A Darwinian apparatchik rallies the faithful.

Latest Cambrian Explosion "Explanation" Qualifies as Propaganda

Evolution News & Views October 9, 2015 10:37 AM

Many of us remember Pravda and Izvestia, the official propaganda organs of the former USSR. Having silenced the free press long ago, these "newspapers" were free to dole out the party line without opposition, giving the impression to unwary readers that there was no opposition. Well, another major science journal has followed this strategy. Fortunately, social media provides a "black market" for samizdat publishing.

To celebrate its 25th anniversary, Current Biology offers a special issue on "The History of Life on Earth." The 16 open-access articles amount to a treasure trove of evolutionary thinking on a wide variety of subjects: RNA World, insect evolution, bird evolution, and more -- all presented by big-name Darwinian proponents who ignore alternative views. A case in point is the primer on "The Cambrian Explosion" by Derek E. G. Briggs. Any mention of Stephen Meyer? No. Or critiques of the Darwinian explanation? Nope. Intelligent design? Are you kidding?

One might think that the editors would find it strategic to allay the fears of readers worried about the challenge to Darwinism raised by Meyer's best seller Darwin's Doubt by answering it. Instead, they chose to ignore it. That seems a risky strategy, considering that Meyer and others cogently responded to their critics' best objections in the follow-up book released this summer, Debating Darwin's Doubt. It's hard to imagine Briggs or the editors being unaware of these books. Apparently they think that enough of their readers don't know of the controversy, or they don't wish to give Meyer publicity. To illustrate our love for freedom of the press, we'll encourage you to hear both sides.

It's interesting to see what Briggs admits about the Cambrian explosion (emphasis added):

1. It's real: "We now know that the sudden appearance of fossils in the Cambrian (541-485 million years ago) is real and not an artefact of an imperfect fossil record," he says.
2. It saw diverse body plans: "In effect, the major body plans or phyla were established during the Cambrian explosion," but how? (Keep reading.)
3. Hard parts were not required: "Exceptionally preservedCambrian fossil deposits, such as the famous Burgess Shale, yield examples of 14 of the 19 soft-bodied phyla" of the ~33 animal phyla recognized today.
4. Not oddballs: "The affinities of some of the Cambrian creatures that were dubbed 'weird wonders' are still debated but phylogenetic analyses have shown that most of them are much less weird than first thought -- they do not represent extinct higher taxa, but are early offshoots of the lineages leading to modern groups."
5. Complex parts: "Various arthropods from the Cambrian of China have recently been shown to preserve evidence of the brain and nervous system, which were fossilized in rapidly precipitating minerals," Briggs says.
6. No answers: "The drivers behind the Cambrian explosion were varied and complex, and there is no simple explanation of either the timing or ecological mechanisminvolved." All he can do is offer possibilities.
7. Bottom line: Briggs still is looking for clues about how "all the major animal groups evolved in a relatively short timeduring the Cambrian explosion."

We see that Briggs doesn't dispute the observable facts. He knows that all the major animal body plans appeared quickly. So what is his explanation?

1. He stretches out the explosion, giving it the largest possible range of 56 million years. 10 million years is more widely accepted, but no matter how many years are granted, the problems of missing ancestors and abrupt appearances remain.
2. He considers the Ediacaran period ancestral to the Cambrian, asserting that this resolves "Darwin's dilemma" about the missing Precambrian fossils. "Darwin's dilemmaregarding the absence of Precambrian fossils was not resolved until the 1940s when a diversity of large animals of Ediacaran age (635-541 million years ago) was discovered in South Australia, providing spectacular evidence of life prior to the appearance of the first shells." This is very misleading, as most biologists do not consider the Ediacaran organisms ancestral to the Cambrian animals.
3. He makes the most of early arrivals: "However, a number ofEdiacaran fossils are interpreted with reasonable certainty as early offshoots (stem taxa) of lineages leading to modern groups -- including sponges (Palaeophragmodictya),cnidarians, and bilaterians such as molluscs (Kimberella) and possibly arthropods." This misdirects attention from the complexity of these phyla, and fails to account for at least 15 more new body plans that exploded onto the scene in the early Cambrian.
4. He puts a lot of trust in molecular inferences: "Molecular clock dates indicate that the ancestors of most modern marine phyla had evolved by the Ediacaran, but identifying their representatives, even among the remarkable range of Ediacaran forms, is not straightforward." His conclusion is more confident: "Phylogenies calibrated by fossil occurrences allow molecular clocks to estimate the timing of branching even where fossil evidence is wanting."
5. He uses the power of suggestion: "The rise of oxygen levels in the earth's atmosphere and oceans has often been implicated in initiating rapid diversification." We responded to this hypothesis before. Another suggestion: "The rise of zooplankton allowed particles to sink to the sea floor as fecal material which significantly augmented the nutrient supply," he speculates. "Such increases in environmental complexity during the Cambrian may well have resulted in a proliferation of diverse ecological strategies that were not present earlier." Should we call this the crap theory?
6. He offers promissory notes: "And in due course, experiments on the role of control genes in the development of animals from embryo to adult may provide clues to how all the major animal groups evolved in a relatively short time during the Cambrian explosion."

