The (In)adequacy of Darwinian Evolution

Jason Dulle

Years ago I was discussing evolution with a co-worker.  I asked her if she thought evolution was true.  She heartily replied, “Yes, I do.”  When I asked, “Why do you think it is true?”, she responded, “I’ll have to get back to you on that.”  While her honesty was atypical, her posture was not.  Many people accept Darwin’s theory of evolution without a sufficient understanding of the theory, and without sufficient evidence.  As Michael Behe once quipped, most people’s knowledge of evolution extends little beyond that of the car decal depicting a fish with feet.1 

In my experience, the reason most people accept Darwin’s theory is because it is the scientific consensus.  They reason that scientists base their claims on the evidence, so if most scientists believe in evolution, it follows that the evidence for evolution must be compelling.  What they fail to understand is that scientists, like everyone else, bring certain biases and philosophical perspectives to the evidence.  Like the proverbial tail that wags the dog, sometimes their conclusions are driven more by their philosophical assumptions than by the empirical evidence itself.  Such is the case when it comes to Darwinian evolution.  While experimental evidence has demonstrated that natural selection working on random mutation can account for trivial changes within species ­­– such as the size of finch beaks and antibiotic resistance in bacteria ­– there is no evidence that Darwin’s mechanism is sufficient to create new biological information and novel biological systems, and hence it cannot account for the proliferation of species as Darwin suggested.  Indeed, recent experimental evidence disconfirms the notion.

What Needs to be Explained

To properly evaluate Darwin’s theory of the evolution of life we must first clarify what is meant by “evolution.”  In its most basic sense evolution refers to small biological changes within a species over time.  Called “microevolution,” or the special theory of evolution, this definition of evolution is relatively uncontroversial and has been empirically confirmed (e.g. drug resistance in bacteria, changes in the size of finch beaks, etc.).  Evolution can also refer to large-scale biological changes2 that, over time, transform one species into another into another ad infinitum.  This kind of evolution is called macroevolution, or the general theory of evolution.  Darwin’s theory entails this latter definition, and thus proof for his theory requires evidence that there are no natural limits to the amount of biological variation an organism can undergo.

Have Darwinists met their burden of proof?  No.  To date, no evidence for macroevolution has been provided.  Darwinists routinely offer the evidence for microevolution as if that is evidence for macroevolution, but this is a methodologically illegitimate extrapolation from the evidence.  Evidence for microevolution is just that: evidence for microevolution.  It is not, in itself, evidence for macroevolution.  To be sure, the reality of microevolution makes macroevolution a plausible concept because it proves organisms are capable of experiencing biological change of some sort, but more than plausibility is required if we are to take Darwinism seriously.  Minimally, Darwinists need to offer (1) empirical proof that there are no natural limits to genetic change, (2) a detailed biological pathway for the transition from one organism to another, as well as (3) evidence that this pathway could reasonably be traversed given the amount of time available.  Without such a demonstration, there is no reason to think macroevolution is anything more than an unsubstantiated hypothesis. 

What does the evidence reveal?  It strongly suggests there is a natural limit to the amount of variation organisms can undergo before they reach an evolutionary ceiling.  As Gilbert, Opitz, and Raff wrote:

The Modern Synthesis is a remarkable achievement. However, starting in the 1970s, many biologists began questioning its adequacy in explaining evolution. Genetics might be adequate for explaining microevolution, but microevolutionary changes in gene frequency were not seen as able to turn a reptile into a mammal or to convert a fish into an amphibian. Microevolution looks at adaptations that concern only the survival of the fittest, not the arrival of the fittest. As Goodwin (1995) points out, “the origin of species—Darwin's problem—remains unsolved.”3

Everything we know about organisms tells us they are more like balloons than Play-doh: They are capable of experiencing a range of change, but only within prescribed limits.  It would be foolish to assume that because we can inflate a balloon to the size of a basketball, given enough time it could be inflated to the size of a planet.  Likewise, it is foolish to think that just because an organism is capable of undergoing small biological changes, given enough time it will become an entirely different organism altogether.  Balloons and DNA are designed with a measure of elasticity, but both have a breaking point beyond which no further change is possible.  While beak sizes may change within a population of finches during seasons of drought, there is no empirical evidence demonstrating that finches can evolve into squirrels given enough time.  The genetic evidence is overwhelmingly in favor of the conclusion that there are natural limits to genetic variability.  And if there are natural limits to genetic variability, Darwinism is proven false.

The Origin of Biological Information

Point Mutations

If macroevolution occurs in biological systems, it must do so at the biochemical level.  Additional genomic information is needed to build the new proteins and biological systems required for large-scale changes.  Where does the new biological information come from?  Mutations?  No.  Point mutations, such as insertions, inversions, or substitutions of nucleotides in existing genes cannot increase the information content of DNA even if they occur in protein-coding regions, and even if the mutations are beneficial to the organism.  At best they can only replace existing information/function with different information/function, so that the overall information content is preserved.4  Macroevolution requires a net increase of biological information, not just a change in existing information. 

The origination of new genetic information requires new proteins, each of which requires hundreds of additional nucleotides arranged in a highly specified order.  How likely is it that chance processes can get the job done?  Next to none!  The chances of producing a functional amino acid sequence of a mere 150 nucleotide bases (which would sequence one of the smallest proteins) is 1 in 10164.5 To put this number in perspective, consider that there have only been 10139 events in the entire universe since the Big Bang.6  Even if every event in the history of the universe was devoted to building a single functional protein, the number of sequences produced thus far would be less than 1 out of a trillion trillion of the total number of events needed to give it even a 50% chance of success!  A reasonable person must conclude, then, that it is beyond the reach of chance to create even the smallest amount of new biological information in an organism.  Add to this the fact that many new proteins are needed to produce new biological systems, and the scenario becomes all the more fantastical.  If chance alone cannot produce the gene for even one protein—yet alone many—macroevolution becomes impossible. 

