When terms are not carefully defined, miscommunication and false leaps of logic can result. For instance, when you see the word "evolution," you should ask, "Which definition is being used?" Typically, there are three common meanings.

>> Evolution #1: Microevolution (defined earlier): Small-scale changes in a population of organisms.

Macroevolution (also defined earlier) can be divided into two parts.

>> Evolution #2: Universal Common Descent: The view that all organisms are related and are descended from a single common ancestor.

>> Evolution #3: Natural Selection: The view that an unguided process of natural selection acting upon random mutation has been the primary mechanism driving the evolution of life.

Sometimes evolutionists purposefully confuse these definitions, hoping you won't notice that they overstated their case. It's not uncommon for an evolutionist to take evidence for microevolution (evolution #1), and claim it supports common descent (evolution #2) or development solely through unguided mechanisms (evolution #3).

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To kick off the celebration of Charles Darwin's 200th birthday (February 11, 2009), Dr. Scott coauthored an essay titled "Don't Call It 'Darwinism.'" Terms have limits, she argued, and this one has got to go. Her reasons for seeking to force the retirement of the term "Darwinism" (and "neo-Darwinism") are weak. And, since her essay appeared, many even on her own side of the evolution debate have declined to take her advice. What can we learn from this failed attempt to impose term limits?

Scott summed up her argument this way:

Evolutionary biology owes much to Charles Darwin, whose discussions of common descent and natural selection provide the foundations of the discipline. But evolutionary biology has expanded well beyond its foundations to encompass many theories and concepts unknown in the 19th century. The term “Darwinism” is, therefore, ambiguous and misleading. Compounding the problem of “Darwinism” is the hijacking of the term by creationists to portray evolution as a dangerous ideology -- an “ism” -- that has no place in the science classroom. When scientists and teachers use “Darwinism” as synonymous with evolutionary biology, it reinforces such a misleading portrayal and hinders efforts to present the scientific standing of evolution accurately. Accordingly, the term “Darwinism” should be abandoned as a synonym for evolutionary biology.

Today "neo-Darwinism" is commonly used to refer to the version of Darwin's theory that has been current since the 1930s (and that represents the majority viewpoint today, with some modifications). For the sake of simplicity, and since the 1930s don't seem so "neo" anymore, it is now common to refer to the contemporary update of Darwin's theory simply as "Darwinism." Consider this sample of publications that have appeared since Eugenie Scott put her warning label on the term “Darwinism” (emphasis mine):

1. Brinkworth, Martin H., and Friedel Weinert. Evolution 2.0: Implications of Darwinism in Philosophy and the Social and Natural Sciences. Heidelberg; New York: Springer-Verlag Berlin Heidelberg, 2012. Part III of this anthology is titled "Philosophical Aspects of Darwinism in the Life Sciences," and it focuses on contemporary biology.
2. Brooks, Daniel R. "The Extended Synthesis: Something Old, Something New." Evolution: Education and Outreach 4, no. 1 (2011): 3-7. See my comments below about Brooks's promotion of Darwinism as the "future of biology."
3. Wilson, Catherine. "Darwinian Morality." Evolution: Education & Outreach 3, no. 2 (2010): 275-287.
4. Deichmann, Ute, and Anthony S. Travis. Darwinism, Philosophy, and Experimental Biology. New York: Springer, 2010. The essays in this anthology include both historical studies and analysis of contemporary biology such as "How Evolutionary Biology Presently Pervades Cell and Molecular Biology," by Michel Morange.
5. Savic, D. J. "Adaptive Mutations: A Challenge to Neo-Darwinism?" Science Progress 92 (2009): 447-468. Dragutin Savic is professor of Molecular Genetics at the Faculty of Sciences, University of Belgrade. He spent several years as a visiting scientist at Johns Hopkins University, Carolinska Institute and Institute J. Monod. This article considers whether certain mutational events are "directed, Cairnsian, or selection-induced."

Let's look a little more closely at a few of the items in this sample bibliography to further document the failure (or very limited success) of Eugenie Scott's terminology blackout memo.

David Vecchi's chapter in the book Evolution 2.0 is called "Taking Biology Seriously: Neo-Darwinism and Its Many Challenges." Vecchi opens a section called "Mapping the Future of Biology" (p. 227-228, emphasis mine) with this comment about evolutionary biology since the 1930s "neo-Darwinism" or "Modern Synthesis":

Of course, we should be critical of any approach that calls for a radical re-interpretation or even abandonment of the neo-Darwinian perspective. What many practitioners seem to be opposing is rather the result of a long-going and multi-faceted process of “hardening” of the Modern Synthesis’ interpretation of Darwinism, as already chronicled in some respects by Gould [6]. However, it should be noted that, historically, some neo-Darwinians have been more open-minded than others, and that Dawkins’ version of neo-Darwinism remains fringe despite its popular success [7]. Furthermore, it is clear enough that we are not on the verge of a Kuhnian revolution in biology, the essential reason being that Darwin got it fundamentally right: life on earth is diverse but interrelated via common ancestry, and it evolves by natural selection. No sensible biologist would deny that selection happens and that it is real. But many people would add that something more happens, as I will try to show in the rest of the paper. Biology is in need of an extension, and the reasons to celebrate Darwin’s genius remain intact.

Even though Vecchi published this with Springer, the publisher behind Evolution: Education and Outreach where Eugenie Scott's D-word essay appeared, apparently he did not get (or admire) Eugenie Scott's blackout memo. Darwinism, he argues, is an important term for the future of evolutionary biology.

Consider this article in the same journal as Eugenie Scott's essay: Brooks, Daniel R. "The Extended Synthesis: Something Old, Something New." Evolution: Education and Outreach 4, no. 1 (2011): 3-7 (p. 3, emphasis mine):

We must extend back in time to recover important aspects of Darwinism that were set aside, and then lost during neo-Darwinism, then move forward beyond neo-Darwinism to encompass new data and concepts. . . . I am attracted to an older concept in which biology needs a covering law to connect it with the rest of the natural sciences. Darwin implicated a “higher law,” but did not specify it. If we can elucidate that law, the Extended Synthesis will become the Unified Theory of Biology called for by Brooks and Wiley 25 years ago.

The same journal, which is aimed at "K-16 students, teachers and scientists," published this article: Wilson, Catherine. "Darwinian Morality." Evolution: Education & Outreach 3, no. 2 (2010): 275-287. What does Wilson recommend for evolution education (p. 275, emphasis mine)?

According to the terms of Charles Darwin’s theory of evolution by natural selection, we human beings are the descendants of ape-like forebears and the remote descendants of one-celled organisms that once floated in a primeval ocean. . . . . It is pointless to ask what the purpose of our existence is. Our species is here because a number of singly improbable events converged to bring our species onto the stage, and there are only the particular purposes that we establish for ourselves. The universe is not in the hands of a powerful and intelligent agent whose benevolence will ensure that everything will turn out for the best.

Many philosophers find these views inspiring, rather than bleak, liberating, rather than dispiriting. The appreciation of our kinship with nonhuman animals and the sense of the unity and coherence of the natural world that Darwinism implies arouse sentiments as respectful as those experienced by religious believers while leaving no doubt that the remediation of social injustice and the restoration and repair of the environment are up to us. Steven Pinker has argued recently that attention to the new human sciences and especially to “evolutionary psychology,” the study of the evolutionary history of attitudes, emotions, and mental capabilities, promises “a naturalness in human relationships, encouraging us to treat people in terms of how they do feel rather than how some theory says they ought to feel” (Pinker 2002, xi).

Without ever giving good reasons, she suggests that the "Darwinism" that she affirms for evolution education can generate ethics that are as exalted as those systems based on traditional religions. Later Wilson states (p. 276) her main contribution to evolution education:

My central argument is that the biological sciences can contribute to moral progress -- not just to the explanation of the origins and formation of moral attitudes and dispositions -- but only by working to dispel the myths and superstitions that sustain oppressive social relations. The existence of measurable physical and psychological differences between individuals and between groups that are the result of random variation on one hand and the selective pressures operating on early humans and their ancestors on the other does not defeat arguments for the moral rightness and practical possibility of greater social equality.

Curiously, she simply asserts the existence of objective "moral rightness" without offering any argument to ground it. Catherine Wilson tries to distance herself from the Darwinian ethics that promoted "forced sterilization" and "genocide" in first half of the twentieth century (p. 277). She also is unsupportive of E. O. Wilson's 1990s version of Darwinian ethics (p. 281). Later, she muses:

Can the biological sciences, whose early racist and militaristic extrapolations were refuted and rejected by the critical social sciences, re-emerge to cooperate with them? Can they do more than defend social inequalities and oppression as natural and inevitable in light of human biological differences? This is the key question for the future of evolutionary ethics. I would insist that the biological sciences can perform in this role but only to the extent that the field of evolutionary ethics can rise to the challenge of exploring the ways in which social oppression is based on mythology and ideology and to the extent that it can replace conventional beliefs with a scientifically more accurate image of people and their world.