Here's another key passage expressing hope for an answer:

Although the fossil record is silent on mechanisms to explainhow morphology could have evolved so rapidly, developmental biology investigates how genetic mechanisms affect body plans. Evolutionary developmental biology (evo-devo) may provide clues to how such a remarkable range of morphology evolved so quickly, at least in organisms amenable to experimental manipulation.

There's really nothing new here. All these hypotheses have been answered in Darwin's Doubt and Debating Darwin's Doubt. Our job is to get the information past the censors, so that the organs of propaganda are defeated by free and open inquiry.

Today's supernatural is tomorrow's scientific revolution.

Science and Credulity

David Klinghoffer January 31, 2013 5:15 AM

The Center for Science & Culture's John West did an interesting interview with the Australian-based commentary/news site Mercator, commenting on the recent Discovery Institute Press book The Magician's Twin: C. S. Lewis on Science, Scientism, and Society ("Exposing scientism"). The interviewer asked about a seeming paradox in Lewis's thought:

MercatorNet: C.S. Lewis claimed that science has made us more gullible. But how can this happen if science is based on empirical facts?

West: Lewis observed that many non-scientists simply checked their critical faculties at the door when they heard claims made in the name of science. People who didn't think we could know anything with confidence about historical figures like Julius Caesar or Napoleon because they lived such a long time ago had no problem accepting the most outlandish claims made about "pre-historic" man, because the latter claims were dressed up as science. Lewis was concerned that this kind of blind deference to scientific authority opened the door to tyranny. That's one of the reasons it's so concerning today when people are routinely attacked as "anti-science" just for raising thoughtful questions about claims made in the name of science. If we want to avoid the abuse of science, we need to encourage that kind of questioning, not suppress it.

This reminded me of a comment I came across by Harvard geneticist George Church, about whom, on reflection, I think I was probably too harsh and quick to judgment the other day when he was in the news on the subject of cloning Neanderthals (see here, here, and here). For which, if so, I apologize. Church has done a lot of important work that we've highlighted at ENV -- in fact, we do so in our current cover story ("Demonstrating, Once Again, the Fantastic Information-Storage Capacity of DNA").

Church has tangled honorably and creditably with Jerry Coyne -- see his response to Coyne's criticism at the end of this post from Why Evolution Is True. Among other things he remarks on the different ways that a "considerable amount of faith drives everyday science."

Incidentally, a noteworthy aspect of Coyne v. Church is that George Church has said things that make Coyne wonder if he's "somewhat of a creationist, or at least sympathetic to intelligent design." Coyne demands from his more distinguished colleague, yes, a statement of faith in Darwinian evolution: "If he's not [an ID sympathizer], and firmly adheres to the naturalistic theory of evolution, let him state that."

Church's reply is intriguing:

I like the theory of evolution -- I even harness it industrially to make practical materials. Perhaps, another less-than-ideal dichotomy here is between "naturalistic" and "supernaturalistic." "Natural" is what is known to science at the moment. If we discover next year quantum computing and/or aliens capable of transferring bits of information to minds or DNA, then we might reconsider past "naturalism." I like a simple Occam's razor, but not if it gets in the way of a revolution.

He "likes" evolution -- microevolution, he means, since that's the only kind you'll ever have a chance of observing at work.

