Butterflies for design

Defects on Purpose Make Butterfly Wings Shine
Evolution News & Views

Illustra Media's film Metamorphosis: The Beauty and Design of Butterflies showcased many dazzling butterfly wings, but didn't have time to discuss the secrets behind those colors. Scientists have long identified the source of the colors as not coming from pigments, but from light interference patterns at the nanoscale. A regularly repeating 3-D structure called a "photonic crystal" reinforces some colors and interferes with others. That's how the dazzling blue of a Morpho butterfly is produced: crystals in the scales of the wings play tricks with light. Grind up the scales and you won't get a pile of blue dust, just brown or gray material. It's the highly-organized nanostructure that generates the brilliant blue of the living insect flapping in the sunlight.

But how does a butterfly grow those crystals? Something has to guide them into position as the wing develops in the chrysalis. Metamorphosis showed the wings taking shape but only touched on the complexity involved. Now, scientists at the University of California, San Diego, have shined some X-ray light onto the process. In a paper in the AAAS open-access journal Science Advances, they used X-ray diffraction to examine the properties of individual scales.

Many organisms in nature have evolved sophisticated cellular mechanisms to produce photonic nanostructures and, in recent years, diverse crystalline symmetries have been identified and related to macroscopic optical properties. However, because we know little about the distributions of domain sizes, the orientations of photonic crystals, and the nature of defects in these structures, we are unable to make the connection between the nanostructure and its development and functionality. [Emphasis added.]
As Illustra showed with electron micrographs, the wings are composed of scales that overlap like shingles on a roof. The scales, made of the protein chitin, begin as individual cells. The cells must manufacture chitin and place it in the right orientation. The scientists found that the crystals of chitin are strongly oriented normal to the plane of the scale (i.e., perpendicular). The crystals apparently grow from the edges of the cell toward the middle, where they meet at domain boundaries.

We report on nondestructive studies of the morphology of chitinous photonic crystals in butterfly wing scales. Using spatially and angularly resolved x-ray diffraction, we find that the domains are highly oriented with respect to the whole scale, indicating growth from scale boundaries. X-ray coherent diffractive imaging reveals two types of crystalline domain interfaces: abrupt changes between domains emerging from distinct nucleation sites and smooth transitions with edge dislocations presumably resulting from internal stresses during nanostructure development. Our study of the scale structure reveals new aspects of photonic crystal growth in butterfly wings and shows their similarity to block copolymer materials. It opens new avenues to exploration of fundamental processes underlying the growth of biological photonic nanostructures in a variety of species.
The domain boundaries, they found, are randomly oriented, yet each crystal is highly organized within each domain. "The photonic crystal is reminiscent of a thin polycrystalline film, with the domains being highly oriented in the direction normal to the scale boundary, which suggests a layer-by-layer crystal growth process starting at the cell membrane," the paper says. The boundaries, furthermore, are "extremely sharp," on the order of one unit cell. "The preferred orientation of the domains, normal to the scale plane, is quite remarkable and is consistent with crystal nucleation at the scale boundary and crystal growth outward." This gives the researchers some ideas about how to manufacture artificial photonic crystals. Again, it's remarkable as well as intriguing:

The discovery of the edge dislocations in the biological photonic crystals is particularly remarkable because artificially manufactured topological defects in photonic crystals lead to interesting optical properties such as Anderson localization of light. Two intriguing questions are whether nature-engineered defects for a particular purpose and whether mimicking similar growth conditions allows for controlled manufacturing of defects in artificial photonic structures.
"Nature-engineered defects for a particular purpose"? Can it be that defects have a function? Indeed they can. The press release from UCSD describes why scientists sometimes "engineer" defects to improve their strength and function:

These crystal dislocations or defects occur, the researchers say, when an otherwise perfectly periodic crystal lattice slips by one row of atoms. "Defects may have a negative connotation, but they are actually very useful in improving materials," explains Singer. "For example, blacksmiths have learned over centuries how to purposefully induce defects into metals to make them stronger. 'Defect engineering' is also a focus for many research teams and companies working in the semiconductor field. In photonic crystals, defects can enhance light-scattering properties through an effect called light localization."
The bug is a feature. Defects consisting of random domain boundaries in the butterfly scale actually enhance the light-scattering properties. Post-doc Adrej Singer describes "tiny crystal irregularities that may enhance light-scattering properties, making the butterfly wings appear brighter."

