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Failed and falsified evolutionary predictions

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1 Failed and falsified evolutionary predictions on Thu Apr 10, 2014 5:48 pm

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Failed and falsified evolutionary predictions

http://reasonandscience.heavenforum.org/t1666-failed-evolutionary-predictions

Can it be falsified?  In fact, Darwin gave several criteria that would falsify his theory, if proven true.  How do these play out?


Irreducible Complexity falsifies Darwins ToE

Now a definition:“Irreducible Complexity”: Occurs when a biological form cannot exist without multiple independent aspects that cannot be reduced further. (Behe)

In other words, an irreducibly complex system would require two or more independent features to be present simultaneously in order to function.  Any thing less would be a meaningless feature, of no value to the host.  Behe gives the mousetrap as an example: if only the board exists, no mice will e caught.  If only the spring exists, no mice will be caught.  If only the latch exists, no mice will be caught.  It takes all three elements to be present for a mouse trap to function.  So the irreducible complexity of the mouse trap is three elements.

Examples of Irreducibly Complex systems:

1. Behe’s flagellum.  Some bacteria have on-board propulsion systems consisting of a rotary motor, a free turning shaft, a bushing around the shaft as it emerges to the outside, and a propeller.  The motor can reverse               directions and go to 100,000 rpm. All components are required in order to function.
2. Bombardier Beetle. The beetle contains two sacs, one which contains a volatile substance and another containing an oxidizing substance; it also has a mixing chamber, an expulsion mechanism, and a movable nozzle for           aiming the ejection of the explosive mixture at a foe.
3. DNA / RNA Interactions.  DNA supplies the blueprint of the required protein to the RNA, which uses the blueprint to manufacture the protein.  One can’t do anything without the other.
4. Stomach.  Digests, yet doesn’t digest itself.
5. Coagulation of blood.  If blood coagulated inside the vein, the entire arterial/venous system would clog shut.  If blood did not coagulate when it needs to, excessive bleeding to the point of death would occur.  A number of       clotting factors are needed in order for blood clotting to perform correctly.
6. First Life.  Requires 9 essential features, all present simultaneously.
7. Feathers.  Extremely complex mechanisms that are not direct off-shoots of hair or scales.
8. Toxic snakes. 3 necessary systems: They generate toxin in a fashion that keeps them immune, they hypodermically inject the toxin without injecting themselves, they consume their own toxin by eating the prey, yet are         unaffected.
9. Giraffe’s neck. Must have extra vascular valves to make the length work.
10. DNA / protein dependency: DNA requires proteins, but proteins require DNA.

These are just a sampling of the myriad systems that are too complex to have occurred with just one step, one mutation.  So Darwin’s first falsification proposition is satisfied.  But there’s more.

A list of irreducible complex systems
http://reasonandscience.heavenforum.org/t2166-a-list-of-irreducible-complex-systems

Catch22, chicken and egg problems in biology and biochemistry
http://reasonandscience.heavenforum.org/t2059-catch22-chicken-and-egg-problems

Irreducible complexity is a undeniable fact
http://reasonandscience.heavenforum.org/t1468-irreducible-complexity#2133


Cerebral Probabilities falsify Darwins ToE

Here is the reason Darwin specifically eliminated the origin of the mind from his theoretical discussion: The complexity of the human brain, let alone the human mind, is far more than any stretch of evolutionary theory can possibly accommodate. So Darwin eliminated it from the evolutionary discussion with a stroke of denial.  (See “Darwin’s Dodge”, in the Paradox section of the Appendix).
We aren’t that naïve or lacking in intellectual integrity.  Here are some stats (1) to consider:
The Cerebral Cortex (part of the brain):
•Contains 9,200,000,000 neurons (9.2 x 10^9);
•Contains 1,000,000,000,000,000  (10^15) neural interconnections.
•The earth is 3,500,000,000 years old, give or take a little.
So,
Assuming gradual mutation of the cortex, say a daily constant rate from the beginning of the earth (A very generous assumption!), the successful mutations required for development of the cortex is:
(10^15) / (3.5x10^9) = 2.86 x 10^7 (interconnects/year)
And,
(2.86 x 10^7) / 365 = 0.78 x 10^5 (interconnects/day)
Or, to restate,
78,000 new, successful new neural interconnections…each and every day, for 3.5 billion years.
The likelihood of this is clearly negligible.  It is another Falsification of Darwinism.
(1) These numbers are taken as reasonable averages of a great number of variations reported.


Falsification by Redundancy

If a system demonstrates back-up systems, the likelihood of this resulting from evolution is negligible.

An example is the Circle of Willis in the human brainpan, where the six (6) arteries that feed the brain come together and terminate into a circular artery which connects them all together.   If any of the main arteries lacks capacity to supply blood, the other arteries can supply it backwards through the Circle of Willis, into the endangered region.

Another example: It is now thought that the “extra” DNA in the helix is actually used for back-up in the repair process, another redundancy.

What are the probabilities of this occurring randomly, by chance mutation?  So close to zero as to be considered negligible.  It is a Falsification of Evolution.

Falsification By Rapid Complexity

Darwinists have been unable to explain away the “instant complexities” that occurred during the Cambrian “explosion”.  In the Pre-Cambrian era, only single celled creatures, algae, and later, a few worms existed.  Then suddenly in the Cambrian era, 35 or possibly all 40 of the world’s phyla (top category) came to exist.   (Stephen C Meyer, PhD, Cambridge U.)

If the world’s history were 24 hours long, the Cambrian era would be one minute.

Is this the result of gradual selection by natural processes?  Hardly likely.  More likely, it is a Falsification of Evolution.

What’s more, in China the discovery of soft-bodied, microscopic sponge embryos in the pre-Cambrian zone, with no sign of higher forms, falsifies the theory that there are not yet enough fossil records, or that pre-Cambrian creatures were too small and soft bodied to leave records. (J. Wells)

The empirical data are that the phyla did not happen slowly from a single source.  A Falsification of Evolution.

Falsification By Skipping Steps

Even more telling is the instant complexities of certain organs, such as the eye.  Coordinated binocular, 3D, range-finding, auto-focusing, auto light-value adjusting, color vision requires 2 coordinated eyes, of very high complexity.

If eyes developed gradually, there would have been numerous creatures with, say, one eye.  Or just a light sensitive spot.

Where is the lineage of animals with the intermediate light spots? Or single eyes? Or just heat sensors?  Why the instantaneous complexity?

It’s a Falsification of Evolution.

The lack of forensic data to fill in the many gaps has caused Gould to propose a different theory from Darwin’s:

Gould’s Punctuated Equilibrium: small isolated populations mutate, then re-populate and dominate the original population.  This would “leave no traces”.

The proof for this theory is that it matches the facts by requiring no evidence.  Actually, so did Darwin’s!  An amazing twist of logic.  And a direct violation of the concepts of empiricism and forensics.  No evidence is just no evidence, nothing more.

In fact there is empirical refutation of the mutated population theories. in the bacterial populations there is a loss of staying power for “selected” populations, which lose out to the parent population.  When stressors are reduced, the original population resumes dominance.  Mutations are weaker, not stronger.

There is no empirical evidence to support Gould’s Theory, which is seen to be a “just so story” in a desperate attempt to shore up a failing theory.


Falsification by Process Interruptus.


At some point, the supposed process of evolution stopped, and changed over to a process of extinction.

Had the process of evolution been driven by natural selection of mutations, new super species would be developing now at a rapid rate, due to the supposed pollution of the earth by man.  Species should develop that are immune to the attack of man, but the process of extinction seems to be the only process active.

Don’t bother to throw in the selection of hardened E-Coli, or other bacteria.  These are not mutations, they are micro-evolved populations, and they are still E-Coli.  They have not become wolves, snakes, or super-humans.  It does not demonstrate macro-evolution.  And when the cause for hardening is removed, the population, like that of Darwin’s Finches, returns to it’s previous configuration.

Extinction is a true process that existed long before mankind.  It is observable.  Evolution is not observable, as is admitted by evolutionist Dawkins.  Process Interruptus is a Falsification of Evolution.

Empirical Falsification.

What is provided by an empirical look at the Theory of Evolution?  Empirical observation is the weapon of choice for Atheists, yet it can’t produce much support for evolution.

1.For example, empirically, life has never been observed to erupt spontaneously.  There is currently a $1 Million reward for anyone who can produce, repeatably, I presume, an organism that contains the nine requirements for life.  The cash is still available, unclaimed.

2.Life is always observed to come from prior life.  It is never seen to spontaneously erupt or self-assemble. This is the Falsification of Evolution that causes Darwinists to deny any involvement in First Life.

3.The Miller Lab Experiments in the 1950’s claiming to have produced amino acids from primordial soup have been falsified.  The existence of primordial soup itself has been falsified.

4.To evolve would require a selection of a new characteristic not present in the current population, i.e. a mutation.  Very few if any mutations are observed (none documented) to be beneficial; in fact most mutations are detrimental and would decrease the creature’s ability to compete.  Statistically, the mutation theory is so weak as to be a Falsification of Evolution.

5.Spontaneous mutations that occur simultaneously are not observed.

Lönnig: Complex systems in nature point to an intelligent origin for life 1

“A scientific hypothesis should be potentially falsifiable, that is, there should be criteria according to which a hypothesis can be disproved and thus be rejected as false. As to the origin of species, Darwin had asserted that evolution proceeds by “infinitesimally small inherited variations”, “steps not greater than those separating fine varieties” and “insensibly fine steps”, “for natural selection can act only by taking advantage of slight successive variations; she can never take a leap, but must advance by the shortest and slowest steps”. This is also the credo of most modern evolutionists (neo-Darwinians) and, in principle, even of the proponents of the punctuated equilibrium theory. However, the idea of slow evolution by “infinitesimally small inherited variations” etc. has been falsified by the findings of palaeontology (abrupt appearance of the Baupläne) as well genetics (origin of DNA and complex genetic information). Yet its adherents principally reject any scientific proof against Neo-Darwinism, so that, in fact, their theory has become a non-falsifiable world-view, to which people stick in spite of all contrary evidence. Their main reason: Without Darwinism, philosophic materialism has lost its battle against an intelligent origin of the world.“

Ignorance + "body plans" + misinformation (lies) + god-of-the-gaps = Intelligent Design Creationism 3


Lantog wrote: Everything we’ve learned from developmental biology and comparative genomics in the last decade is consistent with extant body plans being derived by descent with modification from simpler ones…

That question is the center and core of dispute between evolution and design. No wonder, this question keeps the debates and disputes alive, because we have not yet a clear and fully elucidated picture. In order to know what provokes the origin of body plans, and if the claim that evolutionary mechanisms might explain biodiversity, and the change from one kind or species to another, and the formation of evolutionary novelty, like eyes, wings, legs, finns, ears etc. we need to know first what ontogenetic mechanisms and forces actually provoke body forms. Paul Nelson has not lied in regard of stating that mainstream science has been greatly ignorant to point out clearly what mechanism that is.

EVEN PROPONENTS OF EVOLUTION ADMIT TO NOT KNOWING HOW EVOLUTION SUPPOSEDLY WORKS:

No coherent causative model of morphogenesis has ever been presented. 5

“Although the vast majority of research in evolutionary biology is focused on adaption, a general theory for the population-genetic mechanisms by which complex adaptations are acquired remains to be developed.”
Proceedings of the National Academy of Sciences of the U.S., “Scaling expectations for the time to establishment of complex adaptations”, September 7, 2010, 6

“Students should realize that although virtually all scientists accept the general concept of evolution of species, scientists do have different opinions on how fast and by what mechanisms evolution proceeds.”
The American Association for the Advancement of Science, Educational Benchmarks, (F) Evolution of Life 4

“Scientists are still uncovering the specifics of how, when, and why evolution produced the life we see on Earth today.”
Smithsonian’s National Museum of Natural History’s website, “Foundational Concepts: Evolution” page 7

“But they are trying to figure out how evolution happens, and that’s not an easy job.”
University of California Museum of Paleontology and the National Center for Science Education 8

“Much of the recent experimental work on natural selection has focused on three goals: determining how common it is, identifying the precise genetic changes that give rise to the adaptations produced by natural selection, and assessing just how big a role natural selection plays in a key problem of evolutionary biology—the origin of new species.”
Scientific American Magazine, “The Evolution of Evolution: Testing Natural Selection with Genetics”, December 18, 2008. 9

Science however goes forward, and keeps elucidating what goes on inside the cell, and development biology is opening the black box, and demonstrating how organisms develop. We are slowly getting out of a state of ignorance in regard of what mechanisms determines cell shape, assignment of their planes of division, tendencies to move, directions and rates of movement, modes of differentiation into particular cell types, and cell death (apoptosis).

Two reasons :

One primary feature of oriented cell division is the proper positioning of the mitotic spindle relative to a defined polarity axis. In principle, spindle orientation is achieved through signaling pathways that provide a molecular link between the cell cortex and spindle microtubules. These pathways are thought to elicit ( provoke ) both static connections and dynamic forces on the spindle to achieve the desired orientation prior to cell division. Although our knowledge of the signaling molecules involved in this process and our understanding of how they each function at the molecular level remain limited, collective efforts over the years have shed light on the importance of spindle orientation to animal development and function. Moreover, emerging evidence shows an association between improper spindle orientation and a number of developmental diseases as well as tumor formation. 10

and: Electrical gradients and fields are critical in the 3D function and shape of cells and organs.

Electrical signaling is key for cells to properly interpret their environment, and when this process goes awry, the cells default to a cancer program.
While ion flows control cell-level behaviors such as migration, differentiation, and proliferation, bioelectric signals also function as master regulators of large-scale shape in many contexts: a simple signal can induce complex, highly orchestrated, self-limiting downstream morphogenetic cascades. For example, an unmodulated flux of protons can cause the formation of a complete tail of the right rise and tissue composition. 11

BOTH EXPLANATIONS POINT TO INFORMATION. INFORMATION IS THE KEY. CHANGE THE INFORMATIONAL INSTRUCTIONS, AND THE RESULT IS NOT NEW BODY PLANS, BUT DESEASE, CANCER ETC. IN THE END, THE QUESTION IS: WHERE DOES THE INFORMATION COME FROM THAT DIRECTS THE FORMATION OF NEW BODY PLANS ?

And a second question arises : Why the heck would unicellular protozoans want to evolve into multicellular organisms, if they compartmentalize and are able to work with multiple organs which exercise various tasks just fine, like multicellular organisms do ? As for example : Diplodinium (Epidinium) ecaudatum, which has a kind of "brain" (motorium); 2 - - mouth; 4 - conductive filaments of the pharynx; 5 - fibrils pharynx; 6 - skeletal plate; 7 - endoplasm; 8 - "hindgut"; 9 - poroshitsa; 10 - contractile vacuole; 11 - Ma;Mi-12; 13 - dorsal lip; 14 - dorsal cirri area ??? 2


1) http://dippost.com/2014/03/22/wolf-ekkehard-lonnig-complex-systems-in-biology-overwhelmingly-point-to-an-intelligent-origin-of-living-beings/
2) http://reasonandscience.heavenforum.org/t2308-origin-of-development-and-ontogeny#4757
3) http://sandwalk.blogspot.com.br/2016/02/ingorance-body-plans-misinformation.html#comment-form
4) http://www.project2061.org/publications/bsl/online/ch5/ch5.htm#F
5) http://journals.cambridge.org/action/displayAbstract;jsessionid=79710AE9A71071921BD4A3CAC34D5C80.journals?aid=7928966&fileId=S147355041000025X
6) doi:10.1073/pnas.1010836107.
http://www.pnas.org/content/early/2010/08/30/1010836107.abstract
7) http://www.nmnh.si.edu/paleo/geotime/main/foundation_life3.html
8  http://evolution.berkeley.edu/evolibrary/article/0_0_0/evo_50
9) http://www.sciam.com/article.cfm?id=testing-natural-selection&print=true
10) http://reasonandscience.heavenforum.org/t2090-centriole-centrosome-the-centriole-spindle-the-most-complex-machine-known-in-nature#4759
11) http://reasonandscience.heavenforum.org/t2293-the-recent-groundbreaking-scientific-research-which-explains-the-real-mechanisms-of-biodiversity

Theodore Holden : how evolution is a failed hypothesis.