Catherine Wilson hopes that evolution education (which includes evolutionary psychology as a "human science") will eliminate such traditional "mythology" in the following manner (p. 283):

The new human sciences, predicated on the assumption that not only our bodies but also our minds and feelings as well are the products of a long evolutionary history, can potentially help us to frame a more accurate image of reality than folklore, philosophy, or the imaginations of novelists and dramatists. For as worthwhile as these cultural forms are, they are not sources of moral knowledge uncolored by bias and unwarranted assumptions.

As I noted at the beginning of this essay, human beings have no functions, no purposes, in virtue of which their qualities can be evaluated, except those they themselves decide to adopt. A person is, from the biologist’s perspective, a temporary federation of replicators that are working to be represented in future generations, sometimes threatened, sometimes exploited, and sometimes assisted by other federations of replicators (Dawkins 1999). We exist not to glorify God, nor to exercise rationality, nor to bring about any particular conditions of society, but merely because we are assemblages of successful replicators.

This kind of evolution education is a public relations nightmare for Eugenie Scott. The NCSE under Scott's direction has built strategic alliances with many members of the "faith community." Catherine Wilson's ethical "Darwinism" can't hope to win over many theists. Of course many evolutionary biologists today distance themselves from such views, but the inner logic of Darwinism and neo-Darwinism up to the present day strongly suggests this sort of ethical and educational outcome (or something like it).

What lesson can we learn from Eugenie Scott's failed attempt to impose term limits on "Darwinism" and "neo-Darwinism"? Simply that there are just too many scientists and historians/philosophers of science who will not allow Scott's ideologically driven educational agenda to prescribe how such terms are to be used. Although Eugenie Scott is now about to enjoy her own retirement, "Darwinism" and "neo-Darwinism" (as terms for contemporary thinking about evolution) will probably have many more years of active service before they retire.

Cross-posted at The Christian Post.

Writing about Nagel's Mind and Cosmos in the Chronicle of Higher Education, Michael Chorost's basic point is that scientists and science writers have long been saying that evolution appears to have direction built somehow into it. He is careful to remind us that those who say this aren't in the camp of intelligent design:

Yet some scientists think that increases in complexity also happen "actively," that is, driven by physical laws that directly favor increases in complexity. As a group, these scientists have no sympathy for intelligent design. However, they do see reasons to think that seen as a whole, life does go from simple to complex, from instinctual to intellectual. And they are asking if there are fundamental laws of nature that make it happen.

While not advocates of ID, neither are they orthodox Darwinists -- as demonstrated by the reactions to the piece by actual Darwin proponents. Jerry Coyne calls it "irresponsible," while Richard Dawkins writes in an email to Coyne that the picture of evolution as obeying some source of "teleological attraction" "INFURIATES me."

But Chorost can't be surprised by such reactions. He quotes one evolutionary biologist on exactly how resistant to changes her field really is:

Joan Roughgarden, an ecologist and evolutionary biologist at the Hawaii Institute of Marine Biology, agrees that evolutionary biologists can be nasty when crossed. "I mean, these guys are impervious to contrary evidence and alternative formulations," she says. "What we see in evolution is stasis --- conceptual stasis, in my view -- where people are ardently defending their formulations from the early 70s."

Impervious to contrary evidence! "Conceptual stasis" -- that's a nice formulation. It sounds like she's been reading ENV.

Chorost wonders why Nagel's book, despite being so unshocking, nevertheless got "raked over the coals." He thinks it's partly because Nagel didn't cite the dissenters -- "Mind and Cosmos is not only negative but underpowered, as if Nagel had brought a knife to a shootout" -- even as Nagel does refer respectfully to advocates of ID. He is "alarmingly nice to intelligent-design theorists." That too rankles Coyne:

In the past, Nagel has shown sympathies for Intelligent Design -- he named, for example, Stephen Meyer’s ID book Signature in the Cell as his “book of the year” in the Times Literary Supplement -- but he asserts that he’s an atheist. No, the teleological force isn’t God, but something else. No matter that no respectable evolutionary biologist has ever seen the need for a teleological force: that idea was abandoned years ago because, to paraphrase Laplace, we simply didn’t need it.

Coyne isn't impressed by the dissenters Chorost mentions -- saying, for example, of Stuart Kauffman:

Stuart Kauffmann: a theoretical biologist at the Santa Fe Institute who has suggested that much of evolution really reflects the self-organizing properties of matter. I disagree with him for numerous reasons (one being that “self organization” cannot explain complex adaptations like eyes), but at any rate his views are outliers, far from the mainstream of most thinkers. That doesn’t automatically make them wrong, of course: he’s wrong for reasons other than being an outlier.

It will be interesting to see what folks like Coyne and Chorost make of the middle third of Steve Meyer's forthcoming book, Darwin's Doubt, which is all about how the scientific search for a replacement theory for Darwinism has gone very mainstream. It's no longer possible, in fact, to dismiss it as merely a fringe phenomenon of "outliers" and eccentrics.

There exists three main types of membrane-embedded ATPases: F-type, V-type and P-type. I will discuss here the F-type ATPases (also called ATP synthase). V-type ATPases facilitate the acidification of intracellular organelles, and use the energy from adenosine triphosphate (ATP) hydrolysis to pump protons into cells and organelles (Beyenbach and Wieczorek, 2006). P-type ATPases are involved in the pumping of cations, also using the energy of ATP hydrolysis (Bublitz et al., 2011; Kuhlbrandt, 2004). The F-type ATPase discussed here is unique inasmuch as it, rather than hydrolysing ATP, actively synthesizes it using the energy from the flow of protons down an electrochemical gradient. There are also A-type ATPases which are found in archaea and perform a similar function to F-type ATPases (Bickel-Sandkötter et al., 1998).

ATP synthase has been described as "a splendid molecular machine," and "one of the most beautiful" of "all enzymes" (Boyer, 1997). This "bona fide rotary dynamo machine" (Mulkidjanian et al., 2007) is the key enzyme involved in the biochemical process known as oxidative phosphorylation, which is very closely coupled to the electron transport chain since the electrochemical proton gradient that is produced by electron transport supplies the energy necessary for the production of the ATP from adenosine diphosphate (ADP) and a phosphate group. The ATP synthase machine is able to crank out approximately 100 ATP molecules per second. With its near-100% efficiency, far surpassing human technology, ATP synthase manifests clear evidence not merely of engineering but of brilliant engineering. A recent paper in Nature offered a "resolution map of the H⁺-driven ATP synthase from Thermus thermophilus obtained by electron cryomicroscopy of single particles in ice," (Lau and Rubinstein, 2012).

The electron transport chain and oxidative phosphorylation occur following three previous stages of aerobic respiration (glycolysis, pyruvate oxidation, and the tricarboxylic acid, or TCA, cycle), and differ between eukaryotes and bacteria. For one thing, in eukaryotes, the process takes place within the cell's mitochondria (or chloroplasts), whereas, in bacteria (which lack mitochondria and chloroplasts), the process takes place in the cell's plasma membrane. Other differences relate to the individual proteins involved (eukaryotes use five main protein complexes, whereas bacteria use many different enzymes). The purpose of this article is to unravel the molecular complexity of this nanotechnological marvel. I will dwell only very briefly on the electron transport chain, offering an explanation merely by way of background.

The Electron Transport Chain

Briefly, the electron transport chain involves the flow of electrons through a respiratory chain. Electrons pass through three protein complexes that are embedded in the inner mitochondrial membrane: NADH-Q oxidoreductase (Complex I); Q-cytochrome c oxidoreductase (Complex III); and cytochrome c oxidase (Complex IV). Complex I, a large multi-subunit protein, is the enzyme that catalyzes the transfer of electrons from the reducing agent (electron donor) NADH to coenzyme Q. The electrons are relayed to cytochrome c at Complex III, and Complex IV transfers the electrons to O₂, which is thus reduced to H₂O. There are some substrates, such as succinate which has more positive redox potentials than NAD⁺/NADH, which involve succinate-Q reductase (Complex II) instead of NADH-Q oxidoreductase (Complex I).

Oxidative Phosphorylation

The transmembrane electrochemical gradient across the inner mitochondrial membrane (the matrix side now has a net negative charge) creates a proton motive force that drives the process of ATP synthesis. Complexes I, III and IV serve as proton pumps, transporting protons from the matrix into the intermembrane space. The complexes utilize the energy given up by the flow of electrons. The inner mitochondrial membrane is impermeable to protons, leading to their accumulation in the intermembrane space. Like water behind a dam, this build-up of protons stores potential energy. The principle of ATP synthase is to facilitate the flow of protons down their concentration gradient from the inner membrane space to the matrix, using the energy released in the process to create ATP.

ATP synthase consists of two protein complexes, the F₁ domain and the F₀ domain, each of which is comprised of several different subunits. The F₀ complex is a proton channel and is embedded within the mitochondrial membrane. The F₁ complex is the site of ATP synthesis and is located in the mitochondrial matrix. The F₁ domain is made up of alpha, beta, gamma, delta and epsilon subunits. The alpha and beta subunits, present in three copies each, make up the catalytic core of the F₁ domain, while the gamma subunit comprise the rotating central stalk, which connects the F₁ domain to the F₀ domain. The epsilon subunit is an ATPase inhibitor, and can take two conformations: extended and contracted. The conformation taken depends on the rotational direction of the gamma subunit and the presence of ADP. When it switches from the contracted to the extended conformation (triggered by the presence of ADP), where the c-terminus extends towards the F₁ domain, the epsilon subunit is believed to inhibit ATP hydrolysis (but not synthesis), thereby operating as a safety lock to limit the wasteful hydrolysis of ATP (Feniouk and Junge, 2005).

