Epistemology vs. Darwin.

Evolution May Obscure Reality, Says a Cognitive Scientist and Evolutionist

Sarah Chaffee

Writing here last month, I explained why Darwinian theory directly undermines UC Berkeley psychologist Tania Lombrozo's argument that our reasoning may be getting better because science is getting better. In truth, naturalistic evolution erodes confidence in human reasoning -- the basis of science.

But it's not only evolution skeptics who realize this. For an article in The Atlantic, Amanda Gefter interviewed UC Irvine cognitive scientist Donald D. Hoffman ("The Case Against Reality"):

Gefter: People often use Darwinian evolution as an argument that our perceptions accurately reflect reality. They say, "Obviously we must be latching onto reality in some way because otherwise we would have been wiped out a long time ago. If I think I'm seeing a palm tree but it's really a tiger, I'm in trouble."

Hoffman: Right. The classic argument is that those of our ancestors who saw more accurately had a competitive advantage over those who saw less accurately and thus were more likely to pass on their genes that coded for those more accurate perceptions, so after thousands of generations we can be quite confident that we're the offspring of those who saw accurately, and so we see accurately. That sounds very plausible. But I think it is utterly false. It misunderstands the fundamental fact about evolution, which is that it's about fitness functions -- mathematical functions that describe how well a given strategy achieves the goals of survival and reproduction. The mathematical physicist Chetan Prakash proved a theorem that I devised that says: According to evolution by natural selection, an organism that sees reality as it is will never be more fit than an organism of equal complexity that sees none of reality but is just tuned to fitness. Never.

Gefter: You've done computer simulations to show this. Can you give an example?

Hoffman: Suppose in reality there's a resource, like water, and you can quantify how much of it there is in an objective order -- very little water, medium amount of water, a lot of water. Now suppose your fitness function is linear, so a little water gives you a little fitness, medium water gives you medium fitness, and lots of water gives you lots of fitness -- in that case, the organism that sees the truth about the water in the world can win, but only because the fitness function happens to align with the true structure in reality. Generically, in the real world, that will never be the case. Something much more natural is a bell curve -- say, too little water you die of thirst, but too much water you drown, and only somewhere in between is good for survival. Now the fitness function doesn't match the structure in the real world. And that's enough to send truth to extinction. For example, an organism tuned to fitness might see small and large quantities of some resource as, say, red, to indicate low fitness, whereas they might see intermediate quantities as green, to indicate high fitness. Its perceptions will be tuned to fitness, but not to truth. It won't see any distinction between small and large -- it only sees red -- even though such a distinction exists in reality.

Gefter: But how can seeing a false reality be beneficial to an organism's survival?

Hoffman: There's a metaphor that's only been available to us in the past 30 or 40 years, and that's the desktop interface. Suppose there's a blue rectangular icon on the lower right corner of your computer's desktop -- does that mean that the file itself is blue and rectangular and lives in the lower right corner of your computer? Of course not. But those are the only things that can be asserted about anything on the desktop -- it has color, position, and shape. Those are the only categories available to you, and yet none of them are true about the file itself or anything in the computer. They couldn't possibly be true. That's an interesting thing. You could not form a true description of the innards of the computer if your entire view of reality was confined to the desktop. And yet the desktop is useful. That blue rectangular icon guides my behavior, and it hides a complex reality that I don't need to know. That's the key idea. Evolution has shaped us with perceptions that allow us to survive. They guide adaptive behaviors. But part of that involves hiding from us the stuff we don't need to know. And that's pretty much all of reality, whatever reality might be. If you had to spend all that time figuring it out, the tiger would eat you.

We cannot depend on evolution to give us the ability to grasp truth. Darwinism doesn't necessarily reveal reality to us; it can hide it. Here is research Hoffman published in the Journal of Theoretical Biology making the same argument. The idea that evolution doesn't necessarily generate an ability to grasp truth doesn't just come from advocates of intelligent design. And it has many serious implications.

In her recent book, Finding Truth: 5 Principles for Unmasking Atheism, Secularism, and Other God Substitutes, Nancy Pearcey highlights logical inconsistencies in holding to evolution. She notes: 

An especially damaging form of contradiction is self-referential absurdity -- which means a theory sets up a definition of truth that it itself fails to meet....An example of self-referential absurdity is a theory called evolutionary epistemology, a naturalistic approach that applies evolution to the process of knowing. The theory proposes that the human mind is a product of natural selection. The implication is that the ideas in our minds were selected for their survival value, not for their truth-value. 

But what if we apply that theory to itself? Then it, too, was selected for survival, not truth -- which discredits its own claim to truth. Evolutionary epistemology commits suicide.

