Evolution, Part II: What Genetics Really Tells Us

Evolution: What Genetics Really Tells Us

Read Part I here

While the genetic evidence at first seems like one of the strongest arguments in favor of evolution, it’s ultimately the theory’s largest Achilles heel.  Ironically, the more science has learned about DNA and genetics, the more apparent evolution’s challenges have become.

New genetic discoveries have sparked significant debate within the evolutionary community.  It is important to note that the vast majority of biologists and geneticists still agree that evolution occurs. However, there is tremendous debate over how it occurs1, 2.  This fact is because the latest evidence is not consistent with what the theory demands.

Biological Change Does Occur

As mentioned in part one, biological change clearly occurs.  This fact alone is not proof of Darwinian evolution.  Several questions must be answered before we can decide if such change is driven by purely natural evolutionary processes.  First, we have to naturally explain the origin of biological information (e.g. DNA) and its considerable further expansion.  Secondly, we need to understand if there are limits to the changes that can be caused by natural variations (i.e. mutations) in biological information.  Finally, we need to determine if the combination of random mutations and natural selection can overcome the statistical odds stacked against it to create the biological diversity and complexity surrounding us.  Keeping these questions in mind as we move through parts two through six, let’s address the genetic evidence in favor of evolution that was discussed in part one.

Genetic and Morphological Similarity

The genetic similarities, in both DNA and structures (homologies) among living creatures, are used as compelling evidence that life evolved from common ancestors.  In particular, the fact that humans and chimpanzees share 98% of their DNA is used to point to a common ancestor.

There is one glaring problem with this argument.  While biological similarity is consistent with common descent, it is just as consistent with a common design or designer.  And when we consider the fact that these homologous structures are not necessarily controlled by the same genes within supposedly related organisms3, the argument for common descent takes a significant blow.  Consequently, homologies do not provide strong evidence for evolution, but instead point toward common design.

As with much of evolutionary evidence, homologies are “evidence” that presumes its own conclusion. Evolutionary biologists define homologies as similar structures in creatures derived from a common ancestor.  Then they use that definition to argue that homologies provide evidence for common ancestry.  It is the ultimate circular argument4.

Furthermore, the assertion that humans and chimpanzees share 98% of their DNA is exaggerated.  First, even if there is only a 2% difference, this still represents sixty million genetic letter differences throughout the genome5.  In addition, more recent studies suggest the actual differences in human and chimpanzee DNA are approximately 10%, five times what was previously thought6.  Finally, the types of differences are clearly more important than the quantity.  As such, the gulf between humans and chimpanzees is vast, much greater than either the 2% or 10% genetic variation suggests.

Junk DNA

So-called Junk DNA was once thought to be one of the most compelling genetic arguments for evolution.  It seemed to simultaneously argue for evolution (as evidence of left-over genetic “fossils”) and against creation (since an intelligent designer wouldn’t use junk).  But new genetic discoveries have greatly turned the tables.

The recent ENCODE (Encyclopedia of DNA Elements) project is an international consortium of research groups funded by the National Human Genome Research Institute and represents the leading edge of mainstream genetic research.  One of its major discoveries is that so-called junk DNA is not junk after all.  In fact, whereas scientists used to believe that the non-protein coding “junk” (~95% of human DNA) had no function, ENCODE has discovered important roles for up to 80% of the genome7!  And there is now reason to believe the other 20% also has function that is still to be discovered8.  The non-coding DNA is now known to play important roles in “gene expression” by deciding when to turn select genes “on and off” at the correct times.

By finding purpose for junk DNA, ENCODE has removed one of the greatest genetic arguments for evolution.  There is no left-over “junk” after all.  And with the vast majority, if not all, of the genome active, there is no argument against an intelligent designer.  As evolutionary biologist Dr. Dan Graur says “If the human genome is indeed devoid of junk DNA as implied by the ENCODE project, then a long, undirected evolutionary process cannot explain the human genome.  If ENCODE is right, then evolution is wrong9!”

It is important to note that Dr. Graur is still an ardent supporter of evolution.  He is not suggesting evolution is wrong.  Rather, he believes ENCODE must be wrong and should be shut down10!  However, he believes this because of his own biases, not because of the evidence.  ENCODE represents the forefront of mainstream genetic research.  And it clearly contradicts naturalistic evolution!