Gene Duplication

While single point mutations cannot get the job done, what about whole gene duplication (when a gene is copied twice, thus becoming two identical genes)?  Can this account for new biological information?  No.  The reason is simple: Duplicating a gene does not increase the net information content of the cell, but merely repeats existing information.  There is another reason for thinking gene duplication cannot account for new biological information: Duplicating a gene does not increase the net information content of the cell, but merely repeats existing information.  Do you want more proof?  Here’s a third reason: Duplicating a gene does not increase the net information content of the cell, but merely repeats existing information. 

Surely you just said to yourself, “That’s not three reasons, but one.  You simply repeated yourself three times.”  Exactly!  That’s the point.  Duplicating existing information cannot produce new information.  Just as saying, “duplicating a gene does not increase the net information content of the cell” three times does not triple the information content of the sentence, duplicating a gene cannot increase the information content of the cell.  Gene duplication cannot help an organism perform some new function.  Trying to get new biological information/function by duplicating an existing gene is like thinking you can obtain an engine for your car by making a second steering wheel!

Gene Duplication + Point Mutations

While neither gene duplication nor point mutations can independently increase the information content of DNA, could they do so together?  Some suggest that new information could be gained by gene duplication followed by numerous single point mutations over a long period of time, so that eventually the duplicated gene spells out a different biological message than the original. 

There are some examples in which it is likely that gene duplication followed by point mutations has resulted in a functional gene that differs from the parent gene: e.g. the two gamma-globin coding regions on human chromosome 11.  The second gamma-globin gene probably resulted from a duplication of a single gamma-globin gene, followed by a single point mutation.  It should be noted, however, that only one codon experienced change, no new biological systems were produced, and the function of the second gamma-globin gene differs little from its parent.7  While this is an important biological change, it is impotent to advance macroevolutionary change.

If we are to believe gene duplication followed by point mutations is capable of producing the raw materials for genuine biological innovation, minimally we need to know if the cell is capable of producing enough duplicated genes.  Douglas Futuyma estimates that the gene duplication rate is “about 0.01 duplication[s] per gene per million years.”8  That means it would take 100 million year to duplicate any given gene.  If an organism requires multiple copies of the same gene to produce an adaptable change, its evolution will be extremely slow.  For example, the Antarctic eelpout fish required 30 copies of an anti-freeze gene to survive the icy waters of the Antarctic Ocean.  According to evolutionists the Antarctic eelpout would have had to have experienced all 30 duplications in a period of less than 50 million years.  And yet given Futuyma’s calculations, we could only expect that many duplications after 3 billion years!

The real question is whether gene duplication followed by point mutations is capable of increasing the biological information of an organism and creating new biological systems.  There are numerous reasons to think the answer to these questions is a resounding no.  It is highly unlikely that all point mutations will be beneficial.  Consider something as simple as HTML code.  If one randomly inserts, inverts, and deletes various characters in the code, what are the chances that every change will be beneficial?  The chances are extremely low.  The chances are overwhelmingly greater that most changes will be deleterious to the integrity and function of the code.  Likewise, as soon as one or more harmful mutations accumulate in a critical region of the gene, the gene will either cease to function or function sub-optimally, affecting the organism’s fitness.  And because energy is required to preserve this broken gene in subsequent generations, the organism’s overall fitness will decrease. 

But what if – by chance – every mutation was a beneficial one?  Over time, couldn’t the gene evolve to form new genetic information?  Apart from the extremely unlikely possibility that the duplicate gene would experience beneficial – and only beneficial mutations – is it reasonable to think new genetic information could be gained through such a process?  No, because the gene would need to remain functional throughout the evolutionary process (i.e. it must always convey a biologically functional message) if it is to provide a survival advantage to the organism nature can select for.  How could this be done by changing one nucleotide at a time?  While small amounts of information could conceivably maintain function while undergoing slight, successive evolutionary changes, it is inconceivable that the same could happen for large amounts of biological information.  For example, we could evolve WORD into GENE one letter at a time and preserve meaning throughout the process:


But what if we had to evolve “gene duplication does not provide additional genetic information” into “we have to consider the fact that double point mutations are highly improbable” one letter at a time?  How could the sentence retain meaning at every step of the evolutionary process?  It is impossible, and my analogy only contains 66 characters.  Most genes contain hundreds of genetic characters (nucleotides)!  And yet for macroevolution to occur, this process would need to repeat itself millions of times over. 

On a purely conceptual level alone, it seems inconceivable that random mutations could be responsible for macroevolutionary changes in organisms.  Ultimately, however, it is the empirical data that must decide the matter.  Joseph Bozorgmeh summarizes the empirical data in the abstract of his paper “Is gene duplication a viable explanation for the origination of biological information and complexity?”:

All life depends on the biological information encoded in DNA with which to synthesize and regulate various peptide sequences required by an organism's cells. Hence, an evolutionary model accounting for the diversity of life needs to demonstrate how novel exonic regions that code for distinctly different functions can emerge. Natural selection tends to conserve the basic functionality, sequence, and size of genes and, although beneficial and adaptive changes are possible, these serve only to improve or adjust the existing type. However, gene duplication allows for a respite in selection and so can provide a molecular substrate for the development of biochemical innovation. Reference is made here to several well-known examples of gene duplication, and the major means of resulting evolutionary divergence, to examine the plausibility of this assumption. The totality of the evidence reveals that, although duplication can and does facilitate important adaptations by tinkering with existing compounds, molecular evolution is nonetheless constrained in each and every case. Therefore, although the process of gene duplication and subsequent random mutation has certainly contributed to the size and diversity of the genome, it is alone insufficient in explaining the origination of the highly complex information pertinent to the essential functioning of living organisms.9

In the body of the paper he writes:

The various postduplication mechanisms entailing random mutations and recombinations considered were observed to tweak, tinker, copy, cut, divide, and shuffle existing genetic information around, but fell short of generating genuinely distinct and entirely novel functionality.  Contrary to Darwin’s view of the plasticity of biological features, successive modification and selection in genes does indeed appear to have real and inherent limits: it can serve to alter the sequence, size, and function of a gene to an extent, but this almost always amounts to a variation on the same theme—as with RNASE1B in colobine monkeys.  The conservation of all-important motifs within gene families, such as the homeobox or the MADS-box motif, attests to the fact that gene duplication results in the copying and preservation of biological information, and not its transformation as something original.10

Having determined that gene duplication cannot account for biological novelty, we now turn our attention to what scientific research has revealed about the power of random mutation to create biological novelties.  How much biological change can it account for?

