Welcome to Episode 6 of Foundations Restored, a Catholic Perspective on Origins.
I'm your host, Keith Jones.
This episode continues to expose the failure of the Darwinian icons, and it explains the
foundational flaw of Darwinian evolution, which is the claim that mutations, acting
with natural selection over time, constitute a plausible mechanism for molecules to man
evolution.
This flaw is foundational because once the failure of the Darwinian mechanism is exposed,
it allows us to dismiss the notion that fossil finds will one day arise to support Darwinism.
Welcome to Episode 6 of Foundations Restored, a Catholic Perspective on Origins.
Explaining the failure of the claimed mechanism for evolution will require us to delve into
some details related to the genetic code and certain components of the cell.
To help, we will define some key terms as we go along.
In addition, all of the essential concepts needed to explain the failure of mutations
as a mechanism of evolution can be demonstrated through an analogy that is intuitive and will
be an aid in understanding the more technical discussion to follow.
Biologists Pamela Acker and Dr. Kevin Mark will now introduce the analogy and explain
its relevance to the subsequent technical discussion.
The failure of the claimed neo-Darwinian mechanism for evolution is easy to visualize and explain
once we recall that the genetic code contained in the DNA of living organisms is, in a very
real sense, an instruction manual for how to assemble and maintain each organism.
The instruction manual is made up of specific letters, or nucleotides, that form what is
called the genetic code.
These letters are arranged into strands of DNA, and two DNA strands are paired to form
a double helix, which resembles a spiral staircase.
Since the structure of DNA was first described by Watson and Crick in 1953, we have learned
a great deal about the complexity of the genetic code, but our knowledge pales in comparison
to what we do not yet understand.
For our analogy, we only need to know that the genetic code is the instruction manual
for how to build a specific organism.
We can choose any animal for our analogy, let's just say we're talking about the
genetic code or instruction manual for a squirrel.
Our analogy consists of imagining that the instruction manual for building a squirrel
contains thousands of pages of genetic information, and each paragraph on each page contains useful
information related to some aspect of building and maintaining a squirrel.
Since our assumption is that all information in the instruction manual is useful, it is
readily apparent that anything causing some of the information in the manual to be destroyed
over time will necessarily mean that useful information is lost.
Due to the relatively small amount of information contained in any paragraph, the elimination
of a paragraph or even a page may not result in an immediately noticeable decrease in a
squirrel's functionality, but it is clear that there will be a loss of useful information
and that this will be detrimental in some respect.
Now let's develop our analogy further.
Let's suppose that in North America, there was only one instruction manual printed a
few centuries ago, and because the manual was so rare, the original purchaser never
gave his copy to anyone else.
Nevertheless, the owner of the manual wanted his children to have a copy for their own
studies, and so he allowed his children to painstakingly copy the manual, page for page,
until they at last had their own copy.
In turn, their children had to repeat the same process, painstakingly copying not the
original but the copy that their parents had made.
This process continued generation after generation.
Of course, as this process continues, it is inevitable that there would be copying errors
introduced, and other mistakes could arise if, for example, some pages were torn, became
too worn to read, or were ruined by a water spill.
In each instance, information would be lost and our instruction manual would no longer
convey all of the original details about how to build a squirrel from genetic material.
We will call this loss of information a mutation.
As mutations accumulate from generation to generation, the instruction manuals would
contain an increasing number of errors and the information would be increasingly degraded
compared to the original copy.
Before we go further, let's give a name to the accumulation of copying errors or mutations
over long periods of time.
Since we are talking about the degradation of a genetic instruction manual, a good scientific
description would be the term entropy, which refers to the tendency of everything in the
physical universe to go from a state of order to increasing disorder.
Also, since our make-believe analogy involves degraded copies of an instruction manual,
as it is passed from family members in one generation to the next, and since all members
are genetically related, the phenomena we are talking about can be called genetic entropy.
From our example, it is clear that genetic entropy would increase from generation to
generation due to the presence and accumulation of mutations or copying errors, and that each
new generation would experience further degradation of useful information that used to be present
in the genetic code instruction manual of their parents.
Now here is the key point.
While the information in the instruction manual changes from generation to generation due
to the increasing accumulation of mutations, it would be a real stretch to call this process
evolution, because all that results from genetic entropy is a more imperfectly designed squirrel,
not the emergence of a new animal kind like a fox, or the emergence of a complex and functional
new organ such as a feathered wing that allows the squirrel to fly like a bird.
A new animal kind or feathered wing would require new information, whole new chapters
of information, but mutations do not provide these new chapters, they only degrade the
information in the instruction manual.
To suggest that such degradation would lead to Darwinian evolution is like suggesting
that adding multiple random typos to Macbeth would lead to a new highly acclaimed Shakespeare
play.
In essence, what we have described is what occurs to the genetic code of all living creatures
over time.
All genomes degrade over time due to mutations, information is lost, and we can't expect
new animal kinds and complex new organs to somehow emerge from a genome that can't
even maintain what it has.
The process of genetic entropy, so named by Dr. John Sanford of Cornell University in
his landmark book, effectively deals a death blow to the notion that mutations and natural
selection produced amoeba to man evolution over hundreds of millions of years.
Entropy is a measure of disorder.
The nature of entropy is that it always increases, that is, everything tends to break down.
And so you can see it in your car, you can see it in your house, you can see it in your
own body as we age, and everything's breaking down.
So this entropy problem, this universal degenerative process, is happening within our genome, within
our genes.
And so that's a problem because our genome is the programming that makes us alive.
