Debunking Creationism: "Mutations Are NEVER Beneficial!"


Thumbnail photos: Kaden11a/Wikimedia Commons; Clker-Free-Vector-Images/Pixabay


In their attempts to undermine evolution, some creationists will argue that genetic mutations are never beneficial. As I show here, they are flat wrong about this and there are many such examples of beneficial mutations: enzymes taking on new functions; bacteria changing their size or lifestyle to avoid predation; and humans becoming completely immune from deadly illnesses. In many of these examples, the precise genetic changes that confer the benefits have been identified.

Other creationists concede that yes, beneficial mutations exist, but they occur so rarely that they couldn't possibly be responsible for any significant evolutionary changes! This too is plainly untrue, as scientific research in this area finds that anywhere from 1 to 6% of mutations are beneficial. Creationist attempts to support a much lower percentage come from deeply flawed analyses that don't reliably quantify mutations, or that don't even attempt to characterize mutations. Other creationists simply misstate what the scientific research shows in this area.

Barney Maddox makes the case for this viewpoint in an article for the Institute For Creation Research—exactly the organization I think to consult when I'm looking for trustworthy information on evolution.

You get a good taste of what they think on the subject in the "Store" section of their website, where you can purchase such books as How Darwinism Corrodes Morality by Jerry Bergman. Yes, it starts with a belief in evolution, and before you know it, you're cheating on your wife and smoking crack next to a dumpster!

The subtitle of this book is: "Darwinism, Immorality, Abortion & The Sexual Revolution." Dude, those are like my four favorite things right there!

As Barney writes,


"[Biology textbooks] . . . fail to inform students that unequivocally positive mutations are unknown to genetics, since they have never been observed (or are so rare as to be irrelevant)."


Ok, let's get the obvious out of the way first: saying that beneficial mutations have "never been observed" is different from saying that they have been observed, but they're very rare. This guy doesn't even seem to know what it is that he's arguing in favor of! "Those things that have been occasionally observed have never been observed!"

As is so often the case, creationists on this point are simply wrong about the facts. There have been many documented examples of beneficial mutations taking place in many different kinds of organisms, both in the wild and in the laboratory. I'm just gonna provide a few noteworthy examples here, but trust me when I say that a comprehensive list of every documented example simply wouldn't fit inside of a YouTube video.

In Campbell Biology, we read the following:


"One group tested whether the function of an enzyme called B-galactosidase could change over time in populations of the bacterium Escherichia coli (E. coli). B-galactosidase breaks down the disaccharide lactose into the simple sugars glucose and galactose. Using molecular techniques, the researchers introduced random mutations into E. coli genes and then tested the bacteria for their ability to break down a slightly different disaccharide (one that has the sugar fucose in place of galactose).

They selected the mutant bacteria that could do this best and exposed them to another round of mutation and selection. After seven rounds, the 'evolved' enzyme bound the new substrate several hundred times more strongly, and broke it down 10 to 20 times more quickly, than did the original enzyme.

The researchers found that six amino acids had changed in the enzyme altered in this experiment. Two of these changed amino acids were in the active site, two were nearby, and two were on the surface of the protein. This experiment and others like it strengthen the notion that a few changes can indeed alter enzyme function."

Source: p. 157, Campbell Biology, Ninth Edition. Jane B. Reece et al. 2011.


In a TalkOrigins article written by Richard Harter, we learn about another example:


"Bacteria that eat nylon . . . Well, no, they don't actually eat nylon; they eat short molecules (nylon oligomers) found in the waste waters of plants that produce nylon. They metabolize short nylon oligomers, breaking the nylon linkages with a couple of related enzymes.

Since the bonds involved aren't found in natural products, the enzymes must have arisen since the time nylon was invented (around the 1940s). It would appear this happened by new mutations in that time period. These enzymes which break down the nylon oligomers appear to have arisen by frameshift mutation from some other gene which codes for a functionally unrelated enzyme.

This adaptation has been experimentally duplicated. In the experiments, non-nylon-metabolizing strains of Pseudomonas were grown in media with nylon oligomers available as the primary food source. Within a relatively small number of generations, they developed these enzyme activities."


Think about what this means for the Christian worldview: If this bacteria keeps evolving in this direction, all of those anti-gay preachers that crossdress on weekends are gonna need a new material to make their stockings out of!

