Monday, December 5, 2016

Dennis Venema, Galileo, and Protein-Protein Binding

Don’t Count on the Duchess

We have looked at Dennis Venema’s articles on evidences for common descent here, here, here, here, here, and here. In a recent discussion with Venema, he made the erroneous claim that the mammalian immune system, with its search for, and production of, antibodies, is a good example of why evolving protein-protein binding sequences is not a problem. In fact the mammalian immune system is yet another enormous problem for the theory of evolution. Furthermore, the mammalian immune system is not a good example because it is designed for this job of creating protein-protein binding sequences. It searches a well-defined design space extremely rapidly, and measures the success of its search experiments accurately and quickly. The fact that our immune system successfully designs antibodies in short order does nothing to address the problem of how random mutations occurring throughout the genome is supposed to have found myriad binding sequences, crucial for life. Venema also referred to another example which he has written about. Unfortunately this example also fails to demonstrate Venema’s claim of “evolution producing a new protein-protein binding event.”

The problem with evolving protein-protein binding is that too much gene sequence complexity is required to achieve the needed binding affinity. You could say it is an “all-or-none” type of problem.

One or two mutations will not generally do the job—you usually need more mutations before the two proteins stick together very well. And stick together they must, on a massive scale, in order to perform their necessary tasks. Even the simplest, unicellular, organisms contain massive protein machines, consisting of dozens of different proteins binding together to perform crucial life functions.

The study Venema referred to did a beautiful job in confirming this “all-or-none” character of protein-protein binding sequences. The study showed that in order for a viral protein to perform a relatively simple switch from one protein to a very similar protein required four types of mutations.

Anything less and no dice.

The twist in this study was that subsets of the four mutation types were apparently useful for a different function (strengthening the binding affinity to the original protein). So while in general the evolution of protein-protein binding sequences is astronomically difficult because too many simultaneous mutations are required, in this case the four mutation types could be accumulated, with useful benefit realized at some of the intermediate steps.

This is not a general result. It is not a revolutionary new finding that reverses our understanding of protein-protein binding sequences.

It confirms our knowledge, and adds a fascinating outlier case where the “all-or-none” character is circumvented by intermediate functions which, fortuitously “push” the design in the right direction. As the study explains:

The “all-or-none” epistasis among the four canonical phage mutations implies that it would have been unlikely for the new function to evolve on the scale of our experiments, except for the lucky fact that some of the mutations were beneficial to the phage in performing their current function, thereby pushing evolution toward the new function.

The study provides no indication that the untold thousands upon thousands of protein-protein binding problems in molecular biology would enjoy this type of setup. And if they did, oh what a most suspicious sign of design that would be.

Venema is mistaken in his failed attempt to recruit this study as a solution to the evolution of protein-protein binding sequences.

Strangely enough not only had Michael Behe provided his explanation of this study, but Venema was aware of it at the time of his writing. Venema explained that in his next article he would address Behe’s explanation, but in fact Venema simply rehashed Behe’s original explanation for why protein-protein binding is a problem for evolution.

Venema did not address Behe’s explanation but simply concluded that Behe’s original explanation must be false because, after all, this new study demonstrates the evolution of just such protein-protein binding sequences.

This is an unfortunate misrepresentation of a study that most readers will not understand. Venema completely misappropriated the study, and force-fit it into an evolutionary proof.

Additional problems

In addition to this basic problem of serendipity, this confirmation of the “all-or-none” character of protein-protein binding sequences was possible only with a very contrived, designed, laboratory experiment.

Simply put, a virus population was provided with a willing, and well fed host to live off of. In the meantime, many more host targets awaited the virus population. So a few mutations helped the virus’ infect the initial hosts, and mere single additional mutation then allowed the virus’ to infect the second group of hosts.

It was an entirely artificial, laboratory, environment, that wasn’t even intended to replicate a realistic evolutionary environment. Venema nowhere explained this.

Second, the study also discovered even more serendipity. Not only were there “luckily” intermediate fitness benefits, but the finding of the four mutations types also required certain mutations in the host genome.

Without them, no dice.

Finally, it is worth noting that across the many different virus populations used in the experiment, the virus protein in question did not incur any synonymous mutations. The study attempted to explain this as a sign of selection:

First, all 248 independent mutations in the 51 sequenced J alleles were nonsynonymous, whereas the expected ratio of nonsynonymous to synonymous changes is 3.19:1 under the null model for the ancestral J sequence. This great excess is evident even if we include only the 82 nonsynonymous mutations in the 24 isolates that did not evolve the new receptor function.

