Inside the Human Genome: A Case for Non-Intelligent Design.
The University of California, Irvine’s Distinguished Professor of Ecology and Evolutionary Biology, John C. Avise, is a very productive and highly respected scientist. His popular book, Inside the Human Genome, examines the content and structure of the human genome, but he moves beyond the bald facts about our genomes and tries to discern what they mean. The sequence of the human genome, according to Avise, provides strong evidence for the theory of evolution and even stronger evidence against the theory of intelligent design. More tellingly, Avise thinks that it tells us something profound about the problem of evil.
In the first chapter, Avise introduces the reader to a subject that he turns to repeatedly throughout the book: theodicy. Theodicy is the study of the problem of evil, or how an all-powerful, omniscient, loving God could have created a world that contains vast quantities of seemingly pointless pain, evil, and suffering. The inefficient design of the human genome, which is the subject of the following chapters, is responsible for a great deal of human suffering and presents a substantial challenge to some of the more commonly cited solutions for the problem of evil.
In chapter 2, Avise describes the relationship between many of the genes in the human genome and the biochemical pathways in our cells. These pathways allow cells to degrade food to make energy and then use that energy to make cellular components that grow, heal, or maintain the body. Biochemical pathways rely on proteins called enzymes that catalyze, or increase the rate of, each reaction. Without these enzymes, biochemical reactions would proceed far too slowly to contribute to the life of the cell. Because the replication of the genome is never perfect, mutations or changes in the sequence of our genes occur each time it is copied. Loss-of-function mutations in genes that encode enzymes deprive our cells of these reactions and lead to a host of different types of genetic diseases. Many of these genetic diseases cause rather painful deaths, and on page 42, Avise asks, “Why would an intelligent designer have crafted the innermost machinery of human life to be error prone?”
In chapter 3, Avise discusses the seemingly unnecessary layers of complexity in the human genome. Our genes are encoded by discontinuous sections of DNA and during gene expression (that is, when an RNA copy of the gene is synthesized), the protein-coding regions are clipped out and spliced together. This process generates more opportunities for inactivating mutations that cause genetic diseases. Also, the tortuously complex manner in which genes are regulated in the human genome provides further opportunities for the occurrence of mutations that wreck proper gene regulation and cause genetic diseases. Humans also show a type of genetic regulation called “genetic imprinting” whereby some genes are “expressed when inherited from one parent but not from the other” (90). This gives rise to mutations that cause one type of genetic disease if the mutation is inherited from the father and a completely different syndrome if inherited from the mother. Avise asserts that if a “higher intelligence directly instigated this error-prone genomic complexity, that agent was either highly fallible as a genetic engineer or largely unconcerned about people’s genetic health” (82). However, the real clincher is the power factory of our cells, structures called mitochondria, which contain their own bacterial-like genetic systems. Mutations in these genomes cause devastating genetic diseases. In Avise’s own words: “Why would a wise engineer have put any crucial genes in a caustic cytoplasmic environment where they are exposed routinely to high concentrations of mutagenic oxygen radicals? … Not only is the overall design of mtDNA suboptimal—it is downright ludicrous!” (104). Chapter 4 examines seemingly wasteful sequences that litter the human genome. These include repeated sequences, “pseudogenes,” and transposable elements. Repeated sequences cause problems with chromosome paring during cell division that give rise to chromosomal rearrangements that cause destructive genetic diseases. Pseudogenes are defective copies of genes that are no longer functional. Transposable elements, or stretches of DNA that can sometimes jump from one location in the genome to another, can insert into active genes and cause mutations. Transposable elements also include defective copies of viruses (approximately 8 percent of the human genome is littered with defective retroviruses). Avise asks why “an intelligent designer with human interests at heart would have engineered a genome grotesquely infested with parasitic elements” (129-130).
In the final chapter, Avise summarizes his findings: the overwhelming majority of the human genome consists of molecular gibberish, nucleic acid parasites and the ghosts of genes long past. While our genomes have co-opted some of these transposable elements, pseudogenes and repeated sequences for functional purposes, the vast majority of them simply occupy genomic space. The protein-coding portions of the human genome “have proved to be mere islands of DNA in the vastly larger river of intergenic spacer sequences” (136). This is, in Avise’s view, exactly opposite of what anyone would expect if the theory of Intelligent Design were true. These intrinsic imperfections, which are built into the very fabric of the human genome, demolish William Paley’s argument from design. Insentient forces are a better explanation for a messy, inefficient, error-prone entity like the human genome.
