Does Evolution Prove that Christianity Is False? Part 1

<i>By Adam Lloyd Johnson, Ph.D.</i><br /><br /><p>What if evolution is false? I’ve talked with many people who considered themselves Christians but then, for whatever reason, came to believe that evolution is true. These individuals were greatly troubled because they thought, now that they had accepted evolution, that they’d have to reject Christianity. However, many of them remained confident that the basic tenets of Christianity were true, i.e., God exists, Jesus is God, the Bible is from God, and a person can be forgiven and reconciled back to God through faith in Jesus Christ. With such individuals I’ve tried to lovingly point out that evolution doesn’t prove that Christianity is false. In this article I’ll summarize my argument in the hope it will be a benefit to others. This article will be published in two parts. I’ll begin by stating the obvious: If evolution is false, then certainly it doesn’t prove that Christianity is false. Therefore, in part one of this article, I’ll present the strongest argument against evolution.</p>

By Adam Lloyd Johnson, Ph.D.

Since I’m not a trained scientist, I wanted to have someone with substantial scientific training to evaluate my article to make sure I understood and explained the issues accurately. Thus, I asked Dr. Eric Birgbauer to review my article before I published it. Dr. Birgbauer earned his B.A. in Molecular Biology at the University of California-Berkeley and his Ph.D. in Biology, with an emphasis in cell biology, from MIT (Massachusetts Institute of Technology), one of the most prestigious universities in the world. He currently serves as Associate Professor of Biology at Winthrop University. Dr. Birgbauer wrote the following about my article:

Dr. Johnson has written an excellent paper discussing the theory of evolution from a Christian perspective. He explains our current understanding of evolution and the science behind it. He does not dismiss the science, but analyzes it meticulously. He starts with an explanation of the premises of evolution and the strong scientific data that supports small evolutionary changes by natural selection. He then thoughtfully discusses whether these random processes can be extrapolated to explain the origin of all known organisms in all their diversity, and he provides intelligent evidence for his arguments. Furthermore, Dr. Johnson clarifies the important practical theological issue that the science of evolution does not negate the truth of the gospel of Jesus Christ.

What if Evolution Is False?


I’ve talked with many people who considered themselves Christians but then, for whatever reason, came to believe that evolution is true. These individuals were greatly troubled because they thought, now that they had accepted evolution, that they’d have to reject Christianity. However, many of them remained confident that the basic tenets of Christianity were true, i.e., God exists, Jesus is God, the Bible is from God, and a person can be forgiven and reconciled back to God through faith in Jesus Christ. With such individuals I’ve tried to lovingly point out that evolution doesn’t prove that Christianity is false. In this article I’ll summarize my argument in the hope it will be a benefit to others.

This article will be published in two parts. I’ll begin by stating the obvious: If evolution is false, then certainly it doesn’t prove that Christianity is false. Therefore, in part one of this article, I’ll present the strongest argument against evolution. In part two of this article, which you can read here, I’ll argue that even if evolution is true, this still doesn’t prove that Christianity is false.

What is Evolution?

Before I present the strongest argument against evolution, it’s important to recognize that the word “evolution” is a broad term which is used by different people to mean different things. For example, there’s a sense in which evolution is a proven scientific fact. Its three basic ingredients—trait variation among descendants, the natural selection of those that have superior traits, and the passing on of those traits to descendants—have been repeatedly observed in numerous scientific experiments. The process itself is remarkably simple but, for those who may be new to this conversation, I’ll begin by summarizing the most rudimentary basics. 

When an organism produces offspring, these new organisms are not exact replicas of the original parent; they’re all slightly different from their parent and from one another. Those with superior differences, ones that aid in survival and reproduction within their specific environment, have a greater probability of surviving and thus passing on their superior traits to their offspring. Those with such superior traits out-compete those without them in the struggle for mates and scarce resources over multiple generations until the only ones left are those that possess these superior traits. In this sense an organism changes over time to better adapt to its environment. After numerous generations, the resulting organism can become incredibly different than the original ancestor.

While the details of exactly how this happens have only been uncovered in the last couple centuries, for millennia people have understood these facts about trait variation and hereditary inheritance. In fact, for thousands of years human breeders have made use of this knowledge with animal breeding by artificially selecting descendants who have the particular traits the breeders are trying to develop. To compare artificial selection with natural selection, I’ll summarize below the three-part evolutionary process I described above:

  1. Offspring with varying traits
  2. Nature (the environment they’re in) determines which traits are superior in terms of survival and reproduction value
  3. Hereditarily passing on these traits to descendants                     

Breeders can replace nature in the second step by artificially choosing which offspring to breed again. Through this process, with canines for example, breeders have been able to develop dogs as different from one another as Chihuahuas and Great Danes.1 

The importance of Charles Darwin’s work, who had considerable experience with animal breeding, was to postulate that a process akin to artificial breeding could happen naturally, i.e., natural selection. Darwin acknowledged that others, such as William Charles Wells and Patrick Matthew, had proposed similar ideas but had not developed them fully or presented them as scientific publications. The idea of natural selection is that, instead of humans artificially selecting which offspring to mate, nature could make this selection simply through the harsh environment in which the offspring are competing with each other for mates and scarce resources.