This is most suspicious. According to evolutionary theory, a lack of selection will be manifest in relatively few nonsynonymous mutations. So the ratio of normalized nonsynonymous mutations-to-normalized synonymous mutations (the so-called Ka/Ks ratio) will be less than unity.

On the other hand, strong selection will be manifest in relatively many nonsynonymous mutations. So the Ka/Ks ratio will be greater than unity.

A high Ka/Ks ratio, and hence an inference of strong selection, should be due to relatively many nonsynonymous mutations.

In this study, however, it is in the synonymous mutations where the surprise comes. There were zero.

In other words, the Ka/Ks ratio is infinity.

To pass this off simply as a sign of strong selection is not good science, even within the normal science of evolutionary theory.

Sunday, December 4, 2016

More Teleological Language: Hox Gene Function Was Coopted

When RM+NS Just Doesn’t Cut It

Evolutionists are now saying that in embryonic mammary buds, Hoxd gene regulation evolved “by hijacking” a preexisting regulatory landscape. Or as the press release explains:

A team of geneticists demonstrated that the emergence of mammary glands in placental mammals and marsupials results from recycling certain 'architect' genes. The latter, known as Hox genes, are responsible for coordinating the formation of the organs and limbs during the embryonic stage. Such genes are controlled by complex regulatory networks. In the course of evolution, parts of these networks were reused to produce different functions. Architect genes were thus requisitioned to form the mammary bud and, later, for gestation

Hijacking and recycling?

The teleology becomes particularly obvious, as usual, with the infinitive form: Networks were reused to produce … . And genes were requisitioned to form … .

The incessant use of such Aristotelian language is another sign of the failure of evolutionary thought.

Saturday, December 3, 2016

Another Warfare Thesis Tidbit

The Hits Just Keep on Coming

In his recent Washington Post opinion piece, Harvard astrophysicist Howard Smith began with yet more Warfare Thesis history:

There was a time, back when astronomy put Earth at the center of the universe, that we thought we were special.

Actually we “put Earth at the center of the universe” as a consequence of Aristotelian physics, not because of any anthropomorphism. That is the imaginary history, foisted on us by the Warfare Thesis, which can be traced back to Voltaire, but rose in prominence in the 19th century.

Tuesday, November 22, 2016

About That Genetic Code

A Smoke Screen

We recently looked at the enormous problems that the DNA, or genetic, code pose for evolutionary theory. Here is a paper that seems to have come to the same conclusion. The authors argue that the underlying patterns of the genetic code are not likely to be due to “chance coupled with presumable evolutionary pathways,” (P-value < 10^-13), and conclude that they are “essentially irreducible to any natural origin.”

A common response from evolutionists, when presented with evidence such as this, is that we still don’t understand biology very well. This argument from ignorance goes all the way back to Darwin. He used it in Chapter 6 of Origins to discard the problem of evolving the electric organs in fish, such as the electric eel (which isn’t actually an eel). The Sage from Kent agreed that it is “impossible to conceive by what steps these wondrous organs” evolved, but that was OK, because “we do not even know of what use they are.”

Setting aside the fact that Darwin’s argument from ignorance was a non-scientific fallacy, it also was a set up for failure. For now, a century and half later, we do know “what use they are.” And it has just gotten worse for evolution.

Darwin’s argument has been demolished, once again demonstrating that arguments from ignorance, aside from being terrible arguments, are not good science.

The truth is, when evolutionists today claim that the many problems with their chance theory are due to a lack of knowledge, they are throwing up a smoke screen.

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.

Sunday, November 20, 2016

How the Peppered Moth Backfired

The Poster Child Became the Rebuttal

It has been called one of the best examples of evolution observed in the wild—light colored peppered moths (Biston betularia) became dark colored in response to 19th century industrial pollution darkening the birch trees in their environment. Evolving a darker color helped camouflage the moths, and keep them hidden from predatory birds. And more recently, air pollution reductions lightened the environment and with it, the moths also began to revert to their lighter color. Proof of evolution, case closed, right? From popular presentations and museum exhibits, to textbooks and scientific papers, evolutionists have relentlessly pounded home the peppered moth as an undeniable confirmation of Darwin’s theory in action. There’s only one problem: All of this ignores the science.

