A Review of Immunological Principles in Michael Behe’s Darwin’s Black Box
by Parijata Mackey
“That the creationists have resorted to this subversion should surprise none of us, for the ethical poverty of their actions matches the intellectual poverty of their beliefs.”
-- Peter Atkins
American author and social reformer Upton Sinclair once said, “It is difficult to make a man understand something when his salary depends on his not understanding it.” Likewise, it is difficult for a man to follow evidence to its logical conclusion when the conclusion demands he abandon his primary source of earthly comfort: his faith. Throwing up a web of fancy words and pseudo-facts, man will do whatever he can, for as long as he can, to protect himself and his way of life. Believers of Intelligent Design will exalt any support that appears reputable and well-researched, even if logical flaws, false assumptions and gaping holes riddle its landscape. Although the fallacies in Michael Behe’s Darwin’s Black Box are vast and easy to spot, there are still many who hail his work as proof of the Bible itself.
In chapter six of his crusade, Behe attempts to use immunological arguments to support his attack on Darwinism. He launches a three-pronged attack on the unlikely evolution of three complex immunological systems: clonal selection, V(D)J recombination, and the complement cascade. Behe amasses his evidence, carefully building his argument that the human body is filled with biochemical processes that are irreducibly complex, and therefore impossible to evolve. He explains, “By irreducibly complex I mean a single system composed of several well-matched, interacting parts that contribute to the basic function, wherein the removal of any one of the parts causes the system to effectively stop functioning” (Behe 39). The only way such complicated systems could have arisen, Behe asserts, is through careful and Intelligent Design. Fortunately for
His supposedly professional biological analyses are filled with errors, omissions, and outright untruths. His careful misportrayal of the function of antibodies is as almost as convincing as it is inaccurate. He compares antibodies to toy darts, claiming them to serve only as markers for macrophages, which will then know what to destroy. He goes on to describe the complement system, and the complex set of genes that make up the adaptive immune system’s massive repertoire. Each is dependent on the other, Behe argues; the system is irreducibly complex. Spanning several pages, Behe elaborates on his notion that antibodies serve no purpose other than to mark something for death, and can harm nothing on their own. The most amazing thing about this statement is, it’s just plain wrong.
Hemolin is a protein found in moths, almost identical in sequence to antibodies found in higher vertebrates. It binds, generically, to bacteria, causing it to lyse or precipitate out of the hemolymph (Beck 63). Furthermore, antibodies often serve as catalysts in biochemical reactions.
It is also the role of antibodies to neutralize toxins; by binding to the active site of a molecule of poison, the antibody can effectively deactivate it and render it harmless. This is the principle that allows the DPT vaccine to work; the vaccine stimulates the production of the antibodies that can neutralize the relevant toxins (Robison 8). Moreover, antibodies are capable of binding to and disabling viruses, by wedging themselves into the virus’s molecular “hinge” which allows it to infect a cell (Robison 5). Lastly, antibodies are well-known to precipitate targeted bacterial or viral proteins out of solution; if enough antibodies bind to a structure, it will lose its structure, and by extension, its function.
Behe is also not being entirely truthful when he claims that we have no hypotheses on how the enormous repertoire of antibody diversity could have possibly evolved. The V(D)J-C (Variable, Diversity, Joining - Constant) gene schematic is the mechanism for antibody assembly in gnathostomes through primates. In humans, antibody genes are mixed and matched; a little bit of each kind (V, D, and J) DNA is needed to be complete. An antibody gene consists of one V-segment, one D-segment, one J-segment, and one C-segment, each of which are drawn from huge pools of DNA segments. A human antibody can be labeled as V3(D2)J7-C, or V21(D17)J34-C. But in sharks, the VDJ segments are already assembled; that is, the antibody genes are V5(D5)J5-C, or V21(D21)J21-C. The genes are prearranged in long strings of such assembled genes, called tandem arrays. Our understanding of tandem arrays and the genetic processes that can generate them is well-developed. From these tandem arrays, it is just a short step in evolutionary time to generate the arrangement found in man. Deletions, working in conjunction with secondary expansions caused by tandem duplication, can easily lead to the V(D)J system present in humans (Litman 73). And even if Behe were intelligent enough to argue that this arrangement is useless without the splicing machinery, the presence of a V(D)J system in sharks indisputably disproves Behe’s notion that antibody diversity requires splicing machinery in the first place.