It looks like we will have to add "defect engineering" to our list of intelligent design sciences in action. How strange that the butterfly figured this out before mankind did:

"In the evolution of butterfly wings," he adds, "it appears nature learned how to engineer these defects on purpose."

We can dismiss the references to evolution. Nature does not learn to engineer things for a purpose. Organisms do not evolve sophisticated cellular mechanisms in order to produce optical properties. Minds do that. If our best optical engineers look to butterflies for inspiration to improve their manufacturing, what does that tell you? It implies that engineers do not employ unguided, aimless Darwinian processes of chance. They use intelligent design. By arguing from lesser to greater, we explain what goes on in the "black box" of the chrysalis, where "remarkable" and "sophisticated" engineering generates structure, function, and beauty.

Nature's navigators for design

Oh, Deer: Mammals Use Magnetic Navigation, Too
Evolution News & Views

You're in a herd of deer when a mountain lion is seen approaching. What's your safest retreat? Is it to run directly away? Is it to scatter in all directions? Or is it to run according to a predetermined orientation?

Scientists in Europe were intrigued that roe deer seem to orient in a north-south direction when grazing and when startled, so they decided to investigate. What they uncovered was a novel case of magnetic navigation in the animal kingdom. A Springer news item says:

Why do deer in a group, when startled, suddenly bolt away together and never collide with each other? It's because these deer have an inner compass that allows them to follow a certain direction in order to make their escape. Their getaway is almost always along a north-south axis, thanks to their ability to sense the magnetic field, says Petr Obleser of the Czech University of Life Sciences in the Czech Republic. He and Hynek Burda of the University Duisburg-Essen, Germany, are lead authors of a study in Springer's journal Behavioral Ecology and Sociobiology. [Emphasis added.]
This is a first for large mammals. Illustra Media has shown in Metamorphosis how butterflies use the magnetic field to get to Mexico. They showed in Flight how Arctic Terns navigate from pole to pole, and in Living Waters how salmon and sea turtles use magnetosensing in their long-distance migrations. Suggestions of magnetosensing had been reported for bats and mole rats, but large mammals like deer -- who would have thought they use an inner compass for everyday safety?

One of the authors of the new paper, Dr. Hynek Burda of University of Duisburg-Essen, had contributed to a 2008 study published in PNAS that used Google Earth to find cattle and deer preferentially orienting on a north-south axis. BBC News commented on this finding, saying that this phenomenon "has apparently gone unnoticed by herdsmen and hunters for thousands of years." At the time, the function of this orientation was unknown. One biologist remarked, "We need to think about some really fundamental things that this sensory ability provides in animals."

Since then, Obleser and Burda monitored roe deer from April to August 2014. This species of deer tends to congregate in flat areas on agricultural land, making them easy to observe with binoculars. From 60 locations, they recorded data on the deer's orientation at rest and when startled, monitoring 188 escape behaviors under a variety of conditions.

It was found that roe deer tend to align their bodies along the north-south axis when grazing. When startled, the animals generally fled away from observers. They did not merely make their getaway in the direction directly opposite to the approaching threat, but consistently did so north- or southwards. In fact, they seemed to actively avoid escaping westwards and eastwards, says Obleser. Wind direction or the position of the sun had no influence on the direction of their escape route.
The authors took note of the time of day, odor, wind and other factors; the magnetic orientation still prevailed. If a forest shelter was nearby, however, the herd could override the magnetic tendency and escape directly toward the shelter.