The Creative Power of Mutations Tested and Found Wanting

The heart of the neo-Darwinian synthesis is that evolution advances via the process of natural selection working on random mutations (RM+NS).  Natural selection itself lacks any creative power – it only eliminates what doesn’t work.  Eliminating the unfit, however, does nothing to “explain the origin of the fit”!11  The burden falls entirely on RM to create the biological novelties required by Darwinism to drive evolution forward.  It must be asked, then, whether RM has the creative power required by Darwin’s theory.  Can RM produce the new biological information necessary to drive evolution forward and explain the diversification of all life?  What exactly can RM do?  Michael Behe evaluated these question in-depth in his book, The Edge of Evolution.  Much of wat follows is a summary of Behe’s argument.

When the neo-Darwinian synthesis was set forth some 70 years ago, answers to these questions could not be ascertained.  While the theory was plausible on a conceptual level, there was no way of testing it directly on an empirical level.  Over the last 30 years, however, we have been able to observe both the power and limits of RM+NS at the biological level, and are now in a good position to evaluate the power of RM+NS.  What have we discovered?  We discovered that while RM can produce variability within an organism, it is not capable of producing the kind of changes required by Darwin’s theory.  RM is severely limited in what it can accomplish. 

A Lack of Building Materials

If we are to believe the process of natural selection working on random mutations is capable of creating novel biological information and structures, at least two conditions must be demonstrated empirically: (1) The mutation rate must be such that we can expect the raw materials necessary to create the novel biological information and structures required for macroevolution to both arise and become fixed in a given population within the time limits required for its evolution; (2) The fitness gains provided by each beneficial mutation must be cumulative. 

Demonstrating the first condition has long been a challenge to Darwinism.  In most organisms the mutation rate is 1 nucleotide per 100,000,000, and only a miniscule fraction of these mutations are ever beneficial to an organism.  If, say, an organism requires 10,000 beneficial mutations over a period of 10 million years to evolve from species A into species B, and yet given the population size and mutation rate only 120 beneficial mutations can be expected to become fixed in the population during that time, then it would be impossible for that organism to experience macroevolution.  The problem is analogous to building a brick house.  If one is tasked with building a brick house in 30 days and the job requires 10,000 bricks, but the builder is only provided with two bricks per day, the home cannot be built in the time allotted.  Such is the situation Darwinists find themselves in.  The changes required for macroevolution are enormous, but the raw materials are few because beneficial mutations are so rare. 

As for the second condition, Darwinists have long assumed that fitness gains add up, so the more beneficial mutations the better!  Recent experimental work by Rafael Sanjuán, Andrés Moya, and Santiago F. Elena, however, have undermined this assumption.  Sanjuán et al found that when multiple beneficial mutations occur within an organism12, fitness is not improved but diminished.  In their experiment, rather than working together (synergistic), beneficial mutations were observed to work against one another (antagonistic): “[A]ntagonistic epistasis represents the most abundant type of interaction among beneficial mutations, with several cases showing decompensatory epistasis.”  They describe the importance of this finding as follows:

[W]hen epistasis is decompensatory, both beneficial alleles involved in the interaction cannot spread to fixation in the population, because the double mutant is less fit than each single mutant.  As a consequence, lineages bearing alternative beneficial mutations should compete with each other on their way to fixation and, as a consequence of asexuality and clonal interference, only the best competitor will eventually become fixed in the population.13

This puts Darwinists in a tough spot.  When appearing alone, there are not enough beneficial mutations necessary for macroevolution.  When multiple beneficial mutations arise simultaneously, they fight against one another and decrease the fitness of the organism.  Either way, macroevolution is not possible.

Many biological features require multiple mutations before any adaptive benefit can be conferred on the organism.  Chemical engineer, Douglas Axe, published a paper in BIO-Complexity that sought to determine mathematically how long it would take for such a sequential combination of mutations to arise and become fixed in a population.  To be generous to the Darwinist paradigm, Dr. Axe calculated the odds using asexual organisms.  What did Axe discover?  Assuming a constant population size of 1,000,000,000 organisms that reproduce three times per day every day for billions of years, up to six neutral mutations could become fixed in the population over the course of nearly four billion years (which is longer than the entire history of life on Earth).  If the mutations were maladaptive (negative), then only two mutations could become fixed in a population over the same period of time. 

What does this mean?  Put simply, there is not enough time to generate the number of mutations necessary to confer even minimally-complex adaptive advantages in microorganisms.  When you consider the fact that the population size, reproduction rate, and years in existence of most organisms are orders of magnitude smaller than asexual microorganisms, the chances of such mutations arising in complex, multicellular populations is effectively zero.  As Axe concludes:

[T]he most significant implication comes not from how the two cases contrast but rather how they cohere―both showing severe limitations to complex adaptation. To appreciate this, consider the tremendous number of cells needed to achieve adaptations of such limited complexity. As a basis for calculation, we have assumed a bacterial population that maintained an effective size of 109 individuals through 103 generations each year for billions of years. This amounts to well over a billion trillion opportunities (in the form of individuals whose lines were not destined to expire imminently) for evolutionary experimentation. Yet what these enormous resources are expected to have accomplished, in terms of combined base changes, can be counted on the fingers.14

Microbial Life

The best way to gauge the power of RM is by observing microbial life such as bacteria, parasites, and viruses because their populations are so numerous and their generation times so short.  When it comes to evolvability, the most important factors are mutation rates, population sizes, and reproduction rates, not time.  At an optimal reproduction rate of 30 minutes, a single E. coli bacterium can generate a population size of more than seven quadrillion organisms (7,000,000,000,000,000) in just 24 hours.  Over the course of one year it can spawn 17,520 generations15.  That’s a lot of room for evolutionary advancement!  Mammals cannot come close to such astronomical population sizes and generations, and thus we can learn what RM can do in mammals over a long period of time by observing what it can do in microbial life over a relatively short period of time (“short” from a mammalian perspective). 