A proof or disproof is a kind of a transaction. There is no such thing as absolutely proving or disproving something; there is only such a thing as proving or disproving something to SOMEBODY'S satisfaction. If the party of the second part is too thick or too ideologically committed to some other way of viewing reality, then the best proof in the world will fall flat and fail.
In the case of evolution, what you have is a theory which has been repeatedly and overwhelmingly disproved over a period of many decades now via a number of independent lines reasoning and yet the adherents go on with it as if nothing had happened and, in fact, demand that the doctrine be taught in public schools at public expense and that no other theory of origins even ever be mentioned in public schools, and attempt to enforce all of that via political power plays and lawsuits.
At that point, it is clear enough that no disproof or combination of disproofs would ever suffice, that the doctrine is in fact unfalsifiable and that Carl popper's criteria for a pseudoscience is in fact met.
Once again for anybody who may have missed this earlier:
The educated lay person is not aware of how overwhelmingly evolution has been debunked over the last century.
The following is a minimal list of entire categories of evidence disproving evolution:
The decades-long experiments with fruit flies beginning in the early 1900s. Those tests were intended to demonstrate macroevolution; the failure of those tests was so unambiguous that a number of prominent scientists disavowed evolution at the time.
The discovery of the DNA/RNA info codes (information codes do not just sort of happen...)
The fact that the info code explained the failure of the fruit-fly experiments (the whole thing is driven by information and the only info there ever was in that picture was the info for a fruit fly...)
The discovery of bio-electrical machinery within 1-celled animals.
The question of irreducible complexity.
The Haldane Dilemma. That is, the gigantic spaces of time it would take to spread any genetic change through an entire herd of animals.
The increasingly massive evidence of a recent age for dinosaurs. This includes soft tissue being found in dinosaur remains, good radiocarbon dates for dinosaur remains (blind tests at the University of Georgia's dating lab), and native American petroglyphs clearly showing known dinosaur types.
The fact that the Haldane dilemma and the recent findings related to dinosaurs amount to a sort of a time sandwich (evolutionites need quadrillions of years and only have a few tens of thousands).
The dna analysis eliminating neanderthals and thus all other hominids as plausible human ancestors.
The total lack of intermediate fossils where the theory demands that the bulk of all fossils be clear intermediate types. "Punctuated Equilibria" in fact amounts to an attempt to get around both the Haldane dilemma and the lack of intermediate fossils, but has an entirely new set of overwhelming problems of its own...
The question of genetic entropy.
The obvious evidence of design in nature.
The arguments arising from pure probability and combinatoric considerations.
Here's what I mean when I use the term "combinatoric considerations"...
The best illustration of how stupid evolutionism really is involves trying to become some totally new animal with new organs, a new basic plan for existence, and new requirements for integration between both old and new organs.
Take flying birds for example; suppose you aren't one, and you want to become one. You'll need a baker's dozen highly specialized systems, including wings, flight feathers, the specialized system which allows flight feathers to pivot so as to open on upstrokes and close to trap air on downstrokes (like a venetian blind), a specialized light bone structure, specialized flow-through design heart and lungs, specialized tail, specialized general balance parameters etc.
For starters, every one of these things would be antifunctional until the day on which the whole thing came together, so that the chances of evolving any of these things by any process resembling evolution (mutations plus selection) would amount to an infinitessimal, i.e. one divided by some gigantic number.
In probability theory, to compute the probability of two things happening at once, you multiply the probabilities together. That says that the likelihood of all these things ever happening, best case, is ten or twelve such infinitessimals multiplied together, i.e. a tenth or twelth-order infinitessimal. The whole history of the universe isn't long enough for that to happen once.
All of that was the best case. In real life, it's even worse than that. In real life, natural selection could not plausibly select for hoped-for functionality, which is what would be required in order to evolve flight feathers on something which could not fly apriori. In real life, all you'd ever get would some sort of a random walk around some starting point, rather than the unidircetional march towards a future requirement which evolution requires.
And the real killer, i.e. the thing which simply kills evolutionism dead, is the following consideration: In real life, assuming you were to somehow miraculously evolve the first feature you'd need to become a flying bird, then by the time another 10,000 generations rolled around and you evolved the second such reature, the first, having been disfunctional/antifunctional all the while, would have DE-EVOLVED and either disappeared altogether or become vestigial.
Now, it would be miraculous if, given all the above, some new kind of complex creature with new organs and a new basic plan for life had ever evolved ONCE.
Evolutionism, however (the Theory of Evolution) requires that this has happened countless billions of times, i.e. an essentially infinite number of absolutely zero probability events.
I ask you: What could be stupider than that?
Fruit flies breed new generations every few days. Running a continuous decades-long experiment on fruit flies will involve more generations of fruit flies than there have ever been of anything resembling humans on Earth. Evolution is supposed to be driven by random mutation and natural selection; they subjected those flies to everything in the world known to cause mutations and recombined the mutants every possible way, and all they ever got was fruit flies.
Richard Goldschmidt wrote the results of all of that up in 1940, noting that it was then obvious enough that no combination of mutation and selection could ever produce a new kind of animal.
There is no excuse for evolution to ever have been taught in schools after 1940.



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What false predictions tell us about evolution



Ever since Darwin proponents of evolution have been certain of their theory. They hold that evolution is a fact beyond all reasonable doubt. Proponents of evolution arrive at this conclusion from a wide range of powerful arguments based on contrastive reasoning where evolutionary theory is compared to alternative hypotheses derived from the concept of independent creation. (Hunter 2014) Proponents of evolution have found these alternative hypotheses to be false, leaving evolutionary ideas as the only remaining possibility. This process of elimination, which traces back to the sixteenth and seventeenth centuries, is based on comparing scientific evidence with expectations derived from independent creation. Therefore the motivation, justification and truth claims for evolutionary theory entail metaphysical beliefs about independent creation.
 
This raises the question of how evolution fares without the metaphysics. That is, how does evolution compare with the scientific evidence? Evolutionary theory holds that the biological world (and more generally the cosmos as well), arose from the interplay of chance and natural law. In other words, evolution holds that the species arose spontaneously. From a strictly scientific perspective, this is a high claim. It is perhaps not surprising that, setting the contrasting reasoning aside and focusing exclusively on the science, evolution’s fundamental predictions fail badly. The above sections reviewed several fundamental predictions of evolutionary theory, once held with great conviction, that have all been found to be false, much to the surprise of practitioners.
 
Philosophers have debated the role and importance of predictions in the historical sciences, and how they are related to explanatory capacity. (Cleland 2011; Cleland 2013; Turner) The predictions described above do have strong implications for evolution’s capacity to explain phenomena. For most of these predictions, the falsification has been followed by one or more proposed theory modifications to accommodate the new data. These modifications are often vague and they cause the theory to lose its parsimony. Perhaps most importantly they refute evolution’s common cause argument and remove its so-called “smoking gun.” The proponents of evolution's claim has been that in biology we find a wide range of observations that seem unlikely or bewildering, but that in a stroke evolution parsimoniously explains and makes sense of them. Evolution brings a consilience to the data.
 
The  predictions below illustrate that there is no such consilience. Evolution’s predictions, and associated explanations, do not make sense of the observations. Consider, for example, the pentadactyl structure prediction discussed below. In Darwin’s day the five-digit pentadactyl structure was observed in a wide variety of species. Why should the same type of structure be used for such a wide variety of tasks? Evolution’s common descent provided a single, simple explanation. The pentadactyl structure arose from a single common ancestor. The associated prediction is that the pentadactyl structure should continue to appear in species according to a common descent pattern. The failure of the pentadactyl structure to form this pattern does not merely represent a false prediction. This common cause argument had been celebrated for more than a century as a compelling proof text. It appears consistently in the literature and is one of evolution’s “smoking guns.” The falsification of this prediction means the loss of this compelling argument. And it means the introduction of non parsimonious explanations, calling for the pentadactyl structure to repeatedly evolve and disappear in various lineages, as the data require.
 
Yet contrastive reasoning, proponents of evolution argue, prove that evolution is a fact. This illustrates the tremendous importance of the role of contrastive reasoning. If all we had was the science there would be no basis for believing the species have spontaneously arisen, much less that such an idea is a fact. But evolution is not a typical scientific theory. In spite of the consistent failure of fundamental scientific predictions, there remains no doubt amongst proponents of evolution that evolution is a fact. Its high standing is underwritten by extremely powerful contrastive proofs which render its scientific puzzles less crucial. Those puzzles are interpreted as research questions, not challenges to the fact of evolution. That fact, for proponents of evolution, has already been established by the philosophy and theology that support evolution’s contrastive reasoning. From a strictly scientific perspective, evolution is not a good theory.
 
References
 
Cleland, Carol. 2011. “Prediction and Explanation in Historical Natural Science.” Brit. J. Phil. Sci. 62:551–582.
 
Cleland, Carol. 2013. “Common cause explanation and the search for a smoking gun.” Geological Society of America Special Papers 502:1-9.
 
Hunter, C. 2014. “Darwin’s Principle: The Use of Contrastive Reasoning in the Confirmation of Evolution.” J International Society History of Philosophy of Science 4:106-149.
Turner, Derek. 2013. “Historical geology: Methodology and metaphysics.” Geological Society of America Special Papers 502:11-18.


Why investigate evolution’s false predictions?




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 Darwin and his peers knew about biology. And we can compare what science has discovered with what Darwin’s theory expects.
It is not controversial that a great many predictions made by Darwin’s theory of evolution have been found to be false. There is less consensus, however, on how to interpret these falsifications. In logic, when a hypothesis predicts or entails an observation that is discovered to be false, then the hypothesis is concluded to be false. Not so in science.
When a scientific theory makes a prediction that is discovered to be false, then sometimes the theory is simply modified 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 actually occurred. In fact proponents of evolution 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. (Lakatos) In fact proponents of evolution argue that false predictions made by the theory of evolution are not problems, but rather are signs of scientific progress. With each new finding, proponents of evolution say, we learn more about how evolution occurred. Nonetheless, it is worthwhile to review a theory’s false predictions. A theorys track record can be highly informative. The history of false predictions generated by a theory tells us about its strengths and weaknesses, and how and why the theory is believed to be true. In the case of evolutionary theory, its many false predictions reveal that the theory is not motivated by the science and that the textbook claim that evolution is a fact does not come merely from empirical evidence (see Conclusions). Therefore the objective of this paper is to collect and record, in one place, a sample of the false predictions generated by evolutionary theory.
The predictions examined in this paper were selected according to several criteria. They cover a wide spectrum of evolutionary theory and are fundamental to the theory, reflecting major tenets of evolutionary thought. They were widely held by the consensus rather than reflecting one viewpoint of several competing viewpoints. Each prediction was a natural and fundamental expectation of the theory of evolution, and constituted mainstream evolutionary science. Furthermore, the selected predictions are not vague but rather are specific and can be objectively evaluated. They have been tested and evaluated and the outcome is not controversial or in question. And finally the predictions have implications for evolution’s capacity to explain phenomena, as discussed in the conclusions.
This paper does not maintain that the predictions presented are the only fundamental predictions of evolution, or that evolution does not have successful predictions. Those are well documented in the literature. Nor does this paper maintain that the predictions presented, though false, have not served to produce productive research. Also, this paper does not maintain that these false predictions cannot be remedied or reversed by future scientific findings.
References
Lakatos, Imre. 1970. “History of science and Its rational reconstructions.” Proceedings of the Biennial Meeting of the Philosophy of Science Association 1970:91-136.


Responses to common objections




This section examines various concerns evolutionists often have regarding their theory’s false predictions.
False predictions often have led to productive research
Productive research can come from a great variety of scientific and nonscientific motivations, including false predictions. That productive research may have arisen from some of these predictions does not detract from the fact that they are false.
Proponents of evolution have fixed these false predictions
A proponent of a theory, given sufficient motivation, can explain all kinds of contradictory findings. (Quine) Typically, however, there is a price to be paid as the theory becomes more complex and has less explanatory power.
Ad hominem and denial
Criticism of evolution draws heated responses, and personal attacks are common. Such attacks, however, do not change the fact that evolution has generated many false predictions. Also, evolutionists sometimes ignore or deny the unexpected findings. They attempt to discredit the facts, referring to them as “tired old arguments,” or fallacies without following up such criticisms with supporting details.
Falsificationism is flawed
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 (Popper) and not used here. Evolution’s many false predictions do not demonstrate that evolution is not science or that evolution is false.
False predictions are valuable in judging the quality of a theory, its explanatory power, 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 naïve falsificationism do not give evolutionists a license to ignore substantial and fundamental failures of their theory.
If there are so many problems evolution would have been toppled
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. (Lakatos; Chalmers)
Those quoted believe in evolution
Many scientists doubt evolution, but they are not cited or quoted in this paper. Only material from evolutionists is used to illustrate that even adherents to the theory agree that the predictions are false.
These falsifications will be remedied in the future
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.
There is no better alternative
One way to evaluate a theory is to compare it to alternative explanations. This approach has the advantage of circumventing the difficulties in evaluating scientific theories. But of course 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. (van Fraassen; Stanford) In any case, the success or failure of evolution’s predictions depends on the science, not on any alternative explanations.
No one believes these predictions anymore
Yes, this is the point. It is true that proponents of evolution have, for the most part, dropped many predictions that were once made by proponents of evolution or entailed by the theory. We can learn from this failed track record as it has implications for evolution’s complexity and explanatory power.
What about all the successful predictions?
Proponents of evolution 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. (Klayman, Ha) 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 as evolutionists tend to view the predictions of evolution as overwhelmingly true. False predictions, on the other hand, are usually not viewed as legitimate falsifications but rather 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.
These falsified predictions are not necessary predictions of evolutionary theory. They merely reflect isolated instances of a practitioner’s surprise over specific sets of data.
The predictions were considered to be necessary when they were held. And they represented consensus evolutionary science at the time they were held. They are well documented in both peer-reviewed research papers, popular literature authored by leading evolutionists and interviews of leading evolutionists. They were not merely held by a few, individual evolutionists. Nor were they one of several possible competing predictions. That these predictions are not now considered to be necessary predictions of evolution is a reflection of the malleability of evolutionary theory and is a reminder of why a history of evolution’s false predictions is important.
References
Chalmers, A. F. 1982. What is This Thing Called Science?. 2d ed. Indianapolis: Hackett.
Klayman, Joshua, Young-Won Ha. 1997. “Confirmation, disconfirmation, and information in hypothesis testing,” in W. M. Goldstein, R. M. Hogarth, (eds.) Research on Judgment and Decision Making: Currents, Connections, and Controversies. Cambridge: Cambridge University Press.
Lakatos, Imre. 1970. “History of science and Its rational reconstructions.” Proceedings of the Biennial Meeting of the Philosophy of Science Association 1970:91-136.
Popper, Karl. 1959. The Logic of Scientific Discovery. London: Hutchinson.
Quine, W.V.O. 1951. “Two Dogmas of Empiricism,” The Philosophical Review 60:40.
Stanford, P. Kyle. 2006. Exceeding Our Grasp: Science, History, and the Problem of Unconceived Alternatives. New York: Oxford University Press.
van Fraassen. Bas C.  1989. Laws and Symmetry. Oxford: Clarendon Press.

The DNA code is not unique


Shortly after the discovery of the DNA code, which is used in cells to construct proteins, evolutionists began theorizing how it evolved. The same code was found in very different species which means that the same code was present in their distant, common ancestor. So the DNA code arose early in evolutionary history and remained essentially unchanged thereafter. And since it arose so early in evolutionary history, in the first primitive cell, the code must not be 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.” (Crick) Or as one widely used undergraduate molecular biology text later put it, “The code seems to have been selected arbitrarily (subject to some constraints, perhaps).” (Alberts et. al., 9) And an evolution textbook further explained, “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.” (Ridley, 48)

In other words, somehow the DNA code evolved into place but it has little or no special or particular properties. But we now know that the code’s arrangement uniquely reduces the effects of mutations and reading errors. As one research study concluded, the DNA code is “one in a million” in terms of efficiency in minimizing these effects. (Freeland) Several other studies have confirmed these findings and have discovered more unique and special properties of the code. One found that the DNA code is a very rare code, even when compared to other codes which already have the error correcting capability. (Itzkovitz) Another found that the code does not optimize merely one function, but rather optimizes “a combination of several different functions simultaneously.” (Bollenbach) As one paper concluded, the code’s properties were “unexpected and still cry out for explanation.” (Vetsigian)


Alberts, Bruce., D. Bray, J. Lewis, M. Raff, K. Roberts, J. Watson. 1994. Molecular Biology of the Cell. 3d ed. New York: Garland Publishing.

Bollenbach, T., K. Vetsigian, R. Kishony. 2007. “Evolution and multilevel optimization of the genetic code.” Genome Research 17:401-404.


Crick, Francis. 1968. “The origin of the genetic code.” J. Molecular Biology 38:367-379.


Freeland, S., L. Hurst. 1998. “The genetic code is one in a million.” J. Molecular Evolution 47:238-248.


Itzkovitz, S., U. Alon. 2007. “The genetic code is nearly optimal for allowing additional information within protein-coding sequences.” Genome Research 17:405-412.


Ridley, Mark. 1993. Evolution. Boston: Blackwell Scientific.

Vetsigian, K., C. Woese, N. Goldenfeld. 2006. “Collective evolution and the genetic code.” Proceedings of the National Academy of Sciences 103:10696-10701.