Philosopher Thomas Nagel takes this in a slightly different direction in The View from Nowhere, noting how evolution can't produce our modern science:

In themselves, the advanced intellectual capacities of human beings, unlike many of their anatomical, physiological, perceptual, and more basic cognitive features, are extremely poor candidates for evolutionary explanation, and would in fact be rendered highly suspect by such an explanation. I am not suggesting, as Kant once did..., that reason has negative survival value and could from that point of view be replaced by instinct. But the capacity to form cosmological and subatomic theories takes us so far from the circumstances in which our ability to think would have had to pass its evolutionary tests that there would be no reason whatever, stemming from the theory of evolution, to rely on it in extension to those subjects. In fact if, per impossibile, we came to believe that our capacity for objective theory were the product of natural selection, that would warrant serious skepticism about its results beyond a very limited and familiar range. 

Purely naturalistic neo-Darwinism is self-defeating in its illogic. The consequences of this truth are far-reaching. Those consequences should include, at the very least, treating evolution as an ordinary idea, not as sacred dogma, while being open to considering other possibilities.

Genetic evidence for common ancestry?Or give us a miracle and we'll explain the rest.

Stunning Evidence for Common Ancestry? S. Joshua Swamidass on the Chimp-Human Divergence

Cornelius Hunter

I once had a rare and valuable baseball card I wanted to sell. I placed an ad and was shortly contacted by a collector. But to my dismay he wasn't interested. He had probably looked at hundreds of baseball cards and it only required one look for him to know that my treasured card held no value for him. He did not attempt any negotiating tricks, just a polite "thank you" and off he went. I would have felt better about the encounter if he had tried to haggle with me to lower the price. For I would have had the comfort of knowing my card held at least some value. Apparently it didn't.

I too am a collector of sorts. And like that baseball card collector I have looked at hundreds of specimens. No matter how unlikely the source or the venue, I will go there and have a look. And in short order, I will know exactly what I am looking at, and if there is any value there. But unlike the baseball card collector, I'm not after something you can hold in your hand. 

What I am interested in are the arguments and evidences for evolution. Ever since Darwin, evolutionists have insisted that their idea is undeniable -- beyond all reasonable doubt. I find that complete certainty to be fascinating. So I search out, analyze, and categorize every justification and explanation for that conclusion that I can find.

My goal is to discover the strongest, most powerful, such arguments and evidences, and to understand how thoughtful people can have such certainty. This brings us to S. Joshua Swamidass, a professor in the Genomic Medicine Division at Washington University and author of a recent post at his website, "Evidence and Evolution." Given his credentials, he deserves to be listened to. Swamidass explains that the evidence for evolution is powerful and compelling. This evidence, which he describes as stunning, is definitely a specimen I want to have a look at.

In his post, Swamidass's focus is on human evolution. Evolutionists believe that we humans evolved from a small ape-like creature and that our closest relative on the evolutionary tree is the chimpanzee. The chimpanzee must be our closest relative, they reason, because the chimp's genome is closest to ours, and according to evolution, genetic mutations are the fuel behind evolutionary change.

The problem with this reasoning is that according to many other measures, the chimpanzee is not very similar to humans. There are enormous differences between the two species. Furthermore, in its morphology and behavior, the orangutan is closer to humans than the chimpanzee. Simply put, from an evolutionary perspective the genetic data are not congruent with the other data. Swamidass's evidence will need to overcome this obvious problem.

But that's not all.

The basic idea of humans arising via a long series of genetic mutations is, itself, not indicated by the science and is unlikely to say the least. Remember, the mutations have to be random. According to evolution, you can't have mutations occurring for some purpose, such as creating a design. And natural selection doesn't help -- it cannot induce or coax the right mutations to occur. This makes the evolution of even a single protein, let alone humans, statistically impossible. So this is another enormous problem Swamidass's evidence will need to overcome.

But that's not all.

The incredible designs in the human body are not the only thing those random mutations have to create -- they will also have to create human consciousness. Evolutionists may try to explain consciousness as an "emergent" property that just luckily arose when our brain somehow evolved. Or they may try to explain that consciousness is really no more than an illusion. But these are just more demonstrations of anti-realism in evolutionary thought. By that I mean, evolutionary theory constructs mechanisms and explanations that do not correspond to the real world. So this is another problem Swamidass will need to overcome.

But that's not all.

In recent decades the genomes of humans and chimps have been determined, and in an evolutionary paradigm they make no sense. One of the main problems is that the genes of the two species are almost identical. They are only about 1-to-2 percent different and, if you're an evolutionist, this means you have to believe that the evolution of humans from a small, primitive, ape-like creature was caused by only a tiny modification of the genome.

This goes against everything we have learned about genetics. You can insert far greater genetic changes with far less change arising as a consequence. It makes little sense that tiny genetic changes could cause such enormous design changes to occur. This is yet another problem for Swamidass to overcome.

But that's not all.

Not only is evolution limited to tiny genetic modifications to create the human, but the majority of those modifications would have had to be of little or no consequence. Here is how a 2005 paper on the chimpanzee-human genome comparisons put it:

In particular, we find that the patterns of evolution in human and chimpanzee protein-coding genes are highly correlated and dominated by the fixation of neutral and slightly deleterious alleles.