Richard Lenski has been culturing E. coli for more than 50,000 generations, which is equivalent to approximately 1,000,000 years of human evolution.16  What has RM been observed to produce?  Nothing much.  No new genes, biological information, or biological systems have developed.  According the Lenski, “the most profound change” he has observed is the ability some E. coli evolved to digest citrate.  While this is a bona fide positive change, it is not all that remarkable when you consider the following:

  1. E. coli can normally digest citrate in anaerobic (absence of oxygen) conditions.
  2. The E. coli already possessed the enzymes necessary to metabolize citrate.  They only lacked a way of getting citrate through their membrane in the presence of oxygen.17  The situation is analogous to a fox living on a chicken farm.  While he possesses the ability to digest those chickens, he does not do so because he is separated from them by an impenetrable fence.  Once that fence is breached, however, that fox can and will eat his heart out!
  3. It took 32,000 generations to produce this tiny change. At this rate of evolutionary improvement, it would take billions of years for complex organisms like mammals to change from one species to another (since our population sizes and reproduction rates are orders of magnitude smaller than bacteria), but Darwinism requires that it happen in 10s, 100s, or 1000s of years. 
  4. Why should it take so long for E. coli to develop this transport mechanism, when they’ve been swimming in citrate for so long?
  5. If E. coli could only evolve one major biological improvement in the equivalent of ~500,000 years of human evolution, why think complex organisms have evolved thousands, if not millions of improvements during the same timeframe?
  6. This beneficial change was not achieved by increasing the information content of the E. coli’s genome, but by degrading the genome.  Evolutionary advancement, however, requires that new genetic information be added to the cell, not that it be lost.  While losing genetic information can be beneficial to survival at times, macroevolution cannot be achieved by constantly giving up biological information.  Eventually such a progression will lead to extinction, not advanced evolution.

All of the observed changes in Lenski’s E. coli are examples of microevolution, not macroevolution.  The population began as E. coli,and millions of mutations and thousands of generations later, they remain E. coli.  In fact, rather than gaining complexity and fitness, some of the E. coli populations have been observed to be in a state of devolution.  Some have lost their ability to repair DNA during transcription, resulting in a mutation rate that is 70 times that of normal E. coli.  As a result, they are losing genetic information, not gaining it; devolving, not evolving.18

Dr. Ann Gauger, developmental biologist and senior research scientist at the Biologic Institute, co-authored a paper with Ralph Seelke in BIO-Complexity (“Reductive Evolution Can Prevent Populations from Taking Simple Adaptive Paths to High Fitness,” Vol. 2010) reporting on a laboratory experiment which demonstrates that evolutionary adaptation usually results from eliminating genetic information/machinery rather than building new genetic information/machinery.  Dr. Gauger described her research as follows:

When challenged to grow in medium with very little tryptophan, 14 different populations of cells reduced or eliminated genes for making tryptophan, rather than fixing the broken tryptophan-making gene they carried. (Fixing the gene would have required cells to revert two specific mutations, with each reversion itself conferring a growth advantage.)  Because reducing or eliminating expression of the broken gene was “adaptive,” i.e. it allowed them to reproduce faster than cells still expressing the broken gene, and because there are many more ways to reduce or eliminate gene expression than to fix the gene, the populations always chose to reduce or eliminate gene function.19

Joseph Bozorgmehr also notes that “[i]n many instances...a loss of function and regulation in a harsh or unusual environment can have a beneficial outcome and thus be selected for—bacteria tend to evolve resistance to antibiotics in such a way through mutations that would otherwise adversely affect membrane permeability.”20


Humans have been battling malaria for thousands of years.  The advent of modern medicine provided us with a weapon to finally beat this ravaging parasite once and for all.  Or so we thought.  Unfortunately for us, malaria has been able to develop immunity to every drug we’ve thrown at it.  For example, malaria quickly developed resistance to Atovaquone.  All that was required to circumvent the effectiveness of this drug was a single point mutation at position 268 in a single malarial gene.  The odds of developing this particular mutation are one in a trillion (1012).  While those odds would be difficult to overcome for most organisms (such as human beings or beetles), they are a cinch for malaria due to their staggering population sizes and reproduction rates.  One trillion malarial parasites reside in each infected person, so odds are that at least one malarial parasite will develop resistance to Atovaquone in each and every infected person who takes the drug.  Luckily for us, malaria is not always so lucky.  Resistance to Atovaquone only develops in one out of three infected persons treated with the drug.

We humans would not be outdone by malaria, so we concocted a new drug – Chloroquine – to help us defeat our microscopic enemy.  To develop resistance to this drug, malaria would have to randomly experience two simultaneous and specific point mutations in a single protein.21  While single point mutations are fairly common (1 per 100,000,000 nucleotides per the life of an organism), double-point mutations are extremely rare.22  The odds of developing a double-point mutation like the one malaria would need to develop if it hoped to survive its battle with Chloroquine are 1 in 1020 (one in a hundred billion billion).23  If malaria populations were “small”—say 1,000,000 parasites per infected person—it would take one million years for malaria to meet those odds, but because there are so many malarial parasites (1 trillion per 1 billion people affected = 1,000,000,000,000,000,000,000 malaria parasites living in humans) they can, and have beat the odds.  By chance alone one malarial parasite in every billionth infected person will gain resistance to Chloroquine.  Once that resistant strand of malaria reproduces and spreads to other humans, it undermines the general effectiveness of Chloroquine. 

How long would it take mammals to develop a similar mutation by chance?  Given our tiny population sizes and long reproductive cycles, it would take us twenty billion years!  Not only is this 15 billion years more than the age of Earth, but it is 6 billion years more than the age of the universe itself!  And what would we get for our long wait?  A transformation from one species into another?  No.  A new biological system to help advance us toward the next stage of evolution?  No.  A new protein?  No.  We would simply get our existing cellular machinery broken in a manner that is fortuitously advantageous (micro-evolution of the devolution sort).  This is the biological equivalent of using a TV to plug a hole in a dam.  It may be a functionally acceptable solution to stave off immediate disaster, but it does nothing to build a new and improved dam.