Joe Boxhorn, also on TalkOrigins, provides us with two more examples, these in response to predation:


"In this study [by Shinako et al 1990], an amotile, short (1.5 micrometer) rod-shaped bacterium was grown with the ciliate predator Cyclidium. Medium transfers occurred every seventh day. After 8 to 10 transfers long bacterial cells (up to 20 micrometers) appeared in cultures which had the ciliate. . . . They coexisted with a shorter morph. After appearance of the long form, the density of ciliates in the experimental flasks declined. Feeding experiments showed that the ciliates fed preferentially on the shorter cells.

[Example #2—or I guess #4 or 5, overall. There's so much evolution going on that I'm already starting to lose track of it all!] . . . Chlorella vulgaris is a common unicellular green alga that is used as a 'lab rat' in labs throughout the world. We've grown the same strain of it for thousands of generations on agar and in liquid culture without it losing its unicellular morphology. . . . [In Boraas et al,] steady-state unicellular C. vulgaris cultures were innoculated with the predator Ochromonas vellesiaca, a phagotrophic flagellate. Within less than 100 generations a multicellular form of the Chlorella became dominant in the culture. The alga first formed globose clusters of tens to hundreds of cells. After 10-20 generations in the presence of the flagellate, eight-celled colonies predominated. These colonies retained the eight-celled morphology indefinitely in continuous culture and when plated onto agar. The basis of the change appears to be a change in the cell wall."


For our next example of a beneficial mutation, we're gonna look no further than an article written by another creationist: Alex Williams of


"At this point Darwinists will make a lot of noise about numerous experiments which demonstrate beyond doubt that some mutations can lead to increased fitness, both in humans and in experimental populations. This is certainly true. A recent example is the discovery that a single nucleotide change in ethnic Tibetans (compared with Han Chinese) has allowed them to cope with the chronically low oxygen levels that occur on the high Tibetan plateau."


What's hilarious is that near the start of his article, this same creationist says: "Beneficial mutations are simply assumed to exist because Darwinian theory demands that they exist."

Yes, we're simply assuming the existence of those things that even you provide real-world examples of.

Can we also just stop for a moment to talk about how silly the term "Darwinist" is? It's basically this weird, attempted smear-term that makes it look like we're cultishly bowing down at the altar of Charles Darwin. Yes, he was the originator of the idea—but since he published The Origin Of Species, there's been over 150 years of work and research in this field by countless other scientists. So let's stop pretending like every idea and every scrap of evidence in the field comes from Charles Darwin alone, because that's simply not the case.

And why don't creationists do this with other scientific fields? Why aren't we called "James Huttonists" for accepting the findings of geology? When I say the universe is billions of years old, why am I never smeared as an "Edwin Hubblist"?

It's important to note that in several of the examples I provided, we're not just inferring or assuming that a beneficial mutation has taken place; the exact genetic changes which confer these benefits have been identified—flatly contradicting Barney's claim that "unequivocally positive mutations are unknown to genetics, since they have never been observed."

They have been observed—and this is something that even your fellow creationists can prove to you.

By the way, I don't really care much about credentials—because at the end of the day it's your arguments that matter—but I did find it kind of funny to learn that Barney Maddox, whose credentials are proudly hoisted in front of us by the Institute For Creation Research, is a urology specialist out of Cleburne, Texas. Yeah, if I have any questions about my urine stream, I'll give you a call.

And I have to ask, if humans truly are the perfect creation of God, why would we even have, as an occupation, medical doctors like Barney who specialize in diseased human bodies? Why not just create us without all of these life-ruining ailments? It's a bit puzzling that Barney has the worldview he does because he's basically an expert on the many ways that part of our body has been imperfectly created by God.

The next step creationists will take is to argue that, ok, beneficial mutations do take place—but they're so incredibly rare that there's no way they could produce significant evolutionary changes over time! All of the numbers they use to support this claim come from deeply flawed analyses.

One statistic is from John C. Sanford's creationist propaganda book Genetic Entropy & The Mystery Of The Genome:


"Bergman (2004) has studied the topic of beneficial mutations. Among other things, he did a simple literature search via Biological Abstracts and Medline. He found 453,732 'mutation' hits, but among these only 186 mentioned the word 'beneficial' (about 4 in 10,000)."

Source: p. 26. Genetic Entropy & The Mystery Of The Genome, by John C. Sanford. 2005.