There are two main problems with peppered moths story. First, changing colors is hardly a pathway leading to the kinds of massive biological change evolution requires. It is not as though a change in the peppered moth coloration is any kind of evidence for how the moths evolved, or how any other species, for that matter, could have evolved.

In fact changing the color of a moth not only fails to show how species could evolve, it also fails to show how any biological design could evolve. The peppered moth case doesn’t show 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.

The moths were already there. Their wings were already there. Different colors were already there. The changing of color in moth populations, while certainly a good thing for the moths, is hardly an example of evolution.

Second, research strongly suggests that the cause of the darkening, at the molecular level, is an enormous genetic insertion. In other words, rather than a nucleotide, in a gene, mutating to one of the other three nucleotides, as you learned in your high school biology class, instead what has been found is an insertion of a stretch of more than 20,000 nucleotides. That long inserted segment consists of a shorter segment (about 9,000 nucleotides) repeated about two and one-third times.

Also, the insertion point is not in a DNA coding sequence, but in an intervening region (intron), which have been considered to be “junk DNA” in the past.

This observed mutation (the insertion of a long sequence of DNA into an intron), is much more complicated than a single point mutation. First, there is no change in the gene’s protein product. The mutating of the protein sequence was the whole idea behind evolution: DNA mutations which lead to changes in a protein can lead to a phenotype change with fitness improvement, and there would be subject to natural selection.

That is not what we are seeing in the much celebrated peppered moth example. The DNA mutation is much more complicated (~20,000 nucleotides inserted), and the fact it was inserted into an intron suggests that additional molecular and cellular mechanisms are required for the coloration change to occur.

None of this fits evolutionary theory.

For example, evolutionary theory requires that the needed random DNA mutational change is reasonably likely to occur. Given the moth’s effective population size, the moth’s generation time period, and the complexity of the mutation, the needed mutation is not likely to occur. Evolution would have to be inserting segments of DNA with (i) different sequences, at (ii) different locations, within the moth genome. This is an enormous space of mutational possibilities to search through.

It doesn’t add up. Evolution does not have the resources in terms of time and effective population size to come anywhere close to searching this astronomical mutational space. It’s not going to happen.

A much more likely explanation, and one that has been found to be true in so many other cases of adaptation (in spite of evolutionary pushback), is that the peppered moth coloration change was directed. The environmental change and challenge somehow caused the peppered moth to modify its color. This suggests there are preprogrammed, directed adaptation mechanisms, already in place that are ready to respond to future, potential, environmental changes, which might never occur.

Far from an evidence for evolution, this is evidence against evolution.

So there are at least two major problems with what is celebrated as a key evidence for evolution in action. First, it comes nowhere close to the type of change evolution needs, and the details of the change demonstrate that it is not evolutionary to begin with.

Saturday, November 19, 2016

Fake News From PBS on the DNA Code

Heighten Public (Mis)Understanding

Evolution, according to the highly produced PBS Evolution Project, “determines who lives, who dies, and who passes traits on to the next generation. The process plays a critical role in our daily lives, yet it is one of the most overlooked -- and misunderstood -- concepts ever described. … The Evolution series' goals are to heighten public understanding of evolution and how it works, to dispel common misunderstandings about the process, and to illuminate why it is relevant to all of us.” In other words, the PBS Evolution Project would clear away the ignorance and bring the real news of evolution. And with a long list of evolution luminaries advising the project (including Rodger Bybee, Gerald Carr, John Endler, Paul Ewald, Larry Flammer, Douglas Futuyma, Anne Houde, Les Kaufman, Joseph Levine, David Maddison, Anne Magurran, Justin Marshall, Kenneth Miller, Martin Nickels, Kevin Padian, Diane Paul, David Reznick, Helen Rodd, Chris Schneider, Judy Scotchmoor, Daniel Simberloff, Neil Shubin, Meredith Small, David Wake, and Peter Ward), we would expect nothing less. Here is what they had to say about the DNA code:

Biologically and chemically, there is no reason why this particular genetic code, rather than any of millions or billions of others, should exist, scientists assert. Yet every species on Earth carries a genetic code that is, for all intents and purposes, identical and universal. The only scientific explanation for this situation is that the genetic code was the result of a single historic accident. That is, this code was the one carried by the single ancestor of life and all of its descendants, including us.