And if you corrupt a genome, all our functions start to degrade.
And so we experience this on a personal level, and there's no question about this simple
fact, is there are about three new mutations every cell division.
So every cell in our body gets more mutant every day.
Every day we're more mutant than we were yesterday.
And that is actually the primary reason for aging and death, is mutation.
And it's like rusting out of the car, and it's unstoppable.
So personally, we all are undergoing entropic decay.
First of all, we lose functionality, and eventually we die.
So the same thing happens at the population level.
Because when we have children, we pass on our mutations to our children.
And so we receive mutations from our ancestors, and then we add our own mutations and pass
it on to the kids.
Every generation has to be more mutant than the previous one.
And the rate, mutation rate, how many mutations are passed on to the next generation, is disturbingly
high.
So basically, every generation has 100 more mutations than the previous generation.
It's about 100 mutations per person per generation.
And that's bad news because they're almost universally deleterious mutations.
There are rare, exceedingly rare beneficials, but it's so rare that they don't really even
make a difference.
So this is the problem of genetic entropy.
We experience it personally, and all populations should be subject to it.
Here's a simple way of saying it.
We're not going up, we're not evolving upward, we're going down.
It's down, not up.
It's exactly the opposite of evolution.
And it has profound implications.
It means there was a beginning, and there has to be an end.
There had to be a time when there were no mutations, if you run the video backwards.
And it's clear that at some point, as we accumulate more mutations, all populations must eventually
go extinct.
So it's radically different from the common understanding that things are getting better
and better due to mutation selection.
And so this is something I've studied for 18 years.
I think, I don't know that anybody has studied this issue in as much depth as I have.
So people who want to know more about genetic entropy, they can go to geneticentropy.org
and find out more about it.
Time and mutations are an enemy to any genome, as they only result in degraded genomes, not
the additional information needed for new animal kinds.
Let's add a final twist to our analogy.
Let's assume that after many generations, we learn that in another part of the world,
a second copy of the original instruction manual was printed and purchased long ago,
and that the contents of this manuscript were handed down through the same process of copying
we've previously described.
When the present-day copies handed down from the two original printed versions are compared,
it is not surprising that the copies are found to be different in many instances due to random
mutations that occurred as each manuscript was passed on generation after generation,
but in isolation from each other.
In fact, it is possible that the instructions from the two versions may have diverged from
one another so much that squirrels constructed from the different manuals may no longer be
able to interbreed and produce fertile offspring.
In this case, scientists may describe the two offspring as belonging to two different
species.
But is this really a good example of evolution?
The answer is that it is not evolution in the Darwinian sense at all, because the squirrels
are not on their way to becoming a non-squirrel.
They are only degraded squirrels who can no longer produce fertile offspring.
In this way, mutations in genetic entropy can lead to speciation according to the biological
definition of species, but they will never produce the new information needed for the
emergence of new animal kinds.
As new details emerge about the genomes of living organisms, it is becoming increasingly
clear that genetic entropy is real and that Darwinian evolution is not genetically possible.
Based on our analogy of genetic entropy, viewers may be wondering how evolutionists could argue
that mutations can be a viable Darwinian mechanism.
The answer is that evolutionists make a number of problematic assumptions and ignore the
emerging evidence against mutations as a mechanism, because they have no better naturalistic alternative
and special creation is eliminated for philosophical reasons.
Much of the remainder of the episode will explain the lack of evidence supporting these
problematic assumptions.
First, however, let's illustrate these assumptions by returning once more to our analogy.
Our analogy in the concept of genetic entropy could potentially break down if our assumption
that all pages of the instruction manual contain useful information was not true, and instead
most pages provided no useful information about how to construct a squirrel.
So for example, while our instruction manual on how to build a squirrel was said to contain
thousands of pages, if only 2% of the pages actually contained the needed information
to build a squirrel, then copying errors or mutations could occur in the remaining 98%
of the manual without having a negative effect on the squirrel.
In essence, one could view the 98% of non-functional genetic information as junk information that
is not used.
The existence of large portions of junk in the genetic code instruction manual may allow
mutations to accumulate without having a degrading or detrimental impact.
In fact, over eons of time, there could even be random beneficial mutations that arise
and somehow become functional such that virtually unlimited new characteristics could arise
to produce new squirrel variations and eventually non-squirrel animal kinds.
This may sound far-fetched, but in essence, is the view professed by evolutionists.
But is this view based on fact, or does it amount to a kind of faith?
The remainder of this episode explains that of the two views, the emerging evidence since
2007 clearly supports the concept of genetic entropy with the implication that mutations
fail as a mechanism of evolution and Darwinism is thus not true.
Specifically, following some historical background, we will discuss, firstly, while evolutionists
claimed until recently that 98% of the genome is junk DNA, this is now known to be false.
Virtually all of the genome is now believed to be functional.
The implication of this functionality is that mutations destroy useful information.
Secondly, there are no truly neutral mutations.
All mutations are somewhat harmful since they destroy information to some degree.
Third, even the rare mutation that is claimed to be beneficial comes at a fitness cost.
Fourth, even if a rare mutation were beneficial without incurring any fitness cost, it would
not lead to evolution because it would take so long for beneficial mutations to accumulate
and have an impact.
Meanwhile, the cumulative impact of harmful mutations would destroy much more information
than beneficial mutations could ever replace.
And finally, fifth, all examples of beneficial mutations, such as bacterial resistance to
antibiotics and resistance to HIV, fail to support the claim that mutations are a viable
mechanism of evolution.
We will now transition into a more technical discussion of evolution's supposed mechanism,
starting with a historical overview of its development.
