Everyday miracles.

The Ubiquitous Miracles Of Our Existence
Posted by William J Murray

In another thread, I asked daveS why he was an atheist. He responded:

The proposition “there is no god” also appears to me to be consistent with what I observe in the world.

When asked what that meant, he expanded:

Well, I don’t know of any inconsistencies between this proposition and my observations. For example, I’m not aware of a god blatantly intervening in the world, as some people say happens.

I’ve addressed this in the other thread, but this comment is reflective of what a lot of atheists say is a convincing lack of evidence for god: the supposed lack of observed miracles. Atheists think we live in a world that looks like a world without a god. Of course, that’s circular reasoning based upon a groundless assumption; the assumption that what we experience is what we would be experiencing if there were no god and no supernatural commodities – a world dictated by more-or-less predictable cause-and-effect sequences of matter interacting according to intrinsic properties and orderly patterns.

Unrecognized by atheists, however is that therein lies what I call the ubiquitous miracles of our existence. We don’t consider them miraculous because we take them so utterly for granted that we, for the most part, aren’t even consciously aware of these miracles.  We’re blind to the miraculous because the nature of our very existence is miraculous.

1. The miracle of an orderly, predictable experiential context. What if the universe was not orderly? What if the constants and properties that guide matter into patterned behaviors were not constant at all? What if they fluctuated randomly? Why should matter have any consistent properties at all? What holds these properties and forces at certain values?  Without an orderly universe, how would we have any rational thoughts? Nothing would be coherent.  How would we even come into existence unless something was keeping activity in the universe orderly?

2. The miracle of an individual conscious existence. Why should interacting matter become conscious and have individualistic thoughts? How does such a thing even happen? Why should our thoughts be apparently controllable and orderly? How is it that we can seemingly create a virtually unlimited amount of highly complex, coherent ideas/information on demand?

3. The miracle of mind over matter. How is it that without any knowledge whatsoever of how any of it works, we can simply will an action and cause the correct sequences of countless microscopic physical interactions to properly occur to achieve body movement? I was playing with my year-old great granddaughter the other day and she saw me wiggle my eyebrows, then immediately wiggled hers. Okay, she had no idea how to do that, and couldn’t even see herself doing it. How did she wiggle her eyebrows in response? It can’t be anything other than her, in whatever conscious state she has developed at this point, seeing me do a thing and then willing her body to do the same thing, and the her body immediately and correctly translating a pre-language, entirely uneducated intent into countless physico-chemical events that ended up being her wiggling her eyebrows.


I honestly don’t know how anything gets any more miraculous than that which we take for granted every moment of our existence. IMO, the existence of an orderly, predictable world where conscious entities exist and have intentional control (to a large degree) over their physical bodies and thoughts, and the existence of logic and mathematics as functionally valid correspondences to that experience is far, far more profoundly miraculous than if I saw somebody flying or solving a super-complex problem or parting an inland sea. Frankly, I’ve seen “miraculous” faith healings and all kinds of “miraculous” things that most people would simply not believe unless they experience them (and perhaps not even then), and none of it even remotely compares to the ubiquitous, every-day miracles that allow all of us this incredible experience of being deliberate, conscious entities in an orderly, lawfully predictable universe.

1Samuel Ch.17 the Watchtower Society's commentary.

David Versus Goliath—Did It Really Happen?

Some people wonder if the account about David and Goliath is true history or just myth. Did such a doubt cross your mind as you read the preceding article? If so, please consider the following three questions.


1 | Could a man really be some nine and a half feet (2.9 m) tall?

The Bible says that Goliath’s “height was six cubits and a span.” (1 Samuel 17:4) The cubit in question was 17.5 inches (44.5 cm) long; the span, 8.75 inches (22.2 cm). That adds up to about nine feet six inches (2.9 m). Some insist that Goliath could not have been that tall, but consider: In modern times, the tallest man documented was over 8 feet 11 inches (2.7 m) tall. Is it really impossible that Goliath was six inches (15 cm) or so taller? He was of the tribe of the Rephaim, men who were known for their unusual size. An Egyptian document from the 13th century B.C.E. mentions that some fearsome warriors in the region of Canaan were over eight feet (2.4 m) in height. So Goliath’s height, while unusual, is hardly impossible.


