© 2009, 2010 by Cornelius Hunter
Last updated: February 13, 2010
1.2 Two examples
Charles Darwin presented his theory of evolution in 1859. In
the century and half since then our knowledge of the life sciences has
increased dramatically. We now know orders of magnitude more than
It is not controversial that a great many predictions made by
When a scientific theory makes a prediction that is discovered to be false, then sometimes the theory is simply modified a bit to accommodate the new finding. Broad, umbrella theories, such as evolution, are particularly amenable to adjustments. Evolution states that naturalistic mechanisms are sufficient to explain the origin of species. This is a very broad statement capable of generating a wide variety of specific explanations about how evolution is supposed to have actually occurred. In fact evolutionists often disagree about these details. So if one explanation, dealing with a particular aspect of evolution, makes false predictions, there often are alternative explanations available to explain that particular aspect of evolution. Obviously the theory of evolution itself is not harmed simply because one particular sub-hypothesis is shown to be wrong.
Failed expectations are not necessarily a problem for a theory.  But what if fundamental predictions are consistently falsified? As we shall see this is the case with the theory of evolution. Evolutionists are commonly surprised by the scientific evidences from biology. The evidences do not fit the evolutionary expectations. Evolutionists argue strenuously that these surprises are not problems, but rather are signs of scientific progress. With each new finding, evolutionists say, we learn more about how evolution occurred. Is this true or simply a case of partisanship in science? How can we tell?
Classical physics was elucidated in the seventeenth century. It explained how objects move and the theory worked well for many years until it was found to fail at very high speeds and in the subatomic world. Objects travelling near the speed of light and tiny particles did not obey the venerable laws of physics, and the new areas of physics known as relativity and quantum mechanics were required. Classical physics still worked well for traditional types of problems, but it was now understood to be a special case of the more general descriptions provided by relativity and quantum mechanics. It seems obvious that classical physics ought not to be dropped. It simply has a limited domain of applicability. In this example, it seems reasonable to say that the new findings are not so much a problem for classical physics so much as a refinement. We learned more about how objects move, regardless of the precise relationship between classical physics and quantum mechanics. 
Geocentrism dates back to antiquity. The idea that the objects in the sky rotate around the earth seems quite reasonable. After all, the stars can be seen to move across the sky every night. So do the moon and planets, and the sun by day. Was not the earth at the center of the universe? But there are anomalies in these motions. Sometimes the planets move backwards, for instance, and the geocentric model did not always work very well. Its false predictions, however, could be accommodated by adding adjustments. The anomalous motions of heavenly objects were described with dozens of epicycles. This highly complicated version of geocentrism worked very well. The positions of objects in the sky, and even eclipses, could be predicted in advance. Heliocentrism eventually replaced geocentrism not because it was more accurate, but because eventually it could be made to be so much simpler.  In this example, it seems obvious that the failures of geocentrism are not merely a case of refining the theory. In this case it seems that the theory is false.
The difference between these two examples is not so much in whether there were falsifications but in how the falsifications were accommodated. Both classical physics and geocentrism had their falsifications. But classical physics was understood to have limited domain of applicability whereas geocentrism became tremendously complex—to the point of seeming to be more of an exercise in fitting the data rather than explaining nature. One can always fit the data if one is willing to employ heroic mechanisms and explanations. 
This brings us to the issue of simplicity, or parsimony, in scientific theories. It has long been understood that elaborate explanations can always be contrived in order to explain observations. But why should we believe they are true? The backward motion of planets can be explained by a series of epicycles, designed specifically to fit the peculiar motion. But with heliocentrism no such adjustments are required—the backward planetary motion is a natural outcome.
So while complicated narratives are needed for bed-time stories and soap operas, parsimony is valued in science. Nature, and only nature, should be explained. Scientists become suspicious when a theory becomes increasingly complex to accommodate failed expectations—when particular explanations are needed to adjust to contradictory findings.
Falsifications can also be a sign of problems if they are common. If a theory makes predictions that are consistently wrong, then suspicion again arises. Regardless of how much complexity is needed to explain the contradictory findings, a steady stream of such findings, in itself, can indicate weakness.
Evolution has a long history of false predictions leading to rising complexity. The evolutionist’s claim that all of this is a sign of good science, of learning how evolution actually occurred, is not consistent with evolution’s many falsified predictions and complex adjustments. This document summarizes a representative set of such false predictions. Each prediction was a natural and fundamental expectation of the theory of evolution, and was held by leading, mainstream, evolutionists. Because these predictions were fundamental, their falsification required substantial increases in the complexity of the theory of evolution. In addition to summarizing each prediction and its falsification, this document includes the reactions of evolutionists showing how the contradictory findings were accommodated. Section 7 concludes with an examination of why evolutionists believe their theory is a fact and what this tells us about the theory.
This section examines various objections evolutionists make in defending their theory’s false predictions and added complexities.
A proponent of a theory, given sufficient motivation, can explain all kinds of contradictory findings.  Evolutionists have accommodated its many false predictions. The problems have been “fixed,” but in the process the theory has grown tremendously complicated. Scientists are suspicious of theories that morph in many directions to fit the data.
Criticism of evolution draws heated responses, and personal attacks are common. Such attacks, however, do not change the fact that evolution has, like geocentrism, generated many false predictions and as a consequence grown more complex.
Evolutionists often ignore or deny the problem of unexpected findings and theory complexity. They attempt to discredit the facts, referring to them as “tired old arguments,” or fallacies. Rarely do evolutionists follow-up such criticisms with supporting details. Until such details are provided we cannot know if these criticisms are sound.
It has been argued that in order to qualify as science, ideas and theories need to be falsifiable. Also, falsified predictions are sometimes used to argue a theory is false. Such naïve falsificationism is flawed  and not used here. Evolution’s many false predictions do not demonstrate that evolution is not science or that evolution is necessarily false. The question of evolution’s truth value is not simple, and beyond the scope of this document. Of course these fundamental false predictions would be considerations in such an assessment.
False predictions are valuable in judging the quality of a theory, and for improving our scientific understanding in general. Nonetheless, evolutionists sometimes reject any mention of their theory’s false predictions as mere naïve falsificationism. The failures of falsificationism do not give evolutionists a license to ignore substantial and fundamental failures of their theory.
Sometimes evolutionists simply point out that their theory has not been falsified. There may be many false predictions, but they do not prove evolution to be false. While this is true, it is not a sign of a healthy theory. First, evolutionists consider their theory to be a fact. Its immunity to scientific surprises reveals the degree to which the theory is protected. Second, evolution has become tremendously complicated as it has had to adjust to the scientific data.
This objection falls under the category of naïve falsificationism. Science is a reactive process. New evidence is processed, and theories are adjusted accordingly. But science can also be a conservative process, sustaining substantial problems before reevaluating a theory. Therefore the reevaluation of a theory takes time. The fact that there are problems is no guarantee a theory will have been toppled. [1,6]
Many scientists doubt evolution, but they are not cited or quoted in this document. Only material from evolutionists is used to illustrate that even those who believe in the theory admit to the falsifications and complications. These people believe in evolution, but that does not mean the problems do not exist.
Could it be that the problems are inconsequential, since
those quoted have not given up on evolution? No, not necessarily. Theory
acceptance is complicated. There are many reasons why scientists continue to
believe in weak or problematic theories, including conservativeness, financial
factors, social and institutional pressures, and so forth. While these reasons
may at times be important in the case of
As scientists, we need to evaluate scientific theories according to the currently available data. No one knows what future data may bring, and the claim that future data will rescue evolution is ultimately circular.
One way to evaluate a theory is to compare it to alternative explanations. There are, however, potential pitfalls to this approach. First, any such comparison will crucially depend on what alternative explanations are used in the comparison. If care is not taken good alternatives can be misrepresented or even omitted altogether. And of course there may be alternatives not yet conceived. [7,8]
Also, such comparisons can become a way to protect a theory by shifting attention away from its problems. Comparisons are interesting and important, but they do not eliminate a theory’s track record of performance. Nonetheless, comparisons to evolution’s alternatives have always been fundamental in evolutionary thought and are critical to understanding evolutionary thinking. Section 7 examines this in more detail.
Yes, this is the point. It is true that evolutionists have, for the most part, dropped many predictions that were once made by evolutionists or entailed by the theory. This suggests that the theory does not have a good track record.
Some arguments for evolution are theological or philosophical in nature. Many have concluded that God would never have created the biological world we observe. This includes Darwin as well as many thinkers before and after him. This conclusion suggested evolutionary theories, in one form or another.  Such arguments cannot be countered with scientific evidence so empirical problems, such as falsified predictions, often are less important to evolutionists. Section 7 examines this further.
Evolutionists argue that evolution is a fact, and that we ought to focus on evolution’s successful predictions rather than its false predictions. The tendency to seek confirming evidence over contrary evidence is known as confirmation bias.  One consequence of confirmation bias can be that confirming evidence is viewed as correct and typical whereas disconfirming evidence is viewed as anomalous and rare. Not surprisingly the confirming evidence is more often retained and documented. Rarely are the many false predictions found in evolution texts. Confirmation bias can hinder scientific research, particularly when researchers believe they know the truth, as do evolutionists. They view the important predictions of evolution as predominantly true. False predictions, on the other hand, are usually not viewed as legitimate falsifications. Instead, these are interpreted, more positively, as open research questions which are yet to be resolved. Indeed, evolutionists often make the remarkable claim that there is no evidence that is contrary to evolution.
This is a living document under version control. A new version number is assigned every time the document is changed. The version number increases by one when the table of contents changes. The version number increases by 0.1 when substantial content changes are made. The version number increases by 0.01 when minor content changes are made, such as changes in terminology, clarifications, grammatical corrections, and so forth.
All figures are used under the GNU Free Documentation License or are original.
Version Description of changes
1.1 Two new objections, and additions to the Falsificationism is flawed objection, in Section 1.4. Additions to the Reaction of Section 2.1. Additions to the Falsification and Reaction of Section 3.1.
2.0 Addition of Section 6.1.
3.0 Addition of Section 5.4.
Many predictions of evolution have been falsified, including foundational expectations. Evolutionists have added explanations to their theory to account for these problematic findings. The drawback is that this greatly complicates the theory. Scientific theories are supposed to be parsimonious, explaining future findings with simple explanations rather than explaining past findings with complicated explanations.
Therefore evolutionists are faced with a accuracy-versus-parsimony tradeoff. The scientific findings make their original theory inaccurate. That is, the theory does not fit the empirical evidence well. The only way to increase evolution’s accuracy is to complicate the theory tremendously and sacrifice parsimony. Evolutionists have consistently preferred low parsimony over low accuracy.
The theory of evolution has consistently failed and as a
consequence it has grown far more complex than anything
In stark contrast to these evidential problems, evolutionists believe that their theory is a fact. Evolution is a fact, they say, just as gravity is fact. This remarkable claim is an indicator that there is more to evolution than merely a scientific theory. In light of the scientific evidence, the claim that evolution is a fact may seem to be absurd. But it is not.
The fact of evolution is a necessary consequence of the metaphysical assumptions evolutionists make. Metaphysical assumptions are assumptions that do not derive from science. They are made independent of science. These metaphysical assumptions that evolutionists make would be difficult to defend as necessarily true outside of evolutionary circles, but within evolution their truth is not controversial. All of this means that the scientific problems with evolution are relegated to questions of how evolution occurred. The science cannot bear on questions of whether or not evolution occurred.
I am grateful for the discussions with, and comments from, the reviewers of this work who remain anonymous.
This section examines evolutionary predictions dealing with the DNA (deoxyribonucleic acid) structure, code and replication.
DNA is a double helix. As Fig. 1 illustrates, it contains two strands that are twisted about each other, just as a rope might consist of two smaller ropes wrapped around each other. Both DNA strands consist of a series of molecules bonded together in sequence. The molecules are called nucleotides and if you stretched out the strand the nucleotides would line up in a row, like beads on a string. These nucleotides are the DNA’s information which encodes the genes in the DNA. If each nucleotide represents a letter, then a gene is similar to a paragraph in a book. DNA strands use four different kinds of nucleotides, so in this language there are only four letters.
Figure 1 DNA contains genes and is a double helix consisting of two strands.
A tremendous amount of effort has been spent on understanding how these molecular letters are read. In 1953, before the DNA structure was deciphered using X-ray photographs, the great American chemist Linus Pauling predicted that the nucleotides pointed outwards from a helix. A few years earlier Pauling had successfully predicted the helix structure of proteins. Now he would try to do the same for the DNA structure. If the nucleotides pointed outwards, Pauling reasoned, they could be read without having to pull apart the DNA. But this time Pauling’s intuition failed him.
Not long after that Francis Crick and James Watson, working
Watson and Crick’s new DNA model was a great breakthrough and soon DNA was viewed as the blueprint that was modified over the course of evolution to create new species.
Most evolutionists believe that the first life arose from non-living
chemicals. In a letter
It was not easy to explain how something as complicated as a
living cell could emerge on its own. Evolutionists needed to start with
something far simpler than an entire cell. If some fundamental component of the
cell could arise on its own, perhaps then the other cellular components would
gradually aggregate and eventually build up to a complete cell. The research
was driven not by positive scientific findings so much as the acceptance of
Before Watson and Crick discovered the DNA structure, some evolutionists felt that life began with a single gene. With the gene’s molecular structure explained by Watson and Crick, this genes-came-first view began to take shape. That first gene, it was then understood, would have been a segment of DNA.
Nobel Laureate H. J. Muller had promoted the genes-came-first idea, and the DNA structure did nothing to detract from his convictions. He continued to advocate for the primacy of genes. After all, DNA coded for proteins, not vice-versa. A segment of DNA contained the sequence information for a protein, but a protein did not contain the DNA sequence information.
The great popularizer (and scientist) Carl Sagan also held to this idea that life must have come from non-life via the spontaneous assembly of DNA. Sagan used the term “naked gene” to convey the idea that life began with DNA, absent the other cellular components and environment. 
The prediction that the DNA molecule formed on its own, and then led to the formation of the first life, we now know is problematic for many reasons. For instance, each nucleotide, consisting of its nitrogenous base, ribose sugar and phosphate group, is a fairly large organic molecule. These do not spontaneously form, even when the right ingredients are coaxed together in experiments mimicking some hypothetical primitive, early Earth condition. “There is at present,” concluded one senior researcher recently, “no convincing, pre-biotic total synthesis of any of the nucleotides.” 
Beyond this there remain several more problems. For instance, even if nucleotides could somehow form on their own, they would likely be at low concentrations because there are many alternate conformations they could assume. Also a great many other organic molecules could form in the brew. What is needed is a particular type of molecule, not a menagerie.
And even if the right type of building block molecule could somehow be created at reasonable concentrations, these molecules would have to polymerize (i.e., chemically bond to form a sequence, like beads on a string). This requires energy and precision. Nonetheless, what is needed are long DNA polymers (thousands or at the very least hundreds of nucleotides long).
Next the nucleotides must encode information. Even if DNA polymers could form on their own, they cannot be just any polymer. Long DNA polymers that are functional are rare. One experiment, dealing with randomized protein sequences, showed that about one hundred trillion such sequences are needed before even a simple binding function is obtained.  This result is optimistic because the protein was relatively unstable and short. Most proteins are several times longer, and longer sequences would likely have even lower rates of functionality. Also the function was elementary. Proteins that do something useful do far more than merely bind to a chemical.
