More aspirational hoodoo re:the Darwinian narrative on the origin of sight.

Optimistic Optics: Scientific American Makes Bold Claims About the Origin of the Eye
Jonathan M. June 23, 2011 6:00 AM 

A couple of weeks ago, an interesting article appeared in Scientific American, titled "Evolution Of The Eye." The subheading of the article makes the bold claim, "Scientists now have a clear vision of how our notoriously complex eye came to be." When I saw that this article had been published, I was immediately filled with a sense of intrigue. I looked forward to reading a proposed solution to a fiendishly vexing problem. What the article actually provided, however, was largely disappointing. There was nothing particularly new or original, and (though coated with our modern scientific understanding) the argument took, more or less, the same basic form that has been rehashed for the last century and a half since the publication of Darwin's On the Origin of Species.

The article actually makes explicit mention of intelligent design (ID) and offers the pertinent argument as a rebuttal to the concept of irreducible complexity. The author of the article, Trevor D. Lamb, claims that

... [B]iologists have recently made significant advances in tracing the origin of the eye--by studying how it forms in developing embryos and by comparing eye structure and genes across species to reconstruct when key traits arose. The results indicate that our kind of eye--the type common across vertebrates--took shape in less than 100 million years, evolving from a simple light sensor for circadian (daily) and seasonal rhythms around 600 million years ago to an optically and neurologically sophisticated organ by 500 million years ago. More than 150 years after Darwin published his groundbreaking theory, these findings put the nail in the coffin of irreducible complexity and beautifully support Darwin's idea. They also explain why the eye, far from being a perfectly engineered piece of machinery, exhibits a number of major flaws--these flaws are the scars of evolution. Natural selection does not, as some might think, result in perfection. It tinkers with the material available to it, sometimes to odd effect.
In a nutshell, the claims made by Lamb are as follows:

1. By comparing eye structures and embryological development of the eye in vertebrate species, one can infer that our camera eye has very ancient evolutionary roots.
2. Prior to acquiring the elements required for its operation as a visual organ, its function was simply the detection of light for modulating the circadian rhythms of our distant ancestors.

3. The eye has various design flaws and this is evidence for its evolutionary / dysteleological origin.

4. There are clues in developing embryos which indicate how the eye formed from a light-sensing but nonvisual organ into an image-forming one by around 500 million years ago.

Lamb's article is chiefly concerned with rebuffing intelligent design (and not merely demonstrating common ancestry). In this critique of the article, therefore, I want to focus primarily on the fourth of those points (which I deem to be the crux of the matter), and will also weigh in briefly on the apparent suboptimality of the eye's design.

Folding A Patch Of Photoreceptors
Lamb tells us,
Early in development, the neural structure that gives rise to the eye bulges out on either side to form two sacs, or vesicles. Each of these vesicles then folds in on itself to form a C-shaped retina that lines the interior of the eye. Evolution probably proceeded in much the same way. We postulate that a proto-eye of this kind--with a C-shaped, two-layered retina composed of ciliary photoreceptors on the exterior and output neurons derived from rhabdomeric photoreceptors on the interior--had evolved in an ancestor of vertebrates between 550 million and 500 million years ago, serving to drive its internal clock and perhaps help it to detect shadows and orient its body properly.
This insight is hardly novel. The idea has been espoused by many of the great evolutionary biologists of the 20th century (e.g. Richard Dawkins). Nilsson and Pelger (1994) also articulated a very similar argument (see David Berlinski's critique here).

In such models, it is thought that visual acuity might be improved first by the initially flat patch of photoreceptors becoming concave, and subsequently by increasing the level of indentation. The argument is, of course, predicated on the critical assumption that the change is both hereditable and able to be continued indefinitely (no matter how much indentation and selection has occurred previously).

Moreover, once the indented patch of photoreceptors is equally as deep as it is wide, visual acuity is most effectively enhanced, not by becoming deeper, but by constricting the orifice of the depression until an optimum is achieved with respect to the trade off between visual acuity (as a result of the narrowing of the angle of incident light to each respective photocell) and the reduction in light admitted to the photocells.

The Development And Evolution Of The Lens
Lamb continues,
In the next stage of embryological development, as the retina is folding inward against itself, the lens forms, originating as a thickening of the embryo's outer surface, or ectoderm, that bulges into the curved empty space formed by the C-shaped retina. This protrusion eventually separates from the rest of the ectoderm to become a free-floating element. It seems likely that a broadly similar sequence of changes occurred during evolution. We do not know exactly when this modification happened, but in 1994 researchers at Lund University in Sweden showed that the optical components of the eye could have easily evolved within a million years. If so, the image-forming eye may have arisen from the nonvisual proto-eye in a geologic instant.
This is all based upon one big assumption: that biological tissues are innately plastic. Little attention is given to the biochemical and molecular conundrums which confront such scenarios. In other words, all that we have learned in the last 50 years of genetics and biochemistry is totally ignored. One cannot help but wonder whether the details of biochemistry are ignored as a result of oversight or whether it is, rather, because it presents such a formidable challenge to conventional evolutionary explanations that to pay it due attention would radically undermine the Darwinian paradigm.

