evolutionnewsandviews--2020-05-20--Collateral Damage: Mutations Decrease Fitness in More Ways than One

To improve a sophisticated machine , fire at it with a rifle , blindfolded .
Is that the way to improve the machine ?
Darwinians have no other tool than rifling through random mutations in hopes of adding new functional information to the genomes of living things , making slow progress up Mount Improbable .
But natural selection can only select what random mutations give .
Having sworn off intelligent causes , Darwinians must rely on random mutations to get from the first molecular replicator to the human brain .
A new study gives them bad news and worse news @ @ @ @ @ @ @ deleterious , but many mutations are expected to be neutral , and a few might be beneficial .
A simplistic view of neo-Darwinism focuses on one gene or protein at a time .
The rare beneficial mutation might help a particular gene or protein improve its function , and therefore increase the organism ’ s fitness .
A more realistic view of mutations needs to consider possible unintended consequences : the “ collateral damage ” that can result from an otherwise beneficial mutation .
That ’ s what a group of ten biomolecular @ @ @ @ @ @ @ , set out to investigate .
Led by Jacob D. Mehlhoff , the team published results of their study on “ Collateral fitness effects of mutations.
” Their paper in PNAS begins with an affirmation of Darwin dogma : “ Mutations provide the source of genetic variability upon which evolution acts.
” From there , it ’ s all downhill for Darwin .
The six collateral fitness effects they found were all bad .
In fact , one can look in vain for any evidence of a raw beneficial mutation that did not @ @ @ @ @ @ @ mention of innovation .
There is no mention of novel function .
There is no mention of new information .
In all of the 230 mentions of “ fitness ” in the paper , there is not one clear-cut example of an improvement in fitness — the kind of progress that a Darwinian must hope for to believe in universal molecules-to-man evolution .
The team focused on a version of beta lactamase in E. coli as a prototype for understanding the collateral effects of mutations .
That ’ s part of the bad @ @ @ @ @ @ @ in a protein not only damages the protein , it just as often causes collateral damage somewhere else .
Design advocates understand this ; in car engines , a broken part of an engine is likely to lead to other collateral damage , such as overheating or loss of steering control .
Why would anyone think that a complex cell will perform better when a part goes “ missense ” — meaning its sequence no longer allows it to fold and function ?
The phrase “ may play a role in constraining protein @ @ @ @ @ @ @ collateral damage stops protein evolution in its tracks.
” Stepping on the brakes is a constraint , all right .
How is a hopeful Darwinian going to get a brain for E. coli by slamming on the brakes every time a cosmic ray hits a gene ?
Notice that the collateral damage “ particularly ” affects the very proteins that the hopeful Darwinian needs to evolve the most : ( 1 ) the ones that are highly expressed , ( 2 ) the ones that are under selection for their function , and @ @ @ @ @ @ @ ( “ buffered against deleterious effects on protein activity and protein abundance ” ) .
These are the very proteins that are particularly constrained by the collateral fitness effects of mutations .
A faithful Darwinian might take refuge in exaptation theory : the idea that some idle sequences of amino acids are silently waiting in the wings for their chance in the limelight .
Maybe a duplicated gene or divided gene could take advantage of neo-functionalization or sub-functionalization .
Maybe a pseudogene could come back to life ( but see our article on @ @ @ @ @ @ @ good .
The moment the bench player gets up to bat and becomes “ highly expressed ” or under selection , it also gets in the line of fire for collateral fitness effects when the next mutation comes along .
To keep spirits high , maybe stating more Darwin dogma can help .
Translated , this says , “ We ’ re clueless about one of the most important concepts in evolutionary biology.
” That ’ s odd .
Wasn ’ t Darwin ’ s great achievement the discovery of a “ mechanism @ @ @ @ @ @ @ 169 years later , they can ’ t even measure it ?
Think about this a moment ; if “ fitness ” ( whatever that is ) is measured by fecundity , does that mean that pandas and rhinos are unfit ?
If fitness is measured , on the other hand , by “ survivorship , ” how is that not circular ?
The fit survived because they are fit .
The survivors are fit because they survived .
Measurements based on fecundity and survivorship may indeed be “ very useful for evolutionary @ @ @ @ @ @ @ us little about the underlying mechanisms ” of evolution .
It ’ s hard to find any good news in this paper for doctrinaire Darwinians .
All the fitness ( whatever that is ) goes downward .
In the Discussion , the authors say , Then they list , for the third time , the six kinds of collateral damage they actually witnessed when they tinkered with the sequence of one protein in one bacterium .
There ’ s another important conclusion in this paper .
A molecular biologist can not just study @ @ @ @ @ @ @ see if it folds or not , or has any function at all .
He or she must study it in the context of the cell or organism in which it is embedded in real life .
All damage is bad : This holds out one last hope : compensation .
But do they describe any real-world examples of damage “ offset by beneficial primary fitness effects ” ?
Do they describe any damage compensated by another mutation ?
Guess .
Answer : no .
They just hope that in some other mythical @ @ @ @ @ @ @ .
Maybe in some molecular Eden , the gene will come under positive selection , and human brains will be one step closer .
Or maybe it will just stop having the bad effect ( i.e.
, go neutral ) .
Keep the faith .
Evolutionists keep hoping for the mythical “ evolutionary advantage ” that can make brains from bacteria , but real-world observations continue to disappoint .
The bad news is that beneficial mutations are rare .
The worse news is that they are usually accompanied by collateral damage .
The @ @ @ @ @ @ @ is under selective constraint both to maintain function and to avoid collateral negative effects.
” Advocates of intelligent design do not expect random mutations to do any good .
Instead , they perceive evidence of foresight that prepared cells and organisms for the inevitable harm of mutations , and gave them the tools to repair the damage .

To improve a sophisticated machine, fire at it with a rifle, blindfolded. Is that the way to improve the machine? Darwinians have no other tool than rifling through random mutations in hopes of adding new functional information to the genomes of living things, making slow progress up Mount Improbable. But natural selection can only select what random mutations give. Having sworn off intelligent causes, Darwinians must rely on random mutations to get from the first molecular replicator to the human brain. A new study gives them bad news and worse news.
Bad and Worse
Evolutionists know that mutations can be deleterious, but many mutations are expected to be neutral, and a few might be beneficial. A simplistic view of neo-Darwinism focuses on one gene or protein at a time. The rare beneficial mutation might help a particular gene or protein improve its function, and therefore increase the organism’s fitness. A more realistic view of mutations needs to consider possible unintended consequences: the “collateral damage” that can result from an otherwise beneficial mutation.
That’s what a group of ten biomolecular engineers, primarily from Johns Hopkins University, set out to investigate. Led by Jacob D. Mehlhoff, the team published results of their study on “Collateral fitness effects of mutations.” Their paper in PNAS begins with an affirmation of Darwin dogma: “Mutations provide the source of genetic variability upon which evolution acts.” From there, it’s all downhill for Darwin.
Deleterious protein mutations are commonly thought of in terms of how they compromise the protein’s ability to perform its physiological function. However, mutations might also be deleterious if they cause negative effects on one of the countless other cellular processes. The frequency and magnitude of such collateral fitness effects are unknown. Our systematic study of mutations in a bacterial protein finds widespread collateral fitness effects that were associated with protein aggregation, improper protein processing, incomplete protein transport across membranes, incorrect disulfide-bond formation, induction of stress-response pathways, and unexpected changes in cell properties. [Emphasis added.]