As I say, that's very interesting, coming form a Harvard geneticist. Note the smart deconstruction of "natural" v. "supernatural." This line is a keeper: "'Natural' is what is known to science at the moment." So for science to continue insisting on "naturalistic" explanations of everything guarantees that knowledge can't advance further than it already has done. True.

Yet more iconoclasm II

Lee Spetner on Darwin’s iconic finches

Published on October 9th, 2015

Written by: News

Further to What’s happened since Icons of Evolution (2002)? Well, for one thing, Darwin’s textbook finches took a beating (no speciation)

From The Evolution Revolution by physicist Lee Spetner:

The proximate biochemical signal evoking the change in beak shape [of Galapagos finches] has been discovered to be a protein growth factor Bmp4. The more Bmp4 that is made, the broader and deeper is the bird’s beak. This protein acts as a signal to the development of the craniofacial bones which determines the beak’s shape. If my suggestion is correct that the hormones triggered by environmental inputs affect embryonic development, then those hormones induce these growth factors to form the finch beak….The built-in mechanism of the NREH [Non Random Evolutionary Hypothesis] enables the bird population to adapt to a new environment quickly and efficiently without having to call upon the slow and wasteful neo-Darwinian process of random mutation and natural selection. p. 76

Note from reader:

Spetner’s Non Random Evolutionary Hypothesis proposes that certain genetic traits lie dormant within the genomes of various living things until environmental cues turn them on and they appear in the next generation. In other words, living things are front loaded with a host of options which allow for rapid and specified adaptations for various enviroments. There is neither chance nor selection in this process. Moreover, it also accounts for the rapid return of smaller finch beaks when the drought ceases. It points towards exquisite design and accounts for the variability of Darwin’s finches without invoking the confusions of natural selection. If mutations are random, why is it that thicker, larger beaks appear reliably with every drought on the Galapagos Islands? Why don’t longer tail feathers or unusual colors appear? If natural selection works slowly and imperfectly, why are the changes in beak size so rapid? If the mutations are embedded in the genomes of the birds, why do they disappear so quickly when conditions change?

Here for more on Spetner’s The Evolution Revolution.

It's design all the way down V

Gate-Crashing the Nuclear Pore Complex

Evolution News & Views October 8, 2015 10:14 AM

ho would have thought a hundred years ago that a simple fungus contains high-tech security gates guarded by agents that authenticate cargo before letting it through? That's what advances in imaging are allowing scientists to observe. We must be among the most privileged in history to witness the foundations of biological life coming into focus in all their glory!

You got a simplified glimpse of this gate 13 years ago in the filmUnlocking the Mystery of Life. It's that circular portal that allows the messenger RNA out into the cytoplasm. We've learned a lot since then. We know now that the nuclear pore complex (NPC) is one of the largest and most complex molecular machines in the cell. Each eukaryotic nucleus is studded with NPCs. They resemble portholes with nets, like basketball hoops, but much more sophisticated. They are the gateways for traffic in and out of the nucleus, but not just any molecule can pass through. Each macromolecule needs a ticket and an escort, represented by tags and accessory proteins that first authenticate the cargo then accompany it in or out.

New details of the NPC architecture came to light in a couple of papers in Science this month. Regarding these papers, Katharine S. Ullman and Maureen A. Powers state:

Nuclear pore complexes (NPCs), first observed by electron microscopy 65 years ago, mediate selective transport of macromolecules between the nucleus and cytoplasm of eukaryotic cells. Although the exact size and protein composition of NPCs can vary between species, these massive and complex machines are highly conserved in their overall organization, which consists of multiple copies of ∼30 nuclear pore proteins, or nucleoporins (Nups), in asymmetrical eightfold radial arrangement. Deciphering the structure of this immense complex has required ongoing multifaceted approaches. On page 106 and 56 in this issue, Chug et al. and Stuwe et al., respectively, have employed parallel approaches in very distant species and arrived at remarkably similar and informative structures of an essential subcomplex of the NPC.

What were the "very distant species" with conserved structures? The Chug team used a frog; the Stuwe team studied a thermophilic (heat-loving) fungus. Both teams looked at one element of the eight-fold radial structure at the central inner ring of the pore. They found that this domain has coils of protein that extend out into the pore and make contact with coils from the opposite side. These coils form a net that blocks entry unless the cargo has the right password, consisting of an "usher" of sorts called a nuclear transport receptor (NTR).