So basically, what this guy did was ask: what percent of papers that include the word "mutation" also include the word "beneficial"? And from this, creationists seem to think they're arrived at a reliable estimate of what percentage of mutations are beneficial: 0.04% of them.

Think about how incredibly faulty this analysis is. The word "mutation" could be used in countless contexts that wouldn't involve classifying one unique genetic mutation as either harmful, neutral, or beneficial. The word "mutation" could plausibly be used in papers about speciation, cell reproduction, the testing of a medicine, the milking of cows, crop distributions around the world, gender roles in the X-men movies—literally any subject that relates to biology in some way.

I really doubt that this guy took the time to read all 453,000 papers—or even just the abstracts to ascertain their contents—because even if it just took one minute per paper, this would've taken him over 7,000 hours! Think about all of the scripture you could've read with that time! With 7,000 hours you could've almost made it through the "begats" by now!

I would also add that even if we assumed every usage of the word "mutation" was in the context of a paper that ultimately did focus specifically on genetic mutations, how would this analysis account for overlap where the same mutation is talked about in hundreds or even thousands of different papers? For example, you could have 10,000 papers written about a genetic disease where, at one point or another, they use the word "mutation" to describe how this disease initially came about. Even though all 10,000 papers would be about one particular mutation—say, the one that causes sickle cell disease—according to this analysis, that would be counted as 10,000 hits in the "not a beneficial mutation" ledger.

The assumption being made here is that any paper that includes the word "mutation" is actively categorizing one particular unique mutation as either beneficial, harmful, or neutral. This assumption makes no sense given the countless different ways the subject of mutation could be brought up as well as the repeat discussion of subjects in the literature. These numbers provide us with no meaningful indication whatsoever of what percent of mutations are beneficial.

Alex Williams, in his article, provides another completely useless analysis on this point:


"The Human Gene Mutation Database currently contains records of more than 141,000 mutations. . . A September 2012 summary reported that of these about 6,000 constitute 'disease associated' and 'functional' polymorphisms (different versions of a DNA sequence). Notice that the classification recognizes just two categories—mutations are either 'disease associated' or they are 'functional'. There is no category labelled 'beneficial'."


"There is no category labelled 'beneficial'", he tells us. The implied conclusion is that since none of these 141,000 mutations are beneficial, the occurrence of beneficial mutations must therefore be extremely rare.

There's just one problem with this conclusion: All of the mutations compiled in this database are related to human disease! Just go to their homepage and you'll read that: "The Human Gene Mutation Database (HGMD®) represents an attempt to collate all known (published) gene lesions responsible for human inherited disease."

Even the reference Alex Williams provides us with on this point makes this clear in the very first sentence!


"The Human Gene Mutation Database (HGMD) constitutes a comprehensive core collection of data on germ-line mutations in nuclear genes underlying or associated with human inherited disease."


So you could go to the Haemophilia A section, for example, and look for every recorded instance of a person having a small deletion mutation, or a missense mutation, in the genes associated with that disease. That is the kind of thing that this database collects, so I wouldn't exactly expect it to be brimming with examples of beneficial mutations!

And again, the same problem from earlier rears its ugly head: the very genetic diseases tracked on this website must have been a part of God's creation plan for us. What kind of sick monster would intentionally create people with a disease like haemophilia? I would genuinely like to hear a creationist try to wriggle their way out of this uncomfortable position.

"Uh, hemophilia obviously allows people to have a greater spiritual connection with God! You know who else bled a lot? Jesus, during his crucifixion."

No, let's be clear: The diseases in this database aren't the result of poor lifestyle choices or dietary habits; these are genetic diseases. This entire database is a shining testimony of God's failure during creation.

And even if we do focus on the narrow category of human disease, you can still find several examples of beneficial mutations that have taken place.

Adam Lee writes the following in a BigThink article:


"All humans have a gene for a protein called Apolipoprotein AI, which is part of the system that transports cholesterol through the bloodstream. Apo-AI is one of the HDLs, already known to be beneficial because they remove cholesterol from artery walls.

But a small community in Italy is known to have a mutant version of this protein, named Apolipoprotein AI-Milano, or Apo-AIM for short. Apo-AIM is even more effective than Apo-AI at removing cholesterol from cells and dissolving arterial plaques, and additionally functions as an antioxidant, preventing some of the damage from inflammation that normally occurs in arteriosclerosis. People with the Apo-AIM gene have significantly lower levels of risk than the general population for heart attack and stroke.