There was only one problem: that was fake news. The DNA, or genetic, code was and is, in fact, very special. This was known at the time of the PBS Evolution Project, and since then it has only gotten worse for the evolutionists.

It is the exact opposite of how the evolutionists informed their viewers. They could not have misrepresented the science any more than they did. Because when evolutionists seek to “heighten public understanding,” and “dispel common misunderstandings,” it doesn’t mean teaching science. It means promoting evolution, in spite of the science.

Religion drives science, and it matters.

The DNA Code and Evolution

My Dear Watson

The DNA code is used in cells to translate a sequence of nucleotides into a sequence of amino acids, which then make up a protein. In the past fifty years we have learned four important things about the code:

1. The DNA code is universal. There are minor variations scattered about, but the same canonical code is found across the species.

2. The DNA code is special. The DNA is not just some random, off the shelf, code. It has unique properties, for example that make the translation process more robust to mutations. The code has been called “one in a million,” but it probably is even more special than that. For instance, one study found that the code optimizes “a combination of several different functions simultaneously.”

3. Some of the special properties of the DNA code only rarely confer benefit. Many of the code’s special properties deal with rare mutation events. If such properties could arise via random mutation in an individual organism, their benefit would not be common.

4. The DNA code’s fitness landscape has dependencies on the DNA coding sequences and so favors stasis. Changes in the DNA code may well wreak havoc as the DNA coding sequences are suddenly not interpreted correctly. So the fitness landscape, at any given location in the code design space, is not only rugged but often is a local minimum, thus freezing evolution at that code.

Observation #1 above, according to evolutionary theory, means that the code is the ultimate homology and must have been present in the last universal common ancestor (LUCA). There was essentially zero evolution of the code allowed over the course of billions of years.

This code stasis can be understood, from an evolutionary perspective, using Observation #4. Given the many dependencies on the DNA coding sequences, the code can be understood to be at a local minimum and so impossible to evolve.

Hence Francis Crick’s characterization, and subsequent promotion by later evolutionists, of the code as a “frozen accident.” Somehow the code arose, but was then strongly maintained and unevolvable.

But then there is Observation #2.

The code has been found not to be mundane, but special. This falsified the “frozen accident” characterization, as the code is clearly not an accident. It also caused a monumental problem. While evolutionists could understand Observation #1, the universality of the code, as a consequence of the code being at a fitness local minimum, Observation #2 tells us that the code would not have just luckily been constructed at its present design.

If evolution somehow created a code to begin with, it would be at some random starting point. Evolution would have no a priori knowledge of the fitness landscape. There is a large number of possible codes, so it would be incredibly lucky for evolution’s starting point to be anywhere near the special, canonical code we observe today. There would be an enormous evolutionary distance to travel between an initial random starting point, and the code we observe.

And yet there is not even so much as a trace of such a monumental evolutionary process. This would be an incredible convergence. In biology, when we see convergence, we usually also see variety. The mammalian and cephalopod eyes are considered to be convergent, but they also have fundamental differences. And in other species, there are all kinds of different vision systems. The idea that the universal DNA code is the result of convergence would be very suspect. Why are there no other canonical codes found? Why are there not more variants of the code? To have that much evolutionary distance covered, and converge with that level of precision would very strange.

And of course, in addition to this strange absence of any evidence of such a monumental evolutionary process, there is the problem described above with evolving the code to begin with. The code’s fitness landscape is rugged and loaded with many local minima. Making much progress at all in evolving the code would be difficult.

But then there is Observation #3.

Not only do we not see traces of the required monumental process of evolving the code across a great distance, and not only would this process be almost immediately halted by the many local minima in the fitness landscape, but what fitness improvements could actually be realized would not likely be selected for because said improvements rarely actually confer there benefit.

While these problems obviously are daunting, we have so far taken yet another tremendous problem for granted: the creation of the initial code, as a starting point.

We have discussed above the many problems with evolving today’s canonical code from some starting point, all the while allowing for such a starting point simply to magically appear. But that, alone, is a big problem for evolution. The evolution of any code, even a simple code, from no code, is a tremendous problem.