2 | Was David a real person?
There was a time when scholars tried to relegate King David to the realm of myth, but that has become harder to do. Archaeologists have found an ancient inscription that mentions “the house of David.” Furthermore, Jesus Christ spoke of David as a real person. (Matthew 12:3; 22:43-45) Jesus’ identity as the Messiah is supported by two detailed genealogies showing that he descended from King David. (Matthew 1:6-16; Luke 3:23-31) Clearly, David was a real man.

3 | Did the events described in the account unfold in a real place?

The Bible says that the battle occurred in the Valley of Elah. But it gets still more specific, noting that the Philistines camped on a hillside somewhere between two towns, Socoh and Azekah. The Israelites were stationed across the valley on the opposite hillside. Were these real places?

Note what a recent visitor to the area says: “Our guide—who was not a religious man—took us to the Valley of Elah. We ascended a path that took us to the brow of a hill. As we looked over the valley, he had us read 1 Samuel 17:1-3. Then he pointed across the valley, saying: ‘There, to your left, lie the ruins of Socoh.’ Turning, he said, ‘Over there, to your right, are the ruins of Azekah. The Philistines camped between those towns, somewhere on the hillsides facing you. So we may be standing where the Israelites camped.’ I thought of Saul and David standing right where I was. Then we descended, and on the valley floor, we crossed a streambed, mostly dry, that was full of stones. I could not help but picture David stooping here to pick up five smooth stones, one of which killed Goliath.” That visitor, like many others, was deeply impressed with the authentic details in the Bible record.


There is no real basis for doubting the truthfulness of this historical account. It involves real people and real places. More important, it is part of God’s inspired Word, so it comes from the God of truth, the One who “cannot lie.”—Titus 1:2; 2 Timothy 3:16.

Bomb thrower David Berlinski doing his thing.

Microbiology v. Darwinism.

Thank Goodness the NCSE Is Wrong: Fitness Costs Are Important to Evolutionary Microbiology
Casey Luskin 

The evolution of antibiotic resistance is typically the result of small changes allowing for survival in a microbe or other organism under special circumstances where the organism faces extremely strong selection pressure due to the presence of some antibiotic drug. In other cases, it is the result of the transfer of pre-existing antibiotic resistance genes from one microbe to another, and the selection of such microbes in an environment containing antibiotics. Even in the first example, evolution does not produce a truly new function. In fact the change produced often makes the microbe less fit when the antibiotic is removed--it reproduces slower than it did before it was changed. This effect is widely recognized, and is called the fitness cost of antibiotic resistance. It is the existence of these costs and other examples of the limits of evolution that call into question the neo-Darwinian story of macroevolution.

Fitness costs are real, and biological realities like fitness cost and other limits to evolution play a vital role in shaping strategies used to combat antibiotic resistance, antiviral resistance, and pesticide resistance. In fact, were it not for the existence of fitness cost, in many cases antibiotic resistant bacteria would proliferate and resistant strains would soon replace non-resistant strains. Because of fitness costs, resistant strains are outcompeted by non-resistant bacteria once selection pressure is relaxed, allowing doctors to combat antibiotic resistance through various drug usage strategies.

Yet under the approach adopted by the National Center for Science Education (NCSE) in its critique of Explore Evolution (EE)[1], organisms are treated as if they are nearly infinitely-plastic; evolution is viewed as if it can do anything. If the NCSE were right--which thankfully it isn't--then medical researchers would have little hope in the fight against antibiotic resistant microbes.

Not only is the NCSE's mindset challenged by the evidence [4], but if it were true, the implications for medicine would be drastic: If biological realities like fitness cost and other limits to evolution did not exist, it would be pointless for medical doctors to try to combat antibiotic resistance or antiviral drug resistance, because evolution could always produce an adaptation such that bacteria would become resistant without incurring a fitness cost. Thankfully, Explore Evolution informs students about the realities of limits to bacterial evolution that give doctors and scientists empirically-based hope in the fight against antibiotic resistance.

The NCSE wrongly implies that fitness costs are a minor issue for those trying to fight antibiotic resistance and other forms of resistance, stating, "Mutations do not necessarily impair a protein's normal functioning nor impose a fitness cost." After complaining that "Explore Evolution ... says mutations do confer resistance but with a 'fitness cost,'" the NCSE then claims that "Explore Evolution significantly misrepresents how antibiotic resistance arises in this description." Unfortunately, it appears that the NCSE misunderstands both EE and the importance of fitness costs to evolutionary biologists.