Offspring with traits that are well-suited to a particular environment will thrive there while those without those traits will be less likely to survive and thus mate to pass on their traits. Obviously nature doesn’t “select,” as in “to make a decision” like a human mind does, but it does affect which traits will be passed on to the next generation. This competitive struggle for survival and reproduction is driven by the fact that there are scarce resources to go around, so only the best, the ones most adapted to their particular environment, will pass on their traits. Everything I’ve presented thus far is uncontroversial; everyone affirms these basic facts about evolution, and we can all celebrate Darwin’s brilliant discovery.

The important question to ask is this: how powerful is this evolutionary process? We know empirically that it’s powerful enough, given the appropriate length of time for numerous generations, to transform a canine into a very specialized dog such as a Saint Bernard. But, is it powerful enough, given an even longer time for many numerous generations, to transform a canine into a completely different species? Is it so powerful as to eventually transform a reproducing single-celled organism into a human being? This is what Darwin proposed; hence he titled his book On the Origin of Species. He theorized that eventually enough small changes over time within a species could add up such that it results in the origin of a new species. This hypothesis is the controversial aspect of evolution that many disagree with. For example, in 1997, evolutionary biologist Keith Stewart Thomson wrote: “A matter of unfinished business for biologists is the identification of evolution’s smoking gun” and “the smoking gun of evolution is speciation [the origin of a new species], not local adaptation and differentiation of populations.” Before Darwin, centuries of artificial selection had seemingly demonstrated that species can vary only within a certain limit. “Darwin had to show that the limits could be broken,” wrote Thomson, and “so do we.”2

A Reasonable Hypothesis

Armed with our many observations of small-scale evolution which take place within our own lifetimes, we can certainly hypothesize that evolution is powerful enough to account for the large-scale transformation of the first self-reproducing organism into all the forms of life we see today.3 This hypothesis is a combination of the evolutionary process we directly observe on a smaller scale and the assumption that this process can be extrapolated to a much larger scale. This assumption, that the small-scale evolutionary process we observe can be extrapolated to explain the origin of species, was the very crux of Darwin’s hypothesis.

His assumption here was quite reasonable because extrapolation is a valid method of hypothesis. After all, this is exactly what Isaac Newton did. He experienced gravity on a smaller scale (causing apples to fall from a tree) and extrapolated that to a much larger scale (causing planets to orbit the sun). Unfortunately, Darwin didn’t have access to the scientific tools and knowledge we have today to more fully explore this fundamental assumption. To make matters worse, the vast amount of numerous generations necessary for such proposed large-scale transformations often requires more time (millions of years) than we can fit into a scientific experiment, making it difficult to empirically prove this hypothesis in a laboratory. Thankfully, we have two other ways of ascertaining the real power of this process.

First, there is forensic science, most well-known for being used by crime-scene investigators who attempt to solve crimes by uncovering the past. In this way we can attempt to understand what has happened by studying the available evidence left behind by previous generations. Such evidence would be the fossil record as well as the results of the process thus far, i.e., currently living organisms. Some things have been learned from this endeavor, but without actually observing the large-scale process directly, we can’t be too confident about the results of these types of investigations. Limitations abound in this form of inquiry because we only have a very small fraction of the fossil record. Like a crime scene investigator with access to only a fraction of the evidence, it’s difficult to prove exactly what happened based on only this sort of evidence.   

Second, by better understanding how the evolutionary process happens on a small scale within our lifetime, we can make better judgments on the viability of the hypothesis that these small changes can add up, given enough time, to account for the origin of new species. In other words, by evaluating exactly how the small-scale evolutionary process works, we can try to ascertain the limits, if any, of its ability to transform organisms. Is there anything we’ve learned from the observation of small-scale evolutionary transformations, something inherent in the process, that limits it from accomplishing large-scale species origination?

Dr. Michael Behe has presented a compelling case that, yes, there is a limit to what this evolutionary process can produce. Behe earned his Ph.D. in Biochemistry from the University of Pennsylvania, did postdoctoral work on DNA structure at the National Institutes of Health, and is currently a professor of Biochemistry at Lehigh University. Behe affirms that all life has descended from a common ancestor but, based on his scientific research, has come to reject the idea that evolution is able to produce new species.


It’s hard for some to believe that such large-scale evolution has taken place because they can’t imagine how small, incremental changes over time could lead to the creation of entirely new organs such as the human eye. But just because we have limited imaginations concerning how it might have happened, this doesn’t mean that it didn’t. It’s not a strong enough argument to maintain that just because we can’t imagine how the process produced, say, the human eye, that it must not have happened in this manner. It may just mean our intellects have not yet grasped the how yet. It’s important to keep in mind the opposite is true as well; it would be powerful evidence for evolution if scientists could provide pathway examples of each mutation and how it was beneficial. In other words, it’s not enough to speculate that it could happen, but it needs to be shown empirically that it did. Regardless, when it comes to making an argument against evolution, a more powerful argument would be to show empirically the limitations of the small-scale evolutionary process and how it could not have resulted in large-scale evolution if, in fact, there are such limitations.             