Finally, a possible explanation for these several and significant problems to the evolution of the DNA code is the hypothesis that the code did not actually evolve so much as construct. Just as the right sequence of amino acids will inevitably fold into a functional protein, so too perhaps the DNA code simply is the consequence of biochemical interactions and reactions. In this sense the code would not evolve from random mutations, but rather would be inevitable. In that case, there would be no lengthy evolutionary pathway to traverse.

Now I don’t want to give the impression that this hypothesis is mature or fleshed out. It is extremely speculative.

But there is another, more significant, problem with this hypothesis: It is not evolution.

If true this hypothesis would confirm design. In other words, a chemically determined pathway, which as such is written into the very fabric of matter and nature’s laws, would not only be profound but teleological. The DNA code would be built into biochemistry.

And given Observation #2, it is a very special, unique, detailed, code that would be built into biochemistry. It would not merely be a mundane code that happened to be enabled or determined by biochemistry, but essentially an optimized code.

Long live Aristotle.

The problem is there simply is no free lunch. Evolutionists can try to avoid the science, but there it is.

Tuesday, November 15, 2016

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.

Saturday, November 12, 2016

Tim Ingold’s Question For Andy Gardner Says It All

A Not So Hidden Agenda

Anthropologist Tim Ingold’s question for Andy Gardner at last week’s “New trends in evolutionary biology” Scientific meeting at The Royal Society should disabuse those who still don’t get it. Gardner had finished his talk, “Anthropomorphism in evolutionary biology,” in which he acknowledged the design in biology. But if Gardner's organisms are actually designed, an agitated Ingold demanded, then how would Gardner’s explanation for their origin be any different from William Paley’s natural theology which invoked design?

Anyone who has interacted with evolutionists knows this moment all too well. The metaphysics and religion are always there for evolutionists, crouching at the door and ready to strike at any moment. Whether in lecture, seminar, or writings, the agenda is painfully obvious. As Eva Jablonka put it, “Not God—we’re excluding God.”

Evolution isn’t about the science—it never was. It doesn’t matter what the science shows, evolution must be true. Religion drives science, and it matters.

Friday, November 11, 2016

Here’s That Study That Found Pseudo-Pseudogenes

Evolution is Getting Demolished

It is one of the strongest arguments for evolution: dysteleology, the apparent lack of design in the biological world. And the most obvious and compelling examples of such dysteleology are in the genome. And the most celebrated examples of dysteleology in the genome are the pseudogenes—genes which are broken. They are the long since abandoned junk of the genome. And the most obvious example of such brokenness is a stop codon that has accidentally arisen somewhere in the middle of the gene. These so-called premature termination codons (PTCs) halt the production of proteins in mid-stream. And the most abundant source of pseudogenes is the olfactory receptor families—genes involved in detecting odors. All those pseudogenes are a sure sign that no designer worth his salt would have constructed such a world. Evolution must be true, as evolutionists from Charles Darwin to Jerry Coyne have proclaimed. There’s only one problem—such examples of junk always turn out to be false.

At evolution’s foundation is the claim of lack of function, and that is a terrible argument. First of all, it is metaphysical rather than scientific. It is not a positivist argument—evolutionists have no idea how genes, or anything else for that matter—actually evolved. The argument is that such nonfunctional structures would never have been designed or created. That conclusion does not come from science, and cannot be tested by science. It is a religious argument.

But in addition to the metaphysics, showing that a structure has no function makes no sense to begin with. For one would have to watch the structure, in the organism, for the entire life of the organism. And one would have to be able to measure function—all possible functions. Needless to say, no evolutionist has ever done that.

But it gets worse.

Not only is the dysteleology argument religious and nonsensical, it is also false. At least in the cases that have been investigated. Over and over, the long lists evolutionists make of nonfunctional structures just get shorter and shorter.

That brings us to pseudogenes.

For sometime it has been known that not all pseudogenes are pseudogenes. That is, not all pseudogenes are junk. Some pseudogenes have been found to be performing useful functions. But typically these are onesies, twosies.

Now, a new study has found something more interesting—a PTC in an olfactory receptor pseudogene that, in certain contexts, is not actually a termination codon after all. The gene has a stop codon, and yet the gene is successfully used to create a protein. The translation process somehow can read-through what normally would be a stop codon. The paper suggests this is accomplished with a near-cognate tRNA, which inserts an amino acid rather than causing a halt:

We suggest that read-through is due to PTC recognition by a near-cognate tRNA that allows insertion of an amino acid instead of translation termination.