Finally, even if long, functional DNA polymers could form on their own, they would need helper molecules (such as today’s proteins) to perform the copying, translating and replicating tasks. This chicken-or-the-egg problem arises because DNA alone cannot perform the various tasks needed to form a living entity, no matter how simple.
The theory of evolution motivated the idea that a lone DNA molecule was the starting point for the history of life on Earth, but we now know of several substantial problems with this hypothesis. Alternative theories have not fared well either.
To address these many failures of earlier expectations,
evolutionists have continued to speculate about how first life could have
arisen, constructing a variety of complicated hypotheses. For instance, one
idea is that evolution formed information bearing, functional sequences via
natural selection. The appeal to natural selection certainly fits well within
the theory of evolution, but is rather heroic in this case because selection
requires that many test trials can be run with a mechanism for selection. In
Another hypothesis evolutionists constructed in recent decades is that life began not with DNA but with its cousin molecule, RNA. There is no trace of this today, but evolutionists hypothesized that first life was RNA-based, and then at some point it switched to DNA. This more complicated hypothesis takes advantage of the fact that RNA not only can store information like DNA, but also can accomplish some of the copying tasks by itself, without the help of proteins. Soon the DNA-first hypothesis was replaced with the idea of an “RNA world,” which gave evolutionists substantially more room to speculate. [8,9]
The new RNA world hypothesis was often interpreted as more or less solving the problem of how the first replicating molecule arose. Yet even if this hypothesis completely resolves the chicken-or-the-egg problem, there still remain the other problems we reviewed above, including nucleotide synthesis and low concentration, polymerization and information. As one paper put it, the RNA world is a “prebiotic chemist’s nightmare.” For as Leslie Orgel explained, “The prebiotic synthesis of nucleotides in a sufficiently pure state to support RNA synthesis cannot be achieved using presently known chemistry.”  This has led to the search for substitutes for DNA and RNA which perhaps could do the job initially, and then be replaced by today’s genetic system at some later time. But DNA and RNA have excellent properties and substitutes do not come close to fulfilling their roles. As Robert Shapiro writes:
Gerald F. Joyce of the Scripps Research Institute and Leslie Orgel of the Salk Institute concluded that the spontaneous appearance of RNA chains on the lifeless Earth “would have been a near miracle.” I would extend this conclusion to all of the proposed RNA substitutes that I mentioned above. 
No one can say what future research will tell us, but the evolutionary hypotheses from the early and mid 20th century about how life initially arose have led research down long, circuitous, trails. Consequently evolutionary ideas of how life arose are highly complex, consisting of low-probability events and substantial serendipity.
To avoid this falsification, many evolutionists argue that their theory does not encompass the origin of first life. This is erroneous and in stark contrast to the evolution literature which consistently includes the origin of first life within the theory of evolution. Here are representative textbook examples:
Life may have evolved from inanimate matter, with associations among molecules becoming more and more complex. In this view, the force leading to life was selection; changes in molecules that increased their stability caused the molecules to persist longer. In this text, we … attempt to understand whether the forces of evolution could have led to the origin of life and, if so, how the process might have occurred. 
The next step in our story is the most difficult to understand completely. From the jumbled mixture of molecules in the organic soup that formed in Earth’s oceans, the highly organized structures of RNA and DNA must somehow have evolved. 
A Self-Replication System Evolves … According to the RNA-first hypothesis, RNA would have been the first to evolve, and the first true cell would have had RNA genes. 
Though evolutionists do not know how the first cell could have evolved, they refer to the hypothetical processes leading up to the first cell as chemical evolution, and subsequent processes as biological evolution.  Because these two evolutionary processes are speculative, there can be some degree of overlap in how these processes are conceived. For instance, selection is contemplated as a mechanism for chemical evolution, as well as biological evolution.
Darwin speculated about chemical as well as biological evolution, and since then evolutionists have continued to speculate and search for mechanisms to explain both types of evolution. The prediction that the DNA structure gave rise to first life deals with chemical evolution rather than biological evolution.
DNA is often illustrated as having a twisted ladder shape, where two strands wind around each other to form a helix. What is more difficult to illustrate is the fact that each strand is a sequence of molecules called nucleotides, and that there are only four different types of nucleotides. Each nucleotide is a symbol, or letter, in the DNA code, so each strand can be thought of as a sequence of letters. In this code each word is three letters long. With an alphabet of four letters and words that are three letters long, the total number of possible words is 64 (43).
In the early 1960s Marshall Nirenberg of the National
Institutes of Health broke the code for one amino acid. Nirenberg, Severo Ochoa
The DNA code is sometimes referred to as the genetic code, and its words are referred to as codons. Of the 64 codons, 61 of them code for amino acids which are used to make proteins (the remaining three indicate the end of the gene). A DNA sequence, therefore, translates into a protein sequence. For instance, our sequence ATGACGGAG codes for the amino acids methionine (Met), threonine (Thr) and glutamic acid (Glu), as illustrated in Fig. 2.
Figure 2 A sequence of nucleotides in a DNA strand is translated into a sequence of amino acids, via the genetic code.
Shortly after the discovery of the DNA code, evolutionists began theorizing how it could have arisen. The same code was found in very different species which, for an evolutionist, means that the same code was present in their distant, common ancestor. In other words, according to evolution, the DNA code must have arisen when the common ancestor to all life appeared, and then the code remained essentially unchanged thereafter.
Various theories of the code’s origin soon emerged. Perhaps the code was, to some extent a consequence of chemistry. The codons AAA and AAG, for example, would in this case code for the amino acid lysine because lysine was somehow stereochemically “related” to these two codons. Or perhaps the code evolved to reduce the impact of mutations. On the other hand, perhaps the codon-to-amino acid mapping was simply a matter of chance. These different theories and their variations and intermediates were considered.
It is not easy to generate plausible explanations for how the DNA code evolved and evolutionists were impressed with “the great difficulty of the problem.”  Therefore it is not surprising that no theory emerged as a clear winner. A common thread in evolutionary thinking, however, was that the code was not particularly unique or special. For how could such a code have evolved so early in the history of life? As Nobel Laureate Francis Crick wrote in 1968:
There is no reason to believe, however, that the present code is the best possible, and it could have easily reached its present form by a sequence of happy accidents. 
Regardless of how the code was thought to have evolved, this view became common among evolutionists. As one widely used undergraduate molecular biology text later put it:
The code seems to have been selected arbitrarily (subject to some constraints, perhaps). 
This was in spite of the fact that even a casual inspection of the code reveals substantial structure. Yet evolutionist Mark Ridley explained in his 1993 evolution textbook:
The most popular theory is as follows. The code is arbitrary, in the same sense that human language is arbitrary. In English the word for a horse is “horse,” in Spanish it is “caballo,” in French it is “cheval,” in Ancient Rome it was “equus.” There is no reason why one particular sequence of letters rather than another should signify that familiar perissodactylic mammal … All living species use a common, but equally arbitrary, language in the genetic code. The reason is thought to be that the code evolved early on in the history of life, and one early form turned out to be the common ancestor of all later species … The code is then what Crick called a “frozen accident.” The original choice of a code was an accident; but once it had evolved, it would be strongly maintained. 
In other words, somehow the DNA code evolved into place but it has little or no special or particular properties. Most any other code could have just as well evolved rather than the DNA code we have discovered.
We now understand that the DNA code is anything but arbitrary and the evolutionary prediction has been roundly falsified. As had been noticed, the code’s arrangement reduces the effects of mutations and reading errors. They often result in no change to the amino acid sequence, or merely a slight change as a similar amino acid is used in place of the original amino acid. And the degree of this safeguarding is now better understood. As one research study found, the DNA code is “one in a million” in terms of efficiency in minimizing these effects.  This structure found within the DNA code was “unexpected and still cry out for explanation” evolutionists admit. 
Several other studies have confirmed these findings and yet other studies have discovered even more unique and special properties of the code. For instance, the code’s degeneracy means that it is capable of carrying other messages, in addition to the protein amino acid sequence encoding. That is, such a code can, in theory, allow the DNA sequence to carry multiple, parallel, messages, and this is precisely what researchers have found. For instance, the DNA sequence tells proteins where to bind to the DNA structure and where to splice its duplicate copy that is created when creating new proteins. The DNA sequence also determines the structure of that duplicate copy. In addition to allowing for multiple messages, the DNA code also reduces the effects of harmful errors by increasing the chances that such errors will result in a stop codon.
What is important for our purposes here is not only that the DNA code has these capabilities, but the degree as well. Research has found that the DNA code is a very rare code, even when compared to other codes which already have the error correcting capability. 
The DNA code was discovered almost fifty years ago and it has continued to serve up unanticipated capabilities. As one paper put it:
As we learn more about the functions of the genetic code, it becomes ever clearer that the degeneracy in the genetic code is not exploited in such a way as to optimize one function, but rather to optimize a combination of several different functions simultaneously. Looking deeper into the structure of the code, we wonder what other remarkable properties it may bear. While our understanding of the genetic code has increased substantially over the last decades, it seems that exciting discoveries are waiting to be made. 
Indeed the DNA code has revealed several unusual properties. With each new finding, evolutionists ascribe the capability to an unknown evolutionary process that can generate and test an astronomical number of codes, and select the best one from the group. If yet more capabilities are discovered, there is no reason to think evolutionists will not subsume them as well into their increasingly complicated story. In the meantime, after more than 40 years there still remains no compelling explanation of how the code evolved.
The DNA code is highly optimized yet, because of its universality, it must be regarded by evolutionists as highly difficult to evolve. Somehow the code evolved over an astronomical number of possible codes, and then froze in time. Furthermore, the code would not have evolved merely to reduce error rates, but to attain several advanced capabilities. Evolutionists must say that at a time when life was more primitive, the DNA code fortunately was gearing up to drive the machinery of much more advanced cellular designs.
Carl Woese, a long-time investigator of the code’s evolution,
and co-workers at the
Gone are the ideas that the code’s degeneracy is merely an inefficiency, that the code is mostly arbitrary with perhaps a few constraints, that the code originated via an accidental series of events, and that the code originated via a Darwinian process. The code is a fundamental component of molecular biology but the evolutionary predictions of its origin have proven to be false.
In the twentieth century scientists discovered a great deal about the inner workings of the cell. These details, involving DNA, the genetic code, protein synthesis and an army of molecular machines, revealed many commonalities across the species, and many complex and convoluted designs.
Consider for example DNA replication, a common and central feature of all known cellular life. Cells are the basic unit of life and to replicate themselves they make a copy of the DNA they contain. The DNA consists of pairs of long molecular strands, and a small army of proteins performs a series of fascinating and complex tasks to make a copy of each pair of strands.
This process is essentially the same in all species and begins by separating the two DNA strands at designated starting points. Each strand then serves as a template upon which a new copy of the other, complementary strand, is synthesized. In the end, the result is two pairs of strands where originally there was just one pair. One intriguing aspect of this operation is that the synthesis is performed in opposite directions on each strand. That is, as the strands are unzipped a “Y” is formed. On one of the single strands, the proteins synthesize a new strand, continuously moving toward the intersection of the “Y” as the DNA strands are unzipped. This way, as more strand becomes exposed it quickly is covered with its new paired strand.
On the other single strand, however, the proteins synthesize a new strand in the opposite direction, away from the unzipping action. This makes sense because paired DNA strands are chemically anti-parallel. But this makes for a complex process. As the strand is exposed due to unzipping, the proteins start close to the intersection of the “Y,” at the location that has most recently been exposed. The proteins then move away from the intersection as they synthesize a new paired strand.
At some point the proteins halt, move back toward the intersection of the “Y,” and begin the process again on the newly exposed section of strand. Hence on one of the strands replication is continuous (the “leading” strand), and on the other strand replication is discontinuous (the “lagging” strand). Figure 3 illustrates the process.
Figure 3 DNA replication processes on the leading and lagging strands. Several protein machines perform various tasks to complete the replication.
Figure 3 illustrates how the topoisomerase and helicase protein machines act to unwind and separate the DNA strands. Then in addition to the DNA polymerase machines which synthesize the new complementary strands, a variety of other protein machines perform various tasks in a highly coordinated manner, particularly on the lagging strand. These tasks include priming the lagging strand with temporary nucleotides, later removal of those nucleotides, gap filling and nick sealing.
There is of course a great deal more detail to this process. For our purposes what is important is that this complex and somewhat circuitous process is found in all cellular life. It is a classic example of the type of fundamental molecular processes that evolution predicts to originate in a common ancestor. How could it evolve twice?
Furthermore, once established, such fundamental molecular processes probably could not evolve, for too much depends on them. It would be like changing the size of an inner part at the core of a finely tuned machine.
Therefore, evolution predicts that the fundamental molecular processes within the cell, that perform functions common to all life, are conserved and originate from a common ancestor. In other words, processes that are found in all species must have been present in the common ancestor of all the species.
Initially it appeared that this prediction was confirmed. All species use DNA to store genetic information, the same code to interpret that information, RNA to copy that information, the DNA replication process to pass on that information, and so forth. Evolutionists boldly proclaimed that a key prediction had been verified and that evolution had passed a crucial test. As the leading evolutionist Niles Eldredge put it:
The basic notion that life has evolved passes its severest test with flying colors: the underlying chemical uniformity of life, and the myriad patterns of special similarities shared by smaller groups of more closely related organisms, all point to a grand pattern of “descent with modification.” 
Similarly philosopher Michael Ruse concluded that “molecular
biology has opened up dramatic new veins of support” for evolution, and the
theory is now beyond reasonable doubt. “The essential macromolecules of life
speak no less eloquently about the past than does any other level of the
biological world.”  The
Life is one. This fact, implicitly recognized by the use of a single word to encompass objects as different as trees, mushrooms, fish, and humans, has now been established beyond doubt. Each advance in the resolving power of our tools, from the hesitant beginnings of microscopy little more than three centuries ago to the incisive techniques of molecular biology, has further strengthened the view that all extant living organisms are constructed of the same materials, function according to the same principles, and, indeed, are actually related. All are descendants of a single ancestral form of life. This fact is now established thanks to the comparative sequencing of proteins and nucleic acids. 
Evolutionists believed that the fruits of molecular biology,
The twentieth century’s findings that the fundamental molecular processes within the cell are common to all species was superficial. In later years, as the details were investigated, nuanced differences between species emerged that defied the simplicity of the earlier claims. It seemed that such processes, such as DNA replication, could not have evolved twice, but it now appears this is exactly what must have happened if evolution is true. For too many of the key proteins involved in DNA replication are too different in the various species to be related via the usual Darwinian model of common descent.
Furthermore, scientists have also discovered different DNA replication processes, used to replicate viral and plasmid DNA. These results were not what evolutionists expected. As one evolutionist has written:
It is therefore surprising that the protein sequences of several central components of the DNA replication machinery, above all the principal replicative polymerases, show very little or no sequence similarity between bacteria and archaea/eukaryotes. 
In particular, and counter-intuitively, given the central role of DNA in all cells and the mechanistic uniformity of replication, the core enzymes of the replication systems of bacteria and archaea (as well as eukaryotes) are unrelated or extremely distantly related. Viruses and plasmids, in addition, possess at least two unique DNA replication systems, namely, the protein-primed and rolling circle modalities of replication. This unexpected diversity makes the origin and evolution of DNA replication systems a particularly challenging and intriguing problem in evolutionary biology. 