Many scientific papers discuss the stark reality of fitness costs, supporting the emphasis that EE places on this topic. In fact, one paper cited by the NCSE acknowledges that the reality of fitness costs is vital to help scientists predict whether resistance will spread: "biological cost of resistance might be a more relevant predictor of the risk for resistance development." [5] Another paper published in Environmental Toxicology and Chemistry found that "[t]he topic of fitness costs is a central theme in evolutionary biology" because "fitness costs constrain the evolution of resistance to environmental stress." [6] Yet another paper observed that "[i]t is generally established that drug resistance mutations reduce viral fitness." [7] Regarding the specific case of antibiotic resistance, one study in the Journal of Antimicrobial Chemotherapy observed that "[t]he biological fitness cost of antibiotic resistance is a key parameter in determining the rate of appearance and spread of antibiotic-resistant bacteria." [8] Indeed, science journals are replete with documented examples of fitness costs, as the following selections amply demonstrate:

An article published in the journal Genetics in 2007 by Marciano et al. titled "A Fitness Cost Associated With the Antibiotic Resistance Enzyme SME-1 β -Lactamase" found that blaSME-1 β-lactamase gene, which confers antibiotic resistance to the use of carbapenems, has a fitness cost associated with mutations in its signal sequence. Only by artificially swapping the gene's signal sequence with the signal sequence from a different gene could this fitness cost be alleviated; there was no natural evolutionary elimination of this fitness cost. The article found that identifying this fitness cost barrier to evolution helped them prevent the spread of antibiotic resistant bacteria: "The identification of a SME-1-mediated fitness cost allows the direct application of genetic techniques that have been utilized to understand structural features of β-lactamase function and evolution." See David C. Marciano, Omid Y. Karkouti and Timothy Palzkill, "A Fitness Cost Associated With the Antibiotic Resistance Enzyme SME-1 β-Lactamase," Genetics, Vol. 176: 2381--2392 (August, 2007).
A paper in BiomedCentral's journal Evolutionary Biology titled "Acetylcholinesterase alterations reveal the fitness cost of mutations conferring insecticide resistance" found that some insects exposed to insecticides which target acetylcholinesterase, an important enzyme involved in the nervous system of insects, evolve resistance that comes only at a fitness cost. According to the article, "Our findings suggest that the alteration of activity and stability of acetylcholinesterase are at the origin of the fitness cost associated with mutations providing resistance." As the paper put it, "higher the number of [resistance-conferring] mutations, the lower the stability of the mutant" enzyme. When seeking mutations that compensated for loss of stability in the mutant enzymes, the study found that "no mutation increased the stability of the enzyme, all combinations resulted in proteins still less stable." In other words, there was a clear fitness cost faced by insecticide-resistant mutant insects. See David C. Marciano, Omid Y. Karkouti and Timothy Palzkill, "A Fitness Cost Associated With the Antibiotic Resistance Enzyme SME-1 β-Lactamase," Genetics, Vol. 176: 2381--2392 (August, 2007).
A paper in the Journal of Antimicrobial Chemotherapy, titled "Nitrofurantoin resistance mechanism and fitness cost in Escherichia coli," observes the reality of fitness cost, stating: "The biological fitness cost of antibiotic resistance is a key parameter in determining the rate of appearance and spread of antibiotic-resistant bacteria." The paper found that because of the fitness cost associated with E. coli that are resistant to Nitrofurantoin, "even though resistant mutants will appear in the bacterial population in the bladder, they will be unable to become enriched and establish an infection because of their impaired growth at these therapeutic antibiotic concentrations." The article further observes, "Resistance to antibiotics is most often accompanied by a biological cost, observed as a decrease in fitness, i.e. a reduced growth rate or virulence." Ironically, the paper cited by this study to bolster this claim--a claim that corroborates EE's statements about fitness cost--is Andersson (2006) [see below], the same paper that the NCSE cites to back its claim that "not all mutations produce fitness costs!" It seems that research scientists have interpreted Andersson (2006) differently than the NCSE. See Linus Sandegren, Anton Lindqvist, Gunnar Kahlmeter, and Dan I. Andersson, "Nitrofurantoin resistance mechanism and fitness cost in Escherichia coli," Journal of Antimicrobial Chemotherapy, Vol. 62, 495--503 (2008).
Andersson (2006) explicitly observes that fitness cost is important to understanding whether resistant populations will persist after selection is relaxed:
A key parameter influencing the rate and trajectory of the evolution of antibiotic resistance is the fitness cost of resistance. Recent studies have demonstrated that antibiotic resistance, whether caused by target alteration or by other mechanisms, generally confers a reduction in fitness expressed as reduced growth, virulence or transmission. These findings imply that resistance might be reversible, provided antibiotic use is reduced. However, several processes act to stabilize resistance, including compensatory evolution where the fitness cost is ameliorated by additional mutation without loss of resistance, the rare occurrence of cost-free resistance mechanisms and genetic linkage or co-selection between the resistance markers and other selected markers. Conceivably we can use this knowledge to rationally choose and design targets and drugs where the costs of resistance are the highest, and where the likelihood of compensation is the lowest.
Thus, Andersson (2006) observes that "cost-free resistance mechanisms" are "rare" and that fitness cost is a very common phenomenon, stating that antibiotic resistance "generally confers a reduction in fitness." EE thus properly discusses this common phenomenon, and Andersson (2006) actually bolsters the points of EE. We find it unfortunate that the NCSE has misused this paper in its attempt to downplay the importance and reality of fitness costs. Additionally, Andersson (2006) states, "A rational antibiotic design strategy is therefore to identify targets for which the resistance mechanism has the most negative effect on fitness." This is a good strategy, but it would be pointless if bacteria didn't face evolutionary limits and could essentially always evolve to avoid fitness costs, as the NCSE implies. Again, we see that fitness cost is a real phenomenon and is vitally important to understand as microbiologists seek to slow the spread of antibiotic resistant bacteria. EE is justified in discussing it. See Dan I Andersson, "The biological cost of mutational antibiotic resistance: any practical conclusions?," Current Opinion in Microbiology, Vol. 9:461--465 (2006).