Is there a reason for this behavior? The north-south escape strategy was especially pronounced when the deer were congregated in groups. The authors feel the strategy helps the deer avoid collisions that would be more likely to occur if each animal took off in a random direction. Other possible functions include keeping group cohesion, guiding the deer get back to the previous grazing spot after the danger has subsided, and helping a mother find its fawn it left hiding in the grass.

For the strategy to work, an animal needs hardware and software programmed into its body and brain.

The researchers believe that the tendency of deer to align their bodies with respect to a north-south magnetic field line confirm that they are magnetosensitive and magnetoreceptive. This assists the animals to "read" and comprehend the mental maps they hold of the landscapes they occupy.
The authors did not speculate about the predator. What if it has a compass, too? What if it knows the strategy? Just speculating, it would seem the deer still have an advantage. The lion can't run north and south at the same time, and would have no way of knowing in advance which direction the deer will choose to run. If they split directions, the deer in both groups would still have some safety in numbers. Most of the advantages would appear to accrue to the prey; the wide angle of 180 degrees "would maximize the distance between the animal and the danger," the authors say.

The authors feel this pioneering study points to magnetosensing being common in mammals. It might even reside in us humans!

This is the first study of escape behavior in animals which considers also the role of absolute compass direction. Our findings confirm existence of magnetic alignment and thus magnetosensitivity in the roe deer and provide first evidence for its role as the so-called direction indicator in control of escape behavior in roe deer in particular and in mammals in general. Our results make the speculations more plausible that the magnetic alignment helps to organize and read the mental (cognitive) map of space. (In analogy, humans are more efficient in reading and commenting the map, if it is held in an accustomed direction: with north pointing upwards and if the person aligns with the map and with the visible landmarks.)
Many of us can probably relate to that: facing north and holding a map to try to find our way around when vacationing in an unfamiliar city. It's just by "analogy" the authors say we might also have directional sensing. That deserves further study. Could a latent human ability for magnetosensing be trained? Could it augment orienteering by the sun and the stars? Fascinating thought. Maybe it will put compass makers out of business.

In the new open-access paper, the authors make no use of evolutionary theory to explain the coordinated escape strategy of roe deer with its requirements for magnetosensing equipment. There's no mention of natural selection, fitness or phylogeny. Why would that be, if nothing in biology makes sense except in the light of evolution?

As design theorists, we can identify prerequisites for magnetically-based escape strategy in roe deer and other mammals:

Construction of crystals of iron or protein that respond to the earth's magnetic field.

Neurons that can sense the response of the crystals.

Brain receptors that can process the neural inputs and interpret them.

Mental maps to place the interpretations in a regional context.

Brain regions that can coordinate the magnetic data with other sensory data.

Stored instincts to activate body systems to respond appropriately.

Genes to encode the construction of all the above.

Epigenetic systems to guide the development of the genetic information.

That's a bigger parts list than in the classic mousetrap model of irreducible complexity. In fact, each item on the list could itself be called irreducibly complex.

Needless to say, magnetosensation presupposes a planet with a strong magnetic field. Of the rocky planets in our solar system, the Earth is unique in that regard; Mercury's magnetic field is too weak, Venus has none, and Mars has only patches of magnetism. Many regard a strong magnetic field as a requirement for habitability, to act as a shield from stellar and cosmic radiation. It's one of at least twenty improbable factors listed in The Privileged Planet that point to fine-tuning for habitability.


Intelligence is the only cause we know that is capable of arranging multiple independent factors for a function. The design inference strengthens with the improbability or specified complexity of each factor. With Darwinian evolution apparently of no use in explaining why roe deer know how to escape along a north-south axis, an inference to intelligent design beckons.

Transhumanism's brave new world.

When Atheists Meet Creationism, You Get Creatheism
Brendan Dixon 

Creathiest: It is not a word that rolls easily off the tongue. But I am at a loss for one that better describes the atheists Daniel Jackson describes in a condescending post at The Spectator ("Atheists are embracing Gods and creationism").