The cell’s fundamental molecules are universal



 
In addition to the DNA code, there are other fundamental molecular processes that appear to be common to all life. One intriguing example is DNA replication which copies both strands of the DNA molecule, but in different directions. Evolution predicts these fundamental processes to be common to all life. Indeed this was commonly said to be an important successful prediction for the theory. As Niles Eldredge explained, the “underlying chemical uniformity of life” was a severe test that evolution passed with flying colors. (Eldredge, 41) Likewise Christian de Duve declared that evolution is in part confirmed by the fact that all extant living organisms function according to the same principles. (de Duve, 1) And Michael Ruse concluded that the essential macromolecules of life help to make evolution beyond reasonable doubt. (Ruse, 4)

But this conclusion that the fundamental molecular processes within the cell are common to all species was superficial. In later years, as the details were investigated, important differences between species emerged. For example, key DNA replication proteins surprisingly “show very little or no sequence similarity between bacteria and archaea/eukaryotes.” (Leipe) Also different DNA replication processes have been discovered. These results were not what were expected:


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. (Koonin)

Some proponents of evolution are reconsidering the assumption that all life on Earth shares the same basic molecular architecture and biochemistry, and instead examining the possibility of independent evolution, and multiple origins of fundamentally different life forms. (Cleland, Leipe)

References

Cleland, Carol. 2007. “Epistemological issues in the study of microbial life: alternative terran biospheres?.” Studies in History and Philosophy of Science Part C: Studies in History and Philosophy of Biological and Biomedical Sciences 38:847-861.

de Duve, Christian. 1995. Vital Dust. New York: BasicBooks.


Eldredge, Niles. 1982. The Monkey Business. New York: Washington Square Press.


Koonin, E. 2006. “Temporal order of evolution of DNA replication systems inferred by comparison of cellular and viral DNA polymerases.” Biology Direct 18:1-39.


Leipe, D., L. Aravind, E. Koonin. 1999. “Did DNA replication evolve twice independently?.” Nucleic Acids Research 27:3389-3401.

Ruse, Michael. 1986. Taking Darwin Seriously. New York: Basil Blackwell.

Mutations are not adaptive




In the twentieth century, the theory of evolution predicted that mutations are not adaptive or directed. In other words, mutations were believed to be random with respect to the needs of the individual. As Julian Huxley put it, “Mutation merely provides the raw material of evolution; it is a random affair, and takes place in all directions. … in all cases they are random in relation to evolution. Their effects are not related to the needs of the organisms.” (Huxley, 36) Or as Jacques Monod explained:


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. (Monod, 112)

Ronald Fisher wrote that mutations are “random with respect to the organism’s need” (Orr). This fundamental prediction persisted for decades as a recent paper explained: “mutation is assumed to create heritable variation that is random and undirected.” (Chen, Lowenfeld and Cullis)


But that assumption is now known to be false. The first problem is that the mutation rate is adaptive. For instance, when a population of bacteria is subjected to harsh conditions it tends to increase its mutation rate. It is as though a signal has been sent saying, “It is time to adapt.” Also, a small fraction of the population increases its mutation rates even higher yet. These hypermutators ensure that an even greater variety of adaptive change is explored. (Foster) Experiments have also discovered that duplicated DNA segments may be subject to higher mutation rates. Since the segment is a duplicate it is less important to preserve and, like a test bed, appears to be used to experiment with new designs. (Wright)


The second problem is that organisms use strategies to direct the mutations according to the threat. Adaptive mutations have been extensively studied in bacteria. Experiments typically alter the bacteria food supply or apply some other environmental stress causing mutations that target the specific environmental stress. (Burkala, et. al.; Moxon, et. al; Wright) Adaptive mutations have also been observed in yeast (Fidalgo, et. al.; David, et. al.) and flax plants. (Johnson, Moss and Cullis) One experiment found repeatable mutations in flax in response to fertilizer levels. (Chen, Schneeberger and Cullis) Another exposed the flax to four different growth conditions and found that environmental stress can induce mutations that result in “sizeable, rapid, adaptive evolutionary responses.” (Chen, Lowenfeld and Cullis) In response to this failed prediction some evolutionists now are saying that evolution somehow created the mechanisms that cause mutations to be adaptive.


References

Burkala, E., et. al. 2007. “Secondary structures as predictors of mutation potential in the lacZ gene of Escherichia coli.” Microbiology 153:2180-2189.

Chen, Y., R. Lowenfeld, C. Cullis. 2009. “An environmentally induced adaptive (?) insertion event in flax.” International Journal of Genetics and Molecular Biology 1:38-47.


Chen, Y., R. Schneeberger, C. Cullis. 2005. “A site-specific insertion sequence in flax genotrophs induced by environment.” New Phytologist 167:171-180.


David, L., et. al. 2010. “Inherited adaptation of genome-rewired cells in response to a challenging environment.” HFSP Journal 4:131–141.


Fidalgo, M., et. al. 2006. “Adaptive evolution by mutations in the FLO11 gene.” Proceedings of the National Academy of Sciences 103:11228-11233.


Foster, P. 2005. “Stress responses and genetic variation in bacteria.” Mutation Research / Fundamental and Molecular Mechanisms of Mutagenesis 569:3-11.


Huxley, Julian. 1953. Evolution in Action. New York: Signet Science Library Book.


Johnson, C., T. Moss, C. Cullis. 2011. “Environmentally induced heritable changes in flax.” J Visualized Experiments 47:2332.


Monod, Jacques. 1971. Chance & Necessity. New York: Vintage Books.


Moxon, E., et. al. 1994. “Adaptive evolution of highly mutable loci in pathogenic bacteria.” Current Biology 4:24-33.


Orr, H. 2005. “The genetic theory of adaptation: a brief history.” Nature Review Genetics 6:119-127.

Wright, B. 2000. “A biochemical mechanism for nonrandom mutations and evolution.” J Bacteriology 182:2993-3001.

Competition is greatest between neighbors




Darwin’s basic theory of evolution, by itself, did not account for the tree-like, hierarchical pattern the species were thought to form. Darwin was keenly aware of this shortcoming and wrestled with it for years. He finally conceived of a solution for why modified offspring would continue to evolve away and diverge from their parents. The principle of divergence, the last major theoretical addition before Darwin published his book, held that competition tends to be strongest between the more closely related organisms. This would cause a splitting and divergence, resulting in the traditional evolutionary tree pattern. (Desmond and Moore 1991, 419-420; Ridley, 378-379)

But no such trend has been observed. In a major study of competition between freshwater green algae species, the level of competition between pairs of species was found to be uncorrelated with the evolutionary distance between the pair of species. As the researchers explained, Darwin “argued that closely related species should compete more strongly and be less likely to coexist. For much of the last century, Darwin’s hypothesis has been taken at face value […] Our results add to a growing body of literature that fails to support Darwin’s original competition-relatedness hypothesis.” (Venail, et. al., 2, 9) The team spent months trying to resolve the problem, but to no avail. As one of the researchers explained:



It was completely unexpected. When we saw the results, we said “this can’t be.” We sat there banging our heads against the wall. Darwin’s hypothesis has been with us for so long, how can it not be right? … When we started coming up with numbers that showed he [Darwin] wasn’t right, we were completely baffled. … We should be able to look at the Tree of Life, and evolution should make it clear who will win in competition and who will lose. But the traits that regulate competition can’t be predicted from the Tree of Life. (Cimons)

Why this long-standing prediction was not confirmed remains unknown. Apparently there are more complicating factors that influence competition in addition to evolutionary relatedness.


References

Cimons, Marlene. 2014. “Old Idea About Ecology Questioned by New Findings.” National Science Foundation.

Desmond, Adrian, James Moore. 1991. Darwin: The Life of a Tormented Evolutionist. New York: W. W. Norton.


Ridley, Mark. 1993. Evolution. Boston: Blackwell Scientific.

Venail , P.A., A. Narwani , K. Fritschie, M. A. Alexandrou, T. H. Oakley, B. J. Cardinale. 2014. “The influence of phylogenetic relatedness on competition and facilitation among freshwater algae in a mesocosm experiment.” Journal of Ecology, DOI: 10.1111/1365-2745.12271.

Protein evolution



Protein coding genes make up only a small fraction of the genome in higher organisms but their protein products are crucial to the operation of the cell. They are the workers behind just about every task in the cell, including digesting food, synthesizing chemicals, structural support, energy conversion, cell reproduction and making new proteins. And like a finely tuned machine, proteins do their work very well. Proteins are ubiquitous in all of life and must date back to the very early stages of evolution. So evolution predicts that proteins evolved when life first appeared, or not long after. But despite enormous research efforts the science clearly shows that such protein evolution is astronomically unlikely.

One reason the evolution of proteins is so difficult is that most proteins are extremely specific designs in an otherwise rugged fitness landscape. This means it is difficult for natural selection to guide mutations toward the needed proteins. In fact, four different studies, done by different groups and using different methods, all report that roughly 1070 evolutionary experiments would be needed to get close enough to a workable protein before natural selection could take over to refine the protein design. For instance, one study concluded that 1063 attempts would be required for a relatively short protein. (Reidhaar-Olson) And a similar result (1065 attempts required) was obtained by comparing protein sequences. (Yockey) Another study found that from 1064 to 1077 attempts are required (Axe) and another study concluded that 1070 attempts would be required. (Hayashi) In that case the protein was only a part of a larger protein which otherwise was intact, thus making for an easier search. Furthermore these estimates are optimistic because the experiments searched only for single-function proteins whereas real proteins perform many functions.


This conservative estimate of 1070 attempts required to evolve a simple protein is astronomically larger than the number of attempts that are feasible. And explanations of how evolution could achieve a large number of searches, or somehow obviate this requirement, require the preexistence of proteins and so are circular. For example, one paper estimated that evolution could have made 1043 such attempts. But the study assumed the entire history of the Earth is available, rather than the limited time window that evolution actually would have had. Even more importantly, it assumed the preexistence of a large population of bacteria (it assumed the earth was completely covered with bacteria). And of course, bacteria are full of proteins. Clearly such bacteria would not exist before the first proteins evolved. (Dryden) Even with these helpful and unrealistic assumptions the result was twenty seven orders of magnitude short of the requirement.


Given these several significant problems, the chances of evolution finding proteins from a random start are, as one evolutionist explained, “highly unlikely.” (Tautz) Or as another evolutionist put it, “Although the origin of the first, primordial genes may ultimately be traced back to some precursors in the so-called ‘RNA world’ billions of years ago, their origins remain enigmatic.” (Kaessmann)


References


Axe, D. 2004. “Estimating the prevalence of protein sequences adopting functional enzyme folds.” J Molecular Biology 341:1295-1315.

Dryden, David, Andrew Thomson, John White. 2008. “How much of protein sequence space has been explored by life on Earth?.” J. Royal Society Interface 5:953-956.


Hayashi, Y., T. Aita, H. Toyota, Y. Husimi, I. Urabe, T. Yomo. 2006. “Experimental Rugged Fitness Landscape in Protein Sequence Space.” PLoS ONE 1:e96.


Kaessmann, H. 2010. “Origins, evolution, and phenotypic impact of new genes.” Genome Research 10:1313-26.


Reidhaar-Olson J., R. Sauer. 1990. “Functionally acceptable substitutions in two alpha-helical regions of lambda repressor.” Proteins 7:306-316.


Tautz, Diethard, Tomislav Domazet-Lošo. 2011. “The evolutionary origin of orphan genes.” Nature Reviews Genetics 12:692-702.

Yockey, Hubert. 1977. “A calculation of the probability of spontaneous biogenesis by information theory.” J Theoretical Biology 67:377–398.

Histone proteins cannot tolerate much change




Histones are proteins which serve as the hubs about which DNA is wrapped. They are highly similar across vastly different species which means they must have evolved early in evolutionary history. As one textbook explains, “The amino acid sequences of four histones are remarkably similar among distantly related species. … The similarity in sequence among histones from all eukaryotes indicates that they fold into very similar three-dimensional conformations, which were optimized for histone function early in evolution in a common ancestor of all modern eukaryotes.” (Lodish et. al., Section 9.5) And this high similarity among the histones also means they must not tolerate change very well, as another textbook explains: “Changes in amino acid sequence are evidently much more harmful for some proteins than for others. … virtually all amino acid changes are harmful in histone H4. We assume that individuals who carried such harmful mutations have been eliminated from the population by natural selection.” (Alberts et. al. 1994, 243)

So the evolutionary prediction is that in these histone proteins practically all changes are deleterious: “As might be expected from their fundamental role in DNA packaging, the histones are among the most highly conserved eucaryotic proteins. For example, the amino acid sequence of histone H4 from a pea and a cow differ at only at 2 of the 102 positions. This strong evolutionary conservation suggests that the functions of histones involve nearly all of their amino acids, so that a change in any position is deleterious to the cell.” (Alberts et. al. 2002, Chapter 4)


This prediction has also been given in popular presentations of the theory: “Virtually all mutations impair histone’s function, so almost none get through the filter of natural selection. The 103 amino acids in this protein are identical for nearly all plants and animals.” (Molecular Clocks: Proteins That Evolve at Different Rates)


But this prediction has turned out to be false. An early study suggested that one of the histone proteins could well tolerate many changes. (Agarwal and Behe) And later studies confirmed and expanded this finding: “despite the extremely well conserved nature of histone residues throughout different organisms, only a few mutations on the individual residues (including nonmodifiable sites) bring about prominent phenotypic defects.” (Kim et. al.)


Similarly another paper documented these contradictory results: “It is remarkable how many residues in these highly conserved proteins can be mutated and retain basic nucleosomal function. … The high level of sequence conservation of histone proteins across phyla suggests a fitness advantage of these particular amino acid sequences during evolution. Yet comprehensive analysis indicates that many histone mutations have no recognized phenotype.” (Dai et. al.) In fact, even more surprising, many mutations actually raised the fitness level. (Dai et. al.)


References


Agarwal, S., M. Behe. 1996. “Non-conservative mutations are well tolerated in the globular region of yeast histone H4.” J Molecular Biology 255:401-411.

Alberts, Bruce., D. Bray, J. Lewis, M. Raff, K. Roberts, J. Watson. 1994. Molecular Biology of the Cell. 3d ed. New York: Garland Publishing.


Alberts, Bruce., A. Johnson, J. Lewis, et. al. 2002. Molecular Biology of the Cell. 4th ed. New York: Garland Publishing. http://www.ncbi.nlm.nih.gov/books/NBK26834/


Dai, J., E. Hyland, D. Yuan, H. Huang, J. Bader, J. Boeke. 2008. “Probing nucleosome function: a highly versatile library of synthetic histone H3 and H4 mutants.” Cell 134:1066-1078.


Kim, J., J. Hsu, M. Smith, C. Allis. 2012. “Mutagenesis of pairwise combinations of histone amino-terminal tails reveals functional redundancy in budding yeast.” Proceedings of the National Academy of Sciences109:5779-5784.


Lodish H., A. Berk, S. Zipursky, et. al. 2000. Molecular Cell Biology. 4th ed. New York: W. H. Freeman. http://www.ncbi.nlm.nih.gov/books/NBK21500/


“Molecular Clocks: Proteins That Evolve at Different Rates.” 2001. WGBH Educational Foundation and Clear Blue Sky Productions.

The molecular clock keeps evolutionary time




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 varies from species to species. Emile Zuckerkandl and Linus Pauling reasoned that if such sequence differences were the result of evolutionary change occurring over the history of life, then they could be used to estimate past speciation events—a notion that became known as the molecular clock. (Zuckerkandl and Pauling)

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. (Thomas, et. al.) As the National Academy of Sciences explained, the molecular clock “determines evolutionary relationships among organisms, and it indicates the time in the past when species started to diverge from one another.” (Science and Creationism, 3) 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.” (Jukes, 119, emphasis in original)

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. The 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 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. (Thomas, et. al.; Andrews, 28)

The proteins relaxin, superoxide dismutase (SOD) and the glycerol-3-phosphate dehydrogenase (GPDH), for example, all contradict the molecular clock prediction. 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 roughly the 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.” (Ayala)

Proponents of evolution 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 …” (Thomas, et. al.)

Proponents of evolution 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 warned, “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.” (Schwabe)

References

Andrews, Peter. 1987. “Aspects of hominoid phylogeny” in Molecules and Morphology in Evolution, ed. Colin Patterson. Cambridge: Cambridge University Press.

Ayala, F. 1999. “Molecular clock mirages.” BioEssays 21:71-75.

Jukes, Thomas. 1983. “Molecular evidence for evolution” in: Scientists Confront Creationism, ed. Laurie Godfrey. New York: W. W. Norton.

Schwabe, C. 1986. “On the validity of molecular evolution.” Trends in Biochemical Sciences 11:280-282.

Science and Creationism: A View from the National Academy of Sciences. 2d ed. 1999. Washington, D.C.: National Academy Press.