For the process of DNA replication, the evolutionary prediction that this fundamental molecular process is conserved across all life has been empirically falsified. Not only are key molecular components not conserved, but there is not one, but several types of DNA replication processes.
The response of evolutionists to this finding is to drop the prediction and modify evolution, making it more complex. Now they say that some fundamental molecular processes within the cell, that perform functions common to all life, may not originate from a common ancestor, but perhaps evolve independently. As one paper concluded, “the modern-type system for double-stranded DNA replication likely evolved independently in the bacterial and archaeal/eukaryotic lineages.”  Indeed, some evolutionists are reconsidering the assumption that all life on Earth shares the same basic molecular architecture and biochemistry, and instead examining the possibility of multiple origins of fundamentally different life forms. 
Hence the prediction was never really a falsifiable prediction after all. The direct opposite of the prediction is what is suggested by the research, and evolution is expanded to accommodate this new finding. The theory becomes more complicated as it now must account for unexpected and seemingly contradictory findings.
This section examines predictions dealing with events hypothesized to have occurred early in the evolutionary process.
Usher’s creation date of 4004 B.C. had been influential, as
evidenced by examples such as
This move to “deep time” in geology was crucial for
evolution. Darwin himself advocated a 400 million year or more age for the earth,
which he considered to be required for the new species to evolve. This
requirement became particularly evident when William Thomson (later Lord
Kelvin) contradicted the trend toward longer time periods. Only a few years
The 100 million years that Thomson allowed was not nearly
long enough for evolution to work. “Thomson’s views of the recent age of the
Darwin and Huxley worked to overthrow Thomson’s time
It is now known that evolution has nowhere near the eons of
time predicted and required by
There is, for example, the origin of the first organic cells. The early earth was inundated by meteors wreaking havoc on a global scale. Studies have shown that this process took the better part of a billion years. On the other hand, paleontologists continue to find evidence for ancient life forms, leaving little time for their evolution. As one researcher put it:
I’m much more confident today than I was in 1996 about the likelihood that this is evidence of early [3.8 billion years ago] life. This is not “smoking gun” evidence—we are not seeing fossils—but in every case, the model has come through with flying colors. 
Life seems to have appeared early in earth’s history, leaving little time once the catastrophic meteor impacts ceased. This renders the age of the earth irrelevant. Darwin needed hundreds of millions of years for his evolutionary processes, but it is not available regardless of the age of the earth. Life apparently began rapidly, and this is the first of several “big bangs” of biology. Paleontologists estimate that over the past 600 million years a series of abrupt appearances were made by the major groups in the fossil record. The rule of the fossil record seems to be one of long periods of boredom with short fire drills interspersed.
An example of these big bangs is the “Cambrian Explosion.”
Estimated to have taken place almost 600 million years ago over an order of
magnitude shorter time period than
When Thomson argued that the earth could not be older than 100 million years, he knew that this was less time than evolution needed. “A correction of this kind,” Thomson pointed out, “cannot be said to be unimportant to in reference to biological speculation”  But Huxley had already anticipated the problem, and had argued that, in fact, the “biological speculation,” as Thomson put it, would merely adapt to the new time window:
The only reason we have for believing in the slow rate of the change in living forms is the fact that they persist through a series of deposits which geology informs us have taken a long while to make. If the geological clock is wrong all the naturalists have to do is to modify his notions of the rapidity of change accordingly… It is not obvious that we shall have to alter or reform our ways. 
But Huxley set the tone for evolutionary theory in the twentieth century. Now evolution has been handed dramatically shorter time windows and evolutionists have responded with a substantial modification to the theory. Exemplified in a sub-hypothesis called “punctuated equilibrium,” evolution has now been generalized to accommodate both long, slow change and fast, abrupt change, though how this would actually occur remains speculative.
Huxley represents the post-Darwin evolutionist for whom evolution is a fact. Therefore the theory, with whatever complications are necessary, is used to explain the empirical data, rather than being vulnerable to falsification by the data. Today, evolutionists erroneously view Darwin’s prediction triumphantly. Darwin argued for hundreds of millions of years and geology gave us an order of magnitude more than that. Is this not a successful prediction?
It is not a successful prediction because Darwin predicted that hundreds of millions of years would be available for evolutionary processes. Geology gave us deep time but paleontology made it irrelevant. Evolution must occur much faster than Darwin predicted. Today’s theory of evolution has been modified to account for the shorter time windows, and as a consequence is substantially more complicated. Evolutionists yet again claim success while the empirical data challenge their theory.
In the nineteenth and early twentieth centuries microbiologists observed that the fundamental unit of life—the cell—was in great variety. One obvious distinction was that some cells were larger and revealed more organization, with well defined internal structures. In 1923 Edouard Chatton described these as eukaryotes and the smaller, simpler cells as prokaryotes.
With new instrumentation the twentieth century revealed the dramatic differences between the two cell types. Eukaryotic cells include an array of structures, referred to as organelles, which perform a variety of functions. Eukaryotes also have an internal skeleton, a complex system of internal folded membranes and, perhaps most notably, a nucleus. The nucleus is enclosed by a double membrane with thousands of imbedded protein machines that control the molecular traffic in and out of the nucleus. Inside the membrane is the cell’s main complement of DNA, tightly wrapped around proteins and organized into separate chromosomes. An army of protein machines are stationed around the DNA, some unzipping and copying selected genes or performing other tasks.
By contrast prokaryotes have no nucleus and are missing key organelles, such as the mitochondria—the eukaryote’s powerhouse. There are no internal folded membranes and the smaller, simpler complement of DNA is in a single, simpler chromosome.
Essentially all multicellular organisms, from the tiny hydra to the giant redwood tree, are eukaryotic species. And the vast majority of single celled organisms, such as bacteria, are prokaryotic species. There are some single celled organisms, such as yeast, that are eukaryotic.
There is a dizzying array of prokaryote species and it was difficult for evolutionists to determine their evolutionary relationships. Nevertheless it seemed obvious that the eukaryotes had descended from the prokaryotes. As one 1971 textbook stated, “there can be little doubt that the simpler prokaryotes are the evolutionary antecedents of the more complex eukaryotes.” 
The details of how this transformation could have occurred were less clear, for the eukaryotic cell is a tremendous step from the prokaryote. As one text later admitted, “For many years biologists have wondered how eukaryotic cells evolved from prokaryotic cells.” 
Perhaps some of the eukaryote’s organelles, such as the mitochondria, evolved via a symbiotic merger of an early eukaryotic progenitor and a prokaryote. In this endosymbiotic hypothesis, the eukaryote’s mitochondria is thought to be the descendant of an ancient prokaryote that was engulfed by the eukaryote progenitor. Afterwards, a symbiotic relationship is thought to have developed between the larger cell and its new organelle. But even this hypothesis addresses only a fraction of the complexity of the eukaryote cell. (Some evolutionists considered the possibility that prokaryotes descended from eukaryotes  but leading evolutionists considered it to be unlikely.  In any case, this reverse hypothesis would have fared no better.)
Evolutionists hoped to fill in the missing details of how prokaryotes might have given rise to eukaryotes, but instead the evidence increasingly revealed that no such transformation occurred.
The most obvious problem with the prediction that eukaryotes descended from prokaryotes is the immense gap between the two designs. In decades past it was perhaps possible to imagine that the much larger eukaryotes, with their nucleus and other structures, could have somehow emerged from a precocious prokaryote lineage. But with new and better instrumentation, scientists gradually uncovered the details of how cells work, and the gap between eukaryotes and prokaryotes widened. Here are three representative conclusions made by evolutionists:
If the prokaryote-to-eukaryote transition came about by normal evolutionary mechanisms, then given the enormity of the structural and molecular differences between these two cell types, this transformation must have occurred over a very long period involving numerous intermediate species, each developing limited selective advantages and evolving certain eukaryotic characteristics. However, there is no evidence (living or fossil) for the existence of any such “intermediate” organisms, despite the great diversity of the prokaryotic and eukaryotic organisms that preceded or followed this major change. 
There are no obvious precursor structures known among prokaryotes from which such attributes could be derived, and no intermediate cell types known that would guide a gradual evolutionary inference between the prokaryotic and eukaryotic state. 
Comparative genomics and proteomics have strengthened the view that modern eukaryote and prokaryote cells have long followed separate evolutionary trajectories. Because their cells appear simpler, prokaryotes have traditionally been considered ancestors of eukaryotes. 
Or in other words, as one reviewer summed up our knowledge of prokaryotes and eukaryotes, “The saltational difference cannot be overstated.”  This observed difference between prokaryotes and eukaryotes is reinforced by a more subtle difficulty in trying to draw an evolutionary path between the two: the respective DNA and protein sequences do not reveal an evolutionary pathway.
An interesting side story is that in the 1970s the prokaryotes were found to sub divide into two major categories. Typical bacteria fell into one category while bacteria that are tolerant of certain extreme environments, such as high temperatures, fell into the other category. These extreme environments are thought to be more representative of early earth conditions so this category is referred to as Archaea.
More important for our purposes is the fact that the molecular comparisons between these three categories were ambiguous. The three different cell types were sufficiently different that they could not have evolved from each other. Evolutionists postulated that the three lineages must have had evolved from a single progenitor, as Fig. 4 illustrates below.
Figure 4 Evolutionary tree illustrating the independent evolution of eukaryotes, prokaryotes (bacteria) and archaea.
The eukaryotes were now envisioned not to evolve from prokaryotes (bacteria) or archaea, but rather all three evolved from an unknown ancestor. Having a single progenitor evolve in three different directions would explain how the three lineages could have substantial similarities yet also did not have any direct evolutionary relationship between them. The problem, however, is that the new model was motivated less by the scientific evidence than by the conviction that evolution is true. Not only do the data not suggest such an evolutionary arrangement, the data do not reveal any particular evolutionary pathway. We may interpret the data according to evolution, but the expectation that eukaryotes descended from prokaryotes was not fulfilled
In fact, this new model places a substantial burden on the unknown progenitor and unknown evolutionary processes, in order for it to produce both prokaryotes and eukaryotes. In particular, evolutionists increasingly realize that the progenitor would have to be highly complex. Evolutionists at a recent conference concluded that they had underestimated the complexity of the eukaryotic cell’s precursor. The ancestral cell, they realized, must have had more genes, more structures, and more diverse biochemical processes than previously imagined.  The evolutionary quandary about how the eukaryote cell arose has substantially been pushed back onto its ancestor.
The new model is not a minor, empirically motivated, adjustment to the prediction that eukaryotes descended from prokaryotes. The new model is a substantial departure. The ingredients needed to make a eukaryote were not found in prokaryotes and no evolutionary pathway was evident. So the lineages were separated. Their connection to an unknown ancestor is not a theory-neutral inference, but is based on an evolutionary view. The old model provided specific hypotheses. The prokaryote genome was expected to lead toward the eukaryote genome. The new model allows for a wide range of observables. The relationship between the eukaryote and prokaryote is far more arbitrary and their evolution less compelling. As one leading evolutionist admitted, the evolution of eukaryotes is “one of the greatest enigmas in biology.”  "It’s like a puzzle," remarked another. “People try to put all the pieces together, but we don’t know who is right or if there is still some crucial piece of information missing.” 
The evidence does not indicate an obvious evolutionary pathway leading to eukaryotes so, not surprisingly, evolutionists have produced a wide spectrum of hypotheses.  As one review explained:
There are no obvious precursor structures known among prokaryotes from which such attributes could be derived, and no intermediate cell types known that would guide a gradual evolutionary inference between the prokaryotic and eukaryotic state. Accordingly, thoughts on the topic are diverse, and new suggestions appear faster than old ones can be tested. 
Practically every permutation has been suggested on the basic model of an ancestor splitting three ways to give rise to bacteria, archaea and eukaryotes. As Figure 5 illustrates, perhaps the archaea split off from the eukaryote lineage, or perhaps the bacteria split off from the archaea lineage. Perhaps the bacteria split off from the eukaryote lineage, or perhaps the archaea and bacteria lineages produced a fusion that led to eukaryotes. The problem is that none of the solutions are strongly supported. Very different evolutionary relationships are indicated by different molecular sequences, so it is difficult to choose among them. 
Figure 5 Examples evolutionary relationships that have been hypothesized to account for the data.
In addition to a plethora of evolutionary relationships, evolutionists have also resorted to a variety of new processes or events to explain this early evolution. Genetic annealing, genetic integration, various fusion events and symbiotic relationships have all been proposed. Even viruses have been hypothesized to stimulate the origin of the different cell types.
The scientific evidence does not fit evolution very well, and not surprisingly there is a dizzying array of hypotheses for the origin of the eukaryotes, greatly complicating the theory of evolution. One hypothesis that is not popular, however, is that eukaryotes descended from prokaryotes.
It is no secret that biology is full of complex designs. Molecules
are intricately designed to perform their function, apparently simple bacteria
are in fact extraordinarily complicated, and multi-cellular organisms reveal an
intricate network of organs and structures. Biology presents to us a seemingly
endless list of phenomenally intricate designs and, as
The eye gave
Figure 6 Different visual systems of increasing complexity.
This evolutionary prediction of a historical lineage, from
simple to complex, has strongly influenced evolutionists. In Chapter 10 of
The Eozoön canadense
fossil, or “dawn animal of
The only problem with Eozoön was that it was so simple, it was not entirely clear that it actually was a biological organism. Could it have been nothing more than a mineral formation? This seemed obvious and some scientists argued this in the face of staunch opposition by evolutionists who opposed such skepticism. Eozoön nicely fulfilled their expectations, but eventually they would have to concede. Evolution or no evolution, Eozoön clearly was simply a mineral formation. 
Long after the Eozoön affair, this evolutionary view that the earliest multi-cellular animals were simple has persisted, and it continues to meet with surprises. One example is Funisia dorothea, an ancient tubular organism. Funisia shows evidence of the same growth and propagation strategies used by most of today’s invertebrate organisms. Funisia clearly shows, remarked one researcher, “that ecosystems were complex very early in the history of animals on Earth.” Another researcher agreed that “the finding shows that fundamental ecological strategies were already established in the earliest known animal communities, some 570 million years ago.” [3,4]
This early complexity is also implied by genome data of the lower organisms. As one researcher observed, the genomes of many seemingly simple organisms sequenced in recent years show a surprising degree of complexity. [5,6] In fact, what we consistently find in the fossil record and genomic data are examples of high complexity in lineages where evolution expected simplicity. As one evolutionist admitted:
It is commonly believed that complex organisms arose from simple ones. Yet analyses of genomes and of their transcribed genes in various organisms reveal that, as far as protein-coding genes are concerned, the repertoire of a sea anemone—a rather simple, evolutionarily basal animal—is almost as complex as that of a human. 
Early complexity is also evident in the cell’s biochemistry. For instance, kinases are a type of enzyme that regulate various cellular functions by transferring a phosphate group to a target molecule. Kinases are so widespread across eukaryote species that, according to evolution, they must persist far down the evolutionary tree. Yet the similarity across species of the kinase functions, and their substrate molecules, means that if evolution is true these kinase substrates must have remained largely unchanged for billions of years. The complex regulatory actions of the kinase enzymes must have been present early in the history of life. 