Evolution of Species
Starting with Charles Darwin, evolutionists speculated as to what caused variations that
supposedly worked with natural selection to drive evolutionary processes.
In The Origin of Species, Darwin claimed that he saw no limit to the processes that
produce variation among parents and offspring such that, given enough time, the processes
could account for all animal species.
To support this claim, Darwin relied upon his authority as a scientist and also spent
much time discussing the selective breeding of pigeons and the differing characteristics
that resulted from these artificial breeding experiments.
And yet, even Darwin's staunchest supporters admitted that it was inappropriate to extrapolate
such observations because experimental evidence clearly suggested that there are limits to
variation that could occur in any species.
Additionally, Darwin's claim did not adequately consider the tendency of random breeding to
produce offspring that reverted back to the original type.
Recall, for example, that Lyell noted,
Every naturalist admits that there is a general tendency in animals and plants to vary, but
it is usually taken for granted that there are certain limits beyond which each species
cannot pass under any circumstances or in any number of generations.
This comment reflected the observation that artificial and natural selection could, at
the most, produce what is called adaptive radiation, a form of variations on the same
body plan to fill different ecological niches.
But this limit poses a problem for the creation of new body plans and forms needed for molecules
to man evolution.
It is also interesting to note that Darwin had no idea about what specific and internal
process actually drove the variation he speculated led to new species.
Recall that the day after The Origin of Species was published, he wrote to Huxley,
You have most cleverly hit on one point which has greatly troubled me.
If, as I must think, external conditions produce little direct effect, what the devil determines
each particular variation?
Clearly, a fuller hypothesis about the supposed mechanism of evolution was needed, but it
would not be forthcoming until the next century.
In the early 1900s, several scientists independently rediscovered the important insights of the
Augustinian monk, Gregor Mendel, whose experiments with pea plants fortuitously provided a means
of understanding heredity.
Mendel observed that there did appear to be some physical quantity that was passed from
parent to offspring and determined the traits expressed in the next generation.
In 1905, Danish botanist Wilhelm Johansen introduced the term gene to describe this
heritable material.
Shortly thereafter, Dutch botanist Hugo de Vries speculated that a change or mutation
in a gene could lead to the development of a new species.
Here at long last was a possibility for the naturalistic mechanism that evolutionary biology
had been lacking.
Thomas Hunt Morgan, a biologist at Columbia University, carried out the first notable
experiments studying mutations within a population.
But his discovery of a mutant white-eyed fruit fly in 1909 cast some doubt on de Vries'
hypothesis that a single change in a gene could lead to the development of a new species.
The paradigm needed to be refined.
Ronald Fisher and J.B.S.
Haldane soon shed new light on the issue through their work in population genetics that involved
creating mathematical models to track variations within a population and the favorability of
these variations under certain environmental pressures.
But it was not until Theodosius Dobzhansky, a scientist who had worked in Morgan's so-called
fly room, published Genetics and the Origin of Species in 1937 that a seemingly plausible
role for mutations in the development of new species was fleshed out.
Dobzhansky's work began what eventually came to be known as the modern synthesis,
the fusion of Darwinian evolution theory with molecular biology and Mendelian genetics.
Dobzhansky hypothesized that a large number of mutations are neutral.
They confer neither harm nor benefit on the individuals who carry them.
These neutral mutations, accumulating in populations over time, create new alleles, or alternative
versions of a gene, that give rise to new variations within the population.
These variations could lead to a speciation if reproductive isolation occurred in a population.
Reproductive isolation could include novel cording behavior or geographical separation.
Dobzhansky hypothesized that over long periods of time, as neutral mutations accumulated,
and assuming there was no gene flow or breeding between the two isolated populations, the
two groups would lose the ability to interbreed entirely and become different species.
While Dobzhansky's work represented an advance in the formulation of a mechanism for evolution,
specialists understood that more was needed to explain microbe-to-man evolution.
The mutations that he discussed were primarily what we now call point mutations, or changes
in a single base pair in the DNA.
This kind of change can create alternative versions of a gene, but is not sufficient
to increase genome size.
There must be an increase in genome size if the original common ancestor of all living
things resembled a bacterium, as is widely held by evolutionary biologists.
Using our analogy, there must be a way to introduce new, information-containing chapters
into the instruction manual, not just a way to change an already existing sentence.
By the late 1960s and early 1970s, evolutionary biologists seemed to be making progress in
understanding how genomes could be increased and new genetic material could be introduced
without harming functionality and the fitness of an organism.
Much of the progress centered around the belief that large segments of the genetic code were
non-functional.
As evolutionary biologists studied the supposedly non-functional portion of the genomes, it
was observed that many regions appeared to be altered copies of other functional regions.
Biologists interpreted this to mean that genomes can be increased in size through various
means of duplication, with the result that organisms can possess more functional copies
of particular genes than are necessary.
These extra copies were then assumed to be free from selective pressure because they
were thought to be non-functional, and mutations could theoretically accumulate without affecting
the function of the organism.
Mutations or stretches of DNA that have nearly identical sequences to functional genes but
are not translated into protein are one of the most often cited evidences for this concept
involving duplication and the subsequent accumulation of mutations.
Additional information on pseudogenes will be discussed later in this episode.
Eventually, according to the evolutionary narrative, the accumulated mutations in pseudogenes
or other duplicated regions could somehow become functional.
The now functional duplications were said to give the population the plasticity required
for evolution to occur without the organism having to sacrifice its original advantageous
traits.