. . . a different mutation, in a gene called PCSK9 . . . has a similar effect. People with this mutation have as much as an 88% lower risk of heart disease."


Sarah Williams provides another example in PNAS:


"One percent of Northern Europeans . . . are now known to carry a mutation in a gene called CCR-5 that renders a cellular receptor defective and confers total immunity from HIV infection."


Combine all three of these mutations, and wow, you could start doing whatever you wanted!: having orgies, eating cheesburgers all day—whatever, man!

You're like: "Yes, I could... start doing those things..."

So you can look at this subject from any angle you want to, and the creationist is always going to lose.

Another attempt at supporting the rarity of beneficial mutations is made in an article:


"Evolutionists often speak in generalities about beneficial mutations. They may be rare, we are assured, but they happen. . . . All right, we have some data to look at. We can put a number to the frequency of beneficial mutations in a large sample. The number is zero.

Nature just published results of the Exome Aggregation Consortium (ExAC), the largest survey of human genes to date. (An 'exome' is the portion of the genome that codes for proteins.) The exomes from 60,706 individuals from a variety of ethnic groups have been collected and analyzed. If we multiply 60,000 people by the 20,000 genes in the human genome (the lowest estimate), we get a minimum of 1.2 billion genes that have been examined by ExAC for variants. That sounds like a pretty good sample size for scrutinizing some of those beneficial variations that Darwin said his law of natural selection could add up and preserve.

Out of this high ratio of variants (one in eight bases shows variation, they said), there should be some proportion, even if small, that improves fitness. But we search the paper in vain for any mention of beneficial mutations. There’s plenty of talk about disease. The authors only mention 'neutral' variants twice. But there are no mentions of beneficial mutations. You can't find one instance of any of these words: benefit, beneficial, fitness, advantage . . . improvement, innovation, invention, or positive selection."


Yet again, this is another abortive analysis that doesn't support the conclusion reached by the creationist. They seem to misunderstand what was even done in this research and how one goes about determining whether a mutation is beneficial.

There is no way to sequence an entire genome and then perform some sort of "Control + F" search function that will identify every beneficial mutation that has taken place. I wish it was that easy to search a genetic database because that way we could finally discover what's wrong with the creationist brain!

It's not like you can see, just from your sequencing, that one base pair of an enzyme's gene has changed from an A to a G, and be like "Ahh! That means the active site of this enzyme will match up with its target molecule 10% better than its previous gene!"

No, you ascertain whether mutations are beneficial or not by observing the actual impact of that mutation on that organism relative to other members of the species without the mutation.

"Haha! They didn't identify a single beneficial mutation!"

Yeah, well maybe that's because they weren't looking for them? This was a gene survey—not an analysis of what percentage of mutations were harmful, neutral, or beneficial. The creationist is simply mistaking this survey for a completely different type of scientific of analysis—and then using their misunderstanding as their basis for declaring victory. You can hardly criticize these researchers for not finding something that they didn't even look for.

Barney Maddox goes on to claim that efforts to bring about positive mutations in the laboratory have yielded not a single convincing example:


"In the twentieth century many genetic researchers tried to 'accelerate evolution' by increasing mutation rates. This can be accomplished with ionizing radiation, like x-rays, or chemical mutagens. Researchers gave plants and fruit flies very high doses of radiation or other mutagens in hopes that new life forms, or at least improved organs, would result. Decades of this type of research resulted in repeated failure. Every mutation observed was deleterious to the organisms' survival."


It's ironic that this guy's a urine specialist, because he is completely full of shit. When he says that every observed mutation in mutagenesis experiments has been deleterious, this is just a flat-out lie. Many of these experiments haven't just detected beneficial mutations, but can outright quantify what percent of mutations are beneficial.

Take a 2004 paper by Sanjuán et al, for example:


"The goal of this work is to . . . [create] a collection of single-nucleotide substitution mutants by site-directed mutagenesis on an infectious [vesicular stomatitis virus] cDNA. Then we measure fitness for each member of the collection to infer the statistical properties of the distribution of mutational fitness effects.

. . . We recovered infectious particles for 67 of 91 mutants. . . . Overall, 31 mutations had no significant fitness effect, 32 were deleterious, and 4 were beneficial."

Source: "The distribution of fitness effects caused by single-nucleotide substitutions in an RNA virus," by Rafael Sanjuán et al. PNAS. June 1, 2004, Vol 101, No 22. 8396–8401.


