Darwinists continue to major in minors.

Rapid" Evolution Observed in Guppies? As Always, It Depends on What You Mean by Evolution

David Klinghoffer October 1, 2015 3:31 PM 

Reporting in Proceedings of the Royal Society B, researchers have rigorously demonstrated something totally unsurprising -- only to turn around and offer it as evidence for something quite different and quite surprising. The technical term for that is bait-and-switch.

A team showed that if you take guppies and move them from an environment rich in predators to one that's largely predator-free, this can have an effect on a superficial trait like coloration. Who would have thought otherwise? Given (a) characteristics that vary from generation to generation, (b) heritability, and (c) an environment or other factors that favor one over another, it would be startling if selection didn't result in small-scale change over time, even over rather short periods -- microevolution, in other words, at its finest.

From the Abstract ("Selection analysis on the rapid evolution of a secondary sexual trait"):

Here, we present a study of experimental evolution of male colour in Trinidadian guppies where we tracked both evolutionary change and individual-based measures of selection. Guppies were translocated from a predator-rich to a low-predation environment within the same stream system. We used a combination of common garden experiments and monthly sampling of individuals to measure the phenotypic and genetic divergence of male coloration between ancestral and derived fish. Results show rapid evolutionary increases in orange coloration in both populations (1 year or three generations), replicating the results of previous studies. Unlike previous studies, we linked this evolution to an individual-based analysis of selection. By quantifying individual reproductive success and survival, we show, for the first time, that males with more orange and black pigment have higher reproductive success, but males with more black pigment also have higher risk of mortality. The net effect of selection is thus an advantage of orange but not black coloration, as reflected in the evolutionary response. This highlights the importance of considering all components of fitness when understanding the evolution of sexually selected traits in the wild.

Commenting in Science Daily ("Evolution shown in real time"), an author of the study, UC Riverside biologist David Reznick, points out the relevance to the evolution debate as he sees it:

"People think of evolution as historical. They don't think of it as something that's happening under our nose. It is a contemporary process. People are skeptical; they don't believe in evolution because they can't see it. Here, we see it. We can see if something makes you better able to make babies and live longer," Reznick said. [Emphasis added.]

But the kind of evolution Dr. Reznick and his colleagues observed is not the same thing -- unguided macroevolution, novel biological information fortuitously generating new animals -- that is subject to skepticism by those who "don't believe in evolution because they can't see it." Set aside the gratuitous swipe at skeptics. Show me the most devout creationist and I will show you someone perfectly happy to accept every word of David Reznick's results, and completely untroubled by them.

Don't Darwinists know this? I understand wanting to draw attention to your work by highlighting how it casts light on a hot debate. But first find out what both sides in the debate say, what they're arguing about, andthen tell us how your work ought to figure into the discussion.

Darwinism Vs. the real world XIV

Blood Pressure: Standing Up to Gravity

Howard Glicksman October 1, 2015 3:34 AM

Editor's note: Physicians have a special place among the thinkers who have elaborated the argument for intelligent design. Perhaps that's because, more than evolutionary biologists, they are familiar with the challenges of maintaining a functioning complex system, the human body. With that in mind, Evolution News & Views is delighted to present this series, "The Designed Body." Dr. Glicksman practices palliative medicine for a hospice organization.

The cardiovascular system's job is to provide the cells of the body with what they need to live, grow, and work properly by providing enough blood flow to the tissues. To do this, the heart must pump well enough, there must be enough blood in the arteries, and the arterioles must limit how much blood enters the tissues by applying peripheral vascular resistance. It is these three factors that mainly determine the arterial blood pressure.

But life is a dynamic process, and changes in fluid balance, body position, and physical activity require that each of these factors be constantly adjusted to keep the blood pressure where it needs to be to survive. Just as a car's ability to perform well enough goes above and beyond its mere blueprints, so too, the ability of the body to survive within the laws of nature goes above and beyond its mere DNA.

Anyone who has ever felt dizzy upon standing up knows this to be true. When it comes to being able to stand up to gravity, the numbers regarding blood pressure have to be just right or else we'll find ourselves lying on the ground. Just imagine our ancient ancestors trying to survive if their body couldn't control their blood pressure so as to remain in the upright position for an extended period. Evolutionary biologists seem to forget that explaining how life came about requires showing, not just how it looks, but also how it must work within the laws of nature to survive.

It's important to remember that, barring a local obstruction from a clot, or a hemorrhage from an injury, the blood pressure provides the force resulting in adequate blood flow to the tissues of the body. The blood pressure fluctuates between the diastolic (DP) and the systolic pressure (SP) but it is the mean arterial blood pressure (MAP) that is used when considering blood flow. As noted previously, since systole takes up one third of the cardiac cycle and diastole, two thirds, the MAP can be calculated as 1/3 SP + 2/3 DP. An MAP of 100 mmHg could come from a BP of 150/75 or 120/90 and a BP of 90/60 would give an MAP of 70 mmHg.