Through this process, it was claimed that the mechanism of evolution had finally been
worked out.
To summarize, for mutations to be a sufficient mechanism for naturalistic evolution, a large
part of the genome must be non-functional, allowing it to mutate without causing harm
to the organism.
Most mutations must be effectively neutral, causing neither a selective advantage for
the organism nor harm to the organism.
Some mutations or combinations of mutations must be beneficial, or in some way enable
the organism to survive and reproduce better than other members of its species.
These beneficial mutations must be passed down to the offspring more frequently than
neutral or harmful mutations that would occur in the same genetic space, so that they accumulate
in the population over great periods of time.
This accumulation of beneficial mutations would then give rise to new species and new
kinds of organisms.
Writing with confidence that the mechanism of evolution was confirmed through such evidence,
Richard Dawkins stated in 2004,
Genomes are littered with non-functional pseudogenes, faulty duplicates of functional genes that
do nothing, while their functional cousins get on with their business in a different
part of the genome.
And there's lots more DNA that doesn't even deserve the name pseudogene.
It too is derived by duplication, but not duplication of functional genes.
It consists of multiple copies of junk, tandem repeats, and other nonsense which may be useful
for forensic detectives, but which doesn't seem to be used in the body itself.
Once again, creationists might spend some earnest time speculating on why the creator
should bother to litter genomes with untranslated pseudogenes and junk tandem repeat DNA.
We will now explain why, within only a few years after Dawkins confidently wrote these
words, the entire argument for mutations as a mechanism was demolished, and Dawkins'
statement reveals a rush to judgment based on scientific ignorance and philosophical bias.
As early as the 1970s, scientists were aware that the majority of the human genome was
not translated into protein.
Richard Dawkins wrote in 1976,
As discussed earlier, this non-coding DNA quickly came to be known as junk DNA.
But this misnomer was due to an oversight on the part of the biologists, who initially
thought it was solely the presence of the protein products created from the genetic
information that determined the complexity of the organism.
In reality, the presence or absence of protein products is a tightly regulated, finely tuned
operation of turning genes on and off.
That is, of controlling when the genes are transcribed into RNA and how quickly the RNA
is translated into protein in specific cell types.
In order for an organism to be multicellular, it must not only possess the genetic code
for all the cell types in each cell, but it must have a way to turn the appropriate genes
off and on in each specific type of cell so that the eye cell produces proteins and
structures appropriate to the eye, and the liver cell produces proteins and structures
appropriate to the liver, and so on.
The instructions for all of this finely tuned gene regulation appear to lie in the tremendous
quantities of non-coding DNA present in the genome.
This means that so-called junk DNA is extremely important, an idea that has been confirmed
by recent genetic studies.
The Encyclopedia of DNA Elements, or the ENCODE project, was begun as a follow-on to the Human
Genome Project in 2003 at Stanford University.
The mission of ENCODE is to identify all functional elements in the human genome sequence.
The project is an open consortium and releases data rapidly and publicly so that it is available
to researchers.
After a successful pilot study, ENCODE launched a full-scale investigation of the human genome
in 2007.
The results have been surprising to evolutionists and are completely incompatible with the idea
of large amounts of the genome consisting of useless stretches of DNA.
According to a paper published in the journal Nature, ENCODE had already found some level
of functionality for at least 80% of the human genome by 2012.
Their criteria for functionality included, but was not limited to, being associated with
transcription of RNA or a chromatin event.
RNA, once thought to be limited to its role as a messenger that delivers instructions
from the DNA to ribosomes to facilitate protein production, is now known to have a myriad
of complex biochemical roles in the cell.
The fact that massive amounts of the genome are transcribed into RNA suggests that this
RNA has an identifiable function.
It would be a tremendous waste of energy and resources and surely detrimental, from an
evolutionary standpoint, for the cell to be making biochemical copies of vast amounts
of junk.
Also, the role of DNA in chromatin-associated events suggests that these stretches of the
genome are necessary for 3D and 4D characteristics of DNA.
The speed at which genes are transcribed is determined in large part by the way that DNA
interacts with its associated proteins, and the speed of transcription significantly impacts
the role the genes play in the cell.
ENCODE also identified a large number of enhancer-like and promoter-like regions, as well as regions
in the genome that appear to be under selective pressure, that is, to be specifically preserved
from mutations, likely because change in those regions would be so detrimental to the organism
that it would significantly impact its survival.
But it is not only ENCODE that is doing away with the idea of junk DNA.
Researchers investigating introns, the non-expressed regions of DNA sequence in between the expressed
regions, or exons, in a gene, have also been adding to our understanding of the complex
functionality of the genome.
Just prior to my time in the Corsi lab at the Catholic University of America, the graduate
researchers had identified a sequence in our model organism, C. elegans, that was highly
conserved, meaning it was present in almost identical form across a number of species
of nematodes, the tiny roundworms that belong in the same taxonomic family as C. elegans.
The lab members began to look for a function for this sequence, and discovered through
mutagenesis studies that it performed an important role in the development of the nematode's
muscles.
Further studies confirmed that this piece of supposedly useless intronic DNA was actually
an important binding site for a transcription factor.
Without it, no binding occurred, no protein was produced, and certain muscles just didn't
get built.
In addition to containing binding sequences for transcription factors, the proteins necessary
in gene regulation to turn expression of the gene on, introns within the genes have also
been identified as functioning in alternative splicing of genes.
Alternative splicing is an example of the highly ordered information present in the
genome and the extreme efficiency of the code.
In this process, a single piece of RNA created as a copy of a gene sequence can be cut and
pasted by cellular machinery in multiple ways.