In order to answer this question, the place to focus is the first of the three fundamentals of evolution, summarized again below.

  1. Offspring with varying traits
  2. Nature affecting which traits are superior, in terms of survival and reproduction value
  3. Hereditarily passing on these traits to descendants

These variations among offspring are the fuel that drives the evolutionary process. Without variations, there is nothing for nature to select for, and so the process can’t even begin. As Darwin wrote, “[u]nless profitable variations do occur, natural selection can do nothing.”4 This in-depth investigation of small-scale evolution, specifically of trait variation, couldn’t have been done during Darwin’s time because science had not yet even discovered what causes offspring to have different traits and how those traits are passed on hereditarily. 

It might surprise you to know that in Darwin’s day scientists didn’t know the answer to the following basic questions: How do traits vary? How much can they vary? Is anything new ever created in the variations or are they just different combinations of what is already there? Are these variations sufficient enough fuel to allow organisms to transform into radically different forms given enough time? Are these variations purely random and accidental? Since Darwin’s time, have we discovered answers to these questions which would cause us to conclude that this evolutionary process isn’t powerful enough to create new species? It seems we have.

You’re Wearing Mom’s Genes

During Darwin’s time the underlying reason for variations among offspring was unknown. Darwin “had to simply assume that there was some mechanism, unknown to the science of his age, to generate differences.”5 He famously observed beak variation among finches but did not understand what generated these modifications. It was not until the 1930s, over seventy years since Darwin’s On the Origin of Species was first published, that genes were recognized as the basis for these inheritable variations which fuel the process of evolution.

Later it was discovered that DNA is the molecule that contains genetic information. A gene is simply a portion of DNA material that determines a single functional unit. Inherited traits are then controlled by genes as they are passed from parent to offspring, and thus we “now know that variation in organisms depends on hidden changes in their DNA.”6 This combination of genetic inheritance, discovered by Gregory Mendel in the nineteenth century, and evolution is referred to as the modern evolutionary synthesis and is the basic tenet of modern biology.

The offspring of organisms inherit random mixtures of their parents’ genes. Variation is caused by reproduction because even though “only half of their total genetic complement is contributed to each offspring, it is a different half each time.”7 It’s important to realize that “the genes themselves are not changing. Rather, they are merely being shuffled around, expressing novel combinations of genes that were already present. Combinations of both expressed and unexpressed genes (in the genetic reserve) can give geological populations adaptive potential.”8 

Genes do not lose their identity by being blended; they maintain their identity but are “being combined in different ways.”9 The only change from one generation to the next then is “in the prevalence of certain gene combinations.”10 For example, “dog breeding produces widely differing varieties of dogs not by adding new genetic material to the gene pool but by selecting smaller sets of genes from the larger and richer store of genetic material already in the gene pool.”11 

This has also been seen naturally with the success of the English sparrow as it radically changed to adapt to different geographic areas in America. The original birds from England possessed all the genes necessary to produce the range of body-types and sizes that eventually developed. They just “had yet to develop the specialized combinations of genes that we observe in the American forms of today.”12 At first they were established only in small populations because it took time for specialized gene combinations to emerge, ones that would be naturally selected based on their particular environment. It was new combinations of existing genes that proved advantageous, not the origination of new genes.13 

When a breeder causes a specific trait to appear or disappear, it’s not as though this is creating new information or losing old information. What’s going on is merely the “interplay of dominant genes (whose associated traits are manifest) and recessive genes (whose associated traits are, for the moment, concealed). A trait that is seemingly lost may therefore still be present and reappear. Conversely, a trait that seems to appear out of nowhere may not be new at all but simply the expression of a recessive gene that existed all along. When breeders produce new show dogs or meatier cattle, they are in fact merely shuffling genes to bring formerly recessive genes to expression.”14                     

Mendel’s work actually demonstrates “that living things are remarkably stable.”15 The interplay of dominant and recessive genes provides the necessary stable foundation for a superior trait to become established in a population through natural selection. “Natural selection has a much easier time of it working with and taking advantage of hereditary factors that are stable (as occur in Mendel’s theory). But this very stability stands in the way of these hereditary factors changing sufficiently”16 enough to produce genuinely new traits.

Mendelian genetic inheritance then gives us a much more limited view of evolution than what Darwin proposed. “Mendialian inheritance accounts for breeders producing sweeter corn or fatter cattle through the shuffling of existing genes. At the same time, because of the stability of genes, it also explains the inability of breeders to turn corn into another kind of plant or cattle into another kind of animal. What breeders accomplish is diversification within a given species.”17  

Moth populations that shift in color from light to dark are another example of this small-scale evolution by natural selection. But again, this only illustrates “small changes in the gene frequency of populations. A shift in the dominant moth coloring requires no new genetic information because the alleles (variant genes) are already present in the population.”18 In contrast, large-scale evolutionary change “requires wholesale changes in the physical and behavioral characteristics of organisms, the entry of novel information leading to increases in biological complexity, and, ultimately, the origin of novel types of organisms.”19 The passing on of different gene combinations from parent to offspring just doesn’t accomplish this.


