Blindness in Cave Fish is Due to Epigenetics

Evolutionists Say “We See”

A recent paper out of Brant Weinstein’s and William Jeffery’s laboratories on eye development, or the lack thereof, in blind cave fish has important implications for evolutionary theory (paper discussed here). The study finds that the loss of eyes in fish living in dark Mexican caves is not due to genetic mutations, as evolutionists have vigorously argued for many years, but due to genetic regulation. Specifically, methylation of key development genes represses their expression and with it eye development in this venerable icon of evolution. But the finding is causing yet more problems for evolutionary theory.

Darwin appealed to the blind cave fish in his one long argument for evolution. It is a curious argument in many ways, and the first sign of problems was in Darwin’s presentation where he flipped between two different explanations. At one point he explained the loss of vision in the cave fish as an example of evolutionary change not due to his key mechanism, natural selection. Instead, the Sage of Kent resorted to using the Lamarckian mechanism or law of “use and disuse.” Privately Darwin despised and harshly criticized Lamarck, but when needed he occasionally employed his French forerunner’s ideas.

Elsewhere Darwin hit upon a natural selection-based mechanism for the blind cave fish, explaining that elimination of the costly and unneeded vision system would surely raise the fitness of the hapless creatures.

This latter explanation would become a staple amongst latter day evolutionary apologists, convinced that it mandates the fact of evolution. Anyone who has discussed or debated evolutionary theory with today’s Epicureans has likely encountered this curious argument that because blind cave fish lost their eyes, therefore the world must have arisen by itself.

Huh?

To understand the evolutionary logic, or lack thereof, one must understand the history of ideas, and in particular the idea of fixity, or immutability, of species. According to evolutionists, species are either absolutely fixed in their designs, or otherwise there are no limits to their evolutionary changes and the biological world, and everything else for that matter, spontaneously originated.

Any evidence, for any kind of change, no matter how minor, is immediately yet another proof text for evolution, in all that the word implies.

Of course, from a scientific perspective, the evidence provides precisely zero evidence for evolution. Evolution requires the spontaneous (i.e., by natural processes without external input) creation of an unending parade of profound designs. The cave fish evidence shows the removal, not creation, of such a design.

The celebration of such evidence and argument by Darwin and his disciples reveals more about evolutionists than evolution. That they would find this argument persuasive reveals their underlying metaphysics and the heavy lifting it performs. It is all about religion.

We are reminded of all this with the news of Weinstein’s new study. But we also see something new: The insertion, yet again, of Lamarck into the story. The irony is that the epigenetics, now revealed as the cause of repressed eye development in the cave fish, hearkens back to Lamarck.

Darwin despised Lamarck and later evolutionists made him the third rail in biology. Likewise they have pushed back hard against the scientific findings of epigenetics and their implications.

The environment must not drive biological change.

False.

Well such biological change must not be transgenerational.

False.

Well such inheritance must not be long lasting, or otherwise robust.

False again.

This last failure is revealed yet again in the new blind cave fish findings.

False predictions count. A theory that is repeatedly wrong, over and over, in all of its fundamental expectations, will eventually be seen for what it is.

The rise of epigenetics is yet another such major failure. Evolutionists pushed back against it because it makes no sense on the theory, and that means it cannot now be easily accommodated.

One problem is that epigenetics is complex. The levels of coordination and intricacy of mechanism are far beyond evolution’s meager resources.

It’s not going to happen.

Another problem is the implied serendipity. For instance, one epigenetic mechanism involves the molecular tags places on the tails of the DNA packing proteins called histones. While barcoding often seems to be an apt metaphor for epigenetics, the tagging of histone tails can influence the histone three dimensional structures. It is not merely an information-bearing barcode. Like the tiny rudder causing the huge ship to change course, the tiny molecular tag can cause the much larger packing proteins to undergo conformational change, resulting in important changes in gene accessibility and expression.

This is all possible because of the special, peculiar, structure and properties of the histone protein and its interaction with DNA. With evolution we must believe this just happened to evolve for no reason, and thus fortuitously enabled the rise of epigenetics.

Another problem with epigenetics is that it is worthless, in evolutionary terms that is. The various mechanisms that sense environmental shifts and challenges, attach or remove one of the many different molecular tags to one of the many different DNA or histone locations, propagate these messages across generations, and so forth, do not produce the much needed fitness gain upon which natural selection operates.

The incredible epigenetics mechanisms are helpful only at some yet to be announced future epoch when the associated environmental challenge presents itself. In the meantime, selection is powerless and according to evolution the incredible system of epigenetics, that somehow just happened to arise from a long, long series or random mutations, would wither away with evolution none the wiser.

These are the general problems with epigenetics. In the case of the blind cave fish, however, there is possible explanation. It is a longshot, but since this case specifically involves the loss of a stage of the embryonic development, evolutionists can say that genetic mutations caused changes in the methylating proteins, causing them to be overactive.

This explanation relies on the preexistence of the various epigenetic mechanisms, so does not help to resolve the question of how they could have evolved. What the explanation does provide is a way for evolutionists to dodge the bullet presented by the specter of the cave fish intelligently responding to an environmental shift.

Such teleology in the natural world is not allowed.

So the evolutionary prediction is that these proteins will be found to have particular random changes causing an increase in their methylation function, in particular at key locations in key genes (i.e., the genes associated eye development).

That’s a long shot, and an incredible violation of Occam’s Razor.

My predictions are that (i) this evolutionary prediction will fail just as the hundreds that came before, and (ii) as with those earlier failures, this failure will do nothing to open the evolutionist’s eyes.

Religion drives science, and it matters.

New Study: Transgenerational Epigenetics Can Have a Profound Impact

The Third Rail of Evolution

In the spring of 2006 I gave a talk on the campus of Cornell University and afterwards was joined by then Cornell professors Richard Harrison and Kern Reeve for a sort of panel discussion or debate about biological evidences and origins. I presented a dozen or so interesting and important evidences that I felt needed to be recognized in any discussion of origins. The evidences falsified key predictions of evolution and so needed to be acknowledged and reckoned with, one way or another. One of the items on my list was the so-called directed adaptation mechanisms which, broadly construed, can include everything from non random, directed, mutations to transgenerational epigenetic inheritance. But I was in for a big surprise when Harrison and Reeve gave their response.

Directed adaptation is reminiscent of Lamarckism. Rather than natural selection acting over long time periods on biological variation which is random with respect to need, directed adaptation mechanisms provide rapid biological change in response to environmental challenges. Like physiological responses, directed adaptation can help an organism adjust to shifts in the environment. But those adaptations can then be inherited by later generations. Stresses which your grandparents were subjected to may be playing out in your own cells.

In the twentieth century evolutionists had strongly rejected any such capability. Lamarckism was the third rail in evolutionary circles. And for good reason, for it would falsify evolutionary theory. But empirical evidence had long since pointed toward the unthinkable, and by the twenty first century the evidence was rapidly mounting.

While there was of course still much to learn in 2006 about directed adaptation (as there still is today for that matter), it could no longer be denied, and needed to be addressed. At least, that is what I thought.

I was shocked when Harrison and Reeve flatly denied the whole story. Rick waved it off as nothing more than some overblown and essentially discredited work done by Barry Hall and John Cairns, back in the 1970s and 80s (for example here).

But there was a body of work that had gone far beyond the work of Hall and Cairns. Incredulously I responded that entire books had been written on the subject. Rick was quick to respond that “entire books are written about all kinds of discredited things.”

True enough. It was me versus two professors on their home turf with a sympathetic audience, and there was no way that I was going to disabuse them of what they were convinced of.

Confirmation testing and theory-laden evidence are not merely philosophical notions. They are very real problems. I’m reminded of all this every time a new study adds yet more confirmation to the directed adaptation story, such as the recent paper out of Nicola Iovino’s lab on transgenerational epigenetic inheritance in house flies, which states:

Gametes carry parental genetic material to the next generation. Stress-induced epigenetic changes in the germ line can be inherited and can have a profound impact on offspring development.

The press release gives little indication of the controversy as it admits that these findings were once considered impossible:

It has long been thought that these epigenetic modifications never cross the border of generations. Scientists assumed that epigenetic memory accumulated throughout life is entirely cleared during the development of sperms and egg cells.