The six collateral fitness effects they found were all bad. In fact, one can look in vain for any evidence of a raw beneficial mutation that did not cause collateral damage. There is no mention of innovation. There is no mention of novel function. There is no mention of new information. In all of the 230 mentions of “fitness” in the paper, there is not one clear-cut example of an improvement in fitness — the kind of progress that a Darwinian must hope for to believe in universal molecules-to-man evolution.
The team focused on a version of beta lactamase in E. coli as a prototype for understanding the collateral effects of mutations.
The distribution of fitness effects of mutation plays a central role in constraining protein evolution. The underlying mechanisms by which mutations lead to fitness effects are typically attributed to changes in protein specific activity or abundance. Here, we reveal the importance of a mutation’s collateral fitness effects, which we define as effects that do not derive from changes in the protein’s ability to perform its physiological function. We comprehensively measured the collateral fitness effects of missense mutations in the Escherichia coli TEM-1 β-lactamase antibiotic resistance gene using growth competition experiments in the absence of antibiotic. At least 42% of missense mutations in TEM-1 were deleterious, indicating that for some proteins collateral fitness effects occur as frequently as effects on protein activity and abundance.
That’s part of the bad news; a “missense mutation” in a protein not only damages the protein, it just as often causes collateral damage somewhere else. Design advocates understand this; in car engines, a broken part of an engine is likely to lead to other collateral damage, such as overheating or loss of steering control. Why would anyone think that a complex cell will perform better when a part goes “missense” — meaning its sequence no longer allows it to fold and function?
Why Are Darwinians Surprised?
The surprising prevalence of deleterious collateral fitness effects suggests they may play a role in constraining protein evolution, particularly for highly expressed proteins, for proteins under intermittent selection for their physiological function, and for proteins whose contribution to fitness is buffered against deleterious effects on protein activity and protein abundance.
The phrase “may play a role in constraining protein evolution” is jargon for, “collateral damage stops protein evolution in its tracks.” Stepping on the brakes is a constraint, all right. How is a hopeful Darwinian going to get a brain for E. coli by slamming on the brakes every time a cosmic ray hits a gene?
Notice that the collateral damage “particularly” affects the very proteins that the hopeful Darwinian needs to evolve the most: (1) the ones that are highly expressed, (2) the ones that are under selection for their function, and (3) the ones with armor (“buffered against deleterious effects on protein activity and protein abundance”). These are the very proteins that are particularly constrained by the collateral fitness effects of mutations.
A faithful Darwinian might take refuge in exaptation theory: the idea that some idle sequences of amino acids are silently waiting in the wings for their chance in the limelight. Maybe a duplicated gene or divided gene could take advantage of neo-functionalization or sub-functionalization. Maybe a pseudogene could come back to life (but see our article on pseudogenes). It’s no good. The moment the bench player gets up to bat and becomes “highly expressed” or under selection, it also gets in the line of fire for collateral fitness effects when the next mutation comes along.
To keep spirits high, maybe stating more Darwin dogma can help.
Fitness is one of the most important concepts in evolutionary biology. Despite its importance, fitness can be difficult to measure because it is a combination of many traits that interact in complex ways. Accordingly, researchers generally estimate fitness using fitness components — traits like fecundity and survivorship that are thought to be the result of the most important traits affecting fitness. Although these estimates have been very useful for evolutionary research, they tell us little about the underlying mechanisms of these fitness components.
Translated, this says, “We’re clueless about one of the most important concepts in evolutionary biology.” That’s odd. Wasn’t Darwin’s great achievement the discovery of a “mechanism” for evolution? And now, 169 years later, they can’t even measure it? Think about this a moment; if “fitness” (whatever that is) is measured by fecundity, does that mean that pandas and rhinos are unfit? If fitness is measured, on the other hand, by “survivorship,” how is that not circular? The fit survived because they are fit. The survivors are fit because they survived. Measurements based on fecundity and survivorship may indeed be “very useful for evolutionary research,” but “they tell us little about the underlying mechanisms” of evolution.
No Good News Here
It’s hard to find any good news in this paper for doctrinaire Darwinians. All the fitness (whatever that is) goes downward. In the Discussion, the authors say,
Our results caution against using measures of protein properties as a proxy for biological fitness or employing a nonnative context in DMS [deep mutational scanning] experiments, as the former risks underestimating the fraction of mutations that are deleterious in their native context and the latter risks reporting on nonbiologically relevant collateral fitness effects.
Then they list, for the third time, the six kinds of collateral damage they actually witnessed when they tinkered with the sequence of one protein in one bacterium.
There’s another important conclusion in this paper. A molecular biologist cannot just study an isolated protein in a dish to see if it folds or not, or has any function at all. He or she must study it in the context of the cell or organism in which it is embedded in real life. All damage is bad:
In terms of a mutation’s impact on protein evolution, the cause of the deleterious effects is irrelevant. Collateral fitness costs arise from the mutation’s impact on some cellular process(es) that in turn causes a fitness decrease. These costs will constrain protein evolution, provided they are not offset by beneficial primary fitness effects or mitigated by a second, compensatory mutation that alleviates the effect or lowers expression level.
This holds out one last hope: compensation. But do they describe any real-world examples of damage “offset by beneficial primary fitness effects”? Do they describe any damage compensated by another mutation? Guess. Answer: no. They just hope that in some other mythical environment that damage will work out better. Maybe in some molecular Eden, the gene will come under positive selection, and human brains will be one step closer. Or maybe it will just stop having the bad effect (i.e., go neutral). Keep the faith.
However, it is the fitness across all environments an organism experiences that will govern the gene’s evolution. When the gene comes back under selection, such silenced alleles will be rapidly purged because they are not functional. Environment-dependent regulation of gene expression could alleviate this issue; thus, collateral fitness effects might provide an evolutionary advantage for the evolution of gene expression regulation.
Evolutionists keep hoping for the mythical “evolutionary advantage” that can make brains from bacteria, but real-world observations continue to disappoint.
Nature Fights Mutations
The bad news is that beneficial mutations are rare. The worse news is that they are usually accompanied by collateral damage. The authors know that “protein sequence evolution is under selective constraint both to maintain function and to avoid collateral negative effects.” Advocates of intelligent design do not expect random mutations to do any good. Instead, they perceive evidence of foresight that prepared cells and organisms for the inevitable harm of mutations, and gave them the tools to repair the damage.
Photo: A train wreck, 1895, Montparnasse Station, Paris, via Wikimedia Commons.


evolutionnewsandviews--2020-05-21--Thanks to the Sacrifices of Many, There’s Talk of Censoring Us

Your support for the Center for Science & Culture has allowed us to reach an enormous audience .
Now , because of our impact , the censors have turned their gaze on Evolution News .
An article in the journal BioEssays demands Internet censorship of sources sharing evidence of design in biology .
The author of the article says that if Big Tech entities ( Google , Facebook ) shy away from prejudicial treatment of ID , then the government should step in and “ Make them.
” ID scientists , from their personal experience , would have told you @ @ @ @ @ @ @ .
The upcoming Memorial Day weekend is a time for reflection about sacrifice .
While heroes of the U.S. Armed Forces have given their lives , the scholars who critique scientific atheism and advance the theory of ID offer of themselves in different ways .
They risk destruction of careers and reputations .
Please take a moment to consider them in your prayers , and in your own giving .