Each one of these ways results in a different protein product, making alternative splicing
a highly efficient way to code for traits in the organism.
Introns have also been shown to act as enhancers for genes that are quite distant from the
intron itself.
Changing the length of the intron itself apart from its sequence may play an important
role in gene expression.
Longer introns would result in slower transcription and slower production of a protein product,
while shorter introns would result in quicker production.
This is likely to be yet one more way that cells keep the fine-tuned process of gene
regulation in check.
Even pseudogenes, which have long been put forward by evolutionary biologists as the
prime example of evidence for their theory about genome duplications and the accumulation
of neutral mutations, have recently been shown to have a function.
These genes, once thought to be evolutionary leftovers from duplication events, have been
shown to be transcribed into RNA.
The transcription alone would suggest that the sequences are functional, but this functionality
has been further confirmed by studies that support the idea that these sequences are
involved in RNA interference.
RNA interference, or RNAi, is a recently discovered phenomenon in which non-gene RNA sequences
bind to RNA transcribed from genes and interfere with the production of proteins from the genes,
effectively shutting off a gene that is no longer required at that time in a cell.
This function is sequence-dependent, meaning that the particular sequence of nucleotides
is crucial to the interference effect, and suggesting that the sequence of the pseudogene
is not so free from selective pressure as initially thought by evolutionary biologists.
It also explains why the pseudogene resembles a gene in sequence, but does not function
as a gene.
Several other pseudogenes have been found to code for RNA that is necessary for the
expression of the related gene, suggesting that some pseudogenes have an alternate function
in gene expression.
The scientists at ENCODE concurred with these studies in their paper published in Nature,
where it was reported that a large number of non-coding variants of genes were located
within regions that the ENCODE project had identified as functional.
On the whole, these results suggest that rather than simply being accidental duplications
that have been changed through mutation, pseudogenes are necessary and highly specific sequences
required for the expression of functional genes.
The pseudogene's similarity to its related gene should then be attributed to its function,
not to a purported evolutionary history.
This emerging data, taken together, lead to the logical conclusion that DNA, rather
than including large portions of junk that are free to mutate at the rate required for
molecules to man evolution, is largely or completely functional, and leaves little to
no room for the accumulation of mutations without harmful or deleterious impacts.
Dr. John Sanford, inventor of the gene gun and university professor at Cornell University
for over 30 years, summarizes the findings of the ENCODE project as follows in his book
Genetic Entropy.
ENCODE showed that the human genome is vastly more complex than genome scientists had expected
and that essentially all of the genome is transcribed, most of it in both directions.
They concluded that most nucleotides are not only functional, but are polyfunctional, having
multiple roles.
This means that the genome's functionality exceeds 100% most of both strands of the DNA
are functional.
If all of the genome is functional, I invite viewers to think back to our analogy of the
instruction manual for squirrels and to consider the implications.
The implication of having a fully functional genome is that all mutations must be harmful
or deleterious.
As Dr. Sanford states in light of the demise of junk DNA,
no mutations should be considered perfectly neutral and almost all mutations must be considered
deleterious.
And so, the question for evolutionists is, how can mutations build up a genome and produce
a man from an amoeba if all mutations destroy information and are harmful, even if one in
a million mutations appear to be beneficial, as will be discussed later?
Mutations tear down, they do not build up.
To underscore the truth that mutations destroy information and are therefore not neutral,
we will now introduce the next myth about mutations.
When the modern synthesis of Darwinian evolution and Mendelian genetics was initially developed,
scientists assumed a very low mutation rate, perhaps only on the order of one mutation
per generation.
By the late 1960s, it had become clear that the rate of mutations in organisms was significantly
higher than had been estimated in the 1930s.
Scientists now know that mutation rates vary widely among different species, with human
beings passing along as many as 50 to 160 mutations per generation.
This amount of change in each generation did not mesh well with evolutionary timescales,
especially as some mutations were clearly harmful or deleterious.
To avoid error catastrophe, or the accumulation of so many harmful mutations in a species
that extinction was inevitable, evolutionists had to posit that most mutations are neutral,
having little to no impact on the genome.
Dr. Sanford succinctly describes the biological constraints that require this designation
of neutrality.
The overwhelming majority of mutations should be nearly neutral.
All population geneticists would agree it can be seen by the total number of nucleotides.
On average, each nucleotide position can only contain one three-billionth of the total information
in the human genome.
Experimentally, we can show that most nucleotide positions have very subtle effects on any
given cell function, and only a few mutations are real killers of gene function.
Lastly, the nearly neutral impact of most nucleotides can be seen from the very subtle
role single nucleotides play in genome-wide patterns, codon preferences, nucleosome binding
sites, isochores, etc.
With as infinitesimal as these effects are, they are not zero.
This last point by Dr. Sanford deserves further consideration.
Motu Kimura, a population geneticist famous for developing the neutral theory of evolution,
published a paper describing the statistical distribution of mutations in the Proceedings
of the National Academy of Sciences.
A graphical representation of his calculations showed the relationship between the relative
deleteriousness, or damage done to the genome of the organism by the mutation, and the frequency
of that type of mutation occurring in the population.
As Kimura made visible on his graph, the frequency of mutations in the population decreases nearly
exponentially as their deleteriousness increases.
Thus, the number of highly deleterious mutations is very small compared to the number of nearly
neutral mutations, with the result that most mutations are characterized as neutral.
And while Kimura's representation posits that the large majority of mutations approach
zero effect, he shows that no mutations ever reach the point of having zero effect on the
genome.
