’s solution? The evolution of life was driven by an intelligent designer.
The obvious inference, not argued by Behe, but not missed by his outraged critics, is that Behe’s proposed ‘intelligent designer’ is that Intelligent Designer.
Since his 1998 book, Behe has focused on characterising exactly how much blind Darwinian processes can achieve. After all, bit-by-bit mutations are real. They do have an effect. They may only tinker around the edges, but where exactly is that edge? In his 2008 book, The Edge of Evolution, Behe analysed masses of data from the Malarial parasite and other disease-causing microbes. By quantifying mutation rates and population sizes, Behe said then that purposeful design was needed to explain the central architecture of life. Why? Because the genes underlying the fundamentals of biological structures required too many coordinated DNA changes to be explained by random mutation. While undirected Darwinian processes could explain some features, the best evidence indicated they could only explain life’s more peripheral features. At the time, Behe suspected that random processes could only explain very superficial aspects of life, but he awaited better data to make any conclusive statements.
That better data is now here.
In the last ten years or so, a whole slew of molecular evidence has been made available by tremendous advances in genome sequencing technology. With costs and sequencing times being driven down annually, the ease by which we can read genomes has skyrocketed. This means that biologists are now able to track down the molecular basis for differences between one species and another with relative ease. Behe uses this new data, undreamt of by Darwin when he was formulating his theory, to devastating effect.
First, Behe magnifies the resolution on his Edge of Evolution. Having already established that the core architecture of every biological organism needed design, he wanted to quantify more precisely how much change could be attributed to Darwinian processes, and how exactly that change was produced. By researching famous cases of Darwinian evolution, Behe hunted down their molecular basis. Were they produced by multiple coordinated mutations building new genes? Could it be that the new genetic evidence proves that random mutation can produce complex new biological structures?
The answer is no. As a general rule, Darwinian evolution doesn’t work by building genes. In fact, almost every case of Darwinian evolution relies on breaking genes. This is not precise re-engineering. This is arson.
Take for instance Darwin’s finches. These famous finches have been hailed as a landmark example of Darwinian evolution. Various finch species inhabit the Galapagos Islands. They have different sizes and varying beak shapes. Finches are widely reported to be an astounding example of Darwinian evolution, because the finch population changes rapidly in response to environmental conditions. In some years, only larger and tougher seeds are left out in the open for finches to feed upon. These seeds can only be fed upon by the big-beaked finches, leaving the smaller-beaked finches to die out. Within a matter of years, natural selection is thereby able to dramatically change the ratio of smaller vs. larger-beaked finches. When famine ends, softer seeds abound, and the smaller-beaked finches come back in vogue.
Here’s the thing — this famous example of Darwinian evolution relies on some underwhelming genetic changes. In one of the key genes tracked down to change one beak type into another, just two mutations are needed. And the kicker? Both of them are damaging. The DNA wasn’t reconstructed by Darwinian evolution. It was just broken.
This is a theme that repeats itself throughout Behe’s analysis. When looking into Cichlids, colourful fish that have diversified uniquely in Lake Victoria, he again finds damaging mutations are responsible for some of the key differences between species. To look at them, the fish are clearly variations on the same theme. As far as we can tell, their genetic differences are subtle, and may have even been present in ancestor genomes.
Triangulating this data with numerous other examples, from Hawaiian fruit flies to Caribbean lizards, Behe finds that famous examples of Darwinian evolution only take place below the level of family. Despite oodles of time, diversification seems to be restricted to the level of genus and species. These are the lowest two taxonomic ranks, meaning the differences that they represent are very peripheral. Design is needed to explain almost all core biology of an organism, and what Darwinian evolution can explain, it seems to do so by damaging genomes. To add insult to injury, these taxonomic ranks often bleed into each other, meaning that there’s even less here than meets the eye.
Moreover, though Behe does not mention it, the problem of Orphan Genes is slowly looming onto the evolutionary scene. By their most limited definition, these are genes that are unique to individual species, and are often estimated to comprise 10-20% of every species’ genes. Early evidence suggests that these Orphan Genes play a significant role in producing the distinct characteristics of individual species. While perhaps this research is still not yet fully matured, if factored into Behe’s logic, it would bring the edge of evolution all the way down past the genus level, and even past the species level. As Behe readily admits, defining the edge isn’t a precise art. The edge may be jagged, sometimes going up to family, and sometimes down to species.
Whatever the precise reality is, Behe sets forth clearly that undirected processes can only produce superficial biology. Organisms may Darwinianly Evolve away, but all their core biology will remain intact. While it may not have been intended as a summary of Darwinian evolution, the old adage is certainly true:
The more things change, the more they stay the same.