What appeared to be a pseudogenes is actually functional. It is a pseudo pseudogene.

Furthermore, and importantly, this is not an isolated case. They found other examples, and conclude this could be a “widespread phenomenon.”

Pseudogenes are generally considered to be non-functional DNA sequences that arise through nonsense or frame-shift mutations of protein-coding genes. … We identify functional PTC-containing loci within different olfactory receptor repertoires and species, suggesting that such “pseudo-pseudogenes” could represent a widespread phenomenon.

Widespread phenomenon? This adds yet more support to the Project Encode suggestion, which evolutionists immediately pushed back on, that most of the genome is functional rather than junk as evolutionists had insisted (for example, see here, here, and here).

Pseudogenes comprise only a small fraction of the genome, but they have served as the poster child of junk DNA, and proof of evolution.

Instead, once again history appears to be reliable guide as pseudogenes appear to be going down the same path as those other supposedly “nonfunctional” structures. Instead of nonfunctional, pseudogenes are beginning to look like they may have a rather sophisticated function that was not apparent to evolutionists.

Of course function is often not apparent to evolutionists because they view biology as an accident. Organisms are built on a vast number of chance events so of course they will be found to be full of mistakes.

But in its inexorable march of progress, science always seems to find function. Evolution seeks lack of function, which makes no sense, and science just keeps on finding more function. Evolution and science, it seems, are in an eternal conflict.

Don’t expect contriteness anytime soon though. For evolutionists, the finding of function was never a problem. It simply is an example of evolution finding function for what was nonfunctional. The junk was repaired and took on some new function. In fact, it remains powerful evidence for evolution because it is obviously so quirky. When the supposedly “backward” retina of the mammalian eye was found to be incredibly sophisticated, evolutionists didn’t miss a beat. After all, it was still a kludge of a design. As Richard Dawkins put it, “it is the principle of the thing that would offend any tidy-minded engineer!”

So it really doesn’t matter how much function is found, and how optimal a design is. For man has found nature to be wanting, and so it must have formed by chance. This, in a nutshell, is Epicureanism.

Religion drives science, and it matters.

Thursday, November 10, 2016

BioLogos: A New Book By Dennis Venema

Who Was Adam?

In Dennis Venema’s new book, Adam and the Genome, coauthored with Scot McKnight and available in January, readers will be told that evolution is a well-supported, scientific theory. The publisher explains that the authors “address up-to-date genomics data with expert commentary.” But unless Venema has dramatically changed his views, what readers will find is a series of misrepresentations, turning the evidence upside down in order to prove evolution. See, for example, my reviews of several of Venema’s flawed articles (here and here).

Wednesday, November 9, 2016

The BBC on Evolution: Chris Stringer Puts the Hammer Down

Right There in the Mirror

British anthropologist Chris Stringer of the Natural History Museum in London, a leading proponent of the “Out of Africa” hypothesis, is by any measure a leading light amongst evolutionists. And so not surprisingly religion drives his thinking. He made that clear in Chris Baraniuk’s article for the BBC about why evolution is a fact. As Baraniuk writes:

By comparing how many genes organisms share, we can figure out how they are related. For instance, humans share more genes with apes like chimps and gorillas than other animals, as much as 96%. That suggests they are our closest relatives.

"Try to explain that in any other way than the fact that those relationships are based on a sequence of changes through time," says Chris Stringer of the Natural History Museum in London. "We have a common ancestor with chimpanzees, and we and they have diverged since then from that common ancestor."

In other words, according to Stringer, genetic similarities between humans and apes cannot be explained in any way other than evolution. This sentiment, which runs all through evolutionary thought, is not scientific, it is metaphysical.

Stringer and the evolutionists insist that there is no explanation, other than evolution, for similarities we observe between species, such as the high genetic similarity between humans and chimpanzees.

And since there is no explanation, other than evolution, then we must conclude that “We have a common ancestor with chimpanzees.”

That must be the conclusion.

But this claim makes reference to the set of all possible explanations. You’ve got evolution, and then you’ve got all the others.

This means that Stringer and the evolutionists must have knowledge of all those explanations. All possible theories of origin are known to them.

Creationism comes to mind, but of course there could be different versions of creationism. And of course there could be other theories still.