This is by no means an isolated example. Histones are a class of eukaryote proteins that help organize and pack DNA and the gene that codes for histone IV is highly conserved across species. Again, if evolution is true the first histone IV must have been very similar to the versions we see today.
Years ago it seemed obvious to evolutionists that the first eukaryote evolved from the simpler prokaryote (bacteria) type of cell. This would nicely fulfill the evolutionary expectation of a simple-to-complex lineage, but this too appears difficult to reconcile with the evidence (see Section 3.2). As one team of evolutionists admitted:
Nevertheless, comparative genomics has confirmed a lesson from paleontology: Evolution does not proceed monotonically from the simpler to the more complex. 
Consider, for instance, the so-called third eye which merely provides for light sensitivity in some species. In fact, the third eye contains the same cellular signal transduction pathway that is found in image-forming eyes. As Fig. 7 illustrates, that pathway begins with a photon interacting with a light-sensitive chromophore molecule (11-cis retinal). The interaction causes the chromophore to change configuration and this, in turn, influences the large, trans-membrane rhodopsin protein to which the chromophore is attached.
Figure 7 Illustration of the remarkable cellular signal transduction vision pathway which begins with light interacting with the retinal chromophore molecule.
The chromophore photoisomerization is the beginning of a remarkable cascade that causes electrical signals (called action potentials) to be triggered in the optic nerve. In response to the chromophore photoisomerization, rhodopsin causes the activation of hundreds of transducin molecules. These, in turn, cause the activation of cGMP phosphodiesterase (by removing its inhibitory subunit), an enzyme that degrades the cyclic nucleotide, cGMP.
A single photon can result in the activation of hundreds of transducins, leading to the degradation of hundreds of thousands of cGMP molecules. cGMP molecules serve to open non selective, cyclic nucleotide gated (CNG) ion channels in the membrane, so reduction in cGMP concentration serves to close these channels. This means that millions of sodium ions per second are shut out of the cell, causing a voltage change across the membrane. This hyperpolarization of the cell membrane causes a reduction in the release of neurotransmitter, the chemical that interacts with the nearby nerve cell, in the synaptic region of the cell. This reduction in neurotransmitter release ultimately causes an action potential to arise in the nerve cell.
All this happens because a single photon entered the fray. In short order, this light signal is converted into a structural signal, more structural signals, a chemical concentration signal, back to a structural signal, and then back to a chemical concentration signal leading to a voltage signal which then leads back to a chemical concentration signal.
This incredible cellular signal transduction design is the biochemical foundation in image-forming eyes. But it is also found in the third eye. In fact, the third eye includes two antagonistic light signaling pathways in the same cell. Blue light causes the hyperpolarizing response as described above, but green light causes a depolarizing response. How is this done? By the inhibition of the cGMP phosphodiesterase enzyme. Specifically, there are two opsins, one that is sensitive to blue light which activates the cGMP phosphodiesterase enzyme, and another that is sensitive to green light which inhibits the cGMP phosphodiesterase enzyme. It appears that initially these are two separate pathways and they come together at the point of influencing the cGMP phosphodiesterase enzyme. 
Yet another example of early complexity in eyes is found in the long-extinct trilobite. It had eyes that were perhaps the most complex ever produced by nature. One expert called them “an all-time feat of function optimization.”  Reviewing the fossil and molecular data, one evolutionist admitted that there is no sequential appearance of the major animal groups “from simpler to more complex phyla, as would be predicted by the classical evolutionary model.” 
The evolutionary expectation of a lineage progressing from simple to complex designs has become optional for evolutionists. Where hints of simplicity can be found they are employed, but clear and obvious cases of intricate complexity early in the evolutionary tree are typically said to be the result of an early, rapid evolution process.
But these explanations have become increasingly problematic and some evolutionists are dropping altogether the idea of a simple-to-complex evolutionary trend. Instead, a new evolutionary hypothesis is that early on in the history of life, near the bottom of the evolutionary tree, there appeared a small organism with a Universal Genome that encodes all major developmental programs essential for every animal phylum. In other words, all the important DNA sequences were present in an ancient organism. From there, new species emerged depending on which genes were activated, inactivated, or deleted. 
The feasibility of this hypothesis may be difficult to determine, but what we do know is that another prediction of evolution has failed and consequently the theory has become much more complex.
This section examines evolutionary predictions dealing with the design of life.
Biological designs have always fascinated thinkers even if
those designs were not well understood. Even as late as the nineteenth century,
But Paley worked within the design perspective. With
As evolutionary thinking took hold, organisms were increasingly
viewed as clumsy and happenstance contraptions. In 1871
In 1888 the American evolutionist Joseph Le Conte added to this list of evolutionary leftovers he argued existed in various animals. The whale’s teeth and the embryonic development of fish, revealed the crude works of evolution.
In 1893 German anatomist Robert Wiedersheim added to
All of this means that when new designs were first investigated they often were assumed to be rather simple. If the workings of new biological findings were confusing or not understood, then evolutionists typically would assume a minor function, if any at all. These expectations have consistently been wrong.
The parts of the human body that evolutionists thought to be evolutionary relics have mostly turned out to be important and even contrary to the expected evolutionary trend. The importance of our toes, tonsils and most of Wiedersheim’s other eighty-four parts is now better understood, and comparative anatomy has not fulfilled the evolutionary expectation of decaying structures.
For instance, the pineal gland is now known to be part of the endocrine system that sends chemical messages (hormones) in the blood and interacts with the nervous system. Wiedersheim also claimed the coccyx, a short collection of vertebrate at the end of the spine, was an evolutionary leftover. But the coccyx is the attachment point for several important muscles and ligaments. The thyroid gland consists of two lobes on either side of the wind pipe and produces thyroxine which regulates cellular metabolism. It is important in cold temperatures and in child growth. The thyroid gland also produces calcitonin which helps regulate blood calcium levels. Its malfunction and enlargement—the disease known as goiter—is visible as a swelling of the front of the neck. Both the thymus gland and the appendix contribute to the body’s immune system. Our appendix was thought to be a shriveled-up remnant because it was shorter than that of the rabbit’s. But the appendix has since been found to be larger and more distinct than its counterpart in the other primates. 
Perhaps more important are the many findings of subtle and sophisticated designs in biology that consistently defy the evolutionist’s expectations. Consider, for example, the process of cell division which requires an exacting sequence of elaborate and complex steps to be followed, controlled by an array of biochemicals.  And after the contents of the cell have been duplicated, the cell quickly constructs a short-lived ring structure that contracts and splits the cell into the two daughter cells. 
Figure 8 Illustration of the major steps in eukaryotic cell division.
Imagine an automobile duplicating all of its parts, and then splitting itself in two. One review summarized cell division as a remarkable process “during which cells undergo profound changes in their structure and physiology. These events are orchestrated with a precision that is worthy of a classical symphony, with different activities being switched on and off at precise times and locations throughout the cell.” 
As Bruce Alberts, an evolutionist and President of the National Academy of Sciences, once wrote, “
We have always underestimated cells. Undoubtedly we still do today. But at least we are no longer as naive as we were when I was a graduate student in the 1960s. Then, most of us viewed cells as containing a giant set of second-order reactions: molecules A and B were thought to diffuse freely, randomly colliding with each other to produce molecule AB—and likewise for the many other molecules that interact with each other inside a cell. This seemed reasonable because, as we had learned from studying physical chemistry, motions at the scale of molecules are incredibly rapid. … But, as it turns out, we can walk and we can talk because the chemistry that makes life possible is much more elaborate and sophisticated than anything we students had ever considered. Proteins make up most of the dry mass of a cell. But instead of a cell dominated by randomly colliding individual protein molecules, we now know that nearly every major process in a cell is carried out by assemblies of 10 or more protein molecules. And, as it carries out its biological functions, each of these protein assemblies interacts with several other large complexes of proteins. Indeed, the entire cell can be viewed as a factory that contains an elaborate network of interlocking assembly lines, each of which is composed of a set of large protein machines. […]
Why do we call the large protein assemblies that underlie cell function protein machines? Precisely because, like the machines invented by humans to deal efficiently with the macroscopic world, these protein assemblies contain highly coordinated moving parts. Within each protein assembly, intermolecular collisions are not only restricted to a small set of possibilities, but reaction C depends on reaction B, which in turn depends on reaction A—just as it would in a machine of our common experience. […]
We have also come to realize that protein assemblies can be enormously complex. … As the example of the spliceosome should make clear, the cartoons thus far used to depict protein machines (e.g., Figure 1) vastly underestimate the sophistication of many of these remarkable devices. 
Evolution is not an intelligent process so evolutionists are amazed by what we find in biology. There is another reason why evolution expected cells to be relatively simple, and it stems from a fundamental tenet of evolutionary theory. A key premise of the theory is that genetic mutations are the main fuel for evolutionary change. That is, it has been a fundamental tenet of evolution that DNA gene mutations are an important source of the unguided biological variation upon which natural selection acts to morph one species into the next. Thus evolutionists focused narrowly on the genes in the DNA molecule. As one science writer put it, genes were at the center of the biological universe, much as ancient astronomers believed sun and stars revolved around the earth. 
Evolutionists compared genes across the different species to understand better their evolutionary relationships. For according to evolution, changes in those genes were the main cause of the origin of species. An obvious problem with this view arose when the human and chimp genes were found to be practically identical, with only minor differences between them. These differences could hardly explain the differences between the human and chimp, yet evolutionists ignored these obvious indications that genes play a less important role in determining the organism’s design. Indeed, evolutionists maintained the centrality of genes, and erroneously argued that the high genetic similarity between the human and chimp was powerful evidence for their common ancestry.
Now we know this picture to be substantially misguided. First, genes are far more varied and sophisticated than evolutionists expected. They can be edited in different ways and they even overlap on the same segment of DNA, like a sentence with a different message when read backwards.
And genes are only one part of a far more involved and complex story. Evolutionists were surprised when it was first discovered that genes comprise only a few percent of the DNA in higher organisms. If genes were so important, why did they comprise a tiny fraction of the genome? What was the role of all the non-genic DNA?
Such a large quantity of DNA must, it seemed, have a function. Yet some non-genic DNA varied substantially between even highly similar species. Evolution predicts that important DNA is preserved. It should be similar in similar species. In other words, similar species should not have DNA segments that are both substantially different and important.
The findings did not match evolutionary expectations and evolutionists could only guess at the role of all the non-genic DNA. A variety of minor functions were considered as well as the possibility that the majority of the genome was useless. Terms such as “junk,” “parasitic,” “selfish,” and “greedy” DNA were coined.  The genome increasingly was viewed as a motley collection of DNA, and this view fueled a new powerful argument for evolution, for only evolution would create such chaos.
Again the evolutionary expectations were substantially misleading. Not only have major, fundamental roles been discovered for much of the non-genic DNA, but its various functions are highly complex, far beyond anything evolutionists expected. One phenomenally complex example is the fine-tuned micro RNAs (MiRNAs) that perform a variety of regulatory jobs. 
Evolution did not expect this unseen complexity buried within the cell. As one evolutionist lamented, “The picture that’s emerging is so immensely more complicated than anyone imagined, it’s almost depressing,” 
The reaction of evolutionists to the important functionality discovered in what were believed to be evolutionary leftovers, and to the profound complexity found in biology, has been to ascribe the new found functionality and designs to evolution. All findings are consistently ascribed to the workings of evolution. The new functions and high complexity, say evolutionists, answer questions about how evolution works, not whether evolution works. Indeed, evolutionists are adept at integrating revolutionary findings into the evolutionary narrative. In new studies the once hapless non-coding DNA is now found to be a crucial player in the evolutionary process itself. [14,15,16] “It’s funny,” observed one evolutionist, “how quickly the field is now evolving.” 
Second, all of these failed expectations have not deterred evolutionists from their view of biology as a hodge-podge. Where function is still uncertain, the evolution literature is rife with explanations of evolutionary leftovers and haphazard designs. This is not surprising as this expectation is fundamental to the theory.
The only figure in
9 The only figure in Charles
Darwin’s The Origin of Species, illustrating
Because similar species are thought to share a relatively recent common ancestor, they are assumed to have not had much time to evolve differences between them. That explains why they are similar, and it also predicts that such species do not have significant differences. Their genome differences should be minor. This is because evolution is limited by the rate at which genetic variations can appear and subsequently spread throughout the respective lineages. For instance, consider two species which are supposed to share a common ancestor dating back only a few millions of years, such as the human and chimp. Evolution expected that such cousin species would have quite similar genes. There would be no new genes evolved in such a brief time period. Indeed, for decades evolutionists have cited minor genetic differences between such allied species as powerful evidence for evolution. [1,2,3,4,5]
In order for new genes to arise, a much longer time would be required. Such new genes were predicted to arise via the duplication of an existing gene. [6,7] If such duplications produced a non-functional gene then the gene could begin to mutate. The mutations would not cause problems if the gene was already non-functional. The mutations could accumulate, and perhaps luckily produce a new functional gene at a much later time. Of course none of this explains how genes arose in the first place, but that is a different problem (see Section 2.1).
There certainly are many genetic similarities between allied species, but we now know of dramatic differences and the list is growing. This prediction has been falsified as many unexpected genetic differences have since been discovered amongst a wide range of allied species. Even different variants within the same species have large numbers of genes unique to each variant. Different variants of the Escherichia coli bacteria, for instance, each have hundreds of unique genes. And some of these genes have been found to have important functions, such as helping to construct proteins. 
Massive genetic differences were also found between different fruit fly species. The fruit fly is one of the most intensely researched organisms and in recent years a systematic study of the genomes of a dozen different species was undertaken. Evolutionists were surprised to find novel features in the genomes of each of these different fruit fly species. Thousands of genes showed up missing in many of the species, and some genes showed up in only a single species.  As one science writer put it, “an astonishing 12 per cent of recently evolved genes in fruit flies appear to have evolved from scratch.”  These so-called novel genes would have had to have evolved over a few million years—a time period previously considered to allow only for minor genetic changes. [11,12]
Such findings are not limited to bacteria and insects, and substantial genetic differences, in otherwise allied species, are now undeniable. Furthermore, there is compelling evidence that new genes can be manufactured in response to environmental pressures. For instance, in the 1970s bacteria were found that could metabolize nylon, even though nylon synthesis had begun only a few decades earlier. Bacteria had been exposed to nylon via the waste water from factories, and now the bacteria could live off the new chemical. The bacteria had modified an existing enzyme (mainly via a frameshift) to create a new enzyme that degrades nylon oligomers. The slow, unguided mechanism envisioned by evolutionists could not have reacted so quickly. And furthermore the mechanism is repeatable as the enzyme has been found more than once. As one evolutionist admitted, “The swiftness with which these two enzymes have evolved is truly remarkable, for several decades are but a flash in the evolutionary time scale.” 
More recent genome data also suggest other sophisticated mechanisms of gene creation. For instance, it appears that new genes may arise from shuffling both the modules that comprise genes (called exons) and the nearby regulatory sequences. Such chimeric structures can immediately confer novel functions.  This is one of several potential sophisticated mechanisms that can rapidly create new genes. For instance, another mechanism is retroposition which is the insertion of an edited gene back into the DNA. By inserting the gene next to a different regulatory sequence, the gene can immediately be expressed at different times or conditions. 
