GENEWATCH
 
REVIEWS: GENETICS AND 'INTELLIGENT DESIGN'
By Andrew D. Thibedeau
 

Inside the Human Genome: A Case for Non-Intelligent Design by John C. Avise. Oxford University Press, 240 pp., $19.95

Signature in the Cell: DNA and the Evidence for Intelligent Design by Stephen C. Meyers. HarperOne, 624 pp, $19.99 (paper)

At the bottom of both John C. Avise’s Inside the Human Genome and Stephen C. Meyers’s Signature in the Cell is the same, straightforward question: is the human genome evidence of design or evidence of evolution? Through his discussion of the “inherent design flaws” in human DNA, Avise finds proof of “nonsentient” evolution. Meyers reaches the opposite conclusion, finding confirmation of design in the genetic “information” he describes as encoded in our genes. Ultimately, Meyers is undone by the same factors that secure Avise’s success: logic and evidence.

The “signature” Meyers alludes to in his title is the “information” represented by the so-called genetic code: the four-letter “alphabet” and three-letter “words” that mediate the processing of DNA into functional proteins. Exemplifying the idiom of information theory ubiquitous in microbiology today, Meyers’s book is partially a protracted review of the basic tenets of modern genetics. The four nucleotide bases of DNA—adenine (A), guanine (G), cytosine (C), and thymine (T)—encode “information [and] function as alphabetic characters.” These “characters” combine in three-nucleotide combinations— or “words”—called codons. In turn, each codon specifies a particular nucleic acid. Gene expression is the mediation of the “instructions” represented in our DNA converted by a host of intercellular machinery to become proteins— the “chemical building blocks of life.”

To Meyers, this aspect of DNA—that it contains “functionally specified information”— is “profoundly mysterious.” “Apart from the molecules comprising the gene-expression system,” he argues, “sequences or structures exhibiting such specified complexity or specified information are not found anywhere in the natural—that is, the nonhuman—world.” Describing what he calls the “DNA enigma”—“ the mystery of the origin of the information needed to build the first living organism”—Meyers stakes his central claim: that an intelligent designer is required to explain the human genome. While his theory does not identify the intelligence responsible for the informational content of DNA, “it does affirm that the ultimate cause of life is personal . . . [meaning] a self-conscious, deliberative mind in possession of thoughts, will, and intentions.”

Although Meyers’s invocation of the “mysteries” at the core of his argument foreshadows the theological nature of his claim, he nevertheless defends intelligent design as a legitimate scientific hypothesis, amenable to legitimate scientific scrutiny. “Logically,” Meyers posits, “one can infer the past existence of a cause from its effect, when the cause is known to be necessary to produce the effect in question.” “[U]niform experience,” he reasons, “affirms that specified information—whether inscribed in hieroglyphics, written in a book, encoded in a radio signal, or produced in a simulation experiment—always arises from an intelligent source, from a mind and not a strictly material process.” Thus the “strictly material process” of evolution is inadequate to answer the “DNA enigma.” Rather, Meyers infers the necessary existence of a designing mind to explain the ultimate source of genetic “information.” Despite over six hundred pages of eloquent prose, Meyers’s argument ultimately fails for at least two principal reasons. First, his logic is flawed. Second, he confuses the metaphoric for the literal in his analysis of so-called genetic “information.” His reasoning, though formally valid, truncates at an arbitrary point in a chain of necessary inferences. Put syllogistically, his argument is essentially as follows:

- Intelligence is necessary to the occurrence of “information.” - DNA carries “information.” - Therefore, intelligence is the necessary antecedent to DNA.

The problem with this argument is that it stops here, when its underlying logic compels that it continue. By definition, any intelligence capable of creating the “information” in DNA must itself possess at least the same amount of information. Because, as Meyers claims, intelligence is a necessary antecedent of “information,” it follows that another intelligent designer must have designed the intelligent designer. Each step back in the inferential chain necessitates yet a further step ad infinitum. Meyers meekly confronts this issue by appealing to the claim that “[i]n every worldview or metaphysical system of thought something stands as the ultimate or prime reality, the thing from which everything else comes.” Thus Meyers gladly relies on causation when it suits his argument, then denies its logical force when he finds its demands less palatable. Moreover, even if we grant his latter claim that there can be an unmoved mover, this admission vitiates his argument relying on the causal connection between intelligence and “information.” On this point, Meyers refutes himself.

Secondly, Meyers’s use of the concept of “information” to describe the workings of molecular biology—though the near-universal idiom of that field—is problematic because it conflates the metaphoric with the literal meaning of the term. While it serves certain explanatory and pedagogical aims to speak as if DNA were “written” in a “language,” these are merely metaphors for what are fundamentally causal, bimolecular relationships. To say that DNA carries information about proteins is like saying that smoke carries information about fire. While this may be true in a very weak sense, it would be absurd to claim that fire transmits information about itself via smoke. Because there is no true “information” in DNA—merely a set of biochemical affinities and molecular mechanisms—Meyers’s argument falters yet again. Thus, only by way of a fundamental misunderstanding of the human genome can Meyers conclude that DNA offers evidence of intelligent design.