In light of the scientific discovery of how gene heredity works and the inherent limitation of this process which makes it unable to accomplish large-scale evolution, some have proposed something else as the fuel which drives the variations that lead to large-scale evolution. The key necessary ingredient to bridge the gap from small-scale evolution, which merely shuffles around existing information in the gene pool, to large-scale evolution, which actually builds something new, is new information that isn’t already in the gene pool. Scientists who affirm this proposal, sometimes called neo-Darwinists, think that “genetic mutations provide the raw material”20 which drives large-scale evolution and ultimately generates the new information that leads to the origin of new species.

Mutations are random changes that occur at the molecular level in DNA. They can be caused by such things as radiation, viruses, chemicals, and errors that occur during DNA replication, but they also sometimes occur spontaneously without any known cause. There is overwhelming “evidence that random mutation paired with natural selection can modify life in important ways… however, there is strong evidence that random mutation is extremely limited. Now that we know the sequences of many genomes, now that we know how mutations occur, and how often, we can explore the possibilities and limits of random mutation with some degree of precision for the first time since Darwin proposed his theory.”21 

The only way to understand the evolutionary power of mutations is to track the changes that result from them at the molecular level. As Behe explained, “[p]roperly evaluating Darwin’s theory absolutely requires evaluating random mutation and natural selection at the molecular level.”22 The first important thing to understand about mutation is that it’s a random process because most “mutations are genetic copying errors characterized by probabilities.”23 We can calculate these probabilities because “the rate of mutation has been worked out fairly well… as a rule, the copying of DNA is extremely faithful. On average, a mistake is made only once for every hundred million or so nucleotides of DNA copied in a generation.”24

There are broadly two types of mutations. The first type is point mutations. Here, the change occurs in the “individual nucleotide bases of the DNA.”25 The second type is chromosome mutations, which “involve not individual nucleotide bases but entire sections of DNA.”26 Chromosome mutations are simply the “action of chance rearranging and repositioning the gene.”27 It’s very important to understand that, as Behe explained, “randomly duplicating a single gene, or even the entire genome, does not yield new complex machinery; it only gives a copy of what was already present.”28 This merely reshuffles around existing genes. However, point mutations are quite different:

The only known way to introduce genuinely new genetic information into the gene pool is by mutations that alter the nucleotide bases of individual genes. This is different from chromosome mutation, in which sections of DNA are duplicated, inverted, lost, or moved to another place in the DNA molecule. Point mutations do not merely rearrange but fundamentally alter the structure of existing genes. Such mutations typically result from random copying errors of DNA and are intensified through exposure to heat, chemicals, or radiation.29 

 A point mutation is defined as “a random change in functional information.”30 Most all point mutations are harmful to the organism “while most that are not harmful are merely neutral, neither helping nor hindering the organism.”31

Irreducible Complexity

One of the key questions that arises concerning this proposal that mutations can fuel large-scale evolution is this: is it possible to build something new and complex, for example the human eye, from small step-by-step accidents where every accidental step itself, not just the end result, is useful enough to be picked up by natural selection? In light of the limited scientific knowledge that was available in his day, Darwin himself warned that his theory would be proven false if future scientific discoveries confirmed that biological machines were irreducibly complex when he wrote, “If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight changes, my theory would absolutely break down.”32

This is where Behe’s work on irreducible complexity is helpful. In his book Darwin’s Black Box Behe argued that complex biological machines cannot be built one accidental step at a time because all the pieces of the machine have to be there in order for it to work. If just one piece was missing, then the machine wouldn’t work. Behe used bacterial flagella as a pristine example of this irreducible complexity because their tail mechanism is a tiny little machine, literal nanotechnology, that is almost identical to the rotary engines that we humans have designed and built. This tail mechanism on the flagellum is a literal propellor that moves the bacterium through liquid and includes a rotor, a stator, a driveshaft, a U-joint, bushings, bearings, and a whip-like tail. It can turn up to 100 RPMs in one direction, reverse direction in a quarter of a turn, and go just as fast in the other direction.

This irreducible complexity problem for evolutionists is exacerbated by the fact that every piece of the machine would have to be useful on its own in the evolutionary process for nature to select it, but the machine only works when all the pieces are there working together. Those who reject evolution often use the analogy of a tornado by claiming that the process of evolution is as likely to create complex biological machines as a tornado is, if it went through a junkyard, to create new, fully working cars. Unfortunately, this analogy fails because it misrepresents the theory of evolution; evolutionists claim the process happens slowly one step at a time. However, this actually makes things worse for evolutionists, and I’ll try to illustrate this with a new, more accurate analogy that I’ve developed.