I ’ m thinking of colleagues and friends who left perches in academia , or were thrown out for heresy : Stephen Meyer @ @ @ @ @ @ @ John West , Günter Bechly , Richard Sternberg , and more .
Others miraculously survive in their universities , despite the curses and arrows directed at them : David Gelernter at Yale , Michael Behe at Lehigh , Michael Egnor at Stony Brook .
They all would have been prudent to stay safe , masked and sheltering in place .
Or better yet , go along with the Darwinist mob !
That ’ s a great way to get ahead .
Think of the ominous transformation we see today : many people now @ @ @ @ @ @ @ as controversial and divisive !
Please help us by contributing to Discovery Institute ’ s Center for Science & Culture today .
I ’ m grateful to be part of this enterprise that brings the thought of Darwin skeptics and ID scientists to millions .
We do so through websites like Evolution News , which I edit , on YouTube , in live presentations and video conferences , books , journals , and other publications .
Our culture trembles between recognizing and denying the purpose and meaning behind life .
Meanwhile , electronic @ @ @ @ @ @ @ It ’ s a sickness , and good science , widely publicized , is the cure .
Your generous gift now will help deliver that cure .
Your donation of $ 50 , $ 500 , or $ 5,000 — whatever you can afford at this very difficult time for us all — is crucial .
Thank you !
Photo : Stephen Meyer , David Gelernter , and David Berlinski , “ Uncommon Knowledge with Peter Robinson , ” via Hoover Institution , Stanford University ( screen shot ) .

Your support for the Center for Science & Culture has allowed us to reach an enormous audience. Now, because of our impact, the censors have turned their gaze on Evolution News.
An article in the journal BioEssays demands Internet censorship of sources sharing evidence of design in biology. The author of the article says that if Big Tech entities (Google, Facebook) shy away from prejudicial treatment of ID, then the government should step in and “Make them.”
ID scientists, from their personal experience, would have told you it was only a matter of time. The upcoming Memorial Day weekend is a time for reflection about sacrifice. While heroes of the U.S. Armed Forces have given their lives, the scholars who critique scientific atheism and advance the theory of ID offer of themselves in different ways. They risk destruction of careers and reputations.
Your Prayers, Please
Please take a moment to consider them in your prayers, and in your own giving.
I’m thinking of colleagues and friends who left perches in academia, or were thrown out for heresy: Stephen Meyer, Douglas Axe, Ann Gauger, John West, Günter Bechly, Richard Sternberg, and more. Others miraculously survive in their universities, despite the curses and arrows directed at them: David Gelernter at Yale, Michael Behe at Lehigh, Michael Egnor at Stony Brook.
Stay Safe…Or Join the Mob?
They all would have been prudent to stay safe, masked and sheltering in place. Or better yet, go along with the Darwinist mob! That’s a great way to get ahead.
Think of the ominous transformation we see today: many people now consider supporting the right to free speech as controversial and divisive! Please help us by contributing to Discovery Institute’s Center for Science & Culture today.
I’m grateful to be part of this enterprise that brings the thought of Darwin skeptics and ID scientists to millions. We do so through websites like Evolution News, which I edit, on YouTube, in live presentations and video conferences, books, journals, and other publications.
Our culture trembles between recognizing and denying the purpose and meaning behind life. Meanwhile, electronic media pump out propaganda for nihilism. It’s a sickness, and good science, widely publicized, is the cure.
Your generous gift now will help deliver that cure. Your donation of $50, $500, or $5,000 — whatever you can afford at this very difficult time for us all — is crucial. Thank you!
Photo: Stephen Meyer, David Gelernter, and David Berlinski, “Uncommon Knowledge with Peter Robinson,” via Hoover Institution, Stanford University (screen shot).


evolutionnewsandviews--2020-05-21--On Intelligent Design, an Italian Philosophy Journal Takes a Step in the Right Direction

Philosophers are making some important and interesting contributions to the conversation about biological origins .
Earlier today we saw that philosopher Subrena E. Smith registered a harsh critique of evolutionary psychology in the journal Biological Theory , even saying that evo psych explanations are “ impossible.
” Now , a new paper in the Italian philosophy journal Humana Mente , “ Residuals of Intelligent Design in Contemporary Theories about Language Nature and Origins , ” observes that the arguments of intelligent design proponents are applicable to many explanations of the origins of language .
The authors are cognitive scientists at @ @ @ @ @ @ @ the English translation isn ’ t always easy to follow and some of their ideas about ID are both dated and heavily critical , the openness to taking ID seriously is clear .
They correctly quote Phillip Johnson noting that ID isn ’ t based upon the Bible : “ the first thing that has to be done is to get the Bible out of the discussion , ” and even rightly observe that “ Natural selection is the actual target ” of ID , quoting ID theorists Angus Menuge and Michael Behe @ @ @ @ @ @ @ that ID is potentially compatible with common ancestry , noting that under ID “ evolution can reveal itself as a sequence of related species , but never as a casual variation of structures that come in succession across a selective ecological modeling.
” What you just saw is something rare : scholars recognizing in a mainstream academic journal that ID is not based upon biblical arguments , is compatible with common descent , but takes issue with the causal power of natural selection .
So , Are They Pro-ID ?
Don ’ t @ @ @ @ @ @ @ are pro-ID .
They are not .
The article is peppered with gratuitous rhetorical jabs at ID in which they show their bona fides to fellow academic materialists .
Indeed , their primary information about ID comes from a highly inaccurate and outdated polemic against ID published back in 2004 .
Their ideas are so outdated that they cite “ Discovery Institute ’ s Center for the Renewal of Science and Culture , ” a name we haven ’ t used in over 15 years !
They quote ID proponents such as Michael @ @ @ @ @ @ @ , Phillip Johnson , William Dembski , and Jonathan Wells — calling them “ new gladiators , ” apparently unaware that Johnson passed away last year , some 15 years after their primary source on ID was written .
They use all kinds of outlandish rhetoric , including calling ID “ second generation creationism , ” a “ more sophisticated and dangerous ‘ theistic science ’ tradition , ” and “ a vehicle of philosophical infection , an insidious vehicle because it seems reasonable and moderate.
” In a passage that has to @ @ @ @ @ @ @ How the Hell , Indeed There ’ s no need to for their mystification about the cause behind ID .
Since as human beings we have extensive observations of intelligent agents designing things , we can readily recognize the effects of intelligent agency in the natural world .
Thus , intelligent design is detectible by science , and while it may not have a “ naturalistic mechanism ” it certainly provides a scientifically acceptable cause : intelligence .
You might even call it a “ mechanism ” ( although definitely not one in @ @ @ @ @ @ @ the point of the article is less to attack ID than it is to attack their fellow evolutionists who propose non-direct evolutionary pathways .
They do this , ironically , by claiming that such evolutionists are falling into some traps of ID .
To make this argument , they first note that ID strongly criticizes direct evolutionary pathways : From this point of view two decisive points of evolutionary analysis are brought into question : the first one is that the origin of language has to be obligatorily connected to functions directly linked @ @ @ @ @ @ @ is that , from the point of view of adaptive selection , the functional components acquired with language development might not be considered , or revealed , as an evolutionary advantage ( on the contrary , they even could show themselves as counter-evolutionary features ) .
This second point raised up by Dembski seems to challenge the central mechanism of evolutionary reconstructions .
According to Darwinian dictate , indeed , also the most complex organism derives from “ numerous , successive , and slight mutations ” of their own morphologic structures .