Thomas, J. A., J. J. Welch, M. Woolfit, L. Bromham. 2006. “There is no universal molecular clock for invertebrates, but rate variation does not scale with body size.” Proceedings of the National Academy of Sciences103:7366-7371.

Zuckerkandl, E., L. Pauling. 1965. “Molecules as documents of evolutionary history.” J Theoretical Biology 8:357-366.



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Falsification of common descent predictions



The pentadactyl pattern and common descent

The pentadactyl structure—five digits (four fingers and a thumb for humans) at the end of the limb structure—is one of the most celebrated proof texts for evolution. The pentadactyl structure is found throughout the tetrapods and its uses include flying, grasping, climbing and crawling. Such diverse activities, evolutionists reason, should require diverse limbs. There seems to be no reason why all should need a five digit limb. Why not three digits for some, eight for others, 13 for some others, and so forth? And yet they all are endowed with five digits. As Darwin explained, “What can be more curious than that the hand of a man, formed for grasping, that of a mole for digging, the leg of the horse, the paddle of the porpoise, and the wing of the bat, should all be constructed on the same pattern, and should include similar bones, in the same relative positions?” (Darwin, 382)
 
Such a suboptimal design must be an artefact of common descent—a suboptimal design that was handed down from a common ancestor rather than specifically designed for each species. And the common descent pattern formed by this structure is often claimed as strong evidence for evolution. (Berra, 21; Campbell et. al., 509; Futuyma, 47; Johnson and Losos, 298;  Johnson and Raven, 286; Mayr, 26) One text calls it a “classic example” of evolutionary evidence. (Ridley, 45)
 
But this prediction is now known to be false as the digit structure in the tetrapods does not conform to the common descent pattern. In fact, appendages have various digit structures and they are distributed across the species in various ways. This is found both in extant species and in the fossil record. As evolutionist Stephen Jay Gould explained, “The conclusion seems inescapable, and an old ‘certainty’ must be starkly reversed.” (Gould)
 
This means that evolutionists cannot model the observed structures and pattern of distribution merely as a consequence of common descent. Instead, a complicated evolutionary history is required (Brown) where the pentadactyl structure re-evolves in different lineages, and appendages evolve, are lost, and then evolve again. And as one recent study concluded, “Our phylogenetic results support independent instances of complete limb loss as well as multiple instances of digit and external ear opening loss and re-acquisition. Even more striking, we find strong statistical support for the re-acquisition of a pentadactyl body form from a digit-reduced ancestor. … The results of our study join a nascent body of literature showing strong statistical support for character loss, followed by evolutionary re-acquisition of complex structures associated with a generalized pentadactyl body form.” (Siler and Brown)
 
References
 
Berra, Tim. 1990. Evolution and the Myth of Creationism. Stanford: Stanford University Press.

Brown, R., et. al. 2012. 
Species delimitation and digit number in a North African skink. Ecology and Evolution 2:2962-73.


Campbell, Neil, et. al. 2011. Biology. 5th ed. San Francisco: Pearson.
 
Darwin, Charles. 1872. The Origin of Species. 6th ed. London: John Murray.
http://darwin-online.org.uk/content/frameset?itemID=F391&viewtype=text&pageseq=1
 
Futuyma, Douglas. 1982. Science on Trial: The Case for Evolution. New York: Pantheon Books.
 
Gould, Steven Jay. 1991. “Eight (or Fewer) Little Piggies.” Natural History 100:22-29.
 
Johnson, G., J. Losos. 2008. The Living World. 5th ed. New York: McGraw-Hill.
 
Johnson, G., P. Raven. 2004. Biology. New York: Holt, Rinehart and Winston.
 
Mayr, Ernst. 2001. What Evolution Is. New York: Basic Books.
 
Ridley, Mark. 1993. Evolution. Boston: Blackwell Scientific.

Siler C., R. Brown. 2011. “Evidence for repeated acquisition and loss of complex body-form characters in an insular clade of Southeast Asian semi-fossorial skinks.” Evolution 65:2641-2663.

Serological tests reveal evolutionary relationships



Early in the twentieth century scientists studied blood immunity and how immune reaction could be used to compare species. The blood studies tended to produce results that parallel the more obvious indicators such as body plan. For example, humans were found to be more closely related to apes than to fish or rabbits. These findings were said to be strong confirmations of evolution. In 1923 H. H. Lane cited this evidence as supporting “the fact of evolution.” (Lane, 47) Later in the century these findings continued to be cited in support of evolution. (Berra, 19; Dodson and Dodson, 65)
 
But even by mid century contradictions to evolutionary expectations were becoming obvious in serological tests. As J.B.S.Haldane explained in 1949, “Now every species of mammal and bird so far investigated has shown quite a surprising biochemical diversity by serological tests. The antigens concerned seem to be proteins to which polysaccharides are attached.” (quoted in Gagneux and Varki)
 
Indeed these polysaccharides, or glycans, did not fulfill evolutionary expectations. As one paper explained, glycans show “remarkably discontinuous distribution across evolutionary lineages,” for they “occur in a discontinuous and puzzling distribution across evolutionary lineages.” (Bishop and Gagneux) These glycans can be (i) specific to a particular lineage, (i) similar in very distant lineages, (iii) and conspicuously absent from very restricted taxa only.
 
Here is how another paper described glycan findings: “There is also no clear explanation for the extreme complexity and diversity of glycans that can be found on a given glycoconjugate or cell type. Based on the limited information available about the scope and distribution of this diversity among taxonomic groups, it is difficult to see clear trends or patterns consistent with different evolutionary lineages.” (Gagneux and Varki)
 
References
 
Berra, Tim. 1990. Evolution and the Myth of Creationism. Stanford: Stanford University Press.
 
Bishop J., P. Gagneux. 2007. “Evolution of carbohydrate antigens--microbial forces shaping host glycomes?.” Glycobiology 17:23R-34R.
 
Dodson, Edward, Peter Dodson. 1976. Evolution: Process and Product. New York: D. Van Nostrand Company.
 
Gagneux, P., A. Varki. 1999. “Evolutionary considerations in relating oligosaccharide diversity to biological function.” Glycobiology 9:747-755.
Lane, H. 1923. Evolution and Christian Faith. Princeton: Princeton University Press.

Biology is not lineage specific



Evolution expects the species to fall into a common descent pattern. Therefore a particular lineage should not have highly differentiated, unique and complex designs, when compared to neighboring species. But this has been increasingly found to be the case, so much so that this pattern now has its own name—lineage-specific biology.
 
For example, transcription factors are proteins that bind to DNA and regulate which genes are expressed. Yet despite the importance of these proteins, their DNA binding sites vary dramatically across different species. As one report explained, “It was widely assumed that, like the sequences of the genes themselves, these transcription factor binding sites would be highly conserved throughout evolution. However, this turns out not to be the case in mammals.” (Rewiring of gene regulation across 300 million years of evolution) Evolutionists were surprised when transcription factor binding sites were found to be not conserved between mice and men, (Kunarso et. al.) between various other vertebrates, and even between different species of yeast. So now evolution is believed to have performed a massive, lineage-specific “rewiring” of cellular regulatory networks. (Pennacchio and Visel)
 
There are many more such examples of lineage-specific biology. Although flowers have four basic parts: sepals, petals, stamens and carpels, the daffodil’s trumpet is fundamentally different and must be an evolutionary “novelty.” (Oxford scientists say trumpets in daffodils are ‘new organ’) Out of the thousands of cockroach species, Saltoblattella montistabularis from South Africa is the only one that leaps. With its spring-loaded hind legs it accelerates at 23 g’s and out jumps even grass hoppers. (Picker, Colville and Burrows) An important immune system component, which is highly conserved across the vertebrates, is mysteriously absent in the Atlantic cod, Gadus morhua. (Star, et. al.) The brown algae, Ectocarpus siliculosus, has unique enzymes for biosynthesis and other tasks. (Cock) And the algae Bigelowiella natans has ten thousand unique genes and highly complex gene splicing machinery never before seen in a unicellular organism. It is, as one evolutionist explained, “unprecedented and truly remarkable for a unicellular organism.” (Tiny algae shed light on photosynthesis as a dynamic property)
 
Another fascinating example of lineage-specific biology are the many peculiar morphological and molecular novelties found in disparate, unrelated unicellular protists. As one study concluded, “Both euglenozoans and alveolates have a reputation for ‘doing things their own way,’ which is to say that they have developed seemingly unique ways to build important cellular structures or carry out molecular tasks critical for their survival. Why such hotspots for the evolution of novel solutions to problems should exist in the tree of life is not entirely clear.” (Lukes, Leander and Keeling, 2009a) Or as one evolutionist exclaimed, “this is totally crazy.” (Lukes, Leander and Keeling, 2009b)
 
References
 
Cock, J., et al. 2010. “The Ectocarpus genome and the independent evolution of multicellularity in brown algae.” Nature 465:617-621.
 
Kunarso G., et. al. 2010. “Transposable elements have rewired the core regulatory network of human embryonic stem cells.” Nature Genetics 42:631-634.
 
Lukes, J., B. Leander, P. Keeling. 2009. “Cascades of convergent evolution: the corresponding evolutionary histories of euglenozoans and dinoflagellates.” Proceedings of the National Academy of Sciences 106 Suppl 1:9963-9970.
 
Lukes, J., B. Leander, P. Keeling. 2009. “The corresponding evolutionary histories of euglenozoans and dinoflagellates: cascades of convergent evolution or accumulation of oddities?.” The National Academies.http://sackler.nasmediaonline.org/2009/darwin/julius_lukes/julius_lukes.html
 
“Oxford scientists say trumpets in daffodils are ‘new organ’.” 2011. BBC News February 28. http://www.bbc.co.uk/news/uk-england-oxfordshire-12598054
 
Pennacchio, L., A. Visel. 2010. “Limits of sequence and functional conservation.” Nature Genetics 42:557-558.
 
Picker, M., J. Colville, M. Burrows. 2012. “A cockroach that jumps.” Biology Letters 8:390-392.
 
“Rewiring of gene regulation across 300 million years of evolution.” 2010. ScienceDaily April 12. http://www.sciencedaily.com/releases/2010/04/100409093211.htm
 
Star, B., et. al. 2011. “The genome sequence of Atlantic cod reveals a unique immune system.” Nature 477:207–210.
“Tiny algae shed light on photosynthesis as a dynamic property.” 2012. ScienceDaily November 28. http://www.sciencedaily.com­ /releases/2012/11/121128132253.htm

Similar species share similar genes



The only figure in Darwin’s book, The Origin of Species, showed how he envisioned species branching off of one another. Similar species have a relatively recent common ancestor and have had limited time to diverge from each other. This means that their genes should be similar. Entirely new genes, for instance, would not have enough time to evolve. As François Jacob explained in an influential paper from 1977, “The probability that a functional protein would appear de novo by random association of amino acids is practically zero.” (Jacob) Any newly created gene would have to arise from a duplication and modification of a pre-existing gene. (Zhou et. al.; Ohno) But such a new gene would retain significant similarity to its progenitor gene. Indeed, for decades evolutionists have cited minor genetic differences between similar species as a confirmation of this important prediction. (Berra, 20; Futuyma, 50; Johnson and Raven, 287; Jukes, 120; Mayr, 35)
 
But this prediction has been falsified as many unexpected genetic differences have been discovered amongst a wide range of allied species. (Pilcher) As much as a third of the genes in a given species may be unique, and 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. (Daubin and Ochman)
 
Significant genetic differences were also found between 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. (Levine et. al.) As one science writer put it, “an astonishing 12 per cent of recently evolved genes in fruit flies appear to have evolved from scratch.” (Le Page) These novel genes must have evolved over a few million years, a time period previously considered to allow only for minor genetic changes. (Begun et. al.; Chen et. al., 2007)
 
Initially some 
proponents of evolution  thought these surprising results would be resolved when more genomes were analyzed. They predicted that similar copies of these genes would be found in other species. But instead each new genome has revealed yet more novel genes. (Curtis et. al.; Marsden et. al.; Pilcher)
 
Next proponents of evolution thought that these rapidly-evolving unique genes must not code for functional or important proteins. But again, many of the unique proteins were in fact found to play essential roles. (Chen, Zhang and Long 1010; Daubin and Ochman; Pilcher) As one researcher explained, “This goes against the textbooks, which say the genes encoding essential functions were created in ancient times.” (Pilcher)
 
References
 
Begun, D., H. Lindfors, A. Kern, C. Jones. 2007. “Evidence for de novo evolution of testis-expressed genes in the Drosophila yakuba/Drosophila erecta clade.” Genetics 176:1131-1137.
 
Berra, Tim. 1990. Evolution and the Myth of Creationism. Stanford: Stanford University Press.
 
Chen, S., H. Cheng, D. Barbash, H. Yang. 2007. “Evolution of hydra, a recently evolved testis-expressed gene with nine alternative first exons in Drosophila melanogaster.” PLoS Genetics 3.
 
Chen, S., Y. Zhang, M. Long. 2010. “New Genes in Drosophila Quickly Become Essential.” Science 330:1682-1685.
 
Curtis, B., et. al. 2012. “Algal genomes reveal evolutionary mosaicism and the fate of nucleomorphs.” Nature 492:59-65.
 
Daubin, V., H. Ochman. 2004. “Bacterial genomes as new gene homes: The genealogy of ORFans in E. coli.” Genome Research 14:1036-1042.
 
Futuyma, Douglas. 1982. Science on Trial: The Case for Evolution. New York: Pantheon Books.
 
Jacob, François. 1977. “Evolution and tinkering.” Science 196:1161-1166.
 
Johnson, G., P. Raven. 2004. Biology. New York: Holt, Rinehart and Winston.
 
Jukes, Thomas. 1983. “Molecular evidence for evolution” in: Scientists Confront Creationism, ed. Laurie Godfrey. New York: W. W. Norton.
 
Le Page, M. 2008. “Recipes for life: How genes evolve.” New Scientist, November 24.
 
Levine, M., C. Jones, A. Kern, H. Lindfors, D. Begun. 2006. “Novel genes derived from noncoding DNA in Drosophila melanogaster are frequently X-linked and exhibit testis-biased expression.” Proceedings of the National Academy of Sciences 103: 9935-9939.
 
Marsden, R. et. al. 2006. “Comprehensive genome analysis of 203 genomes provides structural genomics with new insights into protein family space.” Nucleic Acids Research 34:1066-1080.
 
Mayr, Ernst. 2001. What Evolution Is. New York: Basic Books.
 
Ohno, Susumu. 1970. Evolution by Gene Duplication. Heidelberg: Springer.
 
Pilcher, Helen. 2013. “All Alone.” NewScientist January 19.
Zhou, Q., G. Zhang, Y. Zhang, et. al. 2008. “On the origin of new genes in Drosophila.” Genome Research 18:1446-1455.

MicroRNA



Genes hold information that is used to construct protein and RNA molecules which do various tasks in the cell. A gene is copied in a process known as transcription. In the case of a protein-coding gene the transcript is edited and converted into a protein in a process known as translation. All of this is guided by elaborate regulatory processes that occur before, during and after this sequence of transcription, editing and translation.
 
For instance, some of our DNA which was thought to be of little use actually has a key regulatory role. This DNA is transcribed into strands of about 20 nucleotides, known as microRNA. These short snippets bind and interfere with RNA transcripts—copies of DNA genes—when the production of the gene needs to be slowed.
 
MicroRNAs can also help to modify the translation process by stimulating programmed ribosomal frameshifting. Two microRNAs attach to the RNA transcript resulting in a pseudoknot, or triplex, RNA structure form which causes the reading frameshift to occur. (Belew)
 
MicroRNAs do not only come from a cell’s DNA. MicroRNAs can also be imported from nearby cells, thus allowing cells to communicate and influence each other. This helps to explain how cells can differentiate in a growing embryo according to their position within the embryo. (Carlsbecker)
 
MicroRNAs can also come from the food we eat. In other words, food not only contains carbohydrates, proteins, fat, minerals, vitamins and so forth, it also contains information—in the form of these regulatory snippets of microRNA—which regulate our gene production. (Zhang)
 
While microRNAs regulate the production of proteins, the microRNAs themselves also need to be regulated. So there is a network of proteins that tightly control microRNA production as well as their removal. “Just the sheer existence of these exotic regulators,” explained one scientist, “suggests that our understanding about the most basic things—such as how a cell turns on and off—is incredibly naïve.” (Hayden)
 
Two basic predictions that evolutionary theory makes regarding microRNAs are that (i) like all of biology, they arose gradually via randomly occurring biological variation (such as mutations) and (ii) as a consequence of this evolutionary origin, microRNAs should approximately form evolution’s common descent pattern. Today’s science has falsified both of these predictions.
 
MicroRNAs are unlikely to have gradually evolved via random mutations, for too many mutations are required. Without the prior existence of genes and the protein synthesis process microRNAs would be useless. And without the prior existence of their regulatory processes, microRNAs would wreak havoc.
 