Lamb's choice of words in the above seems to imply a spontaneous embryological development of the lens, and he suggests that perhaps evolution happened in much the same manner. The problem is that lens formation does not, in reality, possess such spontaneity -- far from it. Rather, it is triggered by the release of several chemicals, called "inducers," from the optic vesicle. In epithelial cells, release of these chemicals triggers the expression of the genes which are involved in implementing lens development. The inducer triggers the epithelial cells to start producing a transcription factor, which is often called the "master control gene" of eye development (known as Pax6). Pax6 subsequently activates the genes that cause the epithelium to form a lens placode and then a lens vesicle.

Pax6 also plays a role in the initial formation of the optic vesicle, and in differentiation of retinal cells. This gives rise to an interesting question -- how does the same transcription factor perform different roles in different cell types? Its action is carefully modulated by an array of other factors which are particular to the respective tissues and cell types. In the case of epithelial cells, Pax6 works in collaboration with another transcription factor called Sox2. When these two proteins bind together on a specific DNA sequence, it literally acts as a genetic switch -- triggering lens differentiation.

As Lamb himself explains, lens morphogenesis results from "a thickening of the embryo's outer surface, or ectoderm, that bulges into the curved empty space formed by the C-shaped retina. This protrusion eventually separates from the rest of the ectoderm to become a free-floating element."

The lens vesicle subsequently morphs into a lens. The cells of the vesicle's posterior wall become lens fibers, which grow substantially to a length dozens of times greater than their original size (meaning they completely cover the vesicle cavity). There are several important changes which these cells need to undergo in order to take up their role as lens fibers. For one thing, they have to lose their internal organelles to allow the incoming light to be successfully transmitted through them. The lens fibers are also packed very tightly together -- hexagonal in cross-section, and aligned parallel to the axis of the eye.

These lens fibers also produce proteins known as crystallins, and Pax6 (the transcription factor which I mentioned previously) is involved in activating the crystallin genes. The high level of production of these proteins confers an extraordinary high density and hence a high refractive index which is responsible for the lens' light-bending properties.

Now, at this point we potentially run into a problem.

In the case of most proteins, if they accumulated in such a high concentration as this, they would have a tendency to agglomerate and denature. This would entail that the lens would become cloudy and thus lose its transparency. The proteins which are used -- crystallins -- however, are exceptionally stable, and the largest class of these proteins actually serves to stabilise the other crystallins. This class is known as α-crystallin, and these molecules interact to form hollow balls which are connected by other proteins called CP49 and filensin. This forms a structure called a "beaded filament". These structures predominate within the lens fibers. They are absolutely critical for facilitating such a dense concentration of proteins to actually enhance visual capabilities. Even more remarkable is the fact that these proteins are never recycled. Unlike most other proteins, these crystallin molecules do not degrade and thereby result in the lens becoming cloudy. The beaded filament structures actually protect the proteins from such degradation and denaturation. Actually, one of the causes of eye cataracts is a faulty beaded filament structure.

But here's the bottom line: This is not the type of system which one might intuitively expect to be the product of trial-and-error Darwinian-type tinkering. To simply appeal to the addition of a lens is to fundamentally trivialise the matter at hand.

Chicken And Egg
I have really only scratched the surface here. Molecular morphogenesis of the eye extends far deeper than this. Once the optic vesicle has contacted the epithelium, it spreads outwards and folds in on itself. This forms the hollow eyeball. The inner layer of this will develop into the retina. What is particularly remarkable is that, while the optic vesicle is absolutely fundamental for the induction of lens development, subsequent development of the eye depends, in large measure, on factors which are secreted by the developing lens! This casts even further doubt on the sorts of scenarios commonly offered to us by Darwinians such as Lamb, wherein the lens is viewed as a relatively late addition to the eye structure.

Further Problems
In his review of Richard Dawkins' Climbing Mount Improbable, David Berlinski makes the following additional observations:

Light strikes the eye in the form of photons, but the optic nerve conveys electrical impulses to the brain. Acting as a sophisticated transducer, the eye must mediate between two different physical signals. The retinal cells that figure in Dawkins' account are connected to horizontal cells; these shuttle information laterally between photoreceptors in order to smooth the visual signal. Amacrine cells act to filter the signal. Bipolar cells convey visual information further to ganglion cells, which in turn conduct information to the optic nerve. The system gives every indication of being tightly integrated, its parts mutually dependent.
The very problem that Darwin's theory was designed to evade now reappears. Like vibrations passing through a spider's web, changes to any part of the eye, if they are to improve vision, must bring about changes throughout the optical system. Without a correlative increase in the size and complexity of the optic nerve, an increase in the number of photoreceptive membranes can have no effect. A change in the optic nerve must in turn induce corresponding neurological changes in the brain. If these changes come about simultaneously, it makes no sense to talk of a gradual ascent of Mount Improbable. If they do not come about simultaneously, it is not clear why they should come about at all.

The same problem reappears at the level of biochemistry. Dawkins has framed his discussion in terms of gross anatomy. Each anatomical change that he describes requires a number of coordinate biochemical steps. "[T]he anatomical steps and structures that Darwin thought were so simple," the biochemist Mike Behe remarks in a provocative new book (Darwin's Black Box), "actually involve staggeringly complicated biochemical processes." A number of separate biochemical events are required simply to begin the process of curving a layer of proteins to form a lens. What initiates the sequence? How is it coordinated? And how controlled? On these absolutely fundamental matters, Dawkins has nothing whatsoever to say.

