Consider the extraordinary diversity of life on Earth. Does genetic mutation and natural selection offer a strong enough mechanism to account for this diversity? For instance, if a construction team claimed to build a house, they would also be able to explain the mechanism that was used. They might say, “We had a crew of a dozen workers, tools, bulldozers, and a foreman.” This mechanism would account for the construction of the house, and in this case, it would be sufficient. On the other hand, if a foreman claimed that he built the Sears Tower with this same crew in a matter of hours, we wouldn’t accept this as an adequate mechanism. Does the Darwinian mechanism of natural selection acting on random mutation account for the extraordinary diversity of life?
When DNA repeatedly copies itself, it will sometimes make small errors called mutations. This ever so slightly changes the physical makeup of an organism—most of which are damaging to the organism and the species. Darwinist Richard Dawkins explains, “As a matter of fact, virtually all the mutations studied in genetics laboratories—which are pretty macro because otherwise geneticists wouldn’t notice them—are deleterious to the animals possessing them.” Gauger writes, “Natural selection may be good at weeding out mistakes that make the system crash or reduce efficiency, but it’s really bad at innovation.” Therefore, because of genetic mutation, species are constantly changing. This brings us to the second component: natural selection.
As Dawkins explained, virtually all mutations in the genome are harmful—not helpful. However, Darwinism claims to eliminate these harmful mutations by natural selection. Since these less fit mutations lead to extinction, only the helpful ones carry on. If they weren’t helpful, they wouldn’t help the creature pass on their DNA to their offspring. Therefore, Darwinists are quick to point out that Darwinism is random in its mutation—but not in its selection. Since the helpful mutations survive, this leads to constant change and diversity in the species.
Does this mechanism account for the extraordinary diversity of life? Darwinists argue that this mechanism (mutation + natural selection) can be clearly seen in a number of examples.
Evolution in Action
Darwinists often point to a number of examples which contain microevolution. However, paleontologists Erwin and Valentine write,
One important concern has been whether the microevolutionary patterns commonly studied in modern organisms by evolutionary biologists are sufficient to understand and explain the events of the Cambrian or whether evolutionary theory needs to be expanded to include a more diverse set of macroevolutionary processes. We strongly hold to the latter position.
From their perspective, these cases of microevolution are not capable of explaining the extraordinary diversity of life. Of course, as naturalistic paleontologists, Erwin and Valentine simply believe that other naturalistic causes will be discovered to explain this (“…a more diverse set of macroevolutionary processes…”). However, an adequate mechanism hasn’t been found. Fodor and Piattelli-Palmarini concur,
These days biologists have good reasons to believe that selection among randomly generated minor variants of phenotypic traits falls radically short of explaining the appearance of new forms of life.
Davidson and Erwin (2006) argued that known microevolutionary processes cannot explain the evolution of large differences in development that characterize entire classes of animals. Instead, they proposed that the large distinct categories called phyla arise from novel evolutionary processes involving large-effect mutations acting on conserved core pathways of development.
Where there have been morphogenetic explosions, fitness relations become surely non-transitive and plausibly irrelevant. There is no hill climbing, not even a smooth path from each level of fitness to the next; only a jumpy traverse of a maze or a ‘glass-like’ surface with a huge number of neighbouring peaks.
Natural selection can’t be the whole story about how phenotypes evolve. In fact, as we read the current literature and as we’ve seen… that isn’t seriously in dispute these days. Perhaps it never was: certainly Darwin himself didn’t think that natural selection could be the only mechanism of evolution.
Whatever Natural Selection is, it cannot be the mechanism that generates the historical taxonomy of species… Darwin did propose a causal mechanism for the process of speciation, but he got it wrong.
The journal Nature (2008) reported what has been called the “Altenberg 16,” where 16 biologists met in Altenberg, Austria to discuss the limits of neo-Darwinism. John Whitfield recorded some of their criticism:
Graham Budd, a palaeobiologist at the University of Uppsala, Sweden: “The origin of wings and the invasion of the land… are things that evolutionary theory has told us little about.”