In one interesting example that involved retroposition, a
monkey protein that protects against retroviruses appears to have exons from
two other proteins. And like the nylon metabolizing enzyme, the process
apparently was repeated. This unlikely protein has been found in species in
Asia and in
The many novel genes found in bacteria were a surprise finding for evolutionists. Initially some evolutionists thought the mystery would be resolved when more genomes were analyzed. They predicted that similar copies of these genes would be found in other species. But each new genome has revealed yet more novel genes. In fact, as more genomes were decoded the list of novel genes continued to grow. As one study concluded, the evidence indicates that many of these genes are unique to each organism. 
Despite this growing trend and the falsifications above, evolutionists continue to be certain that the genes evolved. One way or another, novel genes must have evolved. As one evolutionist remarked, quoting Sherlock Holmes: “When you have eliminated the impossible, whatever remains, however improbable, must be the truth.”  In this case, the impossible is evolution’s prediction that there are no novel genes in allied species; the improbable is the evolution of such genes.
One of the great challenges in molecular biology is to understand how the DNA sequence affects the organism design—the genotype-to-phenotype relationship. The task is complicated by the astronomical number of possible DNA sequences. Consider a gene consisting of one thousand DNA nucleotide pairs (also referred to as base pairs). There are four different bases (adenine, thymine, guanine and cytosine), so there are 41000 (or equivalently, a one followed by about 600 zeros) different possible DNA sequences in the gene. Such a large number makes it difficult to understand how the sequence affects the organism.
Another complication is that many DNA changes have little or perhaps no effect. There are many more genotypes than phenotypes, and many DNA changes are phenotype-neutral. This is observed experimentally as DNA modifications often cause no perceptible difference in the laboratory organisms. In fact, entire proteins have been swapped between species with no apparent effect
If our example gene codes for a protein, for instance, then many changes to the DNA sequence do not affect the protein’s amino acid sequence. This is because different DNA triplets often code for the same amino acid (see Fig. 2). Mutate a DNA base and the resulting amino acid may remain unchanged. And when it is changed, the genetic code is such that the new amino acid is often similar to the original, minimizing the effect of the change.
And even when the new amino acid is substantially different, that too is likely to have little or no effect on the final protein structure or function. A protein often can sustain many amino acid swaps without significant structural and function change. In fact, two proteins whose amino acid sequences are as much different as alike (i.e., fifty percent sequence identity) may share a common structure and function.
While such proteins may seem to be quite different, in fact they are practically identical in terms of the amino acid sequence. The chances of two random proteins sharing fifty percent sequence identity is roughly 1 in 10200 (a one followed by about 200 zeros). Therefore evolutionists usually think that such similar proteins share a common ancestor, rather than arose independently.
Evolution predicts that more distant species should have greater differences in their genomes. After all, species in distant limbs of the evolutionary tree likely have different evolutionary pressures and have been evolving independently for millions of years. This genome difference should be all the more given that many DNA changes are phenotype-neutral. Such changes can accumulate, independently in the different evolutionary lineages, as they go unchecked by evolution’s selection process.
When DNA changes do influence the phenotype then the prediction becomes more complicated. These DNA changes may be selected for, or against, depending on how they affect the function, and ultimately the reproductive advantage, of the organism. But for DNA segments that are not functionally constrained, the theory of evolution predicts divergence across different species. Or in other words, for functionally unconstrained DNA, similar sequences should not be found in distant species. The corollary to this prediction is that similar DNA sequences found in distant species must be functionally constrained.
This prediction has been falsified, for many examples of functionally-unconstrained highly similar stretches of DNA have been discovered in otherwise distant species. One example is the histones, a class of proteins that help organize and pack DNA. The gene that codes for histone IV is highly conserved among a range of species. Of its hundreds of nucleotides less than half-a-dozen changes are typically found between different species. Not surprisingly, evolutionists predicted that there must be a strong functional constraint on this protein sequence, allowing for only a few mutations in the gene sequence. But experiments showed milder functional constraint than expected. A few mutations in the histone IV sequence in yeast cells do not alter fitness, and those that do usually do not result in the loss of viability. [1,2]
Figure 10 Illustration of the histone assembly and packaging with DNA.
Even more remarkable are the recently discovered ultra-conserved elements (UCEs). Thousands of these DNA segments, hundreds of base pairs in length, have been found across a range of species including human, mouse, rat, dog, chicken and fish. Evolutionists were astonished to discover these highly similar DNA sequences in such distant species. In fact, across the different species some of these sequences are 100% identical. Species that are supposed to have been evolving independently for 80 million years were certainly not expected to have identical DNA segments. “I about fell off my chair,” remarked one evolutionist. 
Evolutionists assumed such highly preserved sequences must have an important function. But even if true, it would be difficult to see how so little sequence variation could be tolerated. The results were not what evolutionists expected, but this was just the beginning. Subsequent laboratory studies failed to reveal any phenotype effects. A variety of knockout experiments were done to determine the function of these sequences that evolution was supposed to have preserved. But in many of the regions no function could be found. One study knocked out several UCE regions, including a stretch of 731 DNA base pairs that was hypothesized to regulate a crucial gene. Evolutionists expected the knock out to result in lethality or infertility but instead found normal, healthy mice. Months of observation and a battery of tests found no abnormalities or significant differences compared to normal mice. As one of the lead researchers explained:
For us, this was a really surprising result. We fully expected to demonstrate the vital role these ultraconserved elements play by showing what happens when they are missing. Instead, our knockout mice were not only viable and fertile but showed no critical abnormalities in growth, longevity, pathology, or metabolism. 
Another study knocked out two massive, highly conserved, DNA regions of 1.5 million and .8 million base pairs in laboratory mice and, again, the results were viable mice, indistinguishable from normal mice in every characteristic they measured, including growth, metabolic functions, longevity and overall development.  “We were quite amazed,” explained the lead researcher. 
Extensive tests have failed to find a function for many of UCEs and these results were surprising to evolutionists. Perhaps some mysterious functions will be discovered in the future, but the years of research at this point indicate evolution’s prediction is false. The best information we have to date, and it is extensive, indicate that the genomes of distant species include highly similar and even identical stretches of DNA that otherwise are not functionally constrained.
It is worth noting that problems posed by this evidence will not all disappear even if some mysterious function is discovered in the future. Highly similar sequences in distant species, functional or not, are simply not consistent with evolution. Because such sequences are in distant species, according to evolution such sequences must date back to a very distant ancestor. In other words, these sequences not only must have important function in the extant organisms in which they are found, but they must have evolved early in the history of life, and they must have been important in a very different organism, under very different conditions.
And whatever the mysterious function is, it must be incredibly sensitive to every detail in the DNA sequence. But how could the sequence initially evolve if little or no variation is allowed? Evolution requires a functional pathway to arrive at the sequence in the first place but the highly restricted UCEs would have none. We would have to believe that functionally important stretches of DNA, hundreds of base pairs in length, just happened to form and then were preserved by evolution. The odds against this are astronomical.
“It can’t be true” was one evolutionist’s reaction to the UCE findings in recent years.  The findings falsify predictions of evolution, but they are true and they have been verified independently. Some evolutionists considered the possibility of sequence armoring. That is, perhaps these highly conserved sequences are a consequence of a strong, local, resistance to mutations at certain locations in the DNA. But it is difficult to imagine how such localized DNA protection could occur, and in any case empirical observations have ruled out this explanation.
Evolutionists have also considered the possibility of functional redundancy. In this case, no deleterious effects are observed in the knockout mice because other DNA regions perform the same function as do the deleted UCE regions. But then this would not explain why the UCE are so highly conserved.
On the other hand, perhaps the deleterious effects of removing an apparently functionless UCE are observed only in subsequent generations. But again, this idea has difficulty explaining why the UCEs are so highly conserved.
Perhaps the most common hypothesis is that many of the UCEs have functions that are difficult to detect. This is certainly possible, but it raises the problem of how evolution could select for such rare sequences and subtle function.
This section examines evolutionary predictions dealing with the process of biological change.
One need not be a biologist to understand that there is
considerable biological variation within a population. There are the taller and
the shorter, the heavier and the lighter, the faster and the slower, and so
forth. It is precisely this biological variation that
Figure 11 Wild horses (Equus przewalskii)
Is biological variation really something that just naturally
arises? A common idea in
Such observations were what inspired Gregor Mendel (1822-1884),
an Austrian monk who made the first discoveries in what would become modern
genetics. In 1865, just six years after
With much hard work and a bit of luck, Mendel was able to infer the fundamental principles of genetics. His findings called for a discrete spectrum of traits rather than the blending of continuous traits, as had been considered. Mendel’s work went unnoticed for many years, and was finally rediscovered at the turn of the century.
It was not an easy task, but Mendel’s findings were eventually merged with the theory of evolution in the early twentieth century. The upshot was that normal biological variation arose from different gene combinations. Breeders achieved their results by manipulating these combinations, but all the while they were operating within a given gene pool. This is why they found limits to the amount of change they could produce. The way to produce greater change would be to use new genes not present in the existing pool, and the way to produce new genes was via mutation.
Great faith was placed in the power of the unguided production of new genes to provide for the raw material with which natural selection would work. A theme in Darwinism is the use of unguided natural processes, and since mutations are unguided they seemed to fit perfectly with evolution. Researchers set about trying to induce mutations in the laboratory to see what new species they could create. This area of work did not fulfill the early expectations, but that is another story. For our purpose here, the point is that modern genetics was explaining how biological variation came about and it was anything but free.
Mendel discovered the foundation of modern genetics, and the twentieth century’s revolution in molecular biology has filled in the details. We now know that the molecular mechanisms that produce genetic variation are incredibly complex. Whereas early evolutionists might have envisioned a simple sort of blending action or random perturbing force, we now have discovered a highly-intricate Mendelian machine behind variation. Biological variation does not simply arise spontaneously.
This is sometimes called the existence problem. Evolution relies on the preexistence of biological variation without understanding from where it came. We now know how variation comes about but not how the machine behind it came about. The shortcoming is particularly awkward because evolution proposes to tell us not only how variation is used but how all the species came about—and its answer is by unguided natural forces. But when we come to the Mendelian machine of variation we must ask how was it that evolution produced such a fine-tuned machine which is, in turn, supposed to be the engine for evolution itself?
Not surprisingly Darwinists claim that evolution created the Mendelian machine that produces biological variation. They must because their theory states that the species arose via evolution. So evolution is supposed to have produced a fine-tuned machine which is, in turn, supposed to be the engine for evolution itself. Without variation natural selection is powerless to work. Yet natural selection is supposed to have created just what it needed—a wonderful source of variation so populations can adapt to changing environments. But biological variation does not occur naturally, it occurs via an intricate machine.
Here we find an element of serendipity in evolutionary theory. Without variation, natural selection was powerless to work, yet somehow a source of variation arose. Speculation is alive and well about how this might have happened; for example, perhaps a simple source of variation somehow arose first and later evolved and gained complexity.
More commonly, however, evolutionists focus on examples of
adaptation as proof of evolution. Amazingly, such adaptation is routinely used
as one of the pillars establishing evolution as a fact. For example, according
to Ernst Mayr, “evolutionary change is also simply a fact owing to the changes
in the content of gene pools from generation to generation.”  Likewise, Isaac Asimov claimed that the
peppered moth changing color proves evolution. 
Steve Jones explains that the changes observed in HIV (the human
immunodeficiency virus) contain
The Galapagos finches have been studied for decades and are now a standard textbook example of evolution in action.  The finches’ beaks were observed to change size and shape during abnormally dry or wet years. The finches’ beaks return to normal during average years and there is no net change, yet evolutionists continue to use this example. As with the other examples, the finch studies demonstrate nothing more than mere adaptation, and ignore the fact that complex adaptation mechanisms are responsible for the changes.
In the early nineteenth century, a generation before
Figure 12 Jean-Baptiste Lamarck (1744-1829).
Charles Darwin’s theory of evolution was a radical break from
Lamarckianism, or any idea that biological change occurs in response to need.
Such ideas imply some sort of designed system that responds to environmental
Mutation merely provides the raw material of evolution; it is a random affair, and takes place in all directions. Genes are giant molecules, and their mutations are the result of slight alterations in their structure. Some of these alterations are truly chance rearrangements, as uncaused or at least as unpredictable as the jumping of an electron from one orbit to another inside an atom; others are the result of the impact of some external agency, like X-rays, or ultra-violet radiations, or mustard gas. But in all cases they are random in relation to evolution. Their effects are not related to the needs of the organisms, or to the conditions in which it is placed. They occur without reference to their possible consequences or biological uses. 
We call these events [the various types of DNA sequence alteration] accidental; we say that they are random occurrences. And since they constitute the only possible source of modifications in the genetic text, itself the sole repository of the organism’s hereditary structures, it necessarily follows that chance alone is at the source of every innovation, of all creation in the biosphere. Pure chance, absolutely free but blind, at the very root of the stupendous edifice of evolution: this central concept of modern biology is no longer one among other possible or even conceivable hypotheses. It is today the sole conceivable hypothesis, the only one that squares with observed and tested fact. And nothing warrants the supposition—or the hope—that on this score our position is likely ever to be revised. 
The essence of Darwinian evolution is that populations [adapt] by producing mutations that are random with respect to the organism’s need, that is those that have random direction in phenotypic space. 
In other words, evolution predicts that biological variation does not vary with environmental pressures or other factors that influence how well the potential designs will perform. Evolutionary change is supposed to have proceeded via the selection of useful designs from a pool of otherwise unguided designs that were independent of need.
This prediction of evolution has been falsified more than
once, by quite different findings. The findings are leading to new
understandings of biology that evolutionists never imagined. Progress has not
always been easy though. These findings are antithetical to evolution and so
have been resisted. As one researcher who investigated the flax plant wrote, the
evidence for environmentally-driven change in flax populations “is unequivocal
but inheritance of acquired changes has been an anathema to evolutionary
biologists ever since
One hint that biology would not cooperate with
The problem is that evolutionary mechanisms are not supposed to work this fast. Clearly these adaptations were induced by environmental change, and the changes appear to be addressing the need rather than independent of the need. If the changes were random with respect to the environmental pressure, then a much longer time period would be needed to evolve such adaptations.
The evidence does not stop at such an inference. In fact, for years evidence has been growing that species have sophisticated adaptation mechanisms to respond to immediate needs, and that they pass on their adaptation information to their offspring.  For instance, water fleas develop defensive spines when exposed to predators, and their offspring also develop such spines.  Plants can be dramatically influenced by the parental light environment  and environmentally induced disease risk can be transmitted to offspring. [12,13]
This sort of rapid adaptation falls under the category of epigenetics and the underlying molecular mechanisms involve gene regulation within the cell. Gene regulation mechanisms determine the timing and degree to which genes are used or not used, but do not alter the genes themselves.
The new findings have immense implications for our understanding of disease and public health. They also have immense implications for evolution, since a fundamental prediction has been falsified. As one evolutionist put it, “The whole discourse about heredity and evolution will change.” That change, however, will not come easily as it is tantamount to heresy within evolution circles.  As one evolutionist admitted, “The really heretical thing to say is that the environment could be pushing the epigenetic information in a direction that is beneficial … that raises the hackles.” 