Since gravity pulls blood down, when the body is upright the MAP in the brachial artery is higher than the one in the arteries leading to the brain. Because the gravitational constant and the distance between the heart and the head are constant, the MAP in the brain, compared to the one in the aorta and in the brachial artery, can be determined.

At rest, the MAP in the aorta, as the blood exits the left ventricle, is usually about 80-110 mmHg. By the time the blood travels to the arms it has lost some energy and the MAP has dropped to 70-100 mmHg. Due the additional effect of gravity, when the body is in the upright position, the MAP in the brain drops to about 60-75 mmHg. Since it is the blood pressure that generates blood flow, this means that, in general, the lower the MAP in a given organ the lower the blood flow.

When you are sitting or standing, the force moving blood to your hands is higher than the one moving blood to your brain. However, despite this relatively low pressure, the brain has a mechanism in place, calledautoregulation, to help ensure adequate blood flow so its metabolic needs can be met.

Autoregulation within a given organ usually takes place independent of nervous or hormonal control and allows for adequate blood flow. It is important to understand that the blood flow (Q) within a given organ is directly related to its MAP (P) and inversely related to the vascular resistance in its arterioles (R). The higher the pressure, the more blood flow and the lower the pressure, the less blood flow. And the higher the arteriolar resistance within a given organ, the less blood flow, and the lower the arteriolar resistance, the more blood flow.

This natural law can be expressed as Q = P/R. One can therefore see that if the MAP drops in the brain, it can try to compensate by reducing its vascular resistance at the same time so it can maintain adequate blood flow to meet its metabolic needs. This is particularly important for brain function because of its high metabolic rate and extreme sensitivity to changes in blood flow.

Vascular resistance is directly related to the degree of muscle contraction around the arterioles.

More contraction causes more resistance and less contraction causes less resistance. When the MAP drops in the brain, autoregulation makes the vascular resistance drop almost immediately by relaxing the arteriolar muscles, increasing blood flow back to where it is supposed to be.

But, like everything else in life, autoregulation and its ability to control the blood flow in the brain does have objective limits. Regarding significant drops in blood pressure, there is only so much relaxation of the arteriolar muscles and reduction in vascular resistance that can take place.

Wince life is a dynamic process where the blood pressure is always fluctuating due to various circumstances, the body has to always keep it under control to prevent brain malfunction.

When you stand up, not only does gravity prevent blood from traveling to the brain, it also makes about 500 mL move from the veins in your chest and abdomen into your legs. This sudden drop in the volume of blood returning to the heart through the veins usually causes a

40 percent drop in the cardiac output and with it, a further drop in the MAP in the brain. So much so that autoregulation is incapable of adequately compensating for this sudden drop in pressure causing reduced blood flow. When this happens, we feel light-headed. If our body doesn't correct the situation or we don't get our head below our heart fast enough, we may pass out.

To fix this problem quickly, so we can remain standing, the body must know that if

Q = P/R, then P = Q x R. This expresses what has already been explained above. The blood pressure (P) is directly related to the total blood flow in the circulation (Q) (which is determined by how well the heart pumps and how much blood is in the arteries) and the peripheral vascular resistance (R). To prevent passing out on suddenly standing up, the body must immediately increase the cardiac output and the peripheral vascular resistance as well.

When it comes to making quick adjustments to blood pressure, it is the sympathetic nervous system, in response to the data it receives from the baroreceptors in main arteries carrying blood to the brain, that acts to solve the problem. When the MAP in the major arteries is in the normal range (70-100 mmHg), the frequency of impulses from the baroreceptors to the brain remains relatively stable. However, as the MAP deviates up or down from normal, the increase or decrease in the stretching of the vessel wall makes the baroreceptors increase or decrease the frequency of their messages. In response, the brain stem stimulates the sympathetic nervous system in an inverse pattern.

An increase in the MAP causes an increase in the frequency of impulses from the baroreceptors and a decrease in sympathetic activity. And a decrease in the MAP (like from standing up too quickly) causes a decrease in the frequency of impulses from the baroreceptors and an increase in sympathetic activity.

When we stand up too quickly, causing the MAP in our brachial artery to drop below 70 mmHg and the MAP in our brain to drop below 50 mmHg, we feel dizzy. By attaching to specific receptors, the increased output of sympathetic neurohormones quickly makes the systemic veins send more blood back into the arteries and the heart pump harder and faster. These quick actions combine to immediately increase the cardiac output (Q). And, increased sympathetic activity makes the muscles surrounding the arterioles in most of the tissues of the body contract more, quickly increasing the peripheral vascular resistance (R) as well.

As noted above, P = Q x R, so this rapid increase in Q and R, brings the MAP in the brain back to a level that allows its autoregulatory mechanism to maintain adequate blood flow. We experience this by our dizziness resolving within a second or two and being able to carry on. So it looks like the system the body uses to control its blood pressure to stand up to gravity seems to know what it's doing.

What has been described here is the real situation that faces human life. Not only must it know how the laws of nature work and have the mechanisms in place to deal with them, it must also do the right thing at exactly the right moment and do it well enough to survive.