A Bug’s Life
Behe’s analysis doesn’t stop there. In fact, it’s only just getting started. Based on his findings so far, he questions the key extrapolation that underpins Darwinian Evolution.
It goes something like this: in the same way that we can see small-scale evolutionary change in finches and cichlids occurring relatively quickly, perhaps every form of life was produced by these small-scale gradual changes occurring over much longer time periods.
Thus according to the conventional Darwinian view, every major innovation since life’s (entirely unexplained) origin came from small-scale gradual changes in a precursor organism. This includes the jump from a prokaryotic to a eukaryotic cell, from Precambrian jellyfish to all the major animal body plans in the Cambrian Explosion, from chimp-like ancestors to Homo Sapiens’ dexterity, upright gait, expanded cranium, language, musicality, mathematical abilities etc…
Behe is rightly sceptical of such boisterous claims on Darwinism’s behalf, and he next turns his gaze to experimental evolution. These are experiments that look at evolution under controlled conditions. The most famous of these is Richard Lenski’s Long Term Evolution Experiment (LTEE). With ingenious techniques, Lenski has replicated E. Coli bacteria over 3 decades, which in E. Coli years is ~70,000 generations. The experiments have shown evolution in action like never before. In this perfect Darwinian, survival of the fittest scenario, only the strongest have survived. Bugs have seen fitness improvements of as much as 70%. Many strands have gotten much bigger. They’re mutating their genomes at rapid rates, and adapting to their dynamic environments before the experimenter’s eyes.
How are these bugs doing all this fine work?
By breaking down their genes. Overwhelmingly, effective mutations degraded genes. Weirdly, this is often to the organism’s favour, in the same way that a plane discharging all its cargo mid-flight would help it fly faster. Of course, the passengers might have a problem with that, but soon the plane can eject them too, and the pilot whizzes to his next destination unencumbered by those overweight humans and their three extra towels each.
With this, Behe demonstrates that both in the wild and in the lab, organisms tend to degrade their genes in order to better adapt to an environment. He bills this the ‘The First Rule of Adaptive Evolution’:
Break or blunt any functional gene whose loss would increase the number of a species’s offspring.
This isn’t an absolute rule — many mutations modify genetic elements, and a very small proportion produce genuinely new genetic innovations. For instance, one example in the LTEE was the evolution of Citrate metabolism on behalf of the E. Coli. They already had the genes to do this in the absence of oxygen, but a part of a bug’s genome was swapped around, meaning that citrate metabolism could happen in the fresh air. But this wasn’t so much the creation of a new gene, rather it was the shuffling of existing genes, and the genome in question was inundated with destructive mutations anyway. Moreover, these destructive mutations set in exponentially quicker than the rare constructive ones. So even if a constructive mutation occurs, it will be swamped by destructive mutations. Genes will be broken long before those rare constructive mutations swing around.
Behe shows that the loss of genetic material is the primary mechanism by which species adapt to their environment. It’s easy to degrade or outright destroy a gene’s function. Usually it just takes one or two random changes at any point along a DNA stretch. On the contrary, to re-engineer a gene function requires highly specific mutations in coordination with each other. In evolution, as in life, it’s easier to throw a spanner in the works than use that spanner to make something new. And in certain situations, that spanner in the works can give an organism an immediate fitness gain over its competitors. Like the longer or shorter beak of the finch, or E. Coli getting bigger, destructive mutations can often sometimes help rather than hinder.
Your Own Worst Enemy
This is all headline news, but it’s Behe’s next insight that elevates his thesis to being truly fatal for Neo-Darwinism. Observing that these destructive but useful mutations happen often, they are subject to positive selection. This means that organisms with these broken genes spread rapidly in a population. But this natural selection is blind. It doesn’t care about the evolutionary potential lost in those broken genes. The carnage is useful right here, right now — so survive they shall. But this short-sightedness means that evolutionary potential is habitually wasted by natural selection acting on degradative mutations. After all, a broken gene can’t and won’t evolve. Even if you get incredibly lucky and somehow reverse the mutations that broke it, it’s likely that more damaging mutations will come along and break it elsewhere.
This shouldn’t be surprising. Dawkins may have called natural selection the blind watchmaker but he’s much too generous. In the words of the Muslim spiritual leader and polymath Hazrat Mirza Tahir Ahmad, natural selection is not just blind, it’s also deaf and dumb. It doesn’t care about the future evolutionary potential of genes. It will burn a bridge just to warm itself up.