What's emerging is a different model from the previously-held vision of pores that dilate and constrict to allow passage. "Instead they suggest arigid pore in which flexible domains called FG repeats fill the channel and form a barrier that can be traversed by receptors that carry cargos across," Valda Vinson explains in a brief summary of the papers inScience. FG repeats are so named for the phenylalanine-glycine amino acid patterns. "Interactions between NTRs and FG repeats are essential for facilitated translocation," Chug's team says.

NPCs grant free passage to small molecules but becomeincreasingly restrictive as the size of the diffusing species approaches or exceeds a limit of ≈30 kD in mass or 5 nm in diameter. This property is critical for keeping nuclear and cytoplasmic contents separate. NTRs, however, are not bound by this size limit. They mediate facilitated NPC passage and ferry cargoes up to the size of newly assembled ribosomal subunits (≈25 nm in diameter) between the two compartments.

For size comparison, consider that the inner ring complex is 425 kilodaltons (kD) compared to the 30kD mass limit of unescorted cargo (one Dalton = one atomic mass unit). The specific order of amino acids in each Nup protein is critical to its structure and function. Nup62, for instance, requires "kinks" that fold it into the pore-traversing domain.

"The kink is stabilized by a network of highly conserved hydrophobic and hydrophilic contacts," the researchers say. Indeed, many of the residues show "extreme evolutionary conservation" in animals as diverse as amoebas, fungi, and higher animals. That's the only context in which Chug et al. mention evolution -- the lack of it.

Stuwe's team also mentioned evolution only in the context of conservation, except for a nonspecific comment in the opening paragraph:

One of the hallmarks of eukaryotic evolution is the enclosure of genetic information in the nucleus. The spatial segregationof replication and transcription in the nucleus from translation in the cytoplasm imposes the requirement of transporting thousands of macromolecules between these two compartments. Nuclear pore complexes (NPCs) aremassive transport channels that allow bidirectional macromolecular exchange across the nuclear envelope (NE) and thus function as key regulators of the flow of genetic information from DNA to RNA to protein.

You can find the word conserved or conservation 16 times in the paper. In one case, structural conservation was found despite low sequence conservation. Mutation experiments, however, usually broke the function or reduced it dramatically; some cases were lethal.

The nuclear pore complex, therefore, is a highly selective filter for macromolecules. Why does that matter? Chug et al. explain:

For transport selectivity, preventing the passage of unwanted material is as important as allowing NTR•cargo species to pass. This is straightforward to explain by an adaptive barrier that seals around a translocating species, particularly because cohesive FG domains readily assemble such self-sealing barriers in the form of FG hydrogels.

But if anything and everything can attach NTRs to let it pass through, selectivity is also lost. "A 'general gate' would therefore stand open at all times and consequently fail as a barrier," they realize. How do the NTRs know which cargo is legitimate? This point is not clear from the papers and probably will require more analysis. It appears that multiple interactions with other nucleoporins (Nups) take part in discrimination against unwanted molecules. But the mechanism is general enough to allow the FG domains to rapidly facilitate passage of a wide range of cargo sizes.

In a news item from Rockefeller University, Professor Michael P. Rout sheds some light on the tradeoff between selectivity and speed:

"Usually, binding between traditionally folded proteins is a time consuming, cumbersome process, but because the FG Nups are unfolded, they are moving very quickly, very much like small molecules. This means their interaction is very quick," explains Rout.

The disordered structure of the FG regions is critical to the speed of transport, allowing for quick loading and unloading of cargo-carrying transport factors. At the same time, because transport factors have multiple binding sites for FG Nups, they are the only proteins that can specifically interactwith them -- making transport both fast and specific.

So in this case, "fuzzy" interactions are an asset. Rout thinks that this is "the first case where the 'fuzzy' property of an interaction is a key part of its actual biological function."

How fast are the NPCs? Chug et al. provide some details about the diffusion rate of large molecules through the pore:

Facilitated translocation is usually completed within 10ms[milliseconds].. NPCs can conduct ≈1000 facilitated translocation events or a mass flow of ≈100 MD [megadaltons] per pore per second, which further implies that NPCs can translocate numerous species in parallel.

With some 2,000 NPCs in a typical vertebrate cell (Wikipedia), that provides a huge capacity for facilitated, authenticated transport.