This distinction between no effect and very little effect is an important one to understanding
a major obstacle to the mutations-as-mechanism explanation of evolution theory.
Evolutionary biologists often dismiss the impact of nearly neutral mutations, which
are really slightly harmful mutations, by simply relabeling them as neutral.
It is easy to see why this is a misnomer for mutations that occur within genes, as changes
in the DNA sequence of a gene often result in changes in the amino acid sequence of protein
coded for by the gene.
And as George Wald, a Nobel laureate, puts it,
"...one is hard put to find a single instance in which the change in one amino acid in a
protein does not change markedly its properties."
But it is a misnomer even for those nucleotides that are not part of a gene, as many of them
are involved in the regulation of genes as we have seen.
And as Dr. Sanford points out, even if a nucleotide were to carry absolutely no information, to
have, in effect, zero impact on any gene or any regulation of any gene, it would then,
by its very presence, have a deleterious impact on the organism, as it would require the expenditure
of energy and raw materials that could have been used elsewhere in a way that actually
benefited or enhanced the functioning of the organism.
These considerations support the conclusion that there are likely no truly neutral nucleotide
sites in the genome, with the logical extension that any mutation that occurs will negatively
affect gene expression in some way, however slight.
And this makes perfect sense in the context of a fully functional genome.
This distinction between truly neutral and nearly neutral mutations, while important,
is not the most problematic piece of evidence that nearly neutral mutations provide for
the mutations-as-mechanism hypothesis.
In Kimura's distribution of mutations, the author notes that the large majority of nearly
neutral mutations fall inside what could be called a no-selection zone.
These are the mutations that lie in the shaded region of the graph.
This means that when these mutations occur in an organism, they result in a deleterious
effect so slight that it is not acted upon by natural selection, and the mutations cannot
be removed from the population through evolutionary processes.
Kimura's premise of a no-selection zone can be seen to be particularly plausible when
we remember that natural selection does not act directly on the genotype or genetic sequence,
but only on the phenotype or physical characteristics of an organism.
A change in a gene sequence may confer a measurable loss of function in a particular protein,
but when this damaged protein is factored into the sum of physiological processes and
anatomical structures that belong to an individual organism, the change might on the whole be
so slight that the individual would not experience a measurable decrease in its fitness or in
its reproductive success.
Thus, the individual would pass down its defective gene to its offspring, which would pass it
down to their offspring, and on through succeeding generations.
When this is the case, these slightly deleterious mutations can become prominent or even fixed
in a population and contribute to an overall decline in fitness of the group of organisms.
But the problem does not stop with slightly deleterious mutations that occur in just one
generation.
Each generation adds its own nearly neutral or slightly deleterious mutations, and these
accumulate over time in the genome.
This means that as the genome is waiting for the rare beneficial mutations to accumulate
and drive the evolutionary process, the rest of the genome is rapidly degrading in relative
terms.
Over time, the genome will accumulate so many harmful mutations that it will eventually
break down due to the cumulative effect of harmful mutations well before Darwinian evolution
can occur.
As Dr. Sanford explains, just as rust slowly building up on a vehicle will one day cause
the vehicle body to fall apart, so will the slow accumulation of mutations lead to an
eventual failure of the organism's body.
Time is the enemy of evolution and the genome, not its friend, and degeneration of the genome
over time is inevitable.
Dr. Sanford concludes,
If the genome is actually degenerating, it is bad news for the long-term future of the
human race.
It is also bad for evolutionary theory.
If mutation selection cannot preserve the information already within the genome, it
is difficult to imagine how it could have created all that information in the first
place.
We cannot rationally speak of genome building when there is a net loss of information every
generation.
Anyone who has taken an introductory biology class will have been exposed to the statement
that it is the rare beneficial mutation that drives evolution.
Along with such statements, there are usually a number of alleged examples of beneficial
mutations provided.
These examples may look plausible on the surface, but a closer examination is required to see
if they truly confer an evolutionary advantage on the organisms they affect without compromising
the overall genetic information available to the organism.
One commonly cited example of a beneficial mutation is the development of antibiotic
resistance in bacteria.
The story of bacterial resistance to antibiotics begins with a single bacterium experiencing
a mutation that makes it immune to the action of the antibiotic.
When the population is exposed to the antibiotic, the non-resistant bacteria die off, leaving
behind only the resistant bacteria, which reproduce until there is a new bacterial population.
Since the new population is descended from the resistant bacterium, the entire population
is now resistant to the antibiotic.
This is seen in real-time in hospitals, where the spread of methicillin-resistant Staphylococcus
aureus, or MRSA, presents a tremendous health concern.
But the question remains, does this provide an example of a truly beneficial mutation,
and if so, is it an example of evolution in action?
Before discussing the details of antibiotic-resistant mutations, it is helpful to understand what
Dr. Sanford has to say about purported beneficial mutations in bacteria in general.
There are a few isolated cases where it is claimed that certain laboratory experiments
demonstrate remarkably high rates of beneficial mutation.
The key to understanding these claims of superabundant, high-impact beneficial mutations is that a
large part, up to 50%, of any microbial genome consists of just-in-case genes which need
to be precisely regulated.
These genes are crucial in the real world, conferring tolerance to a host of specific
stress conditions.
But in an artificial and changing laboratory environment, such genes are just dead weight.
Breaking or deleting such non-essential genes will very often conserve energy and allow
faster growth in the artificial environment.
Under these artificial conditions, many diverse beneficial mutations can arise that involve
the loss of information, loss of function, a genetic degeneration, like stripping down
a car for a race.
