In the past six months, I have encountered a review, by Thomas Nagel in The New York Review of Books (2012), of Alvin Plantinga’s latest book (Where the Conflict Really Lies: Science, Religion, and Naturalism, 2011 ) and a review, by Alvin Plantinga in The New Republic (2012), of Thomas Nagel’s latest book (Mind and Cosmos: Why the Materialist Neo-Darwinian Conception of Nature is Almost Certainly False, 2012). Both authors are regarded as distinguished philosophers. In their respective books, they both criticize what may be called the materialist neo-Darwinian approach to explaining life. Plantinga and Nagel both discuss as a putative alternative to evolutionary explanations, the framework known as intelligent design (ID). Whereas Plantinga appears to support ID, Nagel does not endorse ID but criticizes proponents of evolution for being overly disparaging of ID theorists.
My purpose here is not to review these two books, which I have not read in full and which do not focus solely on ID. Instead, I concentrate on issues that are more appropriately regarded as scientific as opposed to the related philosophical issues. Consequently, I propose to re-visit (Greenspan, 2002) the deep problems with the central tenets of ID, which claims both to identify profound flaws in the standard evolutionary account of living systems and to offer a different explanation in the form of an entity, the intelligent designer, that can somehow specify molecular structures, apparently simultaneously in billions of organisms and possibly trillions of cells, all over this planet. The identity of this “intelligent designer” is left completely unspecified, as are any of its attributes or its modes of operation, which must be extraordinary given that they completely escape all detection.
Proponents of ID have no useful thoughts on how these ID-mediated operations could be implemented within the constraints of physics and chemistry or, and this next point is key, subjected to experimental interrogation of any sort. Their need to rely on the supernatural thus obligates ID advocates to object to what they term “scientific naturalism” or “materialism.” This line of thought leads to re-defining science so that it includes what the vast majority of scientists, and likely many non-scientists, regard as non-science: ideas incapable of serious testing or investigation. Furthermore, I am aware of no advances in the understanding of scientific phenomena that have emanated from the individuals who subscribe to ID. The approach offered by ID embraces cognitive capitulation before any standard scientific conundrum and the acceptance of a recurring deus ex machina (“the intelligent designer did it”), the ultimate realization of intellectual cowardice.
ID proposes that physiological systems, on the molecular level, are “irreducibly complex” and therefore could not have evolved by an undirected process, such as natural selection. “Irreducible complexity,” at least in its initial explication, required that a system would lose all function with the removal of a single component. Since this definition has been routinely refuted by both experiments of nature (see for example: LeFranc et al., 1982; Dean et al., 1996) and by intentionally-manipulated experimental animals (one of many possible examples: Kuida et al., 1995), the definition has now apparently been loosened to mean that an irreducibly complex system must contain a minimum of two parts that are suitably configured to interact.
The central motivation behind the formulations of the original or the seriously weakened definition of “irreducible complexity” for supporters of ID is that that systems they regard as irreducibly complex could not evolve. This assertion is supported by no evidence or arguments that hold up to rigorous scrutiny.
It may be instructive to delve further into the study by Kuida et al., who created and investigated mice rendered deficient, via gene targeting, in the protein Interleukin-1β converting enzyme (ICE), now known as caspase-1. At least in the original study, these caspase-1-deficient mice exhibited no obvious phenotype.
Subsequent experiments (Kayakagi et al., 2011) revealed that the mice rendered caspase-1-deficient were simultaneously rendered caspase-11-deficient. Interestingly, mice deficient for both caspase-1 and caspase-11 were more resistant to a lethal dose of bacterial lipopolysaccharide than mice lacking only caspase-1. Similarly, deficiency of both caspase-1 and caspase-11 was associated with reduced susceptibility to infection by Salmonella typhimurium in comparison to mice with only caspase-1 deficiency. Those who argue that eliminating a single component of a putatively irreducibly complex system destroys all function cannot readily account for these (and many other) results associated with gene-targeted organisms.