Many similar examples could be cited. Given the scientific literature, how can the NCSE seriously maintain that fitness cost is not an important issue in microbiology or that EE is mistaken by highlighting its importance to evolutionary processes? The NCSE asserts that EE "significantly misrepresents how antibiotic resistance arises" when EE states that "[e]xperiments show that once antibiotics are removed from the environment, the original (non-resistant) strain 'out-competes' the resistant strain, which dies off within a few generations." But studies like those discussed here directly corroborate this claim of EE. And the existence of fitness costs are vital to helping biologists to fight antibiotic resistance, antiviral resistance, and pesticide resistance. For the sake of medical progress, thank goodness the NCSE is wrong.

[Note: This post was adapted from Antibiotic Resistance Revisited, a response to the NCSE, which was originally co-authored with Explore Evolution co-author Ralph Seelke, Professor of Biology at University of Wisconsin-Superior.]

References Cited
[1] National Center for Science Education. 2008. Section on "Bacteria" in the NCSE critique of Explore Evolution. Available at http://ncseweb.org/creationism/analysis/bacteria as of January 16, 2009.

[4] See R. Seelke and S. Ebnet. "An unexpectedly low evolutionary potential for a trpA 49V,D60N double mutant In Escherichia coli.," Presented at the 107th Annual Meeting, Abstract R-055, American Society for Microbiology, Toronto, Canada, May 21-25, 2007; R. P. Mortlock (ed.), Microorganisms as Model Systems for Studying Evolution (Plenum Press, New York, 1984). Note: This book contains seven examples of situations in which evolution fails to produce a new function.

[5] Dan I Andersson, "The biological cost of mutational antibiotic resistance: any practical conclusions?," Current Opinion in Microbiology, Vol. 9:461--465 (2006).

[6] Lingtian Xie and Paul L. Klerks, "Fitness costs constrain the evolution of resistance to environmental stress in populations," Environmental Toxicology and Chemistry, Vol. 23(6):1499--1503 (2004).

[7] M. Cong, D.E. Bennett, W, Heneine and J.G. García-Lerma, "Fitness Cost of Drug Resistance Mutations is Relative and is Modulated by Other Resistance Mutations: Implications for Persistance of Transmitted Resistance," Antiviral Therapy, Vol. 10, Suppl 1:S169 (June 7-11, 2005).


[8] Linus Sandegren, Anton Lindqvist, Gunnar Kahlmeter, and Dan I. Andersson, "Nitrofurantoin resistance mechanism and fitness cost in Escherichia coli," Journal of Antimicrobial Chemotherapy, Vol. 62, 495--503 (2008).

A fossil link goes belly up.