It is hard enough to see how organisms can respond intra-lifetime to environmental challenges, but how can it be inherited as well? For epigenetic changes that occur in somatic cells, that information must also enter into the germ line as well. Somehow it must be incorporated into the sperm and/or egg cells.

It is an enormous problem to explain how such capabilities evolved. Not only are a large number of mutations required to make this capability work, it would not be selected for until the particular environmental condition occurred. That means that, under evolution, it would be not preserved, even if it could somehow arise by chance.

Evolutionist: Evolution Is Happening Faster Than We Thought

Not

The fact that we can travel at speeds of hundreds and even thousands of miles per hour does not mean we can go faster than light. We can fly to the Moon in a matter of days, but the propulsion technology that allows us to do that is not scalable to travelling faster than 186,000 miles per second. A fundamentally different technology is required. The creators of Star Trek understood that, and so they created the concept of warp drive, a faster-than-light propulsion technology, fundamentally different from today’s technology. One would have to be very ignorant to confuse the two, but this is precisely what evolutionists do when they cast biological adaptation as confirmatory evidence of evolution. Adaptation and evolution are two very different things.

Biological adaptation relies on the preexistence of populations, organisms, genetics, DNA, genes, alleles, proteins, massive molecular machines, inheritance, cellular and molecular mechanisms such as horizontal gene transfer and epigenetics, directed mutations, and so forth.

Evolution, on the other hand, is a theory that attempts to explain the origin of all those things.

Observations of the former are not evidence of the latter. That is backwards. It also would also introduce enormous serendipity. For it would mean that evolution created the very structures and mechanisms required for, drumroll, evolution.

Evolution, in other words, created itself.

And even if we were to go along with this ridiculous idea, the resulting biological adaptation is not capable of generating evolutionary change. Adaptation does small things, evolution requires big things.

Even evolutionists, in their honest moments, have understood this. Macroevolution is more than repeated rounds of microevolution. As one evolutionist admitted, “the rate of random DNA sequence mutation turns out to be too slow to explain many of the changes observed.” His point, which is not new and has been known for a long time, is not that adaptation cannot occur, but that the idea of mutations (which can fuel adaptation) adding up to result in novel, large-scale evolutionary change doesn’t work.

Adaptation and evolution are fundamentally different “technologies.”

You can’t travel faster than the speed of light by combining liquid hydrogen and liquid oxygen, and you can’t create novel, complex, biological structures via adaptation mechanisms.

This is why evolutionary biologist Menno Schilthuizen’s article from last year in the Sunday Review is of concern. The article is entitled: “Evolution Is Happening Faster Than We Thought,” and it is all about various adaptations observed in city-dwelling species. Unfortunately, Schilthuizen presents those examples of adaptation as examples of evolution, and proof that, amazingly enough, evolution happens orders of magnitude faster than we once thought:

For a long time, biologists thought evolution was a very, very slow process, too tardy to be observed in a human lifetime. But recently, we have come to understand that evolution can happen very quickly

Evolution’s deep time requirement was particularly evident when William Thomson (later Lord Kelvin), only a few years after Darwin had published his book on evolution, argued that the earth could be no older than 100 million years. Thomson later revised that figure downward to as little as 20-40 million years.

This short time window was an enormous problem for evolution. As Darwin wrote, “Thomson’s views of the recent age of the world, have been for some time one of my sorest troubles.” As Darwin’s friend Thomas Huxley explained, “Biology takes its time from Geology.”

Lord Kelvin’s estimate was eventually dropped, but this example illustrates how important deep time was, both to nineteenth and twentieth century evolutionists. And therefore, the rapid evolution that is now commonly celebrated by evolutionists such as Schilthuizen represents an enormous falsification of a major, fundamental, prediction of evolutionary theory.

It also represents terribly flawed thinking. Adaptation is not evolution.

Desert Mice Fur Changes Color to Match the Terrain

An Example of Evolution in Every Detail?

About fifteen years ago researchers discovered genetic differences that probably explain the different fur coloring in desert mice populations in New Mexico and Arizona (see papers here and here). Mice populations living on light colored terrain tend to have light colored fur, and those on dark colored terrain tend to have dark colored fur. Blending in with the terrain helps to camouflage the mice, protecting them from predators. And that is, apparently, exactly what the mice did about a thousand years ago when desert lava flows produced the darkened terrain. But that is where the science is overtaken by the dogma. Evolutionists have misappropriated this research work, casting it as a textbook example of evolution, and creating a highly produced video (see above) used to indoctrinate students.

The first problem in casting the dark colored mice as an example of evolution is that their genetic differences are not known to be the result of random mutations. For evolutionists there simply is no question that the genetic differences that are thought to cause the dark fur color arose from random mutations.

Now that may be correct. But it may not be. We simply do not know.

This is not merely a technical objection—in spite of evolutionary theory which called for random mutations to be the source of change, in recent decades directed mutations have been found to be at work in an ever increasing number of cases. For many years evolutionists have ignored and even resisted these findings. Too often I have debated evolutionists who, when I point to this evidence, simply deny it.

So while the genetic differences in those dark mice may well be the result of random mutations, evolutionists do not even give this a second thought. They simply assume from the start, and inform their audience in no uncertain terms, that random mutations are the cause.

This is an example of what philosophers refer to as a “theory-laden observation.” Science can get into trouble when the measurements and observations themselves, rather than being theory-neutral and independent of the theories which explain them, are in fact intertwined with those theories.

This can become circular very quickly, and this desert mouse case is a good example of that. Evolutionists assume the genetic differences arose from random mutations, and then claim the evidence as a powerful confirmation of evolution.

The second problem in casting the dark colored mice as an example of evolution is that the dark coloration may be the result of multiple genetic changes. In one case, four mutations are identified, all of which perhaps are required to bring about the coloration change.

It very well could be that only a lone, single mutation is required. But that is not known.

And if multiple genetic changes are required, then this quickly transitions from an example of what random mutations can do to an example of what random mutations cannot do. If four mutations are required, then we’ve just found yet another hard failure of evolution. But again, the evolutionists give no hint of this interesting question. If everyone had their “burning curiosity,” (as Clarence Darrow put it) then science would have long since come to an end.

The third problem in casting the dark colored mice as an example of evolution is that the coloration is too precise. The dark colored fur appears on the top of the mice, but not their underbelly. This makes sense since the topside is mainly what is exposed to predators. But in the evolution narrative, there is no fitness advantage to such precision. Darkening the entire mouse would, apparently, work just as well.

Small scale adaptation

Everything we’ve talked about so far is an unknown. Evolutionists are proclaiming a slam dunk, case closed, example when in fact there are many unknowns. Some of them could demolish the evolution narrative altogether.

But there is one big known we haven’t yet mentioned. It is that none of this amounts to evolution in the first place. It would be a deceptive equivocation to label fur coloration change via a few mutations as “evolution” when, in fact, this is nothing more than small scale adaptation.

In their “honest moments,” as Stephen J. Gould once put it, even evolutionists admit that random mutation isn’t enough, and that adaptation mechanisms are not enough, to explain the kind of large scale change evolution requires.

Mice changing fur color does not demonstrate how metabolism, the central nervous system, bones, red blood cells, or any other biological wonder could have arisen by evolution’s random mutations coupled with natural selection.

This is an old myth evolutionists have exploited ever since Darwin. Demonstrate biological change, any biological change no matter how trivial, and claim victory. Evolutionist Steve Jones once claimed that the changes observed in viruses contain Darwin’s “entire argument.” That is a gross equivocation and misrepresentation of the science, designed to mislead audiences.

It is a pathetic canard which evolutionists continue to rely on. In the above video, Sean Carroll states that thanks to these mice, “science has an example of evolution, crystal clear, in every detail.” [6:42-48]

It would be difficult to imagine a more absurd misrepresentation. Mice changing color is not a crystal clear “example of evolution … in every detail.” Not even close. Carroll should be ashamed of himself.

Religion drives science, and it matters.