The paper is written from an evolutionary perspective, assuming that humans and chimpanzees share a common ancestor. Given that a priori assumption, they were forced to conclude that most of the mutations affecting protein-coding genes led to "neutral and slightly deleterious alleles." So not only are evolution's random mutation resources meager, in terms of both quality and quantity as explained above, but even worse, those mutations mostly led to "neutral and slightly deleterious alleles." This is no way to evolve the most complex designs in the world and it is yet another problem for Swamidass to overcome.

But that's not all.

When evolutionists search for genes in the human genome that do show signs of selection, rather than neutral drift (again, under the assumption of evolution), they find only a limited repertoire of functionality. For example, one study found genes involved in the sense of smell, in digestion, in hairiness, and in hearing. In other words, evolution is suggesting that we differ from the chimp mainly in those functions. It is a silly conclusion and another problem for Swamidass to explain.

But that's not all.

That 2005 paper also found a host of chimp-human comparisons that are nonsensical in evolutionary terms. In other words, if you are forced to interpret the genetic comparisons in terms of evolution, you end up with contradictions. For example, if you look at large segments of DNA, corresponding in the human and the chimp, you find unexplainable variations in the chimp-human differences:

Nucleotide divergence rates are not constant across the genome... The average divergence in 1-Mb segments fluctuates with a standard deviation of 0.25%, which is much greater than the 0.02% expected assuming a uniform divergence rate.

To explain these nonsensical findings evolutionists have to resort to a "then a miracle happened" hypothesis. The usual explanatory devices do not work, so they are left only with the claim that local variations in the mutation rate did it -- which amounts to special pleading:

[W]e suggest that the large-scale variation in the human-chimpanzee divergence rate primarily reflects regional variation in mutation rate.

Under evolution there is no scientific reason, beyond hand-waving speculation, for such variations. This is the equivalent of epicycles in geocentrism and so we have yet another problem for Swamidass to address.

But that's not all.

The supposed divergence rate between chimps and humans not only has an unexplainable variation in large, 1-Mb segments of DNA, it also has an unexplainable variation towards the ends of most chromosomes. This is another problem that seems to make no sense under evolution, which Swamidass must explain.

But that's not all.

This supposed divergence rate between chimps and humans also has an unexplainable variation that correlates with chromosomal banding. Again, this makes no sense under evolution. Why should the chimp-human divergence vary with the banding pattern? Evolutionists have only just-so stories to imagine why this would have happened, and it is another problem for Swamidass to address.

But that's not all.

This supposed divergence rate between chimps and humans is not consistent with the supposed divergence rate between the mouse and rat. The mouse-rat divergence is about an order of magnitude greater than the chimp-human divergence. Yet the mouse and rat are much more similar than the chimp and human. It makes no sense under evolution. In fact, before the rat genome was determined, evolutionists predicted it would be highly similar to the mouse genome. As one paper explained:

Before the launch of the Rat Genome Sequencing Project (RGSP), there was much debate about the overall value of the rat genome sequence and its contribution to the utility of the rat as a model organism. The debate was fuelled by the naïve belief that the rat and mouse were so similar morphologically and evolutionarily that the rat sequence would be redundant.

The prediction that the mouse and rat genomes would be highly similar made sense according to evolution. But it was dramatically wrong.

Another approach is to ignore the morphological similarities and reason from the number of generations available to produce the genomic differences between the mouse and rat. The mouse-rat divergence date is estimated by evolutionists to be older than the chimp-human divergence date. Furthermore, the lifespan and generation time for mice and rats are much shorter than for chimps and humans. From this perspective, and given these two effects, one would conclude that the mouse-rat genetic divergence should be much greater -- at least two orders of magnitude greater -- than the chimp-human genetic divergence. But it isn't. It is only about one order of magnitude greater.

So either way the mouse-rat comparison does not help to explain things and is another problem for Swamidass to explain.

Swamidass Explains?

Under evolution, the science makes no sense. If we begin by assuming chimps and humans share a common ancestor, we end up with all kinds of contradictions and failures. So what exactly are Swamidass's arguments and evidences? How is it that he is so certain? What is it in the data that he finds to be so stunning? And most importantly, how does he resolve the above problems?

Well, he doesn't.

Astonishingly, Swamidass doesn't even mention the above problems. It is as though they don't exist. After some stories and claims of high certainty, here is what Swamidass says:

As predicted by common ancestry, human and chimpanzee genomes are extremely similar (greater than 98% similarity in coding regions), much more similar than we would expect without common descent. Remarkably, just as predicted by the fossil record, humans are about 10 times more genetically similar to chimpanzees than mice are to rats.

First, the high chimp-human genomic similarity was not predicted by common ancestry. No such prediction was made and no such prediction is required by common ancestry. Common ancestry would be just fine with very different levels of similarity from 98-99 percent. In fact, this high similarity makes no sense under evolution, for several of the reasons given above.