In his otherwise negative review of Michael Behe’s book The Edge of Evolution, Sean Carrol agreed with Behe “that in most species two adaptive mutations occurring instantaneously at two specific sites in one gene are very unlikely and that functional changes in proteins often involve two or more sites.”24  Microbiologist Allen Orr also agrees: “Given realistically low mutation rates, double mutants will be so rare that adaptation is essentially constrained to surveying—and substituting—one-mutational step neighbors.  Thus if a double-mutant sequence is favorable but all single amino acid mutants are deleterious, adaptation will generally not proceed.”25  In other words, if a certain evolutionary change requires a double point mutation, we can be almost certain the organism will not evolve.  The fact of the matter is that many features of advanced life would require double point mutations and greater, and thus we can be reasonably certain that macroevolution via random mutation is impossible.


The HIV virus mutates at the evolutionary speed limit: 10,000 times faster than malaria.26  Its genome is very small as well (nine genes versus thousands in malaria).27  Its small size combined with a short reproduction time (1-2 days) and super-rapid mutation rate means every single nucleotide in the HIV genome will mutate 10,000 to 100,000 times in every infected person every day, and thus double point mutations like the one that made malaria immune to Chloroquine occur in every person every day.  In fact, every possible double point mutation occurs in every HIV virus in every infected person every day.28  Over the past several decades every possible combination of up to six point mutations has occurred in HIV somewhere in the world.  If RM drives macroevolutionary changes in organisms, then we should observe macroevolution in the HIV virus since it experiences more mutations than any other organism.  But we don’t.  HIV has run the gamut of all possible mutations to its genone, and yet with all of these mutations in a population of 100 billion billion viruses, no new cellular machinery has been created, and no new species has developed!  HIV is still HIV.  It still contains the same number of proteins, still performs the same function, and still binds to its host the same way it always has.  There have been no significant biochemical changes.  Even gene duplication has failed to produce any new biological information.

Imagine for a moment that we were trying to determine whether it was possible to evolve a car into a submarine via naturalistic processes.  The feat would require thousands of new mechanical systems and design changes, which in turn requires a lot of additional parts arranged in a very specific order.  Let’s say random parts are dropped from the sky once a day to help aid the process, but no intelligent agent is allowed near the car to select from among the parts or assemble them together in a particular order.  If, after 100,000,000,000,000,000,000 parts were dropped from the sky over a period of 100 million years, the car remained virtually unchanged, what would you conclude about the theory that cars can evolve into submarines without the aid of intelligence if given enough chances to do so?  Based on the empirical data you would probably conclude that it was highly unlikely, even if the time and parts were tripled in number.  So what would you conclude if it was suggested that a car can evolve into a submarine using only 10% of those parts in 10% of the time?  Surely you would conclude that such was impossible. 

This imaginary scenario is analogous to the debate over Darwinism.  Darwinists ask us to believe that natural selection working on random mutations is capable of developing multiple new complex biological systems in a relatively short period of reproductive time in small populations, even though the empirical data has demonstrated that natural selection working on random mutations is incapable of developing even a single new protein in populations and periods of reproductive time that are magnitudes of orders larger. 

After observing trillions upon trillions of microorganisms over thousands upon thousands of generations we have discovered that RM has achieved very little in the way of biochemical advancement, and hence evolutionary significance.  If RM cannot produce macro-evolutionary changes in bacteria, parasites, or viruses with their huge population sizes and short generation times, then surely there is no reason to think RM can do more in multi-cellular, sexual organisms such as mammals whose population sizes are orders of magnitude smaller, with generation times hundreds and thousands of times longer.  As geneticist Francois Jacob said, evolution is a tinkerer, not an engineer.  By tinkering around with a genome RM may get lucky and produce some functional advantage for an organism that helps it survive, but it does so at the expense of breaking existing biological information.  While burning biological bridges may be functionally advantageous for stopping the advancement of the enemy, and hence one’s survival, it is of no help in building new cellular machinery.  Jerry Coyne and Hopi E. Hoekstra recognized this when they wrote, “Supporting the evo devo claim that cis-regulatory changes are responsible for morphological innovations requires showing that promoters are important in the evolution of new traits, not just the losses of old ones.”29 Physicist Lee Spetner said it best, however: “Whoever thinks macroevolution can be made by such mutations is like the merchant who lost a little money on every sale but thought he could make it up on volume.”30  The biochemical engineering needed to originate new kinds requires the aid of an Intelligent Engineer, not a blind tinkerer. 

Protein-Protein Biding Sites

Most proteins work in teams of six or more.  To fulfill their biological function each protein has to find its other partners among the thousands of proteins in the cell, and then assemble themselves together.  This process of self-assembly is made possible due to binding sites located on each protein.  To bind together, the three-dimensional surface shapes and the chemical properties of the proteins have to match (interlocking) at their binding sites.  A wide rate of variability is needed to produce such specification, otherwise proteins would be able to bind together too easily, and thus they would be unlikely to bind with their intended partners.  This would tend to produce large clumps of proteins in the cell, prohibiting most of them from carrying out their function, and making the organism less fit (or possibly even killing it). 

Unless every protein in a protein team evolved at the same time (which is beyond credulity), each protein’s binding site would need to evolve independently of the others.  The obvious question, then, is how these binding sites gained their specificity?  What are the chances that the binding site of protein A would evolve the exact shape and chemical properties needed to complement the binding site of protein B, and the binding site of protein B would evolve the exact shape and chemical properties needed to complement the binding site of protein C, etc. for all the proteins in the protein team?  The odds of evolving just one new binding site by chance alone are 1 in 1020.  That is already inching toward the edge of what Darwinian evolution can produce, but since we need at least two independent binding sites for combination to occur, the odds are actually 1 in 1040.  That is slightly more than the total number of cells that have ever existed on Earth in the past four billion years, and thus it is beyond the bounds of Darwinian evolution to produce.  But it gets worse.  Since proteins usually work in teams of six or more to fulfill a given biological function, the chances of forming the necessary binding sites required of the average protein team are 1 in 10100That’s 20 orders of magnitude more than all the elementary particles in the observable universe!  And once again, for all this work, what is the reward?  Only the binding together of proteins to perform a specific function within the cell.  No new biological systems.  No new organismal kinds.  No macroevolution.31