So in this experiment, 4 out of 67 mutations were beneficial—or 6% of them. Here is the key takeaway from this research: if I smoke a pack of cigarettes every single day, there's a 6% chance I'll become a superhero.

How about a 2010 study by Joan Peris et al?


"[We used] site-directed mutagenesis to engineer single mutations, an approach particularly suited for viruses due to their small genomes. Here, we used this technique to measure the fitness effect of 100 single-nucleotide substitutions in the bacteriophage f1, a filamentous single-strand DNA virus.

. . . We found that 2 of the 100 mutations examined were significantly beneficial . . . the actual fraction might be higher, since mutations of small effect are difficult to detect."


Lília Perfeito et al, 2007:


"We allowed populations of E. coli to adapt to a given laboratory environment for 1000 generations and followed the allelic distribution of the microsatellite at periodic intervals

. . . Given the estimates for the overall mutation rate in E. coli and its genomic deleterious mutation rate, our estimate of [the beneficial mutation rate] implies that 1 in 150 newly arising mutations is beneficial and that 1 in 10 fitness-affecting mutations increases the fitness of the individual carrying it."

Source: "Adaptive Mutations in Bacteria: High Rate and Small Effects," by Lília Perfeito et al. Science. 317, 813, 2007.


That's an interesting way of quantifying it: Because so many mutations are gonna be neutral and have no effect on the fitness of the organism, Perfeito et al ask what percent of fitness-affecting mutations are beneficial—and they arrive at a number of 10%. If you look at the numbers from that Sanjuán et al paper in this way, you arrive at a similar number: 11% of fitness-affecting genes were beneficial.

Looking at all mutations including those that are neutral, from these three studies, you find that anywhere from 0.7%, 2%, or 6% of mutations are beneficial. Compare the actual scientific data on this question against the bold, ignorant statement made by Barney Maddox:


". . . unequivocally positive mutations are unknown to genetics, since they have never been observed (or are so rare as to be irrelevant)."


According to these studies, 1–6% of mutations are beneficial—so you can hardly describe them as "so rare as to be irrelevant." These are the sort of numbers you arrive at when you perform actual scientific analyses on this question—and not the sort of junk science, data misinterpretations that creationists talk about.

Recall also that Maddox said: "Every mutation observed [in these mutagenesis experiments] was deleterious to the organisms' survival." These studies that I just presented—two of which were publicly available at the time he wrote his article—plainly refute this statement.

One more study in this area by MacLean et al is worth mentioning:


"We selected 288 populations initiated by three different isogenic clones of P. aeruginosa PAO1 carrying missense mutations in rpoB (A455T, A455G, or C1550T) that confer low levels of resistance to [the antibiotic] rifampicin in culture medium supplemented with a high dose of rifampicin.

The response to selection in this experiment was very rapid and uniform: After 1 round of selection, genotypes with beneficial mutations conferring high levels of rifampicin resistance were present at a frequency .1% in only 5% of selection lines, but after two rounds of selection, genotypes carrying beneficial mutations were present at a frequency of .1% in 98% of selection lines.

After four rounds of selection, we isolated a single randomly chosen clone from each selection line. . . . We identified a total of 36 unique beneficial mutations across the three genetic backgrounds, all of which are nonsynonymous."


The reason this study is so noteworthy is that in completely separated populations—after just four rounds of selection—mutations that provided similar benefits to the different populations arose independently on multiple occasions. This is a very clear indication that if the environmental pressure put upon an organism is strong enough, beneficial mutations that arise will be selected for and will become prominent in those populations. And if the very same kind of mutation that provides a very similar, specific benefit arises multiple times over, this is further proof that such beneficial mutations are not at all the astronomically unlikely events that creationists make them out to be.

Also keep in mind the population size of experiments like this. While yes, very large numbers of bacteria can exist on the small agar plates used in the laboratory, out in the real world, you're gonna have population sizes millions of times higher than this, growing on surface areas millions of times larger than those provided in the laboratory. So when you have many more organisms undergoing mutations, it naturally follows that more beneficial mutations will arise and spread.

Obviously researchers are dealing with bacteria and viruses because of their short replication times and the large numbers that can be grown in the lab, but there's absolutely no reason to believe that a similar selective process wouldn't be taking place in larger and more complex organisms, as well. The rate of change would just happen at a slower pace, given their longer life cycles.