Is The Vertebrate Eye Bad Design?
Lamb tells us that,
The vertebrate eye, far from being intelligently designed, contains numerous defects that attest to its evolutionary origin. Some of these flaws degrade image quality, including an inside-out retina that focus light to pass through cell bodies and nerve bodies before hitting the photoreceptors; blood vessels that sprawl across the retina's inner surface, casting undesirable shadows onto the retina; nerve fibers that gather together to push through a single opening in the retina to become the optic nerve, creating a blind spot.
This argument has been addressed many a time. The bottom line is this: Retinal cells require a very large oxygen supply, and hence a very large blood supply. Blood cells absorb light. If blood cells invade retinal cells, the consequence can be blindness. This entails that the retinal cells need to receive a blood supply from vessels which do not block the light. Since red blood cells readily absorb light, this demand requires that the retina be wired in the manner in which it is. As is often pointed out, squids and octopuses have 'correctly' wired retinas that face outward. But these organisms are exothermic -- they do not require the same blood supply to the retina.

For a slightly different perspective on this topic, I refer readers to Richard Sternberg's essay here.

Summary and Conclusions

I have only provided a sketchy overview of a few of the key processes which undergird eye development. I have not even discussed the biochemical and molecular details of vision (for that, I refer readers to Michael Behe's book, Darwin's Black Box, or this article). In addition, Casey Luskin has an excellent critique of the Darwinian account of the eye's origin here. Nonetheless, I hope that this article has given readers a sense for why Darwinists are going to have to do a lot better than they are currently doing if they are to convince us of the plausibility of their model.

I.D as pure science

Defining and Utilizing Intelligent Design in Science
Kirk Durston November 5, 2015 10:21 AM


My introduction to the role of intelligent design (ID) detection in science was a student job in the summer of 1978 working for National Defense Research. My assignment was to write software that could detect Soviet submarines amid the natural background noise of the ocean. I successfully completed the project by utilizing, among other things, a fast Fourier transform applied to the signals from underwater acoustic microphones. The otherwise hidden target signal stood out like a sore thumb.

After graduating with degrees in physics and in mechanical engineering, I spent a few years working as a test engineer, helping to coordinate the build and test of experimental aircraft engines for a major company. During that time, I had the opportunity to interact with different departments, including Design. I could see how a new model of aircraft engine emerged, beginning with an idea in an intelligent mind, which was then encoded into prescriptive information and culminated in a novel, fully functional turbine engine. It was ID in action.

In science, it is essential to define what one is talking about when referring to ID. In my own view it can be defined as follows:

Intelligent Design: an effect that requires an intelligent mind to produce

Examples include the unique acoustic signature of a submarine, a smartphone, the fitness function of a well-designed genetic algorithm, and an artificial protein.

I was invited to consider doing a PhD in Bioinformatics at the University of Guelph. On the condition that my research would focus on the role of information encoded in biopolymers, I applied and was accepted into the Biophysics Masters program with the understanding that if my academic performance was "outstanding" (their term -- and I mention this only to protect the academic integrity of my alma mater), I might be permitted to transfer into a PhD program after the first year. Twelve months later the Biophysics department gave the go-ahead to complete a PhD program.

The first project was to develop a method to measure the minimum level of functional information required to code for a protein family. The results were published, and I then moved on to my first major ID-inspired project. As a result of my experience in testing experimental aircraft engines I observed that an intelligent designer usually specifies a higher degree of information for interdependent components. What if I applied this ID observation to the functional information encoding the 3D structure of globular proteins? My prediction was that it should reveal interdependencies within the primary structure. This, in turn, would reveal key sub-molecular structural components within the larger 3D structure.

To test this hypothesis and prediction, I ran a large multiple sequence alignment for ubiquitin through a pattern discovery program that searched for patterns of high information content between sites in the sequence, and clustered the sites accordingly in a nested hierarchy. I was thrilled when the results revealed a cluster tree that predicted important structural interdependencies as well as key binding areas and possible stages of the folding sequence. Comparison with the known 3D structure for ubiquitin, together with published research on binding areas and unfolding experiments, confirmed that the results were meaningful. These were published in a subsequent paper. This approach could give rise to an enormous ID-inspired research program that would give further understanding into protein structure and folding, should someone decide to pursue it.

I have observed three ways in which ID is firmly entrenched in science:

Design Application: The application of intelligence to first principles of physics to produce a desired effect. (e.g., artificial proteins)

Design Derivation: Beginning with a complex effect, the process of reverse engineering back to first principles in an effort to understand the design and how it works (e.g., genetics is probably the largest reverse engineering/ID project that science has embarked upon).

Design Detection: The analysis of an effect to determine if it requires an intelligent mind (e.g., marking and identification of artificial genomes, proteins and designer drugs, as well as forensic science, archeology, decryption and SETI).

The application of these three areas gives rise to a number of predictions in science, which I will deal with in other posts.

The role of ID in science continues to intrigue me, especially design detection. Over the years, I noticed that wherever there were statistically significant levels of functional information, there was an intelligent mind not far away.

How does one develop a method in science to detect when ID is required? I have observed that different disciplines in science use a variety of approaches. However, I realized there was a hypothesis that could provide a common solution to all design detection problems. Despite the variety of approaches used in forensic science, archeology, SETI, and biology, the core of each method could be reduced to just one, generally assumed hypothesis, which I call the central hypothesis:

Central hypothesis: A unique attribute of an intelligent mind is the ability to produce statistically significant levels of functional information (If).

This hypothesis is testable, falsifiable, verifiable, and provides the basis for a scientific method for design detection as follows:

Step One: Measure the minimum level of If required to produce the effect.