Epigenetic change is not the only way that biological variation adapts to environmental pressures. Evolutionists have been surprised that DNA mutations themselves can also be adaptive. The flax plant, for instance, was found to pass on DNA alterations in response to fertilizer levels. Plants treated with heavy fertilizer were larger, but so were their offspring when compared to plants from parents not treated with heavy fertilizer. The DNA of the heavier plants was found to be altered, and the same alterations were found in separate experiments. 
Yeast cells provide another example of adaptive mutations. Yeast adapt to a variety of adverse environments. One adaption is to form a biofilm on the surface of a liquid for better access to oxygen. Yeasts with this ability were found to have two important DNA alterations associated with a particular gene. One alteration increased the gene activity while the other modified the gene itself, making the protein that it coded for more oily. 
Adaptive mutations have been extensively studied in bacteria. For instance, experiments typically alter the bacteria food supply or apply some other environmental stress, and the bacteria response is observed. In the presence of such environmental stresses bacteria increase their mutation rate to speed their adjustment to the new environment. They also produce mutations that target the specific environmental stress. In other words, the bacteria respond to the stress with DNA alterations that help the bacteria cope with the specific stress. The biological variation is not independent of need, but specifically addresses the need.
As one explanation has it, the bacteria accomplish this feat in a series of steps. First, a gene that can help with the environmental stress is activated. As the gene is being copied mutations are introduced. But due to folds in the gene’s DNA structure, only selected parts of the DNA sequence are available for mutation. The fold structures are determined by its sequence. So not only does the sequence of the gene code for a protein, it also codes for mutability. It designates which parts of the sequence are to be more variable. Although the new mutation arises in the absence of cell division, it will be passed on when the bacteria divides. [17,18,19,20]
Species have a variety of mechanisms to respond to environmental pressure. And these mechanisms are efficient. They alter the organism’s characteristics—its phenotype—to help respond to the specific stress. As one paper concluded, “these mechanisms seem to tune the variability of a given phenotype to match the variability of the acting selective pressure.”  The accumulating evidence has some calling for “a radical rethink of how evolution works.” 
Evolutionists are increasingly recognizing that biological
variation is not independent of need. Indeed, evolutionists involved in these
research areas, knowing that the evidence is substantial and growing, have sought
to incorporate these findings into
There is clear evidence from organisms as diverse as humans and bacteria that genomes do indeed contain information that can focus mutations in certain areas and direct it away from others. Yet students are still taught that evolution works through completely random genetic variation acted upon by natural selection, leading to the survival of those organisms with genes best suited to their environment. Surely it is time to rethink the idea that evolution is purely a game of chance: to accept that genomes could have evolved information that allows them to influence genetic change and affect their own chances of survival? 
According to classical evolutionary theory, phenotypic variation originates from random mutations that are independent of selective pressure. However, recent findings suggest that organisms have evolved mechanisms to influence the timing or genomic location of heritable variability. 
The purpose of this thesis is to put forward a new theme proposed neither by Lamarck or Darwin. We stand on the threshold of the first paradigm change for 150 years. 
And how are these new findings to be integrated into the theory of evolution? The general idea is that in the early stages of evolution, organisms evolved the ability to evolve. We now observe species responding to environmental pressures with non-random, beneficial, variation because long ago random changes accumulated to create complex adaptation mechanisms that respond to environmental pressures. Then in later generations these mechanisms influenced the course of evolution. In other words, organisms have evolved because they first evolved evolvability. As one evolutionist put it, “The ability to evolve and adapt is an acquired skill.”  Or as another put it:
Not only has life evolved, but life has evolved to evolve. … The rates at which the various events within the hierarchy of evolutionary moves occur are not random or arbitrary but are selected by Darwinian evolution. 
In other words, evolution created evolution. One can see why traditional evolutionists might balk at this new paradigm shift. But the evidence must be explained somehow. It is ironic that evolutionists have always claimed examples of organisms adapting to their environment as powerful evidence for evolution. In fact, they are examples of yet another failed prediction that has led to a phenomenal leap in the complexity of evolutionary theory.
In the 1960s molecular biologists learned how to analyze protein molecules and determine the sequence of amino acids that comprise a protein. It was then discovered that a given protein molecule varies somewhat from species to species. For example, hemoglobin, a blood protein, has similar function, overall size and structure in different species. But its amino acid sequence, while similar, is not identical.
Evolutionists Emile Zuckerkandl and Linus Pauling believed that such sequence differences were the result of evolutionary change occurring over the history of life and could be used to estimate past speciation events—a notion that became known as the molecular clock. 
For example, if two species have hemoglobin proteins that are almost identical, then evolutionists infer that the two species have a recent common ancestor on the evolutionary tree. Only recently did the two species diverge because their hemoglobin proteins are so similar. On the other hand, if the two hemoglobin proteins have many differences, then evolutionists believe that the two species have been evolving independently for a longer time. In other words, evolution predicts that molecular differences act like an evolutionary clock.
Figure 13 Schematic of the human hemoglobin protein three-dimensional structure consisting of four globin subunits.
In later decades this concept of a molecular clock, relying on the assumption of a roughly constant rate of molecular evolution, became fundamental in evolutionary biology.  As the National Academy of Sciences once claimed, the molecular clock “determines evolutionary relationships among organisms, and it indicates the time in the past when species started to diverge from one another.” 
Indeed the molecular clock has been extolled as strong evidence for evolution and, in fact, a common sentiment has been that evolution was required to explain these evidences. As a leading molecular evolutionist wrote, the molecular clock is “only comprehensible within an evolutionary framework.” 
The claim that the molecular clock can only be explained by evolution is, however, now a moot point as the mounting evidence shows that molecular differences often do not fit the expected pattern. The molecular clock which evolutionists had envisioned does not exist. As one review of the molecular clock prediction recently concluded:
molecular systematics is (largely) based on the assumption, first clearly articulated by Zuckerkandl and Pauling (1962), that degree of overall similarity reflects degree of relatedness. This assumption derives from interpreting molecular similarity (or dissimilarity) between taxa in the context of a Darwinian model of continual and gradual change. Review of the history of molecular systematics and its claims in the context of molecular biology reveals that there is no basis for the “molecular assumption.” 
In other words, what seemed obvious to earlier evolutionists is now obviously wrong. The evolution literature is full of instances where the molecular clock concept fails. For example, it was found early on that different types of proteins must evolve at very different rates if there is indeed a molecular clock. For example the fibrinopeptide proteins in various species must have evolved more than five hundred times faster than the histone IV protein.
Furthermore, it was found that the evolutionary rate of certain proteins must vary significantly over time, between different species, and between different lineages. [2,6] For instance, it was found that the molecular clock doesn’t seem to work very well for bacteria. The molecular data make closely related bacteria look like distant relatives—as different as insects are from mammals, for example. [7,8]
It was also found that the relaxin protein was anomalous when compared across different species. The pig, for example, was found to be more closely related to a shark than to a rodent. [9,10] Evolutionists admitted that “The conclusion to be drawn from the relaxin sequence data is that they do not fit the evolutionary clock model.” Furthermore, in order to fit the data to the molecular clock hypothesis, one must imagine that different regions of the genome evolve at different rates for a species, and that the same region evolves at different rates in different species.  And there is the serum albumin gene family which shows significant deviations from clock-like evolution. 
Other erratic molecular clocks include those based on the superoxide dismutase (SOD) and the glycerol-3-phosphate dehydrogenase (GPDH) proteins. On the one hand, SOD unexpectedly shows much greater variation between similar types of fruit flies than it does between very different organisms such as animals and plants. On the other hand GPDH shows a more or less reverse trend for the same species. As one scientist concluded, GPDH and SOD taken together leave us “with no predictive power and no clock proper.” 
Indeed, evolutionists are finding growing evidence that the purported rates of molecular evolution must vary considerably between species for a wide range of taxa, including mammals, arthropods, vascular plants, and even between closely related lineages. As one study concluded:
The false assumption of a molecular clock when reconstructing molecular phylogenies can result in incorrect topology and biased date estimation. … This study shows that there is significant rate variation in all phyla and most genes examined, implying a strict molecular clock cannot be assumed for the Metazoa. 
In 2007 new fossil evidence revealed a creature similar to the platypus, an egg-laying mammal. The fossil was estimated to date from about 120 million years ago, and for evolutionists it meant the divergence between different egg-laying mammals was earlier than thought. So early that the divergence violated the molecular clock. As the study concluded, the results “are incompatible with strict molecular clocks and difficult to accommodate even when relaxed molecular clock models.” 
Another problem with the molecular clock prediction is that the clock must be calibrated before it can be used. Evolutionists use fossil data to calibrate the clock. Fossils are used to reconstruct a hypothetical evolutionary tree—a phylogeny—including the geological time since particular speciation events. The molecular differences between species are calibrated to those speciation events. The molecular clock is then used to measure the time since other speciation events. In many cases the molecular clock conflicts with the fossil data. That is, once the clock is calibrated using one part of the fossil record, the clock then conflicts with another part of the fossil record. The molecular and fossil data often do not give similar results. This can be explained, for example, by pointing to possible errors in the fossil record. But the problem in all this is that the molecular clock is being calibrated with the same sort of data that the clock then contradicts. As one researcher put it:
Even if one makes the bold assumption that molecular clock models have little error, there seems little objective reason for accepting a few fossil dates used in calibrations and rejecting as unreliable the much more numerous fossil dates that contradict the resultant molecular estimates. 
The molecular clock hypothesis was formulated in the 1960s and since then has made many false predictions.
Evolutionists have reacted to these contrary findings with an ever increasing list of correction factors. One fundamental correction factor is to adjust the clock depending on which protein is analyzed. This could be necessary if fewer mutations can be tolerated in some proteins. Here is a representative explanation for why this correction factor is needed:
some proteins have accumulated amino acid substitutions more slowly than others and are therefore more constant in composition. These differences have a functional basis. For example, the histones are a class of proteins that are bound to DNA in cells that possess a nucleus. They take part in the formation of nucleosomes. Any change in histones could therefore have a destructive effect on the integrity of the cell. 
In other words, proteins with less variation across different species are conserved by evolution in order to preserve their function. The proteins with more variation must have more flexible designs, but the conserved proteins must be highly constrained in their design. This explanation was an evolutionary assumption, rather than an empirical observation, and has since been disproven. Experiments with histone IV showed little functional sensitivity to sequence substitutions. 
Many more corrections factors have been proposed to fit the data to the molecular clock hypothesis. Perhaps the clock is perturbed by varying DNA replication accuracies in different species, or perhaps the protein under study has somehow changed its function in its evolutionary history. Perhaps the molecular clock depends not only on the number of generations per unit time, but also on the number of germ-line cell divisions per generation. Perhaps a horizontal gene transfer has taken place at some point in the organism's history, or perhaps so many mutations have occurred that the picture has become blurred. For instance, perhaps molecular evolution experiences elevated rates during periods of adaptive radiation. Or maybe slightly deleterious mutants were incorporated during population bottlenecks. Perhaps metabolic rate, environmental factors such as temperature and the hypothesized speciation rate are important. Perhaps different regions of the genome evolve at different rates for a given species, and perhaps the same region evolves at different rates in different species.
As with geocentrism, this dizzying array of correction factors has been used to deal with uncooperative data while the theory becomes dramatically more complicated. Yet still there remain problem cases. Evolutionists continue to use the molecular clock concept, but the many correction factors highlight the fact that the sequence data are being fit to the theory rather than the other way around. As one evolutionist admitted, “It seems disconcerting that many exceptions exist to the orderly progression of species as determined by molecular homologies; so many in fact that I think the exception, the quirks, may carry the more important message.” 
Everyone knows that in any population there is often a gradual variation in traits. Some individuals are taller or shorter, faster or slower, and so forth. Using artificial selection breeders can exaggerate these differences to create very different varieties. Darwin hypothesized that using natural selection over long time periods, evolution could also create very different designs. And indeed the fossil record tells us that life was very different in the past.
But the fossil record also reveals large evolutionary change occurring in relatively short periods with little or no change in between. In some cases new forms appear with little or no precursors. Darwin argued that the fossil record is highly imperfect, recording only a small fraction of the history of life. What we see in the strata, he argued, are snapshots of a gradual evolutionary process.
Charles Darwin predicted was that evolution occurs gradually via variations within populations. His friend Thomas H. Huxley was concerned that Darwin had assumed "an unnecessary difficulty in adopting Natura non facit saltum [nature does not make leaps] so unreservedly." But Darwin's theory would have been much less compelling without it. Imagine if evolution had included the caveat that saltations—rapid leaps—can occur by unknown mechanisms such that new fossil species can appear fully formed. This would have undercut Darwin's premise that species evolve by natural processes and we wouldn’t be talking about him today. Yes the fossil record suggested that nature does take jumps, but it was safer for Darwin to question the data than to admit them into his theory.
In order for evolution to succeed Darwin would need to steer clear of the supernatural, or anything that could be interpreted as supernatural, and argue for a strictly naturalistic origin of species. Darwin could hardly argue for a naturalistic origin, and then propose a theory that suggested a supernatural interpretation. As Darwin explained:
As natural selection acts solely by accumulating slight, successive, favourable variations, it can produce no great or sudden modifications; it can act only by short and slow steps. Hence, the canon of “Natura non facit saltum,” which every fresh addition to our knowledge tends to confirm, is on this theory intelligible. We can see why throughout nature the same general end is gained by an almost infinite diversity of means, for every peculiarity when once acquired is long inherited, and structures already modified in many different ways have to be adapted for the same general purpose. We can, in short, see why nature is prodigal in variety, though niggard in innovation. But why this should be a law of nature if each species has been independently created, no man can explain. 
Darwin also used gradualism as a solution to the problem of complexity. He admitted that complex structures, initially at least, might seem unlikely to have evolved:
To suppose that the eye, with all its inimitable contrivances for adjusting the focus to different distances, for admitting different amounts of light, and for the correction of spherical and chromatic aberration, could have been formed by natural selection, seems, I freely confess, absurd in the highest possible degree. 
Darwin’s solution to this apparent absurdity was his gradualistic approach:
Although the belief that an organ so perfect as the eye could have been formed by natural selection, is enough to stagger any one; yet in the case of any organ, if we know of a long series of gradations in complexity, each good for its possessor, then, under changing conditions of life, there is no logical impossibility in the acquirement of any conceivable degree of perfection through natural selection. 
But how could we know of such a long series of gradations? It is true that nature often provides various examples which can help, but even these usually do not reveal a truly gradual sequence. On the other hand, Darwin explained, if it could be shown that no such gradation could possibly exist then his theory must be false:
If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down. But I can find out no such case. 
In this view, gradualism did not need to be empirically compelling, it merely needed to escape falsification. Here Darwin departed from the traditional approach in science. Instead of arguing that ones hypothesis is empirically compelling, he argued merely that his hypothesis had not been falsified. Indeed, it is not clear that such falsification is even possible. What has become clear, however, is that it gradualism is not well supported.
In its first century evolution maintained Darwin’s view that the fossil record was incomplete. Aside from a few heretics such as Richard Goldschmidt and his so-called hopeful monsters, most evolutionists avoided the problem of stasis and abruptness in the fossil record and rigidly adhered to gradualism.
But the fossil record was not the only area of evidence that revealed problems for gradualism. Other areas such as comparative anatomy and genetics raised difficult questions as well. It increasingly looks doubtful that minor biological variations can lead to the large-scale change evolution requires. As one evolutionist put it, macroevolution is more than repeated rounds of microevolution. 