In their never-ending retreat against the facts, creationists will concede, yes, beneficial mutations do take place, and yes, you can point to studies that support this position—but the types of mutations that are called beneficial might not be so beneficial after all!

Barney Maddox makes this argument about antibiotic resistance:


"Virtually all the 'beneficial mutations' known are only equivocally beneficial, not unequivocally beneficial. In bacteria, several mutations in cell wall proteins may deform the proteins enough so that antibiotics cannot bind to the mutant bacteria. This creates bacterial resistance to that antibiotic. Does this support evolutionary genetic theory? No, since the mutant bacteria do not survive as well in the wild as the native (non-mutant) bacteria. That is, the resistant (mutant) bacteria will only do well in an artificial situation, where it is placed in a culture medium with the antibiotic. Only then can it overgrow at the expense of the native bacteria. In the wild, the native bacteria are always more vigorous than the mutant bacteria."


Here's a good rule of thumb: Whenever a creationist makes a concrete, testable, statement of fact, they're probably very wrong. Never take what they say at face value and always investigate their claims, because whenever they present you with what seems like a scientific fact, it's probably the exact opposite of what the science actually shows. This example is no exception.

He claims that "the mutant . . . bacteria do not survive as well in the wild as the . . . (non-mutant) bacteria. . . . In the wild, the native bacteria are always more vigorous than the mutant bacteria."

Anita Melnyk et al take a close look at this subject in a 2015 review of theirs. I'm gonna remove their 30,000 references in the quotes I provide just to make things more aesthetically pleasing, but every one of these claims is supported by scientific evidence. As they write,


"In this review, we performed a meta-analysis to investigate the fitness costs associated with single mutational events that confer resistance. Generally, these mutations were costly, although several drug classes and species of bacteria on average did not show a cost.

Clinical studies have shown that in some cases, resistant bacteria remained abundant in the population or even increased in frequency despite the absence of drug. . . . the fitness costs incurred by resistance mutations may be compensated by second-site mutations that increase fitness without compromising resistance. Such compensatory evolution has been observed in both in vitro, in vivo, and in clinical studies.

. . . the pleiotropic costs of resistance among mutations may [also] be so highly variable as to sometimes include 'no-cost' mutations, those that have fitness indistinguishable from (or even greater than) their antibiotic-sensitive ancestor in the absence of antibiotic.

. . . the literature contains a number of reports of putatively cost-free mutations, including streptomycin resistance in the rpsL locus of Mycobacterium smegmatis, isoniazid resistance in katG of Mycobacterium tuberculosis using a mouse model and quinolone resistance in gyrA and parC of Streptococcus pneumoniae."


So while yes, there are cases where the resistant strains do suffer fitness reductions in other areas relative to non-resistant strains, there are plenty of other cases where their fitness is the same or even greater than the fitness of non-resistant strains in those same areas.

Set aside the fact that he's just factually wrong on this point, and you'll see that there's another problem with his analysis. This dichotomy that he presents us with doesn't match up with the way the world actually is. He frames it as if resistant bacteria are only at a fitness advantage in controlled, laboratory environments that don't at all reflect bacterial competition in the real world. He seems to forget that outside of the laboratory, antibiotics of one form or another are widely used in many different contexts, whether we're talking about the treatment of illness, the housing of livestock, or the production of food.

It's also pretty widely accepted that antibiotics are overused in this country—and I'm sure Maddox himself is prescribing them almost every single day through his work as an MD!

Maddox: "Alright, I'm gonna go ahead and write you a 10-day prescription for amoxicillin and you should be all set."

"What? I'm not even here for a doctor visit; I'm just the Jimmy John's guy delivering your lunch!"

Antibiotics do exist in the real world—not just the laboratory. So whenever a population of bacteria finds itself in an environment where antibiotics are present, it will be at a fitness advantage relative to non-resistant strains. It'll continue to survive and reproduce whereas non-resistant strains will be quickly killed off.

Whether a given mutation is advantageous or not depends entirely upon the environment that an organism finds itself in. Let's say the color of a beetle changes from green to black. Is this a beneficial mutation? It totally depends on his environment. If he lives in the forest among bright-green plant matter, changing to black will make him more visible to predators—and it'll thus be a harmful mutation. But if he lives on patches of dark volcanic rock, the black coloration will help him blend in and avoid predation.