There are many more fascinating clues to possible evolutionary origins to the adaptive immune system which are conveniently absent from Behe’s arguments. The intriguing similarities in molecular structure of antibodies to those involved in immune recognition, and especially those involved in cell-to-cell (non-immune) recognition. Why the resemblances? The recombination machinery which builds antibodies is, interestingly, active in vast regions of the brain; could antibodies have evolved from cell-to-cell recognition molecules? It certainly seems likely.
After reviewing Behe’s lack of immunological understanding, it is easy to conclude that his ideas about Intelligent Design are just as unsound. However, even if his biology was accurate, his central argument is hopelessly flawed, his logic doomed; even if his descriptions of the “irreducibly complex” systems were correct, even if there were no misleading omissions or subtle manipulation of the facts, his pretenses still, inevitably, collapse.
Remember that all of these cases are attempts by Behe to demonstrate the irreducible complexity of the immune system. He uses his favorite example, the mousetrap, to illustrate: a mousetrap has a clearly defined function (squashing mice), and is composed of several interacting parts (platform, spring, bait, metal bar for squashing, etc). Behe describes this system as irreducibly complex; if you remove any one of the interacting parts, the mousetrap will no longer be able to perform its function, and no mice will be squashed by that particular mousetrap.
This metaphor, Behe maintains, extends into the biochemical processes that keep us alive. Behe’s claim is that the adaptive immune system is so complex, with each antibody binding perfectly to its antigen, that there is no way it could have evolved. “There are billions of different kinds of antibodies… Could this system have evolved step-by-step? … In a simplified scheme, we are left with three critical ingredients: (1) the membrane-bound form of the antibody; (2) the messenger; and (3) the exported form of the antibody. If any of these parts is missing, the system fails to function” (Behe 124). As Behe rightly states, we gain nothing by replacing a problem with a miracle, so it is best to disregard statistically impossible explanations. In so doing, Behe rejects any possible Darwinian explanation for the evolution of such a complex system. This, however, is a fatal error: a solution does exist.
Ignoring the possible but highly unlikely chance that all genetic mechanisms to produce the immune system arose at the same time, or the idea that the parts of this “irreducibly complex” system evolved separately for other purposes and then joined together by accident to create adaptive vertebrate immunity, there is a very simple, and very Darwinian, explanation.
A system deemed irreducibly complex can be built step-wise, through the gradual addition of parts that are, initially advantageous, but become, because of later changes in the system or environment, essential for proper functioning. Imagine that gene X encodes a protein that performs a certain function. Somehow, gene Y is acquired through mutation, and is selected for because it coincidentally helps with the function of gene X. Gene Y is not, at first, crucial, it simply improves upon what already occurs. Eventually, whether through changes in the organism or environment, gene Y becomes an essential part of the function initially only performed by gene X. This compounds over time, and can easily, over billions of years, become “irreducibly complex.” This step-wise refutation of irreducible complexity originates in 1918, refined later in 1939, with the writings of H. J. Muller, giant in genetics, and winner of the 1946 Nobel Prize in medicine for his work on artificially-induced mutations and genes.
This is also one of the thrusts behind the Red Queen Theory of Evolution, named after Lewis Carroll’s character in Through the Looking Glass. In her world where the landscape was a treadmill, the Red Queen said, “It takes all the running you can do, to keep in the same place.” It suggests that a species may have to evolve quickly just to hold on to its particular niche, which would plausibly explain the emergence of “irreducibly complex” systems.