Consider the process of trying to write a book one letter at a time where each letter can only be selected if it “works” on its own, that is, if it makes sense with what’s already there. In English we have 26 letters, and we’ll graciously throw in a “space” as a 27th random possibility. In this analogy the “author” can function as “nature” and select the next sequential letter but only if it “works,” that is, if it adds something that is helpful and makes sense to the existing word, sentence, or paragraph that is being “built.” The book, in fact every paragraph, sentence, and word, would have to start with an a, an i, or an o because only those three letters “work” on their own, in other words, only those letters complete a word on their own. If a is “selected,” then the next letter would have to be a b, d, h, l, m, n, s, t, w, x, y or “space” because only those letters would “work” on their own; that is, only those letters add something to the existing word (a) that also forms a whole word in combination with a—in this example you’d have ab, ad, ah, al, am, an, as, at, aw, ax, ay, or a then a “space.” This step-by-step process would have to be repeated without ever contemplating ahead of time a particular vision of where the sentence, paragraph, or story could or should go. Someone could easily set up a random generator of these 27 possibilities, but for every accidental step, the first of these 27 random possibilities that work would have to be selected. I trust you can see that it’s impossible for a full-fledged book with chapters, plot, character development, foreshadowing, climax, epilogue, etc. to come about through such a process. This analogy illustrates that it’s impossible to build a complex biological machine through such an accidental step-by-step process as evolutionists have proposed.

I find this irreducible complexity argument against large-scale evolution to be quite compelling. However, it seems to have developed into a stalemate between those who reject large-scale evolution and those who affirm it. Those who reject large-scale evolution, based on this irreducible complexity argument, conclude that it’s impossible for a complex biological machine to be built one accidental haphazard step at a time whereas those who affirm large-scale evolution respond by claiming that they can conceive how this could have happened. Such individuals have proposed various ideas of how this might have happened, but of course it would be more impressive if they could actually provide empirical examples instead of conceptual models. Unfortunately, this is something they can’t provide because the process takes millions upon millions of generations. It would be so very helpful to be able to observe this process at work over many generations because then we could directly see what accidental mutations and natural selection can actually accomplish. It may surprise you to know that, in fact, we do have several such scenarios where we can observe this evolutionary process at work over millions and millions of generations.

The Edge of Evolution

In Behe’s book The Edge of Evolution he evaluates these scenarios to see what evolution actually accomplishes over millions of generations and shows empirically that random mutation does not provide the fuel necessary for large-scale evolution. The classic example of this comes from fruit fly experimentation. These flies make great test subjects for this type of research because their life span is so short that scientists can literally watch this process in action. Because they bombard the flies with radiation to increase the rate of mutations, scientists have been able to develop a clear idea of what kind of mutations can occur. 

From these experiments scientists have learned that “even though there are trillions upon trillions of possible simple mutations to an insect’s genome, all but a handful are irrelevant.”33 The reason they’re irrelevant is that they don’t aid the fruit fly at all, and most of them are extremely detrimental to its ability to survive or reproduce. They’ve observed that even in nature these same handful of mutations arise within insects as different as the “mosquito and fly because no others work. This limitation compounds the limitation noted earlier, that most mutations decrease an organism’s overall functioning—they are destructive, not constructive, even among tiny fractions of mutations that ‘work.’”34 

Thus, we can focus our attention on these few mutations that do work. It’s critically important to recognize that even these mutations don’t create new information. With the fruit flies there’s no evidence of mutations “creating new structures. Mutations merely alter existing structures.”35 How these mutations become successful, as well as the limits of their success, have become more clearly defined as scientists have studied virus mutations.   

Malaria and HIV

Scientific studies of Malaria and HIV provide us with the very best direct evidence of the power of random mutation to drive evolution. Why? Behe explained that the “reason is simple: numbers. The greater the number of organisms, the greater the chance that a lucky mutation will come along, to be grabbed by natural selection.”36 Malaria, for instance, “grows to huge population numbers—numbers that are much greater than those of mammals or other vertebrates.”37 We can watch it mutate over trillions of generations in just a few years.

Malaria is a terrible disease caused by a parasite most often transmitted by mosquitoes. On average 400,000 die every year as the result of Malaria. “The evolutionary pressure on humanity to come up with some mutational monkey wrench to counteract malaria is about as intense as it can get. If malaria were much more deadly or contagious than it is, there wouldn’t be any humanity left to worry about.”38 Malaria has been described as:

An ancient scourge of humanity; in some regions of the world malaria kills half of all children before the age of five. In the middle part of the twentieth century miracle drugs were discovered that could cure the dreaded disease, and hopes swelled that it could even be totally eradicated. But within a decade the malarial parasite evolved resistance to the drugs. New drugs were developed and thrown into the fight, but with only fleeting effect… the take-home lesson of malaria is: Evolution is relentless, brushing aside the best efforts of modern medicine.39 

On the other side of this evolutionary warfare, within humans, there is sickle cell mutation. Most people are familiar with sickle cell disease. Behe explained the difference between sickle cell mutation and sickle cell disease as follows: 

It takes two copies (one from each parent) of the mutated sickle gene to get the disease. People who have just one copy do not have the disease, but they do have resistance to malaria, and they often live when others die. 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.40

Hemoglobin is the protein in blood whose job it is to carry oxygen. It collects oxygen by binding tightly to it in the lungs and then dumps off the oxygen throughout the body where it’s needed. This requires hemoglobin to be specifically shaped and have a particular amino acid sequence. There are many genetic diseases where a single amino acid change destroys its ability to carry oxygen effectively. In sickle cell hemoglobin, for instance, one single amino acid differs from normal hemoglobin. It doesn’t significantly alter its ability to carry oxygen, but it has other profound effects. 