No bleak darkness for these disbelievers. No existential angst enters their minds. No despair over the vast emptiness in which Earth floats, seemingly alone with life. Creathiests have the comforts of religion without the commitment of a creed. Post-humanity will bring an end to all ills. Eternal life arrives when we can upload ourselves into a machine. And Elon Musk admitted to a Creator when, a couple of weeks ago, he suggested that the odds of our living in a simulation to be "a billion to one."

Jackson writes:

Elon Musk, the billionaire inventor and entrepreneur, the twenty-first century's answer to Howard Hughes, believes we are living in a computer simulation.

...

His argument -- that, given the increasing pace of progress in computer technology, we will eventually be able to synthesise reality and consciousness -- is an abbreviated version of a 2003 paper by Nick Bostrom, a philosophy Professor at Oxford.

The paper suggests that if we aren't living in a simulation, civilisation will end before we are able to reach the 'posthuman' age. The detail and the terminology isn't important; the idea is bunkum, the sort of thing that's fun to think about on psilocybin, but not much use otherwise.

What's interesting is the way in which atheists are embracing the idea -- or at least the possibility -- of creationism. If we are living in a simulation, someone or something had to create it.

It brings a kind of pleasure to watch someone apparently without religion call attention to the religiosity of the supposedly irreligious devoted to demolishing religion. It is, truly, ironic.

After all, only the religiously devoted would shut down rational discussion over their creation myth: evolution by means of random change and natural selection. Why else would otherwise very smart, well-read, articulate people fall for and promote the silly, unfounded "just so" stories with which evolutionary research is generously stocked? What else can explain the consistent misrepresentation of alternative views and the refusal to engage counterarguments? Only because it serves creathiests as their creation myth is evolution held with such irrational passion against the evidence of design.

The same fervor promotes the ungrounded faith in a coming Singularity, when computers will transcend us, perhaps leading to our demise. It is not a logical result drawn from the data. It is a wild extrapolation that fails to admit the vast amount we don't know and the limits of our technological successes. It is not a short leap from a pattern-matching, game-playing machine -- such as Google's AlphaGo -- to awe-inspiring AI super-intelligence. It is a blind leap of religious faith.


For everyone engaged in the evolution debate, a calm, rational discussion would be best. Religious devotion, no matter how sincere, cannot alter the evidence or up-end the challenge. Let's leave our a priori commitments behind and look closely at what we're seeing, following the evidence wherever it leads.

Darwinism Vs.the real world XXXIV

The Kidney's Irreducibly Complex Systems
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.

If a unicellular organism is like a microscopic island that can get what it needs and get rid of what it doesn't need through its surrounding water, the body, consisting of trillions of cells, is like a huge land mass that must move what it needs and doesn't need in and out of its interior so it can survive. The cells of the body need the right amount of oxygen and carbon dioxide to work right, so the lungs, at the direction of the respiratory center in the brain, take care of that.

They also need to have the right amount of water, sugar, salt, and other nutrients, which is taken care of by the gastrointestinal system, at the direction of the nervous system. And to transport what it needs into and out of its continental mass of cells, the body uses the cardiovascular system to move blood containing these chemicals to where they need to go so they can be on- or off-loaded.

Evolutionary biologists are good at imagining how the molecular structures for life may have come about, as long as they don't have to reckon with the objective standards those structures must meet to keep the cells and the body alive. To survive within the laws of nature, the cell must be able to control its volume and chemical content. So too, for the body to survive within the laws of nature, it must also control its volume and chemical content.

Stephen Meyer has described the complexity of the cell, the numerous systems within it, and what they must do for it to work properly. But each cell, no matter where it is located, is blind to the overall needs of the body. We have seen this in how the water content and blood levels of sodium, potassium, calcium, and nitrogen (protein) affect organ function and body survival. The common pathway the body uses to control all of these chemical parameters leads through the kidney.

The functioning unit in the kidney is the nephron, and there are about one million per kidney. The nephron filters fluid out of the blood by squeezing it through a specialized capillary system called the glomerulus. The kidneys filter about 7.5 liters of fluid, with its chemical content, out of circulation per hour. This fluid enters tubules, which wind their way through the tissue of the kidney on its way to becoming urine. As the fluid moves along the cells lining, the tubules reabsorb or secrete different chemicals to the degree that is necessary for body survival.