The @ @ @ @ @ @ @ internal laws that rule them , is called by ID supporters a « direct Darwinian pathway » ( Dembski & Well , 2008 , p. 151 ) .
They believe that language is amenable to such direct evolutionary pathways : They then take aim at those who use non-direct explanations to account for human language — oddly linking this somehow to a flaw in ID : They then delve into the debate about the best way to explain the evolutionary origin of language .
Here ’ s their view : We prefer to @ @ @ @ @ @ @ , note that some theorists are deeply skeptical that the origin of human language is amenable to a detailed evolutionary explanation , appealing to adaptive benefits alone .
For example : In a very real sense , the two principal peculiarities of human language are an evolutionary embarrassment .
It is not easy to picture the scenarios that would confer selective fitness on , specifically , syntactic classes and structure-dependent rules .
While linguists advise us that these are formal properties without which human language can not be modeled , it is not @ @ @ @ @ @ @ language are served specifically by these formal properties .
Perhaps recursiveness is such a property ; it may depend on syntactic classes .
Let us pretend that it does : I , at least , do not see how to realize recursiveness without syntactic classes .
These classes afford the kind of abstract representation in which the rewrite rules , needed for recursiveness , can be easily realized .
But if this is correct , even in the weak sense that syntactic classes provide an economical or simple access to recursiveness , the @ @ @ @ @ @ @ no less an evolutionary embarrassment .
I challenge the reader to reconstruct the scenario that would confer selective fitness on recursiveness .
Language evolved , it is conjectured , at a time when humans or protohumans were hunting mastodons .
Having language would be a benefit to them .
They could do social planning , discuss strategies together , lay plans for specific contingencies .
Now the alleged advantage of recursiveness is not simply unlimited sentences , but even more perhaps , the compacting of information .
Would it be a great advantage @ @ @ @ @ @ @ alongside the embers , to be able to remark : “ Beware of the short beast whose front hoof Bob cracked when , having forgotten his own spear back at camp , he got in a glancing blow with the dull spear he borrowed from Jack ” ?
Human language is an embarrassment for evolutionary theory because it is vastly more powerful than one can account for in terms of selective fitness .
It ’ s difficult to know how to make sense of all of it .
These philosophers take ID seriously @ @ @ @ @ @ @ relevant arguments accurately .
Yet they heavily criticize design theory , with trite and easily answered low-brow objections .
One of the main points on which they take ID seriously seems to be a misapplication of ID ideas : they critically compare invoking the arguments of ID theorists to linguists who adopt non-direct evolutionary explanations for the origin of human language .
Of course ID proponents are some of the most vocal critics of those who promulgate indirect evolutionary explanations .
Why ?
Because such explanations are weak , difficult to test , @ @ @ @ @ @ @ evolutionary explanations almost sound teleological .
Again , the English translation of this paper is rough .
Perhaps the article rejects indirect evolutionary pathways because those pathways seem too goal-directed .
Perhaps the authors intuit that material causes don ’ t work very well to guide an evolutionary pathway toward a specific , complex endpoint .
If this is the way they see things , then they ’ re exactly right .
But then what they don ’ t appreciate is that there is a cause that can operate with an end-goal in @ @ @ @ @ @ @ highly complex function .
In the words of Stephen Meyer : “ The answer is : intelligence .
Conscious activity .
The deliberate choice of a rational agent.
” Photo : Socrates , a bust displayed in the Vatican Museum , via Wikimedia Commons .

Philosophers are making some important and interesting contributions to the conversation about biological origins. Earlier today we saw that philosopher Subrena E. Smith registered a harsh critique of evolutionary psychology in the journal Biological Theory, even saying that evo psych explanations are “impossible.” Now, a new paper in the Italian philosophy journal Humana Mente, “Residuals of Intelligent Design in Contemporary Theories about Language Nature and Origins,” observes that the arguments of intelligent design proponents are applicable to many explanations of the origins of language. The authors are cognitive scientists at the University of Messina, and although the English translation isn’t always easy to follow and some of their ideas about ID are both dated and heavily critical, the openness to taking ID seriously is clear.
First, the authors semi-accurately describe ID arguments, noting:
ID’s current and general criticism — not only to evolutionism but also to biological science — is not that complex phenomena can’t be explained without the participation of a creator God, but rather that they can’t be entirely solved inside a radically monistic theory. In other words, they can’t be exposed to a naturalistic reduction…
They correctly quote Phillip Johnson noting that ID isn’t based upon the Bible: “the first thing that has to be done is to get the Bible out of the discussion,” and even rightly observe that “Natural selection is the actual target” of ID, quoting ID theorists Angus Menuge and Michael Behe to this effect. They even recognize that ID is potentially compatible with common ancestry, noting that under ID “evolution can reveal itself as a sequence of related species, but never as a casual variation of structures that come in succession across a selective ecological modeling.” What you just saw is something rare: scholars recognizing in a mainstream academic journal that ID is not based upon biblical arguments, is compatible with common descent, but takes issue with the causal power of natural selection.
So, Are They Pro-ID?
Don’t take this to mean that the authors are pro-ID. They are not. The article is peppered with gratuitous rhetorical jabs at ID in which they show their bona fides to fellow academic materialists. Indeed, their primary information about ID comes from a highly inaccurate and outdated polemic against ID published back in 2004. Their ideas are so outdated that they cite “Discovery Institute’s Center for the Renewal of Science and Culture,” a name we haven’t used in over 15 years! They quote ID proponents such as Michael Behe, Angus Menuge, Michael Behe, Phillip Johnson, William Dembski, and Jonathan Wells — calling them “new gladiators,” apparently unaware that Johnson passed away last year, some 15 years after their primary source on ID was written. They use all kinds of outlandish rhetoric, including calling ID “second generation creationism,” a “more sophisticated and dangerous ‘theistic science’ tradition,” and “a vehicle of philosophical infection, an insidious vehicle because it seems reasonable and moderate.” In a passage that has to make you laugh, they state:
If nothing is ascribable to structural transformations generated by natural selection, but neither comes out already equipped by a demiurge’s mind, how the hell we can explain the ID foundational phenomena, or the irreducible and specific complexity in range of a carefully regulated universe? [Emphasis added.]
How the Hell, Indeed
There’s no need to for their mystification about the cause behind ID. Since as human beings we have extensive observations of intelligent agents designing things, we can readily recognize the effects of intelligent agency in the natural world. Thus, intelligent design is detectible by science, and while it may not have a “naturalistic mechanism” it certainly provides a scientifically acceptable cause: intelligence. You might even call it a “mechanism” (although definitely not one in the materialistic sense).
Nonetheless, the point of the article is less to attack ID than it is to attack their fellow evolutionists who propose non-direct evolutionary pathways. They do this, ironically, by claiming that such evolutionists are falling into some traps of ID.
To make this argument, they first note that ID strongly criticizes direct evolutionary pathways:
From this point of view two decisive points of evolutionary analysis are brought into question: the first one is that the origin of language has to be obligatorily connected to functions directly linked to reproductive advantage; the second one is that, from the point of view of adaptive selection, the functional components acquired with language development might not be considered, or revealed, as an evolutionary advantage (on the contrary, they even could show themselves as counter-evolutionary features). This second point raised up by Dembski seems to challenge the central mechanism of evolutionary reconstructions. According to Darwinian dictate, indeed, also the most complex organism derives from “numerous, successive, and slight mutations” of their own morphologic structures. The pure reconstruction of these transformations and the internal laws that rule them, is called by ID supporters a «direct Darwinian pathway» (Dembski & Well, 2008, p. 151).
