Editor’s note: This is Part 4 of a 10-part series based upon Casey Luskin’s chapter, “The Top Ten Scientific Problems with Biological and Chemical Evolution,” in the volume More than Myth, edited by Paul Brown and Robert Stackpole (Chartwell Press, 2014). The full chapter can be found online here. Other individual installments can be found here: Problem 1, Problem 2, Problem 4, Problem 5, Problem 6, Problem 7, Problem 8, Problem 9, Problem 10.
In 2008, 16 biologists from around the world convened in Altenberg, Austria, to discuss problems with the modern neo-Darwinian model of evolution. The journal Nature covered this “Altenberg 16” conference, quoting leading scientists saying things like:
- “[T]he origin of wings and the invasion of the land . . . are things that evolutionary theory has told us little about.”49
- “You can’t deny the force of selection in genetic evolution . . . but in my view this is stabilizing and fine-tuning forms that originate due to other processes.”
- “The modern synthesis is remarkably good at modeling the survival of the fittest, but not good at modeling the arrival of the fittest.”
In Problem 3, we learned that mutations cannot generate many complex traits in living organisms on reasonable evolutionary timescales. But mutations are only part of the standard evolutionary mechanism — there is also natural selection. And Darwinian evolution not only commonly fails to explain the “arrival of the fittest” via mutations, but also often struggles to explain the “survival of the fittest” via natural selection.
Evolutionary biologists often assume that once mutations produce a functionally advantageous trait, it will easily spread (become “fixed”) throughout a population by natural selection. For example, imagine a population of brown-haired foxes which lives in a snowy region. One fox is born with a mutation which turns its fur coat white, rather than brown. This fox now has an advantage in hunting prey and escaping predators, because its white fur provides it with camouflage in the snow-filled environment. The white fox survives, passing its genes on to its offspring, which are also adept at surviving and reproducing. Over time, the white-haired trait spreads throughout the population.
This is how it’s supposed to work — in theory. In the real world, however, merely generating a functionally advantageous trait does not guarantee it will persist, or become fixed. For example, what if by chance the white fox trips, breaks a leg, and gets eaten by a predator — never passing on its genes? Random forces or events can prevent a trait from spreading through a population, even if it provides an advantage. These random forces are lumped together under the name “genetic drift.” When biologists run the mathematics of natural selection, they find that unless a trait gives an extremely strong selective advantage, genetic drift will tend to overwhelm the force of selection and prevent adaptations from gaining a foothold in a population.
This underappreciated problem has been recognized by some evolutionary scientists who are skeptical of the ability of natural selection to drive the evolutionary process. One of those scientists is Michael Lynch, an evolutionary biologist at Indiana University, who writes that “random genetic drift can impose a strong barrier to the advancement of molecular refinements by adaptive processes.”50 He notes that the effect of drift is “encouraging the fixation of mildly deleterious mutations and discouraging the promotion of beneficial mutations.”51 Likewise, Eugene Koonin, a leading scientist at the National Institutes of Health, explains, genetic drift leads to “random fixation of neutral or even deleterious changes.”52
In Lynch’s view, there are many cellular systems which aid in survival, but are redundant. As a result, they serve as backup mechanisms that are only used when a highly effective primary system fails. Because they are only seldom used, these systems are only occasionally exposed to the sieve of selection. Yet these systems can be extremely complex and efficient. How can a system which is only rarely used, or only occasionally needed, evolve to such a high and efficient level of complexity? After observing the many “layers” of complex cellular mechanisms which are involved in processes like DNA replication, Lynch poses a crucial question:
Although these layered lines of defense are clearly advantageous and in many cases essential to cell health, because the simultaneous emergence of all components of a system is implausible, several questions immediately arise. How can selection promote the establishment of additional layers of fitness-enhancing mechanisms if the established primary lines of defense are already highly refined?53
Lynch doesn’t believe natural selection is up to the task. In a 2007 paper in Proceedings of the U.S. National Academy of Sciences titled “The frailty of adaptive hypotheses for the origins of organismal complexity,” he explains that among evolutionary biologists, “What is in question is whether natural selection is a necessary or sufficient force to explain the emergence of the genomic and cellular features central to the building of complex organisms.”54 Using similar language, a paper in the journal Theoretical Biology and Medical Modelling concludes that “it is important for biologists to realistically appraise what selection can and cannot do under various circumstances. Selection may neither be necessary nor sufficient to explain numerous genomic or cellular features of complex organisms.”55 Lynch is clear in his views: “there is no compelling empirical or theoretical evidence that complexity, modularity, redundancy or other features of genetic pathways are promoted by natural selection.”56