The alpha and beta subunits are attached to the central stalk and form a hexameric cylindrical structure that surrounds it: Each also possesses a substrate-binding site (the ones on the alpha subunits are regulatory, while the ones on the beta subunits are catalytic). There is also a peripheral stalk, which extends from the membrane to the top of the F₁ domain and is comprised of b and d subunits. It is attached to the α3β3 hexamer by the delta subunit. The purpose of the peripheral stalk is to anchor the alpha and beta subunits of the F₁ domain, preventing them from rotating as the central stalk rotates.

The principle subunits in the F₀ domain are a, b and c. Ten to fifteen (depending on the species) c-subunits form a transmembrane ring known as the "c ring", which is the rotor of the F₀ domain (Meier et al., 2005). The F₁ domain has its own rotor, comprised of the central gamma subunit inside the cylinder formed by the alpha and beta subunits. The rotors move in opposite directions. When the c ring rotor dominates, it uses the energy of the proton motive force to drive the reverse rotation of the gamma subunit rotor (clockwise), facilitating the production of ATP (Okuno et al., 2011; Yasuda et al., 2001). When the gamma subunit rotor dominates, it uses the energy from the hydrolysis of ATP to drive the reverse rotation of the c ring rotor (counter-clockwise), and protons are pumped against their electrochemical gradient.

Proton flow through the F₀ domain causes the complex to rotate, driving ATP synthesis in the F₁ domain. Some bacterial species, such as the obligate anaerobe Propionigenium modestum, use sodium ions instead (Dimroth et al., 1999; Dimroth, 1992; Laubinger and Dimroth, 1989). As the axis rotates, the conformation of the alpha and beta subunits in the F₁ complex's active site is altered such that it switches from an "open" state (where ADP and phosphate can enter the active site) to a "closed" state (where ADP and phosphate are bound loosely) to a "tight" state (where the ADP and phosphate molecules are forced together, covalently bonding to form ATP) (Boyer, 1997). The active site then undergoes a further conformational change, resulting in the breaking of the hydrogen bonds that were stabilizing the ATP in the active site (releasing the newly-formed molecule), and reverting back to the original open state, ready for another reaction cycle.

How does the flow of protons cause rotation of the F₀ domain? Site-directed mutagenesis studies in Escherichia coli have determined that two amino acid residues are crucial to the function of the F₀ motor (Fillingame et al., 2002; Valiyaveetil and Fillingame, 1997). These are: "aArg-210 in one of the transmembrane α-helices (TMH), TMH4, of the a-subunit and cAsp-61 in the outer TMH of each c-subunit, the primary proton binding sites located in the middle of the membrane hydrophobic layer," (Aksimentiev et al., 2004).

Garrett and Grisham (2008) explain the remarkable process of motor rotation:

The a-subunit contains two half-channels, a proton inlet channel that opens to the intermembrane space and a proton outlet channel that opens to the matrix. The c-subunits are proton carriers that transfer protons from the inlet channel to the outlet channel only by rotation of the c-ring. Each c-subunit contains a protonatable residue, Asp⁶¹. Protons flowing from the intermembrane space through the inlet half-channel protonate the Asp⁶¹ of a passing c-subunit and ride the rotor around the ring until they reach the outlet channel and flow out into the matrix... Each c-subunit in the c-ring has an inner helix and an outer helix. Asp⁶¹ is located midway along the outer α-helix. When protonated, the Asp carboxyl faces into the adjacent subunit. Rotation of the entire outer α-helix expses Asp⁶¹ to the outside when it is protonated. Arg²¹⁰, located midway on a transmembrane helix of the a-subunit, forms hydrogen bonds with Asp⁶¹ residues on two adjacent c-subunits. The half-channels of the a-subunit extend up and down from Arg²¹⁰. The inlet channel terminates in Asn²¹⁴, whereas the outer channel terminates at Ser²⁰⁶.

The structure of the c-subunit complex is exquisitely suited for proton transport. When a proton enters the a-subunit inlet channel and is transferred from a-subunit Asn²¹⁴ to c-subunit Asp⁶¹, the α-helix of that c-subunit rotates clockwise to bury the Asp carboxyl group. Each Asp⁶¹ remains protonated once it leaves the a-subunit interface, because the hydrophobic environment of the membrane interior makes deprotonation (and charge formation) highly unfavorable. However, when a protonated Asp residue approaches the a-subunit outlet channel, the proton is transferred to Ser²⁰⁶ and exits through the outlet channel. The a-subunit Arg²¹⁰ side chain orients adjacent Asp⁶¹ groups and promotes transfers of entering protons from a-subunit Asn²¹⁴ to Asp⁶¹ and transfers of existing protons from Asp⁶¹ to a-subunit Ser²⁰⁶. Arg²¹⁰, because it is pronated, also prevents direct proton transfer from Asn²¹⁴ to Ser²⁰⁶, which would circumvent ring rotation and motor function.

For further discussion of the rotary mechanism of ATP synthase, see Arechaga and Jones (2001).

An interesting review article reported on the incredible engineering found in the F₀ motor (von Ballmoos et al., 2009):

The rotational mechanism of the ATP synthase demands ingeniously designed interfaces between rotor and stator subunits, particularly between the rotating c ring and the laterally abutted subunit a, because rotation speeds up to 500 Hz must be tolerated in the absence of a stabilizing rotor axis. This proteinous interface also acts as the critical scaffold for torque generation and ion translocation across the membrane. To prohibit charge translocation without rotation, ion leakage at the interface must be efficiently prevented.

For non-specialists it can often be difficult to visualize, from a written description alone, exactly what is going on at the molecular level. This is why computer animations can prove invaluable in understanding the operation of these systems. To get a better handle on how rotation of the F₀ component drives the conformational changes of the active site in the F₁ component, readers are referred to this animation. For a much closer inspection of the conformational changes that take place in the F₁ complex at the molecular level, readers are directed to this animation. For an animated overview of the whole process from electron transport to oxidative phosphorylation, see this video.

The Evolution of ATP Synthase

ATP synthase is found almost ubiquitously across life, and is even found in fermentative organisms that lack the electron transport chain and do not undergo oxidative phosphorylation, such as Clostridium pasteurianum (Das and Ljungdahl, 2003). This is because many cellular processes use energy from the proton motive force rather than ATP. The motor is reversible, and hydrolysis of ATP by the α3β3-catalytic hexamer can supply the torque for the rotation in the opposite direction, catalyzing the active transport of protons from inside to outside the cell. Hydrolysis of ATP sometimes has to be halted in the cell (e.g. during hornworm moulting or during glucose deprivation). V-type ATPases have a nifty trick in this regard. In such cases, the V₁ domain has been observed to reversibly detach from the V₀ domain (Drory and Nelson, 2006; Beyenbach and Wieczorek, 2006; Iwata et al., 2004), owing to the "socket like function" of subunit C "in attaching the central-stalk subunits of the V1 domain," (Iwata et al., 2004).

ATP synthase bears similarity in some respects to other systems. Ion channels are very common in biology -- for example, bacterial flagella are also driven by a proton motive force across the membrane (although some bacteria, such as Vibrio species, use a flow of sodium ions instead). FliI serves as an inessential ATPase involved in the flagellar export apparatus, and it exhibits significant degrees of homology to the alpha and beta subunits of ATP synthase (Imada et al., 2007; Vogler et al., 1991). FliI also has a homologue in Yersinia pestis called YscN, which serves to energize the type III secretion system (Woestyn et al., 1994). It is hypothesized by some that an F or V-type ATPase was recruited by these systems (Pallen et al., 2006; Blocker, 2003; Aizawa, 2001). What is interesting, however, is that the ATPase of these systems lacks the characteristic central stalk found in F and V-type ATPases (Mulkidjanian et al., 2007).

The hexameric structure formed from the three alpha and three beta subunits also resembles hexameric DNA helicases which, like the ATP synthase, form a ring with a central channel, and three-fold rotational symmetry. DNA helicases also possess ATPase activity, and use the energy from ATP hydrolysis to move directionally along the phosphodiester backbone of DNA and separate the two nucleic acid strands.

How could a complex macromolecular machine like ATP synthase have evolved by natural selection? No other enzyme works in the same way. One hypothesis is that a proton motor came to be associated with a DNA or RNA helicase, and the ATPase of the helicase was driven forcibly in reverse by the proton motor (Mulkidjanian et al., 2007; Walker, 1998; Doering et al., 1995). It's certainly an elaborate story, but biology doesn't work like that. Molecular machines are not Lego bricks. They don't spontaneously combine to form new machines. Furthermore, explaining the F-type ATPases in terms of other ATPases only begs the question of the origin of ATPases in the first place. The ability of the F₀ domain to cause such specific conformational changes in the active site of the F₁ domain via proton-driven rotation requires foresight and planning, and ingeniously designed interaction.