By only describing how life looks, and not how it actually works, evolutionary biologists claim to have shown how life came into being by chance and the laws of nature alone. This means that all of the control mechanisms needed for all the chemical and physiological parameters to support life must have come about the same way.

Moreover, it is interesting to consider that in the last century, by using their intellectual powers to measure these parameters and sometimes do something about them, medical scientists have only recently been able to do what the body has had to do, by necessity, since the very beginning of its existence. For, as the next two articles in this series will demonstrate, when circumstances arise to overwhelm the body's ability to keep its blood pressure where it needs to be, real numbers matter.

Why sex fails as an engine for Darwinian evolution.

Can Sex Explain Evolution?

Denyse O'Leary September 29, 2015 3:54 AM 

Last time out, we looked at Darwin's theory of natural selection, alleged by some to be the single best idea anyone ever invented. The mere process of eliminating unfit examples of a type in a given environment builds up information over time, resulting in huge new layers of complexity.

But if no one can say what is fit or unfit according to natural selection, because nature has no direction, why must we pay attention to claims about natural selection? Why is there supposed to be anything to know?

Then there is Darwin's theory ofsexual selection, with its famous exemplar: the peacock's tail. An illustration may help us see why reasonable persons continue to doubt.

Picture a triplex: Tom, a world class cribbage addict in Apartment A, does no work and has no money (apart from social assistance and charity). Dick, in Apartment B, works eight shifts a week in trucking, so has no trouble paying his bills. Harry, formerly in Apartment C, went off and became a multimillionaire (legally) in packaging and shipping for the software industry.

Does work alone explain Harry's success? Did he work a thousand times harder and more often than Dick? Is that even possible? Or is it all an accident of fate, such that Tom or Dick might have stumbled down the same way and done the same thing?

Most human beings tend to doubt that it is so simple. Also, there are not a billion generations between Tom, Dick, and Harry. Not even one, actually.

And if each of these guys somehow ends up with fertile heirs, is any of them "unfit"?

Very well, so let us now look at Darwin's other theory, sexual selection:

Reproduction is expensive and can exert an additional evolutionary pressure. Darwin defined this pressure as sexual selection. Sexual selection operates through some members of a species having an advantage over others in terms of mating. It is the selection for traits that are solely concerned with increasing the mating success of an individual.

So fitter animals pass on their genes more frequently, so we don't know anything except that they do pass them on.

Traditionally, that has often been interpreted as, a more combative male wins more mates and sires more offspring, furthering evolution via his genes.

From a common sense perspective, there is a problem with the underlying assumption: The combative male may get himself seriously injured and be unable to protect his offspring. He may also be susceptible to a serious Y-linked disease to which the vanquished males are immune. So it is unclear whether fitter offspring reliably result from success in sexual competition.

Incidentally, human breeding is not a good analogy because breeders are "designers" who avoid breeding aggressive animals or those with serious genetic disease in their pedigree.

After a fruit fly experiment, some researchers offered an additional reason why sexual dominance does not necessarily speed evolution:

Females are frequently harassed and harmed by males attempting to obtain matings. When these males are also "choosy" with their courtship, there may be negative consequences to the species' ability to adaptively evolve.

Similarly, another study revealed many secrets of the convoluted sex lives of crickets, including the fact that "dominant males had fewer mates than subordinate males, but they had similar numbers of offspring."

Recently, a key sexual selection theory, Bateman's theory that promiscuity benefits males but not females, was subjected to replication studies (repeating the experiment to see if it works out) and it didn't replicate.

Sexual selection, despite its immense cultural popularity as an idea, does not seem to work as a mechanism for major evolutionary changes.

We are still stuck for a mechanism that replaces intelligence.

Beclouded by ego

Self-Image as a Bulwark of Darwinian Orthodoxy
David Klinghoffer September 25, 2015 11:49 AM


Carrying on the wonderful legacy of the noble Chuck Colson, the guys at BreakPoint -- John Stonestreet and Eric Metaxas -- are some of the more insightful commentators we know on the passing scientific scene. Stonestreet has a nice one this week ("Sensationalist Science"), noting the distorting role that pride plays in research, leading to some recent embarrassments.

Last month, psychology suffered a major blow when it was reported how often studies in the field fail the test of reproducibility -- better than half the time, in fact. Stonestreet asks:

Why are so many scientists apparently exaggerating and misinterpreting their findings? [Benedict] Carey [in the New York Times] points to what the scientists themselves describe as "a hypercompetitive culture across science that favors novel, sexy results and provides little incentive for researchers to replicate the findings of others, or for journals to publish studies that fail to find a splashy result."

In other words, sensationalist science is its own undoing. But there's more to it. Norbert Schwarz, a psychology professor at the University of Southern California, tells the Times that many senior researchers bristle at the thought of a younger, less experienced scientist critiquing their work. "There's no doubt," he said, "that replication is important, but it's often just [seen as] an attack, a vigilante exercise."

In other words, the real flaw in a lot of research isn't technical or methodological. It's just old-fashioned human pride. And it's not restricted to psychology or the social sciences. Dr. John Ioannidis, director of Meta-Research at Stanford, hints that the peer-review climate could be even more toxic in other fields, like cell biology, economics, neuroscience, clinical medicine, and animal research, calling the reliability of science itself into question.