Increasingly evolutionists have recognized the need for some other mechanism.  An early and prominent example of this came in the mid twentieth century when geneticist Richard Goldschmidt hypothesized that species were separated by “bridgeless gaps” and that single mutations could alter embryonic development and cause major phenotypic changes in a single generation. Such so-called macromutations were envisioned to produce unique organisms, or as Goldschmidt memorably put it, “hopeful monsters.”
Goldschmidt and other skeptics of gradualism hypothesized about the mechanisms that could bring about such saltational change. Ultimately their ideas had limited success, but their concern that gradualism alone was not sufficient to explain the origins of species continued to be supported by the empirical data. And one evolutionist recently explained:
[U]p to now the empirical basis of strict gradualism is weak at best. For instance, with its abrupt transitions, the fossil record provides little evidence for a gradual evolution of new forms. Also the branching patterns of higher taxa in both animals and plants as revealed by cladistics and systematics do not support the idea that the major features of body plans and their constituent parts arose in a gradual way. … Unfortunately, the Synthetic Theory and its contemporary derivatives have major shortcomings, for example in explaining evolutionary novelties and constraints, and the evolution of body plans 
In recent years evolutionists have employed Neo-Goldschmidtian, or saltational evolution, for a variety of problems. Here are some examples:
As nature does jump, exclusive gradualism is dismissed. Saltatory evolution is a natural phenomenon, provided by a sudden collapse of the thresholds which resist against evolution. The fossil record and the taxonomic system call for a macromutational interpretation. 
We offer evidence for three independent instances of saltational evolution in a charismatic moth genus with only eight species. … Each saltational species exhibits a markedly different and discrete example of discontinuous trait evolution 
Major transitions in biological evolution show the same pattern of sudden emergence of diverse forms at a new level of complexity. The relationships between major groups within an emergent new class of biological entities are hard to decipher and do not seem to fit the tree pattern that, following Darwin’s original proposal, remains the dominant description of biological evolution. The cases in point include the origin of complex RNA molecules and protein folds; major groups of viruses; archaea and bacteria, and the principal lineages within each of these prokaryotic domains; eukaryotic supergroups; and animal phyla. In each of these pivotal nexuses in life’s history, the principal “types” seem to appear rapidly and fully equipped with the signature features of the respective new level of biological organization. No intermediate “grades” or intermediate forms between different types are detectable. 
Here we provide for the first time evidence of major phenotypic saltation in the evolution of segment number in a lineage of centipedes 
Titles of research papers, which include phrases such as “farewell to Darwinism, neo- and otherwise,” “when natura non facit saltum becomes a myth,” “Saltational evolution: hopeful monsters are here to stay,” and “a Neo-Goldschmidtian view of unicellular hopeful monsters,” highlight this falsification of evolution’s prediction that it proceeds gradually.
Evolutionary studies have increasingly appealed to saltational evolution to explain a variety of species and designs. Today saltational evolution is probably here to stay.
After Darwin evolutionists continued to maintain a gradualist view. With the coming of the new synthesis, which integrated Mendelian genetics into Darwin’s theory, leading evolutionists such as Ronald Fisher, Theodosius Dobzhansky, Hermann Muller, Kenneth Mather and Julian Huxley continued to advocate gradualism.  Some of their arguments were based on theory that would not hold up in later years, but at the time Goldschmidt did not help his scientific reputation by promoting saltational change. 
Today things are different and it is acceptable to speak of macromutations, saltational evolution and even a Neo-Goldschmidtian view. Darwin’s and the new synthesis’s gradualism is yet another falsified prediction leading to a tremendously more complicated theory which is needed to fit the awkward patterns in biology.
This section examines evolutionary predictions dealing with behavior.
Darwin’s theory of evolution states that beneficial variations within a population tend to be passed down to subsequent generations. Here, a beneficial variation is defined as any variation that leads to increased reproduction. The idea is very simple. Biological modifications that yield more progeny will, of course, be more common in later generations than modifications that yield less progeny.
In a world of struggle and predation, this rule of natural selection seems to make sense. If a modification confers a higher survival rate, for instance, then it will more likely persist. It is not surprising that evolution has often been viewed as a sort of biological arms race, summed up with the pithy phrase, survival of the fittest.
But what about kindness, love and self-sacrifice? Do these virtues make sense within the evolutionary framework? Indeed, such altruistic behavior may even place one in harms way. How does evolution deal with the virtue of loving our enemies?
Figure 14 Mother Theresa, founder of the international Missionaries of Charity.
In Origins, Darwin did not examine the question of altruistic behavior in great detail. But he did not leave the question untouched, and at points made relevant statements about what we should expect if evolution is true. Clearly, natural selection could not result in destructive behavior. Here are two representative statements from Origins:
we may feel sure that any variation in the least degree injurious would be rigidly destroyed. 
Natural selection will never produce in a being any structure more injurious than beneficial to that being, for natural selection acts solely by and for the good of each. 
And again, the terminology is not ambiguous. When Darwin explains that natural selection would not produce anything “more injurious than beneficial,” he is using those terms strictly in reference to reproduction. Under the theory of evolution, the design of an organism, ranging from the organs to the behavior, will move toward increased reproduction.
But are not examples of such biological altruism obvious? When the rattlesnake rattles its tail, is this not injurious to its hunt for food, and ultimately to its reproductive chances? Darwin argued that this and other such examples are signals to frighten away enemies, not warn the intended prey.
Other examples of apparent altruism were known in Darwin’s time, but today the breadth and depth of our understanding of altruistic structures and behaviors has grown tremendously. We know of many examples of unambiguous altruism, and in far greater detail. It is not controversial that the evolutionary prediction Darwin issued has been falsified many times over. Indeed, there is a plethora of designs that are “injurious” and even “more injurious than beneficial” to reproduction. They are found everywhere, from the mindless, single-cell bacteria to the many subtle behavior patterns of humans.
In bacteria, for example, phenomenally complicated mechanisms have been found which carefully and precisely destroy the individual. Clearly, this suicide mechanism is more injurious than beneficial to the bacteria’s future prospects. One such mechanism consists of a toxic gene coupled with an antitoxic gene. The toxic gene codes for a protein that sets the act of suicide into motion and so ultimately kills the bacteria. The antitoxic gene inhibits the toxic gene from executing its mission. Except, that is, when certain problems arise. Lack of proper nutrients, radiation damage and problems due to antibiotics can all cause the antitoxin to be diluted, thus allowing the toxin to perform its mission. [3,4,5,6]
This bacterial suicide is probably good for the bacteria population on the whole. If nutrients are running low, then better for some bacteria to die off so the neighbors can live on. Not only will the reduced population require less nutrients, but the dismantled bacteria help to replenish the food supply. Therefore, as we shall see below, evolutionists can explain the suicide mechanism as having evolved not for the individual bacteria, but for the population. But the explanation introduces major problems for the theory.
At the other end of the spectrum, many examples of altruism are found in human behavior. Consider those who choose to have few or no children. Such behavior is not uncommon, and it certainly is injurious to one’s reproductive success. Nor does it compare well with Darwin’s oft-repeated edict that “every single organic being may be said to be striving to the utmost to increase in numbers.” 
Other examples of humanity’s altruism include giving blood and donating organs, giving to charities, helping the needy, and heroic wartime acts such as smothering a grenade or rescuing prisoners. Such acts of love and kindness falsify the evolutionary expectation that organisms should be oriented toward high levels of reproductive success.
In the last fifty years evolutionists have proposed several explanations for altruistic behavior. As a consequence the theory has become enormously more complex and incredible. First, the hypothesis of kin selection was proposed by William Hamilton in the early 1960s.  It has since become fundamental in evolutionary explanations of altruism. The idea is that altruistic behavior is a consequence of shared genes. For example, consider a genetic modification that encourages siblings to help each other. Such altruism increases the reproductive success of the sibling. If the sibling shares the genetic modification (as they well might), then the altruistic gene ends up helping to propagate a copy of itself. Thus the behavior is not quite so altruistic after all. From the evolutionary perspective of reproductive success, altruistic behavior makes sense where there are shared genes.
Therefore, the hypothesis of kin selection implies that altruism will be greatest where gene sharing is greatest, such as between siblings and between parent and child, in human relationships. On the other hand, altruism will be weaker when there is less gene sharing (e.g., between cousins).
In addition to the degree of gene sharing, the hypothesis of kin selection also implies that altruism will depend on the number of individuals being helped. A person will be more inclined to aid multiple siblings, for there would be more shared genes at stake. As Hamilton put it, the hypothesis implies that while no one is prepared to sacrifice his life for any single person, everyone will sacrifice it for more than two brothers, or four half-brothers, or eight first-cousins. 
A more complicated selection process
Within a few years kin selection was used to explain a wide range of behaviors in addition to altruism. [e.g., 9,10] But these explanations brought with them an enormously complex evolutionary process. Consider altruism between siblings. Evolution’s unguided genetic modifications must have somehow created this complex behavior. This new modification created a medium level of altruism toward people that could be recognized as sisters or brothers. It was not too much altruism or too little. It was not toward females rather than males, short people rather than tall people, or blondes rather than brunettes. Presumably all these, and many more, types of behavior would be just as likely to have arisen as was the needed sibling altruism. So evolution must have constructed, tested and selected from an enormous set of potential behaviors before finding the few, rare behaviors that fit the kin selection criteria.
And the testing of these behaviors would not be simple. Initially, a new behavior, such as sibling altruism, would not fit the kin selection criteria. This is because, initially, the genes for the new behavior are in only a single individual. Not until the next generation could the genes possibly be distributed amongst siblings. And when that time does come, there is the question of whether the altruistic behavior would actually enhance the reproductive chances of the sibling. Being kind to a sibling does not necessarily do the job the first time. Many generations might be needed, as kin selection can only occur when an altruistic act genuinely improves the reproductive success of the sibling.
Evolution’s creative powers
Even more of a problem for evolution is the creation of these complex behaviors. Somehow unguided genetic modifications must have resulted in genes for a wide range of attitudes and behaviors. The list is staggering. There are of course the obvious behaviors such as love, hate, guilt, retribution, social tendencies and habits, friendship, empathy, gratitude, trustworthiness, a sense of fulfillment at giving aid and guilt at not giving aid, high and low self esteem, competition, and so forth.
These behaviors are supposed to have evolved according to the kin selection criteria, along with many more nuanced behaviors. For instance, love not only evolved, but in varying degrees depending on the degree of shared genes. It is weaker within the extended family than within the family. Low self esteem behavior not only evolved, but the art of not hiding it can be advantageous and so also evolved. Sibling rivalries evolved, but only to a limited degree. In wealthy families, it is more advantageous for siblings to favor sisters while in poor families siblings ought to favor brothers. So those behaviors evolved. Mothers in poor physical condition ought to treat daughters as more valuable than sons. Likewise, socially or materially disadvantaged parents ought to treat daughters as more valuable than sons.
Evolutionists explain all these nuanced behaviors according to the calculus of kin selection. For instance, consider sympathy and compassion. According to evolution, compassion and sympathy are nothing more than cleverly disguised manipulations. For while we may like to think our sympathy is pure, in fact it comes at a price. The unspoken yet universal expectation is: “you owe me one.” As one science writer put it, “Exquisitely sensitive sympathy is just highly nuanced investment advice. Our deepest compassion is our best bargain hunting.”  What such explanations fail to explain is the enormous complexity now added to the theory. Yes, the altruism is explained as advantageous, but such nuanced behaviors must somehow have arisen in the first place, in order to be later selected.
And, evolutionists warn, we should not be fooled by our intuition that certain behaviors are “obvious,” or “right.” For instance, love for one’s children and grief at the death of a child may seem to be natural reactions, but evolutionists explain that what seems to us to be common sense is, itself, merely a manifestation of our evolved behaviors. Yes we love our children, but only because such a behavior was selected. We have evolution to thank for our heartfelt emotions.
But do not many of our moral sentiments and behaviors reflect right and wrong? Are not loyalty, sacrifice, honor, our sense of justice, obligation and shame, remorse and moral indignation more than merely the result of mutations and selection? No, warn evolutionists, such appeals only reveal the power of evolution. As one writer put it, “It is amazing that a process as amoral and crassly pragmatic as natural selection could design a mental organ that makes us feel as if we’re in touch with higher truths. Truly a shameless ploy.” 
In fact, evolutionists explain, evolution has constructed elaborate deception mechanisms. Children use temper tantrums to manipulate parents. Parents countered this with the ability to discern and children, in turn, refined their manipulation with heartfelt whining. All a result of the complexities of natural selection. Cheating, suspicion, exaggeration, embellishment, hypocrisy, displays of morality, false compliments, self-serving dishonesty, boasting and self-deprecation are all evolved behaviors in accordance with natural selection.
Deception is rampant and evolutionists believe it evolved in biology to enhance reproduction. In turn, the ability to recognize deception has evolved, which in turn spurred the evolution of some degree of self deception, to better fool the opponent. This self deception should not be underestimated. It really means that we are, to a certain degree, truly deceived about the world around us. Our brains did not evolve to know truth, but some skewed version of reality. As one evolutionist concluded, “the conventional view that natural selection favors nervous systems which produce ever more accurate images of the world must be a very naïve view of mental evolution.” 
Here evolution aligns itself with radical skepticism. Nothing can be known to be true. If evolution is true, then not only are our minds nothing more than the product of unguided natural processes, but those very processes inbred a certain degree of falsehood. The evolutionist’s claim that evolution is a fact is self-refuting, for it leads to the conclusion that they cannot know that evolution is a fact.
Regardless of how deceived we are, we do know that evolution now calls for unguided genetic variation to create an incredible menagerie of complex and nuanced behavior. The enormous inventory of human behavior, which was selected, is only a tiny fraction of what must have been created. It would be swamped by the myriad behaviors which were not advantageous. In order to explain altruism, evolutionists now make a staggering claim about what must have arisen in nature. But the claim is a trade secret, as it is rarely discussed. Evolution has become a theory of seemingly endless speculation about behavior with little explanation of how the specific behaviors actually are supposed to have arisen. Evolutionists speculate at length about how behaviors could have been advantageous, with little consideration of the origin of such behaviors. Here is a representative example of this speculation, regarding an imagined behavioral strategy called “Selfish Punisher,” which exploits altruists and punishes other selfish individuals.
Individuals who behave altruistically are vulnerable to exploitation by more selfish individuals within their own group, but groups of altruists can robustly out-compete more selfish groups. Altruism can therefore evolve by natural selection as long as its collective advantage outweighs its more local disadvantage. All evolutionary theories of altruism reflect this basic conflict between levels of selection. It might seem that the local advantage of selfishness can be eliminated by punishment, but punishment is itself a form of altruism. For instance, if you pay to put a criminal in jail, all law-abiding citizens benefit but you paid the cost. If someone else pays you to put the criminal in jail, this action costs those individuals something that other law-abiding citizens didn’t have to pay. Economists call this the higher-order public goods problem. Rewards and punishments that enforce good behavior are themselves forms of good behavior that are vulnerable to subversion from within. 
Sub hypotheses such as this are now rampant within evolutionary theory. They are required to explain the wide range of behaviors in biology, and they force evolution to unprecedented levels of complexity. Unguided genetic change must be capable of somehow generating a wide array of behaviors with incredible precision.