Given the failure of the first prediction, it is not surprising that the second prediction has also failed. The microRNA genetic sequences do not fall into the expected common descent pattern. That is, when compared across different species, microRNAs do not align with the evolutionary tree. As one scientist explained, “I've looked at thousands of microRNA genes and I can't find a single example that would support the traditional [evolutionary] tree.” (Dolgin)
 
While there remain questions about these new phylogenetic data, “What we know at this stage,” explained another evolutionist, “is that we do have a very serious incongruence.” In other words, different types of data report very different evolutionary trees. The conflict is much greater than normal statistical variations.
 
“There have to be,” added another evolutionist, “other explanations.” One explanation is that microRNAs evolve in some unexpected way. Another is that the traditional evolutionary tree is all wrong. Or evolutionists may consider other explanations. But in any case, microRNAs are yet another example of evidence that does not fit evolutionary expectations. Once again, the theory will need to be modified in complex ways to fit the new findings.
 
In the meantime, scientists are finding that imposing the common descent pattern, where microRNAs must be conserved across species, is hampering scientific research:
 

These results highlight the limitations that can result from imposing the requirement that miRNAs be conserved across organisms. Such requirements will in turn result in our missing bona fide organism-specific miRNAs and could perhaps explain why many of these novel miRNAs have not been previously identified. (Londin)
 
Evolutionary theory has been limiting the science. While the common descent pattern has been the guide since the initial microRNA studies, these researchers “liberated” themselves from that constraint, and this is leading to good scientific progress:
 

In the early days of the miRNA field, there was an emphasis on identifying miRNAs that are conserved across organisms … Nonetheless, species-specific miRNAs have also been described and characterized as have been miRNAs that are present only in one or a few species of the same genus. Therefore, enforcing an organism-conservation requirement during miRNA searches is bound to limit the number of potential miRNAs that can be discovered, leaving organism- and lineage-specific miRNAs undiscovered. In our effort to further characterize the human miRNA repertoire, we liberated ourselves from the conservation requirement … These findings strongly suggest the possibility of a wide-ranging species-specific miRNA-ome that has yet to be characterized. (Londin)
 
The two microRNA predictions have been falsified and, not surprisingly, the evolutionary assumption has hampered the scientific research of how microRNAs work.
 
References
 
Belew, Ashton T., et. al. 2014. “Ribosomal frameshifting in the CCR5 mRNA is regulated by miRNAs and the NMD pathway.” Nature 512:265-9.
 
Carlsbecker, Annelie, et. al. 2010. “Cell signalling by microRNA165/6 directs gene dose-dependent root cell fate.” Nature 465:316-21.
 
Dolgin, Elie. 2012. “Phylogeny: Rewriting evolution.” Nature 486:460-2.
 
Hayden, Erika Check. 2010. “Human genome at ten: Life is complicated.” Nature 464:664-7.
 
Londin, Eric, et. al. 2015. “Analysis of 13 cell types reveals evidence for the expression of numerous novel primate- and tissue-specific microRNAs.” Proc Natl Acad Sci USA 112:E1106-15.
Zhang, L., et. al. 2012. “Exogenous plant MIR168a specifically targets mammalian LDLRAP1: evidence of cross-kingdom regulation by microRNA.” Cell Research 22:107-26.

Genomic features are not sporadically distributed



A fundamental concept in evolutionary theory is the inheritance of genetic variations via blood lines. (Forbes) This so-called vertical transmission of heritable material means that genes, and genomes in general, should fall into a common descent pattern, consistent with the evolutionary tree. Indeed, such genes are often cited as a confirmation of evolution. But as more genomic data have become available, an ever increasing number of genes have been discovered that do not fit the common descent pattern because they are missing from so many intermediate species. (Andersson and Roger 2002; Andersson and Roger 2003; Andersson 2005; Andersson, Sarchfield and Roger 2005; Andersson 2006; Andersson et. al. 2006; Andersson 2009; Andersson 2011; Haegeman, Jones and Danchin; Katz; Keeling and Palmer; Richards et. al 2006a; Richards et. al 2006b; Takishita et. al.; Wolf et. al.)
 
This type of pattern is also found for genome architecture features which are sporadically distributed and then strikingly similar in distant species. In fact these similarities do not merely occur twice, in two distant species. They often occur repeatedly in a variety of otherwise distant species. This is so widespread that evolutionists have named the phenomenon “recurrent evolution.” As one paper explains, the recent explosion of genome data reveals “strikingly similar genomic features in different lineages.” Furthermore, there are “traits whose distribution is ‘scattered’ across the evolutionary tree, indicating repeated independent evolution of similar genomic features in different lineages.” (Maeso, Roy and Irimia)
 
One example is the uncanny similarity between the kangaroo and human genomes. As one evolutionist explained: “There are a few differences, we have a few more of this, a few less of that, but they are the same genes and a lot of them are in the same order. We thought they’d be completely scrambled, but they’re not.” (Taylor)
 
It is now well recognized that this prediction has failed: “Vertical transmission of heritable material, a cornerstone of the Darwinian theory of evolution, is inadequate to describe the evolution of eukaryotes, particularly microbial eukaryotes.” (Katz) And these sporadic, patchy patterns require complicated and ad hoc scenarios to explain their origin. As one paper explained, the evolution of a particular set of genes “reveals a complex history of horizontal gene transfer events.” (Wolf et. al.) The result is that any pattern can be explained by arranging the right mechanisms. Features that are shared between similar species can be interpreted as “the result of a common evolutionary history,” and features that are not can be interpreted as “the result of common evolutionary forces.” (Maeso, Roy and Irimia)
 
These common evolutionary forces are complex and must have been created by evolution. They can include horizontal (or lateral) gene transfer, gene loss, gene fusion, and even unknown forces. For instance, one study concluded that the best explanation for the pattern of a particular gene was that it “has been laterally transferred among phylogenetically diverged eukaryotes through an unknown mechanism.” (Takishita et. al.) Even with the great variety of mechanisms available, there still remains the unknown mechanism.
 
References
 
Andersson, J., A. Roger. 2002. “Evolutionary analyses of the small subunit of glutamate synthase: gene order conservation, gene fusions, and prokaryote-to-eukaryote lateral gene transfers.” Eukaryotic Cell 1:304-310.
 
Andersson, J., A. Roger. 2003. “Evolution of glutamate dehydrogenase genes: evidence for lateral gene transfer within and between prokaryotes and eukaryotes.” BMC Evolutionary Biology 3:14.
 
Andersson, J. 2005. “Lateral gene transfer in eukaryotes.” Cellular and Molecular Life Sciences 62:1182-97.
 
Andersson, J., S. Sarchfield, A Roger. 2005. “Gene transfers from nanoarchaeota to an ancestor of diplomonads and parabasalids.” Molecular Biology and Evolution 22:85-90.
 
Andersson, J. 2006. “Convergent evolution: gene sharing by eukaryotic plant pathogens.” Current Biology 16:R804-R806.
 
Andersson, J., R. Hirt, P. Foster, A. Roger. 2006. “Evolution of four gene families with patchy phylogenetic distributions: influx of genes into protist genomes.” BMC Evolutionary Biology 6:27.
 
Andersson, J. 2009. “Horizontal gene transfer between microbial eukaryotes.” Methods in Molecular Biology 532:473-487.
 
Andersson, J. 2011. “Evolution of patchily distributed proteins shared between eukaryotes and prokaryotes: Dictyostelium as a case study.” J Molecular Microbiology and Biotechnology 20:83-95.
 
Haegeman, A., J. Jones, E. Danchin. 2011. “Horizontal gene transfer in nematodes: a catalyst for plant parasitism?.” Molecular Plant-Microbe Interactions 24:879-87.
 
Katz, L. 2002. “Lateral gene transfers and the evolution of eukaryotes: theories and data.” International J. Systematic and Evolutionary Microbiology 52:1893-1900.
 
Keeling, P., J. Palmer. 2008. “Horizontal gene transfer in eukaryotic evolution,” Nature Reviews Genetics 9:605-18.
 
Maeso, I, S. Roy, M. Irimia. 2012. “Widespread Recurrent Evolution of Genomic Features.” Genome Biology and Evolution 4:486-500.
 
Richards, T., J. Dacks, J. Jenkinson, C. Thornton, N. Talbot. 2006. “Evolution of filamentous plant pathogens: gene exchange across eukaryotic kingdoms.” Current Biology 16:1857-1864.
 
Richards, T., J. Dacks, S. Campbell, J. Blanchard, P. Foster, R. McLeod, C. Roberts. 2006. “Evolutionary origins of the eukaryotic shikimate pathway: gene fusions, horizontal gene transfer, and endosymbiotic replacements.” Eukaryotic Cell 5:1517-31.
 
Takishita, K., Y. Chikaraishi, M. Leger, E. Kim, A. Yabuki, N. Ohkouchi, A. Roger. 2012. “Lateral transfer of tetrahymanol-synthesizing genes has allowed multiple diverse eukaryote lineages to independently adapt to environments without oxygen.” Biology Direct 7:5.
 
Taylor, R. 2008. “Kangaroo genes close to humans,” Reuters, Canberra, Nov 18.
Wolf, Y., L. Aravind, N. Grishin, E. Koonin. 1999. “Evolution of aminoacyl-tRNA synthetases--analysis of unique domain architectures and phylogenetic trees reveals a complex history of horizontal gene transfer events.” Genome Research 9:689-710.


Gene and host phylogenies are congruent



Evolution predicts that genetic change drives evolutionary change. Genetic changes that confer improved fitness are more likely to be selected and passed on. All of this means that evolutionary trees based on comparisons of genes should be similar, or congruent, with evolutionary trees based on comparisons of the entire species. Simply put, gene trees and species trees should be congruent. But while this has often been claimed to be a successful prediction, it is now known to be false. As one study explained, “Perhaps most unexpected of all is the substantial decoupling, now known in most, although not all, branches of organismal life, between the phylogenetic histories of individual gene families and what has generally been accepted to be the history of genomes and/or their cellular or organismal host lineages.” (Ragan, McInerney and Lake)
 
The molecular and the visible (morphological) features often indicate “strikingly different” evolutionary trees that cannot be explained as due to different methods being used. (Lockhart and Cameron) Making sense of these differences between the molecular and the morphological features has become a major task, (Gura) so common that it now has its own name: reconciliation. (Stolzer, et. al.)
 
The growing gap between molecular analyses and the fossil record, concluded one researcher, “is astounding.” (Feduccia) Instead of a single evolutionary tree emerging from the data, there is a wealth of competing evolutionary trees. (de Jong) And while the inconsistencies between molecular and fossil data were, if anything, expected to be worse with the more ancient, lower, parts of the evolutionary tree, the opposite pattern is observed. As one study explained, “discord between molecular divergence estimates and the fossil record is pervasive across clades and of consistently higher magnitude for younger clades.” (Ksepka, Ware and Lamm)
 
One interesting example is the Orangutans which share many similarities with humans. These “people of the forest,” as they have been called, have more in common with humans than do the other great apes. This includes features of anatomy, reproductive biology and behavior. But there is one feature in which orangutans are not the closest species to humans: the genome. The chimpanzee has the closest genome to the human genome, so it is thought to be our closest relative. The molecular and morphological comparisons point to incongruent phylogenies. As one paper concluded:
 

There remains, however, a paradoxical problem lurking within the wealth of DNA data: our morphology and physiology have very little, if anything, uniquely in common with chimpanzees to corroborate a unique common ancestor. Most of the characters we do share with chimpanzees also occur in other primates, and in sexual biology and reproduction we could hardly be more different. It would be an understatement to think of this as an evolutionary puzzle. (Grehan)
 
If it weren’t for DNA, it would be the orangutan rather than the chimp pictured next to the human in the evolutionary tree.
 
References
 
de Jong, W. 1998. “Molecules remodel the mammalian tree.” Trends in Ecology & Evolution, 13:270-275.
 
Feduccia, A. 2003. “‘Big bang’ for tertiary birds?.” Trends in Ecology & Evolution 18:175.
 
Gura, T. 2000. “Bones, molecules...or both?.” Nature 406:230-233.
 
Grehan J. 2006. “Mona Lisa smile: the morphological enigma of human and great ape evolution.” The Anatomical Record Part B: The New Anatomist 289B:139-157.
 
Ksepka, D. T., J. L. Ware, K. S. Lamm. 2014. “Flying rocks and flying clocks: disparity in fossil and molecular dates for birds.” Proceedings of the Royal Society B 281: 20140677.
 
Lockhart, P., S. Cameron. 2001 “Trees for bees.” Trends in Ecology and Evolution 16:84-88.
 
Ragan, M., J. McInerney, J. Lake. 2009. “The network of life: genome beginnings and evolution.” Philosophical Transactions of the Royal Society B 364:2169-2175.
Stolzer, M., et. al. 2012. “Inferring duplications, losses, transfers and incomplete lineage sorting with nonbinary species trees.” Bioinformatics 28 ECCB:i409–i415.


Gene phylogenies are congruent



Just as evolution predicts that gene trees and species trees should be congruent, it also predicts that different gene trees should be congruent. In 1982 David Penny and co-workers tested this prediction. They wrote that “The theory of evolution predicts that similar phylogenetic trees should be obtained from different sets of character data.” Their character data came from five different proteins and they concluded “there is strong support from these five sequences for the theory of evolution.” (Penny, Foulds and Hendy) But in later years, as more genetic data became available, it was clear that different genes led to very different evolutionary trees. As one study explained, the sequences of genes, “often disagree and can seldom be proven to agree.” (Doolittle and Bapteste) It is now well understood that “Gene and genome trees conflict at many levels” (Haggerty, et. al.) and that “Incongruence between gene trees is the main challenge faced by phylogeneticists in the genomic era.” (Galtier and Daubin) For evolutionists this failed prediction will require more complicated models of evolutionary history. As Penny now writes, he is “not rejecting the tree per se but enriching the tree concept into a network.” (Penny)
 
References
 
Doolittle, W., E. Bapteste. 2007. “Pattern pluralism and the Tree of Life hypothesis.” Proceedings of the National Academy of Sciences 104:2043-2049.
 
Galtier, N., V. Daubin. 2008. “Dealing with incongruence in phylogenomic analyses.” Philosophical Transactions of the Royal Society B 363:4023-4029.
 
Haggerty, L., et. al. 2009. “Gene and genome trees conflict at many levels.” Philosophical Transactions of the Royal Society B 364:2209-2219.
 
Penny, D. 2011. “Darwin’s Theory of Descent with Modification, versus the Biblical Tree of Life.” PLoS Biol 9:e1001096.
Penny, D., L. Foulds, M. Hendy. 1982. “Testing the theory of evolution by comparing phylogenetic trees constructed from five different protein sequences.” Nature 297:197-200.


The species should form an evolutionary tree




Ever since Darwin the universal evolutionary tree has been a unifying principle in biology. Evolution predicted that this universal tree can be derived by arranging the species according to their similarities and differences. And as more data became available, particularly from the dramatic breakthroughs in molecular biology in the latter half of the twentieth century, expectations were high for the determination of this tree. As one paper explains, “Once universal characters were available for all organisms, the Darwinian vision of a universal representation of all life and its evolutionary history suddenly became a realistic possibility. Increasing reference was made to this universal, molecule-based phylogeny as the ‘comprehensive’ tree of the “entire spectrum of life” (O’Malley and Koonin) But those expectations were dashed: “By the mid-1980s there was great optimism that molecular techniques would finally reveal the universal tree of life in all its glory. Ironically, the opposite happened.” (Lawton)
 
As one study explained, the problem is so confusing that results “can lead to high confidence in incorrect hypotheses.” And although evolutionists thought that more data would solve their problems, the opposite has occurred. With the ever increasing volumes of data, incongruence between trees “has become pervasive.” (Dávalos) As another researcher explained, “Phylogenetic incongruities can be seen everywhere in the universal tree, from its root to the major branchings within and among the various taxa to the makeup of the primary groupings themselves.” (Woese) These incongruities are not minor statistical variations and the general failure to converge on a single topology has some researchers calling for a relaxation from “tree-thinking.” (Bapteste, et. al.) Nor are these incongruities limited to protein-coding genes. As one research commented, “I’ve looked at thousands of microRNA genes, and I can’t find a single example that would support the traditional tree.” (Dolgin)
 
These incongruities have forced proponents of evolution to filter the data carefully in order to obtain evolutionary trees. As one paper explains, “selecting genes with strong phylogenetic signals and demonstrating the absence of significant incongruence are essential for accurately reconstructing ancient divergences.” (Salichos and Rokas) But this raises the question of whether the resulting tree is real: “Hierarchical structure can always be imposed on or extracted from such data sets by algorithms designed to do so, but at its base the universal TOL [tree of life] rests on an unproven assumption about pattern that, given what we know about process, is unlikely to be broadly true.” (Doolittle and Bapteste).
 