Swamidass's claim that this evidence is a stunning confirmation of common ancestry is utterly at odds with the science. It is in stark contrast to the scientific facts.

Second, Swamidass's claim that mouse-rat divergence, compared with the chimp-human divergence, is "just as predicted by the fossil record" is also blatantly false. While evolutionists can always combine various explanatory mechanisms to rationalize just about any comparison, that does not make for stunning evidence that is "just as predicted."

Finally, the real strength of Swamidass's argument lies in its metaphysics. The professor states that the chimp-human genome comparison is "much more similar than we would expect without common descent."

Without common descent?

The evolutionist has just made an unbeatable (and unfalsifiable) argument.

This is not science. Swamidass's claim about what is and isn't likely "without common descent" is not open to scientific scrutiny.

Scientists, qua scientists, do not have knowledge of all possible explanations for the origin of life. This is why scientists, qua scientists, make statements about theories, not about the complement of a theory. A scientist cannot know that something is unlikely "without" his theory. That implies knowledge of all other possible theories. And that knowledge does not come from science.

This is the strength of Swamidass's argument. Notice that with this metaphysical knowledge, all of the scientific problems melt away. No wonder he does not address them. They are inconsequential. At worst, they are simply interesting puzzles. The truth of the matter is already known.

If Swamidass is correct then, yes, of course, the genomic data must be strong evidence for common ancestry. But it all hinges on his metaphysics. This is not about science. It never was.

As 'Just so' as it gets II

Rafting Monkeys "Fill a Gap" in Evolutionary Theory?

David Klinghoffer 

Among evolutionary icons -- peppered moth, Darwin's finches, Haeckel's embryos -- arguably the most risible is the rafting monkey. Even Darwinists seem to understand this.

A Washington Post article includes an interview with an author of a new Science paper, "Oligocene primates from China reveal divergence between African and Asian primate evolution," that once again renews the demand for belief in seafaring monkeys. We've covered this paradox before -- monkeys can't swim much less sail. Just last month evolutionary theorizing dodged a bullet by avoiding the spectacle of rafting foxes on the world's oceans.

The researcher, Christopher Beard, explained to reporter Sarah Kaplan how it must be the case that tarsier-like monkeys, evidenced by fossil teeth found in China, sailed on clumps of earth and felled trees, 30-40 million years ago, across an aquatic void separating Asia from Africa, which was then an island:

"It's a little complicated," Beard said, almost sheepishly.

You don't say.

This more convoluted version of our history begins in the Eocene, some 40 million years ago. At this time, Earth's climate was hot and humid, and the continents were just beginning to move into the positions they hold today. India was zooming headlong toward the bottom of Asia (the inevitable collision would one day give rise to the Himalayas). An inland sea flooded the center of the Eurasian land mass. And Africa was an island continent, separated from Asia and Europe by a narrow stretch of ocean.

Early anthropoid (humanlike) monkeys were flourishing in Asia at that time. But they also, somehow, found a way to migrate across the watery barrier to Africa. And since monkeys don't really swim, scientists' best theory about their migration is -- I kid you not -- that they sailed across on rafts made of trees.

"You're laughing," Beard said, "but it's now known that this happened repeatedly. Because of the greenhouse conditions, a lot of monsoons were hitting Asia at the time. When that happens, rivers would flood, riverbanks erode. A half an acre of land with a bunch of trees growing out of it falls into a river and floats out to sea."

"And if there are a bunch of monkeys hanging out in the trees when that happens," he continued, "suddenly those monkeys become sailors."

"I kid you not." "You're laughing, but it's now known that this happened repeatedly." It is "known" not because anyone can picture the scenario without cracking up or feeling "sheepish" but because the theory demands it. See here for Casey Luskin's earlier comments on the "biogeographical conundrum" posed by these Chinese monkeys.

And look here for pictures of how the drifting continents were disposed in the relevant time period between the Oligocene and the Eocene. From Asia to Africa by sea was a considerable distance, and monkeys are supposed to have accomplished this feat while clinging for dear life to bits of earth and tree debris? On Lake Washington near our home, I beg my wife and kids not to row out even close to shore on a store-bought inflatable raft!

Science Daily has additional thoughts from Dr. Beard on the "'mother lode' of a half-dozen fossil primate species." A half-dozen is a "mother lode"? More:

These primates eked out an existence just after the Eocene-Oligocene transition, some 34 million years ago. It was a time when drastic cooling made much of Asia inhospitable to primates, slashing their populations and rendering discoveries of such fossils especially rare.