Stuart Newman, a developmental biologist at New York Medical College: “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.”
Scott Gilbert, an evo-devo researcher at Swarthmore College in Pennsylvania: “The modern synthesis is remarkably good at modeling the survival of the fittest, but not good at modeling the arrival of the fittest.”
Regarding the origin of life in the fossil record, Hickman (et al.) write, “Many species remain virtually unchanged for millions of years, then suddenly disappear to be replaced by a quite different, but related, form. Moreover, most major groups of animals appear abruptly in the fossil record, fully formed, and with no fossils yet discovered that form a transition from their parent group. Robert Carroll (a paleontologist at McGill University) argues, “The extreme speed of anatomical change and adaptive radiation during this brief time period requires explanations that go beyond those proposed for the evolution of species within the modern biota.”
Darwinists currently debate the causal mechanism for the diversity of species. For a condensed treatment of this debate among Darwinists, see the 2014 debate in Nature between Kevin Leland and Gregory Wray.
1. Black peppered moths (or Galapagos Island Finches)
Science textbooks regularly refer to the black peppered moths as a clear-cut proof of evolution. The majority of peppered moths were white, until the Industrial Revolution began to spread soot on many of the trees. Because the white moths were now resting on black trees, they became an easy target for predators. Thus, Darwinists argue that this is evolution in action. However, there are several problems with this evidence.
First, it merely shows adaptation—not creation. This story shows the survival of members in this species, but it does not show the arrival of this species. In fact, the environmental change of the Industrial Revolution did not create the black peppered moth. Instead, it merely changed the proportion of black moths to white moths. Put another way, light colored moths never evolved into black colored moths, according to this account.
Second, it doesn’t account for reversals in change. Jonathan Wells compares this to a stock promoter. He writes, “Like a stock promoter who claims a stock might double in value in twenty years because it increased 5 percent in 1998, but doesn’t mention that it decreased 5 percent in 1999, [this evidence] misleads the public by concealing a crucial part of the evidence.” In the same way, environmental changes might cause change, but they also eliminate this change just as quickly.
Third, these classic pictures of peppered moths turned out to be staged. British biologist Bernard Kettlewell was one of the first to run experiments on the proportion of black to white moths. However, since this time, his work has undergone severe criticism. Wells points out, “Since 1980, however, evidence has accumulated showing that peppered moths do not normally rest on tree trunks.” According to Wells, these classic pictures in biology textbooks were created by gluing dead moths to tree trunks.
2. Fruit-flies or Dog-breeding
There are several cases of fruit flies being bred in labs that produce change in the species. In fact, two-winged fruit flies have been changed into four-winged fruit-flies. However, there are a number of observations that can be made regarding this evidence:
First, in most of these cases, they have documented minor changes—not major. For example, these lab fruit flies will have more hair on their legs, or they will lick themselves more than other fruit flies.
Second, this is not an example of NATURAL selection. In the confines of the lab, certain flies are supernaturally selected by the scientists—not naturally selected. Wells writes, “Four-winged fruit flies do not occur spontaneously. They must be carefully bred in the laboratory from three artificially maintained mutant strains.” Nature doesn’t select species like this. In other words, these cases are the product of intelligence—not naturalism. ID advocate Phillip Johnson comments, “When domesticated animals return to the wild state, the most highly specialized breeds quickly perish and the survivors revert to the original wild type. Natural selection is a conservative force that prevents the appearance of the extremes of variation that human breeders like to encourage.”