In Inside the Human Genome, John C. Avise offers a different perspective on the (non)workings of human DNA. Observing that “most [genetic] mutations range from neutral to highly deleterious for human health . . . leav[ing] in their wake countless shattered bodies and destroyed lives,” he suggests that “[t]hese are probably not the kinds of biological outcomes that one would wish to attribute to the direct hand of an all-powerful and loving God.” Genetic malfunctions, and their consequent diseases, are legion—ranging from the mild to the gruesome. Trimethylaminuria, for example, is an incurable genetic disorder that inhibits proper metabolism of trimethylamine (a by-product of digestion). While it carries no serious health effects, trimethylaminuria’s one notable symptom is that it can cause those afflicted to smell like rotten fish. Another, more horrific example is Lesch-Nyhan syndrome. Resulting from the mutational substitution of a single nucleotide among some three billion, Lesch-Nyhan syndrome causes severe neurological dysfunction as well as compulsive vomiting and selfmutilation. Affecting mostly children, it is not uncommon for the afflicted to chew off their lips and their fingers.

At the end of the day, the strength of Avise’s argument is its focus on evolution’s ability to explain phenomena— namely, systematic flaws in the human genome—that the theory of intelligent design cannot answer. For example, one curious inhabitant of the intracellular world is the mitochondrion. Known as “powerhouses” of the cell, these organelles oxidize hydrogen to produce adenosine triphosphate (ATP), “a cell’s biochemical equivalent of electrical power.” Unique among their cytoplasmic fellows, mitochondria house their own DNA (mtDNA), comprised of 16,596 nucleotide base-pairs that encode thirty seven genes. Curiously, these 37 genes translate to only a portion of the proteins necessary for proper mitochondrial functioning. The remaining critical proteins are encoded in the cell’s nuclear DNA. In other words, mtDNA “is just a tiny snippet of DNA that by itself would be absolutely helpless, to itself and to the organism in which it is housed.”

Like nuclear DNA, mtDNA is also subject to mutations that compromise molecular operation. What’s more, in quintessentially baroque fashion, nuclear DNA and mtDNA are incompatible in such a way as to require a parallel system of gene transcription for each. The complexity of this strange arrangement opens the door to numerous opportunities for genetic error. Abundant metabolic disorders derive from faulty nuclear-mitochondrial interaction. In fact, “[a]n emerging paradigm is that many of the degenerative diseases of aging have their etiologies in mitochondria, either as deleterious mutations in the populations of mtDNA molecules themselves or as operational flaws in nuclear-mitochondrial interaction.”

“The serious health problems that arise from mitochondrial mutations,” Avise argues, “immediately challenge any claim for omnipotent perfection in mitochondrial design.” The energy-producing function of mitochondria is essential to cellular metabolism. “[W]hy in the world,” Avise rhetorically asks, “would an intelligent designer have entrusted so much of the production process to a mitochondrion, given the outrageous molecular features this organelle possesses?” Why would a wise creator engineer mtDNA and mtDNA expression in a manner so fundamentally different from that of their nuclear counterparts? This arrangement simply “make[s] no (theo)logical sense.”

In contrast to intelligent design’s inability to explain this mtDNA enigma, the endosymbiotic theory of mitochondrial evolution offers a straightforward explanation of mitochondrial origin and function. This evolutionary hypothesis posits that some two billion year ago, proto-mitochondria—ancestral analogs to bacteria—somehow took up residence in primitive eukaryotic cells. At first, the proto-mitochondrial genome carried all the genes needed for its own survival. As time passed and the symbiotic relationship drew closer, however, the majority of these genes were shifted to the host genome. Thus the divergent molecular processes required to transcribe mtDNA and cellular DNA reflects mitochondria’s extracellular origin.

The enigma of mtDNA offers a clear example of Avise’s central thesis. “From scientific evidence gathered during the last century, and especially within recent decades,” he explains, “we now understand that the human genome and the metabolic processes it underwrites are riddled with structural and operational deficiencies.” “These defects register not only as deleterious mutational departures from some hypothetical genomic ideal,” Avise observes, “but also as universal architectural flaws in the standard genomes themselves.” Intelligent design cannot explain these features of the human genome. Indeed, these “universal architectural flaws” offer strong evidence against the possibility of intelligent design. Moreover, what intelligent design theory is incapable of illuminating, evolutionary processes neatly explain. In Avise’s words: “[e]xactly how a Fall from Grace in the Garden of Eden might have become translated into these molecular defects is mechanistically unclear.” “By contrast,” he concludes, “how such genomic flaws arise and persist poses no insuperable mystery from the scientific perspective of evolutionary genetics.”

Ultimately, Avise’s slim tome carries far more weight than Meyers’s opus. Both authors set out to make a scientific case in support of their argument. Avise succeeds in his task by pointing to the powerful explanatory force of evolution— its ability to make sense of the otherwise baffling, haphazard nature of the human genome. Granting Meyers the benefit of the doubt, his arguments fall prey to fatal logical flaws and a deeply confused concept of “information” and the role it plays in genetics. In the end, intelligent design cannot meet the rigorous demands of scientific proof, whereas evolution is again affirmed as the predominant illuminating force in molecular biology.

Andrew Thibodeau is a fellow of the Council for Responsible Genetics.

 
 
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