Not sufficiently impressed yet? Consider that the entire nuclear envelope breaks down at cell division, all the parts are duplicated (including all the genetic information, which is also error-checked), and the entire nucleus, NPCs and all, is reassembled in both daughter cells, ready to go sometimes in just minutes. That's intelligent design!

On the incomprehensible comprehensibility of the cosmos

Putting Scientism in Its Place

David Klinghoffer October 7, 2015 3:38 AM 

Nautilus has a brief and elegant essay, "Why Science Needs Metaphysics," extracted from a forthcoming book by Oxford philosopher Roger Trigg.

He concludes:

There is such a thing as scientific progress, and it happens through systematic trial and error or, in Karl Popper's terminology, conjecture and refutation. A "scientific realist" has to be wary, though, about how such realism is defined. A realism that makes reality what contemporary science says it is links reality logically to the human minds of the present day. Science is then just a human product, rooted in time and place. Bringing in future science -- or ideal science -- may sound more plausible, but even then there is a distinction between science reflecting (or corresponding to) the nature of reality and it being simply a human construction. Once the logical independence of reality from science is accepted, the question is why reality has a character that enables it to be understood scientifically. The intelligibility and intrinsic rationality of reality cannot be taken for granted. Even the greatest scientists, such as Einstein, have seen that the intelligibility of the world is a mystery. He famously remarked that "the eternally incomprehensible thing about the world is its comprehensibility."⁴ Like the way in which mathematics seems to map the intrinsic rational structure of the physical world, this is presupposed within science and cannot be given a scientific explanation. It appears to be a metaphysical fact, and the explanation for which, if there can be one, must come from beyond science.

The comment from Einstein is a keeper.

Trigg splendidly puts scientism in its place. We take it for granted that nature is a book that is not only decipherable but eager to be read, as if written to be so. The remarkable mystery of why we can even begin to understand the universe, topped by the enigmatic fact of our physical situation on earth being so extremely convenient for scientific discovery, has of course been a frequent theme of intelligent design advocates.

Darwinism Vs. the real world XV

Low Blood Pressure and Evolutionary Biology

Howard Glicksman October 6, 2015 3:39 AM 

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

The body is made up of trillions of cells which must each receive what they need to live. The cardiovascular system circulates blood throughout the body to accomplish this task. However, being made of matter, the body must follow the laws of nature. These laws demand that there be enough power to move the blood against natural forces such as inertia, vascular resistance, and gravity.

The blood pressure is the force the blood applies against the arterial walls as it flows by, and represents the energy that moves the blood where it needs to go. It's like how a city must supply its residents with enough water to meet their hygienic needs. If the pressure in the city's water system isn't high enough, then customers won't be serviced properly. The same thing applies to the blood pressure and the body. If there isn't enough blood pressure in the systemic arteries, the organs of the body won't be serviced properly and they'll malfunction or die because their metabolic needs aren't being met.

The three main things that affect arterial blood pressure are how well the heart pumps blood, how much blood is in the arteries, and the vascular resistance applied to blood flow by the downstream arterioles. The body controls its blood pressure mainly through systems which involve the brain, the heart, the kidneys and the blood vessels. Evolutionary biologists only show how these systems look and then imagine how they may have come about without considering how they actually work within the laws of nature to keep the body functioning properly. The last article in this series showed what it takes for the body to be able to stand up to gravity, something that would have been absolutely necessary for the survival of our earliest ancestors. But sometimes circumstances can still overwhelm the body's control mechanisms to allow the blood pressure to go too low.

It is important to understand that the lower limit of blood pressure resulting in blood flow is directly related to the metabolic needs of the organs. It's the same as having enough gas and air entering a car's engine so it has enough energy to perform properly. Without enough blood pressure to provide enough blood flow to the organs, they are as good as dead.

My previous article showed that vital organs like the brain use autoregulation to maintain a constant blood flow. They do this by changing the vascular resistance in their arterioles to adjust to constant changes in blood pressure. The normal range of the mean arterial pressure (MAP) that results in proper blood flow in the brain, without the need for autoregulation, is 70-100 mmHg. This translates into a BP of 90/60-140/80.

However, when it comes to significantly low blood pressure, there are limits to how low the vascular resistance in the arterioles can go in an attempt to maintain adequate blood flow. For critical organs like the brain, this lower limit of MAP is about 50 mmHg, which is equal to a blood pressure of only 70/40.