References
 
Bapteste E., et. al. 2005. “Do orthologous gene phylogenies really support tree-thinking?.” BMC Evolutionary Biology 5:33.
 
Dávalos L., et. al. 2012. “Understanding phylogenetic incongruence: lessons from phyllostomid bats.” Biological Reviews Cambridge Philosophical Society 87:991-1024.
 
Dolgin, E. 2012. “Phylogeny: Rewriting evolution.” Nature 486:460-462.
 
Doolittle, W., E. Bapteste. 2007. “Pattern pluralism and the Tree of Life hypothesis.” Proceedings of the National Academy of Sciences 104:2043-2049.
 
Lawton, G. 2009. “Why Darwin was wrong about the tree of life.” New Scientist January 21.

 
O’Malley, M., E. Koonin. 2011. “How stands the Tree of Life a century and a half after The Origin?.” Biology Direct 6:32.
 
Salichos L., A. Rokas. 2013. “Inferring ancient divergences requires genes with strong phylogenetic signals.” Nature 497:327-331.
Woese C. 1998. “The universal ancestor.” Proceedings of the National Academy of Sciences 95:6854-6859.



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Complex structures evolved from simpler structures


“To suppose that the eye,” wrote Darwin, “could have been formed by natural selection, seems, I freely confess, absurd in the highest possible degree.” But Darwin argued that we must not be misled by our intuitions. Given natural selection operating on inheritable variations, some of which are useful, then, if a sequence of numerous small changes from a simple and imperfect eye to one complex and perfect can be shown to exist, and if the eye is somehow useful at each step, then the difficulty is resolved. (Darwin, 143) The key was to identify “a long series of gradations in complexity, each good for its possessor” which could lead to “any conceivable degree of perfection.” (Darwin, 165)
 
But ever since Darwin the list of complex structures in biology, for which no “series of gradations in complexity” can be found, has continued to grow longer. Both the fossil record and genomic data reveal high complexity in lineages where evolution expected simplicity. As a proponent of evolution explained:
 

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. (Technau)
 
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 widespread across eukaryote species and so they must persist far down the evolutionary tree. And the similarity across species of the kinase functions, and their substrate molecules, means that 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. (Diks)
 
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. So again, the first histone IV must have been very similar to the versions we see today. An 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.” (Levi-Setti, 29) Reviewing the fossil and molecular data, a proponent of evolution explained 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.” (Sherman) And as one team of proponents of evolution concluded, “comparative genomics has confirmed a lesson from paleontology: Evolution does not proceed monotonically from the simpler to the more complex.” (Kurland)
 
References
 
Darwin, Charles. 1872. The Origin of Species. 6th ed. London: John Murray.
http://darwin-online.org.uk/content/frameset?itemID=F391&viewtype=text&pageseq=1
 
Diks, S., K. Parikh, M. van der Sijde, J. Joore, T. Ritsema, et. al. 2007. “Evidence for a minimal eukaryotic phosphoproteome?.” PLoS ONE 2.
 
Kurland, C., L. Collins, D. Penny. 2006. “Genomics and the irreducible nature of eukaryote cells.” Science 312:1011-1014.
 
Levi-Setti, Riccardo. 1993. Trilobites. 2d ed. Chicago: University of Chicago Press.
 
Sherman, M. 2007. “Universal genome in the origin of metazoa: Thoughts about evolution.” Cell Cycle 6:1873-1877.
Technau, U. 2008. “Evolutionary biology: Small regulatory RNAs pitch in.” Nature 455:1184-1185.


Structures do not evolve before there is a need for them


A fundamental premise of evolutionary theory is that evolution has no foresight. It is a blind process responding to current, not future, needs. This means that biological structures do not evolve before they are needed. But many examples of this have been discovered in recent years. For instance, in the embryonic stages of a wide variety of organisms, the development of the vision system is orchestrated by similar control genes known as transcription factors. As one paper explained, “All eyes, invertebrate and vertebrate, develop through a cascade of similar transcription factors despite vast phylogenetic distances.” (Wake, Wake and Specht) Because these transcription factors are so prevalent across the evolutionary tree, they must have evolved in the very early stages of evolution, in an early common ancestor. But that was before any vision systems had evolved. The vision system is just one of several such examples showing that the genetic components of many of today’s embryonic development pathways must have been present long before such pathways existed. Evolutionists now refer to the appearance of these genetic components, before they were used as such, as preadaptation:
 

Genome comparisons show that the early clades increasingly contain genes that mediate development of complex features only seen in later metazoan branches. … The existence of major elements of the bilaterian developmental toolkit in these simpler organisms implies that these components evolved for functions other than the production of complex morphology, preadapting the genome for the morphological differentiation that occurred higher in metazoan phylogeny. (Marshall and Valentine)
 
Such preadaptation extends beyond embryonic development. For example, several key components of the human brain are found in single-celled organisms called choanoflagellates. Therefore these key components must have evolved in single-celled organisms, long before animals, brains and nerve cells existed. As one evolutionist explained, “The choanoflagellates have a lot of precursors for things we thought were only present in animals.” (Marshall)
 
Another example is the molecular machines for protein transport across the mitochondria inner membrane which must have evolved long before mitochondria existed. (Clements et. al.) As one evolutionist explained, “You look at cellular machines and say, why on earth would biology do anything like this? It’s too bizarre. But when you think about it in a neutral evolutionary fashion, in which these machineries emerge before there’s a need for them, then it makes sense.” (Keim)
 
References
 
Clements, A., D. Bursac, X. Gatsos, et. al. 2009. “The reducible complexity of a mitochondrial molecular machine.” Proceedings of the National Academy of Sciences 106:15791-15795.
 
Keim, Brandon. 2009. “More ‘Evidence’ of Intelligent Design Shot Down by Science.” Wired Aug. 27. http://www.wired.com/wiredscience/2009/08/reduciblecomplexity/
 
Marshall, Michael. 2011. “Your brain chemistry existed before animals did.” NewScientist September 1.
 
Marshall C., J. Valentine. 2010. “The importance of preadapted genomes in the origin of the animal bodyplans and the Cambrian explosion.” Evolution 64:1189-1201.
Wake D., M. Wake, C. Specht. 2011. “Homoplasy: from detecting pattern to determining process and mechanism of evolution.” Science 331:1032-1035.


Functionally unconstrained DNA is not conserved



As different species evolve, their DNA segments are preserved only if they contribute to the organism’s fitness. DNA segments that are not functionally constrained should mutate and diverge over time. The result is that similar yet functionally unconstrained DNA segments 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 in the many examples of functionally-unconstrained, highly similar stretches of DNA that have been discovered in otherwise distant species. For instance, thousands of so-called ultra-conserved elements (UCEs), hundreds of base pairs in length, have been found across a range of species including human, mouse, rat, dog, chicken and fish. 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. (Lurie) “It can’t be true” another commented. (Pennisi)
 
Proponents of evolution assumed such highly preserved sequences must have an important function. But laboratory studies failed to reveal any significant effects in mice. A variety of 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 deleted several UCE regions, including a stretch of 731 DNA base pairs that was hypothesized to regulate a crucial gene. 
Proponents of evolution expected the removal 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. (Ahituv, et. al.) 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. (Mice thrive missing ancient DNA sequences)
 
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. (Nobrega, et. al.) “We were quite amazed,” explained the lead researcher. (Westphal)
 
References
 
Ahituv, N., Y. Zhu, A. Visel, A. Holt, V. Afzal, L. Pennacchio, E. Rubin. 2007. “Deletion of ultraconserved elements yields viable mice.” PLoS Biol 5:e234.
 
Lurie, Karen. 2004. “Junk DNA.” ScienCentral July 20.
 
“Mice thrive missing ancient DNA sequences.” 2007. ScienceDaily September 6. http://www.sciencedaily.com/releases/2007/09/070904151351.htm
 
Nobrega, M., Y. Zhu, I. Plajzer-Frick, V. Afzal, E. Rubin. 2004. “Megabase deletions of gene deserts result in viable mice.” Nature 431:988-993.
 
Pennisi, Elizabeth. 2004. “Disposable DNA puzzles researchers.” Science 304:1590-1591.
Westphal, S. 2004. “Life goes on without ‘vital’ DNA.” New Scientist June 3.


Cell death


According to evolutionary theory, biological variation that supports or enhances reproduction will increase in future generations—a process known as natural selection. The corollary to this is that biological variation that degrades reproduction will not be selected for. Clearly, natural selection could not result in destructive behavior. Here are two representative statements from Origins:
 

we may feel sure that any [biological] variation in the least degree injurious would be rigidly destroyed. (Darwin, 63)
 
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. (Darwin, 162-3)
 
But are not examples of such “injurious” behavior 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.
 
But today we have many examples of injurious behavior that falsify Darwin’s prediction that natural selection “will never produce in a being any structure more injurious than beneficial to that being.” In bacteria, for example, phenomenally complicated mechanisms 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. (Chaloupka, Vinter; Engelberg-Kulka, Hazan, Amitai; Engelberg-Kulka, Amitai, Kolodkin-Gal, Hazan; University Of Nebraska)
 
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 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.
 
Suicide is probably good for the bacteria population, on the whole, in challenging conditions. Since gene sharing within a bacteria population is at its maximum, evolutionists have no problem explaining such altruism as a result of kin selection (see Altruism). Such a facile response, however, misses the profound problem of how such a design could arise in the first place, for the mechanism is immensely complex.
 
In this example of bacteria suicide, the antitoxic gene normally inhibits the toxic gene from executing its mission. When the antitoxic gene is diluted then the toxic gene can 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.” (Amitai) 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 random 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. This is highly unlikely and adds considerable complexity to the theory.
 
References
 
Amitai, Shahar, Ilana Kolodkin-Gal, Mirit Hananya-Meltabashi, Ayelet Sacher, Hanna Engelberg-Kulka. 2009. “Escherichia coli MazF leads to the simultaneous selective synthesis of both ‘death proteins’ and ‘survival proteins’.” PLoS Genetics 5:e1000390.
 
Chaloupka, J., V. Vinter. 1996. “Programmed cell death in bacteria.” Folia Microbiologica, 41:6.
 
Engelberg-Kulka, Hanna, Ronen Hazan, Shahar Amitai. 2005. “mazEF: a chromosomal toxin-antitoxin module that triggers programmed cell death in bacteria.” J Cell Science 118:4327-4332.
 
Engelberg-Kulka, Hanna, Shahar Amitai, Ilana Kolodkin-Gal, Ronen Hazan. 2006. “Bacterial programmed cell death and multicellular behavior in bacteria,” PLoS Genetics 2:e135.
University Of Nebraska. 2007. “New Hope For Fighting Antibiotic Resistance,” ScienceDaily April 27.

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Failed Predictions of evolutionary theory

Despite their protests, proponents of evolution do depend on “Junk DNA,” and LOTS of It!  1




As important functions are found for more and more junk DNA, some proponents of evolution are trying to claim it is not all that important to evolution.

Once Susumu Ohno coined the term “junk DNA” and called it the remains of extinct genes1, junk DNA started to become the darling of the evolutionary community. First, it was seen as an effective argument against creationism or intelligent design. After all, why would the Creator put so much useless DNA into His creation? More importantly, however, it was considered an integral component of evolution. After all, evolution requires that genetic mutations acted on by natural selection produced genes with novel functions. However, it is difficult to expect that to work when the mutations occur in genes that the organism needs. Thus, one of the major mechanisms of genetic evolution involves gene duplication. In this view, a gene is duplicated, and one copy continues to produce the protein it always produced, while the other is free to mutate wildly. Waving the magic wand of time, the evolutionist then says that a large number of these mutating copies will become useless junk, but a small number of them will develop into novel genes. As you can see, then, junk DNA is integral to evolution, and according to evolution, most organisms should have a lot of it.


This, of course, is why Dr. Jerry Coyne says the following in his book, Why Evolution Is True:2,


When a trait is no longer used, or becomes reduced, the genes that make it don’t instantly disappear from the genome: evolution stops their action by inactivating them, not snipping them out of the DNA. From this we can make a prediction. We expect to find, in the genomes of many species, silenced, or ‘dead,’ genes: genes that once were useful but are no longer intact or expressed. In other words, there should be vestigial genes…Our genome—and that of other species—are truly well populated graveyards of dead genes.


Unfortunately for proponents of evolution, function is routinely being found for this supposed “junk DNA.” As a result, some proponents of evolution have realized that they need to back away from the claim that junk DNA is integral to the process of evolution.
For example, Dr. Larry Moran has tried to rewrite the history of evolutionary thought. In discussing Dr. Jonathan Wells’s book The Myth of Junk DNA. Hewrites:


The IDiots have a bit of a problem. In order to make this book look important they have to first establish that the concept of abundant junk DNA in our genome was a “pillar” of support for evolution. That’s hard to do when their understanding of evolution is so flawed that they don’t see the difference between “Darwinism” and evolution by random genetic drift. Their claim that evolutionary theory PREDICTED the presence of huge amounts of junk DNA in our genome is just plain false. (emphasis his)

Not surprisingly, its Moran’s statement that is 100% false, and its falsehood can be demonstrated quite clearly simply by reading a recent paper written by two young-earth creationists and published in a secular, peer-reviewed scientific journal. —Sigh— Yes, both creationists and intelligent design advocates write papers about evolution that are published in the secular, peer-reviewed literature. Anyone who says otherwise spends little time reading such literature.
This particular paper was written by Chase W. Nelson and world-renowned geneticist J.C. Sanford. They examined the program Avida, which attempts to simulate evolution using “digital organisms.” In the digital world of Avida, the organisms are replicating “creatures” whose “DNA” is composed of strings of computer instructions. As these creatures replicate, mutations change those instructions. Avida has shown that over time, these mutations (acted on by a digital form of natural selection) produce creatures that can perform new logic operations, which would be the digital equivalent of new biological characteristics. In other words, Avida produces a digital simulation of evolution using strings of computer instructions as DNA and logic operations as biological traits. It is considered the gold standard when it comes to digital simulations of evolution.
The problem that Nelson and Sanford point out in their excellent paper3 is that Avida uses only high-impact mutational events – events that produce a lot of fitness very quickly. However, such high-impact mutational events are extremely rare in nature. To be more realistic, the authors conclude, Avida should use digital mutation events that are more like real-life mutational events when it comes to their effect on the fitness of the organism. When the authors do this, they find that Avida is unable to produce new logic operations. In other words, when you make the simulation more realistic, you no longer see the evolution of new traits. This, of course, is precisely what creationism predicts, but it is not all that surprising. As I have already pointed out, the longest-running experiment on evolution shows that the changes mutations can make in the genome are extremely limited.
What I found interesting was another point they make in their paper. They say that an integral part of the Avida program is…wait for it… junk DNA:


The ancestral genome devotes about 15 instructions to the essential replication code, while the remaining 85 positions are occupied by benign no-operation instructions, analogous to inert “junk DNA” that can be used as raw material for evolutionary tinkering.


Now remember, Moran claims that a large amount of junk DNA is not a pillar of support for evolution. Contrary to that assertion, the standard digital simulation of evolution starts out with a genome that is 85% junk DNA. I don’t know about Moran, but to me, a genome that is 85% junk does, indeed, represent a genome with “huge amounts” of junk DNA, and that is the beginning assumption of the standard computer simulation of evolution. As this makes clear, a vast amount of junk DNA in most creatures’ genomes is an integral component of evolutionary theory, and like most things, the more we learn about genetics, the more we realize how wrong that integral component is.