If “junk” DNA is not junk, the supposed shared mutations within it are no such thing.  Since these genes have specific functions, there is strong reason to believe they are not mutations at all and are rather examples of common design just like other genetic similarities.

There is another key point about junk DNA we must consider.  Ironically, even if junk DNA is actually junk, it would still argue against Darwinian evolution.  This fact is because leftover, junk DNA would be evidence of devolution, not evolution.  If 95% of the genome has lost function over time, it is an indication that the vast majority of genetic information has been destroyed, which is moving in the exact opposite direction that evolution requires to account for increasing biological diversity and complexity.

Further, if evolution is true, one has to wonder how it could be so inefficient as to expend energy maintaining a genome that is 95% useless.  There is presumably no survival benefit from carrying around and maintaining so much useless genetic material.  This should not occur since evolution is supposedly so efficient at “rejecting that which is bad, preserving and adding up all that is good”11.  Consequently, however “junk DNA” is viewed, evolutionary theory is challenged, not reinforced.

Genetic Information

There is a tremendous amount of information contained in the human genome.  In fact, each microscopic strand of human DNA contains the equivalent of 2 million pages of information12!  And DNA also contains the means to copy, edit, and self-correct this information.  In fact, Bill Gates (who is not a creationist) acknowledges that “DNA is like a computer program, only far more advanced than anything man has ever created.”13  Despite the fact that functional computer programs will never write themselves, even with billions of years, evolutionists would have us believe that “far more advanced” DNA did exactly that.

If evolution is true, it must account for a few significant facts about this information.  First, evolution must be able to explain how it arose naturally in the first place.  Secondly, evolution must show how this information has increased dramatically over time.  As an example, the DNA of a “simple” single-celled E. coli bacterium contains roughly 4 million letters whereas human DNA contains over 3.5 billion letters14.  If all life evolved from simple single-celled organisms, evolution must be able to explain how genetic information increased ~90,000%, countless times, to account for the massive genetic diversity on earth.

The proposed mechanism behind Darwinian evolution is the combination of random mutation and natural selection.  This mechanism can, and does, easily account for limited genetic change.  But it cannot account for either an increase in genetic information or the development of new, functional biological structures.  It is fundamentally the wrong mechanism15.

Mutations are copy mistakes and almost invariably destroy information16.  This is true even of “beneficial” mutations such as antibiotic resistant bacteria17 and the famous Lenski E. coli experiments18.  In fact, there are no known instances of mutations increasing the amount of functional genetic information19, 20.  Even Richard Dawkins famously failed to think of a single example when asked this question21.

If mutations destroy information, how can they be the primary driver behind the mind-boggling increase of genetic information required to move from single-celled organisms to the vast array of diverse and complex animals present today?  This is a key point.  The question is not about how to explain the development of new biological traits.  These can occur via mutations.  But new information does not.  Trying to answer this question is what creates so much debate within the evolutionary community22.  Evolutionists have offered many suggestions, but none has proven adequate.

Furthermore, to get a fundamental change in morphology (body plans and parts) requires more than a single mutation.  There would have to be multiple, coordinated, interdependent mutations23.  Given that mutations are almost always negative, the chances of getting multiple, coordinated, interdependent, and beneficial mutations to occur at once is practically nil.

In effect, a reliance on random mutation is the biological equivalent to serendipity.  While serendipity has occasionally produced good outcomes like penicillin, it rarely does so and is hardly the cornerstone of modern medicine or science.  If we rely on intelligence and planning to drive our own production of information, why do we believe that the creation of vastly more and more complex biological information is due to luck?  Still, evolutionists have offered several explanations to attempt and solve this problem.

Gene Duplication

The mutation known as gene duplication is the evolutionists’ favorite proposal for how to create new genetic information.  With gene duplication, a particular gene is mistakenly copied twice in the genome.  This second copy does not technically create new information just as a second copy of a page in a book does not add to the story.  However, once the copy is made, it is now free to mutate as well.  Consequently, new information can result over time as the duplicate gene changes from subsequent mutations and gains new function.