Stonestreet draws a couple of appropriate conclusions for BreakPoint's Christian readers and listeners, including:

[T]his should remind us that science doesn't have all the answers. In fact, the more political, ideological, or lucrative the stakes, the more likely those "splashy results" are to be fish stories. And Christians know the reason: because inside every white lab coat and bow tie is a fallible human being, just like you and me.

The only thing this leaves out is an aspect of pride, and that is: prestige. In the context of evolution, it's all-important. It's not possible to exaggerate the place of self-image as a bulwark of Darwinian orthodoxy. Experience has taught us, again and again, how often otherwise thoughtful people refuse to consider alternative understandings of life's origins because that would potentially lead them down a socially uncomfortable path.

Yes, for scientists there are real professional dangers that go with opening your mouth to say something critical of the reigning evolutionary theory. Even for the tenured scholar, and all the more so for the untenured and the graduate student, a great deal of looking over your shoulder and anticipating damnation goes with the thought of admitting that Darwinism faces serious scientific challenges, or that evidence of design in nature might conceivably be worth a look.

Some folks in other professions -- journalism, notably -- face similar pressures, potentially impacting careers in very practical ways.

For many others -- not scientists but lay people -- it's the cloud of prestige around certain ideas, not the evidence or arguments behind them, that really matters. That's why Darwin defenders so typically respond to ID not with evidence and arguments of their own but with emotional manipulation based on their listeners' self-image.

The strategy has evolved with the times. It used to be that Darwin skeptics were tarred predominantly with language suggestive of religious fundamentalism. Hence the popularity of conflating intelligent design with creationism, resulting in the fanciful chimera of "Intelligent Design Creationism." More recently the tactic has shifted somewhat, with Darwin advocates making increased use of the weaponized terms "science denial" and "science denier." Here the idea is to subtly associate skepticism with something not just embarrassing but utterly vile -- Holocaust denial.


So, yes, as John Stonestreet says, pride plays its unacknowledged but important role in science discussions. Boy, does it ever.

On how natural flight makes the case for design

Ideology first/good science whenever

Junk Science at Smithsonian's Hall of Human Origins

Casey Luskin September 27, 2015 3:38 PM |

This past week I was in Washington, DC (no, not to see the Pope) and had the opportunity to spend a couple hours at the Smithsonian Institution's National Museum of Natural History. I had long looked forward to seeing its David H. Koch Hall of Human Origins.

Ever since the hall opened in 2010, I'd been hearing that the exhibit was not just biased in favor of evolution, but had an unabashed evangelical motive to promote evolution to the public. In fact, in 2010 I heard Rick Potts (director of the Smithsonian's Human Origins Program) speak at an American Scientific Affiliation conference where he essentially admitted just that. He more or less told the audience that the purpose of the Smithsonian's human origins displays was to encourage the public -- especially religious communities -- to accept evolution.

Marvin Olasky recently reviewed the museum in World Magazine, but I needed to see it for myself. I love museums, and I love fossils, and I don't mind at all when museums talk about evolution. What I found is that the Hall of Human Origins is so zealous in its agenda that it was willing to promote junk science to achieve its goals.

One thing that really struck me is how the exhibit repeatedly called early hominins "early humans" even though they're very far from humanlike. This apparently is an effort to make you think that these creatures are really "us" and we are "them."

For example, early on I watched an interactive video display that showed a young paleoanthropologist discussing "early humans." I thought I heard her mention Paranthropus robustus as an example of an "early human," but I wasn't sure I heard that correctly. Surely, I mused, nobody would call Paranthropus robustus an "early human" when it's thought, even by mainstream paleoanthropologists, to belong to a distant side branch that was far removed from human origins. So I stuck around to listen to the whole video over again to make sure I hadn't misheard.

Unfortunately, I hadn't misheard.

So why was the exhibit calling Paranthropus robustus an "early human" -- when its very name means "parallel to man" because it's not thought to be in our line of ancestry, but was a distinct creature that probably lived alongside early Homo? The rest of my visit helped explain what was going on.

This same pattern repeated throughout the exhibit. Again and again, it promotes as "ancient humans" fossils that virtually no scientist would call "human" -- and clearly don't belong in the genus "Homo." Here's one example:

• Another display said, "From at least 6 to 3 million years ago, early humans combined apelike and humanlike ways of moving around." These must be really early humans because there were no humans around back then, and nothing that looked human or walked or thought or behaved like humans. Yet the exhibit calls these "early humans" apparently so visitors will think that these non-human species are connected to us.
• Another display says "For the first several million years of human evolution, early humans lived only in Africa." The display makes it clear they're talking about species prior to 1.8 million years ago. But again, prior to that time it's not clear that Homoexisted. The species from that period were not human.
• Yet another display shows a chimp, an australopithecine, and a modern young lady and calls the australopithecine "early human." A similar display portrays an "early human" that is 3 million years old next to a "modern human" eating a slice of pizza. The problem, of course, is that 3 million years ago there was nothing around that should be called "human," whether "early " or otherwise.
• Finally, one panel calls Sahelanthropus tchadensis an "early human" though it is from about 6 million years ago, and all we have of this species is a skull that some have said resembles a gorilla.