Third, when radical mutations occur, they are not helpful. This concurs with Richard Dawkins point from above: most mutations are harmful to the species. In one case, breeders were able to create a fruit fly with four wings—instead of two. However, these two wings were non-functional, and they couldn’t reproduce with other normal two-winged flies. This would be an example of downward evolution—not upward. Wells writes, “Biologists have known since the 1950s that the extra wings on bithorax mutants lack flight muscles. The hapless insect is thus disabled, and the disability increases with the size of the mutant appendages. In aerodynamic terms, a triple-mutant four-winged fruit fly is like an airplane with an extra pair of full-sized wings dangling loosely from its fuselage… Because of this, four-winged males have difficulty mating, and unless the line is carefully maintained in a laboratory it quickly dies out.”
3. Insects with DDT
Insects have been able to survive DDT—a poison used to exterminate them. For instance, evolutionist Francisco Ayala writes, “More than two hundred insect and rodent species, for example, have developed resistance to the pesticide DDT in parts of the world where spraying has been intense.”
While this offers persuasive evidence of micro changes in the insect species, it doesn’t show macro change. In fact, in each of these examples above, we see this same pattern. Evolution works to adapt a species to its environment. However, can we infer the overwhelming diversity of life from these examples of change? Paleontologists Erwin and Valentine explain, “Thus, the move from micro to macro forms a discontinuity.”
Darwinists argue that these cases of microevolution (e.g. special theory of evolution) can be measured to infer macroevolution (e.g. general theory of evolution). To illustrate, consider measuring the height of a child for an entire day. When you don’t measure any growth in his stature, you might conclude that he never will grow, and he will be doomed to be three and a half feet tall for the rest of his life. On the other hand, if you measure him over the course of a year, he might get a few inches taller. From this, you could extrapolate his future height. However, if you monitored the growth of an infant for six months, you might extrapolate that he would be eight feet by the time he reaches the age of six! You can see that the debate over extrapolation can be confusing. In these instances listed above, we find that the case for microevolution is strong, but these cases cannot be extrapolated as the mechanism for macroevolution.
Testable and observable limits to the mechanism of natural selection acting on random mutation
According to the standard neo-Darwinian account, given enough mutations and generations, natural selection acting on random mutation can account for the extraordinary diversity of life. Yet to test this account, in his book The Edge of Evolution (2007), Michael Behe offers three examples of the limited capability of natural selection acting on random mutation.
E. coli (Prokaryotic life—bacteria with no nucleus)
Professor Richard Lenski (of Michigan State University) created an experiment to watch evolution in action. He grew Escherichia coli (or E. coli), which only has a generation span of roughly 24 minutes. His team began growing the samples in the early 1990’s. Over the entire experiment, he grew roughly 10 trillion bacteria in lab flasks. Since these organisms out compete each other, Darwinian selective pressure still exists—even within the safety of the laboratory. Yet biochemist Michael Behe comments, “The lab bacteria performed much like the wild pathogens: A host of incoherent changes have slightly altered pre-existing systems. Nothing fundamentally new has been produced. No new protein-protein interactions, no new molecular machines.”
Antibiotic Resistant Bacteria (Eukaryotic life—organisms with a nucleus)
Bacteria quickly evolve to the antibiotics hurled at them. Bacteria rapidly reproduce and mutate (mutation), and then certain strands are able to survive the antibiotic (natural selection). In fact, bacteria evolve so quickly that this has become an epidemic in medical circles. However, while the antibiotic resistant bacteria do demonstrate evolution, they also demonstrate the limits of evolution.
Consider malaria. A person with malaria has roughly a trillion malarial cells in their body. Needless to say, malaria mutates rapidly! Therefore, the human immune system has tremendous selective pressure to combat and resist malaria. Yet one mutation has been found to combat malaria, making humans malaria resistant. The mutation has occurred in the human respiratory system, and it is called sickle-cell hemoglobin. Unfortunately, this produces anemia, which is deadly to humans.