The body is always taking in different amounts of various chemicals through the gastrointestinal system, while simultaneously losing them through metabolism. Therefore, the ongoing chemical needs of the body are always in flux and the kidneys must constantly adjust to these changes by changing how much of a given chemical they keep or release from the body through the urine. We will look at the five vital chemicals mentioned above, water, sodium, potassium, calcium, and nitrogen, and explain how the body, through the kidneys, adjusts them to stay alive.

Evolutionary biologists may be good at describing how kidneys look and imagining how they evolved, but they never seem to mention how they work or what they would have had to do to keep the transitional organisms they belonged to alive.

Water is vital for life and is the commonest molecule in the body, making up sixty percent of its weight. Two-thirds of the body's water is inside the cells and one third is outside, either between the cells or inside the blood. If the body loses one-quarter of its water (10 liters), it dies. Since the kidneys filter 7.5 liters of fluid per hour this means that if they didn't take back any of it, the body would die in about ninety minutes.

Water can move freely in and out of the cell, so cell volume reflects the body's water content. In general, if the body's water content is below normal, then the volume of its cells will be below normal as well. The hypothalamus contains shrink-sensitive cells that can detect this drop in cell volume. These osmoreceptors react to worsening cell shrinkage by making more Anti-Diuretic Hormone (ADH) be released. ADH travels in the blood and attaches to specific receptors on certain tubules within the kidneys and tells them to bring more water back into the body from the urine in production. By using osmoreceptors in the brain, ADH, and its specific receptors on certain kidney tubules, the body is able to take of control of its water content.

Sodium is vital for life and dissolves in the body's water as an Na+ ion. The fluid outside the cells contains about ninety percent of the body's total sodium and is ten times more concentrated than the fluid inside the cells. Since water generally follows Na+ ions wherever they go in the body, this means that the relatively high concentration of sodium in the fluid outside the cells is responsible for not only its water content but also the blood volume. Much like water, if the body loses about one-quarter of its sodium, it dies. The amount of sodium in the blood is so high that the 7.5 liters of fluid the kidneys filter out per hour contains about one-half of the body's total sodium. If the kidneys didn't take back any of this filtered sodium, the body would die in about a half hour.

Since blood volume is dependent on water content and water content is dependent on sodium content, this means that the wall motion that takes place as blood flows into a blood vessel or chamber is a reflection of the body's sodium content. One set of sensors, called mechanoreceptors, detect this wall motion within the kidneys, where blood enters to be filtered, and another is in the walls of the atria. The sensory cells in the kidneys release a hormone, called renin. The amount of renin released is inversely related to how much wall motion the sensors detect. The more the walls stretch, indicating more blood volume, the less renin is sent out, and the less the walls stretch, indicating less volume, the more renin is sent out. In contrast, the atrial cells send out a hormone, called Atrial Natriuretic Peptide (ANP), in an amount that is directly related to how much wall motion they detect. The more the walls stretch, indicating more blood volume, the more ANP is sent out, and vice versa.

Renin results in the formation of a hormone called angiotensin II which binds to specific receptors in the adrenal glands and tells them to release another hormone called aldosterone. Aldosterone travels to the kidneys and attaches to specific receptors on the cells lining some of its tubules. This tells them to bring more sodium back into the body. So, the less blood volume, the more renin, resulting in more angiotensin II and aldosterone, and more sodium the kidneys reabsorb. In contrast, the more blood volume, the more ANP attaches to specific receptorson the same tubules in the kidneys and tells them to release more sodium. In other words, the effects of renin and ANP counterbalance each other. By using mechanoreceptors in the kidneys and atria, renin and ANP and specific aldosterone and ANP receptors on certain kidney tubules, the body is able to take of control of its sodium content.