Describing such mutations as beneficial is really a misnomer.
They actually represent adaptive degeneration.
This is best seen in the famous long-term Escherichia coli experiment by Lenski and
colleagues.
E. coli did indeed adapt to a certain artificial environment and on a specific medium could
grow slightly faster.
But when the enabling beneficial mutations were analyzed, they all involved loss of function
events, either broken genes or broken promoters.
Genome size consistently shrank.
This is clearly not how genomes are built and speaks directly to the problem of genetic
degeneration.
If this analysis by Dr. Sanford is correct, we would expect to see broken genes in the
antibiotic-resistant strains of bacteria.
Or in other words, we should expect to see loss or diminishment of function in a gene
that the bacterium needs to survive.
The antibiotic resistance should only be an accidental side effect of this loss of function
and not the gain of an independent newly acquired function.
And this is exactly what we do see in the mutation that leads to methicillin resistance
in Staphylococcus aureus or MRSA.
MRSA strains express a protein variant of a normal protein involved in cross-linking
the bacterial cell wall.
In non-resistant bacteria, methicillin binds to this protein and prevents cross-linking,
weakening the cell wall and leading to the death of the bacterium.
The mutation found in MRSA causes the cross-linking protein to have an altered affinity for methicillin.
In other words, the antibiotic binds to the mutated protein less efficiently than it does
to the normal protein.
This makes therapeutic doses of the antibiotic ineffective.
While this benefits the bacterium in the presence of the antibiotic, it actually also weakens
the cross-linking in the cell wall.
So MRSA has weaker cell walls than non-resistant strains of Staphylococcus aureus because of
the inefficient cross-linking by the mutated protein.
Because of this weakness, MRSA is readily out-competed by non-resistant Staphylococcus
aureus when antibiotics are removed.
The mutation, while beneficial in one situation, is highly detrimental in others.
MRSA is not alone in demonstrating that antibiotic resistance involves broken genes.
Certain species of the Klebsiella genus are resistant to the antibiotic streptomycin.
In bacteria that are not resistant, streptomycin passes across the cell membrane and binds
to the bacterial ribosomes, the protein-making factories inside the cells.
The attachment of the antibiotic to the ribosome prevents protein synthesis, and the lack of
proteins results in the death of the bacterium.
Resistant bacteria have modifications in the site on the ribosome where streptomycin
would normally attach, which keeps the antibiotic from binding and disrupting protein synthesis.
While this disrupted binding site results in greater fitness of the individual bacterium
under the selective pressure of the antibiotic, the ribosomes of the resistant bacteria were
significantly less efficient at protein synthesis than the ribosomes of the bacteria that were
not resistant.
Experiments showed that the non-resistant bacteria, who could still make proteins properly,
quickly out-competed the resistant bacteria when the two populations were mixed together
in the absence of the antibiotic.
This is yet another example of how it is the loss of function of a crucial component of
the bacterium that results in the antibiotic resistance, and this loss of function is ultimately
detrimental to the organism.
In both of these examples, it can easily be seen that the organisms have gained new functions
at the expense of losing something and their already existing functions.
One might think of an organism, or even of a single cell, in some ways as a zero-sum
game.
In order for one function to be improved, another function must be changed, modified,
or perhaps destroyed.
We have to look at what is going on both at the level of the organism and its interactions
with the environment, and the DNA sequence.
Just because something looks functional on the outside, like antibiotic resistance, it
does not mean that from a genetic and molecular perspective that any new information is being
added to the genome.
In fact, the reverse is most often true.
The mutation is causing an overall loss of specificity at the molecular level, and it's
hard to imagine how things getting more and more formless could lead to the kind of molecules
demand transitions that evolution requires.
But what about organisms other than bacteria?
We will examine here a notable example of beneficial mutation in humans and determine
whether these benefits derive from the input of new information into the genome, or from
a similar loss of specificity to what we observed in the bacterial world.
A recent example of purported beneficial mutation in human beings is a mutation in CCR5, a protein
normally present on the surface of human immune cells.
The gene for the mutant protein is missing 32 base pairs that are present in the normal
gene.
This mutation causes a frameshift or an alternate reading of the genetic code, introducing an
early stop signal and making the mutant protein short by 137 amino acids.
The absence of these amino acids makes T-cells resistant to infection by the deadly HIV-1
virus and also has been associated with lower numbers of circulating viruses in individuals
that are infected.
Because of this resistance, the deletion confers a potentially life-saving benefit to individuals
exposed to the virus.
Unfortunately, the loss of this part of the protein also makes CCR5 incapable of being
properly placed in the cell membrane.
When it cannot be positioned in the membrane, it cannot perform its normal role as an important
receptor for chemical messengers that are integral to the human immune response.
Because of this loss of function, the deletion is associated with serious liver disease and
early death in patients with multiple sclerosis.
The loss of these 32 base pairs can certainly be considered a loss of function.
We see again the same pattern of a supposed benefit being the result of a broken protein
that negatively impacts the overall health and well-being of the individual.
As Dr. Donald Batten of the University of Sydney explains,
Evolutionists are continually holding up examples of evolution via adaptive mutations to try
to convince us that it really does work.
However, the sorts of examples they provide include loss of Satan cavefish and cave salamanders,
loss of functional wings in beetles on a windy island, loss of control of the enzyme action
or a defective uptake channel causing antibiotic resistance, and a defective gene in tomcod
fish that helps them survive in water polluted with PCBs.
This repeated loss cannot lead to the gains necessary to drive molecule-to-main evolution.