However, here’s the point: malaria has never been able to overcome sickle hemoglobin. In order for malaria to overcome hemoglobin (i.e. sickle-cell anemia), it would need to have multiple simultaneous mutations. Yet in the thousands of years of pitting sickle-cell hemoglobin against malaria, malaria has never been able to overcome this combination. Behe writes,
The gene that carries the sickle mutation arose in a human population in Africa perhaps ten thousand years ago. The mutation itself is a single, simple genetic change—nothing at all complicated. Yet despite having a thousandfold more time to deal with the sickle mutation than with modern drugs, malaria has not found a way to counter it. While the evolutionary power of malaria stymies modern medicine, a tiny genetic change in its host organism foils malaria.
Consider the trillions upon trillions of combinations that malaria has tried in the countless bodies of human beings. Malaria has population pools that are astronomically large, incurring innumerable mutations. Yet malaria has never been able to overcome sickle-cell hemoglobin. Behe comments, “Here we have genetic studies over thousands upon thousands of generations, of trillions upon trillions of organisms, and little of biochemical significance to show for it.”
HIV (Evolution in viruses)
HIV mutates 10,000 times faster than malaria. Behe notes, “Viruses contain much less genetic material, but it mutates so rapidly, and there are so many copies of it, that HIV alone, in just the past fifty years, has undergone more of at least some kinds of mutations than all cells have experienced since the beginning of the world.” The virus replicates every day or two: “Over the course of ten years a single person will produce more than a thousand generations of HIV, or up to 1013 viruses.” Moreover, HIV is resistant to every drug we’ve ever developed to counter it. Darwinists use this as a clear case of evolution in practice.
However, while HIV has performed an incommensurable amount of mutations (i.e. more than all cells on Earth combined), there are no significant changes to the virus whatsoever. Behe writes,
Over the years its DNA sequence has certainly changed. HIV has killed millions of people, fended off the human immune system, and become resistant to whatever drug humanity could throw at it. Yet through all that, there have been no significant basic biochemical changes in the virus at all… A hundred billion billion mutant viruses later, HIV continues to do exactly the same thing, to bind the same way. If a mutant virus developed the ability to enter other kinds of cells by binding to other kinds of proteins, it might replicate more effectively and thus outcompete its siblings. That hasn’t happened. Neither has much else happened at a molecular level. No new gizmos or basic machinery. There have been no reports of new viral protein-protein interactions developing in an infected cell due to mutations in HIV proteins. No gene duplication has occurred leading to a new function. None of the fancy tricks that routinely figure in Darwinian speculations has apparently been of much use to HIV.”
HIV, therefore, actually serves as a case study on how little a virus will change—even given inexhaustible mutations.
 Of course, Dawkins goes on to write, “Ironically I’ve met people who think that this is an argument against Darwinism!” However, given the non-adaptive quality of these mutations, it is difficult to see how this specious mechanism could be responsible for the extraordinary extrapolation required for the diversity of life. Dawkins, Richard. The Blind Watchmaker: Why the Evidence of Evolution Reveals a Universe without Design. New York: Norton, 1996. 233.
 Gauger, Ann, Douglas Axe, and Casey Luskin. Science and Human Origins. Seattle, WA: Discovery Institute, 2012. 26.
 Emphasis mine. Douglas, Erwin, and James W. Valentine. The Cambrian Explosion: The Construction of Animal Biodiversity. Greenwood Village, CO: Roberts. 2013. 10.
 Fodor, Jerry A., and Massimo Piattelli-Palmarini. What Darwin Got Wrong. New York: Farrar, Straus and Giroux, 2011. 21.
 Fodor, Jerry A., and Massimo Piattelli-Palmarini. What Darwin Got Wrong. New York: Farrar, Straus and Giroux, 2011. 40.
 Fodor, Jerry A., and Massimo Piattelli-Palmarini. What Darwin Got Wrong. New York: Farrar, Straus and Giroux, 2011. 53.
 Fodor, Jerry A., and Massimo Piattelli-Palmarini. What Darwin Got Wrong. New York: Farrar, Straus and Giroux, 2011. 95.
 Fodor, Jerry A., and Massimo Piattelli-Palmarini. What Darwin Got Wrong. New York: Farrar, Straus and Giroux, 2011. 2.