It's simple: The Smithsonian's Human Origins hall is overwhelmingly animated by the desire to sell Darwinism. That isn't surprising. After all, during the California Science Center case, we discovered that internal Smithsonian emails said ID is officially "against SI/MNH policy." And that's true enough. The Smithsonian punished evolutionary biologistRichard Sternberg just for publishing a peer-reviewed article by Stephen Meyer in a technical biological journal.

As an institution, the Smithsonian is zealous for Darwinism -- so much so that it is willing to promote claims that are obviously bad science.

Not the planet of the apes.

Recent Genetic Research Shows Chimps More Distant From Humans, Neanderthals Closer
Casey Luskin April 29, 2010 9:04 AM 

Research published in Nature over the past few months is showing a much greater genetic distance between humans and chimps than previously thought, while revealing a closer one between humans and Neanderthals.

A Nature paper from January, 2010 titled, "Chimpanzee and human Y chromosomes are remarkably divergent in structure and gene content," found that Y chromosomes in humans and chimps "differ radically in sequence structure and gene content," showing "extraordinary divergence" where "wholesale renovation is the paramount theme." Of course, the paper attributes these dramatic genetic changes to "rapid evolution during the past 6 million years."

One of the scientists behind the study was quoted in a Nature news article stating, "It looks like there's been a dramatic renovation or reinvention of the Y chromosome in the chimpanzee and human lineages." The news article states that "many of the stark changes between the chimp and human Y chromosomes are due to gene loss in the chimp and gene gain in the human" since "the chimp Y chromosome has only two-thirds as many distinct genes or gene families as the human Y chromosome and only 47% as many protein-coding elements as humans." According to the news piece, "Even more striking than the gene loss is the rearrangement of large portions of the chromosome. More than 30% of the chimp Y chromosome lacks an alignable counterpart on the human Y chromosome, and vice versa, whereas this is true for less than 2% of the remainder of the genome."

But not wishing to offend the "myth of 1%", the Nature news article carefully adds, "The remainder of the chimp and human genomes are thought to differ in gene number by less than 1%."

While this research takes us genetically further from apes, a more recent report in Nature news takes us genetically much closer to Neanderthals. Titled, "Neanderthals may have interbred with humans," the article explains that "A genetic analysis of nearly 2,000 people from around the world indicates that such extinct species interbred with the ancestors of modern humans twice, leaving their genes within the DNA of people today." According to this new article:

[I]t may help explain the fate of the Neanderthals, who vanished from the fossil record about 30,000 years ago. "It means Neanderthals didn't completely disappear," says Jeffrey Long, a genetic anthropologist at the University of New Mexico, whose group conducted the analysis. There is a little bit of Neanderthal leftover in almost all humans, he says.
Given the high degree of skeletal similarity between humans and Neanderthals, the notion that we interbred is nothing new. They have been called a possible "race" of our own species, as studies have found their body shape is highly similar to that of modern human variation. Indeed, the discovery of "morphological mosaics" indicates that they likely interbred with modern humans. The finding of a modern-humanlike hyoid bone in a Neanderthal implies that they may have had language capabilities.

Textbooks often depict Neanderthals as primitive, bungling brutes with a vaguely human-like form (see above)--an attempt to instill the ape-to-human icon in students. But as Time Magazine reported in 1999, there's increasing evidence showing that this evolutionary interpretation was wrong, and Neanderthals were essentially "all just people":

The real message, [a Washington University paleoanthropologist Erik] Trinkaus believes, is that to people living in the Stone Age, Neanderthals were just another tribe. "They may have had heavier brows or broader noses or stockier builds, but behaviorally, socially and reproductively they were all just people."
(Michael D. Lemonick, "A Bit of Neanderthal in Us All?," Time Magazine (April 25, 1999).)


Some ID proponents might disagree with me on this particular point, but it's my view that Neanderthals were a race of human beings that ultimately went extinct. Either way, it's becoming increasingly clear that Neanderthals do nothing to bolster the case that humans evolved from more primitive hominids.

Would you know it if you saw it?

A world-famous chemist tells the truth: there’s no scientist alive today who understands macroevolution.

Professor James M. Tour is one of the ten most cited chemists in the world. He is famous for his work on nanocars (pictured above, courtesy of Wikipedia), nanoelectronics, graphene nanostructures, carbon nanovectors in medicine, and green carbon research for enhanced oil recovery and environmentally friendly oil and gas extraction. He is currently a Professor of Chemistry, Professor of Computer Science, and Professor of Mechanical Engineering and Materials Science at Rice University. He has authored or co-authored 489 scientific publications and his name is on 36 patents. Although he does not regard himself as an Intelligent Design theorist, Professor Tour, along with over 700 other scientists, took the courageous step back in 2001 of signing the Discovery Institute’s “A Scientific Dissent from Darwinism”, which read: “We are skeptical of claims for the ability of random mutation and natural selection to account for the complexity of life. Careful examination of the evidence for Darwinian theory should be encouraged.”