People who have a blood pressure less than 90/60 mmHg are said to have hypotension. Many of them have to live relatively sedentary lives because they suffer from fatigue, weakness and dizziness on standing up. Since cardiac performance is a major determinant of blood pressure, it is not surprising that many people with heart failure, valvular disorders and arrhythmias commonly suffer from hypotension. People with disorders of the sympathetic nervous system, as seen in diabetics and people with neurological conditions like Parkinson's Disease and Multiple Sclerosis, are particularly prone to severe drops in blood pressure when standing up, sometimes to the point of passing out (syncope). This condition is called orthostatic hypotension and takes place because the body cannot compensate fast enough through the sympathetic nervous system to the sudden drop in blood pressure brought on by the force of gravity.

Recall, from the last article, that when the MAP drops below 70 mmHg, the baroreceptors in the main arteries supplying blood to the brain trigger the sympathetic nervous system to increase the cardiac output and peripheral vascular resistance to keep the MAP where it is supposed to be. However, sometimes circumstances arise that overwhelm the body's ability to maintain an MAP above 50 mmHg. When this happens, the body is unable to adequately perfuse its organs and tissues and it is said to be in circulatory shock (as opposed to emotional shock).

Without aggressive resuscitation, irreversible cellular dysfunction and multi-organ failure is likely, often leading to death. Since blood pressure is largely dependent on three factors, blood volume, cardiac performance, and vascular resistance, shock is generally divided into three categories that reflect this reality.

A significant and quick drop in total blood volume can lead to what is called hypovolemic shock. Severe and rapid blood loss from traumatic rupture of a large blood vessel or a major organ or severe bleeding from the gastrointestinal tract are some of the more common causes. Non-hemorrhagic fluid loss, such as severe and persistent vomiting and diarrhea, or extensive third degree burns, can cause hypovolemic shock as well.

Conditions of the heart resulting in a marked reduction in cardiac output can quickly lead to what is called cardiogenic shock. A sudden heart attack causing severe damage to the left ventricle and a marked reduction in contractility and stroke volume or the sudden rupture of the mitral valve, are common causes of cardiogenic shock. Additionally, an already damaged and failing heart that suddenly starts beating too slowly or too quickly can lead to a quick drop in cardiac output and cardiogenic shock as well.

In my last article I showed that the relationship between blood pressure, blood flow and vascular resistance can be expressed as P = Q x R. Blood pressure (P) is directly related to total blood flow (Q) and the vascular resistance (R) in the tissues. As noted above, hypovolemic and cardiogenic shock are caused by a significant reduction in cardiac output (Q) due to reduced total blood volume and inefficient cardiac function, respectively. The body's natural response to both hypovolemic and cardiogenic shock is to increase the vascular resistance through the sympathetic nervous system and other hormones in an attempt to bring the blood pressure back towards normal.

In contrast to both hypovolemic and cardiogenic shock, the third type of shock involves a significant reduction in the peripheral vascular resistance. Since P = Q x R, a major drop in R can also lead to severe hypotension in what is called distributive shock. In this setting, the muscles surrounding the arterioles throughout the body relax and allow too much blood to enter the capillaries which results in excessive loss of fluid into the tissues.

One of the commonest causes of distributive shock is severe infection, often in the bloodstream. Another name for it is septic shock, or SIRS (systemic inflammatory response syndrome). Not only do the bacteria release toxins that cause the muscles surrounding the arterioles to relax too much causing a catastrophic drop in the vascular resistance, but the body's immune system in trying to fight the infection does the same thing as well.

The body has many different mechanisms in place to overcome the laws of nature and thus survive in the world. The fact that we die indicates that eventually these mechanisms become overwhelmed, resulting in cardiopulmonary arrest and brain death.

As is common with many of the chemical and physiological parameters the body must control to stay alive, blood pressure must follow theGoldilocks principle. Everything has to be just right for the body to be able to function well enough to survive. The current theory of evolution does not even begin to explain how any of this works in real life. Real numbers have real consequences and clinical experience bears this out by showing that not only is low blood pressure hazardous to your health, but so is high blood pressure. That's what we'll consider next time.

Self-Correcting huh?