Michael Behe sums up the problem this presents for Darwinism quite well:

The development of protein features, such as protein-protein binding sites, that require the participation of multiple amino acid residues is a profound, fundamental problem that has stumped the evolutionary biology community until the present day….  It is a fundamental problem because all proteins exert their effects by physically binding to something else, such as a small metabolite or DNA or other protein, and require multiple residues to do so. The problem is especially acute for protein-protein interactions, since most proteins in the cell are now known to act as teams of a half-dozen or more, rather than individually. Yet if one can’t explain how specific protein-protein interactions developed, then it is delusional to claim that we can explain how anything that depends on them developed, such as the molecular machinery of the cell. It’s like saying “we understand perfectly well how a car could evolve; we just don’t know how the pieces could get fit together.”32

The Fossil Record

What about the fossil record?  Doesn’t it show evidence of evolution?  No.  While the fossil record suggests gradualism from simpler to more complex organisms, this in itself does not require Darwinian evolution.  A design model could equally account for the data: God could have created different kinds of organisms over a long period of time, utilizing previous design patterns to create new, more complex organisms.  Of course, this doesn’t necessarily mean every distinct organism in the fossil record was independently created by God.  Some could be the result of micro-evolution within kinds, producing distinct species. 

I think the Cambrian explosion reveals the superiority of the design model, however.  For 85% of life’s history life was simple, consisting mostly of one celled organisms and simple fauna, then in the equivalent of six geological minutes complex multi-cellular life burst on the scene, with 95% of all body plans that have ever existed emerging at that time, and without evidence of earlier, simpler ancestors.  Darwin recognized the problem this posed to his theory.  And 150 years later, that problem remains.  Even Richard Dawkins has admitted, “The Cambrian strata of rocks, vintage about 500 million years, are the oldest ones which we find most of the major invertebrate groups.  And we find many of them already in an advanced state of evolution, the very first time they appear.  It is as though they were just planted there, without any evolutionary history.”33

Secondly, there are large gaps in the fossil record and few plausible transitional forms.  Organisms seem to just appear out of nowhere fully formed with no evolutionary history.  If Darwinism is true, we would expect to find a fairly detailed account of each step in the macro-evolutionary process preserved in the fossil record (including thousands of ill-formed animals unfit for survival) just as Darwin predicted.  What do we find?  Nothing.  New species appear suddenly with no trace of ancestors, persist for several million years,34 then disappear in the same manner that they appeared: without a trace.  Famed Harvard paleontologist Stephen J. Gould called this the “trade secret” of paleontologists. 

Third, the fossil record lacks any explanation of causal relationship between fossils.  The evolutionary lines drawn in our textbooks constituting the evolutionary tree of life are supplied by the imagination of men who first presuppose the truth of common descent, not by the fossil record itself.35  As Henry Gee, senior editor of biological sciences for Nature, wrote in 1999: “The intervals of time that separate fossils are so huge that we cannot say anything definite about their possible connection through ancestry and descent. … To take a line of fossils and claim that they represent a lineage is not a scientific hypothesis that can be tested, but an assertion that carries the same validity as a bedtime story—amusing, perhaps even instructive, but not scientific.”36  Thinking one can establish evolutionary relationships between such large gaps in the fossil record is like thinking one can reconstruct War and Peace based on the discovery of 13 pages, or thinking the discovery of Hawaii demonstrates that it is possible to walk from California to China!37

What one may think is an evolutionary relationship of descent between fossils may not be one at all.  Consider how many species of dogs can be produced through artificial selection.  Though all are dogs, they bear many morphological differences.  Now imagine someone in the distant future who unearths fossil remains of these dogs without any knowledge of their origin.  Given their morphological similarities, they might very well conclude that at least some of them evolved from others.  It would be easy to see an evolutionary pattern between them based on their morphological similarities alone.  While they may conclude that A evolved into B, B into C, and C into D, the fact of the matter is that there was no evolution at all.  All of them are of a single dog kind; all of them were created within a few hundred or thousand years of one another; and none of them originated through the Darwinian process of random mutation and natural selection (they were created by artificial selection through breeding).  Couldn’t evolutionary paleontologists be making similar mistakes in their assessment of the fossil record?  Couldn’t it be that what we perceive as an evolutionary relationship between fossils is nothing more than various species of the same general kind?  It is highly subjective, if not illegitimate, to claim evolutionary relationships between fossils based on morphology alone.

That morphology is not an adequate basis for determining ancestry has also been demonstrated by molecular studies.  These studies yield evolutionary trees quite different from those constructed from morphological analysis alone.  As Masami Hasegawa et al wrote in the Journal of Molecular Evolution, “That molecular evidence typically squares with morphological patterns is a view held by many biologists, but interestingly, by relatively few systematists.  Most of the latter know that the two lines of evidence may often be incongruent.”38  A good example of this is the story of horse (equid) evolution.  A recent study in the eminent journal, Proceedings of the National Academy of Sciences,not only discovered that a DNA-based evolutionary tree is inconsistent with a morphologically-based evolutionary tree, but also that some equid fossils thought to be different species based on their morphological differences turned out to be variations of the same species when their DNA was examined.39  This is a real-life example demonstrating the reality of the error I spoke of in the previous paragraph. 

Fourth, while the fossil record cannot be ignored when exploring the question of biological history, it is not sufficient in itself for demonstrating macro-evolution.  It’s not enough to say that because fossil B looks similar to fossil A that precedes it and fossil C that follows it, it must be a transitional form between the two.  While that is a possibility, one needs to do more than just point to morphological similarities (homology) between fossilized organisms to demonstrate macro-evolution.  One needs to lay out a plausible biochemical pathway that would produce the hundreds of thousands of morphological/systemic/functional transformations needed to evolve one kind of organism into another, and show that this pathway could be traversed in the amount of time required by the fossil evidence.40  Nobody is doing this.  One has to just take it on faith in Darwinism that such transformations are possible.  Given what we’ve discovered about the limits of RM+NS to generate the required biological information, that faith would have to be blind.  RM+NS cannot produce the types of changes needed to produce the diversification of life we observe in the fossil record. 