"At the Eocene-Oligocene boundary, because of the rearrangement of Earth's major tectonic plates, you had a rapid drop in temperature and humidity," said K. Christopher Beard, senior curator at the University of Kansas' Biodiversity Institute and co-author of the report. "Primates like it warm and wet, so they faced hard times around the world -- to the extent that they went extinct in North America and Europe. Of course, primates somehow survived in Africa and Southern Asia, because we're still around to talk about it." Because anthropoid primates -- the forerunners of living monkeys, apes and humans -- first appeared in Asia, understanding their fate on that continent is key to grasping the arc of early primate and human evolution.

Sarah Kaplan's article in the Post speaks more than once of the fossils as "fill[ing] in the gaps":

The fossils "fill a gap," in our understanding of our evolutionary history, Stony Brook University primatologist John Fleagle, who was not involved in the study, told the Christian Science Monitor. They illustrate "a whole aspect of primate evolution that wasn't clearly documented before."

But the value of "filling a gap" lies in reducing the distance you have to leap in order to believe something seemingly far-fetched. More about rafting animals surely makes the challenge for evolution tougher, not easier. I would have said reducing, not increasing, the number of such unlikely sailors would "fill a gap."

Darwinism vs. the real world XXIX

Calcium's Role in the Body -- and a Note on the Origin of This Series

Howard Glicksman 

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 is delighted to offer this series, "The Designed Body." For the complete series, see here. Dr. Glicksman practices palliative medicine for a hospice organization.

museum of natural history and you are likely to see human skeletons displayed next to those of other animals. Often, without any explanation as to the molecular and cellular structure of bone or its impact on calcium metabolism, this is intended to convince visitors that chance and the laws of nature alone are responsible for the origin of human life. 

In contrast, visit a museum of science and technology and you are likely to see the remains of many different inventions, starting with the prototypes followed by the developmental models in between and ending with the most modern versions. Often, by explaining the science behind the technology, describing the intellectual hurdles that had to be overcome, and displaying the equations, calculations, and blueprints, they show the observer the ingenuity of the inventors. 

About a dozen years ago I woke in the middle of the night with a thought. It was that if people understood what makes up bones and their relationship with the calcium metabolism and how it impacts their survival, they would cease to believe in the theories of evolutionary biologists and realize that we are the product of intelligent design. This series has resulted from that middle of the night awakening. The next several articles will put flesh to the bones of this skeletal notion.

We live in a world made from matter. Matter is made up of atoms and molecules that follow the laws of nature. All life is made up of atoms and molecules that are organized into cells. Our body has trillions of them. Calcium is a chemical element that is vital for life. 

Everyone knows that we must eat food and drink liquids that contain calcium to have strong bones. Most people realize that it is the digestive system that brings calcium into the body and puts it into the blood so it can be used to build up the skeleton. Some people know that the digestive system controls how much calcium enters the body and that the kidneys regulate how much calcium goes out of the body through the urine. But what most people do not understand and appreciate is how, in addition to strengthening the bones, calcium plays a major role in clotting and heart, nerve, gland, and muscle function. 

The body must make sure it has enough calcium, not only inside the bones, but within the blood and its cells too. Having the right amount of calcium in the right places is not as simple as eating food or drinking liquids that contain calcium. Nor is it as simple as having properly working digestive and cardiovascular systems, bones, and kidneys. Without the body's ability to 

control the amount and location of calcium within it, life as we know it would be impossible. The proof of this is that when our body loses control of its calcium, we die. In other words, control is the key to life. But how does the body do it? Let's first look at the cellular and molecular structure of bones and their relationship with the calcium content of the body. 

There are over two hundred bones in the human body. Look at a complete skeleton and you will see a skull, two clavicles, twenty-four ribs, a sternum, and the bones that make up the pelvis, the upper and lower extremities, and the spinal column. The bones provide support and protection for many important organs. The skull protects the brain, the vertebrae protect the spinal cord, and the ribs and sternum protect the heart and lungs from external injury. The bones also contain the marrow tissue that makes the blood cells, like red blood cells to carry oxygen, white blood cells to fight infection, and platelets to prevent bleeding. 

The bones are the frame to which the muscles are attached by tendons. This allows us to breathe, move around, and manipulate things. There are many joints in the body where two or more bones come together that can be moved in one or more directions by muscular contraction. The bones in these joints are held together by strong bands of tissue called ligaments. In addition, where the ends of each bone meet, there is a specialized tissue called cartilage. Cartilage acts both as a shock absorber to cushion the bones within the joint and to reduce friction, allowing the bones to glide across each other smoothly. The upper body has the shoulders, elbows, wrists, and joints of the hands and the lower body has the hips, knees, ankles, and joints of the feet. There are many other joints between the vertebrae in the spinal column, both ends of the ribs, 

and even the jaw and temporal bone so we can open the mouth to talk and eat.

Bone is a specialized connective tissue formed by living cells containing organic material and minerals. There are mainly two types of bone cells directly involved in the formation, growth, and turnover of bone. These cells live within the bone itself. To make bone, the osteoblast lays down a firm organic mesh, called osteoid, which is mainly made up of protein. It then mineralizes the osteoid by depositing calcium crystals into it. It is the calcium in our bones that gives them the strength to withstand the forces of nature, so if we fall, gravity usually won't shatter them like glass. The other bone cell is the osteoclast, which reverses what the osteoblast does by removing the calcium crystals and the osteoid from the bone tissue. 