A scientist, qua scientist, cannot have such knowledge. This is why Mr. Nelson was so careful to teach you in seventh grade science class that “The Scientist” works from observation to hypothesis to prediction to experiment. Scientists deal with hypotheses and theories, which they deduce and test.

They don’t make all-encompassing truth claims. The claim that Theory A explains Observation B is scientific. The claim that no theory except Theory A explains Observation B is metaphysical. A slight change in the language makes an enormous difference in the claim.

One is scientific, one is religious.

But it gets worse.

Because, as stated above, Stringer and the evolutionists are making claims about creationism. Stringer’s point is that God would not create genomes with so much similarity. This claim traces back to the Principle of Plenitude. That is the label that historian Arthur Lovejoy gave to a long running religious tradition in the history of thought about, simply put, how God would design the world.

The Principle of Plenitude is very much with us today, as much as it was with Plato, Anselm, Bruno, and Leibniz.

Evolutionists aren’t merely making some vague claims about colored marbles in an urn. They are making very specific claims about what God would and would not do.

That’s religious.

But it gets worse.

Not only are Stringer and the evolutionists driven by religious sentiment, but it forces them into a completely untenable position. If you genuinely want to test theories against the evidence, it is evolution that fails. In this case we’re talking about the comparisons between the species. How are they similar, and how are they different?

And these data demolish evolutionary theory.

The data do not fit the evolutionary model, not even close. One way to measure this is with the so-called consistency index, which consistently shows, pun intended, no consistency. The observables are closer to the random “null hypothesis” model than to the evolution model.

So while evolutionists criticize the skeptics for being religiously-driven, anti-science, smuggling metaphysics into science, and insisting on terrible theories, all those criticisms are, actually, right there in the mirror.

Religion drives science, and it matters.

Tuesday, November 8, 2016

The Big Day Has Finally Arrived

What Will The Decision Be?

After years of battling and debating, we have finally reached the big day with its big decisions. Tensions are running high as the old-guard status quo battles the radical new ideas—it is the “New Trends in Evolutionary Biology” meeting at the Royal Society where evolutionists are finally reckoning with the science which makes no sense on the theory. The problem is that species adapt not according to the random mutations coupled with natural selection, but according to mechanisms that respond directly to the environment. The Big Day Has Finally Arrived.

Ross Pomeroy Reminds us of P-Value Problems

But it is Much Worse

Ross Pomeroy’s article in yesterday’s Real Clear Science was a much needed reminder about the dangers of statistical hypothesis testing. But while Pomeroy rightly points out important problems, particularly with the so-called P-value, out here on the ground, the problem is much worse.

One of Pomeroy’s several legitimate concerns is the use of what is essentially a default value of 0.05 for P. Too often scientists don’t realize that, as David Colquhoun has pointed out, this will lead to false conclusions at least 30 percent of the time. Pomeroy also points out the common fallacy of interpreting the P value as the probability that the null hypothesis is true.

The result of such mishandling of hypothesis testing is that, “Quite simply, a large amount of published research is false.”

Would that it would end there. Unfortunately, when it comes to evolutionary studies, fixing these problems is like rearranging the deck chairs on the Titanic. These concerns about selecting a good alpha value and understanding the nuances of what P actually means, while important, pale in comparison to a much larger infraction: using the P-value to mask what is, in fact, a strawman argument.

One of the key, underlying, assumptions in using the P-value is that there are only two alternatives, the null and alternative hypotheses. These two hypotheses must be complementary—they must be distinct, mutually exclusive, and exhaustive. In other words, one of them must be true, and the other must be false. They cannot both be true, or both be false. They cannot overlap, and there can be no other possibilities.

And while such a perfect pair of hypotheses is possible in simple academic problems such as colored marbles in an urn, real world problems often are more complicated. Take something as seemingly simple as the question of whether or not it will rain today. Is it not binary? Either it will rain, or it will not rain. Right?

Well no. The weather has a multitude of complexities. It is spatially and temporally varying, with an infinite degree of variation. What if it sprinkles? What if the rain evaporates before it reaches the ground? How do you define the time and location? What if it rains in one location but not another?

What the P-value, and its null hypothesis, allows is for trivial null hypotheses to be erected and easily knocked down like strawmen, thus “proving” ones favored explanation.