On Professor Tour’s Website, there’s a very revealing article on evolution and creation, in which Tour bluntly states that he does not understand how macroevolution could have happened, from a chemical standpoint (all bold emphases below are mine – VJT):

Although most scientists leave few stones unturned in their quest to discern mechanisms before wholeheartedly accepting them, when it comes to the often gross extrapolations between observations and conclusions on macroevolution, scientists, it seems to me, permit unhealthy leeway. When hearing such extrapolations in the academy, when will we cry out, “The emperor has no clothes!”?

…I simply do not understand, chemically, how macroevolution could have happened. Hence, am I not free to join the ranks of the skeptical and to sign such a statement without reprisals from those that disagree with me? … Does anyone understand the chemical details behind macroevolution? If so, I would like to sit with that person and be taught, so I invite them to meet with me.

In a more recent talk, entitled, Nanotech and Jesus Christ, given on 1 November 2012 at Georgia Tech, Professor Tour went further, and declared that no scientist that he has spoken to understands macroevolution – and that includes Nobel Prize winners! Here’s what he said when a student in the audience asked him about evolution:

… I will tell you as a scientist and a synthetic chemist: if anybody should be able to understand evolution, it is me, because I make molecules for a living, and I don’t just buy a kit, and mix this and mix this, and get that. I mean, ab initio, I make molecules. I understand how hard it is to make molecules. I understand that if I take Nature’s tool kit, it could be much easier, because all the tools are already there, and I just mix it in the proportions, and I do it under these conditions, but ab initio is very, very hard.

I don’t understand evolution, and I will confess that to you. Is that OK, for me to say, “I don’t understand this”? Is that all right? I know that there’s a lot of people out there that don’t understand anything about organic synthesis, but they understand evolution. I understand a lot about making molecules; I don’t understand evolution. And you would just say that, wow, I must be really unusual.

Let me tell you what goes on in the back rooms of science – with National Academy members, with Nobel Prize winners. I have sat with them, and when I get them alone, not in public – because it’s a scary thing, if you say what I just said – I say, “Do you understand all of this, where all of this came from, and how this happens?” Every time that I have sat with people who are synthetic chemists, who understand this, they go “Uh-uh. Nope.” These people are just so far off, on how to believe this stuff came together. I’ve sat with National Academy members, with Nobel Prize winners. Sometimes I will say, “Do you understand this?”And if they’re afraid to say “Yes,” they say nothing. They just stare at me, because they can’t sincerely do it.

I was once brought in by the Dean of the Department, many years ago, and he was a chemist. He was kind of concerned about some things. I said, “Let me ask you something. You’re a chemist. Do you understand this? How do you get DNA without a cell membrane? And how do you get a cell membrane without a DNA? And how does all this come together from this piece of jelly?” We have no idea, we have no idea. I said, “Isn’t it interesting that you, the Dean of science, and I, the chemistry professor, can talk about this quietly in your office, but we can’t go out there and talk about this?”

If you understand evolution, I am fine with that. I’m not going to try to change you – not at all. In fact, I wish I had the understanding that you have.

But about seven or eight years ago I posted on my Web site that I don’t understand. And I said, “I will buy lunch for anyone that will sit with me and explain to me evolution, and I won’t argue with you until I don’t understand something – I will ask you to clarify. But you can’t wave by and say, “This enzyme does that.” You’ve got to get down in the details of where molecules are built, for me. Nobody has come forward.

The Atheist Society contacted me. They said that they will buy the lunch, and they challenged the Atheist Society, “Go down to Houston and have lunch with this guy, and talk to him.” Nobody has come! Now remember, because I’m just going to ask, when I stop understanding what you’re talking about, I will ask. So I sincerely want to know. I would like to believe it. But I just can’t.

Now, I understand microevolution, I really do. We do this all the time in the lab. I understand this. But when you have speciation changes, when you have organs changing, when you have to have concerted lines of evolution, all happening in the same place and time – not just one line – concerted lines, all at the same place, all in the same environment … this is very hard to fathom.

I was in Israel not too long ago, talking with a bio-engineer, and [he was] describing to me the ear, and he was studying the different changes in the modulus of the ear, and I said, “How does this come about?” And he says, “Oh, Jim, you know, we all believe in evolution, but we have no idea how it happened.” Now there’s a good Jewish professor for you. I mean, that’s what it is. So that’s where I am. Have I answered the question? (52:00 to 56:44)

Professor Tour’s online talk is absolutely fascinating as well as being deeply moving on a personal level, and I would strongly urge readers to listen to his talk in its entirety – including the questions after the talk. You won’t regret it, I promise you. One interesting little gem of information which I’ll reveal is that it was Professor Tour who was largely instrumental in getting Nobel Laureate Richard Smalley, winner of the 1996 Nobel Prize in Chemistry, to reject Darwinian evolution and accept Old Earth creationism, shortly before he died in 2005. It was Tour who persuaded Smalley to delve into the question of origins. After reading the books “Origins of Life” and “Who Was Adam?”, written by Dr. Hugh Ross (an astrophysicist) and Dr. Fazale Rana (a biochemist).. Dr. Smalley explained his change of heart as follows:

Evolution has just been dealt its death blow. After reading “Origins of Life”, with my background in chemistry and physics, it is clear evolution could not have occurred. The new book, “Who Was Adam?”, is the silver bullet that puts the evolutionary model to death.