Step Two: Determine if the level of If is statistically significant.

Step Three: If If is statistically significant, the artifact/signal/effect tests positive for ID.


In the future, I hope to discuss an application of this method for design detection in science, together with its implication for the protein families of biology.

Apparently contemptous sneering remains Darwin defenders strongest argument

From Biochemist Larry Moran, More Gratuitous Misrepresentations

Ann Gauger November 6, 2015 10:25 AM 

Biochemist Larry Moran at the University of Toronto has posted another piece arguing with us about the Cambrian explosion, and specifically the view given by Stephen Meyer in his book Darwin's Doubt. I do wish Moran would state his case without inserting gratuitous misrepresentations. If he's read the book, he should know by now what intelligent design theorists like Stephen Meyer really think. So all I can conclude is that Moran's little slurs are an attempt to prejudice his readers.

Here it comes:

Meyer ... believes that a supernatural being visited the Earth about 540 million years ago and noticed that it was teeming with life -- lots of plants, algae, fungi, protozoa, and bacteria. The god(s) thought there should be some bigger creatures called "animals" so he/she/it/they built a few and let them loose to reproduce and evolve.

Meyer believes no such thing. He thinks that the appearance of most of the animal phyla over 10 million years represents a considerable increase in biological information. Ten million years is nothing on the geologic time scale, and information isn't had for free. New body plans and new ways of living require new cell types, new organs, new nervous systems -- at a minimum, new ways of using existing genes and the acquisition of new ones. This represents an incredible increase in biological information.

The prior existence of algae, fungi, protozoa and bacteria is not disputed by Meyer. (Plants came later, Professor Moran.) The existence of these organisms also needs explanation. For them to exist at all required massive amounts of information. Scientists can't explain how the first cell, the first molecule of DNA, or the first protein came to be, or where the information to make them came from. Meyer thinks that DNA, RNA, and proteins require explanation first of all, which Moran should know from reading either Signature in the Cell or Darwin's Doubt.

More Moran:

Most biologists don't agree with Meyer's explanation (surprise!). Instead, they look for real evidence to inform them of what happened at this point in the history of life. One of the ways they do this is to construct phylogenetic trees from sequence data. This should be a test of whether all these species popped into existence at once or whether they have an evolutionary history.

Molecular phylogenies should also reveal whether the various phyla are related to each other or whether they were all poofed into existence independently within a few days, or weeks, or years, as Stephen Meyer suggests.

Really, Larry? You were doing so well! I thought maybe we could have a legitimate discussion of the science. Then poof, more misrepresentations appear.

I have already said Meyer does not think that all these animals poofed into existence over the span of days, weeks or years. He acknowledges the existence of the fossil record and the time span of ten million years over which animal life made its appearance. He does dispute the accuracy of the trees, however, for reasons Moran describes quite well in his post. The molecular clocks are equivocal about both the timing of the event and the relationships between groups. And the fossils are still missing.

To be fair, Moran acknowledges that Meyer may actually have some points worth discussing. (Why not discuss them, Larry?) Where Moran and Meyer part ways is on how to account for the appearance of these animals.

Perhaps the major animal phyla evolved from earlier species. Plenty of ID advocates accept that. And we all accept evolution in the sense of change over time. What we dispute is the mechanism responsible forchange over time.

Meyer disagrees with the interpretation that is placed upon the Cambrian by Moran and other evolutionary biologists, primarily because they fail to account for the sudden appearance (10 million years) of so much biological information. They assume that a purely materialistic evolution is capable of accounting for all that biological information. The problem is, it does no good to push the origins of animal life further and further back in time, because the information problem hasn't been answered. Meyer states very clearly that the information to make animals, whether from prior organisms or not, came from an intelligent designer. Why? Because intelligence is the one source we know that is capable of generating that kind of information.

If Moran could just leave out the misrepresentations, perhaps we could have a legitimate discussion about the evidence. But why try when your opponent can't stick to the facts?

Darwinism Vs. the real world.XIX

Vasoconstriction and Platelet Aggregation Defy Evolutionary Explanations

Howard Glicksman November 6, 2015 4:25 AM

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

To feed the cells of the body so they will live, grow, and work properly, the heart must pump blood with enough pressure through the circulatory system. However, just as water under pressure can leak out of a pipe that has burst, so too a ruptured blood vessel can result in blood loss. Moreover, depending on how much blood is lost and where it takes place in the body, this can lead to significant health risks. Our earliest ancestors needed to live active lives and, just like us, were constantly at risk of blood loss from injury. If the body didn't have the wherewithal to prevent significant blood loss, humanity could never have survived or reproduced.

As I noted in my last article, the process that performs the important task of preventing blood loss is called hemostasis. Hemostasis involves the quick and almost simultaneous actions of the injured blood vessel, the platelets, and the clotting factors to form a fibrin clot to stop the bleeding.

But the body faces another dilemma. A clot in a major vessel like an artery supplying blood to the brain, or the heart, or the lungs, can cause significant damage. In other words, hemostasis and the clots it forms must turn on only when it's actually needed and must turn off and stay offwhen it's not. It's like the sprinkler system in a factory and an air bag in a car. They must deploy only when needed. Let's consider the first two components of hemostasis: blood vessel vasoconstriction and platelet aggregation.