In fact, over 2,700 gene-targeted mouse strains exhibit no abnormal phenotype (http://www.informatics.jax.org/javawi2/servlet/WIFetch?page=mpAnnotSummary&id=MP:0002169). Similarly, only about 20% of genes in the yeast, Saccharomyces cerevisiae, are essential for growth in rich glucose medium (Giaever et al., 2002). It is to be expected that the identities of the genes that are essential will vary with growth conditions and with genetic background.
Furthermore, the claim that systems with at least two specifically interacting components cannot evolve has actually been subjected to experimental test using organisms that evolve in realistic time frames in the laboratory and shown to be incorrect (e.g., see: Meyer et al., 2012). Unfortunately, as noted by Sean Carroll (2007), an eminent practitioner of evolutionary developmental biology, ID proponents routinely refuse to take note of new results that do not fit comfortably into their pre-conceived scheme. Irrespective of the acceptance or rejection of supernatural explanations, the willful failure to take account of evidence already obtained cannot be labeled as “science” or as reputable scholarly activity of any sort.
A similar problem afflicts the arguments, in connection with ID, of both Plantinga and Nagel, both of whom, however intelligent and philosophically sophisticated, lack familiarity with the numerous domains of relevant primary literature relating to evolutionary phenomena. There is also no evidence that either individual adequately understands basic and relevant concepts in evolutionary biology, genetics, biophysics, biochemistry, microbiology, and immunology. That their arguments are taken seriously reveals more about the appreciative audience than the plausibility of their specific assertions relevant to existing scientific results. The positions of Plantinga and Nagel bring to mind a statement of a prominent philosopher made in the context of a 1998 review in The New Republic, of a book by Alan Sokal and Jean Bricmont attacking post-modernism: “We may hope that incompetents who pontificate about science as a social phenomenon without understanding the first thing about its content are on the way out, …” That philosopher was Thomas Nagel.
Although the claims of Plantinga and Nagel are certainly not identical to those targeted for derision by Sokal and Bricmont, and are more carefully reasoned, they, like the post-modernist theorists, lack sufficient knowledge of the pertinent science, as opposed to philosophical positions related to or about that science, to seriously evaluate the scientific plausibility of ID. Like some ID supporters, Plantinga and Nagel appear to have almost no appreciation for the subtleties of proteins and genes and fail to recognize the pervasiveness of pleiotropy, the range and diversity of mutations other than single nucleotide substitutions, or the surprising resilience, due in part to functions shared by different molecules or pathways, of biological systems in the face of perturbations. I offer the preceding judgments despite having previously appreciated a number of Professor Nagel’s articles in a variety of publications.
As biological investigation continues, new pathways for stepwise protein evolution, of the sort that ID advocates claim is not possible, continue to be documented (Blount et al., 2012; Näsvall et al., 2012). Irrespective of the philosophical arguments of Plantinga and Nagel, the plausibility of ID continues to shrink. ID proponents already have acknowledged the existence of some evolutionary processes, such as the development of antibiotic resistance, and on one memorable occasion involving a direct interrogation, even speciation. If evolutionary theory requires revision, a plausible position given current controversies within biology, it will not be in ways that favor acceptance of the arguments associated with ID theorists.
Nagel T. A philosopher defends religion, The New York Review of Books, September 27, 2012. http://www.nybooks.com/articles/archives/2012/sep/27/philosopher-defends-religion/ (Accessed on 2/28/13).
Plantinga, A. Where the Conflict Really Lies: Science, Religion, and Naturalism. Oxford University Press, 2011.
Plantinga A. Why Darwinist materialism is wrong. The New Republic, November 16, 2012. http://www.newrepublic.com/article/books-and-arts/magazine/110189/why-darwinist-materialism-wrong (Accessed on 2/28/13).
Nagel, T. Mind and Cosmos: Why the Materialist Neo-Darwinian Conception of Nature is Almost Certainly False. Oxford University Press, 2012.