Although bone is a very solid and rigid material, it nevertheless has a very dynamic metabolism. All of the bones in the body continually undergo a process of turnover called remodeling. The osteoclasts break down bone and then osteoblasts build it back up again. The remodeling of bone usually involves anywhere from 5 to 20 percent of the body's total bone mass each year. The remodeling of bone is thought to allow the skeleton to adapt to ongoing changes in mechanical stress, from weight-bearing and multi-directional movements that take place with everyday activities. A person who leads a very sedentary life or is forced to remain in a chair or bed for prolonged periods of time may lose significant amounts of bone mass. In fact, astronauts have been shown to experience loss of bone mass as a result of prolonged weightlessness in space unless they undergo exercise programs. Despite its present knowledge of what happens during bone remodeling, medical science has a very limited understanding of what factors control this process.

About 99 percent of the calcium in the body is located within our bones. And about 99 percent of the calcium within our bones is in crystalline form called calcium hydroxyapatite. Because it's a solid, the calcium within these calcium crystals is not available to the rest of the body.    

The remaining 1 percent of the calcium inside our bones is dissolved as calcium phosphate in the bone tissue fluid that surrounds the bone cells. The bone tissue fluid is in direct contact with the capillaries and in communication with the body through circulation. From the calcium phosphate dissolved in this pool of bone tissue fluid, the osteoblasts take calcium to make the calcium crystals needed for bone. Calcium is deposited in this pool of bone tissue fluid as calcium phosphate when the osteoclasts remove the calcium crystals from the bone. The body is able to supply the bone and itself with its calcium needs through this bone tissue fluid. In other words, through its tissue fluid and circulation, the bones act as a reservoir for the body's calcium metabolism.

Now that you understand the molecular and cellular structure of bone and its relationship with the body's content of calcium, you are ready to explore the roles that calcium plays within the fluid inside and outside the cell. Maybe natural history museums could better educate the public about the origin of life by adding what you've learned here about the relationship between bones and the calcium metabolism to their skeletal displays. Visitors might then see how 

life actually works and not just how it looks.

Twenty years later and proto-life is more irreducibly complex than ever

Galloping Flagella and Cilia Railroads -- Getting Ready to Celebrate Twenty Years of Darwin's Black Box

Evolution News & Views 

ary of the publication of Darwin's Black Box (it appeared on August 2, 1996, to be precise). Michael Behe's book inspired a generation of Darwin discontents and showed that intelligent design was (and still is) firmly based on cutting-edge science. Among other highlights, he showcased two cellular organelles to illustrate his concept of irreducible complexity: the cilium and the flagellum. 

These organelles, protruding from the cell into the environment, could not be built by a Darwinian mechanism, he argued, because they are composed of multiple, independent parts required for function. Like a mousetrap, they could not work unless all the parts were present together at the same time.

All true, but in the intervening years molecular biologists have learned a great deal more about cilia and flagella. The revelations keep coming, like down to the day before yesterday.

Galloping Cilia

In fascinating news from the University of Cambridge, we learn that "Algae use their 'tails' to gallop and trot like quadrupeds." (Those tails are Behe's famous flagella, though differing in structure from the bacterial flagella.) You can see for yourself in the embedded videos that single-celled algae named Chlamydomonas use their flagella in coordinated ways "to achieve a remarkable diversity of swimming gaits."

When it comes to four-legged animals such as cats, horses and deer, or even humans, the concept of a gait is familiar, but what about unicellular green algae with multiple limb-like flagella? The latest discovery, published in the journal Proceedings of the National Academy of Sciences, shows that despite their simplicity, microalgae can coordinate their flagella into leaping, trotting or galloping gaits just as well.[Emphasis added.]

They trot. They gallop. They leap in a manner similar to the "pronk" of a springbok, where the animal arches its back and springs all four feet off the ground together. The resemblance is uncanny, despite a difference in size of many orders of magnitude. The cells even know two different galloping gaits: a rotary gait and a transverse gait. How is this possible for single-celled organisms lacking neurons?

In vertebrates, gaits are controlled by central pattern generators, which can be thought of as networks of neural oscillators that coordinate output. Depending on the interaction between these oscillators, specific rhythms are produced, which, mathematically speaking, exhibit certain spatiotemporal symmetries. In other words, the gait doesn't change when one leg is swapped with another -- perhaps at a different point in time, say a quarter-cycle or half-cycle later.

It turns out the same symmetries also characterise the swimming gaits of microalgae, which are far too simple to have neurons. For instance, microalgae with four flagella in various possible configurations can trot, pronk or gallop, depending on the species.