Potassium is also vital for life and dissolves in the body's water as a K+ ion. The fluid inside the cells contains about ninety-eight percent of the body's total potassium and is over thirty times more concentrated than the fluid outside the cells. The relatively low K+ ion level in the fluid outside the cells must be maintained within a very narrow range to make sure the difference between the electrical charge inside and outside the cell allows for proper heart, nerve, and muscle function. The relative amount of potassium in the blood is a lot lower than it is for sodium, and if the kidneys did not bring any of it back from the 7.5 liters of fluid it filters per hour, the body would die in about a day.

The body uses sensors in specialized cells within the adrenal glands to detect the ratio between the K+ and Na+ ion concentration in the blood. If the ratio rises, due to an increase in K+ ion concentration or a decrease in Na+ ion concentration, these cells send out more aldosterone. Conversely, if the ratio drops, due to a decrease in K+ ion concentration or an increase in Na+ ion concentration, it sends out less aldosterone.

Aldosterone travels in the blood and attaches to specific receptors on the cells lining certain tubules in the kidneys and tells them to release K+ ions out through the urine and bring Na+ ions back in. More aldosterone, due to an increase in the ratio between K+ ions and Na+ ions, makes more K+ ions leave the body and more Na+ ions come back in. Less aldosterone, due to a decrease in this ratio, makes less K+ ions leave the body and less Na+ ions come back in. By using receptors that detect the ratio between K+ and Na+ ions in the adrenals and aldosterone and its specific receptor on certain tubules in the kidneys, the body is able to take control of its potassium content.

Calcium is vital for life and the bones of the body house over ninety-nine percent of its content. However, the remaining one percent is just as important for survival. Calcium dissolves in the body's water as Ca++ ions and its concentration in the blood is about ten thousand times more than within the cell. Besides creating the skeleton, bone also acts as a reservoir for the calcium needs of the body, which include heart, nervous, glandular, muscle function, and clotting. The total content of calcium is over one thousand milligrams and if the kidneys did not bring back any of it from the 7.5 liters of fluid that it filters per hour, the body would lose its entire supply in about two months.

The cells of the four parathyroid glands have sensors that can detect the calcium level in the blood. In response to a drop in serum calcium, they release more parathormone (PTH). PTH travels in the blood and not only makes the bone release more Ca++ ions into the circulation but tells the kidneys to activate Vitamin D so the gastrointestinal tract can absorb more calcium. It also attaches to specific receptors within the tubules and tells them to bring more calcium back into the body. By using calcium sensors, PTH, and its specific receptors in the kidneys, the body is able to take control of its calcium content.


Nitrogen is mainly present in the amino acids that make up the proteins of the body. Protein metabolism produces a highly toxic nitrogen-containing molecule called ammonia, which the liver converts into less toxic urea to be released from the body through the kidneys. The amount of fluid filtered by the glomeruli of the kidneys is called the Glomerular Filtration Rate (GFR) and is normally about 125 mL/min (7.5 liters/hr). The body's ability to keep its blood level of nitrogen-containing substances under control is directly related to its kidney function.

Especially in people with long-standing hypertension and diabetes, worsening kidney function causes the level of urea and other nitrogen-containing substances to rise. In fact, when the GFR is less than ten percent of normal, severe weakness, nausea, and confusion are common symptoms. In addition, there is often retention of sodium and water. This results in fluid build-up in the lungs, which in turn can cause shortness of breath and high levels of potassium, both of which can lead to cardiopulmonary arrest. It is at this time that a person may be considered for dialysis, which artificially cleans the blood of urea and other nitrogen-containing substances and stabilizes its water, sodium, and potassium levels.

The kidney may not be as sophisticated as the brain or the liver, but it definitely has a lot of roles to play when it comes to human life. Each of the control systems mentioned above is irreducibly complex in that all of the parts must be present for it to do its job. And to get the job done right so the body can survive within the laws of nature requires a natural survival capacity -- an inherent knowledge of what is required.