Here is Why Steven Novella is Wrong About That Harvard Experiment

Going Nowhere Fast

Steven Novella, neurologist at Yale University School of Medicine, has commented on a recent Harvard University experiment for visualizing bacterial adaptation to antibiotics. The Harvard researchers constructed a giant petri dish with spatially-varying antibiotics to watch how bacteria adapt over time and space (the researchers came up with a great name for the experiment: The microbial evolution and growth arena [MEGA]–plate). And adapt they did. Those adaptations, however, were instantly claimed as an example of evolution in action. The researchers wrote that the “MEGA-plate provides a versatile platform for studying microbial adaption and directly visualizing evolutionary dynamics.” And the press release informed the public that the experiment provided “A powerful, unvarnished visualization of bacterial movement, death, and survival; evolution at work, visible to the naked eye.” Likewise, Novella called it “a nice demonstration of evolution at work in a limited context.” There’s only one problem: The experiment did not demonstrate evolution, it falsified evolution.

First off, Novella deserves some credit for acknowledging at least some limitations in the experiment’s results:

Of course, this one piece of evidence does not “prove” something as complex and far ranging as the evolution of life on Earth.

Novella also deserves credit for acknowledging that evolutionary change that requires a few mutations, rather than merely one, is a big problem. Novella has solutions which he believes resolve this problem (as we shall see below), but at least he acknowledges what too often is conveniently ignored.

What Novella does not acknowledge, however, is that bacteria adaptation research, over several decades now, has clearly shown non evolutionary change. For instance, bacterial adaptation has often been found to be rapid, and sensitive to the environmental challenge. In other words, when we look at the details, we do not find the evolutionary model of random variation slowly bringing about change, but rather environmentally directed or influenced variation.

That is not evolution.

And indeed, the Harvard experiment demonstrated, again, very rapid adaptation. In just 10 days the bacteria adapted to high doses of lethal antibiotic. As one of the researchers commented, “This is a stunning demonstration of how quickly microbes evolve.”

True, it is “stunning,” but “evolve” is not the correct term.

The microbes adapted.

The ability of organisms to adapt rapidly falls under the category of epigenetics, a term that encompasses a range of sophisticated mechanisms which promote adaptation which is sensitive to the environment. Given our knowledge of bacterial epigenetics, and how fast the bacteria responded in the Harvard experiment, it certainly is reasonable to think that epigenetics, of some sort, may have been at work.

Such epigenetic change is not a new facet of evolution, it contradicts evolution. Not only would such complex adaptation mechanisms be difficult to evolve via random mutations, they wouldn’t provide fitness improvement, and so would not be selected for, even if they did somehow arise from mutations.

Epigenetic mechanisms respond to future, unforeseen conditions. Their very existence contradicts evolution. So the Harvard experiment, rather than demonstrating evolution in action, is probably yet another example of epigenetic-based adaptation. If so, it would contradict evolution.

Another problem, that Michael Behe has pointed out, is that it appears that most of the mutations that occurred in the experiment served to shutdown genes. In other words, the mutations broke things, they did not build things. This is another way to see that this does not fit the evolutionary model. It’s devolution, not evolution. Novella begs to differ, and says Behe has made a big mistake:

Behe is wrong because there is no such thing as “devolution.” Evolution is simply heritable change, any change, and that change can create more complexity or more simplicity. Further, altering a protein does not “degrade” it – that notion is based on the false premise that there is a “correct” sequence of amino acids in any particular protein. Evolution just makes proteins different. Proteins perform “better” or “worse” only in so much that they contribute to the survival and reproduction of the individual. If it is better for the survival of the organism for an enzyme to be slower, then the slower enzyme is better for that organism.

First, Novella ignores the fact that many of the mutations introduced stop codons, and so did not merely slow an enzyme but rather shut it down altogether.

Secondly, it is not Behe here who is making the mistake, it is Novella. He says “Evolution is simply heritable change …”

But this is an equivocation.

On the one hand, evolutionists want to say that shutting down or slowing a gene is “evolution,” but on the other hand, evolutionists say that a fish turning into a giraffe is “evolution.”

Unfortunately evolutionists routinely make this equivocation. This is because they don’t think of it as an equivocation. In their adherence and promotion of the theory, the distinction is lost on them. All change just smears together in one big long process called evolution. You can see other examples of this here and here.

So the comments, press releases, and articles send a misleading message. Readers are told that the researchers have seen “evolution in action.” The message is clear: This is evolution, the evolution. But it isn’t. There is nothing in these findings that show us how a fish turns into a giraffe.

Multiple mutations

As mentioned above, Novella also believes that evolution coming up with designs requiring multiple mutations is not a problem. Novella’s reasoning is that while this would be a problem if most mutations are harmful, they aren’t. Most mutations are neutral, so evolutionary drift can introduce the many needed mutations, and once the set of required mutations are in place, then you have the new design.

This is a profound misunderstanding of the problem evolution faces. You can’t evolve a protein, for example, with drift. That most mutations are neutral does not suddenly resolve the curse of dimensionality and resolve this astronomical search problem. There just is no free lunch.

Similarly, Novella makes yet another profound mistake involving what he calls “the lottery fallacy.”

The first is basically the lottery fallacy – considering the odds of John Smith winning the lottery by chance alone and concluding it could not have happened by chance. Rather, you should consider the odds that anyone would win the lottery. This is actually pretty good. Behe looks at life on Earth and asks – what are the odds that this specific pathway or protein or whatever evolved by chance alone. He is failing to consider that there may have been billions of possible solutions or pathways down which that creature’s ancestors could have evolved. Species that failed to adapt either migrated to an environment in which they could survive, or they went extinct. In other words, Behe should not be asking what the odds are that this bit of complexity evolved, but rather what are the odds that any complexity evolved. It is difficult to know the number of potential complexities that never evolved – that number may dwarf the odds of any one bit evolving. Right there Behe’s entire premise is demolished …

This is a terribly flawed argument for several reasons. First, life needs proteins. All life that we know of needs proteins.

Thousands of proteins.

Yet proteins are far beyond evolution’s reach. It is true, per Novella’s point, that there are a whole lot of ways to make a given protein. There are many, many different amino acid sequences that give you a globin. But “many, many” is like a grain of sand compared to the astronomical amino acid sequence search space.

There just is no free lunch.

But Novella goes further than this, and this brings us to the second flaw. Novella is not merely arguing there are many different ways to construct life as we know it. He is pointing out that there are, or at least there could be, a whole bunch of different ways to make life, in the first place.

If you take them all together, you could have a pretty big set of possibilities. Perhaps it is astronomical. So what we got in this world—the life forms we observe, are not point designs in an otherwise lifeless design space. Rather, the design space could be chocked full of life forms. And hence, the evolution of life becomes likely, and “Right there Behe’s entire premise is demolished.”

What Novella is arguing for here is unobservable. He is going far beyond science, into an imaginary philosophical world of maybe’s.

Not only is Novella clearly appealing to the unobservable, but even that doesn’t work. At least for any common sense approach. There is no question that the design space is full of useless blobs of chemicals that do nothing. A speculative claim? No, that is what this thing called science has made abundantly clear to us. Even the simple case of a single protein reveals this. Only a relatively few mutations to most proteins rob them of their function. Protein function is known to dramatically reduce as different amino acids are swapped in.

Of course this is all obvious to anyone who understands how things work. Sure, Novella may be right that there are other, unknown, solutions to life. But that isn’t suddenly going to resolve evolution’s astronomical search problem. That problem was never contingent on the life we observe being the only possible life forms possible

Novella calls himself a skeptic. In fact, he is exactly the opposite.

Michael Skinner on Epigenetics: Stage Three Alert

Over the Top Lies

Readers here will know that Darwin’s God has covered the topic of epigenetics extensively for many years now, and so we were interested to read Michael Skinner’s Aeon article on this subject, which appeared last week. Skinner’s piece reminds us of the old maxim that truth passes through three stages. First, it is ridiculed. Second, it is violently opposed. Third, it is accepted as being self-evident. If we can slightly modify these three stages as follows, then we have the history of how evolution has struggled and opposed the scientific findings we now refer to as epigenetics:

1. Reject and persecute
2. Delegitimize and minimize
3. Rename and incorporate

Skinner’s position represents the move, which has been taking place in recent years, into Stage 3 (for example, see here).

Skinner’s Aeon article provides an excellent rundown of findings, both old and new, that confirm and elucidate what evolutionists have aggressively and violently opposed for a century: that epigenetics is not only real, but significant in causing long-term biological change. Natural selection plays no role in this process.