Admittedly, the gene duplication proposal at least provides a theoretically possible means of generating new information.  But there are several glaring problems with this process, especially if it is to be the key mechanism driving biological progression and evolution.

First of all, there is a huge difference between being theoretically possible and actually occurring.  Despite years of looking, there is not a clear example of this type of scenario occurring and creating net new information24.  While it works in theory, it does not appear to do so in practice.

Part of the reason gene duplication doesn’t work in practice is because, like most mutations, it is deleterious and ultimately harmful25.  The genome has a functional and highly specific architecture, so unplanned insertions tend to disrupt its operation26.  The addition of unneeded genes can disrupt cell size and function and significantly impact the regulation of gene expression27.  A common instance of gene duplication in humans is Down Syndrome.  People born with this condition have an extra copy of the 21st chromosome.  But they can hardly be said to benefit from this extra genetic information or from subsequent mutations in it.

Further, gene duplication faces the same challenges that every other form of mutation faces28.  As stated previously, mutations are mistakes that invariably degrade genetic information.  The fact that gene duplications give incremental genetic material doesn’t change that fact.  The duplicated gene will be subject to degradation as well.  While some of these mutations may occasionally prove beneficial, the vast majority will not.

Hox Genes

Another area where evolutionists have sought to demonstrate that large-scale body changes and new information can result is from mutation in so-called Hox genes.  Hox genes regulate the expression and operation of protein-coding genes.  The evolutionists beloved “proof case” of this concept is where geneticists have been able, by manipulating Hox genes of fruit flies, to make an additional pair of wings or create a set of legs where antennae should be!

But this example fails to actually show evolution in action.  Rather, it serves to discredit it.  First of all, while the change is certainly dramatic, it is not in any way beneficial.  In fact, these mutations are catastrophic.  Such is the case in known instances of Hox mutations precisely because they impact so many other genes29.  Further, while extra wings or legs can be grown, the corresponding musculature and other requirements for them to be functional, does not result30!  Consequently, Hox mutations actually demonstrate the extreme improbability of getting multiple, coordinated mutations to create new, functional morphologies (body plans).  Finally, Hox genes only regulate other, existing genes.  If the required information is not already present, they can do nothing with it31.


The area of epigenetics, which refers to genetic information outside of DNA, has also been proposed as a means of driving major biological change, the origin of new body parts and plans, and therefore evolution.  However, epigenetics as a mechanism for evolution also faces major obstacles.  First, epigenetics are less vulnerable to mutation and alteration than DNA32.  Secondly, when epigenetic information is altered, it is overwhelmingly likely to have harmful or catastrophic consequences33.  Genetic information that is hard to change, and highly negative when it is changed, is not a promising mechanism for creating vast biological diversity!

Natural Selection

Another common response from evolutionists is to trust natural selection to come to the rescue.  Random mutations alone can’t account for the increase of information and body structures.  But random mutation combined with natural selection can because natural selection maintains those changes that are good and eliminates the ones that are bad.  Or so goes the theory.

Richard Dawkins speaks of how natural selection and vast evolutionary time allow life to scale “Mount Improbable” and overcome the incredible odds stacked against it.  In essence, natural selection and long time periods allow evolution to be broken down into many small, incremental steps34.  Consequently, the end result appears exceedingly rare, but each individual step is no problem.  While Dawkins’ proposal sounds good, he is really just putting lipstick on a pig.

First, climbing Mount Improbable one step at a time does nothing to address the information problem described above.  Mutations destroy information.  You cannot scale Mount Improbable if your chosen mechanism is actually digging a hole deeper vs. climbing higher!

Secondly, natural selection holds nowhere near the mythological power that Dawkins ascribes it.  While it has an impact on genetic variation, it is actually very inefficient and less impactful than random chance35.  Consequently, the probability of reproduction for a given organism is more often impacted by its environment and circumstances than by its genetics.  In reality, we see “survival of the luckiest” more often than survival of the fittest36.