Ida's Critics Demolish Claims That Fossil Is Human Evolutionary Link
Casey Luskin

Remember Ida? The fossil hailed as the "eighth wonder of the world" whose "impact on the world of palaeontology" would be like "an asteroid falling down to Earth"? She was promised to be "the link that connects us directly with the rest of the animal kingdom." She was touted on a History Channel / BBC documentary, but then there was the bust. Well, Ida's critics have now gotten around to publishing technical articles critiquing the hyped view promoted to the public last year. A recent news release at the University of Texas, "Recently Analyzed Fossil Was Not Human Ancestor As Claimed, Anthropologists Say," explains:
A fossil that was celebrated last year as a possible "missing link" between humans and early primates is actually a forebearer of modern-day lemurs and lorises, according to two papers by scientists at The University of Texas at Austin, Duke University and the University of Chicago.
In an article now available online in the Journal of Human Evolution, four scientists present evidence that the 47-million-year-old Darwinius masillae is not a haplorhine primate like humans, apes and monkeys, as the 2009 research claimed.

They also note that the article on Darwinius published last year in the journal PLoS ONE ignores two decades of published research showing that similar fossils are actually strepsirrhines, the primate group that includes lemurs and lorises.

"Many lines of evidence indicate that Darwinius has nothing at all to do with human evolution," says Chris Kirk, associate professor of anthropology at The University of Texas at Austin. "Every year, scientists describe new fossils that contribute to our understanding of primate evolution. What's amazing about Darwinius is, despite the fact that it's nearly complete, it tells us very little that we didn't already know from fossils of closely related species."

The big question now is, will BBC and The History Channel publish documentaries retracting their prior claims about Ida's importance as a "human ancestor," or will they leave the public with the impression that Ida is a "missing link"? Perhaps they might publish a documentary about the scientific community's tendency to overhype fossils as part of a crusade for Darwin? I'm a huge fan of The History Channel (or at least I used to be when they focused on real history instead of broadcasting UFO / "2012" material), but I'm not holding my breath.

A lack of evidence proves Darwinism?

Smithsonian's New Human Origins Exhibit Targets Students Who Doubt Darwinism
Casey Luskin

The Smithsonian has a new human origins exhibit, "What does it mean to be human?" specially targeted at swaying student visitors who might doubt Darwinian evolution.

The most amusing part of the exhibit proudly explains that evolution predicted we'd lack evidence for evolution; that's how we know it's true!

That's right, this is how the nation's most prestigious natural history museum presents evolution: evolution predicts that evolution is supported both when we do and when we don't find confirming fossil evidence. Consider the following from the educator's guide:

Misconception: Gaps in the fossil record disprove evolution.
Response: Science actually predicts gaps in the fossil record. Many species leave no fossils at all, and the environmental conditions for forming good fossils are not common. The chance of any individual organism becoming fossilized is incredibly small. Nevertheless, new fossils are constantly being discovered. These include many transitional fossils--e.g., intermediary fossils between birds and dinosaurs, and between humans and our primate ancestors. Our lack of knowledge about certain parts of the fossil record does not disprove evolution.

Did you get that? Ignoring the fact that transitional fossils are often missing even among taxa whose records are very complete, now Darwin's defenders argue that their theory "predicts gaps in the fossil record." How convenient!

(Now I fully understand the evolutionary explanation as to why transitional fossils are purportedly missing, and I've written on it extensively in the past, so if you want a critique, go there.)

What's ironic, however, is that if you ask the question How Do We Know Humans Evolved? the answer you're given is, "Fossils like the ones shown in our Human Fossils Gallery provide evidence that modern humans evolved from earlier humans." So whether you find fossils or you don't, that's evidence for evolution.

And some of the "transitional" fossils listed in the gallery are quite dubious.

Ardipithecus ramidus is offered as an alleged "a human-African ape common ancestor," yet the exhibit doesn't disclose that when "Ardi" was first discovered it was reportedly "crushed to smithereens" such that it resembled "Irish stew."

The exhibit also touts Sahelanthropus tchadensis as the "oldest fossil human," even though this species is known from only one skull and a few jaw fragments, which some paleoanthropologists have suggested might have belonged to a female gorilla.

But the exhibit gives no evidence of dissent from the official party line, such as an admission from Ernst Mayr in 2004 that "[t]he earliest fossils of Homo, Homo rudolfensis and Homo erectus, are separated from Australopithecus by a large, unbridged gap," and therefore we're in a position of "[n]ot having any fossils that can serve as missing links."

I guess according to the Smithsonian's exhibit, this large, unbridged gap is just more evidence for evolution.