From 18th century observations of plants adapting to hotter temperatures, to Conrad Waddington fruit fly experiments in the 1950s (for more tidbits see here), to more recent observations of a range of species, Skinner provides an accessible summary and makes the inescapable conclusion:

Much as Lamarck suggested, changes in the environment literally alter our biology. And even in the absence of continued exposure, the altered biology, expressed as traits or in the form of disease, is transmitted from one generation to the next.

Much as Lamarck suggested? That is an astonishing admission given how evolutionists have, in the past century, vilified Lamarck and anyone who would dare associate with his ideas. And to this day such resistance continues, but it is waning. Hence evolutionists such as Skinner can broach the truth.

Skinner also comes clean on the problem that evolution’s basic source of biological variation, DNA mutations, is insufficient:

the rate of random DNA sequence mutation turns out to be too slow to explain many of the changes observed. Scientists, well-aware of the issue, have proposed a variety of genetic mechanisms to compensate: genetic drift, in which small groups of individuals undergo dramatic genetic change; or epistasis, in which one set of genes suppress another, to name just two. Yet even with such mechanisms in play, genetic mutation rates for complex organisms such as humans are dramatically lower than the frequency of change for a host of traits, from adjustments in metabolism to resistance to disease.

Mutations are too slow for evolution? Again, this is an astonishing admission. The last time mathematicians reported this inconvenient truth they were told by evolutionists that it didn’t matter because, after all, we all know that evolution is true. Nothing like contradicting the science. Skinner admits that a paradigm shift is needed.

Unfortunately for Skinner and his readers that is where the light ends and smoke begins. Qua evolutionist, Skinner must present this contradictory biology as, somehow, consistent with evolution. The first sign that Skinner will firmly plant himself in the Stage Three lie (Rename and incorporate) is the opening sentence:

The unifying theme for much of modern biology is based on Charles Darwin’s theory of evolution, the process of natural selection by which nature selects the fittest, best-adapted organisms to reproduce, multiply and survive.

Evolution is the unifying theme for much of modern biology? This not so secret handshake is such an over-the-top misrepresentation that it hardly seems worthwhile to dignify it with a rebuttal. Given how evolutionists are consistently surprised by biology, one would hope they at least could stop with this lie. But there it is.

Unfortunately it doesn’t stop there. Skinner’s next Big Lie, and the thesis of his article, is that the long rejected epigenetics will now fit conveniently into evolutionary theory. It was all a big misunderstanding and rather than rejecting epigenetics, we should see it as merely another component in the ever increasingly complex theory called evolution.

This is Stage Three: Rename, recast, retool, reimagine, and incorporate the new idol into our modern-day Epicureanism.

With enough massaging and story-telling evolutionists will forget the contradictions and convince themselves, and their fawning audiences, that the fit is perfect and epigenetics is, in fact, yet more proof of evolution.

There’s only one problem. This is all absurd.

What Skinner and the evolutionists won’t tell you is that all of this makes no sense on their theory. With epigenetics the biological variation evolution needs is not natural. It is not the mere consequence of biophysics—radiation, toxins or other mishaps causing DNA mutations. Rather, it is a biological control system.

It is not simple mistakes, but complex mechanisms.

It is not random, but directed.

It is not slow, but rapid.

It is not a single mutation that is selected, but simultaneous changes across the population.

This is not evolution.

And as Skinner inconveniently realizes, such epigenetics are found across a wide range of species. They are widely conserved and, for evolution, this is yet more bad news. It means the incredible epigenetics mechanisms must have, somehow, arisen very early in the history of evolution.

What the evolutionists will never admit is that epigenetics contradicts evolutionary theory. Not only must such incredibly complex mechanisms have evolved early on, and not only must they have arisen from chance mutation events, and so not only must evolution have created evolution, but they would have persisted in spite of any fitness advantage.

The whole idea behind the evolution mythology is that natural selection saves the day by directing the blind, chance mutations. Setting aside the silliness of this idea which we have discussed many times, the problem with epigenetics is that if they were to arise from chance mutations (and “oh what a big if”), they would not increase the organism’s fitness.

Epigenetics mechanisms are helpful at some future, unknown, time when the environmental challenge finally presents itself. They are useless when they initially arise, and so would not be preserved by evolution’s mythical natural selection.

Of course evolutionists will contrive yet more complex, silly, just-so stories about how epigenetics mechanisms arose from pre existing parts used for other purposes (the ridiculous co-adaptation argument), and about how they just happened to provide some other functions so as to improve fitness.

Skinner’s presentation of how to integrate epigenetics with evolution is entirely gratuitous. He has empirical evidence for the former, and religious dogma for the latter. There is no scientific need for the addition of evolution—it is a multiplied entity and is gratuitous. But Skinner needs it.

These are all the usual lies, which will be trotted out as yet more “facts.” Evolutionists must tell these lies. Otherwise they would have to move beyond Stage Three, and admit the science contradicts the theory.

And that is not going to happen. Old scientists don’t change their minds, they just die.

Religion drives science, and it matters.

How Did Birds Get Their Wings? Bacteria May Provide a Clue to the Genomic Basis of Evolutionary Innovation, Say Evolutionists

30 Days of Evolution

That evolution occurred is known to be a fact but how evolution occurred is not known. In particular we are ignorant of how evolutionary innovations arose. Of course biological novelties and innovations arose from a series of random chance events, but it is less than reassuring that we cannot provide more detail. How exactly did the most complex designs spontaneously arise? What mechanisms overcame, over and over, the astronomical entropy barriers, by sheer luck of the draw? As Craig MacLean’s and Andreas Wagner’s, and coworker’s, new PLOS Genetics paper begins, “Novel traits play a key role in evolution, but their origins remain poorly understood.” Could it be that evolution is not actually a fact? No, not according to evolutionists. And this new paper claims to provide the basis for how the seemingly impossible became the mundane.

The paper begins by summarizing the many proposed genetic mechanisms for the evolution of biological innovations:

An evolutionary innovation is a new trait that allows organisms to exploit new ecological opportunities. Some popular examples of innovations include flight, flowers or tetrapod limbs [1,2]. Innovation has been proposed to arise through a wide variety of genetic mechanisms, including: domain shuffling [3], changes in regulation of gene expression [4], gene duplication and subsequent neofunctionalization [5,6], horizontal gene transfer [7,8] or gene fusion [9]. Although innovation is usually phenotypically conspicuous, the underlying genetic basis of innovation is often difficult to discern, because the genetic signature of evolutionary innovation erodes as populations and species diverge through time.

1. Mayr E. Animal Species and Evolution. Cambridge: MA: Harvard University Press; 1963.

2. Pigliucci M. What, if anything, is an evolutionary novelty? Philos Sci. 2008;75: 887–898. Available:http://philpapers.org/rec/PIGWIA

3. Patthy L. Genome evolution and the evolution of exon-shuffling—a review. Gene. 1999;238: 103–14. Available: http://www.ncbi.nlm.nih.gov/pubmed/10570989 pmid:10570989

4. True JR, Carroll SB. Gene co-option in physiological and morphological evolution. Annu Rev Cell Dev Biol. 2002;18: 53–80. doi: 10.1146/annurev.cellbio.18.020402.140619. pmid:12142278

5. Zhang J. Evolution by gene duplication: An update. Trends Ecol Evol. 2003;18: 292–298. doi: 10.1016/S0169-5347(03)00033-8.

6. Bergthorsson U, Andersson DI, Roth JR. Ohno’s dilemma: evolution of new genes under continuous selection. Proc Natl Acad Sci U S A. 2007;104: 17004–9. doi: 10.1073/pnas.0707158104. pmid:17942681

7. Boucher Y, Douady CJ, Papke RT, Walsh DA, Boudreau MER, Nesbø CL, et al. Lateral gene transfer and the origins of prokaryotic groups. Annu Rev Genet. 2003;37: 283–328. doi: 10.1146/annurev.genet.37.050503.084247. pmid:14616063

8. Wiedenbeck J, Cohan FM. Origins of bacterial diversity through horizontal genetic transfer and adaptation to new ecological niches. FEMS Microbiol Rev. 2011;35: 957–976. doi: 10.1111/j.1574-6976.2011.00292.x. pmid:21711367

9. Thomson TM, Lozano JJ, Loukili N, Carrió R, Serras F, Cormand B, et al. Fusion of the human gene for the polyubiquitination coeffector UEV1 with Kua, a newly identified gene. Genome Res. 2000;10: 1743–56. pmid:11076860 doi: 10.1101/gr.gr-1405r

The unspoken problem here is, as usual, serendipity. The various proposed genetic mechanisms for the evolution of biological innovations all suggest an amazing bit of fortuitous luck. For random chance events just happened to create these various complicated structures and mechanisms (such as horizontal gene transfer and protein domains their shuffling) which then produced new evolutionary breakthroughs.