 John Whitfield, “Biological theory: Postmodern evolution?” Nature, 455: 281-284 (September 17, 2008). Cited in Luskin, Casey. More than Myth: Seeking the Full Truth about Genesis, Creation, and Evolution. Chartwell Press, 2014. 20.
 C.P. Hickman, L.S. Roberts, and F.M. Hickman, Integrated Principles of Zoology, p. 866 (Times Mirror/Moseby College Publishing, 1988, 8th ed). Cited in Luskin, Casey. More than Myth: Seeking the Full Truth about Genesis, Creation, and Evolution. Chartwell Press, 2014. 25-26.
 Robert L. Carroll, “Towards a new evolutionary synthesis,” Trends in Ecology and Evolution, 15(1):27-32 (2000). Cited in Luskin, Casey. More than Myth: Seeking the Full Truth about Genesis, Creation, and Evolution. Chartwell Press, 2014. 26.
 Leland, Kevin (et al.) and George Wray (et al.). “Does Evolutionary Theory Need a Rethink?” Nature. Volume 514. October, 2014. 161-164.
 Wells, Jonathan. Icons of Evolution: Science or Myth: Why Much of What We Teach about Evolution Is Wrong. Washington, DC: Regnery Pub., 2000. 175.
 Wells, Jonathan. Icons of Evolution: Science or Myth: Why Much of What We Teach about Evolution Is Wrong. Washington, DC: Regnery Pub., 2000. 149.
 Wells, Jonathan. Icons of Evolution: Science or Myth: Why Much of What We Teach about Evolution Is Wrong. Washington, DC: Regnery Pub., 2000. 150-151.
 Wells, Jonathan. Icons of Evolution: Science or Myth: Why Much of What We Teach about Evolution Is Wrong. Washington, DC: Regnery Pub., 2000. 178.
 Johnson, Phillip E. Darwin on Trial. 2nd ed. Downers Grove, IL: InterVarsity, 1993. 17-18.
 Wells, Jonathan. Icons of Evolution: Science or Myth: Why Much of What We Teach about Evolution Is Wrong. Washington, DC: Regnery Pub., 2000. 186.
 Ayala, Francisco José. Darwin and Intelligent Design. Minneapolis: Fortress, 2006. 61.
 Douglas, Erwin, and James W. Valentine. The Cambrian Explosion: The Construction of Animal Biodiversity. Greenwood Village, CO: Roberts. 2013. 11.
 Behe, Michael J. The Edge of Evolution: The Search for the Limits of Darwinism. New York: Free, 2007.
 Behe, Michael J. The Edge of Evolution: The Search for the Limits of Darwinism. New York: Free, 2007. 143.
 Francisco Ayala writes, “When an individual receives an antibiotic that specifically kills the bacteria causing a disease—say, tuberculosis—the immense majority of the bacteria die, but one in a million may have a mutation that provides resistance to the antibiotic. These resistant bacteria will survive and multiply, and the antibiotic will no longer cure the disease. This is the reason why modern medicine treats bacterial diseases with cocktails of antibiotics.” Ayala, Francisco José. Darwin and Intelligent Design. Minneapolis: Fortress, 2006. 61.
 Behe, Michael J. The Edge of Evolution: The Search for the Limits of Darwinism. New York: Free, 2007. 58.
 Behe, Michael J. The Edge of Evolution: The Search for the Limits of Darwinism. New York: Free, 2007. 15.
 Behe, Michael J. The Edge of Evolution: The Search for the Limits of Darwinism. New York: Free, 2007. 140.
 Behe, Michael J. The Edge of Evolution: The Search for the Limits of Darwinism. New York: Free, 2007. 13-14.
 Behe, Michael J. The Edge of Evolution: The Search for the Limits of Darwinism. New York: Free, 2007. 138.
 Behe, Michael J. The Edge of Evolution: The Search for the Limits of Darwinism. New York: Free, 2007. 139.