Just like in a garden hose, there is a central channel or lumen through which blood flows in a blood vessel. The tissue that lines the lumen is called the endothelium. The endothelium does much more than just act as a barrier between the blood and the underlying support tissue, which in most blood vessels contains a protein called collagen and is surrounded by muscle. When a blood vessel is injured, local chemical changes related to the endothelium trigger the surrounding muscle to automatically contract in an attempt to close down the lumen to prevent further blood loss.

This short-lived vasoconstriction plays a major role in hemostasis and often in small arteries and arterioles can almost totally shut off the blood vessel, allowing the platelets and clotting factors to work together, forming a clot to permanently seal the injured site. Vasoconstriction acts like the person who has to sit on an over-packed suitcase so the top and bottom can be brought close enough together for the lock (platelet plug and fibrin clot) to be applied. Without vasoconstriction, the task of the platelets and clotting factors would be impossible.

Adequate hemostasis to prevent recurrent serious bleeding would have required our earliest ancestors to have blood vessels with normal function. There are several rare medical conditions in which the body has abnormal blood vessels that have difficulty contracting upon injury. Some chronic illnesses cause significant vascular fragility. These conditions put people at very high risk for bleeding from minimal trauma, resulting in life-threatening hemorrhage if a major organ or blood vessel is involved.

Evolutionary biologists may imagine how blood vessels came into being, but clinical experience shows that the complicated structure of blood vessels must not only allow for adequate blood flow, but also have a mechanism in place that helps to minimize bleeding when injury takes place. For our earliest ancestors, this would be the difference between life and death.

The second action needed for clot formation and hemostasis is the activation of the platelets. Platelets, also known as thrombocytes, are small disc-shaped, cell-like structures in the blood. They are about one-quarter to one-half the size of red blood cells. Platelets form in the bone marrow and, once released into the bloodstream, survive for only about ten days.

Platelet production in the bone marrow is controlled by a hormone called thrombopoietin. This hormone is produced mainly in the liver and the kidneys. It works by attaching to specific receptors on the stem cells in the bone marrow to start the production of platelets. How the body regulates thrombopoietin production has only recently been explored, and where the thrombopoietin receptor on the stem cells originated is still unknown. But rest assured, this lack of knowledge does not deter evolutionists from speculating on how platelets with their important function must have come into being only by chance and the laws of nature alone.

Normally, platelets circulate in the bloodstream without interacting with each other or the blood vessel wall. This occurs because the endothelium releases chemicals that prevent the platelets from sticking to each other and repels them from the vessel wall. Vascular injury activates the platelets by disrupting the secretion of these endothelial chemicals and exposes the platelets to the collagen just below the endothelium as well. This allows the platelets passing by the damaged region to attach to the vessel wall, change shape, and stick together.

Activated platelets also release chemicals that cause further vasconstriction and recruit more passing platelets to the site of injury. This piling on of several layers of platelets sticking to each other is called platelet aggregation, and it ultimately results in the formation of a soft platelet plug. Since the vessel walls on either side of the injury still have an intact endothelium, platelet activation and plug formation tends to be limited mainly to the site of injury. In this way, progression of the platelet plug in either direction from the vessel injury is usually prevented. The total absence of platelets is incompatible with life.

For minor injuries in very small blood vessels, the platelet plug is often all that is needed to stop the bleeding and allow healing to take place. Think of it like what a beaver must do to fix a breach in its dam. If it is very small with only a trickle of water going through, then using small amounts of soft leaves and sticks joined together by thin mud may be all that is needed. But if it is larger and has a torrent of water going through, then lots of large logs and flexible branches combined with solid sticks, soft leaves, and lots of thick mud will be needed to seal the breach.

For most of the traumatic injuries our earliest ancestors encountered in trying to win the battle for survival, it is the latter situation that applied. Next time, we'll look at how the third component needed for adequate hemostasis, the clotting factors, bring about fibrin clot formation to prevent excessive blood loss.

Darwinism Vs. The real world XVIII

Blood Clotting Requires Four Different Processes Working Together
Howard Glicksman October 26, 2015 4:17 AM

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

Let's review some of the lessons that this series has so far provided about human life. The body is made up of trillions of cells, each of which must control its volume and chemical content while receiving what it needs from the blood to live, grow, and work properly. Since the body is made up of matter, it is subject to the laws of nature, which demand that it have enough energy to do what it needs to do to survive.

The body must constantly take in oxygen through the respiratory system to provide itself with the energy it needs to live because, unlike glucose, oxygen can't be stored for future use. About one-quarter to one-half of the energy the body uses while at rest is just for the sodium-potassium pumps within the plasma membrane of its trillions of cells. These pumps push Na+ ions out of the cell and bring K+ ions back in. This action not only maintains the volume and chemical content of the cell, but also the 2/3:1/3 ratio of water inside and outside the cells.

Combined with the control of its water and sodium content and the production of albumin, this process allows the body to maintain enough blood volume. The sodium-potassium pumps also maintain the electrical resting membrane potential of the cell. This is particularly important for proper heart, nerve, and muscle function.

When the cells in the brainstem die (the ones that tell the body to breathe, control its circulation, and make it conscious of its surroundings) the body is considered dead. However, the commonest cardiopulmonary arrest is the most common cause of death. Without respiration the body can't bring in new supplies of oxygen and get rid of toxic carbon dioxide, and without the heart pumping, there isn't enough blood flow to the brain. Together, this causes it to malfunction.