Evolution didn’t know what was coming. Evolution did not plan this out, it did not realize that horizontal gene transfer would lead the way to new biological worlds. The evolution of horizontal gene transfer would require a long sequence of random mutations, many of which would not provide any fitness advantage. And when the construction project was completed, and the first horizontal gene transfer capability was possible, there would be no immediate advantage.

This is because there would have been no genes to transfer. The mechanism works only when it is present in more than one, neighboring, cells. One cell gives, and another cells receives. By definition the mechanism involves multiple cells.

But it doesn’t stop there. Even if the first horizontal gene transfer capability was able to spread across a population, and even if it did provide a fitness advantage to the fortunate citizens, there would not be even a hint of the enormous world of biological innovations that had just been opened.

In other words, what this evolutionary narrative entails is monumental serendipity. Biological structures and mechanisms (horizontal gene transfer in this case, but it is the same story with the other hypotheses listed above) are supposed to have evolved as a consequence of a local, proximate, fitness advantage: a bacteria could now have a gene it didn’t have before.

But it just so happened that the new structures and mechanisms would also, as a free bonus, be just what was needed to produce all manner of biological innovations, far beyond assisting a lowly bacteria increase its fecundity.

This is monumental serendipity.

The science contradicts the theory

Undaunted, the new paper finds that one of the other mechanisms, gene duplication and subsequent neofunctionalization, is a key enabler and pathway to biological innovations.

That conclusion resulted from what otherwise was a fine piece of research work. The experimenters exposed different populations of Pseudomonas aeruginosa, a dangerous infectious bacteria, to 95 new sources of its favorite food: carbon.

The bacteria had to adjust to the new flavors of carbon and they did so with various genetic modifications, including various genetic mutations. In the most challenging cases (where the new carbon sources were most difficult for the bacteria to adjust to), the bacteria often produced mutations in genes involved in transcription and metabolism. And these mutations often occurred in genes where there were multiple copies, so the mutations occurred in one copy while the other copy could continue in its normal duties.

The problem is, these genetic duplicates were preexisting in the P. aeruginosa genome. This is yet another instance of serendipity.

Why? Because preexisting duplicates are not common. Only about 10% of the genes have duplicates lying around, and fortunately, the genes needed for adaptation (involving transcription and metabolism) just happened to have such duplicates.

Now there were a few instances of de novo gene duplication. That is, once the experiment began, and after the P. aeruginosa populations were exposed to the challenging diets, a total of six genes underwent duplication events. But in each and every case, the duplication events occurred repeatedly and independently, in different populations (for each of the 95 different carbon sources, the experimenters ran four parallel trials with independent populations).

This result indicates directed gene duplication. This is because it is highly unlikely that random, chance, gene duplication events just happened hit on the same gene in different populations. Here is an example calculation.

Let’s assume that in the course of the experiment, which ran for 30 days and about 140 generations of P. aeruginosa, some genes may undergo duplication events by chance. Next assume there is a particular gene that needs to be duplicated and modified in order to for P. aeruginosa to adapt to the new food source. (Note that there may be several such genes, but as we shall see that will not affect the conclusion). Given that there are four separate, independent trials, what is the probability that the gene will be duplicated in two or more of those trials?

Let P_dup be the probability that any gene is duplicated in the course of the experiment. For our gene of interest, it may be duplicated in 0, 1, 2, 3, or all 4 of the trials. The binomial distribution describes the probability, P, of each of these outcomes. To answer our question (i.e., What is the probability that the gene will be duplicated in two or more of those trials?) we sum the binomial distribution’s value for N = 2, 3 and 4. In other words, we calculate P(2) + P(3) + P(4).

This will give us the probability of observing what was observed in the experiment (i.e., the duplication events occurred repeatedly and independently, in different populations, in all 6 cases where duplication events were observed).

Well for a reasonable value of P_dup, the probability that any gene is duplicated in the course of the experiment, such as 0.0001, the probability of observing multiple duplications events for any given food source (i.e., P(2) + P(3) + P(4)) is about 60 in one billion, or 6  times 10^-8. Even worse, the probability of observing this in all 6 cases where duplication events were observed is about 5 times 10^-44.

It isn’t going to happen.

Exceptionally high rates of gene duplication, in particular genomic regions of Salmonella typhimurium, in a high growth rate medium, were observed to be about 0.001 and even slightly above 0.01 in rare cases.

If we go all out and set P_dup to an unrealistically high 0.1, our results are still unlikely. The P(2) + P(3) + P(4)) is .05, and the probability of observing this in all 6 cases where duplication events were observed is about 2 times 10^-8.

In order to raise these probabilities to reasonable levels, such that what was observed in the experiment is actually likely to have occurred, we need to raise P_dup to much higher values. For example, for a P_dup of .67 (two-thirds probability), P(2) + P(3) + P(4)) is .89, and the probability of observing this in all 6 cases where duplication events were observed is about .5.

But even this doesn’t work. For if we were to imagine unrealistically high P_dup values of 0.1 or higher, then massive numbers of duplication events would have been observed in the experiments.

But they weren’t.

Once again, the science contradicts the theory. Our a priori assumption that evolution is a fact, and that the P. aeruginosa adaptations to the new food sources were driven by random mutations, did not work. The theory led to astronomically low probabilities of the observed results.

What the observed gene duplications are consistent with is directed gene duplications. Just as mutations have been found to be directed in cases of environmental challenges, it appears that gene duplications may also be directed.

The paper’s premise, that biological innovations such as flowers and wings are analogous to bacteria adapting to new nutrient sources, is fallacious. But setting that aside, the experimental results do not make sense on evolution’s mechanism of random mutations and natural selection. Instead, the results indicate directed adaptation.

Evolution Arguments Are Not Holding Water

Absurd and Pathetic

Being an evolutionist means never having to say you’re sorry. Just look at Richard Dawkins who will say pretty much anything at any time, no matter how much it contradicts science or just plain logic. If he ever gets into trouble he can always lapse back into a rant about those creationist rascals and the audience will automatically erupt with applause. And so arguing evolution with an evolutionist is a lot like the Monty Python argument skit. They will pull out all manner of canards, misdirections, and fallacies, depending on their mood at the moment. One common example is the use of normal science as confirmatory evidence.

As Thomas Kuhn pointed out, science sometimes operates in paradigms. Scientific research on a particular problem can embrace a type of solution, or paradigm. The research tries to elaborate on and refine the paradigm, but otherwise does not question the paradigm. Paradigms provide a stable framework, within which concepts and terminology can be developed to support scientific thinking.

But because the paradigm is taken for granted and assumed from the start, the research conclusions do not generally confirm or prove the paradigm. The research work develops and critically examines concepts within the paradigm, but not the paradigm itself. Kuhn called the research work done with a paradigm normal science.

Evolutionary theory very much works this way. Normal science, within the evolution paradigm, takes it for granted that the world evolved—that everything arose from strictly naturalistic, chance events. That is, that the world arose spontaneously. Therefore in evolutionary research, the evidence is interpreted according to evolution. You could say the evidence is theory-laden.

A typical evolutionary research study goes as follows: Given that X evolved, here is how X probably evolved. All of this is at odds with the empirical evidence, and so the results inevitably lack all kinds of detail normally required in science, and include all kinds of improbable events normally unacceptable in science. It is a kind of storytelling underwritten by the paradigm.

This evolutionary normal science formula has produced a tremendous volume of literature, ranging from journal papers to popular works. And, one of the favorite lines of argumentation, when evolution is rightly questioned, is to point to this “mountain” of evidence. A simple internet search can usually be counted on to produce dozens of papers advertising “The Evolution of Echolocation in Bats” or whatever wonder the skeptic has in mind as problematic for evolution.