Avise believes these conclusions also have far-reaching religious implications. Evolution, you see, lets God “off the hook” for natural evil. He writes:
No longer need we agonize about why a Creator God is the world’s leading abortionist and mass murderer. No longer need we query a Creator God’s motives for debilitating countless innocents with horrific genetic conditions…. Instead we can put the blame squarely on the agency of insentient, natural evolutionary causation (157-158).
Thus Avise’s true inspiration for this book is that the theory of evolution solves not only the origin of the human genome, but also the problem of evil.
Inside the Human Genome is a very well written, powerfully argued, and beautifully crafted book that anyone with even a fleeting interest in the origin of the human genome should read. Nevertheless, I have two concerns with the book. First of all, the main subject of the book is theodicy; the human genome is merely a foil for discussing the problem of evil. However, Avise has read neither broadly nor deeply about theodicy. The bibliography lists none of the main Christian works on theodicy in the last century and no such ideas are even considered. Even classical works on theodicy receive only a brief and rather cursory mention. Thus, there are potential theological explanations for these observations that were simply not considered.
Secondly, when it comes to his critique of Intelligent Design, Avise has not criticized the strongest case his opponents present. To explain the structure of the human genome, Intelligent Design theorists have co-opted the work of particular molecular biologists like James Shapiro and Richard von Sternberg. These scientists have observed in a series of papers that many organisms like bacteria, puffer fish (Fugu) and the weed-like flowering plant Arabidopsis possess compact genomes.1 The existence of extra sequences in the human genome (and other genomes) begs the question why such sequences are there. According to Shapiro and von Sternberg, the maintenance of such large quantities of “junkDNA” suggests that these sequences are serving some other function that promotes the irretention within genomes. Shapiro and von Sternberg view junk DNA as signals that “format” the genome, much like formatting signals dictate the accessibility of data files in a computer program. Junk DNA integrates protein-coding regions into computationally accessible systems and subsystems that allow the cell to execute various complex cellular processes. The fact that many functions have been discovered for a variety of “junk DNA” sequences tends to provide some evidence for their view. For example, almost 25 percent of all transposable elements in the human genome contribute to “promoters,” which are the regions of genes that determine when they should be expressed. Also, many repeated sequences and transposable elements compose important chromosomal structural features like telomeres, which cap chromosome ends, centromeres, which allow the cell division machinery to grab hold of chromosomes and properly segregate them during cell division, and attachment sites, where DNA sticks to the nuclear matrix. While the perspective of Shapiro and von Sternberg does not represent the majority opinion within molecular genetics, it is an intriguing and potentially fecund idea that is testable. Had Avise addressed this viewpoint, which has been the subject of several discussions by Intelligent Design advocates on the Internet and is featured in Stephen Meyer’s book, The Signature of the Cell, he would have presented a much stronger case.
In conclusion, despite its shortcomings, this book does represent the attempts of a contemporary scientist to wrestle honestly with the meaning of modern scientific findings withintegrity. It deserves a wide reading.
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Footnotes
- James A. Shapiro, “Repetitive DNA, Genome System Architecture and Genome Reorganization,” Re-search in Microbiology 153 (2002): 447–453; Richard von Sternberg, “On the Roles of Repetitive DNA Ele-ments in the Context of a Unified Genomic Epigenetic System,” Annals of the New York Academy of Sciences981 (2002): 154-158; James A. Shapiro, “Retrotransposons and Regulatory Suites,” Bioessays 27 (2005): 122-125; James A. Shapiro and Richard von Sternberg, “Why Repetitive is Essential to Genome Function,”Biological Reviewsof the Cambridge Philosophical Society 80 (2005): 1-24; and Richard von Sternberg and JamesA. Shapiro, “How Repeated Retroelements Format Genome Function,” Cytogenetic and Genome Research110 (2005): 108–116.