They believe that language is amenable to such direct evolutionary pathways:
In human language, for example, a “direct Darwinian pathway” can be rebuilt taking into account the original structural constraint story (peripheral and central structures of hearing-vocal system) and the interaction between ecologic and environmental constraint (bio-geographic, for example) and social structure constraints, produced in turn by morphogenetic and cognitive constraints (from human female’s hidden ovulation, to the “sentence” of semantic and syntactic categorization caused by vocal articulation). In short an intersection between different restrictions, but all “inside” a natural perspective.
They then take aim at those who use non-direct explanations to account for human language — oddly linking this somehow to a flaw in ID:
[U]ntil recently many explicative models, born in the field of cognitive sciences, have unconsciously adopted this dangerous dualism surreptitiously brought by ID in their attempt to explain complexity in human language without using the “right way”: an evolutionary explanation linked only to the progressive variation of morphologic structures.
Explaining Language
They then delve into the debate about the best way to explain the evolutionary origin of language. Here’s their view:
Direct Darwinian pathway goes through the analysis of body morphology: organisms narrate an evolutionary story made by phylogenetic heredity and species-specific changes. The functions that every organism show depend by constraints given by its body shape and by the interaction with the habitat he lives. Human language, as any cognitive function, showed itself only when sapiens’ morphology reached a “usable minimum threshold”, a discreet ergonomic target and a system of neural control that make possible compositional segmentation (Wray, 2002) and constant articulation of vocal sounds. In this way, it is possible to explain the presence of a communicative and representative complex function as human language without “intelligent” residuals, without necessarily using an external substance, and without spasmodically researching the adaptivity of every linguistic component to demonstrate evolutionary continuity.
We prefer to stay out of this fight. However, note that some theorists are deeply skeptical that the origin of human language is amenable to a detailed evolutionary explanation, appealing to adaptive benefits alone. For example:
In a very real sense, the two principal peculiarities of human language are an evolutionary embarrassment. It is not easy to picture the scenarios that would confer selective fitness on, specifically, syntactic classes and structure-dependent rules. While linguists advise us that these are formal properties without which human language cannot be modeled, it is not at all clear what functional properties of language are served specifically by these formal properties. Perhaps recursiveness is such a property; it may depend on syntactic classes. Let us pretend that it does: I, at least, do not see how to realize recursiveness without syntactic classes. These classes afford the kind of abstract representation in which the rewrite rules, needed for recursiveness, can be easily realized. But if this is correct, even in the weak sense that syntactic classes provide an economical or simple access to recursiveness, the, peculiarities of human language would remain no less an evolutionary embarrassment. I challenge the reader to reconstruct the scenario that would confer selective fitness on recursiveness. Language evolved, it is conjectured, at a time when humans or protohumans were hunting mastodons. Having language would be a benefit to them. They could do social planning, discuss strategies together, lay plans for specific contingencies. Now the alleged advantage of recursiveness is not simply unlimited sentences, but even more perhaps, the compacting of information. Would it be a great advantage for one of our ancestors, squatting alongside the embers, to be able to remark: “Beware of the short beast whose front hoof Bob cracked when, having forgotten his own spear back at camp, he got in a glancing blow with the dull spear he borrowed from Jack”? Human language is an embarrassment for evolutionary theory because it is vastly more powerful than one can account for in terms of selective fitness. (David Premack, “‘Gavagai!’ or the future history of the animal language controversy,’ Cognition (19), 1985, pp. 207-296, emphasis added)
Back to the Humana Mente Article
It’s difficult to know how to make sense of all of it. These philosophers take ID seriously, at least enough to describe the relevant arguments accurately. Yet they heavily criticize design theory, with trite and easily answered low-brow objections. One of the main points on which they take ID seriously seems to be a misapplication of ID ideas: they critically compare invoking the arguments of ID theorists to linguists who adopt non-direct evolutionary explanations for the origin of human language. Of course ID proponents are some of the most vocal critics of those who promulgate indirect evolutionary explanations. Why? Because such explanations are weak, difficult to test, and just highly unlikely. Sometimes indirect evolutionary explanations almost sound teleological.
Again, the English translation of this paper is rough. Perhaps the article rejects indirect evolutionary pathways because those pathways seem too goal-directed. Perhaps the authors intuit that material causes don’t work very well to guide an evolutionary pathway toward a specific, complex endpoint. If this is the way they see things, then they’re exactly right. But then what they don’t appreciate is that there is a cause that can operate with an end-goal in mind to guide evolution to produce a highly complex function. In the words of Stephen Meyer: “The answer is: intelligence. Conscious activity. The deliberate choice of a rational agent.”
Photo: Socrates, a bust displayed in the Vatican Museum, via Wikimedia Commons.


evolutionnewsandviews--2020-05-21--Biology Journal: Evolutionary Psychology Is “Impossible”

The field of evolutionary psychology ( “ evo psych ” ) claims that virtually all of human behavior can be explained by past selection pressures shaping our brains .
This means that not only did everything below your neck evolve , but so did everything above it .
That includes not just base behaviors like your desire to eat an orange or cuddle with your significant other , but even your higher activities , like appreciating music , creating art , and worshipping God .
If evo psych ’ s insights are correct , then all of your higher behaviors @ @ @ @ @ @ @ selection on your Pleistocene hominid ancestors .
If that sounds a little far-fetched , you ’ ll find some agreement from a new paper in the journal Biological Theory .
Philosopher Subrena E. Smith at the University of New Hampshire asks , “ Is Evolutionary Psychology Possible ?
” Smith comes out swinging from the abstract : In this article I argue that evolutionary psychological strategies for making inferences about present-day human psychology are methodologically unsound .
Evolutionary psychology is committed to the view that the mind has an architecture that has been @ @ @ @ @ @ @ our psychology can be fruitfully understood in terms of the original , fitness-enhancing functions of these conserved psychological mechanisms .
But for evolutionary psychological explanations to succeed , practitioners must be able to show that contemporary cognitive mechanisms correspond to those that were selected for in the environment of evolutionary adaptedness , that these present-day cognitive mechanisms are descended from the corresponding ancestral mechanisms , and that they have retained the functions of the ancestral mechanisms from which they are descended .
I refer to the problem of demonstrating that these conditions obtain @ @ @ @ @ @ @ argue that evolutionary psychology does not have the resources to address it , and conclude that evolutionary psychology , as it is currently understood , is therefore impossible .
In an interview with Gizmodo , “ This Philosopher Is Challenging All of Evolutionary Psychology , ” Smith further boils the problem down : Her argument is well reasoned and compelling .
She says we simply lack the data to establish the veracity of many evo psych claims .
How About Some Standards ?
She argues that proponents of evo psych ought to be @ @ @ @ @ @ @ For example : If you claim that a particular modern behavior is caused by a particular psychological structure that arose due to particular selection pressures , then you need to show that a particular structure causes that behavior and that it was in fact selected to produce that behavior .
Her argument is so reasonable , and so obvious , it ’ s a bit concerning that she needed to say this at all .
Did evolutionary scientists not understand these things already ?
Might Not Be Enough Yet even meeting such basic @ @ @ @ @ @ @ the claims of evo psych .