It is interesting that even though "the stalk domains of the more closely related A₁ and V₁ are remarkably similar in shape and dimensions, and are different in these respects from the F₁-ATPase", nonetheless, "A₁A₀ and F₁F₀ enzymes function as ATP synthases in cells whereas the V₁V₀ ATPase works as an ATP-driven ion pump," (Gruber et al., 2001). What is even more curious is that comparison of the F-type and V-type ATPases reveals non-homology between the subunits of the central stalk of the two systems (a component that is essential for rotation catalysis), even though there is homology between their membrane and catalytic subunits (Mulkidjanian et al., 2007; Gruber et al., 2001). One hypothesis that takes this into account is that "the conserved head structure, the membrane portion and the peripheral stalk (or stalks) together could have formed a translocase that coupled ATP hydrolysis to the transfer of RNA and/or proteins across the membrane, with the translocated polymer occupying the place of the central stalk," (Mulkidjanian et al., 2007). Such a hypothesis is interesting. After all, there are helicase/F₁ATPase-like DNA translocases involved in bacterial chromosome segregation during cytokinesis (Graham et al., 2010) and in bacterial conjugation (Tato et al., 2005; Gomis-Rüth et al., 2001). Protein translocases are also common (e.g. Papanikou et al., 2007). Since the central stalks of the F and V-type ATPases are not homologous, such a scenario would entail that the nucleic acid or protein translocase was independently converted into an ion-translocating ATPase (unless the central stalk was later replaced following divergence from a single common ancestor, but this doesn't seem plausible). Moreover, it is hypothesized that the ATPase system underwent at least two, and possibly three, reversals in function; "from a progenitor proton-pumping ATPase to a proton-driven ATP synthase" and subsequently "transforming the synthase back into a proton-pumping ATPase" before perhaps transforming it "from an ATPase back to an ATP synthase" (Cross and Muller, 2004).

Such a scenario would suggest that a translocating protein somehow got stuck in a protein translocase, and subsequently evolved into the central stalk of the membrane ATPase. This hypothesis seems less than convincing to me, however. For one thing, the central stalk has to somehow be coupled to the c-ring (in F-type ATPases) or the A subunit (in V-type ATPases) in order for it to rotate. Are we to expect the broken protein translocase to stick around through multiple generations while we wait for it to evolve into the membrane ATPase system? In any case, protein (and nucleic acid) translocation is dependent upon ATP hydrolysis, so these systems already possess ATPase activity (which is left unaccounted for). ATP synthases also appear to be essential in nearly all life-forms, and ATPases more generally are absolutely essential in all known life. It should be noted, however, that the F-type ATPase described in this article appears to be non-essential in some life forms, since they are not found in any member of the bacterial phylum Deinococcus-Thermus (where V-type ATPases are the only category of membrane ATPase) (Lapierre et al., 2006). Moreover, a small subset of obligate parasitic bacteria, such as the BCc strain of Buchnera aphidicola (an endosymbiont of cedar aphid Cinara cedri), are able to get by without ATP synthase (Charles et al., 2011). This organism is an obligate parasite, however, meaning that it is unable to survive outside of its host organism. With the essential nature of the ATPases in mind, it seems highly unlikely that the ATPases could have evolved gradually by natural selection.

Conclusion

ATP synthase is truly a marvel of nanotechnology. With its ingenious design and remarkably high efficiency and speed, this amazing molecular energy turbine stands among the numerous examples of complex macromolecular machines that bear the unmistakable imprints of intelligence and foresight. As one recent review paper stated, the "unique energy transmission mechanism [found in ATP synthase] is not found in other biological systems. Although there are other similar man-made systems like hydroelectric generators, F₀F₁-ATP synthase operates on the nanometer scale and works with extremely high efficiency," (Okuno et al., 2011). If such a unique and brilliantly engineered nanomachine bears such a strong resemblance to the engineering of manmade hydroelectric generators, and yet so impressively outperforms the best human technology in terms of speed and efficiency, one is led unsurprisingly to the conclusion that such a machine itself is best explained by intelligent design.

The newsworthy novelty of U. gibba, the humped bladderwort, is that it gets by on a much more concise genome than other plants: just 3 percent of its genome does not code for proteins. That suggests to some wishful thinkers that perhaps here is the proof that "junk DNA" is junk after all. If the bladderwort can get by without it, so could we.

The occasion for the collective cry of "See, we told you so!" is a paper in Nature, "Architecture and evolution of a minute plant genome." From the abstract:

Despite its tiny size, the U. gibba genome accommodates a typical number of genes for a plant, with the main difference from other plant genomes arising from a drastic reduction in non-genic DNA. Unexpectedly, we identified at least three rounds of WGD in U. gibba since common ancestry with tomato (Solanum) and grape (Vitis). The compressed architecture of the U. gibba genome indicates that a small fraction of intergenic DNA, with few or no active retrotransposons, is sufficient to regulate and integrate all the processes required for the development and reproduction of a complex organism.

The L.A. Times is relieved:

How’s this for spring cleaning? Scientists have discovered that a carnivorous plant deletes so much of its own junk DNA that it has hardly any left. The finding, published online in Nature, hints that such noncoding DNA may not be as important as some scientists believe.

"Junk DNA is probably well named as junk. There doesn’t seem to be any glorious reason or function behind it," said Victor Albert, a University at Buffalo molecular evolutionary biologist and one of the lead authors on the study.

Live Science exults: "'Junk' DNA Mystery Solved: It's Not Needed"!

But this is just silly. There are many examples in plants of non-protein-coding
DNA that plays essential roles in metabolism and development. Generalizing the results from one plant (and an atypical one, at that) to all plants and animals is about as illogical as you can get.

See Chapters 4-7 of Jonathan Wells's The Myth of Junk DNA. Or go to PubMed and do a search on "microRNAs in plants." Here, we've done it for you. For more on the general subject, look at the dozens of papers that were published last September by researchers with the ENCODE project, though those focused mainly on animals. And don't forget to make use of our archives at ENV: search for "junk DNA." You're welcome, we've done that for you too.

By the same token, we know that offspring differ from parents; they might be taller or shorter; thinner or heavier. But “indefinite departure from the original type,” to use A.R. Wallace’s phrase, likewise has never been observed -- outside the confines of textbooks or theoretical treatises. What we do observe is small variations fluctuating around a mean.

On the other hand, a concept of evolution not unlike the Darwinian one is validly applied to human constructions. Language may be the best-known example. Latin evolved into French over a two-thousand-year period. Roman documents in Latin survive, and the language is still used by the Catholic Church. We have two millennia of documentation showing how Latin morphed into its daughter languages.

“Yes, language evolves -- that is, language changes over time, and those changes accumulate to create completely new languages,” says the linguist Noel Rude. He goes on (in a private communication):

The origin of language is an entirely different matter. The kind of changes we observe -- changes in sound, grammar, and semantics -- do not explain how language came to be in the first place.

In a parallel way, we can confidently say that we no more know how life emerged from non-life after Darwin than we did before Darwin.

Just as Darwin hoped to explain organisms by positing an accumulation of parts, each addition helpful to the emerging organism, so linguists sought to explain languages from the “bottom up.” It was assumed that their development was determined by the physiological abilities and limitations of the speakers as well as by the stream of sound that they created.

After Darwin many theories about the origin of language began to be discussed. Some were so silly that in 1866 la Société de Linguistique de Paris banned such speculation. The dam was broken when Philip Lieberman published On the Origins of Language, in 1975. Here’s Noel Rude again:

Lieberman argued that until man evolved a bent vocal tract he couldn't have produced vowel contrasts and therefore he didn't speak. This was thought profound until somebody pointed out that parrots do quite well with just a beak.

This approach to the origin of language resembles the attempt to decipher written messages by studying the ink, the script, and the paper on which they were written. But this can’t get us very far. As Noel Rude adds, “we still need a top-down linguistics that addresses the problem of logic and meaning.”

How friendly are modern linguists to such a top-down study? The answer, to simplify, is that they generally are not friendly. Beyond that the complications build up quickly and get us into Noam Chomsky territory. He went part of the way toward the “top” and was critical enough of Darwinism to have annoyed Daniel Dennett en route. Dennett said that Chomsky sounded like a creationist.

This brings us to both a similarity and a divergence between the evolution of species and the evolution of language. First the similarity: language does evolve but it is not teleological. It does not aim to approach an end state, and in that sense it is Darwinian. The changes in Latin that led to French were not all along aiming to produce something elegant enough to please the Academie francaise (created in 1635); or indeed aiming to produce anything in particular.

The difference is this. The evolution of language has been observed, and recorded in detail. But in every instance it is produced by intelligent agents, namely human beings. Parrots can utter words, sometimes with disconcerting precision, but they don’t understand those words when considered as elements of a sentence.

The problem for Darwinists is that they insist that intelligence can play no role in their materialist, bottom-up scheme. They believe in -- they insist on -- the occurrence of evolution without intelligence. In contrast, proponents of intelligent design assert intelligence yet they deny the sufficiency of the Darwinian evolutionary mechanism. Or, if they don’t deny it, they insist on being shown the evidence.