And not only must all these varied and nuanced behaviors have arisen via unguided genetic modifications, but orders of magnitude more behaviors, which were not advantageous, must also have arisen. If unguided genetic variations were able to generate such pinpoint behaviors from which selection could choose, then there must also have been a vast menagerie of bizarre behaviors that were not selected. For the genetic variations were unguided. There was no foreknowledge of which behaviors were advantageous and which were not. The latter vastly outnumber the former, and so any given variation was most likely selected against. Only the rare exceptions were advantageous and evolutionary history must be chocked full of never observed pathologies that would not pass evolution’s test.
Problem of non reciprocal altruism
In addition to the tremendous complexity that kin selection adds to the theory of evolution, there is the problem that it does not explain altruistic behaviors for which no advantage to the individual can be imagined. Why do soldiers smother grenades? Why do rescuers risk their lives? Why does Mother Theresa help the needy in far away countries? Kin selection does not explain altruistic acts where there is no advantage to one’s own genes.
To explain such altruism, evolutionists must turn to unlikely speculation. For instance, a popular explanation is that in earlier ages our ancestors lived in small clans and villages where blood relations where more common. If most everyone in the village was a relative of yours, then altruistic behaviors would be advantageous more often. By the time civilization expanded into cities and nations, the altruistic behavior had evolved. So now we give aid to unrelated people because our evolved genes consider all people to have at least some relation to us.
In this model today’s examples of altruism that do not seem explainable using kin selection are viewed as vestigial behaviors. They were selected in the past, but now are operating outside the scope of kin selection. So although, as we saw above, evolution must have tremendous precision in creating finely tuned, nuanced behaviors, here evolution becomes a crude instrument. When needed, evolution can act with surgical precision. But when problems arise, evolution is suddenly clumsy. It is remarkable that, on the one hand Mother Theresa is left clueless that orphans on the other side of the world do not share her genes, yet on the other hand evolution can precisely construct detailed behaviors such as the Selfish Punisher strategy, the detailed altruism profiles between wealthy and poor families, and so forth. Mother Theresa falsifies the evolutionary expectations. As a consequence the theory is forced to adopt low probability, high complexity modifications. The theory is not explaining the data, it is adapting to the data.
Several other explanations have also been contemplated. Perhaps there is a way to explain such behaviors as aiding the individual. For instance, perhaps these actions enhance one’s status and attractiveness. Perhaps selection occurs at higher levels than the gene. [15, 16] Or perhaps what seems to be selfless altruism actually plays to self-centered motives. Yes, “Mother Theresa is an extraordinary person,” explained one evolutionist, “but it should not be forgotten that she is secure in service of Christ and the knowledge of her Church’s immortality.”  Ultimately, even helping the poor on the other side of the world can be rationalized with natural selection. With these and other explanations, evolutionists are able to provide some sort of selection rationale for practically any behavior.
What about the example of bacteria suicide, discussed above? Recall that the suicide is probably good for the bacteria population on the whole if, for instance, nutrients are running low. Since gene sharing within a bacteria population is at its maximum, evolutionists have no problem explaining such altruism as a result of kin selection. Such a facile response, however, misses the profound problem of how such design could arise in the first place, for the mechanism is immensely complex.
One bacteria suicide mechanism that has been discovered consists of a toxic gene coupled with an antitoxic gene. As explained above, the toxic gene codes for a protein that sets the act of suicide into motion and so ultimately kills the bacteria. The antitoxic gene normally inhibits the toxic gene from executing its mission. But certain problems, such as a lack of proper nutrients or radiation damage, cause the antitoxin to be diluted, thus allowing the toxin to perform its mission.
The toxin does not, however, single-handedly destroy the cell. The toxin is an enzyme that cuts up the copies of DNA (i.e., messenger RNA, or mRNA) that are used to make other proteins. By slicing up the mRNAs, the cell no longer produces the proteins essential for normal operation. But the toxin does not cut up all mRNAs. Some mRNAs escape unscathed, and consequently a small number of proteins are produced by the cell. These include death proteins that efficiently carry out the task of disassembling the cell.
Death proteins are not the only proteins that the toxin allows to be produced. As researchers reported, the toxin “activates a complex network of proteins.”  While some of the proteins bring death to the bacteria, others can help the cell to survive. The result is that most cells in the population are destroyed, but a fraction is spared. This of course makes sense. The suicide mechanism would not help the bacteria population if every individual was destroyed. Instead, some survive, and they can be the founders of a new population when conditions improve.
This suicide mechanism and “behavior” is altruistic. Some bacteria die off to save others. And the explanation that this bacteria suicide is due to kin selection adds tremendous complexity to the theory of evolution. Kin selection can select from only that which is available. This elaborate suicide mechanism must have just happened to arise from some combination of unguided mutations, and then remained in place until the time when it would succeed in surviving a stressful environment. The toxin and antitoxin genes with their clever functionality, the death and survival proteins, the inter cellular communications—all these were needed to be in place and to be coordinated before the kin selection could even begin to act. How many mutations would be required for this is difficult to say, but obviously this adds considerable complexity to the theory.
Darwin’s theory of evolution led him to several expectations and predictions, regarding behavior in general, and altruism in particular. We now know those predictions to be false. Furthermore, in order to explain many of the behaviors we find in biology, evolutionists have had to add substantial serendipity to their theory. The list of events that must have occurred to explain how evolution produced what we observe is incredible and the theory has become profoundly complex.
The various false predictions and resulting theory complications presented above are merely examples. Since 1859 the theory of evolution has encountered myriad surprises and adjustments. It might seem that evolutionists would waver in light of such evidential problems, but this is not the case. Indeed, today evolutionists are as confident as they have ever been, perhaps even more so. The reason for this is that evolutionists are convinced that their theory is a fact. This has been claimed for more than a century, and no less so today. Given this conviction, the many problems with the theory, such as those presented above, are interpreted as mere technical details to be resolved. They are research problems regarding how evolution occurred, not if evolution occurred.
The key to understanding evolutionary thinking is to understand why evolutionists believe their theory is a fact. They arrive at this remarkable conclusion by the process of elimination. And while this is a perfectly valid method of reasoning, in the case of evolution everything hinges on key premises which are largely unheard of outside evolutionary circles. These premises are, themselves, not from science, but they underwrite the wholesale evolutionary interpretation of volumes of scientific evidence.
The process of elimination is a method of reasoning that concludes a hypothesis is true by falsifying all the alternatives. For instance, without knowing how many blue balls are in an urn, a statistician could conclude they are a majority because less than 50% of the balls are red. The fact that the red balls are not a majority means that the blue balls must be a majority. Of course this conclusion depends on there being only red and blue balls in the urn. If there are white balls in the urn as well, then the statistician’s conclusion is not sound.
In science the process of elimination can be more complicated. With different colored balls in an urn, there are only a limited set of easily defined competing hypotheses. In science it often is not clear how to define competing hypotheses, or even how many there are. Imagine a geocentrist who concludes that the universe revolves about the earth because, after all, it does not revolve about the sun. He has concluded that his favorite explanation is true by comparing it to a straw man explanation.
Evolutionists also use the process of elimination to conclude their theory is a fact. There are many difficulties with the theory, but evolutionists have ruled out the alternatives. As the leading twentieth century evolutionist Ernst Mayr wrote:
The greatest triumph of Darwinism is that the theory of natural selection, for 80 years after 1859 a minority opinion, is now the prevailing explanation of evolutionary change. It must be admitted, however, that it has achieved this position less by the amount of irrefutable proofs it has been able to present than by the default of all the opposing theories. 
Indeed, if there was even a single irrefutable proof for macroevolution
by natural selection then the default of the opposing theories would be irrelevant.
But there are none. The many proofs given in the evolution literature are from
the process of elimination. Evolutionary thinking is deeply indebted to a
contrastive approach. In fact this mode of proving theories in the historical
sciences long predates
A century before
A generation later the great philosopher Immanuel Kant reiterated the argument. Why do planets revolve about the sun in the same direction, asked Kant. The solar system must have evolved via natural laws, concluded Kant, because if God had designed the solar system it would not have the patterns we observe:
It is clear that there is no reason why the celestial bodies must organize their orbits in one single direction. … Thus, God’s choice, not having the slightest motive for tying them to one single arrangement, would reveal itself with a greater freedom in all sorts of deviations and differences. 
And after Kant the great French mathematician and scientist, Pierre Laplace repeated the argument. Laplace and Kant are, to this day, credited with elucidating the foundational thesis of the evolution of the solar system. They both were quite certain their reasoning had led to a new truth. This was no mere hypothesis or theory.
The key here is that random design was viewed as the default option against which natural evolution is tested. Random design was, in twentieth century terminology, the null hypothesis. Null hypothesis testing was formalized in the last century, but it was alive and well in the eighteenth century as well.
Like astronomy, biology also reveals many patterns. And like
Bernoulli, Kant and Laplace,
Figure 15 For evolutionists the possible explanations are random design and evolution. They conclude that evolution must be true because patterns in nature we have found demonstrate the natural world is not randomly designed.
The random design null hypothesis is sufficient to prove
evolution is true. If one agrees that evolution is the only alternative, then
the patterns in nature certainly mandate that evolution is true. But this is
not the only way to eliminate the competition. Evolutionists have developed
several other arguments that also prove their theory by the process of
elimination. And like the random design null hypothesis, these other arguments
Many of these arguments are also explicitly theological. For instance, the seventeenth century cleric Nicolas Malebranche argued that God would not create the evil we see in nature. Instead, God allowed for the evil to arise as a consequence of using simple, law-like natural processes to create the world. According to Malebranche, God wanted to use simple mechanisms, and so He allowed for evil to arise as a consequence. This notion of having natural laws, rather than divine action, be responsible for nature helps to absolve God from responsibility for the evil in the world. It was a popular idea, and Darwin and evolutionists to this day strenuously argue that evolution must be true since God never would have intended to create this nasty world. 
While Malebranche was formulating his response to the problem of evil, others were reacting similarly to the apparent inefficiency and lack of design in the world. Yet others argued the God would not intervene in creation with miracles. For instance, a leading eighteenth century German philosopher and Lutheran, Christian Wolff was certain that God would never use miracles after the initial creation of the world. Others argued that the creation of the details of this world would be beneath the dignity of God, and others warned that we ought not view God as creating material things as people do. These various, but related, traditions laid a foundation for the move toward a strictly naturalistic explanation of origins, and the theory of evolution. Darwin and evolutionists after him were no different. They agreed with these convictions, and have argued that they mandate evolution by the process of elimination.
Aside from these explicitly theological issues, another category of argument deals with the intellectual necessity of naturalism, and how science must proceed. These arguments require that science be strictly and exclusively limited to naturalistic explanations because otherwise problems arise. For instance, one argument is that the alternatives to evolution are not testable, and all scientific theories must be testable. Another argument is that alternatives to evolution lead to an infinite regress. For example, if nature’s complexity implies a designer, then who designed the designer?
With these theological and epistemological arguments in mind,
evolutionists insist that their theory (in one form or another) must be true.
Figure 16 illustrates these various arguments that evolutionists have used in their process of elimination. Example thinkers are given who promoted the different arguments, in their chronological order.
Figure 16 Illustration of the various evolutionary premises (black) and example advocates (red).
Evolution is a fact by the process of elimination, and the criteria fall into two broad categories: theological criteria about God and epistemological criteria about science. The theological criteria eliminate competing theories by falsification. That is, according to the theological criteria, competing theories are false. The epistemological criteria, on the other hand, eliminate competing theories by rejection. That is, according to the epistemological criteria, the competing theories do not qualify as legitimate science.
The epistemological criteria mandate that scientific explanations must strictly appeal only to natural laws and processes. Anything else, say evolutionists, violates the scientific method. Science, however, is a wide ranging set of activities that is difficult to circumscribe. In fact many have attempted to distinguish science from non-science, but without success. Activities that everyone thinks of as science end up being defined as not science.  The evolutionist’s epistemological criteria, for instance, would outlaw the Search for Extra Terrestrial Intelligence (SETI) project.
But let us ignore this potential problem and grant the evolutionists their epistemological criteria. Their mandating of strictly naturalistic explanations is tantamount to scientists placing a constraint on reality. The fact that evolutionary science can only reckon with naturalistic explanations does not mean that only those explanations are true. This would be like an automobile mechanic claiming that jet aircraft cannot be real because, after all, he does not possess the knowledge or tools to work on them. Evolutionists lack the tools to test and evaluate theories that are not strictly naturalistic, but this does not mean such theories are necessarily false.
The irony here is that evolutionists make naturalism unscientific according to their own criterion of testability. This is because naturalistic explanations are the only explanations that are allowed. They therefore cannot be tested because they are true by definition. The only testing that can be done is between different sub-hypotheses of naturalism. Gradualism can be compared with punctuated equilibrium, drift can be compared with selection, and so forth. But naturalism has been defined as the only scientific option available.
Imagine if the species were designed, as they appear to be. Imagine that the DNA code, the bat’s sonar system, the towering redwood trees, and the other biological wonders were designed. If this were true, it would not be allowed within evolutionary science. How can evolutionists claim their theory is a fact while simultaneously ruling out certain explanations? They can do this by claiming that only scientific explanations are factual. The world outside of science may be beautiful, awesome, intriguing, enchanting, and so forth, but it is not factual. In a word, science deals with facts while non-science deals with values.
The is the fact-value split, 
and it does not come from science. As Galileo long ago supposed, religion deals
with how to go to heaven whereas science deals with how the heavens go. It may
sound reasonable but by
It is now common for otherwise sophisticated evolutionary thinkers to claim simultaneously that strictly naturalistic evolution (of one form or another) is a fact, and that anything else is ruled out a priori. Evolutionists say that evolution is a fact and that non-natural theories do not qualify as science and cannot even be evaluated. 
Such claims can be deceptive because they appear to be the conclusion of a scientific evaluation. Ironically, they are not. They are the necessary consequence of theological assumptions. Now we can understand what the claim “evolution is a fact” actually means. Evolutionists explain that evolution is a fact every bit as much as gravity. They arrive at this conclusion by using non-scientific assumptions to rule out the alternatives, in spite of contrary scientific evidence. The claim that evolution is a fact is not arrived at via an analysis of the scientific data; rather, it allows for the many problems in the data to be inconsequential.
In the century and a half since Charles Darwin proposed his
theory of evolution, science has discovered a plethora of contradictory
information. Many predictions of the theory have been falsified, including
foundational expectations. The theory has consistently failed and as a
consequence it has grown far more complex than anything
In stark contrast to these evidential problems, evolutionists believe that their theory is a fact. Evolution is a fact, they say, just as gravity is fact. This remarkable claim is an indicator that there is more to evolution than merely a scientific theory. In light of the scientific evidence, the claim that evolution is a fact may seem to be absurd. But it is not.
The fact of evolution is a necessary consequence of the metaphysical assumptions evolutionists make. Metaphysical assumptions are assumptions that do not derive from science. They are made independent of science. These metaphysical assumptions that evolutionists make would be difficult to defend as necessarily true outside of evolutionary circles, but within evolution their truth is not controversial. All of this means that the scientific problems with evolution are relegated to questions of how evolution occurred. The science cannot bear on questions of whether or not evolution occurred.