Greenspan, N.S. Opinion – Not-so-intelligent design. The Scientist, 16:12, 2002.
Lefranc MP, Lefranc G, Rabbitts TH. Inherited deletion of immunoglobulin heavy chain constant region genes in normal human individuals. Nature. 1982 Dec 23;300(5894):760-2. PubMed PMID: 6817143.
Dean M, Carrington M, Winkler C, Huttley GA, Smith MW, Allikmets R, Goedert JJ, Buchbinder SP, Vittinghoff E, Gomperts E, Donfield S, Vlahov D, Kaslow R, Saah A, Rinaldo C, Detels R, O’Brien SJ. Genetic restriction of HIV-1 infection and progression to AIDS by a deletion allele of the CKR5 structural gene. Hemophilia Growth and Development Study, Multicenter AIDS Cohort Study, Multicenter Hemophilia Cohort Study, San Francisco City Cohort, ALIVE Study. Science. 1996 Sep 27;273(5283):1856-62. Erratum in: Science 1996 Nov 15;274(5290):1069. PubMed PMID: 8791590.
Kuida K, Lippke JA, Ku G, Harding MW, Livingston DJ, Su MS, Flavell RA. Altered cytokine export and apoptosis in mice deficient in interleukin-1 beta converting enzyme. Science. 1995 Mar 31;267(5206):2000-3. PubMed PMID: 7535475.
Kayagaki N, Warming S, Lamkanfi M, Vande Walle L, Louie S, Dong J, Newton K, Qu Y, Liu J, Heldens S, Zhang J, Lee WP, Roose-Girma M, Dixit VM. Non-canonical inflammasome activation targets caspase-11. Nature. 2011 Oct 16;479(7371):117-21. doi: 10.1038/nature10558. PubMed PMID: 22002608.
Broz P, Ruby T, Belhocine K, Bouley DM, Kayagaki N, Dixit VM, Monack DM. Caspase-11 increases susceptibility to Salmonella infection in the absence of caspase-1. Nature. 2012 Oct 11;490(7419):288-91. doi: 10.1038/nature11419. Epub 2012 Aug 15. PubMed PMID: 22895188; PubMed Central PMCID: PMC3470772.
Mammalian Phenotype Ontology Annotations. http://www.informatics.jax.org/javawi2/servlet/WIFetch?page=mpAnnotSummary&id=MP:0002169 (Accessed on 2/27/2013).
Giaever G, Chu AM, Ni L, Connelly C, Riles L, … Davis RW, Johnston M. Functional profiling of the Saccharomyces cerevisiae genome. Nature. 2002 Jul 25;418(6896):387-91. PubMed PMID: 12140549.
Meyer JR, Dobias DT, Weitz JS, Barrick JE, Quick RT, Lenski RE. Repeatability and contingency in the evolution of a key innovation in phage lambda. Science. 2012 Jan 27;335(6067):428-32. doi: 10.1126/science.1214449. PubMed PMID: 22282803; PubMed Central PMCID: PMC3306806.
Carroll, S.B. God as genetic engineer. Science. 2007 Jun 8;316(5830):1427-1428. doi:10.1126/science.1145104
Nagel, T. Review of: Fashionable Nonsense: Postmodern Intellectuals’ Abuse of Science, by Alan Sokal and Jean Bricmont. The New Republic, October 12, 1998.
Blount ZD, Barrick JE, Davidson CJ, Lenski RE. Genomic analysis of a key innovation in an experimental Escherichia coli population. Nature. 2012 Sep 27;489(7417):513-8. doi: 10.1038/nature11514. Epub 2012 Sep 19. PubMed PMID:22992527; PubMed Central PMCID: PMC3461117.
Näsvall J, Sun L, Roth JR, Andersson DI. Real-time evolution of new genes by innovation, amplification, and divergence. Science. 2012 Oct 19;338(6105):384-7. doi: 10.1126/science.1226521. PubMed PMID: 23087246.