Of course, if anyone were ever actually to read the produced papers (and usually the evolutionist presenting the paper has not), that person would find a marked absence of any actual scientific description of how echolocation, or whatever, actually did, in fact, evolve.

Normal science is used inappropriately as confirmatory evidence. When we explained, for example, that epigenetics in plants contradicts evolution, an evolutionist caustically responded with a paper subtitled: “The Evolution of a Complex Epigenetic Pathway in Flowering Plants.”

And did that paper actually explain “The Evolution of a Complex Epigenetic Pathway in Flowering Plants”?

No. The paper presupposed “The Evolution of a Complex Epigenetic Pathway in Flowering Plants.” As we explained, the paper presents several dubious “findings” of how epigenetics evolved which, in fact, are not supported by the science and instead are completely beholden to the assumption that evolution is true.

The paper’s highly unlikely scenarios of how evolution occurred are underwritten and mandated by the a priori assumption that (drumroll), evolution occurred.

And when we pointed this out, the evolutionist next retorted:

In the same way NASA and ESA assume the Earth is a globe and not flat every time they launch a satellite into orbit. What were those dumb space scientists and engineers thinking using assumptions??

Which brings us back to Monte Python and the argument skit. There’s always another canard. After inappropriately using normal science as confirmatory evidence, and having the fallacy explained in no uncertain terms, the evolutionist effortlessly switches over to the next available fallacy: riding the coattails of science.

The analogy between the age-old Epicurean claims that the world spontaneously arose, and space flight, is of course absurd and pathetic. It reveals how silly is evolutionary thought. But like the Monte Python skit, evolutionists will always have another argument.

Religion drives science, and it matters.

RNA-Directed DNA Methylation: The Evolution of a Complex Epigenetic Pathway in Flowering Plants

Nada

The problem with epigenetic mechanisms is that they respond to future, unforeseen, environmental challenges. They don’t work in the present, and so even if random mutations somehow created such mechanisms, they would not be selected for. In other words, epigenetic mechanisms contradict evolutionary theory—there is no fitness improvement at the time of origin by random mutations, so there is no selection. Nor do evolutionists have an explanation for this—they don’t even try. Consider a paper discussing a particular epigenetic mechanism subtitled: “The Evolution of a Complex Epigenetic Pathway in Flowering Plants.”

The paper discusses a complicated cellular process in which different segments of DNA are copied (creating RNA transcripts). The RNAs work together to methylate the DNA at a particular location. The methylation “mark” helps to regulate gene expression. But how did this epigenetic mechanism evolve?

This epigenetic mechanism involves a small army of molecular machines. For instance, the different RNAs are transcribed, from the DNA, by different copying machines. These copying machines consist of a dozen protein subunits. The paper states that two of the copying machines—which are central to the epigenetic mechanism—each evolved from a third copying machine. Why?

The idea of the two copying machines evolving from the third copying machine is problematic because there are significant differences between them. The paper gives no justification for such an unlikely event. It gives no justification because there is none, save for the presupposition that evolution is true. Under evolutionary theory it must have occurred.

In other words, there is no empirical evidence that the two copying machines evolved from the third copying machine and there are enormous problems with the idea. But it is taken as a given because evolution is assumed to begin with.

The point here is that in attempting to explain the evolution of a complex epigenetic pathway the paper presupposed evolution a priori.

Similarly, the paper states that the two copying machines “are evolving rapidly.” Again, where did this come from? Does the science actually show this to be true? Does the science even merely provide any evidence at all for this astonishing claim?

Again, no and no.

Nowhere does the science demonstrate or prove that the two copying machines “are evolving rapidly.” In fact, the science doesn’t even provide any evidence at all for this.

Nada.

What the science shows is that the proteins in the two copying machines have significant differences compared to the corresponding proteins in the third copying machine. The two copying machines are more different from the third copying machine, than would normally be expected if they had evolved from that third copying machine.

But since evolution is assumed to be true to begin with, then those two copying machines must be “evolving rapidly.”

Again, the claim is driven by the belief that evolution is true. There is no empirical evidence that the two copying machines are evolving rapidly, let alone that they even evolved at all.

This is all dogma. There is no science here.

The paper then spends considerable effort attempting to reckon with the various problems that arise when their evolutionary history is assumed. There are duplication events and introns are mysteriously inserted. There are fusion events to explain unexpected differences, and other cases are simply unknown. There must have been a complex series of evolutionary events the reasons for which “remain obscure,” and the evolutionary origin of one gene is “a mystery.”

It is a long sequence of just-so stories. A long sequence of special events just happened to happen, which luckily produced this new epigenetic mechanism.

And then, after all of this, it would not be selected for. All of these events, and the resulting epigenetic mechanism would not improve the evolutionary fitness.

This evolutionary tale is not supported by the empirical evidence. Instead, it is supported by the prior assumption that evolution occurred.

Name It / Claim It: Epigenetics Now Just Another Evolutionary Mechanism

In Spite of the Cognitive Dissonance

It is often said that all truth passes through three stages. First, it is ridiculed. Second, it is violently opposed. Third, it is accepted as being self-evident. And so it is with epigenetics which evolutionists opposed and blackballed for a century before finally appropriating it as just another mode of evolutionary change. (see here, here, and here for more discussion of this history of misdirections regarding Lamarckism and epigenetics). Here is an example of evolutionists, after a century of denial and rejection, claiming epigenetics as their own.

Our example comes from this 2011 review paper on epigenetics in plants. Since plants are sessile they cannot simply move away from environmental challenges that occur. Therefore they need adaptation mechanisms. And since seeds are dispersed not too far from the parent plant, the next generation is likely to face the same environmental challenge. Therefore the adaptation mechanisms should be transgenerational, or heritable. Finally, since environmental challenge may be relatively short lived, lasting only a few generations, there is insufficient time for evolution by random mutations and natural selection to act. Therefore the adaptation mechanisms need to be fast-acting and reversible. These various requirements make epigenetics an “attractive alternative”:

The heritability of reversible epigenetic modifications that regulate gene expression without changing DNA sequence makes them an attractive alternative mechanism.

Note the design language. Not only are evolutionists naming and claiming the once evil epigenetics as just another mode of evolution, they also identify it as “an attractive alternative mechanism,” which is precisely how engineers discuss their design options.

Note, as we have discussed, the notion that such epigenetic mechanisms are just another mode of evolution makes no sense for several reasons. Unlike evolutionary change which is slow, epigenetics is fast. Unlike evolutionary change which propagates through the population from a single mutation occurring in a single individual, epigenetics works in parallel, occurring in many individuals across the population. Unlike evolutionary change which must come about by the selection of changes that must not be induced by the environment, epigenetics is induced by the environment. Unlike evolutionary change which generally is not repeatable, epigenetics is repeatable.

Furthermore, epigenetic mechanisms are, themselves, sophisticated designs. Their origin is far beyond evolution’s meager resources. Random mutations are not going to produce such directed adaptation mechanisms. And even if such a miracle were to occur, it would not survive, because it would not be selected for. This is because such mechanisms provide a differential reproductive advantage, and therefore a fitness improvement, not under the current conditions, but under some future, unforeseen conditions. There is no fitness improvement at the time of origin by random mutations.

There is a reason why evolutionists have so vehemently opposed this Lamarckian idea—it contradicts evolutionary theory. But like saltationism which was once rejected (by Darwin) due to its obvious implications, only to be guardedly accepted years later when the coast was clear (though it makes no sense on evolution), so too epigenetics must be accepted while downplaying the cognitive dissonance it forces on evolution.

Andrew Xiao Confirms Adenine Methylation in Mammals—Thinks it Evolved

This Isn’t Working

Evolutionists are going to need a bigger rug as Yale professor Andrew Xiao now has a new pile of stuff he is absurdly trying to ascribe to evolution. Xiao’s team has confirmed that in mammals the fundamental epigenetic signal—the methyl group—is sometimes attached to a second type of DNA base. DNA is made up of four types of bases (cytosine [C], guanine [G], adenine [A] and thymine [T]) and, as in the lower species, methyl groups are sometimes attached to adenine in mammals as well.

Such epigenetic signals help to cause directed adaptation in organisms—the ability to rapidly respond to new environmental challenges. And this new finding means that not just with cytosine, but with adenine as well, random mutations must have created the proteins (i) to attach the methyl groups and (ii) to remove them.