The word intelligence comes from the Latin words inter and lego which means to choose between, to choose one outcome from all possible outcomes. Most people would look at the complicated structure of the kidney and what it takes for the body to control its water content and blood levels of sodium, potassium, calcium, and nitrogen, and conclude that an intelligent agent, a mind, was at work here.


Funny thing about intelligence though; you must have it in order to detect it. One hopes, in the near future, students will learn the truth about how life really works, and not just how it looks, and with this knowledge see the inadequacy of neo-Darwinism as an explanation for biological origins.

universal common ancestry in the hot seat VII

The Placenta Problem: How Common Descent Fails
Ann Gauger 

Editor's note: For previous replies by Dr. Gauger to Dr. Torley in this series, see here, here, and here.

Philosopher Vincent Torley (and Washington University's Professor Josh Swamidass) have been trying to persuade me that common descent is the only rational view to affirm, the only intellectually consistent and respectable choice. What they don't seem to realize is that I see the evidence for common descent. I know its strength. The reason I doubt common descent is not because of the ways that it succeeds, but the ways that it fails.

Writing at Uncommon Descent, Torley poses the following challenge in "Consider the Opossum," thinking to trap me into either accepting the argument for common descent as the only evidence-based conclusion, or denying the evidence in order to escape the logic:

Do you accept that if hypothesis A readily explains an empirical fact F and hypothesis B does not, then F (taken by itself) constitutes scientific evidence for A over B? Or putting it another way, if a fact F is predicted by hypothesis A, and compatible with hypothesis B but not predicted by B, then do you agree that F constitutes scientific evidence for A over B? If not, why not?

Do I accept Torley's logic? Yes. Do I think common descent is explanatory (A) and design is not (B)? No. Do I think that common descent is predictive (A) and design not (B)? No. The reason is that the syllogisms cut both ways. Design is both explanatory and predictive, particularly when dealing with pattern breaking observations in biology, where common descent doesn't work as an explanation. Thus the onus of proof is not on design alone, as Professor Swamidass thinks, but on common descent as well.

Let me show you. According to the theory of common descent, all true mammals are supposed to have descended from a common ancestor with a placenta. This is a trait common to all mammals. However, it has been a puzzle for some time that placentas differ in the form they take among different mammalian clades.

In the year 2000, French researcher Thierry Heidmann and coworkers found that genes derived from endogenous retroviruses (ERVs) appear to have been coopted to perform an essential role in placental formation. These genes, which resemble the ERV envelope gene env, make a protein that originally promoted fusion of the virus with its host cell's membrane, but now acts to promote fusion of membranes between the embryo and the lining of the uterus. These "repurposed" proteins are called syncytins. They are essential for placental formation, yet are of independent origin in different kinds of mammals -- primates have one kind, mice another, rabbits, cows, and carnivores yet others. They are clade-specific. In fact, in 2015 a functional syncytin was found in several marsupials, extending the presence and essential function of the protein to all placental mammals examined. All syncytins are lineage-specific, meaning that each mammalian clade has its own syncytin, with a unique sequence and location in the genome. They must have inserted themselves (or been placed there) after the separation of the mammals into different clades! This means there must have been multiple independent acquisitions of these syncytins to participate in an essential process that is common to all mammals. Why should there be unique syncytins in each clade?

What we have to explain is the unique and independent group-specific cooption of syncytins for a function that is essential for placental development, a feature common to all mammalian groups. Six independent origins for the placenta! There is no evidence of a grand ancestral syncytin shared by all groups that was later replaced by other syncytins, so the common descent explanation of the placenta in mammals fails.

I repeat: distinct syncytins for cows, carnivores, rodents, primates, rabbits, and even tenrecs (a species thought to retain features of primitive mammals). We all recognize these clades based on their traits -- cows are different from carnivores, which are different from rodents, which are different from chimpanzees. Even nursery school children can tell the difference. And they are all thought to have descended from a common ancestor, the proto-mammal. Well, apparently, these well-defined clades of mammals make their placentas using analogous but distinct proteins. This perhaps explains why the placentas of each clade differ in their structures. But it flies in the face of the idea that all mammals are descended from a single kind of ancestor with a single kind of placenta.