As Smith continues : If present-day human behaviors are caused by special-purpose cognitive structures , and that was also true of our stone age ancestors , and if there is a high degree of concordance between the structures populating the modern mind and those that populated the minds of our prehistoric ancestors , this would still fall short of securing evolutionary psychological inferences .
This is because it might be the case that the similarities between prehistoric and modern cognitive architectures are due to ontogenetic processes — @ @ @ @ @ @ @ the brain .
For a contemporary trait to be a strong vertical homolog of an ancestral trait , the contemporary trait must be of the same kind as the ancestral one .
It must also have the same function as the ancestral one , and must be related by descent to that ancestral trait as part of a continuous reproductive lineage extending back to the EEA .
Additionally , it must be the case that the contemporary trait and the ancestral trait are of the same kind and have the same function because @ @ @ @ @ @ @ ancestral trait .
In principle , it might be that a present-day trait and an ancestral trait are of the same kind and have the same function without one being descended from the other .
If this is the case , then the architecture of the minds of present-day humans would resemble that of early humans without it being the case that this architecture was selected for and genetically transmitted through the generations .
In other words , it ’ s not sufficient for evolutionary psychologists to speculate about the advantage that some @ @ @ @ @ @ @ Pleistocene ancestors in the environment that shaped our brains ( what she calls the “ EEA ” ) .
They need to demonstrate that the contemporary behavior would be similar to the ancient one , and that our ancestors had the same genetically related cognitive machinery producing their trait as we have producing ours .
This sounds reasonable , too .
Smith maintains that some evo psych explanations entail traits that were acquired too recently to be the product of natural selection .
Thus , attempts to explain them in evo psych terms @ @ @ @ @ @ @ not solve what she terms the “ matching problem.
” That means “ evolutionary psychological claims fail unless practitioners can show that mental structures underpinning present-day behaviors are structures that evolved in the EEA for the performance of adaptive tasks that it is still their function to perform.
” To solve the matching problem , as Smith explains in a blog post at The Evolution Institute , three criteria must be met : Ancestral and present-day psychological structures have to match in the way that is needed for evolutionary psychological inferences to succeed @ @ @ @ @ @ @ be met .
First , determine that the function of some contemporary mechanism is the one that an ancestral mechanism was selected for performing .
Next , determine that the contemporary mechanism has the same function as the ancestral one because of its being descended from the ancestral mechanism .
Finally , determine which ancestral mechanisms are related to which contemporary ones in this way .
It ’ s not sufficient to assume that the required identities are obvious .
They need to be demonstrated .
Solving the matching problem requires knowing about @ @ @ @ @ @ @ .
But it is difficult to see how this knowledge can possibly be acquired .
We do not , and very probably can not , know much about the prehistoric human mind .
In its typical fashion , evo psych feels little need to meet these basic standards of proof .
Why ?
Because “ There seems to be a tacit assumption amongst evolutionary psychologists that the needed identities between contemporary psychological mechanisms and ancestral ones are so obvious that they do not need to be established.
” Smith argues in her paper @ @ @ @ @ @ @ evo psych study about attitudes toward sexual fidelity .
The research surveyed college students to purportedly show that males are more concerned about the fidelity of their female partner than females are about that of their male partner .
Smith notes that such a study could never solve the matching problem : A skeptical reader might be thinking at this point , “ Fine , but let ’ s give evo psych a break !
Brains and behaviors don ’ t fossilize , so it isn ’ t fair to expect researchers to @ @ @ @ @ @ @ much less to show that we have modules that existed in our ancestors.
” Smith is ready for this objection .
If the data aren ’ t available , that doesn ’ t give you the right to engage in data-free speculation : Smith also charges that evo psych engages in “ circular ” reasoning when “ individuating ” behaviors .
Individuating means identifying specific behaviors based upon their specific effects , functions , or causes .
To individuate a behavior based on its effects , “ one needs to establish that the @ @ @ @ @ @ @ ( structures ) are strong vertical homologs , ” but she explains that evo psych has no mechanism for doing this .
To individuate a behavior based on its function entails “ circularity , ” because it “ illegitimately supposes that a behavior was selected for and then uses this supposition as evidence that the behavior was selected for.
” To individuate a behavior based on its causes falls into the same trap , because “ it relies on the principle that cognitive mechanisms are individuated by the behaviors that they bring about @ @ @ @ @ @ @ mechanisms that supposedly cause them.
” In light of these difficulties , Smith asks : “ Is evolutionary psychology possible ?
” The answer is no .
She concludes : “ Evolutionary psychologists simply do not have the methodological resources to justify the claim that the psychological causes of contemporary behaviors are strong vertical homologs of the psychological causes of corresponding behaviors in the EEA.
” It ’ s remarkable and encouraging to see such clear thinking in a mainstream scientific journal .
Even evolutionary biologist P. Z. Myers jumped on this bandwagon @ @ @ @ @ @ @ psych , “ None of their prior claims are valid , and they don ’ t fit with what we do know about evolution and the brain !
” But will these criticisms have any effect on the field itself ?
Myers concludes that evo psych is too insular for that : At Gizmodo , however , Smith attributes the resistance to criticism among evo psych practitioners to their “ ideological biases.
” She warns of potential consequences of their unwillingness to listen : The evolutionary psychologists I engage with are not silly @ @ @ @ @ @ @ about these matters .
However , the attractiveness of evolutionary theory coupled with peoples ’ ideological biases forces them to not be as careful as they might be otherwise .
I think that the consequences for our world when we misappropriate evolutionary accounts are really serious .
People are saying that people of color have smaller brains , which is not true , or that women aren ’ t as great as men , which is not true… I think we have a special responsibility , when we say evolution made us that @ @ @ @ @ @ @ read “ innate ” or “ hardwired ” as synonymous with evolution .
We should be especially careful to not be making claims like these , which can have consequences .
If you say evolution made us so , then governments can rightly say you don ’ t have the capacity to do something , so we won ’ t use our resources to make you do stuff you can ’ t do .
This is about the science and politics — making sure that we ’ re not misappropriating the science to @ @ @ @ @ @ @ suit interests , be they my interests or their interests .
If I have interests inconsistent with what the science says , I don ’ t think I should be given a pass .
But my view is that I don ’ t see the framework of evolutionary psychology as-is providing us with an explanation of human behavior that we can get behind .
Just to be clear : Smith is not anti-evolution .
As she writes at The Evolution Institute , she believes “ The human mind was fashioned by evolutionary forces @ @ @ @ @ @ @ be successful.
” But as for evo psych ’ s ability to demonstrate specific hypotheses about how that happened ?
There , she argues , great skepticism is warranted .

The field of evolutionary psychology (“evo psych”) claims that virtually all of human behavior can be explained by past selection pressures shaping our brains. This means that not only did everything below your neck evolve, but so did everything above it. That includes not just base behaviors like your desire to eat an orange or cuddle with your significant other, but even your higher activities, like appreciating music, creating art, and worshipping God. If evo psych’s insights are correct, then all of your higher behaviors are no more than the result of selection on your Pleistocene hominid ancestors.