REFERENCES

1. Susumu Ohno, “So Much ‘Junk’ DNA in Our Genome,” Evolution of Genetic Systems. Brookhaven symposia in biology23:366-370, 1972.
Return to Text

2. Jerry A. Coyne, Why Evolution Is True, Viking, 2009, pp 66-67
Return to Text

3. Chase W Nelson and John C Sanford, “The effects of low-impact mutations in digital organisms,” Theoretical Biology and Medical Modeling8:9, 2011 (Available online)

With Enough Faith You Can Believe Anything!  2



The fish in the above public-domain photograph is a ninespine stickleback fish. It gets its name from the nine spines that stick up from its back. A similar fish, the threespine stickleback, looks very similar but (you guessed it!) has only three spines sticking out its back. Both fish have two spines sticking down from their pelvis, but those spines are typically larger in the threespine stickleback. These similar species of fishes have shown us more examples of the failed predictions of evolution.
Both species of stickleback live in the ocean but swim upstream to reproduce in freshwater. According to the evolutionary story, some populations of each species were trapped in lakes when they did this, so they changed their lifestyles to live exclusively in freshwater. Interestingly enough, when they did this, they lost their pelvises and the spines that grew from them.
Why did this happen? The argument is that such spines are very beneficial to fishes that live in the ocean, because if a predator fish tries to eat a stickleback, the stickleback can extend its spines (the ones on its back and the ones on its pelvis) to defend itself. This could also be protective in freshwater, but there is a catch. There are some predators in freshwater that can actually use the stickleback’s pelvic spines to more easily catch and eat the stickleback.
Dragonfly larvae, for example, live in freshwater. A larval dragonfly has a labium, which is essentially a big “claw” it can extend from under its mouth. It can use that “claw” to grab onto a fish and pull it in to eat it. Here is a quick (and AWESOME) video of how that works:





Amazing, isn’t it? Well, it turns out that the pelvis and pelvic spines of a stickleback make it very easy for a predator like a dragonfly larva to use its labium to grab onto the fish and pull it in for a nice meal. As a result, proponents of evolution say that freshwater sticklebacks have lost their pelvises and pelvic spines over the years.
Now, of course, 
proponents of evolution would want us to believe that this happens because of random mutations in certain genes. By sheer coincidence, a mutation occurs that produces less prominent (or weaker) pelvic spines, and because of this, the “lucky” fish was more likely to live and pass on that trait to its progeny. When another mutation occurred that resulted in even smaller or weaker spines or pelvises, it would be naturally selected. Over time, then, the sticklebacks lost their pelvises and pelvic spines simply because a bunch of lucky mutations happened over the years, and those lucky mutations were acted on by natural selection.
Since evolutionists assume the threespine and ninespine sticklebacks are closely-related, they thought that essentially the same genes would control the loss of the pelvis and pelvic spines in each species. As a result, they predicted that when they compared freshwater threespine and ninespine sticklebacks, they would find that essentially the same genes were mutated in each species. Of course, like most evolutionary predictions, it turns out that this evolutionary prediction was dead wrong.
The genes responsible for the loss of the pelvis and pelvic spines in ninespine and threespine sticklebacks are on different chromosomes. In the ninespine stickleback, the responsible gene is on chromosome four. In the threespine stickleback, it is on chromosome 7. The authors think they have ruled out that the same gene somehow “jumped” chromosomes, so they think that these two incredibly similar fish simply found different genetic solutions to the same problem.
To me, this failed prediction of evolution is not the real “meat” of the story. You get to that if you read a bit further. The researchers also found that while gender is determined by genes on chromosome twelve in ninespine sticklebacks, the gender-determining genes on threespine sticklebacks are found on chromosome nineteen. This is incredibly surprising. As the Science Daily article linked above says:


“This is very surprising because these species are fairly closely related,” even though they diverged 13 million years ago, Shapiro says, noting that “mammals have not changed their sex-determination mechanism in more than 150 million years.”

Now, of course, those “millions of years” ideas require one to use scientifically irresponsible dating techniques. However, his point is clear. Evolution would predict that the genetic control of gender would be very similar in species that are supposed to be so closely-related. However, it is not.
So is this just another example of a failed evolutionary prediction? It is actually a little more than that. It is an example of the absurd lengths to which one must go in order to believe in evolution. Remember, Shapiro (the scientist quoted above) is forced to believe that these two species of sticklebacks are closely-related, because he must continue to believe in evolution. So what does he do when he sees that the gender determination genes are different between the species? He simply assumes that one species changed how it determined its gender.
Think about that for a moment. The species are supposed to be closely-related, so it is assumed that their “recent” common ancestor had a genetic means by which it determined gender. Thus, both of theses species inherited that mechanism. However, for some unknown, mystical reason, one (or both) of the fish species studied here found a “better” mechanism for gender determination (through random mutation, of course) and thus “changed” to a new mechanism over time.
There is no explanation as to why the ancestor’s mechanism wasn’t good enough. There is no explanation as to how one mechanism of gender determination could be in place until the other became fully functional. There is no explanation as to how the old mechanism could be “turned off” once the other one was ready to go. Instead, there is only a fervent belief that these two species MUST be closely-related, and therefore any changes between them must be the result of evolution that took place after they each evolved from their common ancestor. Wow! That’s some amazing faith! It’s certainly more than I can muster!




http://www.evolutionnews.org/2009/06/darwins_failed_predictions_an021311.html

Darwinian evolution indeed makes predictions -- which, however, routinely fail. This requires evolutionary scientists to come up with increasingly baroque additions to and speculations upon their theory to make the data fit with the theory. It all becomes increasingly, suspiciously complicated. For example, Darwinism has a very hard time explaining altruism. Selflessness, especially toward those outside one's family, is not what you'd expect from the evolutionary scenario. Darwinists strain to come up with explanations, resulting in many serendipitous just-so stories that are less and less tethered to scientific fact.

evolution predicts many similarities in species that are close together in the evolutionary tree, and few similarities in species that are far apart in the evolutionary tree. And we find such evidence in biology. But we routinely find significant contradictions as well. So the prediction becomes a soft prediction rather than a hard prediction. The prediction predicts the pattern where the pattern is found, but not where the pattern is not found. So the prediction is really not very meaningful or interesting.



Another Failed Evolutionary Prediction 

In science, one of the most important things a hypothesis can do is make predictions that can be verified by experiment or observation. If a hypothesis makes predictions that are then confirmed by experiment or observation, its scientific value is high. The more confirmed predictions it makes, the more likely it is to be a good, scientific explanation for whatever phenomenon it is describing. However, if a hypothesis makes several predictions that are shown to by false by experiment or observation, its scientific value becomes questionable.

Dr. Cornelius Hunter has done an excellent job detailing many of evolution’s failed predictions. I have discussed a few on this blog as well (here, here, here, here, here, and here). Not surprisingly, as more and more research is being done, more and more evolutionary predictions are being falsified. The latest one involves bats and insects.

As most people know, bats have an amazing echolocation system that allows them to hunt in the dark. They send out high-frequency sound waves that bounce off anything in front of them. They receive the reflected sound waves, analyze them with sophisticated mathematics, and determine all sorts of useful information, such as the size, position, and speed of what’s in front of them. This amazing echolocation system allows bats to hunt and eat insects even when it is pitch black outside.

Well, it turns out that some insects are able to hear these high-frequency sound waves. This alerts them to the fact that a bat is hunting them, and they are then able to take evasive maneuvers. For many, many years, evolutionists have claimed that this kind of hearing in insects evolved after bats evolved. For example, a book that discusses the echolocation systems found in bats and dolphins says:1

The evolution of ultrasound sensitivity in nocturnal insects evolved in response to predation pressures exerted by echolocating bats.

Another evolutionary book makes a very similar statement:2

…before bats evolved…moths and other nocturnal insects owned the night sky, flitting about unmolested by predators. The appearance of bats forced them to evolve a novel antibat strategy – a way of hearing the echolocating calls of hunting bats, in effect a radar detector.

So evolution predicts that the high-frequency hearing in some insects arose after bats evolved, as a response to the bats’ new way of finding prey among the insects.

Like most evolutionary predictions, however, this turns out to be dead wrong.


Dr. Roy E. Plotnick and Dr. Dena M. Smith studied well-preserved fossils of crickets and katydids from the Green River Formation found in the western United States. According to questionable evolutionary dating techniques, these fossils are supposed to be 50 million years old. This is roughly the same age that evolutionists date the first definitive bat fossils. So…assuming that these insects did evolve their ability to hear high-frequency sound waves in response to the appearance of bats, what would you expect these researchers to find when they studied the hearing organs found in those supposedly 50-million-year-old insect fossils? The hearing organs should look quite different from those of their modern counterparts, right? After all, the insects wouldn’t have yet had a chance to evolve their high-frequency hearing, given that the fossils are supposed to be just as old as the earliest bat fossils.

What Drs. Plotnick and Smith actually find? Here’s how they put it:3

Here we describe and document the exceptionally well preserved tympanal ears found in crickets and katydids from the Eocene Green River Formation of Colorado, which are virtually identical to those seen in modern representatives of these groups.

In other words, the fossil evidence indicates that crickets and katydids had essentially the same hearing before and after the supposed evolution of bats. If Dr. Plotnick and Dr. Smith’s analysis is correct, then, these insects did not evolve their ability to hear high-frequency sound in response to the predation of bats. How will evolutionists explain the evolution of high-frequency hearing in some insects now? Here’s how a web article puts it:

The findings suggest that this group of insects evolved their supersensitive hearing long before bat predators came to be, the researchers say.

“Their bat-detecting abilities may have simply become apparent later,” Smith said.

That’s pretty convenient. Evolution just happened to prepare these insects for bat predators long before the bats actually evolved! What an interesting way to explain around this most recently-falsified prediction of the evolutionary hypothesis.

Darwins doubt pg.273

There is another remarkable aspect of the hierarchical organization of information in animal forms.  Many of the same genes and proteins play very different roles, depending upon the larger organismal and informational context in which they find themselves in different animal groups. For example, the same gene (Pax-6 or its homolog, called eyeless), helps to regulate the development of the eyes of fruit flies (arthropods) and those of squid and mice (cephalopods and vertebrates, respectively). Yet arthropod eyes exemplify a completely different structure from vertebrate or cephalopod eyes. The fruit fly possesses a compound eye with hundreds of separate lenses (ommatidia), whereas both mice and squid employ a camera-type eye with a single lens and retinal surface. In addition, although the eyes of squid and mice resemble each other optically (single lens, large internal chamber, single retinal surface), they focus differently. They undergo completely different patterns of development and utilize different internal structures and nerve connections to the visual centers of the brain. Yet the Pax-6 gene and its homologs play a key role in regulating the construction of all three of these different adult sensory structures. Moreover, evolutionary and developmental biologists have found that this pattern of "same genes, different anatomy" recurs throughout the bilaterian phyla, for features as fundamental as appendages, segmentation, the gut, heart, and sense organs .This pattern contradicts the expectations of textbook evolutionary theory. Neo-Darwinism predicts that disparate adult structures should be produced by different genes. This prediction follows directly from the neo-Darwinian assumption that all evolutionary (including anatomical) transformations begin with mutations in DNA sequences—mutations that are fixed in populations by natural selection, genetic drift, or other evolutionary processes. The arrow of causality flows one way from genes (DNA) to development to adult anatomy. Thus, if biologists observe different animal forms, it follows that they should expect that different genes will specify those forms during animal development. Given the profound differences between the fruit-fly compound eye and the vertebrate camera eye, neo-Darwinian theory would not predict that the "same" genes would be involved in  building different eyes in arthropods and chordates.



1) http://blog.drwile.com/?p=6167
2) http://blog.drwile.com/?p=923
3) http://blog.drwile.com/?p=2900
4) http://blog.drwile.com/?p=6828



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44 Reasons Why Evolution Is Just A Fairy Tale For Adults 1


The theory of evolution  is just a fairy tale for adults based on ancient pagan religious philosophy that hundreds of millions of people around the world choose to believe with blind faith.  When asked to produce evidence for the theory of evolution, most adults in the western world come up totally blank.  When pressed, most people will mumble something about how “most scientists believe it” and how that is good enough for them.  This kind of anti-intellectualism even runs rampant on our college campuses.  If you doubt this, just go to a college campus some time and start asking students why they believe in evolution.  Very few of them will actually be able to give you any real reasons why they believe it.  Most of them just have blind faith in the priest class in our society (“the scientists”).  But is what our priest class telling us actually true?  When Charles Darwin popularized the theory of evolution, he didn’t actually have any evidence that it was true.  And since then the missing evidence has still not materialized.  Most Americans would be absolutely shocked to learn that most of what is taught as “truth” about evolution is actually the product of the overactive imaginations of members of the scientific community.  They so badly want to believe that it is true that they will go to extraordinary lengths to defend their fairy tale.  They keep insisting that the theory of evolution has been “proven” and that it is beyond debate.  Meanwhile, most average people are intimidated into accepting the “truth” about evolution because they don’t want to appear to be “stupid” to everyone else.
In this day and age, it is imperative that we all learn to think for ourselves.  Don’t let me tell you what to think, and don’t let anyone else tell you what to think either.  Do your own research and come to your own conclusions.  The following are 44 reasons why evolution is just a fairy tale for adults…


#1 If the theory of evolution was true, we should have discovered millions upon millions of transitional fossils that show the development of one species into another species. Instead, we have zero.
#2 When Charles Darwin came up with his theory, he admitted that no transitional forms had been found at that time, but he believed that huge numbers certainly existed andwould eventually be discovered…


“Lastly, looking not to any one time, but to all time, if my theory be true, numberless intermediate varieties, linking closely together all the species of the same group, must assuredly have existed. But, as by this theory, innumerable transitional forms must have existed, why do we not find them embedded in countless numbers in the crust of the earth?”


#3 Even some of the most famous proponents of evolution in the world acknowledge the complete absence of transitional fossils in the fossil record. For example, Dr. Colin Patterson, former senior paleontologist of the British Museum of Natural History and author of “Evolution” once wrote the following…
“I fully agree with your comments about the lack of direct illustration of evolutionary transitions in my book. If I knew of any, fossil or living, I would certainly have included them …. I will lay it on the line – there is not one such fossil for which one could make a watertight argument.”


#4 Stephen Jay Gould, Professor of Geology and Paleontology at Harvard University, once wrote the following about the lack of transitional forms…
“The absence of fossil evidence for intermediary stages between major transitions in organic design, indeed our inability, even in our imagination, to construct functional intermediates in many cases, has been a persistent and nagging problem for gradualistic accounts of evolution.”


#5 Evolutionist Stephen M. Stanley of Johns Hopkins University has also commented on the stunning lack of transitional forms in the fossil record…
“In fact, the fossil record does not convincingly document a single transitionfrom one species to another.”
#6 If “evolution” was happening right now, there would be millions of creatures out there with partially developed features and organs.  But instead there are none.
#7 If the theory of evolution was true, we should not see a sudden explosion of fully formed complex life in the fossil record. Instead, that is precisely what we find.


#8 Paleontologist Mark Czarnecki, a proponent of evolution, once commented on the fact that complex life appears very suddenly in the fossil record…
“A major problem in proving the theory has been the fossil record; the imprints of vanished species preserved in the Earth’s geological formations. This record has never revealed traces of Darwin’s hypothetical intermediate variants –instead species appear and disappear abruptly, and this anomaly has fueled the creationist argument that each species was created by God.”


#9 The sudden appearance of complex life in the fossil record is so undeniable that even Richard Dawkins has been forced to admit it…
“It is as though they [fossils] were just planted there, without any evolutionary history. Needless to say this appearance of sudden planting has delighted creationists. Both schools of thought (Punctuationists and Gradualists) despise so-called scientific creationists equally, and both agree that the major gaps are real, that they are true imperfections in the fossil record. The only alternative explanation of the sudden appearance of so many complex animal types in the Cambrian era is divine creation and both reject this alternative.”


#10 Nobody has ever observed macroevolution take place in the laboratory or in nature.  In other words, nobody has ever observed one kind of creature turn into another kind of creature.  The entire theory of evolution is based on blind faith.
#11 Evolutionist Jeffrey Schwartz, a professor of anthropology at the University of Pittsburgh, openly admits that “the formation of a new species, by any mechanism, has never been observed.”
#12 Even proponent of evolution Stephen J. Gould of Harvard University has admitted that the record shows that species do not change. The following is how he put it during a lecture at 
Hobart & William Smith College
“Every paleontologist knows that most species don’t change. That’s bothersome….brings terrible distress. ….They may get a little bigger or bumpier but they remain the same species and that’s not due to imperfection and gaps but stasis. And yet this remarkable stasis has generally been ignored as no data. If they don’t change, its not evolution so you don’t talk about it.”


#13 Anyone that believes that the theory of evolution has “scientific origins” is fooling themselves.  It is actually a deeply pagan religious philosophy that can be traced back for thousands of years.
#14 Anything that we dig up that is supposedly more than 250,000 years old should have absolutely no radiocarbon in it whatsoever.  But instead, we find it in everything that we dig up – even dinosaur bones.  This is clear evidence that the “millions of years” theory issimply a bunch of nonsense…
It’s long been known that radiocarbon (which should disappear in only a few tens of thousands of years at the most) keeps popping up reliably in samples (like coal, oil, gas, etc.) which are supposed to be ‘millions of years’ old. For instance, CMI has over the years commissioned and funded the radiocarbon testing of a number of wood samples from ‘old’ sites (e.g. with Jurassic fossils, inside Triassic sandstone, burnt by Tertiary basalt) and these were published (by then staff geologist Dr Andrew Snelling) in Creation magazine and Journal of Creation. In each case, with contamination eliminated, the result has been in the thousands of years, i.e. C-14 was present when it ‘shouldn’t have been’. These results encouraged the rest of the RATE team to investigate C-14 further, building on the literature reviews of creationist M.D. Dr Paul Giem.
In another very important paper presented at this year’s ICC, scientists from the RATE group summarized the pertinent facts and presented further experimental data. The bottom line is that virtually all biological specimens, no matter how ‘old’ they are supposed to be, show measurable C-14 levels. This effectively limits the age of all buried biota to less than (at most) 250,000 years.