Strong words indeed, for a Nobel scientist. Readers can find out more about Professor Richard Smalley’s change of views here.

Why should we believe macroevolution, if nobody understands it?

Now that Professor Tour has informed the world that even Nobel Prize-winning scientists privately admit that they don’t understand macroevolution, a layperson is surely entitled to ask: “Well, if even they don’t understand it, then why should we believe it? How can we possibly be obliged to believe in a theory which nobody understands?”

That’s a good question. And it’s no use for Darwinists to trot out the standard “party line” that “even if we don’t yet understand how it happened, we still have enough evidence to infer that it happened.” At the very most, all that the current scientific evidence could establish is the common descent of living organisms. But that’s not macroevolution. Macroevolution requires more than a common ancestry for living organisms: it requires a natural mechanism which can generate the diversity of life-forms we see on Earth today from a common stock, without the need for any direction by an Intelligent Agent. But the mechanism is precisely what we don’t have evidence for. So the question remains: why should we believe in macroevolution?

The decline of academic freedom

Given the massive uncertainty about the “how” of macroevolution among scientists working in the field, you might think that a wide variety of views would be tolerated in the scientific arena – including the view that there is no such process as macroevolution. However, you would be sadly mistaken. As Professor Tour notes in his online article on evolution and creation, an alarming academic trend has emerged in recent years: a growing intolerance of dissent from Darwinism. This trend is so pronounced that Professor Tour now advises his students not to voice their doubts about Darwinism in public, if they want a successful career:

In the last few years I have seen a saddening progression at several institutions. I have witnessed unfair treatment upon scientists that do not accept macroevolutionary arguments and for their having signed the above-referenced statement regarding the examination of Darwinism. (I will comment no further regarding the specifics of the actions taken upon the skeptics; I love and honor my colleagues too much for that.) I never thought that science would have evolved like this. I deeply value the academy; teaching, professing and research in the university are my privileges and joys…

But my recent advice to my graduate students has been direct and revealing: If you disagree with Darwinian Theory, keep it to yourselves if you value your careers, unless, of course, you’re one of those champions for proclamation; I know that that fire exists in some, so be ready for lead-ridden limbs. But if the scientific community has taken these shots at senior faculty, it will not be comfortable for the young non-conformist. When the power-holders permit no contrary discussion, can a vibrant academy be maintained? Is there a University (unity in diversity)? For the United States, I pray that the scientific community and the National Academy in particular will investigate the disenfranchisement that is manifest upon some of their own, and thereby address the inequity.

It remains to be seen if other countries will allow their young scientists to think freely about the origin of life, and of the various species of organisms that we find on Earth today. What I will say, though, is that countries which restrict academic freedom will eventually be overtaken by countries which allow it to prosper. There is still time for America and Europe to throw off the dead hand of Darwinism in academic circles, and let their young people breathe the unaccustomed air of free speech once again.

Where imagination and storytelling trump observation and analysis

When Theory Trumps Observation: Responding to Charles Marshall's Review of Darwin's Doubt

Stephen C. Meyer October 2, 2013 4:25 PM 

'm pleased that the journal Scienceassigned my book Darwin's Doubt for review to the distinguished UC Berkeley paleontologist Charles Marshall. His is the first critical review ("When Prior Belief Trumps Scholarship," September 20, 2013) to grapple with the book's main arguments about the inability of standard evolutionary mechanisms to explain the origin of morphological novelty in the Cambrian period. Though Marshall does address the main problem discussed in the book, his review also demonstrates -- if inadvertently -- the severity of that problem, and that leading Cambrian paleontologists and evolutionary biologists (such as Dr. Marshall) are nowhere close to solving it.

In coming days I will offer four responses to the four main critiques that Marshall presents of Darwin’s Doubt in his review. I begin here by addressing Marshall’s claim that developmental gene regulatory networks (dGRNs), which are necessary for the development of animals, could have been more labile or flexible in the past.¹ Marshall made this claim to challenge my contention in Chapter 13 of Darwin’s Doubt that the observed inflexibility of these regulatory networks represents a major impediment to the evolutionary transformation of one animal body plan into another.² Not so, he argues. As he asserted in his review, “today's GRNs have been overlain with half a billion years of evolutionary innovation (which accounts for their resistance to modification), whereas GRNs at the time of the emergence of the phyla were not so encumbered."³