Other human artifacts can also be said to have evolved, for example automobiles. In 1968, the Smithsonian Institution published a book by Ritchie Calder entitled The Evolution of the Machine. It is a proper use of the word evolution. Charts showing the “ancestry” of automobile companies over the past 100-odd years can be viewed online today. Cars of course display both intelligent design and teleology. The companies that design and make them deliberately pursue goals of comfort, efficiency and so on.

But Darwinism want to establish evolution as a “fact” and as something that happened without any guiding intelligence at all. Whether anything other than chaos can be achieved by such restricted means is very much open to doubt.

Image credit: Anthony M./Wikicommons.

An open-access paper in PNAS shows that part of the rotary motor of ATP synthase -- a vital molecular machine for almost all living things -- has experienced mutation and selection. We recently featured a dramatic animation of how this motor works. As an exquisite, irreducibly complex device, it looks like evidence par excellence for design. Yet it mutated, and it still works. In the case of alkaliphilic bacterium Bacillus pseudofirmus OF4, it works better with the mutation.

The data indicate a direct connection between the precisely adapted ATP synthase c-ring stoichiometry and its ion-to-ATP ratio on cell physiology, and also demonstrate the bioenergetic challenges and evolutionary adaptation strategies of extremophiles. (Emphasis added.)

Let's begin with several unquestioned facts:

1. It's still ATP synthase.
2. The structure and mechanism work the same.
3. The mutated version fits well within known variations of the motor.
4. This bacterium lives in a highly stressed, high-alkaline environment.
5. The unmutated version of the motor works in the bacterium, albeit not as efficiently.
6. The mutation amounts to a substitution of one amino acid for another.
7. ATP synthase is otherwise "highly conserved" from bacteria to humans.
8. The mutation has no bearing on the origin of the machine.

Here's some background: In the c-ring (the portion of the machine that rotates like a merry-go-round around a central pore), protons attach to c-subunits and drive the rotation so that the other primary domain can synthesize ATP. The number of c-ring subunits varies between species from 5 to 17. This kind of bacterium normally has 12, but the extremophile version has 13.

C-ring subunits contain a conserved motif of glycine repeats (G) in the form GxGxGxG. In Bacillus pseudofirmus OF4, however, the researchers found alanine had replaced the glycine, producing AxAxAxA. This had the effect of creating a 13-subunit ring, with a tighter fit. The modification improved proton pumping, but only in highly alkaline environments (pH > 10). Protons are hard to come by in alkaline environments. Anything that improves the efficiency of utilizing the weakened proton motive force (pmf) would be adaptive.

Glycine and alanine are two of the simplest amino acids. Glycine has a hydrogen (H) for its side group, whereas alanine has a methyl group (CH₃). The codons for the two are also similar. Any of these triplets can code for glycine: GGU, GGC, GGA, and GGG. Any of these triplets can code for alanine: GCU, GCC, GCA, and GCG. It's clear that a single point mutation, like from GGU to GCU, could switch from one to the other. Such variations within an enzyme are common if they do not destroy function of the enzyme.

Consider the extreme environment of this bacterium. It lives in highly alkaline soils. Any individual with a mutation that improves its ability to extract proton fuel for its motors is likely to proliferate. The mutant is not creating a new function; it's merely conserving an existing function. The structure and operation of the motor remain the same; the authors said, "several high-resolution structures of isolated rotor rings have demonstrated an overall conserved structural appearance and functionality." The mutation has the effect of creating a tighter and stabler fit that improves pumping efficiency in the extreme alkaline environment. If it were as effective in more neutral or acidic environments, why would the GxGxGxG motif be so highly conserved?

In other words, because the environment of this bacterium is stressful, extreme conditions call for desperate measures. More importantly, the mutational pathway for its adaptation is simple, well within the "edge of evolution" accessible to natural variation and selection as described by Michael Behe in his book, The Edge of Evolution (2008). Behe described mutational pathways, consisting of one or two mutations, that allow malaria to escape when stressed by chemical agents trying to kill it. He demonstrated that the probability of those lifesaving mutations do not exceed the probabilistic resources available; adding more required mutations, though, quickly exceeds them.

The authors indicated that the mutations they found are within the range of functional variation:

Our data indicate that B. pseudofirmus OF4 can assemble and operate ATP synthases with different stoichiometries of c-rings in the range of c11 to c15, but robust growth at high pH is restricted to strains with a majority of c-rings with at least the c13 stoichiometry.

When protons are in short supply, having more c-ring subunits helps. That's why this extremophile benefits with the alanine motif, because it adds a subunit and tightens the fit of the c-ring in the membrane. It's only when the pH gets above 10 that the mutation is beneficial. Otherwise, if it were a generally beneficial change, all species would use it. Instead, the GxGxGxG motif is the conserved form, even in similar bacteria that live in neutral environments.

The authors say that the location of the particular mutation is a mutational hotspot. Other extremophiles are known to have particular variations there. But one cannot mutate these delicate motors willy-nilly:

The changes in the tertiary structure of these mutants have no influence on complex stability with respect to pH, temperature, or detergent, but further mutations finally destabilize the c-ring.

The authors end by stating that this mutation could have spread quickly in the population. With i indicating the number of c-ring subunits, the rate of ATP production is i x pmf (proton motive force). The mutant proliferates because it has a slightly improved production rate of ATP:

The alanine motif is a necessary, but insufficient, adaptation of alkaliphilic Bacillus bacteria. It has a direct influence on the c-ring stoichiometry and its indigenous property to determine the ATP synthase i value, and thus directly modulates the cell's physiology and bioenergetics, facilitating growth at pH >10. Remarkably, and in agreement with previous work, this observation also suggests that i can be adapted by just one or two selected mutations. This property enables adaptation to new environmental challenges, a process that can occur within a rather short evolutionary time frame.

It's an interesting paper that demonstrates adaptive selection on a small scale. But since the changes are well within the edge of evolution, since they only affect bacteria in a stressed environment, and since they do not alter the irreducible complexity of functional parts, the findings do not alter the inference to design. If anything, they show the weakness of evolutionary theory. It can only permit small-scale adaptations under special conditions, provided the changes do not destabilize the complex machinery.

And who knows; it could be argued that the "mutational hotspot" that permits this adaptability to environmental challenges was itself designed.

Named after George Boole, a 19th-century mathematician, Boolean logic is the basis of digital circuit design. For example, the AND function means that both conditions must be on to trigger the circuit. In notational form, where 1 means present and 0 means absent,

1 AND 1 = true or "on"
0 AND 0 = false or "off"
1 AND 0 = false or "off"

In the OR function, either one (or both) of the inputs can be on to trigger the circuit:

1 OR 1 = true or "on"
0 OR 0 = false or "off"
1 OR 0 = true or "on"

Negation of these functions, called NAND and NOR, reverse the outputs. For a logic gate with two inputs and one output, such as a transistor, there are 16 possible operations (AND, NAND, OR, NOR, XOR, XNOR, ...). All but the last two, XOR (exclusive OR, true if the inputs are different, but false if the inputs are the same), and XNOR (its negation), had been engineered in bacteria, but those two were more challenging.

Now the journal Science has announced the implementation of XOR and XNOR in bacterial circuits by a team at Stanford and another team at MIT. With the logical operator set complete, the way is paved for more advanced digital signal processing using biological circuits. Networks of biological circuits could be used to "study and reprogram living systems, explore biomolecular computing, and improve cellular therapeutics," according to the Stanford team.

Both teams were able to manipulate and regulate the inputs and outputs of DNA transcription, using the readily available enzymes in bacteria (promoters, terminators, recombinases, integrases and other cofactors). The presence or absence of the machines determines the output -- the amount of messenger RNA produced for a given gene. In bacteria, with the DNA arranged in plasmids (circular loops), the ingredients are easier to manipulate: add the ingredients (input) and measure the mRNA produced (output). The Stanford team called their transistor-like mechanism a "transcriptor."

The team realized that they were simply altering an already-existing biological logic. "Organisms must process information encoded via developmental and environmental signals to survive and reproduce," they said (emphasis added). They recognized, further, that their operations are trivial compared to what living organisms do. "Researchers have also engineered synthetic genetic logic to realize simpler, independent control of biological processes."

In the same issue of Science, Yaakov Benenson, from the Swiss Institute of Technology, agreed that living organisms use recombinatorial logic:

Logic gates evoke images of circuit boards, but cells are arguably equally good in relying on logic computations. A classic example is the Lac operon, which activates itself upon the condition "lactose AND NOT glucose". In recent years, there have been multiple reports on rationally designed, genetically encoded logic gates and circuits in living cells. Just like the Lac operon, these gates receive two or more molecular signals (inputs) and generate a product (output) whose level is logically linked to the inputs.