Since blood has mass, the heart has to pump it throughout the body against natural forces like inertia, friction and gravity that would prevent it from moving. As blood moves through the circulatory system, it applies a pressure against the vessel walls. This represents the energy that is generating its flow.

In clinical practice, the blood pressure is taken in the upper arm and is a measure of the force of blood against the walls of the brachial artery. The blood pressure is dependent on how well the heart pumps, how much blood is in the systemic arteries, and the resistance to blood flow applied by the downstream arterioles that control how much blood enters the capillaries. Blood flow (Q) is directly related to the blood pressure (P) and inversely related to the vascular resistance (R). This law of nature can be expressed as Q = P/R. The more blood pressure the more blood flow and the less blood pressure the less blood flow. The more vascular resistance the less blood flow and the less vascular resistance the more blood flow.

When we stand up and feel momentarily dizzy, our body must inherently know that if Q = P/R, then P = Q x R. In other words, blood pressure is directly related to the blood flow and vascular resistance. More blood flow and vascular resistance increases the blood pressure and less blood flow and vascular resistance decreases the blood pressure.

Standing up allows gravity to prevent blood from returning to the heart from the veins in the chest, abdomen and legs. It also keeps it from going from the heart to the brain, which reduces the blood pressure and blood flow to the brain. That's what makes us feel dizzy. The body detects these changes and reacts by sending out nerve messages to make the heart pump harder and faster, pushes blood from the veins back toward the hear,t and increases the vascular resistance applied by the arterioles by increasing the contraction of their surrounding muscles. The first two actions increase blood flow (Q) and the last one increases the vascular resistance (R), so the blood pressure (P) rises and our dizziness usually resolves in a matter of seconds.

The above demonstrates just some of the ways the body takes control and follows the rules in line with the Goldilocks principle: the real numbers must be "just right." After all, life doesn't take place within a vacuum or the imaginations of evolutionary biologists. As was the case with our earliest ancestors, to survive we must remain active, exposing our body, and our blood vessels, to the random forces of nature.

Experience tell us that when we run, jump, climb, roll, fall, and generally bang into or scrape up against solid or sharp things, natural forces like friction, momentum, pressure, sheer and gravity all contribute to blood vessel damage, bleeding and blood loss. This takes place because, with damage to the blood vessel wall, the pressure that sustains blood flow within it naturally pushes blood out through the opening. Think of it like when a water pipe in your home bursts. The water flowing through it is under pressure and when the walls of the pipe rupture water naturally flows out. Depending on the location and the severity, if the body can't stop the bleeding fast enough it runs the risk of serious problems. So to follow the rules that the laws of nature impose on it, the body must have a mechanism in place to prevent excessive bleeding from its blood vessels when they undergo injury.

Experience teaches that when we cut ourselves, a clot forms at the injured site to stop the bleeding and allow healing to take place over the next several days. This process is called hemostasis (Greek: haima = blood + stasis = halt).

Hemostasis generally involves three actions that occur almost simultaneously. Vasoconstriction is contraction of the muscles surrounding the injured blood vessel, which tries to totally close down the opening in the wall. Platelet aggregation is the formation of a soft plug by the platelets coming together and sticking to each other to fill the gap in the blood vessel wall. And activation of the clotting factors is the formation of thousands of sticky strands of fibrin which wrap around the platelet plug to form a molecular meshwork that entraps red blood cells and plasma to form a fibrin clot which closes off the damage and stops the bleeding.

However, when it comes to preventing blood loss from blood vessel injury through hemostasis, the laws of nature present the body with another dilemma. It's important that the clotting mechanism turn on only when it's needed, not only to not waste the body's supply of platelets and clotting factors, but also to prevent the sudden blockage of blood flow to vital organs. A poorly placed blood clot within an artery supplying blood to the heart muscle can cause a heart attack, or to the brain, a stroke, or to the lungs, a sudden drop in oxygen availability. Any one of these situations can result in serious and permanent debility or sudden death.


So, in addition to being able to turn on at the right time, the body must also have a mechanism in place to take control so that hemostasis will turn off and stay off at the right times. How does the body do it and how does evolutionary biology explain how it works in real life? That's what we'll begin to look at next time.

Is artificial selection analogous to Darwinism?

Animal Breeding as Evolution "In Action"?

Michael Flannery November 5, 2015 12:21 PM

Ann Gauger's post "Is Evolution Random? Answering a Common Challenge" is an excellent answer to those who still today affirm Darwin's contention that domestic breeding offers an example of evolution "in action." But there is more to say. Alfred Russel Wallace wrote in his famous Ternate letter:

Again, in the domesticated animal all variations have an equal chance of continuance; and those which would decidedly render a wild animal unable to compete with its fellows and continue its existence are no disadvantage whatever in a state of domesticity. Our quickly fattening pigs, short-legged sheep, pouter pigeons, and poodle dogs could never have come into existence in a state of nature, because the very first step towards such inferior forms would have led to the rapid extinction of the race; still less could they now exist in competition with their wild allies. The great speed but slight endurance of the race horse, the unwieldy strength of the ploughman's team, would both be useless in a state of nature. If turned wild on the pampas, such animals would probably soon become extinct, or under favourable circumstances might each lose those extreme qualities which would never be called into action, and in a few generations would revert to a common type, which must be that in which the various powers and faculties are so proportioned to each other as to be best adapted to procure food and secure safety, -- that in which by the full exercise of every part of his organization the animal can alone continue to live. Domestic varieties, when turned wild, must return to something near the type of the original wild stock, or become altogether extinct.