Sickle cell disease causes red blood cells to be shaped as sickles instead of the normal round-donut shape. This causes hemoglobin to stick to each other, one after another, until most all the hemoglobin in the cell has stuck together. They accumulate into a gelatinous mess inside each red blood cell. Eventually the stiffened, odd-shaped cells can get stuck in the narrow capillaries, much like an accidental dam of twigs and brush. This leads to extreme pain, the deterioration of body tissue due to lack of oxygen, and ultimately death. However, if these misshapen red blood cells make it to the spleen, they are there recognized as abnormal and destroyed. 

When someone inherits this mutated gene from only one of their parents, but not both, the effects are not fatal. It’s only when two carriers mate that their offspring have a one in four chance of getting the sickle cell gene from both parents and inheriting the full disease. The reason why natural selection doesn’t weed this harmful mutation out, like so many other random, accidental mutations, is because inheriting the mutation from only one parent gives a person resistance to Malaria. Inside the first person to ever have this particular mutation, a “tiny mistake happened when either the sperm or egg was made. The machinery for faithfully copying the parent’s DNA, which does an almost flawless job, slipped. Instead of an exact copy, one (one!) of the billions of the nucleotide components of the DNA was changed.”41

The DNA in that reproductive cell provided half of that person’s genetic information. When a malarial cell was injected into this person through a mosquito, it made its normal trip to the liver. As the parasite fed, the inside of the red blood cell changed. Molecular motions cause individual hemoglobin to bump into each other, but in this person they stuck together. More and more clung to each other and soon the liquid solution of the red cell gelled up. This gelatinous mass pressed against the virus and against the red blood cell membrane, distorting its shape. Before the parasite had time to anchor to the walls of a vein, the infected cell passed through the spleen, which did its job of removing damaged blood cells. It grabbed the warped cell and destroyed it along with the malaria virus hidden inside. 

When only half of a person’s hemoglobin takes the sickle form, it will not solidify into a gel on its own. It needs a further push to make it do so, a push that’s supplied by the invasion of the malarial parasite. The parasite raises the amount of acid in the cell, triggering the accumulation of the hemoglobin so only the infected cells are destroyed by the spleen. But when all the hemoglobin in a red blood cell is sickle, it does this on its own. These are the people that have the deadly, full-fledged sickle cell disease.

This mutation has “been touted by Darwinists as among the best, clearest examples of Darwinian evolution.”42 There’s no doubt that this is clearly a result of natural selection acting on random mutation. “By studying the DNA of many human populations, scientists have concluded that this particular mutation has arisen independently no more than a few times in the past ten thousand years-possibly only once.”43 The more important question is this: can advocates of large scale evolution “jump directly from this pristine example to the conclusion that all of life—the complex machinery of the cell, the human mind, and everything in between—can be explained the same way”?44 Malaria and this sickle gene mutation offer some of the best examples of Darwinian evolution in action, “but that evidence points both to what it can, and more important, what it cannot do.”45 

Over these thousands of years, the battle between humans and malaria has resulted in a stalemate. Neither side has accumulated additional mutations upon these existing ones in order to overcome the other. “The thrust and parry of human-malaria evolution did not build anything—it only destroyed things.”46 At its root the sickle gene is a harmful mutation because it hampers the normal functioning of the overall human body by causing “anemia and other detrimental effects. In happier times they would never gain a foothold in human populations. But in desperate times, when an invasion threatens the city, it can be better in the short run to burn a bridge to keep the enemy out.”47 Without the ancillary, anti-malarial effect, this normally detrimental mutation would be weeded out. This is similar to antibiotic resistance which “tends to reduce reproduction rates, so that when the antibiotic is removed, the original bacteria (the ‘wild type’ with higher reproduction rates) reemerge and again dominate the population.”48 

HIV is another excellent example because it virtually “mutates at the evolutionary speed limit—Darwinian evolution just can’t go any faster.”49 Because “there are approximately fifty million people worldwide infected with the virus, the math points to a total of about 10 (to the 20th power) copies of the virus having been produced in the past several decades.”50 Consider, with all of these generations, all of the opportunities that HIV has had to mutate and develop. 

And exactly what has all that evolution of HIV wrought? Very little. Although news stories rightly emphasize the ability of HIV to quickly develop drug resistance, and although massive publicity makes HIV seem to the public to be an evolutionary powerhouse, on a functional biochemical level the virus has been a complete stick-in-the-mud. 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.51

It’s rightly noted that HIV has an amazing ability to quickly evolve resistance to our man-made drugs. Even after all these trillions of generations, HIV is just another example of small-scale evolutionary change. “It turns out that HIV employs the same modest tricks that Malaria uses to evade drugs—mostly simple point mutations to decrease the binding of the poison to its pathogen target. For example, a change of just one amino acid at position 184 of one particular HIV enzyme causes a little bump that interferes with one drug.”52 On the other side, some humans have developed a resistance to “HIV because they burn the bridge that the virus uses to invade the cell: they have a broken copy of the gene for a coreceptor.”53 Behe summarizes the situation as follows:

Despite huge population numbers and intense selective pressure, microbes as disparate as malaria and HIV yield similar, minor, evolutionary responses. Darwinists have loudly celebrated studies of finch beaks, showing modest changes in the shapes and sizes of beaks over time, as the finches’ food supplies changed. But here we have genetic studies over thousands upon thousands of generations, of trillions upon trillions of organisms, and little biochemical significance to show for it.54

Random mutation is an adequate explanation for some features of life but not for others; its power is limited. From our best empirical evidence, the human maladies of malaria, sickle cell disease, and HIV, we have learned that “random mutation wreaks havoc on a genome. Even when it ‘helps,’ it breaks things much more easily than it makes things and acts incoherently rather than focusing on building integrated molecular systems. Random mutation does not account for the ‘mind-boggling’ systems discovered in the cell.”55 Evolution is a powerful tool of adaptation, but we have empirically observed that there’s a limit to what it can do.

Clearing a Path

There is another important point to be made about evolution which is fueled by random mutations: nature can only select for mutations that are immediately beneficial. The evolutionary process can’t look ahead towards some goal it’s trying to achieve. Therefore, evolution is correctly described as blind because it can’t envision the future so as to prepare or adjust for it. Natural selection only holds onto a random mutation if it helps within that organism’s lifetime. In other words, “evolution proceeds without plan or purpose.”56 

Though it’s been empirically demonstrated that mutations can’t originate new, complex, structural information for natural selection to grab onto, it’s still possible to imagine a scenario where enough of these beneficial accidents could accumulate over time to account for the arrival of a new complex system. Dembski insightfully noted that it’s “perhaps imaginable that wind and erosion could sculpt Mount Rushmore, but it’s not a realistic possibility.”57 Jerry Coyne and Allen Orr, who affirm large-scale evolution, agree that imagination is not enough. They wrote that “the goal of theory, however, is to determine not just whether a phenomenon is theoretically possible, but whether it is biologically reasonable—that is, whether it occurs with significant frequency under conditions that are likely to occur in nature.”58 Behe summarized the problem as follows:

A Darwinian process would have to take numerous coherent steps, a series of beneficial mutations that successively build on each other, leading to a complex outcome. In order to do so in the real world, rather than just in our imaginations, there must be a biological route to the structure that stands a reasonable chance of success in nature. In other words, variations, selection and inheritance will only work if there is also a smooth evolutionary pathway leading from biological point A to biological point B.59

Dembski concurred with this assessment when he wrote that it’s “not just that certain biological systems are so complex that we can’t imagine how they evolved by Darwinian pathways. Rather, we can show conclusively that direct Darwinian pathways are causally inadequate to bring them about and that indirect Darwinian pathways, which have always been more difficult to substantiate, are utterly without empirical support.”60

Geneticist François Jacob famously wrote that Darwinian evolution is a tinkerer and not an engineer.61 This is a fitting description because:

If Darwinism is a tinkerer, then it cannot be expected to produce coherent features where a number of separate parts act together for a clear purpose, involving more than several components. Even if someone could envision some long, convoluted, gradual route to such complexity, it is not biologically reasonable to suppose random mutation traversed it. The more coherent the system, and the more parts it contains, the more profound the problem becomes.62

While referring to the situation with Malaria and sickle cell, Behe wrote that “[s]lowing and eventually damming the flow of water doesn’t require sophisticated structures—just a lot of debris. Genetic debris can accumulate in cells, too. If it accidentally does some good, then it can be favored by natural selection.”63 Behe’s conclusion that there’s a limit, an edge, to what evolution can accomplish seems quite reasonable. He summed up his case as follows:

The structural elegance of systems such as the cilium, the functional sophistication of the pathways that construct them, and the total lack of serious Darwinian explanations all point insistently to the same conclusion: They are far past the edge of evolution. Such coherent, complex, cellular systems did not arise by random mutation and natural selection, any more than the Hoover Dam was built by the random accumulation of twigs, leaves and mud.64

Conclusion to Part 1

Charles Darwin’s ideas and assumptions may not explain all of biological life, but “from the moment they were published in 1859 all biologists have realized that they do explain a great deal.”65 This is why evolution makes sense to so many people—because there’s a lot of truth to it as I explained above. It explains much of the diversity that we see, such as the different beaks among finches, different colors among moths, different sizes among dogs, and different traits among human races. However, Darwin’s mistake was to assume that the small-scale evolutionary process he observed could be extrapolated to large-scale evolutionary change, i.e., the origin of new species. His misunderstanding is reasonable; extrapolation is a valid form of hypothesis, and he didn’t have access to the advanced scientific tools and knowledge we have today to understand the basis of offspring variations, genetics, and DNA mutations. 

As these scientific fields have developed over the last century, many scientists have recognized the difference between observed small-scale evolutionary changes and the hypothesis of large-scale evolutionary changes. Small-scale evolutionary changes and large-scale evolutionary changes are distinguished from each other by referring to them as microevolution and macroevolution. Some claim that these terms were invented by those opposed to evolution, but the following quotes will show that that’s not true.   