Benenson believes that "natural evolution" had a harder time encoding the XOR and XNOR operations, but for that assertion, he passed the buck to Leslie Valiant of Harvard in the references. Valiant's 2009 paper in the Journal of the Association for Computing Machinery seems highly speculative. Utterly dependent on the validity of natural selection, Valiant's theory (or rather "suggestion" or "notion") starts with an embarrassing admission about Darwin's theory:

Darwin's theory of evolution suggests that such mechanisms evolved through variation guided by natural selection. However, there has existed no theory that would explain quantitatively which mechanisms can so evolve in realistic population sizes within realistic time periods, and which are too complex. In this article, we suggest such a theory. We treat Darwinian evolution as a form of computational learning from examples in which the course of learning is influenced only by the aggregate fitness of the hypotheses on the examples, and not otherwise by specific examples. We formulate a notion of evolvability that distinguishes function classes that are evolvable with polynomially bounded resources from those that are not.... We suggest that the mechanism that underlies biological evolution overall is "evolvable target pursuit", which consists of a series of evolutionary stages, each one inexorably pursuing an evolvable target in the technical sense suggested above, each such target being rendered evolvable by the serendipitous combination of the environment and the outcomes of previous evolutionary stages.

Our uniform experience with computer circuits that use logic operations is that they originated from intelligent causes. The inference to the best explanation for biological circuits that employ logic operations is that they, too, are the work of intelligent causes.

It doesn't matter if the Stanford team and commentator Benenson "believe" that bacterial logic somehow evolved by natural selection, despite the problem of getting "mechanisms...which are too complex" to evolve "in realistic population sizes within realistic time periods." They can choose to believe that if they want. What matters is the logic behind their work. In this case, they are implying, "Do as I do, not as I say."

As Josh says, this casts the human being who murders as a fundamentally blameless animal, like a man-eating tiger. We would cage or even shoot such a tiger, but we could not blame it for acting as it does.

Profoundly, I thought, Josh's article suggests how remote from human experience a guy like Coyne must travel if he wants to carry his Darwinian materialism to its seemingly logical conclusions.

As Thomas Nagel reminds us in Mind & Cosmos, the entity that we all know most intimately -- our own consciousness -- is that which most powerfully argues against a materialist understanding of reality. We know our conscious experience is not a material thing. So how did a purely material process like Darwinian evolution produce it? There's an obvious contradiction in terms there. Darwinism forces believers to deny their experience of being alive and conscious.

So too with the tiger. As Josh says, we may not know what it's like to be a tiger, but we can be pretty sure it's very little like being you or me. A worldview that demands that we equate a human with a tiger has cut itself totally free from the reality we know best. It tells us to believe what we know most surely not to be true.

Darwin persuasively taught that life is the product of blind, meaningless, purposeless churning, making all life, not just human, hardly anything more special or dignified than cosmic refuse. Indeed in a Darwinian worldview, life is cosmic refuse. While accused abortion butcher Kermit Gosnell may be an outlier, he is an emblematic personality in our Darwin-tutored culture. However the good news is that the latest science demonstrates that for hundreds of millions of years a purpose, an intelligent design, has been working itself out through the history of complex life.

Very far from being galactic garbage, life was intended from the start, with human life as the peak expression of the designer's creative intention.

That's the bottom-line takeaway of Darwin's Doubt: The Explosive Origin of Animal Life and the Case for Intelligent Design, by Discovery Institute senior fellow Stephen Meyer. As ENV readers will know well, you can and should go here and get your 43% discount when you pre-order NOW!

Image: Churning vortex of a north polar storm over Saturn, NASA/JPL-Caltech/SSI.

Psychiatry, though, was supposed to be better. Its practitioners had to earn an MD. It had a widely accepted, peer-reviewed guidebook, the Diagnostic and Statistical Manual of Mental Disorders (DSM), published by its professional society, the American Psychiatric Association. With its focus on observable symptoms, presumably rooted in biology, it had all the trappings of science. The things being said about psychiatry now, though, on the eve of publication of its latest upgrade, the DSM-5, are revealing it to be a science in crisis -- if it ever was a science at all. As we list the problems, ponder whether many of the same criticisms could be leveled against Darwinism.

DSM-5, coming out on May 22, is the latest edition of the official diagnostic "bible" for psychiatrists that had its genesis in 1952. Writing for Nature, David Dobbs says,

Each such manual, DSM or others, has tried to improve on its predecessor. All have failed, says psychotherapist Gary Greenberg in his entertaining, biting and essential The Book of Woe. But none has failed so spectacularly as the DSM-5. (Emphasis added.)

DSM-5 removes some diagnoses, like Asperger's syndrome, reclassifies others, and adds a number of new conditions that are, to most of us, just weird: like "Skin Picking Disorder," "Sluggish Cognitive Tempo," and "Compulsive Hoarding." What about the new "Hypersexual Disorder"? Are psychiatrists just giving excuses for irresponsible behavior? Is psychiatry "cutting nature at its joints" or just manufacturing artificial pigeonholes?

Writing for New Scientist, psychiatrist Allen Frances doesn't believe that one manual should dictate U.S. health research. The new diagnoses and reductions in thresholds for old ones "expand the already stretched boundaries of psychiatry and threaten to turn diagnostic inflation into hyperinflation," he says. By inflation, he's speaking of the tendency to overdiagnose, as when too many boys are diagnosed with "Hyperactivity Disorder" and given ritalin to calm down what might in other contexts be considered normal boyish behavior. Worse, the DSM threatens psychiatry's standing as a science:

In my opinion, the DSM-5 process has been secretive, closed and sloppy -- with confidentiality restraints, constantly missed deadlines, botched field testing, the cancellation of an important quality control step, and a rush to publication. A petition for independent scientific review endorsed by 56 mental health organisations was ignored. There is no reason to believe that DSM-5 is safe or scientifically sound.

According to Nick Craddock, professor of psychiatry at Cardiff University, also writing for New Scientist, psychiatry is still waiting for its "Higgs boson moment," when some prediction-come-true from biological theory will actually confirm its legitimacy. He says, "Not since Freud's pseudoscientific theories early last century has psychiatry claimed any broad theoretical basis for making sense of our normal and abnormal feelings, thinking and social behaviours -- the complexities at the heart of being human." In other words, psychiatry never made it to scientific status in the first place. Its claims remain "atheoretical," he believes, even though he is optimistic its day will come.

In another article for New Scientist, "Psychiatry divided as mental health 'bible' denounced," Andy Coghlan and Sara Reardon point out other problems, like internal squabbling:

The world's biggest mental health research institute is abandoning the new version of psychiatry's "bible" -- the Diagnostic and Statistical Manual of Mental Disorders, questioning its validity and stating that "patients with mental disorders deserve better". This bombshell comes just weeks before the publication of the fifth revision of the manual, called DSM-5.

Even though the DSM has been "the mainstay of psychiatric research for 60 years," practitioners are rising up against it:

The DSM has been embroiled in controversy for a number of years. Critics have said that it has outlasted its usefulness, has turned complaints that are not truly illnesses into medical conditions, and has been unduly influenced by pharmaceutical companies looking for new markets for their drugs.

Thomas Insel, director of the National Institute of Mental Health, calls for "diagnoses based on science not symptoms." Sounds good, but that would require theoretical bases for linking genes and neurons to behavior, a devilishly hard business. Insel believes it will take a decade to achieve the "precision medicine" desired. But what if it never comes? Michael Owen at the University of Cardiff says, "These are incredibly complicated disorders. To understand the neuroscience in sufficient depth and detail to build a diagnosis process will take a long time, but in the meantime, clinicians still have to do their work." That implies that psychiatrists are treating patients on a non-scientific basis. And now, many are abandoning all they have -- their official guidebook. As MD's they might be qualified to diagnose physiological symptoms that could affect behavior, but on what scientific basis could they diagnose mental disorders any better than a pastor, rabbi or wise older person?

Dobbs's review in Nature of Gary Greenberg's new book, The Book of Woe: The DSM and the Unmaking of Psychiatry, is the most devastating critique of psychiatry as a science. Dobbs writes under the headline: "Psychiatry: a very sad story." He notes that a century ago, psychiatrists considered "masturbatory insanity" and "wedding night psychosis" as mental illnesses. That those categories were dropped and new ones added in the interim suggests psychiatry lacks scientific footing, and instead evolves according to cultural norms. Yet the APA vigorously defends DSM-5, partly because it relies on sales for revenue. Greenberg writes about the sordid history of the DSM:

From the adventure in bookmaking-by-committee that followed, Greenberg builds a splendid and horrifying read. He digs up delicious dirt; extracts from the rivalrous main players a treasure chest of kvetching, backbiting, rebuttal, regret, sibling rivalry, Oedipal undercutting and just plain pithy talk. He relates gruesome sausage-making stories about the APA's tortured attempts to refashion rusty diagnoses or forge shiny new ones. (The aetiology of that new temper-dysregulation disorder? You'll throw a fit.)

Greenberg is not just an outsider. He participated in a clinical trial. "The process proved so convoluted that he wanted to apologize to one patient for the 'inadequacy, the pointlessness, the sheer idiocy of the exercise,'" Dobbs writes.

Psychiatrists are fallible members of the human race they're trying to diagnose. On Live Science, Tanya Lewis uncovered the "cutthroat side of science" -- how not a few scientists lie, cheat and steal to gain recognition. "In light of all these problems, science loses some of its luster," she said, excusing it because "scientists are humans, too."

In his book, Greenberg alleges that many psychiatric diagnoses are "constructs of convenience rather than descriptions of biological ailments." It only pretends to accomplish anything: the DSM "dresses up symptoms as diseases that are not real and then claims to have named and described the true varieties of our suffering." The APA has been more concerned about consistency and consensus than about truth.