In addition, as mentioned above, true evolution between various taxa requires the creation of wholly new body parts and plans.  These require much more than a single mutation.  For example, simply evolving from an ape foot to a human foot requires changes to many bones, ligaments, muscles, and neurons37.  The chances of all these mutations happening at once is nil and yet, unless they do, there is nothing beneficial for natural selection to select!  In fact, simply putting human feet on an ape would not be beneficial either.  There would also need to be changes to the legs, knees, hips, backbones, etc.38!  If these mutations occurred in the absence of the others, the resulting creature would actually be less fit and should be selected against!

In summary, Dawkins greatly oversimplifies the analogy of climbing Mount Improbable by simply taking small steps.  Even these supposedly small steps are still vast gulfs that are statistically impossible.


Beyond the failure to account for an increase of information, evolutionists have failed even worse at trying to describe how such information arose in the first place.  We will cover this particular issue more in-depth in part 5 of the series.

The fact is that humans have only ever witnessed information occur from intelligent, intentional sources.  It has never been observed occurring naturally.  Secular scientists acknowledge this fact in every instance other than evolution.  A perfect example is the Search for Extraterrestrial Intelligence (SETI).  SETI is a project that has spanned more than six decades and spent tens of millions of dollars on trying to answer the question of whether intelligent alien life exists.  How do they look for this intelligent life?  By searching the cosmos for signs of information such as radio signals with complex, non-random patterns (e.g. a string of prime numbers).  If information as basic as a transmission of prime numbers in space is irrefutable proof of intelligent life, why is massively more complex information found in living beings somehow evidence of random, natural processes?

The bottom line is that evolution, driven by random mutation, completely fails to account for both the initial creation and eventual and dramatic increase of genetic information.   Both of these factors must be answered for any theory about life to remain credible.


  1. Meyer, Dr. Stephen. Darwin’s Doubt.  New York, NY: HarperCollins Publishers 2013.  Prologue ix-xi
  2. Rana, Dr. Fazale and Ross, Dr. Hugh. Who Was Adam?  RTB Press 2015.  144
  3. Wells, Dr. Jonathan. Zombie Science: More Icons of Evolution. Seattle, WA:  Discovery Institute 2017.  41
  4. Pg. 42
  5. Sanford, Dr. John and Rupe, Christopher. Contested Bones.  FMS Publications 2017.  295.
  6. Ibid, Pg. 295.
  7. Meyer, Dr. Stephen. Cit. Pg. 400.
  8. Rana, Dr. Fazale and Ross, Dr. Hugh. Op. Cit. Pg. 343
  9. Wells, Dr. John. Op. Cit. Pg. 130
  10. Pg. 130.
  11. Dawkins, Dr. Richard. The God Delusion. New York, NY:  New Mariner Books 2008.  190
  12. Carl Sagan, The Dragons of Eden. New York, NY: Random House 1977.  25
  13. Meyer, Dr. Stephen. Op. Cit. Pg. 359.
  14. Lennox, John C., PhD. God’s Undertaker. Oxford, England:  Lion Books 2009.  137
  15. Meyer, Dr. Stephen. Op. Cit. Pg. 281.
  16. Sanford, Dr. John. Genetic Entropy.  FMS Publications 2014. Pg. 15
  17. Pg. 17.
  18. Pg. 29
  19. Pg. 17.
  20. Sarfatti, Dr. Jonathan. Refuting Evolution 2.  Green Forest, AR: Master Books, Inc. 2005. Pg. 56
  21. https://www.youtube.com/watch?v=YddmGJofbL0
  22. Meyer, Dr. Stephen. Op. Cit. Prologue ix
  23. Pg. 233
  24. Sanford, Dr. John. Op. Cit. Pgs. 17, 226
  25. Pg. 224.
  26. Pg. 227.
  27. Pg. 225.
  28. Pg. 223-227
  29. Meyer, Dr. Stephen. Cit. Pg. 318
  30. Pg. 318-319
  31. Pg.320
  32. Pg. 285
  33. Pg. 285
  34. Dawkins, Dr. Richard. Cit. Pg. 147
  35. Sanford, Dr. John. Op. Cit. Pgs. 64, 100
  36. Pg. 100
  37. Sandard, Dr. John and Rupe, Chris. Cit. Pg. 286
  38. Pg. 287