In 1937, Theodosius Dobzhansky noted that there was no hard evidence to connect small-scale changes within existing species (which he called “microevolution”) to the origin of new species and the large-scale changes we see in the fossil record (which he called “macroevolution”). According to Dobzhansky, “there is no way toward an understanding of the mechanisms of macroevolutionary changes, which require time on a geological scale, other than through a full comprehension of the microevolutionary processes observable within the span of a human lifetime.” He therefore concluded: “For this reason we are compelled at the present level of knowledge reluctantly to put a sign of equality between the mechanisms of macro- and microevolution, and proceeding on this assumption, to push our investigation as far ahead as this working hypothesis will permit.”66

In addition, in “1940 Berkeley geneticist Richard Goldschmidt published a book arguing that ‘the facts of microevolution do not suffice for an understanding of macroevolution.’ Goldschmidt concluded: ‘Microevolution does not lead beyond the confines of the species, and the typical products of microevolution, the geographic races, are not incipient species.’”67 For a more recent example, consider that “in 2001, biologist Sean B. Carroll wrote in Nature: ‘A long-standing issue in evolutionary biology is whether the processes observable in extant populations and species (microevolution) are sufficient to account for the larger-scale changes evident over longer periods of life’s history (macroevolution).’”68

From observing the mutations in the battle with malaria and HIV, we can conclude that random mutation is not sufficient to account for large-scale evolutionary changes. In other words, “known material mechanisms capable of causing genetic modification cannot account for the vast increases in functional information required for macroevolution.”69

In part two of this article, I’ll consider these questions: What if I’m wrong? What if macroevolution is true? Would that mean that Christianity is false?


[1] William A. Dembski and Jonathan Wells, The Design of Life: Discovering Signs of Intelligence in Biological Systems (Dallas: The Foundation for Thought and Ethics, 2008), 26.

[2] Ibid., 94.

[3] The process that took place to go from non-life to the first self-reproducing organism, which is a huge jump since self-reproduction is the most amazing and complicated feat of organisms, cannot be explained by this hypothesis because it needs self-reproduction to even begin. So the scope of this hypothesis is solely the transformation from the first self-reproducing organism to the many organisms we see in the world. It does not and cannot explain how the first self-reproducing organism came into existence, which very well may be even a larger and more difficult step than the transformation of this first self-reproducing organism to the various forms of life we see today.

[4] Ibid., 28.

[5] Michael J. Behe, The Edge of Evolution: The Search for the Limits of Darwinism (New York: Free Press, 2007), 65.

[6] Ibid., 10.

[7] Dembski, 36.

[8] Ibid., 35.

[9] Ibid., 33.

[10] Ibid., 34.

[11] Ibid., 31.

[12] Ibid., 34.

[13] Ibid., 35.

[14] Ibid., 31.

[15] Ibid., 32.

[16] Ibid.

[17] Ibid.

[18] Ibid., 43.

[19] Ibid., 32.

[20] Ibid., 51.

[21] Behe, 3.

[22] Ibid., 10.

[23] Dembski, 172.

[24] Behe, 11.

[25] Dembski, 38.

[26] Ibid.

[27] Ibid., 39.

[28] Behe, 74.

[29] Dembski, 43.

[30] Ibid., 38.

[31] Ibid.

[32] Charles Darwin, On the Origin of Species by Means of Natural Selection, or the Preservation of Favoured Races in the Struggle for Life (London: John Murray, 1859), 189.

[33] Behe, 77.

[34] Ibid.

[35] Dembski, 44.

[36] Behe, 140.

[37] Ibid., 76.

[38] Ibid., 20.

[39] Ibid., 14.

[40] Ibid., 15.

[41] Ibid., 24-25.

[42] Ibid., 12.

[43] Ibid., 26.

[44] Ibid., 29.

[45] Ibid., 13.

[46] Ibid., 42.

[47] Ibid., 34.

[48] Dembski, 39.

[49] Behe, 137.

[50] Ibid., 138.

[51] Ibid., 139.

[52] Ibid.

[53] Ibid.

[54] Ibid., 140.

[55] Ibid., 164.

[56] Dembski, 26.

[57] Ibid., 157.

[58] Behe, 103.

[59] Ibid., 5.

[60] Dembski, 160.

[61] Behe, 119.

[62] Ibid.

[63] Ibid., 81.

[64] Ibid., 102.

[65] Ibid., 64.

[66] Dembski, 102.

[67] Ibid., 103-104

[68] Ibid., 104. 

[69] Ibid., 109.


Barr, Stephen M., Modern Physics and Ancient Faith. Notre Dame, Ind.: University of Notre Dame Press, 2003.

Behe, Michael J., The Edge of Evolution: The Search for the Limits of Darwinism. New York: Free Press, 2007.

Darwin, Charles. On the Origin of Species by Means of Natural Selection, or the Preservation of Favoured Races in the Struggle for Life. London: John Murray, 1859.

Dawkins, Richard, The God Delusion. New York: Houghton Mifflin Company, 2006.

Dembski, William A. and Jonathan Wells, The Design of Life: Discovering Signs of Intelligence in Biological Systems. Dallas: The Foundation for Thought and Ethics, 2008.

Convincing Proof