Thus, the selection of domestic breeders (artificial selection) is both quantitatively and qualitatively different from natural selection -- quantitatively because breeder selection is much stronger, and qualitatively because breeder selection is more obviously goal-directed toward things unrelated to fitness. This argument from analogy is, therefore, false on its face. Wallace was right in pointing it out in 1858 and it remains true today.

But there's a further problem. As Bert Theunissen points out in his paper "Darwin and his pigeons. The analogy between artificial and natural selection revisited," Darwin didn't even have a full appreciation of what breeders actually did. Selection is only a broad gloss on the subject. Crossing and inbreeding are also important factors used by conscious breeders in creating domestic animals.

Theunissen notes that Darwin believed most breeds were of ancient origin; they are not. Bottom line: Darwin's analogy simply doesn't work. So while his brand of natural selection may not be considered in an entire and literal sense "random," neither does it involve the kind of careful thought and pre-selection planning of the domestic breeder. Nor is it the sort of blind, random, purposeless, wholly natural causes operating to produce speciation that Darwin himself insisted upon. Darwin himself stated in his Autobiography:

The old argument from design in Nature, as given by Paley, which formerly seemed to me so conclusive, fails, now that the law of natural selection has been discovered. . . . There seems to be no more design in the variability of organic beings, and in the action of natural selection, than in the course which the wind blows.

But there are many more design options than that offered by Paley, and more to the point, domestic breeders don't achieve their purposes by the whimsy of the wind either.

This matters for two reasons. First, because the argument from breeding was extremely important to Darwin. His first two chapters inOrigin are devoted to it. As Jean Gayon has argued in Darwin's Struggle for Survival:

The use of the domestic analogy was not a pedagogic device. It was methodological essential, without it, the subtle interrelationship between variation, heredity and modification, so characteristic of the Darwinian hypothesis of selection, would have been nothing more than empty speculation without any empirical content.

Second, it matters because it demonstrates how different the respective evolutionary theories of Charles Darwin and Alfred Russel Wallace really were. Darwin was interested in individual competition leading to variation, while Wallace was concerned more broadly with competition and variation within a biogeographical context of group dynamics. On Darwin's behalf it should be said that such significant differences between the two need to be carefully considered by those leveling charges of plagiarism or a "Darwin conspiracy" theory.

The doubt is still going strong.

Darwin's Doubt Passes 700 Review Mark on Amazon

Andrew McDiarmid November 3, 2015 12:56 PM

Stephen Meyer's book Darwin's Doubt: The Explosive Origin of Animal Life and the Case for Intelligent Design has reached 700 customer reviews on Amazon.com. It's the most-reviewed book in the categories of Organic Evolution and Paleontology. It's the 7th most-reviewed non-fiction book in Evolution, a category that includes over 50,000 titles. It's even in the top 200 of most-reviewed books in Science & Math, a top-level category that includes over 1.3 million offerings. Meyer's book now joins Michael Behe's book Darwin's Black Box as the two most-reviewed books on Amazon on the topic of biological origins.

I point this out because, slowly but surely, Darwin's Doubt has taken root in the collective consciousness of Amazon customers, and by extension, the American public at large. According to a 2014 poll from Pew Research, 87 percent of American adults use the Internet. Of those, 61 percent use the Internet to shop, and Amazon attracts business from 86 percent of adults shopping online. So Amazon stats mean something. Darwin's Doubt has regularly been a #1 bestseller in Organic Evolution, Paleontology, and other related Amazon book categories.

Although Amazon reviews are by no means the most critical measure of a book's success, it does reveal one thing of note. Our effort to communicate the arguments for intelligent design through alternative channels, beyond what often seems like the echo chamber of mainstream science media, is paying off. Although the book was reviewed in such notable publications as Science, The New Yorker,National Review, and The American Spectator, most science journals and the mainstream media have maintained a wary distance. Despite this,Darwin's Doubt is a national bestseller and continues to engender intense interest and debate.

And it's not just laypeople who are enjoying it. One recent five-star review comes from a PhD biochemist and former director of the Biochemistry and Molecular Biology Department at the Southern Research Institute/UAB, Birmingham, AL. He recommends that both critics and proponents of intelligent design read the book. This is to say nothing of the dozens of PhD scientists and other professional scholars who have endorsed the book before or after its publication in 2013.

Not everyone is happy with Darwin's Doubt, and a browse through the Amazon reviews reveals a passionate minority who are critical of Meyer's work (15 percent are one- or two-star reviews). All the usual tired arguments against intelligent design are rehearsed, but a recent detractor broke new ground with a lament for the trees that were used to create the book: "Utter trash. Complete nonsense. I feel sorry for the trees that have lost their life to print these words on the paper made from their sacrifice. Please do not allow your children to read this." It's interesting that this individual would warn against children being exposed to alternative viewpoints on important scientific topics. That is more revealing than the reviewer probably realizes.

Has the enigma of Cambrian explosion been solved? Can scientists now demonstrate how natural processes alone can build an animal? No on both counts. And while the debate over the evidence goes on, Darwin's Doubt continues to have its important impact, making steady, incremental progress just like that of science itself.

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Loved to death?

National Science Standards Reflect a Growing Anxiety on the Part of Evolution Advocates

Sarah Chaffee November 2, 2015 3:46 PM

Teach science critically -- except when it comes to evolution. In discussions of how to improve public school education in the U.S., that's the message that advocates of national science standards typically convey. Yet that wasn't always the case.