For the Darwinian explanation of the fossil record to be compelling, it needs to do more than account for the general trend toward higher complexity.  It needs to account for the sudden emergence of complex multicellular life, the sudden emergence of nearly all phyla, the lack of intermediates, and long periods of stasis.  If Darwinism cannot provide an adequate empirical explanation for this phenomenon, then it should not be considered the best explanation of the fossil record.  Indeed, the fossil record better fits the notion of progressive creation events by a designing intelligence.  Not only can Intelligent Design equally explain the gradual and increasing complexity found in the fossil record, but it can also explain why it doesn’t begin simple, how so many new phyla appeared in such a short period of geological time, why it lacks transitional forms, and why stasis—not change—is the norm.


The scientific evidence is not confirming the neo-Darwinian synthesis, but falsifying it.  The empirical evidence points to the regular involvement of an Intelligent Designer in the history of life.  If modern science had not committed itself to the philosophy of methodological naturalism (in which only naturalistic explanations are allowed for natural phenomenon) Darwinism would be laughed out of court for paucity of evidence. 
Darwinism has prevailed, not because it is the best explanation of the data, but because it is the best naturalistic explanation of the data – the only kind of explanation many scientists are willing to consider based on their a priori commitment to naturalism.  If one begins by assuming philosophical or methodological naturalism, then something like Darwinism has to be true even in the absence of evidential confirmation and explanatory value.  As Richard Dawkins has admitted, “Even if there were no actual evidence in favor of the Darwinian theory…we should still be justified in preferring it over all rival theories.”41 (emphasis mine)  Why?  Because Darwinism is a naturalistic theory, while others are not.  Darwinism wins the day, not because it has prevailed over the competition, but because it has eliminated the competition by definitional fiat, rooted in a philosophical bias.  When you define your league so narrowly that only one team is allowed to play, is it any surprise that you win the World Series? 

The question that scientists need to ask themselves – and that you need to ask yourself – is what the goal of science is.  Is the goal to find the right answers, or the right kind of answers; i.e. philosophically acceptable ones?  I think Greg Koukl answers this question best: “The object and domain of science should be the physical world, but its goal should be truth, not merely physical explanations.  Though science is restricted to examining physical effects, when causes are inferred, there should be no limitation.”42  The goal of science should be discovering the truth about physical reality, and if the evidence points to the involvement of an intelligent agent, then so be it.  Indeed, that is where the evidence points, and it does so with a neon sign.