A slippery deal, but essential. For by formalizing this scheme, psychiatry can claim medical legitimacy and accompanying insurance coverage and pay rates so that it can help people. Unfortunately, writes Greenberg, this scheme has led everyone, psychiatrists included, to talk about and treat DSM's conceptual constructs as if they are biological illnesses -- a habit that has bred troubles ranging from overconfidence to incestuous liaisons with Big Pharma.

All this talk of "scheming" sounds political, not scientific. Indeed, Dobbs points out that some practitioners feel it's time to start over. Yet here is a major field of "science" with important consequences for human beings. Some patients, trusting their psychiatrist, come to think they are "wired differently" and have a medical excuse for their behavior. Maybe psychiatry should just recognize variations in normal human behavior rather than categorize people as having biological dysfunctions. Who decided that a person grieving for more than two weeks over the loss of a loved one should be diagnosed with clinical depression?

Dobbs ends with an indictment of psychiatry as a (so far) failed science:

For more than 100 years, psychiatry has been getting by on pseudo-scientific explanations and confident nods while it waited for the day, always just around the corner, in which it could be a strictly biological undertaking. Part of the DSM-5's long delay occurred because, a decade ago, APA leaders actually thought that advances in neuroscience would allow them write a brain-based DSM. Yet, as former APA front liner Michael First, a psychiatrist at Columbia University in New York, confirms on Greenberg's last page, the discipline remains in its infancy.

Greenberg shows us vividly that psychiatry's biggest problem may be a stubborn reluctance to admit its immaturity. And we all know how things go when you won't admit your problems.

1. Long history of failure.
2. No theoretical basis grounded in biological reality.
3. Reliance on a book.
4. Conflicts of interest.
5. Lack of quality control.
6. Ignoring critics.
7. Focus on symptoms instead of causes.
8. Category errors: confusing arbitrary classification with reality.
9. Attempting to pigeonhole complex entities into simple categories.
10. Concern for consistency and consensus over empiricism.
11. Tortured attempts to fashion theories.
12. Formalizing schemes to gain legitimacy.
13. Promissory notes to do better in the future.
14. Hopes that other sciences will legitimize it.

Evolutionists would probably argue against our using #2, 4, and 5 as criticisms of neo-Darwinism, and would quibble about 3, 8, 11 and perhaps others. But Darwin skeptics could charge, and have charged, evolutionists with all these flaws. Let's briefly see if psychiatry's failures also apply to Darwinists:

1. Failure to explain the Cambrian Explosion since Darwin.
2. Extrapolating natural selection far beyond the evidence.
3. Continuing to exalt Darwin and his Origin.
4. Scheming to keep criticisms of Darwin out of journals and classrooms.
5. Flimsy assertions that "it evolved," with little rigor.
6. Refusing to hear or publish scientific critiques of Darwinism.
7. Use of homology as evidence and explanation for adaptation.
8. Inventing terms like "kin selection" and "evo-devo."
9. Attributing the whole biosphere to undirected causes.
10. Claiming the consensus accepts evolution in every meaning of the word.
11. Applying natural selection recklessly to everything, even the universe.
12. Scheming to prevent intelligent design from gaining a hearing.
13. Always saying "more research is needed."
14. Misappropriating genetics, computer science, and development to support it.

To the extent that these kinds of criticisms should debunk psychiatry as a science, they should also debunk Darwinism as science. Science is a noble word. Its standards should be high. Often, however, the word is applied too broadly; it stands for too little because it stands for too much. Having a degree in science, belonging to a scientific society, or getting one's ideas published in a journal are no guarantee you are "getting the world right" when it comes to describing entities as complex as human behavior or the biosphere.

If psychiatry doesn't survive its current crisis, it will demonstrate that an entrenched, respected field can collapse, even after over a century of trying to act like a science. We shouldn't think that Darwinism is impregnable. Many of the same criticisms apply. Darwinism's collapse will occur when insiders are no longer afraid to level the same long-standing criticisms that outsiders have lodged for decades. Keeping those critiques alive is key. A true science endures criticism. A pseudoscience ignores it or tries to squelch it. Darwinists should invite scrutiny, for as Darwin himself said, "A fair result can only be obtained by fully stating and balancing the facts and arguments on both sides of each question."

Image: Freud's couch, roberthuffstutter/Flickr.

After all, biologists should have the opportunity to air their views in a semi-private professional setting without "creationists" barging in and telling the unwashed masses that many scientists have already given up on the Darwinian paradigm and are seeking post-Darwinian alternatives. Even though it's true, still it's wrong to publicize the fact, thereby leading the common folk astray and confirming their prejudice in favor of seeing life and the universe as reflecting some purpose.

Of course in this, I'm optimistically assuming that the critics will read the book before attacking Steve Meyer, or at least read something informative about it. That was not the case with Dr. Meyer's previous book, Signature in the Cell, which was denounced by some biologists who had zero idea even what Meyer was arguing. If I'm right in my prediction, it will be interesting to keep in mind the parallel complaint against our Discovery Institute colleague Wesley J. Smith.

Parallel yet also intriguingly different. At his National Review Online blog Human Exceptionalism, Wesley writes about being "bitterly criticized" by bioethicist Udo Schüklenk, editor of the journal Bioethics ("Bioethics Hates the Light"). What does Schüklenk have against Wesley Smith? Wesley's offense is that, writing at the Daily Caller, he exposed another professional journal, the Journal of Medical Ethics, for publishing an article that advocated the permissibility of post-birth abortion. Yes, you read that right.

The authors, Alberto Giubilini and Francesca Minerva, suggested that it should be ethically defensible to kill babies if their mothers somehow missed the opportunity to abort them while still in the womb. Read the shocking abstract ("After-birth abortion: why should the baby live?"):

Abortion is largely accepted even for reasons that do not have anything to do with the fetus' health. By showing that (1) both fetuses and newborns do not have the same moral status as actual persons, (2) the fact that both are potential persons is morally irrelevant and (3) adoption is not always in the best interest of actual people, the authors argue that what we call 'after-birth abortion' (killing a newborn) should be permissible in all the cases where abortion is, including cases where the newborn is not disabled.

Now along comes Udo Schüklenk of Queen's University in Canada who harshly upbraids Smith for threatening "academic freedom" and putting "bioethics journals under siege." Dr. Schüklenk complains about Smith being an "employee" of the "creationist lobby group" Discovery Institute who publishes his articles "pretty much exclusively in religious outlets."

This is just one untruth after another, of course. As Smith points out, he is a Discovery Institute senior fellow, not an employee. DI isn't a "lobbying group," nor do we argue for or otherwise support "creationism." In fact, some creationists criticize intelligent design specifically for not being creationism. Well, they've got their facts straight on that point, unlike our fine ethics scholar Dr. Schüklenk. And Smith predominantly publishes in secular/non-religious outlets, including some academic and legal journals.

The key passage in Schüklenk's article is this:

Academic journals finding themselves under sustained attacks from lobby groups do find themselves in a difficult situation. While political activism is legitimate -- in fact, desirable -- it can become so intense and well-orchestrated that it begins to threaten academic freedom.

So the problem with exposing what goes on in academic journals is that if the enterprise becomes too "intense" or "well-orchestrated" -- that is, too successful in getting out the word -- then that crosses over into an illegitimate "threat" to "academic freedom." On the other hand, if it's sotto voce or otherwise limp, mute and inept, then I guess it's OK in the eyes of the bioethical community. Citizens may turn the pages of the Journal of Medical Ethics so long as -- when they see an article supporting the deliberate murder of healthy but unwanted babies -- they don't get all upset and start talking about it worriedly with lots of other people.

That's one way that in writing Darwin's Doubt, Stephen Meyer is likely to be found at fault: he blows the lid off the pact of silence and secrecy that has so far kept the evolution controversy among mainstream scientists themselves from gaining wider public awareness.

The difference between Smith's expose and Meyer's is that Smith probably will not draw down fire on the academics whose work he rightly condemns -- fire, I mean, from their ethicist colleagues. In fact, his condemnation likely wins them esteem in their own professional circles -- even as, thank goodness, it may put off the day when such evil ideas are put into practice in the United States.

Stephen Meyer, on the other hand, is casting light on a previously hidden discussion not to condemn but in praise of innovative, forward-thinking scientists who are groping their way forward toward truths we've been advocating for years: not intelligent design but the recognition that Darwinism doesn't explain the enigma of life's evolution; something else is going on.

Dr. Meyer does this, I know, with full awareness that not only will it win him condemnation from the Darwin enforcers. But so too, advocates of post-Darwinian views in the science world will draw fire from their own professional circles for "giving aid and comfort to creationist enemies of science." Which of course is what they're already saying about maverick atheist philosopher Thomas Nagel. If it's any comfort, at least, Dr. Nagel doesn't seem to have sustained any real injuries from that assault.

Models are useful in science. They've been used since Victorian times. William Thomson (Lord Kelvin) said that unless he can build a model of something he can't really understand it. The models of 19th- and 20th-century scientists have usually been testable against the real world. Observation provides important tethers to models, so that they don't fly off into fairyland.