An article at Ars Technica recounts the development of the most recent set of proposed standards: the Next Generation Science Standards (NGSS), finalized in 2013. Ironically, teaching students to engage in scientific inquiry, rather than simply expecting them all to absorb the same "facts," was the main impetus.

NGSS began as separate projects of the American Association for the Advancement of Science (AAAS) and National Academies of Sciences (NAS). Their efforts were eventually merged and became the NGSS. John Timmer at Ars Technica writes:

Inspired by the visit of Halley's comet in the 1980s, the AAAS started Project 2061, an attempt to envision where the organization would like to see science literacy in the year the comet would return. Jo Ellen Roseman, Project 2061's Director, told Ars that the goal was to "characterize what the knowledge, skills, and habits of mind would constitute adult science literacy."

Instead of insisting on a "just the facts" approach, the AAAS focused on training young people to think like scientists. After all, the body of knowledge would change over the decades, but the process of scientific inquiry would not.

"While we had no idea what the world would be like, we could guarantee that it would be shaped by science, mathematics, and technology," Roseman said. "And therefore every citizen of the US, every high school graduate had to be literate in those fields."

... Driven by this concept, AAAS gathered scientists and educators to produce a document called Science for All Americans. This publication, while not a set of education standards, laid out the ideas they should contain. Written in prose, it describes basic facts about the Universe that people should know.But over half the document is focused on the nature of science, technology and math, the historic development of these fields, and the "habits of mind" essential for scientific literacy.

The NAS's National Research Council (NRC), meanwhile, produced itsNational Science Education Standards, with a similar emphasis:

"The NRC document took a very strong position about scientific inquiry," Roseman said. "It went beyond what kids should know and be able to do and really articulated what should be going on in classrooms. Students should be engaged in inquiry."

Exactly! At Discovery Institute, we advocate teaching the controversy about evolution. That is for several reasons. Students should learn the full range of evidence on evolution. Teaching the controversy aids in developing critical thinking. And it trains students to think like scientists. Jo Ellen Roseman's comments highlight a further advantage to this pedagogic strategy: that while the content of science may change, the process of scientific inquiry remains vital and valid.

The documents produced by the AAAS and NAS, Science for All Americans and the National Science Education Standards, are persuasive in explaining the importance of critical thinking. Science for All Americansnotes:

In science classrooms, it should be the normal practice for teachers to raise such questions as: How do we know? What is the evidence? What is the argument that interprets the evidence? Are there alternative explanations or other ways of solving the problem that could be better? The aim should be to get students into the habit of posing such questions and framing answers.

Avoid Dogmatism

Students should experience science as a process for extending understanding, not as unalterable truth. This means that teachers take care not to convey the impression that they themselves or the textbooks are absolute authorities whose conclusions are always correct. By dealing with the credibility of scientific claims, the overturn of accepted scientific beliefs, and what to make out of disagreement among scientists, science teachers can help students to balance the necessity for accepting a great deal of science on faith against the importance of keeping an open mind.

The NAS document, National Science Education Standards, recommends:

Students at all grade levels and in every domain of science should have the opportunity to use scientific inquiry and develop the ability to think and act in ways associated with inquiry, including...thinking critically and logically about relationships between evidence and explanations, constructing and analyzing alternative explanations, and communicating scientific arguments.

Building on this foundation, the set of current national science standards, the NGSS, agrees that critical analysis is important. The NGSS were developed in two phases. First, the National Academy of Sciences laid out the basic scientific information students should learn. Second, states worked together to develop specific grade-level standards. The document produced in the first phase, A Framework for K-12 Science Education, takes a very positive view of critical analysis:

Chief among these features [of science] is a commitment to data and evidence as the foundation for developing claims. The argumentation and analysis that relate evidence and theory are also essential features of science; scientists need to be able to examine, review, and evaluate their own knowledge and ideas and critique those of others. Argumentation and analysis include appraisal of data quality, modeling of theories, development of new testable questions from those models, and modification of theories and models as evidence indicates they are needed.

Major science journals also hold that inquiry is central to quality science education. Yet when it comes to evolution, the NGSS abruptly switch gears, rejecting inquiry-based learning and opting for dogmatism.

In middle school, we read, "students can analyze data from the fossil record to describe evidence of the history of life on Earth and can construct explanations for similarities in organisms. They have a beginning understanding of the role of variation in natural selection and how this leads to speciation."

In high school, students are to "demonstrate understanding of how multiple lines of evidence contribute to the strength of scientific theories of natural selection and evolution." This seems to be nearly the opposite of what Science for All Americans says:

Students should experience science as a process for extending understanding, not as unalterable truth. This means that teachers take care not to convey the impression that they themselves or the textbooks are absolute authorities whose conclusions are always correct.

It is inconsistent to oppose the freedom to critically analyze evolutionary thinking, while proclaiming that inquiry is the cornerstone of quality science education. The inconsistency, though, is not all that surprising. It's plainly defensive, a circling of wagons around a theory under increasing pressure from scientific criticisms. The NGSS reflect the anxious mood on the part of evolution defenders in the larger debate about origins.

Students deserve better. If we really want nationwide scientific literacy by the time Halley's comet returns in 2061, we should teach young people to question and analyze across the board, whether the context is biological origins or any other scientific field.