Both types of proteins are needed to make the epigenetic response work. With either protein alone, you just have chaos.

You also need the network of signals and regulation to set these proteins in action at the proper times, and only at the proper times. And of course these epigenetic signals must somehow influence the transcription process.

This isn’t going to happen with random mutations. And, no, natural selection doesn’t help.

But this is only the beginning.

In the lower species, attaching the methyl group to adenine caused gene activation. But in the mammals studied, the new research found that adenine methylation caused gene inactivation. In other words, the exact same methylation signal attached to the same nitrogen atom in the same base, somehow reversed polarity.

That makes no sense. Any change in polarity in the circuitry logic would throw the system into chaos. Imagine your thermostat now works in reverse. When you adjust the temperature lower, the heater rather than the air conditioner, turns on. You wanted it to be cooler, but instead it got even hotter.

Such a change in polarity in the circuitry would have to take place simultaneously, at several functions throughout the logic. This isn’t going to happen with random mutations. And, no, natural selection doesn’t help.

This is all a bad joke. The science makes no sense on evolution, and like the drunk at the party, evolutionists are the only ones who don’t get it.

A Tunable Mechanism Determines the Duration of the Transgenerational Adaptations

Tuning the Duration of Directed Adaptations

Organisms adapt to environmental challenges. In fact, many different organisms adapt in non-homologous ways to many different, unforeseen, environments. This contradicts evolution. For we are not talking about random changes occurring by chance, occasionally getting luck enough to confer an adaptation, and then propagating throughout the population. We’re not talking about an evolutionary process of random mutations and natural selection. That would take a long time. What we’re talking about are adaptations that specifically address environmental challenges, and occur in a good fraction of the population, over a few generations, or perhaps within a generation. Such directed adaptation occurs quickly.

That contradicts evolution because random mutations are not going to create such a complicated adaptation capability. Furthermore, they are not going to do this over and over, in so many different species, for so many different environments. And even if, by some miracle, this did occur, it would not be selected. That is because the adaptation capability is not for the current environment the organism faces, but for an unforeseen, hypothetical, future environment. The moment it arises, the adaptation capability is of no use, and would not be selected for.

But that’s not all.

As with Lamarck’s inheritance of acquired characteristics, these rapid, directed, adaptations are transgenerational. From parent to offspring, the progeny inherit the adaptation from the progenitor.

So now we must not only believe that evolution’s random mutations constructed these unbelievably detailed, complicated, unique adaptation capabilities, but that evolution also constructed the incredibly complicated means to transmit the adaptations to the next generation. As we saw recently, new research has demonstrated such transgenerational inheritance to be genetic, rather than via the parent’s behavior, breast milk, etc.

So again, random mutations must have created yet another complex design (the ability to pass along adaptations for an unforeseen environmental challenge), and it would have been worthless until that particular environmental challenge arose.

But that’s not all.

New research out of Tel Aviv University explains how these acquired adaptations persist through the later generations. Previously, these inherited adaptations were assumed simply to decay or “peter out” over a few generations. But the new research has uncovered proteins that manage and govern the duration of the adaptations. The adaptations are transmitted by small RNA molecules, and the proteins provide a tunable mechanism to govern the duration of the adaptation, over the generations. As the title of the paper explains:

A Tunable Mechanism Determines the Duration of the Transgenerational Small RNA Inheritance

Again, random mutations are not capable of producing such designs, and the designs would not be selected for. None of this makes any sense on evolution.

So now we must not only believe that evolution’s random mutations constructed these adaptation capabilities, and the means to transmit them to later generations, but also to control precisely their duration.

The science contradicts evolution.

Debate Debrief: The Two-Prong Canard Demonstrated Within 24 Hours

The Curious Case of Nylonase

Organisms have remarkable adaptation capabilities and evolutionists, ever since Darwin, have insisted that is powerful evidence of evolution. This is a blatant misrepresentation of science—when a heater turns on to warm the room do you think it must have therefore evolved?—and it is being revealed in the findings of epigenetics and directed adaptation. As I recently explained (The New Epigenetic Lie), rather than acknowledge and reckon with these findings, evolutionists have resorted to a two-prong canard: (i) claim that evolution knew it all along and (ii) claim that directed adaptation is simply a mode of evolutionary change. In other words, after resisting and rejecting directed adaptation for a century—and holding back science in the process—evolutionists are now claiming it as their own. Readers may have doubted my reporting. Do evolutionists really commit such a flagrant and bogus misdirection? But that was before last night’s “What’s Behind It All? God, Science, and the Universe” debate.

Within twenty four hours of my explaining the evolutionist’s two-prong canard, evolutionist Denis Lamoureux, in a futile attempt to refute the overwhelming science that Stephen Meyer alluded to regarding the impossibility of the chance origin of a protein-coding gene, gave a live demonstration of the canard. Lamoureux cited nylonase—enzymes that rapidly arose in bacteria, in the last century, and are able to breakdown byproducts of the nylon manufacturing process. Lamoureux made the non scientific claim that such enzymes demonstrate that the chance origin of a protein-coding genes is not a problem. They could have evolved with no problem, after all, we just witnessed it occur with the origin of nylonase.

This is the second prong: “directed adaptation is simply a mode of evolutionary change.” In other words, evolution is directed adaptation writ large.

That is a blatant misdirection.

Unfortunately, many in the audience were fooled by this canard. Evolutionists often make scientific-sounding claims, laden with jargon, and those not familiar with the scientific details are none the wiser.

In the case of nylonase, as with all cases of directed adaptation, the adaptation was in response to the environment. In other words, the environment influenced the adaptation. This is not a case of evolutionary change. The nylonase enzymes did not arise from a random search over sequence space until the right enzymes were luckily found and could be selected for. That would have required eons of time. Instead, cellular structures rapidly formed new enzymes in an evolutionary nano second.

Such adaptation to nylon manufacture byproducts has been repeated in laboratory experiments. In a matter of months bacteria acquire the ability to digest the unforeseen chemical. Researchers speculate that mechanisms responding to environmental stress are involved in inducing adaptive mutations.

That is not evolution. In fact it refutes evolution. Evolution does not have the resources to have created directed adaptation mechanisms. And even if it did, such mechanisms would not have been selected for because they provide no immediate fitness improvement.

And it is not evidence that protein-coding genes can evolve by chance. A new gene, arising within a modern cell responding to an environmental challenge, is not analogous to chance origin. Unfortunately evolutionists have a long history of inappropriately claiming otherwise.

There is still much to learn about directed adaptation. Unfortunately, evolutionists continue to obfuscate the path.

The New Epigenetic Lie: How Easily a Failure Becomes a Friend

Phony History

In graduate school I had an evolution professor who made the absurd claim that he had solved the protein folding problem—one of the most challenging conundrums in molecular biology. And did he have any examples? No, that was left to the student. It was embarrassing. At another time he referenced a proof of evolution. But again, it was a hollow claim. Unfortunately this sort of phony science is what evolution is all about. The latest example is in how evolutionists are handling epigenetics.

As the old proverb has it, first they'll reject the truth and then they'll appropriate it and say they knew it all along. In the case of epigenetics, after resisting and rejecting it for a century—and holding back science in the process—evolutionists are now entering the “we knew it all along” phase.

In this latest version of Whig history evolutionists have a two-pronged canard. First, they say Darwin proposed Lamarck’s inheritance of acquired characteristics. It was temporarily set aside later due to a lack of scientific evidence, but now in the emerging field of epigenetics, we see Darwin was right all along.

Second, as more and more cases of directed adaptation can no longer be denied, evolutionists are now suddenly referring to it as a new version of evolution. Their old enemy is now their new toy. In fact it resolves so many quandaries. How did new species appear so suddenly in the fossil record? Well now we see evolution occurring before our eyes.

My gosh, evolution works even better than we ever imagined.

For example, one paper concludes that the directed adaptations brought about by a genetic modification “have clear evolutionary implications,” for “this mechanism can give rise to a selectable, coordinated set of mutations under particular environmental stresses that can result sizeable, rapid, adaptive evolutionary responses.”

An evolutionary response? How easily a failure becomes a friend. Never mind that it refutes evolutionary theory. We solved the protein folding problem didn’t we?