When Darwin published his Origin of Species, he did a disservice to the scientific community
by introducing confusion regarding the concept of animal kinds.
Prior to Darwin, naturalists grouped animals into kinds, which roughly corresponded to
families in the Linnaean system of classification.
For example, lions, tigers, and cheetahs, while today we would consider them separate
species, all fall under a common can't kind.
Though some mistakenly held to a complete immutability of species, variation within
a kind was still seen as part of God's plan for creation and not as evidence of a naturalistic
mechanism for the development of animals.
By discussing species instead of kinds, Darwin used a clever sleight of hand to distract
his readers from the lack of evidence he presented for how novel body forms could be
developed.
Today, nearly 160 years after the Origin of Species, there are still no empirically verified
examples of one kind of organism ever evolving into another kind.
Today, scientists use at least 26 different conceptions of the idea of a species.
The most common definition is the biological species definition, which emphasizes reproductive
isolation.
Under this definition, two organisms are considered to be of the same species if they can successfully
reproduce fertile offspring.
But even this seemingly straightforward definition poses a problem for evolutionary biology.
One of the most often cited examples of evolution in action are the Galapagos finches.
As discussed in episode 5, within the last 25 years, it has been discovered that interbreeding
among most of Darwin's finch species produces fertile offspring.
According to the biological definition of species, this would force us to conclude that
most of the finches do not constitute separate species.
Rather than demonstrating evolution, the finches show limited variation within a species, not
the development of a new species, and certainly not the development of a new kind.
This limited variation within a species is observed over and over again in the laboratory.
Fruit flies, Drosophila melanogaster, have been a favorite organism for mutation studies
in the laboratory since Morgan's Fly Room in the early 1900s.
Yet despite increasing mutation rates in Drosophila by up to 15,000%, scientists have
never observed a change that has resulted in anything other than a fruit fly.
And the mutations that are observed are often evolutionary dead ends.
One notable example of this is the four-winged fruit fly.
The fly sports not only the normal wings on the first thoracic segment, but a second pair
of fully developed wings on a second thoracic segment.
The fly seemed to be an almost irresistible visual aid for textbook writers at the turn
of the 21st century.
Looking at it, one might easily imagine that mutation and natural selection could give
rise to new body forms.
But what is really happening at the genetic level?
A series of three artificially crossed mutations caused a normal body structure of the fly,
the halter, to develop instead into a wing.
The halter, while small, is essential to Drosophila for maintaining balance during flight.
So, the mutant fly lost a normal body structure, and this normal structure was replaced, not
by a new structure, but by a structure that the fly already had coded in its DNA, which
was simply repeated at another position on the fly's body.
Also, while the new wings look impressive, they are not attached to any musculature within
the body of the fly, and so are not operational.
Instead, they are dead weight and impair the mutant's ability to fly and to mate with
other flies.
Without special preservation within the laboratory, the four-winged fly would very quickly die
out and be nothing more than an interesting footnote in mutational studies.
It would certainly not constitute evidence for the evolution of a new kind of animal,
especially since it had no way of passing on its genes.
Even within bacteria, the easiest organism to mutagenize, we see an incredible tendency
towards a lack of evolution into anything other than slightly modified bacteria.
Despite the over 2.5 million generations that could be cultured in 100 years, biologists
have not observed the development of a new kind of organism.
Even MRSA, with its antibiotic resistance, is not a new organism, but only a modified
version of Staphylococcus aureus.
According to Pierre Grasse,
For millions or even billions of years, bacteria have not transgressed the structural frame
within which they have always fluctuated and still do.
This observation leads him to the conclusion that
to vary and to evolve are two different things.
While evolutionists claim that variation within species can be extrapolated into variation
between species and the development of completely novel species or kinds, the evidence, as we
have seen, is to the contrary.
Despite over 100 years of studies of mutations in bacteria, fruit flies, nematodes, mice,
and other model organisms, there has not been a single documented case of an organism giving
rise to a new kind of organism, but only to a variation on the theme of the organism
being mutagenized.
The changes that are observed in the laboratory sometimes appear dramatic, as with the four-winged
fruit fly, but they involve loss of function and loss of information, and extrapolating
them into evidence for molecules to man evolution is simply unreasonable.
In conclusion, evolution requires a tremendous amount of junk DNA for the accumulation of
mutations, but as we have seen, the vast majority of the genome has at least a putative function,
if not an experimentally verified function, which would be disrupted by mutation.
Evolution requires that a large number of mutations are neutral and some are beneficial,
but as we have seen, all cases of mutation that have been observed experimentally involve
the loss of information in the affected gene and the loss of function in the protein for
which the gene codes.
These mutations would result in reduced reproductive success if they were visible to natural selection
and the accumulation of slight damage to the genome in each successive generation if
they are not.
Evolution requires that the accumulation of mutations give rise to new kinds of organisms,
but as we have seen, though some kinds show tremendous variety and adaptability, one kind
has never been shown to give rise to another.
And, in fact, animal kinds seem to have a remarkable inherent stability and tendency
to revert to the mean under changing selection pressures.
As we have seen, evolution fails.
It fails to take into account a complete or nearly complete lack of room for error in
the genome, to establish any examples of known mutations that do not destroy useful information
in the genome, or to directly demonstrate that the accumulation of mutations leads to
a new organism.
Mutations, as a reasonable mechanism to explain the diversity of life, belong to the realm
of mythology rather than science, and scientific study will continue to be impeded as long
as the false view of mutations as a viable mechanism for evolution remains unchallenged.