Dr. Kirsty Wan was amazed when she first observed this, saying, "I realised immediately that this behaviour could only be due to something inside the cell rather than passive hydrodynamics." Think of how this expands the argument for irreducible complexity:

The researchers determined that it is in fact the networks of elastic fibres which connect the flagella deep within the cell that coordinate these diverse gaits. In the simplest case of Chlamydomonas, which swims a breaststroke with two flagella, absence of a particular fibre between the flagella leads to uncoordinated beating. Furthermore, deliberately preventing the beating of one flagellum in an alga with four flagella has zero effect on the sequence of beating in the remainder.

Dr. Behe will be pleased to see this additional level of design. "The findings also raise intriguing questions about the evolution of the control of peripheral appendages, which must have arisen in the first instance in these primitive microorganisms," one of the paper's authors comments. Surely the first question should be, "Did it evolve at all?"

Two-Lane Highways in the Cilium

Any freshman confronted with an electron micrograph of a cilium must be impressed by the beautiful symmetry of its 9x2 structure (see the figure in Behe, p. 60). The elements of the structure are microtubules: long filaments that look like white dots in cross section. They are arranged in pairs around the periphery. The question is, "Why"? Until now, scientists were not sure. Science Magazine has just now come out with the answer: "Microtubule doublets are double-track railways for intraflagellar transport trains." One microtubule is for going up; the other is for coming down!

Cilia contain a well-ordered array of microtubule doublets along their length. A longstanding question in cilium structure and function is why the microtubule arrangement in cilia is so complex. Stepanek and Pigino developed a time-resolved correlative fluorescence and three-dimensional electron microscopy method to show that the doublets provide directionality to intraflagellar transport. One microtubule in the pair moves cargoes up to the ciliary tip. Meanwhile, the other microtubule moves cargoes back to the cell body. These results explain why the axoneme is built out of microtubule doublets and suggest a mechanistic picture of how the logistics of bidirectional intraflagellar transport are regulated.

What's really interesting about the paper is the constant use of railroad terminology. There are "cargo trains" with "motors" that ride on microtubule "tracks" for "transportation." They function as "railways for intraflagellar transport" (IFT). Nowhere is a discussion of evolution to be found. Maybe that's because everyone knows train transportation systems are intelligently designed.

Ludek Stepanek and Gaia Pigino from the Max Planck Institute observed the trains going up and down, but never colliding. They wondered how the trains avoid collisions; do they swing around each other, like using a passing lane? No; it turns out that they each have dedicated lanes.

Moreover, the upward-moving (anterograde) cargo trains use kinesin-II motors, the downward-moving cargo trains use dynein motors. How does each one know the lane to use, since the microtubules are made of the same track material? It appears there may be post-translational modifications of the track proteins (tubulins) that allow the engines to recognize the right lane to use. The situation gets even more complex from there:

This might contribute to the efficiency of IFT by providing optimized tracks for kinesin and dynein motors in addition to the IFT train segregation. Nevertheless, the effect of such modifications on the control of IFT in vivo remains unclear. Alternatively, a specific molecular machinery to direct trains to the correct microtubule could be present at the base and tip of the axoneme. More complex motor regulation could be necessary in the sensory cilia of Caenorhabditis elegans, where the B-microtubules do not extend beyond the middle segment of the flagellum. There, the kinesin-II moves only in the middle segment, and an additional motor, OSM-3, is required to bring cargo to the tip along the A-microtubules. Regardless of the mechanisms involved in the recognition of the microtubules by the motors, our work highlights the critical role played by microtubule doublets in the assembly of cilia.

Cilia are present on most eukaryotic cells and are involved in many essential functions, such as clearing the throat of debris (in which they wave in coordinated sweeping motions), and sensing the environment like antennae. Defects in cilium construction cause debilitating diseases or death, underscoring Behe's concept of irreducible complexity.

It's satisfying to report these new discoveries about cilia and flagella, confirming, as they do, Behe's original insights. The case for intelligent design gets stronger all the time.

Putting the Darwinian debate in its place.

David Berlinski: Does Darwin Matter?

David Berlinski

you write about affect the way we live? Why should the Darwin question matter to people who don't normally concern themselves with scientific theories?

DB: I think of the Darwinian debate in the way that Dickens thought of Jardynce v Jarndyce in Bleak House. It is awfully easy to be sucked into it, and once suckered, awfully difficult to get out. I have seen it so often. A man wakes and because has read a book or scanned an essay, he is persuaded that he can make a contribution. He is eager to make it. He offers his opinion on the Internet and is gratified by the prospect of the congratulations that he is shortly to receive. No one pays the slightest attention. He then discovers that to be heard, it is necessary that he amplifies his level of abuse. He does that, referring to the Discovery Institute as the Dishonesty Institute. Repeating the phrase as he moves his bowels affords him an unexpected pleasure. As his influence remains insignificant, his indignation mounts. In the morning, he scuttles to his computer to check his own postings; satisfied when he finds them, and beside himself when he fails. His appetite for conflict sharpens. He becomes determined to exaggerate every issue; and to magnify trivialities. Sooner or later, his Internet presence seems real, and his real life unreal. He ends in the state achieved by almost every Internet blogger: He commences to gibber repetitively. Glen Davidson, who posts to David Klinghoffer's blog, has recently entered the gibbering state.