Swinging from the Abstract
If that sounds a little far-fetched, you’ll find some agreement from a new paper in the journal Biological Theory. Philosopher Subrena E. Smith at the University of New Hampshire asks, “Is Evolutionary Psychology Possible?” Smith comes out swinging from the abstract:
In this article I argue that evolutionary psychological strategies for making inferences about present-day human psychology are methodologically unsound. Evolutionary psychology is committed to the view that the mind has an architecture that has been conserved since the Pleistocene, and that our psychology can be fruitfully understood in terms of the original, fitness-enhancing functions of these conserved psychological mechanisms. But for evolutionary psychological explanations to succeed, practitioners must be able to show that contemporary cognitive mechanisms correspond to those that were selected for in the environment of evolutionary adaptedness, that these present-day cognitive mechanisms are descended from the corresponding ancestral mechanisms, and that they have retained the functions of the ancestral mechanisms from which they are descended. I refer to the problem of demonstrating that these conditions obtain as “the matching problem,” argue that evolutionary psychology does not have the resources to address it, and conclude that evolutionary psychology, as it is currently understood, is therefore impossible.
In an interview with Gizmodo, “This Philosopher Is Challenging All of Evolutionary Psychology,” Smith further boils the problem down:
The matching problem is really the core issue that evolutionary psychologists have to show that they can meet: that there is really a match between our modules and the modules of the prehistoric ancestors; that they’re working the same way then as now; and that these modules are working the same way because they are descended from the same functional lineage or causal lineage. But I don’t see any way that these charges can be answered.
Her argument is well reasoned and compelling. She says we simply lack the data to establish the veracity of many evo psych claims.
How About Some Standards?
She argues that proponents of evo psych ought to be held to basic standards of evidence. For example:
Evolutionary psychologists argue that behaviors in the present are caused by cognitive systems that operate today as they did in the past. In their view, each module was selected for because of its specific fitness-enhancing effects in the EEA [environment of evolutionary adaptedness], and each of them is domain-specific — that is, responsive only to the kinds of inputs for which they are adaptations. Evolutionary psychological inferences are secure only if it is possible to determine that particular kinds of behavior are underwritten by particular structures. Further, these must have the evolved function of producing behaviors of just these kinds.
If you claim that a particular modern behavior is caused by a particular psychological structure that arose due to particular selection pressures, then you need to show that a particular structure causes that behavior and that it was in fact selected to produce that behavior. Her argument is so reasonable, and so obvious, it’s a bit concerning that she needed to say this at all. Did evolutionary scientists not understand these things already?
Might Not Be Enough
Yet even meeting such basic standards might not be enough to demonstrate the claims of evo psych. As Smith continues:
If present-day human behaviors are caused by special-purpose cognitive structures, and that was also true of our stone age ancestors, and if there is a high degree of concordance between the structures populating the modern mind and those that populated the minds of our prehistoric ancestors, this would still fall short of securing evolutionary psychological inferences. This is because it might be the case that the similarities between prehistoric and modern cognitive architectures are due to ontogenetic processes — similar experiences producing similar functional differentiation in the brain. For a contemporary trait to be a strong vertical homolog of an ancestral trait, the contemporary trait must be of the same kind as the ancestral one. It must also have the same function as the ancestral one, and must be related by descent to that ancestral trait as part of a continuous reproductive lineage extending back to the EEA. Additionally, it must be the case that the contemporary trait and the ancestral trait are of the same kind and have the same function because the present-day trait is descended from the ancestral trait. In principle, it might be that a present-day trait and an ancestral trait are of the same kind and have the same function without one being descended from the other. If this is the case, then the architecture of the minds of present-day humans would resemble that of early humans without it being the case that this architecture was selected for and genetically transmitted through the generations.
In other words, it’s not sufficient for evolutionary psychologists to speculate about the advantage that some modern-day behavior might have yielded in our Pleistocene ancestors in the environment that shaped our brains (what she calls the “EEA”). They need to demonstrate that the contemporary behavior would be similar to the ancient one, and that our ancestors had the same genetically related cognitive machinery producing their trait as we have producing ours. This sounds reasonable, too.
Necessarily Fruitless
Smith maintains that some evo psych explanations entail traits that were acquired too recently to be the product of natural selection. Thus, attempts to explain them in evo psych terms must be fruitless:
If the idea that mental structure can be acquired ontogenetically seems dubious, consider the area of the brain called “the visual word-form area” that is specialized for reading (it is a “reading module”). Written language emerged only around 3500 years ago, so it is too recent for reading to have been selected for. This shows that cognitive mechanisms can be acquired by learning. [Citations omitted.]
Evolutionary psychology cannot solve what she terms the “matching problem.” That means “evolutionary psychological claims fail unless practitioners can show that mental structures underpinning present-day behaviors are structures that evolved in the EEA for the performance of adaptive tasks that it is still their function to perform.” To solve the matching problem, as Smith explains in a blog post at The Evolution Institute, three criteria must be met:
Ancestral and present-day psychological structures have to match in the way that is needed for evolutionary psychological inferences to succeed. For this, three conditions must be met. First, determine that the function of some contemporary mechanism is the one that an ancestral mechanism was selected for performing. Next, determine that the contemporary mechanism has the same function as the ancestral one because of its being descended from the ancestral mechanism. Finally, determine which ancestral mechanisms are related to which contemporary ones in this way. It’s not sufficient to assume that the required identities are obvious. They need to be demonstrated. Solving the matching problem requires knowing about the psychological architecture of our prehistoric ancestors. But it is difficult to see how this knowledge can possibly be acquired. We do not, and very probably cannot, know much about the prehistoric human mind.
In its typical fashion, evo psych feels little need to meet these basic standards of proof. Why? Because “There seems to be a tacit assumption amongst evolutionary psychologists that the needed identities between contemporary psychological mechanisms and ancestral ones are so obvious that they do not need to be established.” Smith argues in her paper:
Unless the challenge can be overcome, evolutionary psychological explanations fail. Put more strongly, if the matching problem cannot be solved, evolutionary psychology is impossible.
She gives an example of an evo psych study about attitudes toward sexual fidelity. The research surveyed college students to purportedly show that males are more concerned about the fidelity of their female partner than females are about that of their male partner. Smith notes that such a study could never solve the matching problem:
Faced with evidence that 21st-century male American college students are more doubtful of the future sexual fidelity of their mates than their female counterparts are, the authors make two assumptions. The first is that male college students’ skepticism is caused by a hardwired, domain-specific cognitive module. The second is that this module existed in Pleistocene males, and produced behaviors of the same sort as the contemporary behavior. These assumptions are supposed to underwrite the conclusion that the sexual suspiciousness of contemporary males is caused by a cognitive mechanism with the evolutionary function of enhancing their fitness by preventing cuckoldry. Goetz and Causey do not provide support for their claim that the psychological mechanism driving contemporary male sexual skepticism is a strong vertical homolog of the mechanism that drove (hypothesized) prehistoric anti-cuckoldry behavior. Consequently, their inferences about the evolutionary origin of the male students’ attitudes is unjustified.
Give Them a Break
A skeptical reader might be thinking at this point, “Fine, but let’s give evo psych a break! Brains and behaviors don’t fossilize, so it isn’t fair to expect researchers to demonstrate the existence of ancient behaviors, much less to show that we have modules that existed in our ancestors.”Smith is ready for this objection. If the data aren’t available, that doesn’t give you the right to engage in data-free speculation:
It might be thought that I am unfairly holding evolutionary psychology to a much higher epistemic and methodological standard than is normally used in evolutionary biology. But this is not the case. Evolutionary psychological inferences commonly fail to satisfy reasonable epistemic criteria. When making evolutionary inferences about paradigmatically biological traits, biologists use experimental manipulations, comparative methods, the fossil record, and optimality models to determine that selection has taken place and that the items under consideration have retained their selected-for functions. Evolutionary psychologists are impeded by the fact that these methods are unavailable to them. … evolutionary psychological hypotheses turn on inferences about hypothetical cognitive structures — the mental modules — for which there is a dearth of empirical support … and there is no evidence that the minds of our prehistoric ancestors possessed this sort of cognitive architecture.