The right to die?Pros and Cons

Survival of the heroic?

Could We All Get Together and Evolve as a Group?
Denyse O'Leary October 5, 2015 3:21 AM 

In our quest to understand how evolution happens, we have looked at horizontal gene transfer and epigenetics, each of which gives a small amount of genuine, though generally unheralded, change.

Talk to the Fossils.jpgNatural selection and sexual selection are widely publicized theories, developed in detail by Darwin. They became iconic, in part one must think, because of the instant media recognition. The subtle self-flattery that comes of thinking that one is naturally or sexually selected to survive.
The evidence is sparse.

But what if it is not individuals, but groups that are selected to somehow survive?

No subject apart from religion has vexed Darwin's followers more than why people sacrifice themselves for others. They have embraced the ambiguous term "altruism" because it does not clearly mean "compassion" or "heroism." Rather, it is to be seen as the same natural force that causes worker ants to pass on their genes by serving their queen, who lays lots of eggs, instead of reproducing themselves (kin selection). Maybe this force creates the change we are looking for.

Altruism has been described as "an anomalous thorn in Darwin's side" and a "conundrum that Darwinians would need to solve, given their view of the ruthless struggle among living beings for survival." One outcome has been the curious recent paper war between Darwinian evolutionary biologist E. O. Wilson and those Darwinists who had espoused his earlier theories.

Wilson deserves an introduction. He is widely hailed as the founder of sociobiology (about 1975), which morphed into evolutionary psychology.

Christians have long been encouraged to look up to Wilson (once an evangelical Christian) as the gentlemanly author of The Creation (2006), which begins "Dear Pastor, We have not met, yet I feel I know you well enough to call you friend." (The fact that Wilson attempted to undermine everything the pastors believe was, apparently, irrelevant.)

His group selection theory has a history. It stretches back to 1955 when British geneticist J. B. S. Haldane said, we are told, that he would risk his life for two brothers or eight cousins, to preserve enough of his own genes to justify his death (kin selection). Evolutionist William Hamilton described the idea mathematically, calling it inclusive fitness. His calculations have been used ever since, and were a key inspiration for Richard Dawkins' The Selfish Gene.

But then Wilson dramatically abandoned kin selection in 2010 in a Nature paper, "The evolution of eusociality," co-authored with mathematicians. He argued that strict Darwinism (natural selection) "provides an exact framework for interpreting empirical observations," dispensing with the other theories he had promoted for decades. Over 140 leading biologists signed a letter to Nature, attacking the 2010 paper. Some called his new, strictly Darwin model "unscholarly," "transparently wrong," and "misguided."

What? All this is said of a Darwin-only model?

New atheist evolutionary biologist Jerry Coyne has also weighed in, saying that Wilson et al. are "wrong--dead wrong." Curiously, he admitted, "The "textbook" explanation, based on a higher relatedness of workers to their sisters than to their own potential offspring, no longer seems feasible. ... But we've known all this for years!"

If so, he and fellow evolutionary biologists have been very economical with their accounts of the failures.

How else to account for the -- to most people, incomprehensible -- uproar?

Evolutionary psychologist David Sloan Wilson, defending E. O. Wilson, scolded, "This degree of illiteracy about foundational issues is an embarrassment for the field of evolutionary biology."

He is perhaps telling us more than he realizes there. Neuroscientist Michael Gazzaniga, attempting to defend E.O. Wilson, writes:

In the end, Mr. Wilson comes down on the side of what is called multi-level selection--the view that evolution involves a combination of gene selection, individual selection, kin selection and group selection. Although he says his new theory opposes the idea of kin selection, in another sense he is simply maintaining that everybody is right. Genes are being selected to benefit the individual and their kin. Genes are also being selected that encourage the individual to participate in a group.

So if Wilson thinks everybody is right, why is Wilson sowrong? As John Gray put the matter at The New Republic,the debate is "an exercise in sectarian intellectual warfare of the kind that is so often fought in and around Darwinism."

It sounds so much like a family row. But if we are not part of the family, why be involved? Maybe the rest of us should continue to look for answers elsewhere.

How about life forms that do not evolve at all, or not significantly? We might learn something there. What happens when evolution doesn't happen?


See the rest of the series to date at "Talk to the Fossils: Let's See What They Say Back."

A line in the sand XXIII