1. Michael Behe, “Darwin’s Hostages: A decision in Kansas to Question Evolution Dogma has Given Rise to Hysteria and Intolerance”; available from; Internet; accessed 12 January 2010.
2. These changes are usually understood to be the product of purely unguided, natural processes rather than intelligent agency.
3 . Scott Gilbert, John Opitz, and Rudolf Raff, “Resynthesizing Evolutionary and Developmental Biology,” Developmental Biology, Vol. 173, 1996, p. 361.
4. If the mutations are harmful to the organism, they will result in a loss of information.  
5. To make this number more meaningful, it is equivalent to 100 trillion trillion trillion trillion trillion trillion trillion trillion trillion trillion trillion trillion trillion trillion trillion trillion trillion trillion trillion trillion trillion trillion trillion trillion trillion trillion trillion.  Written out, it looks like this: 100,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000.  6. William Dembski calculated this figure by multiplying together the number of elementary particles (1080), the number of seconds since the Big Bang (1016), and the number of particle interactions per second (1043).
7. Michael Behe, “Even More from Jerry Coyne”; available from; Internet; accessed 13 January 2011.
8. Douglas Futuyma, Evolution (2005), 470.
9. Joseph Esfandier Hannon Bozorgmeh, “Is gene duplication a viable explanation for the origination of biological information and complexity?”, Complexity, DOI: 10.1002/cplx.20365, published online 22 December 2010; available from; Internet; accessed 31 December 2010.
10. Joseph Esfandier Hannon Bozorgmeh, “Is gene duplication a viable explanation for the origination of biological information and complexity?”, Complexity, DOI: 10.1002/cplx.20365, published online 22 December 2010; available from; Internet; accessed 31 December 2010.
11. George Sim Johnston, “An Evening With Darwin in New York”, Crisis magazine, April 2006, pp. 32-37; available from; Internet; accessed 05 April 2006.
12. They used RNA viruses since their genomes are smaller and can respond quickly to mutations.
13. Rafael Sanjuán, Andrés Moya, and Santiago F. Elena, “Evolution: The contribution of epistasis to the architecture of fitness in an RNA virus,” Proceedings of the National Academy of Sciences USA, 10.1073/pnas.0404125101, Published online before print October 18, 2004.  Discussed at Creation-Evolution Headlines, “Neo-Darwinism Falsified in the Lab”; available from; Internet; accessed 04 January 2011.
14. Douglas Axe, “The Limits of Complex Adaptation: An Analysis Based on a Simple Model of Structured Bacterial Populations,” BIO-Complexity, Vol. 2010; available from; Internet; accessed 07 January 2011.  Reviewed by Casey Luskin, “BIO-Complexity Paper Shows Many Multi-Mutation Features Unlikely to Evolve in History of the Earth”; available from; Internet; accessed 07 January 2011.
15. It would take humans approximately 300,000 years to experience the same number of generations, and yet after all that time we wouldn’t come within a hair’s breadth close to the population size of malaria.  More malarial cells have existed in just the last 50 years than all mammals combined over the entire course of mammalian evolution (250,000,000 years).
16. The replication rates of his E. coli are only seven times per day.
17. New Scientist, available from
18. Michael Behe, “New Work by Richard Lenski,” available from; Internet; accessed 22 October 2009.  Reported on at
19. Ann Gauger, interview with David Klinghoffer, “Michael Behe's Challenge: A Conversation with Biologist Ann Gauger”; available from; Internet; accessed 13 December 2010.
20. Joseph Esfandier Hannon Bozorgmeh, “Is gene duplication a viable explanation for the origination of biological information and complexity?”, Complexity, DOI: 10.1002/cplx.20365, published online 22 December 2010; available from; Internet; accessed 31 December 2010.
21. While most resistant strains have the same two mutations, some strains lack the A220S mutation, but contain other novel mutations that likely have the same effect.  The important point is not which mutations result in Chloroquine resistance, but that multiple mutations are required for resistance to arise, and that it only does so once for every 1020 tries. There are “1012 possible double-point mutations…yet only a handful are known to be useful to the parasite in fending off the antibiotic, and only one is very effective — the multiple changes in PfCRT. It would be silly to think that just any two mutations would help. The vast majority are completely ineffective.” (Michael Behe, “Waiting Longer for Two Mutations, Part 5”; available from; Internet; accessed 21 November 2010.
22. That’s why malaria quickly developed a resistance to Atovaquone, because all that is required is a single point mutation at position 268 in a single malarial protein.  The odds of doing so are 1 in a trillion (1012).  Since 1 trillion malarial parasites reside in an infected person, the odds are that malaria will develop a resistance to Atovaquone in each and every infected person.  Usually, however, it occurs in every 3rd person.
23. This is not a mathematical speculation, but based on actual data provided by the eminent malariologist Nicholas White.  See Nicholas White, “Antimalarial drug resistance,” J Clin Invest, 2004, 113:1084-1092.
24. Sean Carroll, “God as Genetic Engineer”, Science, June 8, 2007.
25. Allen Orr, “A minimum on the mean number of steps taken in adaptive walks”; Journal of Theoretical Biology. 220:241-47, as quoted in Michael Behe, The Edge of Evolution: The Search for the Limits of Darwinism (New York, NY: Free Press, 2007), 106.
26. On average, a new mutation will occur every time a copy of the virus is made.  Compare this to human beings.  Though our genome is 1,000,000 times larger than HIV’s, the typical human being will only experience 1 mutation over the course of an entire lifetime, and trillions upon trillions of copies.
27. Its genome is less than 1/1000th the size of the malaria genome, and 1/1,000,000th the size of the human genome.
28. Michael Behe, “Response to Ian Musgrave’s “Open Letter to Dr. Michael Behe,” Part 3”; available from; Internet; accessed 19 November 2010.
29. Hopi E. Hoekstra and Jerry A. Coyne, “The Locus of Evolution: Evo Devo and the Genetics of Adaptation,” Evolution, Vol. 61-5: 995-1016 (2007).
30. Physicist Lee Spetner, Not by Chance!  Shattering the Modern Theory of Evolution (Brooklyn, NY: The Judaica Press, 1997).
31. Michael Behe, The Edge of Evolution: The Search for the Limits of Darwinism (New York, NY: Free Press, 2007), 123-34, 146.
32. Michael Behe, “‘The Old Enigma,’ Part 1 of 3”; available from; Internet; accessed 21 November 2010.
33. Richard Dawkins, The Blind Watchmaker (New York: W. W. Norton, 1986), 229.
34. Some organisms, such as comb jellyfish, have experienced no substantial change from their first appearance in the fossil record 500 million years ago to today.  How is it that the process of RM+NS is so powerful that it is purportedly responsible for evolving countless organisms from one kind into another many times over throughout the last 500 million years, and yet that same process has done nothing to change the jellyfish during that same period of time?  How can the same blind and random process do so much in one organism, and so little in another?  If RM+NS transformed the jellyfish’s neighbors many times over in the last 500 million years, how did jellyfish escape its power?  This evolutionary disparity cannot be explained by a lack of selective pressure on the jellyfish, because they would be under the relatively same selective pressure as their ocean neighbors who supposedly experienced numerous macroevolutionary changes during this period.  Furthermore, given the fact that mutation rates are fairly consistent between species, and mutations are responsible for creating the biological novelties upon which natural selection acts, it follows that we should see comparable biological changes in jellyfish that we see in other organisms who are said to form an evolutionary lineage of common descent.  And yet, we don’t.  Why is that?  Biological stasis over such a long period of time is inconsistent with a Darwinian model.  The data supports the contention that while the genome is flexible, it is relatively stable and thus incapable of undergoing the kinds of changes required by Darwinism.

Other examples of “living fossils” include horseshoe crabs, which have remain unchanged for 450 million years; scorpions have remain unchanged for 410-440 million years; the coelacanth has remain unchanged for 420 million years; sharks have remain unchanged for 400 million years; cockroaches have remain unchanged for 300 million years; dragonflies have remain unchanged for 155 million years; shrimp have remain unchanged for 200 million years; and tortoises have remain unchanged for 200 million years.
35. Evolutionists engage in circular reasoning because they assume an interrelatedness between fossils based on common descent, set out to find a pattern of ancestral relations, and then use that imagined pattern as proof that such an evolutionary relationship of common descent exists. 
36. Henry Gee, In Search of Deep Time: Beyond the Fossil Record to a New History of Life (New York: The Free Press, 1999), 23, 116-117.
37. Constance Holden, “The Politics of Paleoanthropology,” Science (1981), 737.
38. Masami Hasegawa, Jun Adachi, Michel C. Milinkovitch, "Novel Phylogeny of Whales Supported by Total Molecular Evidence," Journal of Molecular Evolution, Vol. 44, pgs. S117-S120 (Supplement 1, 1997), as quoted in “Peter Atkins Dramatically Overstates the Evidence for Evolutionary Phylogenies”; available from; Internet; accessed 26 February 2008.
39. Ludovic Orlando et al, “Revising the recent evolutionary history of equids using ancient DNA,” Proceedings of the National Academy of Sciences, published December 9, 2009, doi: 10.1073/pnas.0903672106.  The relevant excerpts are available from
40. For example, if it could be shown that it would take 300 million years to traverse the pathway, and yet the transitional form is only separated from its predecessor and successor by 25 million years, then it becomes clear that fossil B cannot be a transitional form between fossils A and C.  
41. Richard Dawkins, The Blind Watchmaker (New York: Norton, 1986), 287.
42. Greg Koukl, Solid Ground, July/Augusts 2005 issue, 3.

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