I'll quote a review paper on syncytins. These are the people who discovered syncytins, and they have done great work. Yet they are forced into a corner by their own work and the idea of common descent. I have italicized the key features of syncytins that must be explained, and bolded the explanations offered:

... syncytins are 'new' genes encoding proteins derived from the envelope protein of endogenous retroviral elements that have been captured and domesticated on multiple occasions and independently in diverse mammalian species, through a process of convergent evolution. Knockout of syncytin genes in mice provided evidence for their absolute requirement for placenta development and embryo survival, via formation by cell-cell fusion of syncytial cell layers at the fetal-maternal interface. These genes of exogenous origin, acquired 'by chance' and yet still 'necessary' to carry out a basic function in placental mammals, may have been pivotal in the emergence of mammalian ancestors with a placenta from egg-laying animals via the capture of a founding retroviral env gene, subsequently replaced in the diverse mammalian lineages by new env-derived syncytin genes, each providing its host with a positive selective advantage.

Rather than postulating six independent, random capture events in placental development, they are now postulating at least one more, a founding syncytin leading to a primitive placenta, then the other syncytins to replace that one in each lineage. Each replacement must have had a clear selective advantage as time went on to make the replacement possible, and each must be the outcome of a random series of events. To say it again, the common descent prediction is that there must have been a founding syncytin in the first mammal with a placenta, or something else that functioned in syncytin's place, in order for the primitive placenta to arise and subsequently be passed to all mammalian clades. For which there is no evidence, and may never be.

Can common descent explain the unexpected observation of six independent origins for the placenta? No. Could it predict it? No.

Common design has an explanation, but not one that will be palatable to my interlocutors. The designer used the same idea six different times to produce the same outcome in six different "designs" (clades). That's another way of saying all these clades have the same outcome, the placenta, but achieved by independent uses of the same idea.

This can be stated as a general principle. Design predicts that we should find other examples where there are similar but independent ways of performing an essential function or of solving a common biological problem. The means may differ between groups, but the outcome is the same across groups. Or to put it another way, multiple independent paths converge on a common solution. There are many examples of this known already, at the molecular and organismal level. It's known in evolutionary terms as convergent evolution, but I'll call it convergent design.

Convergent design is to be expected under the design hypothesis because the designer is not constrained by an evolutionary tree. He can reuse ideas that work in one setting in a different place. In fact, he can mix and match his methods to get to any outcome he wants. I am thinking of echinoderms (sea stars and sea urchins) that look alike as adults but get there by very different developmental paths, or two very different animal groups that come up with similar molecular solutions to create a new function, echolocation.

Convergent design is clearly observable across biology but has no evolutionary mechanism. There are proposed reasons for it but no demonstration. I can hear in my head the arguments of evolutionary biologists: intrinsic constraints, canalization, living in similar environments or ecological niches, you have no demonstration either...

So then maybe the answer comes down to probability.

In considering these alternative explanations, ask yourself, how likely is it that a retrovirus would infect, invade the germ line (the cells that make eggs and sperm), then insert itself at random in locations in the genome that are expressed in the developing embryo or primitive uterus at the proper time, then promote fusion of membranes to permit the formation of a placenta, with all this happening at least six separate times in the six lineages tested so far? We should also make clear, expressing a syncytin by itself is unlikely to be enough to make a placenta, which is a complex organ requiring interactions between mother and embryo, and the ability to exchange nutrients and oxygen.

Let me close by posing Torley's questions to him, concerning syncytins:

Do you accept that if hypothesis A readily explains an empirical fact F and hypothesis B does not, then F (taken by itself) constitutes scientific evidence for A over B? Or putting it another way, if a fact F is predicted by hypothesis A, and compatible with hypothesis B but not predicted by B, then do you agree that F constitutes scientific evidence for A over B? If not, why not?


Evidence for and against common descent. It's not nearly so open and shut a case as some believe, unless there is an a priori commitment to materialistic explanations.