#15 The odds of even a single sell “assembling itself” by chance are so low that they aren’t even worth talking about.  The following is an excerpt from Jonathan Gray’s book entitled “[url=http://books.google.com/books?id=f16kK5zk5cMC&pg=PA43&lpg=PA43&dq=Even+the+simplest+cell+you+can+conceive+of+would+require+no+less+than+100,000+DNA+base+pairs+and+a+minimum+of+about+10,000+amino+acids,+to+form+the+essential+protein+chain.+Not+to+mention+the+other+things+that+would+also+be+necessary+for+the+first+cell.&source=bl&ots=VFrEn8RL_l&sig=qbbwE7uqNtoQS0i6_NbZR2Vs5PU&hl=en&sa=X&ei=lcnNUoCIMor7oATc5YLIBg&ved=0CCoQ6AEwAA#v=onepage&q=Even the simplest cell you can conceive of would require no less than 100%2C000 DNA base pairs and a minimum of about 10%2C000 amino acids%2C to form the essential protein chain. Not to mention the other things that would also be necessary for the first]The Forbidden Secret[/url]“…
Even the simplest cell you can conceive of would require no less than 100,000 DNA base pairs and a minimum of about 10,000 amino acids, to form the essential protein chain. Not to mention the other things that would also be necessary for the first cell.
Bear in mind that every single base pair in the DNA chain has to have the same molecular orientation (“left-hand” or “right hand”)? As well as that, virtually all the amino acids must have the opposite orientation. And every one must be without error.
“Now,” explained Larry, “to randomly obtain those correct orientations, do you know your chances? It would be 1 chance in 2110,000, or 1 chance in 1033,113!
“To put it another way, if you attempted a trillion, trillion, trillion combinations every second for 15 billion years, the odds you would achieve all the correct orientations would still only be one chance in a trillion, trillion, trillion, trillion … and the trillions would continue 2755 times!
“It would be like winning more than 4700 state lotteries in a row with a single ticket purchased for each. In other words…impossible.”



#16 How did life learn to reproduce itself?  This is a question that proponents of evolution do not have an answer for.
#17 In 2007, fishermen caught a very rare creature known as a Coelacanth.  Proponents of evolution originally told us that this “living fossil” had gone extinct 70 million years ago.  It turns out that they were only off by 70 million years.
#18 According to proponents of evolution, the Ancient Greenling Damselfly last showed up in the fossil record about 300 million years ago.  But it still exists today.  So why hasn’t it evolved at all over the time frame?
#19 Darwinists believe that the human brain developed without the assistance of any designer.  This is so laughable it is amazing that there are any people out there that still believe this stuff.  The truth is that the human brain is amazingly complex.  The following is how a PBS documentary described the complexity of the human brain: “It contains over 100 billion cells, each with over 50,000 neuron connections to other brain cells.”
#20 The following is how one evolutionist pessimistically assessed the lack of evidence for the evolution of humanity…
“Even with DNA sequence data, we have no direct access to the processes of evolution, so objective reconstruction of the vanished past can be achieved only by creative imagination.”


#21 Perhaps the most famous fossil in the history of the theory of evolution, “Piltdown Man”, turned out to be a giant hoax.
#22 If the neutron were not about 1.001 times the mass of the proton, all protons would have decayed into neutrons or all neutrons would have decayed into protons, and therefore life would not be possible. How can we account for this?
#23 If gravity was stronger or weaker by the slimmest of margins, then life sustaining stars like the sun could not exist. This would also make life impossible. How can we account for this?
#24 Why did proponent of evolution Dr. Lyall Watson make the following statement?…
“The fossils that decorate our family tree are so scarce that there are still more scientists than specimens. The remarkable fact is that all of the physical evidence we have for human evolution can still be placed, with room to spare, inside a single coffin!”


#25 Apes and humans are very different genetically.  As DarwinConspiracy.com explains, “the human Y chromosome has twice as many genes as the chimpanzee Y chromosome and the chromosome structures are not at all similar.”
#26 How can we explain the creation of new information that is required for one animal to turn into another animal?  No evolutionary process has ever been shown to be able to create new biological information.  One scientist described the incredible amount of new information that would be required to transform microbes into men this way…
“The key issue is the type of change required — to change microbes into men requires changes that increase the genetic information content, from over half a million DNA ‘letters’ of even the ‘simplest’ self-reproducing organism to three billion ‘letters’ (stored in each human cell nucleus).”


#27 Proponents of evolution would have us believe that there are nice, neat fossil layers with older fossils being found in the deepest layers and newer fossils being found in the newest layers.  This simply is not true at all…
The fossil layers are not found in the ground in the nice neat clean order that evolutionists illustrate them to be in their textbooks. There is not one place on the surface of the earth where you may dig straight down and pass through the fossil layers in the order shown in the textbooks. The neat order of one layer upon another does not exist in nature. The fossil bearing layers are actually found out of order, upside down (backwards according to evolutionary theory), missing (from where evolutionists would expect them to be) or interlaced (“younger” and “older” layers found in repeating sequences). “Out of place” fossils are the rule and not the exception throughout the fossil record.


#28 Proponents of evolution believe that the ancestors of birds developed hollow bones over thousands of generations so that they would eventually be light enough to fly.  This makes absolutely no sense and is beyond ridiculous.
#29 If dinosaurs really are tens of millions of years old, why have scientists found dinosaur bones with soft tissue still in them?  The following is from an NBC News report about one of these discoveries…
For more than a century, the study of dinosaurs has been limited to fossilized bones. Now, researchers have recovered 70 million-year-old soft tissue, including what may be blood vessels and cells, from a Tyrannosaurus rex.


#30 Which evolved first: blood, the heart, or the blood vessels for the blood to travel through?
#31 Which evolved first: the mouth, the stomach, the digestive fluids, or the ability to poop?
#32 Which evolved first: the windpipe, the lungs, or the ability of the body to use oxygen?
#33 Which evolved first: the bones, ligaments, tendons, blood supply, or the muscles to move the bones?
#34 In order for blood to clot, more than 20 complex steps need to successfully be completed. How in the world did that process possibly evolve?
#35 The information stored in  DNA is so incredibly complex that it is absolutely absurd to suggest that such a language system could have “evolved” all by itself by accident…
When it comes to storing massive amounts of information, nothing comes close to the efficiency of DNA. A single strand of DNA is thousands of times thinner than a strand of human hair. One pinhead of DNA could hold enough information to fill a stack of books stretching from the earth to the moon 500 times.
Although DNA is wound into tight coils, your cells can quickly access, copy, and translate the information stored in DNA. DNA even has a built-in proofreader and spell-checker that ensure precise copying. Only about one mistake slips through for every 10 billion nucleotides that are copied.



#36 Can you solve the following riddle by Perry Marshall?…
1) DNA is not merely a molecule with a pattern; it is a code, a language, and an information storage mechanism.
2) All codes are created by a conscious mind; there is no natural process known to science that creates coded information.
3) Therefore DNA was designed by a mind.
If you can provide an empirical example of a code or language that occurs naturally, you’ve toppled my proof. All you need is one.



#37 Proponents of evolution simply cannot explain why our planet is so perfectly suited to support life.
#38 Shells from living snails have been “carbon dated” to be 27,000 years old.
#39 If humans have been around for so long, where are all of the bones and all of the graves?  The following is an excerpt from an article by Don Batten…
Evolutionists also claim there was a ‘Stone Age’ of about 100,000 years when between one million and 10 million people lived on Earth. Fossil evidence shows that people buried their dead, often with artefacts—cremation was not practised until relatively recent times (in evolutionary thinking). If there were just one million people alive during that time, with an average generation time of 25 years, they should have buried 4 billion bodies, and many artefacts. If there were 10 million people, it would mean 40 billion bodies buried in the earth. If the evolutionary timescale were correct, then we would expect the skeletons of the buried bodies to be largely still present after 100,000 years, because many ordinary bones claimed to be much older have been found. However, even if the bodies had disintegrated, lots of artefacts should still be found.


#40 Proponents of evolution claim that just because it looks like we were designed that does not mean that we actually were.  They often speak of the “illusion of design”, but that is kind of like saying that it is an “illusion” that a 747 airplane or an Apple iPhone were designed.  And of course the human body is far more complex that a 747 or an iPhone.
#41 If you want to be part of the “scientific community” today, you must accept the theory of evolution no matter how absurd it may seem to you.  Richard Lewontin of Harvard once made the following comment regarding this harsh reality…
We take the side of science in spite of the patent absurdity of some of its constructs, . . . in spite of the tolerance of the scientific community for unsubstantiated commitment to materialism. . . . we are forced by our a priori adherence to material causes to create an apparatus of investigation and set of concepts that produce material explanations, no matter how counterintuitive, no matter how mystifying to the uninitiated. Moreover, that materialism is absolute, for we cannot allow a Divine Foot in the door.


#42 Time Magazine once made the following statement about the lack of evidence for the theory of evolution…
“Yet despite more than a century of digging, the fossil record remains maddeningly sparse. With so few clues, even a single bone that doesn’t fit into the picture can upset everything. Virtually every major discovery has put deep cracks in the conventional wisdom and forced scientists to concoct new theories, amid furious debate.”


#43 Malcolm Muggeridge, the world famous journalist and philosopher, once made the following statement about the absurdity of the theory of evolution…
“I myself am convinced that the theory of evolution, especially the extent to which it’s been applied, will be one of the great jokes in the history books of the future. Posterity will marvel that so very flimsy and dubious an hypothesis could be accepted with the incredible credulity that it has.”


#44 In order to believe the theory of evolution, you must have enough blind faith to believe that life just popped into existence from nonlife, and that such life just happened to have the ability to take in the nourishment it needed, to expel waste, and to reproduce itself, all the while having everything it needed to survive in the environment in which it suddenly found itself. Do you have that much blind faith?
For years, I have been looking for someone that can explain to me the very best evidence for the theory of evolution in a systematic way.  My challenge has been for someone to lay out for me a basic outline of the facts that “prove” that evolution is true.

1) http://thetruthwins.com/archives/44-reasons-why-evolution-is-just-a-fairy-tale-for-adults

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An Essential Prediction of Darwinian Theory Is Falsified by Information Degradation








Editor's note: We are delighted to welcome Kirk Durston as a new contributor. Dr. Durston is a scientist, philosopher, and clergyman with a PhD in Biophysics, an MA in Philosophy, a BSc in Mechanical Engineering, and a BSc in Physics.
I was struck, but not surprised, by a statement made recently by Neil Turok, Director of the Perimeter Institute for Theoretical Physics here in Waterloo, Ontario. Speaking of the apparent collapse of evidence for a critical component of the Big Bang theory, he responded, "Even though hundreds or thousands of people are working on an idea, it may still be wrong."
His statement is a harbinger of a much greater collapse looming on the scientific horizon, also involving thousands of scientists. There is mounting evidence that most, if not all the key predictions of the neo-Darwinian theory of macroevolution are being falsified by advances in science. Here, I will look at a fundamental prediction that Darwinism makes regarding the increase of genetic information.
Computer information is digitally encoded using just two symbols ("1" and "0"). We now know that the instructions for the full diversity of life are digitally encoded in the DNA of all living things using a four-symbol alphabet. In more technical terms, this is referred to as functional information.
In the neo-Darwinian scenario for the origin and diversity of life, the digital functional information for life would have had to begin at zero, increase over time to eventually encode the first simple life form, and continue to increase via natural processes to encode the digital information for the full diversity of life.
An essential, falsifiable prediction of Darwinian theory, therefore, is that functional information must, on average, increase over time.
Interestingly, a prediction of intelligent design science is quite the opposite. Since information always degrades over time for any storage media and replication system, intelligent design science postulates that the digital information of life was initially downloaded into the genomes of life. It predicts that, on average, genetic information is steadily being corrupted by natural processes. The beauty of these two mutually incompatible predictions in science is that the falsification of one entails verification of the other. So which prediction does science falsify, and which does science verify?
Ask computer programmers what effect ongoing random changes in the code would have on the integrity of a program, and they will universally agree that it degrades the software. This is the first problem for neo-Darwinian theory. Mutations produce random changes in the digital information of life. It is generally agreed that the rate of deleterious mutations is much greater than the rate of beneficial mutations. My own work with 35 protein families suggests that the rate of destruction is, at minimum, 8 times the rate of neutral or beneficial mutations.
Simply put, the digital information of life is being destroyed much faster than it can be repaired or improved. New functions may evolve, but the overall loss of functional information in other areas of the genome will, on average, be significantly greater. The net result is that the digital information of life is running down.
The second series of falsifying observations is indicated by actual organisms we have studied most closely. First, the digital information for the bacterial world is slowly eroding away due to a net deletional bias in mutations involving insertions and deletions. A second example is the fruit fly, one of the most studied life forms in evolutionary biology. It, too, shows an ongoing, genome-wide loss of DNA across the entire genus.
Finally, humans are not exempt. As biologist Michael Lynch points out in a paper inPNAS, "Rate, molecular spectrum, and consequences of human mutation":


[A] consideration of the long-term consequences of current human behaviour for deleterious-mutation accumulation leads to the conclusion that a substantial reduction in human fitness can be expected over the next few centuries in industrialized societies unless novel means of genetic intervention are developed.
We continue to discover more examples of DNA loss, suggesting that the biological world is slowly running down. Microevolution is good at fine-tuning existing forms within their information limits and occasionally getting something right, but the steady accumulation of deleterious mutations on the larger scale suggests that mutation-driven evolution is actually destroying biological life, not creating it.
This is hardly a surprise, as every other area of science, except for evolutionary biology, grants that natural processes degrade information, regardless of the storage media and copying process. For neo-Darwinian macroevolution to work, it requires something that is in flat-out contradiction to the real world.

1) http://www.evolutionnews.org/2015/07/an_essential_pr097521.html

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Neo-Darwinism, the Modern Synthesis and selfish genes: are they of use in physiology? 2

Darwin himself was not so sure; in the first edition of The Origin of Species (Darwin, 1859) he wrote ‘I am convinced that natural selection has been the main, but not the exclusive means of modification’, a statement he reiterated with increased force in the 1872, 6th edition. As many evolutionary biologists now acknowledge, the Modern Synthesis (neo-Darwinism) requires extending (Jablonka & Lamb, 2005; Pigliucci & Muller, 2010b).

Neo-Darwinism falsified 1

Evolutionary theory itself is already in a state of flux…

all the central assumptions of the Modern Synthesis (often also called Neo-Darwinism) have been disproven

Denis Noble
Physiology is rocking the foundations of evolutionary biology
Nice to hear the truth for a change. The paper drew on the work of James Shapiro (who by the way had co-authored a paper with Discovery Institute Fellow, Richard Sternberg here).

Jerry Coyne has a dislike of Shapiro’s writings:

I hate to give attention to my Chicago colleague James Shapiro’s bizarre ideas about evolution, which he publishes weekly on HuffPo rather than in peer-reviewed journals. His Big Idea is that natural selection has not only been overemphasized in evolution, but appears to play very little role at all. Even though he’s spreading nonsense in a widely-read place, I don’t go after him very often, for he just uses my criticisms as the basis of yet another abstruse and incoherent post. Like the creationists whose ideas he appropriates, he resembles those toy rubber clowns that are impossible to knock down…..

His never-ending attacks on natural selection and neo-Darwinian evolution should be an embarrassment to HuffPo, which will apparently publish anything since they don’t have to pay for it; but they’re also an embarrassment to me, for Shapiro works at my university and, in my view, his writings impugn our reputation for excellence in evolutionary biology.

So again, I tender my challenge: tell us, Dr. Shapiro: you’re always banging on about new sources of genetic variation, but you never seem quite able to tell us how that variation is translated into adaptive evolution. If it’s not natural selection, what is it?

Jerry Coyne James Shapiro goes after natural selection again (twice) on HuffPo
Coyne thinks Shapiro has appropriated creationist ideas. Shapiro’s ideas are referenced in the above peer-reviewed article. I’d say that’s progress.

Coyne laments elsewhere of the battle between molecular biologists and evolutionary biologists:

Virtually all of the non-creationist opposition to the modern theory of evolution, and all of the minimal approbation of Shapiro’s views, come from molecular biologists. I’m not sure whether there’s something about that discipline (the complexity of molecular mechanisms?) that makes people doubt the efficacy of natural selection, or whether it’s simply that many molecular biologists don’t get a good grounding in evolutionary biology.
Coyne laments molecular biologists haven’t been sufficiently indoctrinated with evolutionary biology. Paul Nelson once observed:

molecular biology graduate students (for instance) don’t know much, or any, evolutionary theory… Students don’t see the point of storytelling. They could take a Fiction Writing course for that.

Paul Nelson
It was nice to see Coyne’s name not mentioned in this article, and the only mention of Richard Dawkins was in reference to Dawkins mistakes.

1) http://www.uncommondescent.com/darwinism/peer-reviewed-paper-neo-darwinism-falsified/
2) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3060581/

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