Where, though, are the connections to reality in a paper by Isaac Salazar-Ciudad and Miquel Marín-Riera, published in Nature? One will look in vain for any mention of fossils, mammals, arthropods, or any other animal. The nearest natural thing they discuss is a tooth -- but even that is an idealized, virtual tooth in their dreamed up world of visions and simulations.

The University of Barcelona describes their approach: "3D simulation shows how form of complex organs evolves by natural selection." Notice that they call theirs the first simulation of its kind:

Researchers at the Institute of Biotechnology at the Helsinki University and the UAB have developed the first three-dimensional simulation of the evolution of morphology by integrating the mechanisms of genetic regulation that take place during embryo development. The study, published in Nature, highlights the real complexity of the genetic interactions that lead to adult organisms' phenotypes (physical forms), helps to explain how natural selection influences body form and leads towards much more realistic virtual experiments on evolution. (Emphasis added.)

Keep in mind that the Darwinian evolutionists' burden is to demonstrate that natural selection actually produced novel, innovative structures, the classic examples being an eye or a wing. It's not convincing to look at existing eyes or wings and simply assert that they evolved by unguided processes. Nor is it convincing to look at existing genes and make that assertion. Skeptics of neo-Darwinism will suggest other explanations for the observations, such as genetic drift or intelligent design.

Salazar and Marin-Riera seem to know this. That's why they make a glaring admission in explaining why they couldn't be realistic, but had to go virtual:

"Right now we have a lot of information on what changes in what genes cause what changes in form. But all this is merely descriptive. The issue is to understand the biological logic that determines which changes in form come from which changes in genes and how this can change the body", explains Isaac Salazar, a researcher at the University of Helsinki and in the Department of Genetics and Microbiology of the UAB, and lead author of the article. In nature this is determined by embryo development, during the life of each organism, and by evolution through natural selection, for each population and species.

But in the field of evolution of organisms it is practically impossible to set up experiments, given the long timescale these phenomena operate on. This means that there are still open debates, with hypotheses that are hard to prove experimentally. This difficulty is compensated for by the use of theoretical models to integrate in detail the existing experimental data, thus creating a virtual simulation of evolution.

Even so, it's astonishing to read on and find out that with all the freedom in their imaginary world, they still couldn't get natural selection to accomplish much. We are offered three "visions" of evolution (an instructive choice of words). The first "vision" was that any change was adaptive. That one got shot down, leaving two others with little for natural selection to do:

This simulation enables a comparison of the different hypotheses in the field of evolution regarding which aspects of morphology evolve most easily. The first vision is that all metric aspects of form contribute to adaptation and that, consequently, all are fine-tuned by evolution over time. The second vision is that some aspects of form have greater adaptive value and that the remainder evolve collaterally from changes in these. The third is that no aspect of form is intrinsically more important, but what is important adaptively is a complex measurement of the form's roughness.

"What we have found is that the first hypothesis is not possible and that the second is possible in some cases. Even if ecology favoured this type of selection (the first vision), embryo development and the relationship between genetic and morphological variation imposed by this is too complex for every aspect of morphology to have been fine-tuned. In one way, what we are seeing is that natural selection is constantly modelling body forms, but these are still a long way from perfection in many ways", points out Salazar.

By "roughness," they are referring to another theoretical construct in evolutionism, the "fitness landscape" imagined by Sewall Wright. The fitness landscape has peaks and valleys. An organism might attain a local optimum fitness but get stuck there, with no way to climb to a higher peak without having to decrease its fitness first. Interesting as the fitness landscape concept is, it's incidental. What matters is that Salazar's entire evolutionary model is adrift in virtual space -- and even there, natural selection doesn't do much.

Remember, this was not some backwoods thought experiment, but was published in the leading science journal in the world, Nature. And it got good press. In the same issue of Nature, P. David Polly gives his perspective on the paper, under the headline, "Evolution: Stuck between the teeth." Here's the upshot:

A computer model of tooth evolution designed to assess the impact of developmental dynamics on natural selection reveals that complexity reduces the likelihood of maximum fitness being attained.

Polly's digression into real teeth doesn't help, therefore, because he admits that "the authors created artificial populations of developing teeth that they subjected to mutation and selection." It's all simulation that cannot be tested in the real world. Remember? It takes too long.

When we see what the authors did, we have to sigh: "There you go again." They snuck information into their evolutionary algorithm. That's the only way they could get evolution to (at least partially) work. Look at all the free parameters in their arbitrary scheme:

Fitness was assigned to each individual on the basis of either its phenotypic or its functional similarity to an arbitrarily chosen target phenotype. The latter can be thought of as the phenotype that conveys the greatest fitness in the ecological context of the simulation -- a peak on the adaptive landscape, as described by the geneticist Sewall Wright. The fittest individuals were then selected as the parents of the next generation and the simulation was repeated.

Salazar-Ciudad and Marín-Riera have shown that not only are suboptimal dead ends an evolutionary possibility, but they are also exceedingly likely to occur in real, developmentally complex structures when fitness is determined by the exact form of the phenotype.

However, the authors also found that when fitness was determined by functional properties instead of the phenotype itself, the adaptive peak was usually reached. This is because many different phenotypes can have the same functional properties -- a herbivorous mammal, for example, simply needs grinding and chewing surfaces on its teeth, regardless of how the surfaces are constructed. Thus, there are many more paths to a functional adaptive peak than to a phenotypic one, especially for a phenotype that has a complex developmental system, such as a tooth.

Polly is impressed by the work, but ends with a series of questions that reveal the Darwinian mechanism as a series of promissory notes with no deadlines. Pay special notice to his reference to "knowledge gaps":

The authors' results highlight interesting questions. If phenotypic evolution is likely to get stuck on suboptimal adaptive peaks, what happens to the evolving populations? Do they simply persist in a suboptimal state? Do their ecological relationships change to fit their phenotype, thereby creating new adaptive peaks? Or do they become extinct as they are out-competed by populations that can reach a more optimal phenotype? Salazar-Ciudad and Marín-Riera's focus on teeth -- which can be studied empirically in living populations, among distantly related clades and in the fossil record -- offers considerable potential for testing their evolutionary predictions and closing the knowledge gaps between genetics, development and macroevolution.

Image: Fairies Looking Through a Gothic Arch, John Anster Fitzgerald/Wikicommons.

Ball hits the nail on the head when it comes to one of the difficulties in having a reasoned discussion on dearly held theories:

Why this apparent reluctance to acknowledge the complexity? One roadblock may be sentimentality. Biology is so complicated that it may be deeply painful for some to relinquish the promise of an elegant core mechanism. In cosmology, a single, shattering fact (the Universe's accelerating expansion) cleanly rewrote the narrative. But in molecular evolution, old arguments, for instance about the importance of natural selection and random drift in driving genetic change, are now colliding with questions about non-coding RNA, epigenetics and genomic network theory. It is not yet clear which new story to tell...When the structure of DNA was first deduced, it seemed to supply the final part of a beautiful puzzle, the solution for which began with Charles Darwin and Gregor Mendel. The simplicity of that picture has proved too alluring.

Another aspect of human nature is that we are competitive (which Darwinists readily acknowledge), so conceding that the other side may have a point is, for most of us, a hard pill to swallow. We've found again and again that defenders of Darwinian theory typically have a difficult time even accurately characterizing what the theory of intelligent design says, much less giving proper credit to the strength of its challenge. That's how deep the competitive impulse goes.

For years, ID proponents have been writing and reporting on research that seems to fly in the face of neo-Darwinian theory. Scientists at Biologic Institute have conducted research demonstrating problems with current theories on enzyme evolution. ID theorists have published books on the extent and limits of evolutionary processes on things like drug resistance of malaria-carrying mosquitoes. They have written books on the explanatory inadequacy of current chemical evolution theories, and books discussing the fine-tuning of the universe.

Even if one does not care for the idea of design detection in nature, these works as well as the research reported here at ENV raise important questions for evolutionary theory. When a theory leads, as Darwinism does, to mistaken conclusions about the non-coding regions of DNA, or oversimplifies genetics to the point that epigenetic factors have been largely ignored, then that theory may need, at the very least, to be modified if not scrapped and replaced by a better explanation.

Originally, in sitting down to write this, we planned to report on yet another finding of the complexity of DNA, specifically relating to the number of proteins involved in the replication process. Replication is a key precondition for natural selection to operate, yet studies show that even replication requires multiple proteins operating in a complex, intricate process that is too highly integrated to be explicable by the current Darwinian narrative.

And while this is an interesting paper, and worth reading (see here) -- perhaps we'll have more to say on it later -- Philip Ball's commentary provides the even more interesting and important philosophical background to why we were going to report on that paper in the first place.

My challenge to you? I'm curious to hear how, using these same 1000 words (here), you would briefly summarize the idea of intelligent design. Or better yet, the whole Intelligent Design versus Darwinism debate. For instance:

"Someone, a mind long ago, decided there would be different types of animals that would change over time."

"No, we're here because of chance. Animals just happened. I hate you!"

And unlike me in the example above, be fair to both sides! Let me know what you come up with.