It is all very sad. I have warned about the phenomenon many times.

Does Darwin matter? Yes, of course it matters. It matters a great deal. It matters whether the theory is true because for better or worse we value the truth and struggle to find it; but it would matter far more were we able to say once and for all that the theory is false. Darwinism involves a way of thought in biology, and were it to go, it would take a great many assumptions along with it. Just think of vitalism, for example. To say a word in its favor is at once to be accused of the cheapest kind of intellectual sentimentality. We know better and if we do not know better, theydo. But hold on, please do. If by vitalism one means something like the 19th century idea of a vital fluid that informs living systems, then I am with them. That is so much sentimentality. But if by vitalism one means the thesis that living systems cannot be completely explained in terms of their physics or their chemistry -- what then? Something must explain the difference, no? And if it is not a fluid, as naïve 19th-century biologists sometimes thought, it does not follow that it is nothing.

Nothing in biology makes sense except in the light of evolution.

This remark is half right: Nothing in biology does make sense. It is for the biology of the future to start making sense of it. If that in the end involves religious ideas or even religious I, that's fine with me. Let's ask the questions first, and reject the wrong answers when we know that they are wrong.

Pakistan:a country with an army or an army with a country?:Pros and Cons.

Leviathan vs.Darwin

Crocodile eyes are fine-tuned for lurking
By Jonathan Webb

A new study reveals how crocodiles' eyes are fine-tuned for lurking at the water surface to watch for prey.
The "fovea", a patch of tightly packed receptors that delivers sharp vision, forms a horizontal streak instead of the usual circular spot.
This allows the animal to scan the shoreline without moving its head, according to Australian researchers.
They also found differences in the cone cells, which sense colours, between saltwater and freshwater crocs.
Published in the Journal of Experimental Biology, the findings suggest that although the beasts have very blurry vision underwater, they do use their eyes beneath the surface.

This is because light conditions are different in salt and freshwater habitats, but only underwater - and the crocodiles' eyes show corresponding tweaks.
"There's generally more blue light in saltwater environments, and more red light in freshwater environments. Animals tend to adapt to this," explained Nicolas Nagloo, a PhD student at the University of Western Australia.
He and his colleagues studied eyeballs from juvenile "salties" and "freshies", shipped to the university from a crocodile farm in Broome.
When they measured the light absorbed by single photoreceptors in the retina, they found that those of the freshwater crocs were shifted towards longer, redder wavelengths compared with their saltwater cousins.

Finding this skewed sensitivity in crocodiles was unexpected, Mr Nagloo said, because the famous predators were only semi-aquatic and did their hunting, feeding and mating on land."It's surprising because these guys can't actually focus underwater. [But] light sensitivity seems to be important to them," he told BBC News.
"That tells us there's potentially some aspect of their behaviour underwater that we're not aware of yet."
The team also studied the density of receptors across the crocodile retina. In this regard, the two species were more similar.
Overall, crocodile vision appears to be less precise than ours, achieving a clarity some six or seven times lower than the human eye. But their "foveal streak" is a striking adaptation that suits their lifestyle perfectly.
The fovea is a dent in the retina, containing a huge concentration of receptor cells. The indentation arises because other cells, which transmit visual information to the brain, are shifted to the sides."Typically, the fovea is circular and located in the centre of the retina. It provides animals with an area of very high visual clarity, in a small area of their visual environment," Mr Nagloo said.
It is this small patch of high-resolution information that allows us, for example, to read; but we humans have to move our eyes around to drink in details across a scene.
"In the case of crocodiles... it's spread across the middle of the retina, and it gives them maximum clarity all along the visual horizon."
This arrangement reflects the predator's iconic ability to lurk with just its eyes above the water, waiting motionless for prey to wander too close to the river's edge.Other animals, particularly mammals like deer and rabbits that live in open spaces and themselves face predation, are known to possess a similar "visual streak". But that is a more subtle feature than the furrow-shaped fovea of the crocodile, Mr Nagloo said.
"A visual streak is just an elevated cell density, in an elongated shape. A fovea takes that to the extreme - the number of photoreceptors is so high that they have to move the transmitters away, to make room for them. So the wiring is different.
"I haven't seen any other animals with this kind of specialisation."

Darwinism and S.D.L algorithm II

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

This is monumental serendipity.

The science contradicts the theory

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

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

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

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

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

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

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

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

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

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

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

It isn’t going to happen.

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

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

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

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

But they weren’t.

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

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

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

Posted by Cornelius Hunter