Yet, contrary to Marshall’s speculation about how dGRNs might have functioned in the past, all available observational evidence establishes that dGRNs do not tolerate random perturbations to their basic control logic. Indeed, mutagenesis experiments conducted on the genes present in dGRNs have repeatedly shown that even modest mutation-induced changes to these genes either produce no change in the developmental trajectory of animals (due to pre-programmed buffering or redundancy) or they produce catastrophic (most often, lethal) effects within developing animals. Disrupt the central control nodes, and the developing animal does not shift to a different, viable, stably heritable body plan. Rather, the system crashes, and the developing animal usually dies.⁴ As developmental biologist Eric Davidson has noted:

There is always an observable consequence if a dGRN subcircuit is interrupted. Since these consequences are always catastrophically bad, flexibility is minimal, and since the subcircuits are all interconnected, the whole network partakes of the quality that there is only one way for things to work. And indeed the embryos of each species develop in only one way.⁵

Thus, to claim, as Marshall does in his review of Darwin’s Doubt, that dGRNs might have been more elastic in the past contradicts what developmental biologists have learned over several decades investigating how these networks actually function from mutagenesis studies of many different biological "model systems," includingDrosophila (fruit flies), Caenorhabditis (nematodes), Strongylocentrotus(sea urchins), Danio (zebrafish) and other animals.⁶ Moreover, as Marshall himself has noted elsewhere, there is a good reason for this inflexibility. As Marshall explains, “many of the characters that evolved during the origin of the phyla are no longer able to change. The reason for this is that selectable variation is absent: either the characters are invariant or mutants that carry this variation are sterile or lethal.”⁷

Of course, Marshall thinks that these networks could have had a different, more flexible, character in the past. Yet, given what dGRNs do, namely, that they enable different cell types to organize themselves, and differentiate themselves from each other, in precise ways at precise times during the development of specific animal forms, it is hard to see how dGRNs could have functioned as regulatory networks and also exhibited the kind of flexibility that Marshall envisions. Developmental gene regulatory networks are control systems. A labile dGRN would generate (uncontrolled) variable outputs, precisely the opposite of what a functional control system does. It is telling that although many evolutionary theorists (like Marshall) have speculated about early labile dGRNs, no one has ever described such a network in any functional detail -- and for good reason. No developing animal that biologists have observed exhibits the kind of labile developmental gene regulatory network that the evolution of new body plans requires. Indeed, Eric Davidson, when discussing hypothetical labile dGRNs, acknowledges that we are speculating "where no modern dGRN provides a model" since they "must have differed in fundamental respects from those now being unraveled in our laboratories."⁸

By ignoring this evidence, Marshall and other defenders of evolutionary theory reverse the epistemological priority of the historical scientific method as pioneered by Charles Lyell, Charles Darwin and others.⁹Rather than treating our present experimentally based knowledge as the key to evaluating the plausibility of theories about the past, Marshall uses an evolutionary assumption about what must have happened in the past (transmutation) to justify disregarding experimental observations of what does, and does not, occur in biological systems. The requirements of evolutionary doctrine thus trump our observations about how nature and living organisms actually behave. What we know best from observation takes a back seat to prior beliefs about how life must have arisen.

In the next installment in this series, I’ll address Marshall’s claim that building Cambrian animals would not have required large amounts of new genetic information --  as I argue in Darwin’s Doubt -- but instead could have been produced by the “rewiring” of preexisting developmental gene regulatory networks.

NOTES:

(1) Charles R. Marshall, "When Prior Belief Trumps Scholarship," Science341 (September 20, 2013): 1344.

(2) Stephen C. Meyer, Darwin’s Doubt: The Explosive Origin of Animal Life and the Case for Intelligent Design. HarperOne, 2013, 264-270.

(3) Charles R. Marshall, "When Prior Belief Trumps Scholarship," Science341 (September 20, 2013): 1344.

(4) See Eric H. Davidson, "Evolutionary Bioscience as Regulatory Systems Biology," Developmental Biology, 357 (September 1, 2011): 35-40. See also the discussion in Darwin's Doubt, pp. 264-70.

(5) See Eric H. Davidson, "Evolutionary Bioscience as Regulatory Systems Biology," Developmental Biology, 357 (September 1, 2011): 40.

(6) See, for example, the discussion of the model systemStrongylocentrotus purpuratus in: P. Oliveri, Q. Tu, and E. H. Davidson, “Global Regulatory Logic for Specification of an Embryonic Cell Lineage,” Proceedings of the National Academy of Sciences USA, 105 (2008): 5955-62. For a diagrammed schematic of the dGRN network ofStrongylocentrotus purpuratus see Figure 1D in this article.

(7) See N.H. Shubin and C.R. Marshall, “Fossils, Genes, and the Origin of Novelty,” Paleobiology 26, no. 4, Supplement (2000): 335. (Emphasis added).

(8) Eric H. Davidson, "Evolutionary Bioscience as Regulatory Systems Biology," Developmental Biology, 357 (September 1, 2011): 40.

(9) See Charles Lyell, Principles of Geology: Being an Attempt to Explain the Former Changes of the Earth's Surface, by Reference to Causes Now in Operation. 3 vols. London: Murray, 1830-33, pp. 75-91.