Damned if You Appeal to Selection, Damned if You Don’t
In place of natural selection, however, evolutionary biologists like Lynch propose random genetic drift to explain the origin of complex biological features. According to Lynch, “many aspects of complexity at the genomic, molecular and cellular levels in multicellular species are likely to owe their origins to these non-adaptive forces, representing little more than passive outcomes…”57 But he recognizes that these “nonadaptive forces of evolution are stochastic in nature.”58
Stochastic, of course, means random. Can a strictly random force — which has no reason to preserve features that might provide some advantage — explain the highly complex biological features — like DNA replication or bioluminescence — which appear finely tuned to perform useful biological functions? Biologist Ann Gauger is skeptical of Lynch’s explanation, as she observes that he “offers no explanation of how non-adaptive forces can produce the functional genomic and organismal complexity we observe in modern species.”59 Jerry Coyne similarly points out the major deficiency in appeals to genetic drift:
Both drift and natural selection produce genetic change that we recognize as evolution. But there’s an important difference. Drift is a random process, while selection is the anti-thesis of randomness. … As a purely random process, genetic drift can’t cause the evolution of adaptations. It could never build a wing or an eye. That takes nonrandom natural selection. What drift can do is cause the evolution of features that are neither useful nor harmful to the organism.60
Coyne further observes: “The influence of this process on important evolutionary change, though, is probably minor, because it does not have the molding power of natural selection. Natural selection remains the only process that can produce adaptation.”61 But in a sense agreeing with Lynch, even he recognizes that “genetic drift is not only powerless to create adaptations, but can actually overpower natural selection.”62
The debate over whether natural selection, or genetic drift, is more influential in evolution will undoubtedly continue. But there is little reason to believe that whichever side wins this debate, a viable materialistic solution will be offered. Evolutionary biology now finds itself facing a catch-22:
- Natural selection is too inefficient a mechanism to overcome random forces and fix the sort of complex adaptations we observe in populations because it is easily overpowered by random forces like genetic drift.
- Life is full of highly complex and efficient adaptations, but random genetic drift offers no justifiable reason to believe that such features will have any reason to arise.
In essence, genetic drift is like invoking the “mutation-selection” mechanism, but minus all of the selection. This subjects drift to all of the difficulties we saw in Problem 3, where random mutations were unable to build biochemical features like functional proteins, or simple protein-protein interactions, because multiple coordinated mutations were required to produce those traits. Absent selection, there is no reason for random mutations alone — i.e. genetic drift — to produce anything useful.
Unfortunately, the public is rarely made aware of these problems or this debate. According to Lynch, natural selection is typically portrayed as an “all powerful (without any direct evidence)”63 mechanism that can build complex biological features. He warns that “the myth that all of evolution can be explained by adaptation continues to be perpetuated by our continued homage to Darwin’s treatise in the popular literature.”64 The reality is that neither non-random forces like natural selection, nor random forces like genetic drift, can explain the origin of many complex biological features.
[49.] Scott Gilbert, Stuart Newman, and Graham Budd quoted in John Whitfield, “Biological theory: Postmodern evolution?” Nature, 455: 281-284 (September 17, 2008).
[50.] Michael Lynch, “Evolutionary layering and the limits to cellular perfection,” Proceedings of the U.S. National Academy of Sciences, www.pnas.org/cgi/doi/10.1073/pnas.1216130109 (2012).
[51.] Michael Lynch, “The frailty of adaptive hypotheses for the origins of organismal complexity,” Proceedings of the U.S. National Academy of Sciences, 104: 8597-8604 (May 15, 2007).
[52.] Eugene V. Koonin, “Darwinian evolution in the light of genomics,” Nucleic Acids Research (2009): 1-24, doi:10.1093/nar/gkp089
[54.] Michael Lynch, “The frailty of adaptive hypotheses for the origins of organismal complexity,” Proceedings of the U.S. National Academy of Sciences, 104: 8597-8604 (May 15, 2007).
[55.] Chase W. Nelson and John C. Sanford, “The effects of low-impact mutations in digital organisms,” Theoretical Biology and Medical Modelling, 8:9 (2011).
[56.] Michael Lynch, “The evolution of genetic networks by non-adaptive processes,” Nature Reviews Genetics, 8:803-813 (October, 2007).
[58.] Michael Lynch, “The frailty of adaptive hypotheses for the origins of organismal complexity,” Proceedings of the U.S. National Academy of Sciences, 104: 8597-8604 (May 15, 2007).
[59.] Ann Gauger, “The Frailty of the Darwinian Hypothesis, Part 2,” Evolution News & Views (July 14, 2009), at http://evolutionnews.org/2009/07/the_frailty_of_the_darwinian_h_1
[60.] Jerry A. Coyne, Why Evolution is True, p. 123 (Viking, 2009).
[61.] Ibid., p. 13.
[62.] Ibid., p. 124.
[63.] Michael Lynch, “The frailty of adaptive hypotheses for the origins of organismal complexity,” Proceedings of the U.S. National Academy of Sciences, 104: 8597-8604 (May 15, 2007).