Behe depends upon his “irreducibly complex” argument to attack biochemical cascades, in particular the blood-clotting and the complement cascades. He states, “Because of the nature of a cascade, a new protein would immediately have to be regulated. From the beginning, a new step in the cascade would require both a proenzyme and also an activating enzyme to switch on the proenzyme at the correct time and place. Since each step necessarily requires several parts, not only is the entire blood-clotting system irreducibly complex, but so is each step in the pathway” (Behe 87). This statement is earlier contradicted by Behe himself, when he describes how the blood-clotting cascade is capable of starting on its own: “it seems there is always a trace of thrombin in the bloodstream. Blood clotting is therefore auto-catalytic, because proteins in the cascade accelerate the production of more of the same proteins” (Behe 83). (Interestingly enough, it is often the hypothesis of an auto-catalytic set that would bolster the idea of our primordial soup origins, as complex systems analysis grows as a field, we uncover more and more data illuminating the evolution of auto-catalytic biophysical systems (Waldrop 87).)
Behe’s skill at manipulation is not to be underestimated; his gentle, confident tone and tactically humble encouragement of the reader to double-check the facts are handy tools to maintain the illusion of his authority. Behe does not hold a degree in evolutionary biology; he is a biochemist by education and practice. Evolutionary biologists have openly questioned his knowledge of basic evolutionary concepts such as soft selection, Muller’s ratchet, or the Fundamental Theorem of Natural Selection (Orr 7). The problem with his reasoning is that it is an “argument from ignorance” (Robison 2); Behe is saying that because we don’t know how the “irreducibly complex” immune system evolved, it didn’t evolve. This painful, pseudo-logic has led Behe to arrive at a conclusion based on a lack of information.
Even if Behe had provided us with an interesting and valuable critique to evolution, which closer evaluation reveals is not the case, his reasoning falls apart when he tries to use arguments against evolution as support for intelligent design. This pathetic, unscientific logic is another of Behe’s mental traps; it is like trying to show how healthy Coca-Cola is, using evidence that Pepsi is unhealthy. This sort of negative argumentation is utterly useless without an alternative and testable hypothesis.
This trap, along with the deliberate omission of information about the function of antibodies, misleading metaphors, and unfounded assumptions, whether tactical or sincere, are quite suspicious when viewed alongside stunningly false statements, such as the one appearing on page 179: “There has never been a meeting, or a book, or a paper on details of the evolution of complex biochemical systems.” Ignoring papers such as the four published by a single lab5 in 1985, 1988, 1990, and 1994 on the evolution of the pentose phosphate pathway, and a 1993 paper on glycogen biosynthesis, which cite other analyses of Krebs cycle evolution, published in 1981, 1981, 1985, 1987, 1987, and 1992; there were two entire books published on the subject within three years of his writing. Behe also decides to ignore the paper published a month before Darwin’s Black Box, entitled, “The puzzle of the Krebs citric acid cycle: Assembling the pieces of chemically feasible reactions, and opportunism in the design of metabolic pathways during evolution” (Mendelez-Hevia 1996).
Behe’s brand of criticism consists of disregarding relevant facts, pretending that data does not exist, and claiming that the lack of the data he intentionally ignores proves his theory. Convinced of his own brilliance, Behe writes that the discovery of intelligent design is “So significant that it must be ranked as one of the greatest achievements in the history of science… rivaling those of Newton and Einstein, Lavoisier and Schrodinger, Pasteur, and Darwin.1” The rest of the scientific community can only shake their heads in amazement, wondering how an openly religious scientist, with a clear creationist agenda, and very untrained in evolutionary biology, can get such a fancy publication deal on a subject he clearly knows nothing about.
“Just don’t pull the knot tight before being certain that you have got hold of the right end.”
2. Litman, Gary. “Sharks and the Origins of Vertebrate Immunity.” Scientific American. November 1996; 60-66.
3. Beck, Gregory. Habicht, Gail. “Immunity and the Invertebrates.” Scientific American. November 1996; 67-71.
4. Melendez-Hevia, Waddell & Cascante. “The puzzle of the Krebs citric acid cycle: Assembling the pieces of chemically feasible reactions, and opportunism in the design of metabolic pathways during evolution.” Journal of Molecular Evolution, Sep 1996, 43: 293-303.
5. H. J. Muller, "Reversibility in Evolution Considered from the Standpoint of Genetics". Biological Reviews 14 (1939): 261–80.
6. Orr, Allen H. “
7. Robison, Keith. “
8. Waldrop, Mitchell. Complexity: The Emerging Science at the Edge of Order and Chaos.
Simon & Schuster. 1992.