As for the other prong, it is a good lie because, like all good lies, it contains a grain of truth. Yes, Darwin proposed Lamarck’s inheritance of acquired characteristics, but only under duress. Darwin’s relationship with Lamarckism was complex. He privately castigated the French biologist’s ideas, but publicly employed them at his convenience.

One problem for Darwin was that the blending inheritance idea he used in his theory of evolution were being demolished, for example by Fleeming Jenkin. The problem was sufficiently troubling that Darwin resorted to giving a nod to Lamarck’s inheritance of acquired characteristics.

Darwin did not accept or advocate inheritance of acquired characteristics; rather, Lamarck’s idea was Darwin’s backup plan. The Monday morning claim that Darwin’s proposing of the inheritance of acquired characteristics was a serious theoretical move is absurd. It is Whig history all over again. You can read more about this here.

But that now is becoming the ever more popular claim of evolutionists. As epigenetics becomes increasingly undeniable—an idea that is the polar opposite of evolution—evolutionists increasingly are resorting to this two-prong canard: We knew it all along, and after all it’s actually just another mode of evolutionary change.

Nothing strange here, move along.

Consider a new paper out of Johannes Beckers’ group on transgenerational epigenetic change in mice. The research used in vitro fertilization to confirm that epigenetic inheritance of obesity and diabetes in mice is transmitted via the gametes, and not via other factors such as behavior of the parents or lactation.

It is yet another confirmation of how epigenetics works, and another opportunity to advance the canard. As Beckers absurdly claims:

From the perspective of basic research, this study is so important because it proves for the first time that an acquired metabolic disorder can be passed on epigenetically to the offspring via oocytes and sperm--similar to the ideas of Lamarck and Darwin.

There you have it—Darwin knew it all along.

Religion drives science, and it matters.

Chuan He: Evolution Created Epigenetics

Because Nature Takes Advantage of What it Evolves

They never predicted it, then they denied it could be heritable, and then they denied it could cause lasting change. “It” in this case is epigenetics and in spite of being wrong, wrong and wrong again, and in spite of the fact that there is no scientific explanation for how epigenetics could have evolved, evolutionists nonetheless insist that it, in fact, must have evolved. Evolution loses every battle but claims to win the war. All of this became abundantly clear this past week when the finding of a new epigenetic signal was announced:

The epigenetic mark of DNA methylation, once thought to be rare if not nonexistent in worms and flies, occurs throughout the genomes of these organisms and in algae on the base adenine, not the cytosine known to be modified in mammals

and, in reference to said findings, evolutionist Chuan He explained that “If nature evolves something, it tends to take advantage of it,” both of which are non scientific claims.

First, there is no scientific evidence that nature evolved epigenetics. That is a religiously-driven, absurd claim.

Under evolution, the protein machines that attach the epigenetic markers must have fortuitously evolved from random mutations. But placing markers would not have helped if they were not in the right place, and in response to the right environmental signals. In fact, such protein machines could easily wreak havoc if they weren’t working just right.

But even given all that, such a marvel would do no good. That is because a tiny methyl group, or any other epigenetic marker, must be interpreted by other molecular machines. In other words, there must also have evolved the machines needed to recognize and perform the appropriate regulatory actions, as indicated by the given marker.

Evolution requires an enormous sequence of random mutations to occur before fitness improvements could be realized.

There is no scientific evidence that any such thing occurred. Perhaps future findings will reveal such an amazing feat, but today science gives us no such indication and in fact reveals that such an evolution would be heroic.

Second, He’s claim that nature “tends to take advantage of” what it evolves is a Darwinian personification of evolution which, as usual, is underwritten by Aristotelian teleology—none of which is scientific.

A long history of false predictions followed by absurd truth claims—this is not science.

Here’s That New Study Demonstrating the Inheritance of Directed Change

An Example of Science at Work

Ever since Darwin, evolutionists have resisted the idea of directed change. The twentieth century’s neo Darwinism codified the idea that biological variation must be random with respect to need. And with that codification came certainty. As Jacques Monod unequivocally proclaimed in 1971:

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.

That is a good example of evolution’s metaphysical certainty. And that certainty led to dogma. Evolutionists dismissed, delegitimized and blackballed anything and anyone hinting of directed change.

But as with the other predictions of evolution, this one turned out to be false as well. What Monod proclaimed as the “sole conceivable hypothesis” is now routinely refuted. In fact this has been known for many years but progress has been slow due to evolutionary resistance.

To this day many evolutionists continue to fight the science. But with the inexorable march of science, it just continues to get worse for evolution. Last week a new study out of UC Santa Cruz added yet more confirmation. It showed at the molecular level how certain kinds of directed changes are inherited across generations. As one report explained:

A growing body of evidence suggests that environmental stresses can cause changes in gene expression that are transmitted from parents to their offspring, making “epigenetics” a hot topic. Epigenetic modifications do not affect the DNA sequence of genes, but change how the DNA is packaged and how genes are expressed. Now, scientists have shown how epigenetic memory can be passed across generations and from cell to cell during development.

The lead researcher explained that this field has been controversial:

“There has been ongoing debate about whether the methylation mark can be passed on through cell divisions and across generations, and we’ve now shown that it is,” said corresponding author Susan Strome, a professor of molecular, cell and developmental biology at UC Santa Cruz.

That “ongoing debate” is mainly due to evolutionists resisting the science because it is fundamentally at odds with their theory. With this new study the science becomes that much more difficult to deny:

“Remarkably, when we watch the chromosomes through cell divisions, the marked chromosomes remain marked and stay bright, because the enzyme keeps restoring the mark, but the naked chromosomes stay naked, division after division,” Strome said. “That shows that the pattern of marks that was inherited is being transmitted through multiple cell divisions.”

These sorts of findings, which are becoming increasingly difficult to deny, are splitting evolutionists into different factions. For years now some evolutionists have recognized these findings and have carefully and diplomatically suggested evolutionary theory needs some modification. Other evolutionists, however, continue to vigorously hold that neo Darwinian change remains a fact and these new findings are merely a minor addition to the story.

What none of these factions have seriously reckoned with is that these directed change mechanisms and processes are contrary to and make no sense on evolution. This is an utter refutation of traditional evolutionary theory. There is no scientific explanation of how these directed change mechanisms and processes evolved.

Given this and so many other contrary findings, what we need to do is back off of the high claims. We need to drop the metaphysics and dogma. Yes organisms adapt and change—in that sense evolution is true. But that is a very different kind of evolution than how the term is normally understood. Let’s narrow the scope of the term “evolution” to what we know from science.

Lee Spetner: The Evolution Revolution

A New (and Much Better) Way of Doing Science

I just received my copy of Lee Spetner’s new book, The Evolution Revolution which follows his earlier Not By Chance! In these books Spetner lays out a new theory of origins, a new way of looking at biology, and really a new way of doing science, at least in the life sciences. I couldn’t agree more with his approach. Spetner’s overarching point is not that evolution does not occur, but that it is very different from how we normally understand that word. Spetner’s new approach—which he calls the nonrandom evolutionary hypothesis (NREH)—is data driven. NREH is an empirical idea, based on observations, not a rationalist idea based on a priori axioms. Mutations are effective, not random; evolution is directed to the need, not undirected; evolution occurs rapidly not slowly; and evolution occurs at the level of the individual, not at the population level. All of this points to the conclusion that evolution, like physiological responses, is a built-in capability, not a default, external process. And as Spetner points out, as research increases, the case for NREH is just getting stronger:

When I proposed my nonrandom evolutionary hypothesis (NREH) about fifteen years ago in my book Not By Chance!, the suggestion—that environmental inputs could affect the genome, leading to the possibility that an organism can change its physiology and behavior in response to an external input—was somewhat sketchy. A distinguishing feature of a good theory is that evidence for it grows after it has been formulated. Since I suggested the NREH, the following discoveries have been made that provide a solid mechanism for it, showing how organisms can show an adaptive heritable response to environmental inputs: … [63]

Bravo for Lee Spetner. Let’s bring science back to its rightful role of figuring out how nature works rather than promoting religious dogma. Rather than battle with new findings as evolution is forced to do, Spetner shows us how we can make progress with science, advancing with new findings rather than adding new epicycles with each new study.