Mutations are context-dependent, and it thus wouldn't make sense to just broadly dismiss an entire category of mutation that in some contexts, reduces overall fitness—because in other contexts, they would enhance fitness.

This is basically what the creationist is arguing: "This mutation is only beneficial in environments where the mutation is beneficial!"

Yeah, that's kind of how evolution works!

He's also overlooking the fact that even if certain observed evolutionary changes are only advantageous in a lab environment, such experiments are nonetheless demonstrating the general evolutionary process that takes place out in the real world! The exact same mechanisms would be operative in the wild, so there's no reason to believe that evolution would take place only in the laboratory.

Barney makes another argument that's almost embarrassingly absurd:


"The recent decoding of the human genome has allowed scientists to determine that cystic fibrosis is caused by a random change of three nucleotides in a gene that codes for a 1480-amino acid-long ion transport protein. The human genome has three billion nucleotides, or base pairs, in the DNA. Since a random change of three nucleotides in a three-billion-part genome is fatal . . . how is it remotely possibly that a chimp could be the evolutionary cousin of a human? The lowest estimate of the genetic differences between our DNA and that of chimps is at least 50 million nucleotides."


The simple answer to this challenge is that not all mutations are equal. Some are harmful; some have no fitness effect whatsoever; others are beneficial.

He seems to be making the classic mistake of assuming that evolution is an entirely random process—so how could this difference of 50 million nucleotides not have introduced an enormous amount of harm into the organisms? That's because the nucleotide mutations that took place either didn't affect the organism's fitness or provided a benefit—and that's why that particular lineage survived and passed on its genes. Any mutations in that population that were harmful would've put those organisms at a reproductive and survivalistic disadvantage relative to the other members of its population, and its particular set of genes therefore would not have been passed down.

The answer to his question can be encapsulated in a single word: selection. Yes, the location and impact of the mutations themselves would be random, but the selective process is not random: it favors organisms with good genes and disfavors the ones with bad genes.

His argument would be analogous to talking to an architect or a structural engineer, and saying: "Look, if I make this one particular change to the design of the building, the entire thing would collapse! So how could these 200 changes that you're proposing not cause it collapse 200 times over!?"

"Uh, it's because the changes I'm making would strengthen and improve the building—not degrade its structural integrity."

The same concept applies to the divergence between humans and chimps.

And as a matter of fact, I was actually at the zoo the other day and when a chimp heard this argument, he was like "Ok, that's just fucking ridiculous."

I was like: "What the fuck?! I didn't know chimps could talk!"

He's like: "Yeah bro, it's called evolution. Ever heard of it before? What are you, some kind of fuckin' retard or something?"

I'm like: "Whoah, man, relax! I'm on your side here."

He's like: "Sorry, I just... get really frustrated sometimes. Being pent up here in this cage all day, it really taxes the mind. Anyway, if you'll excuse me, I need to get back to swinging from branches and throwing feces at people."

In a similar vein, Georgia Purdom, in an Answers In Genesis article, writes the following:


"But even if there were a clearly beneficial mutation, this would by no means 'prove' the mechanism for evolution (for one thing, beneficial, information-gaining mutations would have to be a regularly occurring phenomenon and would have to 'build' on previous mutations so as not to be 'undone' and to keep the evolution going 'uphill')."


Yes, if only there was some process whereby this occurred naturally, almost as if there was some form of selection going on!

Apparently without even knowing it, Georgia is basically describing the process of natural selection here. Exactly the thing she says needs to take place does take place.

A beneficial mutation arises in an organism, allowing it to somehow outcompete other members of the species, pass down its genes more often, ultimately sweeping that gene to predominance and making it the new norm in that species. Then another beneficial mutation arises, and it too eventually becomes the norm. Then the same thing happens with another mutation, and another, and another, until eventually, you reach the point where the organism is a human being doubting the existence of the very process that led to them being born in the first place.

To recap the key points made here, beneficial mutations do take place in organisms—and they take place at a rate more than sufficient to drive evolutionary change. Whether we're talking about enzyme activity, antibiotic resistance, or disease immunity, there are many available examples of beneficial mutations that have been observed—something that even some creationists will agree with.

The claim that mutations like antibiotic resistance are only beneficial in the lab doesn't match up with the facts, as many such mutant organisms have a comparable or even greater fitness than those without the mutations. Beneficial mutations can accumulate over time via natural selection, and creationist attempts to provide data on this question depend upon horribly flawed analyses.

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