Darwinism's just so stories are almost as substantive as kipling's

Brangelina Fever Gets Its Own Darwinian Just-So Story
Jonathan Witt

Darwinists love just-so stories. Why are cheetahs fast? Because natural selection preferred the slightly faster cheetah ancestors, thanks to the fast cats being able to catch more prey and impress the lady cats. Why are turtles slow? Well, maybe being fast was a waste of energy, so turtle evolution at some point wandered down an evolutionary alley committed to a defensive strategy that, et cetera, et cetera.

Why are chimps clever? Because being clever gave their ancestors a survival advantage over their stupider cousins. Got a dimwitted species? No problem for Darwinism. Those animals didn't need cleverness in their ecological niche. Bigger brains would just have been a waste of calories.

The Maestro of Magic -- Natural Selection -- and His Sexy Assistant

Any attribute that makes a creature faster, smarter, stronger, stealthier, sturdier, more efficient -- there's a Darwinian just-so story waiting in the wings involving an animal hero, usually some poor duffer getting squeezed out in the competition for food or safety or conjugal warmth, and often as not, some damsel in either heat or distress who needs a hero almost as much as Bonnie Tyler does.

What about all those zany things on the nature shows so impractical that natural selection would never vote them on to the next round of mother nature's great big unmerciful game of Jeopardy? Well then, Darwinism has just the little beauty you're looking for. That's right, folks, sexual selection -- natural selection's winsome, whimsical, and wondrous assistant. Sexual selection is where, say, peahens prefer the peacocks with the bigger tail feathers, never mind how impractical those tails might become for running and flying. Presto! Peacocks have evolved whimsically enormous peacock tails.

Together, natural and sexual selection can whip up a just-so story for any biological marvel you want to throw at them.

The Monkey Business Behind Brangelina Fever

But wait. There's more. Enter movie star couple Brad Pitt and Angelina Jolie.

Angela Chen of The Verge tackles the vexing question of why so many of us give a rip about the Hollywood soap opera that is Brangelina. A big part of her answer, of course: evolution. You see, "our brains adapted long ago to be deeply interested in the beautiful and famous among us, says Daniel Kruger, a psychologist at the University of Michigan."

Chen then summarizes a Duke University study where they showed four monkeys a series of pictures of other monkeys they knew:

Each time they looked at a picture, they received a certain amount of cherry juice. They got more juice for looking at pictures of lower-status monkeys and less juice for pictures of the alpha monkeys. The monkeys loved the juice, and yet were willing to sacrifice it for a glimpse at the alphas. They were transfixed by their power.
Why? "In prehistoric times, our ancestors lived in societies of around 200 people and it was important to know what everyone was up to," Chen explains. "You had to know who you could trust, who was strong, and who could teach you how to be like them. All this could help you get ahead."

We keep tabs on the rich and famous, Chen continues, "because they might reveal the secrets to success. On some level, our brains really do believe that stars are just like us and that lessons from millionaires can improve our own sad lives."

Evolutionary psychologist Frank McAndrew seconds all this. "People who didn't care what people were up to just didn't do very well. We're the descendants of the ones who gossiped, so we're programmed to pay attention to people who are socially important."

What about that brilliant mathematician or inventor or artist too busy discovering, inventing, or creating things to bother with gossip or the latest Brangelina dustup? He's descended from, what -- the dummies at the edge of the camp playing Dungeons & Dragons?

Darwinism is Like a Party Balloon -- Highly Flexible, and Mostly Empty

The Wall Street Journal story on the monkey experiment quotes Paul Glimcher, associate professor of neural science and psychology at New York University:

"All primates living in complex societies have evolved this drive to study what's around them," Dr. Glimcher explained. "People are willing to pay money to look at pictures of high-ranking human primates. When you fork out $3" for a celebrity gossip magazine, "you're doing exactly what the monkeys are doing."
Ain't evolution grand! Probably explains our love of bananas, too. What about the banana haters in our midst, you say? They, of course, are descended from a now extinct subspecies of banana-hating monkeys.

I kid, I kid. The point is that Darwinian just-so stories are so flexible they're able to explain almost any zoological phenomenon and its opposite.

The other problem: Except in some cases of microevolutionary adaptation, these Darwinian just-so stories explain things hardly any better than a Rudyard Kipling tale about how the leopard got his spots or the camel his hump. All of the truly creative action in these Darwinian stories -- that is, the long train of genetic mutations necessary to gradually build the oh-so-helpful pair of wings or the way-cool set of gills or claws or fingers -- generally takes place off stage, out of the spotlight and far away from the paparazzi.


That's bad show business, and bad science.