But a theory that breaks genes will never make those genes in the first place, and they certainly won’t make the irreducibly complex structures that typify life. Genetic devolution cannot explain biological evolution. Purposeful design is needed.
This is Behe’s thesis, and the consummation of three decades of painstaking research.
It has not been favourably received.
Reviewing the Reviews
As a medical doctor I’m familiar with biochemistry, genetics and the physiology of at least one well-regarded organism on the planet. So while I’m not exactly a layman, I’m certainly no specialist in molecular genetics. Thus it can be difficult to be certain of how strong Behe’s thesis really is. What if all the evidence is being misrepresented? What if there are swathes of data being omitted? It’s for that reason that I’m pleased to report that there has been a chorus of professional outrage from evolutionary biologists keen to rebuff Behe. Nothing has convinced me more that Behe is correct than reading and analysing the criticisms levelled against him.
So far there has been a review in Science Magazine, co-authored by no less a figure than Richard Lenski, whose Long-Term Evolutionary Experiment was discussed above; various blog posts by Lenski and his co-authors; a Jerry Coyne Washington Post article; and a professional response from Behe’s colleagues at Lehigh University. These have all been collected at the book’s website, along with all the requisite responses. The debate is lengthy, and needs to be individually explored, but here are some personal highlights:
- The Science review claiming Behe never responded to criticism in a book chapter; in reality, Behe literally wrote a chapter in the same book in response.
- One set of reviewers claiming Behe is misrepresenting data on Polar Bear genetics, when it turned out they were actually misrepresenting it.
- Jerry Coyne doing a great impression of someone who hasn’t read the book he’s supposed to be reviewing.
However the real highlight was Richard Lenski claiming that his LTEE was in fact not a good example of how evolution works in the real world. Why? Because the environment isn’t varied enough to simulate real life, which would generate more genetic innovation.
“The LTEE was designed (intelligently, in my opinion!) to be extremely simple in order to address some basic questions about the dynamics and repeatability of evolution, while minimizing complications. It was not intended to mimic the complexities of nature, nor was it meant to be a test-bed for the evolution of new functions.”
This is of course not true. This is classical Darwinian evolution, hence the massive fitness gains. This micro-evolution itself creates a dynamic environment to which other bacteria adapt, especially in earlier generations. Behe effectively dispatched with these criticisms here and here, but what’s more interesting is that Lenski didn’t seem to mind when Richard Dawkins practically made the LTEE the centrepiece of his book “The Greatest Show on Earth: The Evidence for Evolution” (2009).
As I recall, Lenski’s experiment was essentially the only evidence Dawkins could muster to show that Random Mutation & Natural Selection can account for life’s diversity. In Chapter 5, Dawkins explained Lenski’s work at length, before writing:
“Lenski’s research shows, in microcosm and in the lab, massively speeded up so that it happened before our very eyes, many of the essential components of evolution by natural selection: random mutation followed by non-random natural selection; adaptation to the same environment by separate routes independently; the way successive mutations build on their predecessors to produce evolutionary change; the way some genes rely, for their effects, on the presence of other genes. Yet it all happened in a tiny fraction of the time evolution normally takes.
There is a comic sequel to this triumphant tale of scientific endeavour. Creationists hate it. Not only does it show evolution in action; not only does it show new information entering genomes without the intervention of a designer, which is something they have all been told to deny is possible (‘told to’ because most of them don’t understand what ‘information’ means); not only does it demonstrate the power of natural selection to put together combinations of genes that, by the naïve calculations so beloved of creationists, should be tantamount to impossible; it also undermines their central dogma of ‘irreducible complexity’. So it is no wonder they are disconcerted by the Lenski research, and eager to find fault with it.”
We look forward to Lenski’s request to Dawkins for a retraction of these comments. After all — the overwhelmingly degradative mutations in the LTEE have very little to do with real-world evolution.
This review has tried to summarise Behe’s thesis, but of course it can do no real justice to the power of the book’s arguments in their long form. As a writer, Behe has a rare ability to neither overwhelm the reader with technicalities, nor slide into a pop-culture reference on every page. In terms of structure and pacing, the book’s first part is slightly slower than the subsequent parts, but this is perhaps needed to set the stage. The rest of the book moves along nicely, and the evidence is clearly presented. The book’s final chapter finds a lyrical Behe discussing the need to recognise the effect of purpose and mind in science:
“The reunion of science and purpose should come easily, because the chief problem that divided them—neo-Darwinian materialism—has dissipated. Neo-Darwinian materialism is false, because the assumptions of neo-Darwinism are largely false. Random mutation and natural selection cannot build a brain or even coherently modify one.”
And after 300 pages of evidence, one cannot help but agree.