Circular Reasoning
Smith also charges that evo psych engages in “circular” reasoning when “individuating” behaviors. Individuating means identifying specific behaviors based upon their specific effects, functions, or causes. To individuate a behavior based on its effects, “one needs to establish that the contemporary and ancestral causes of the behavior (structures) are strong vertical homologs,” but she explains that evo psych has no mechanism for doing this. To individuate a behavior based on its function entails “circularity,” because it “illegitimately supposes that a behavior was selected for and then uses this supposition as evidence that the behavior was selected for.” To individuate a behavior based on its causes falls into the same trap, because “it relies on the principle that cognitive mechanisms are individuated by the behaviors that they bring about while these behaviors are individuated by the mechanisms that supposedly cause them.”
In light of these difficulties, Smith asks: “Is evolutionary psychology possible?” The answer is no. She concludes: “Evolutionary psychologists simply do not have the methodological resources to justify the claim that the psychological causes of contemporary behaviors are strong vertical homologs of the psychological causes of corresponding behaviors in the EEA.”
It’s remarkable and encouraging to see such clear thinking in a mainstream scientific journal. Even evolutionary biologist P. Z. Myers jumped on this bandwagon, writing about the field of evo psych, “None of their prior claims are valid, and they don’t fit with what we do know about evolution and the brain!” But will these criticisms have any effect on the field itself? Myers concludes that evo psych is too insular for that:
Not that any of this will have any effect on EP at all — that’s a field that relies more on an emotional belief that they can study the past entirely by imposing their desired conclusions on weak data. Smith, on the other hand, has a strong understanding of logic and recognizes where these Evolutionary Psychologists have made a huge leap beyond what the data entails.
Ideology and Consequences
At Gizmodo, however, Smith attributes the resistance to criticism among evo psych practitioners to their “ideological biases.” She warns of potential consequences of their unwillingness to listen:
The evolutionary psychologists I engage with are not silly people. They are thoughtful and philosophical about these matters. However, the attractiveness of evolutionary theory coupled with peoples’ ideological biases forces them to not be as careful as they might be otherwise. I think that the consequences for our world when we misappropriate evolutionary accounts are really serious. People are saying that people of color have smaller brains, which is not true, or that women aren’t as great as men, which is not true… I think we have a special responsibility, when we say evolution made us that way, to recognize that people will read “innate” or “hardwired” as synonymous with evolution. We should be especially careful to not be making claims like these, which can have consequences. If you say evolution made us so, then governments can rightly say you don’t have the capacity to do something, so we won’t use our resources to make you do stuff you can’t do. This is about the science and politics — making sure that we’re not misappropriating the science to underwrite our politics in a way to suit interests, be they my interests or their interests. If I have interests inconsistent with what the science says, I don’t think I should be given a pass. But my view is that I don’t see the framework of evolutionary psychology as-is providing us with an explanation of human behavior that we can get behind.
Just to be clear: Smith is not anti-evolution. As she writes at The Evolution Institute, she believes “The human mind was fashioned by evolutionary forces in ways that allowed our ancestors to be successful.” But as for evo psych’s ability to demonstrate specific hypotheses about how that happened? There, she argues, great skepticism is warranted.
Image: Pleistocene humans stalk a Glyptodon, by Heinrich Harder (1858-1935) / Public domain.


evolutionnewsandviews--2020-05-22--Harvard Molecular Geneticist Vindicates Michael Behe’s Main Argument in Darwin Devolves

When Michael Behe ’ s book Darwin Devolves came out last year , critics were quick to pounce .
Skeptic Magazine wrote that “ In Darwin Devolves , Michael Behe continues to dig himself further into the hole he opened 20 years ago with Darwin ’ s Black Box.
” Three Quarks Daily stated that Behe ’ s central thesis in the book , “ is clickbait , the book title misleading , and the argument long since rebutted.
” That thesis is what Behe calls the “ first rule of adaptive evolution , ” namely that Darwinian processes tend @ @ @ @ @ @ @ gene whose loss would increase the number of a species ’ s offspring.
” A review in the journal Science called Behe ’ s arguments “ quixotic ” and charged that “ [ t ] here are indeed many examples of loss-of-function mutations that are advantageous , but Behe is selective in his examples ” — so much so that Behe “ misrepresents theory and avoids evidence that challenges him.
” A response in the journal Evolution had this to say : You can find many responses to the critics here , but @ @ @ @ @ @ @ relevant questions : Did Behe mislead readers in emphasizing the importance of loss-of-function mutations ?
Did Behe misrepresent evolutionary theory and ignore evidence by claiming that adaptations tend to involve degradative mutations ?
Did Behe dig himself into a hole by claiming that constructive mutations are less common than those that break or diminish functions ?
If a new article Current Biology means anything , the critics are not just not just rude but plain wrong : The author , Andrew Murray , is a professor of molecular genetics at Harvard .
He @ @ @ @ @ @ @ typical evolutionary biologist who believes that unguided material mechanisms can produce all the diversity of life .
But like Behe , he recognizes that loss-of-function is very important to the evolutionary process : Also much like Behe , Murray knows what the data say .
He reviews multiple examples where Darwinian evolution proceeded via mutations that caused loss or degradation , rather than gain or improvement , of function .
After predicting that when “ there are the same number of genes where loss-of-function mutations improve fitness ( i.e .
are deleterious for @ @ @ @ @ @ @ beneficial for the organism ) as the number of genes that are targets for gain-of-function mutations and both classes of mutations confer similar fitness increases , the loss-of-function mutations will dominate the initial response to selection , ” he observes that this hypothesis is supported by empirical data : Two forms of evolutionary novelty support the inferences from these calculations : laboratory evolution and agricultural domestication .
A variety of laboratory experiments have selected for novelty .
One of the earliest such experiments exposed a bacterial species , Pseudomonas fluorescens , to unstirred @ @ @ @ @ @ @ shaken flask .
In response , two new phenotypes appeared , clones that formed mats on the surface of the medium and those that formed aggregates at the bottom of the flask , with both phenotypes caused by loss-of-function mutations .
Further experiments led to even more complex phenotypes and these too were dominated by loss-of-function mutations .
In budding yeast , two novel phenotypes have been experimentally evolved : multicellularity and a circadian oscillator .
In both cases , most of the mutations that combined to produce the novel phenotypes were loss-of-function @ @ @ @ @ @ @ multicellularity to proliferate successfully on low sucrose concentrations , four different biological functions were altered by loss-of-function mutations : the transcriptional network inducing cleavage of the shared cell wall that holds mothers and daughters together after cytokinesis , catabolite repression — the functional module that represses metabolism of other carbon sources when cells are grown on glucose — the transcriptional mediator complex and a module that represses cell growth and division in response to carbon starvation .
He further observes that genetic analysis of domesticated corn crops often differ greatly from their wild @ @ @ @ @ @ @ the result of loss-of-function mutations : But it ’ s not just artificially selected organisms like corn that have experienced degenerative mutations .
Murray finds that loss-of-function mutations have been “ drivers ” of evolution in humans : Lest you think that Murray believes that loss-of-function mutations occur but are mere unimportant curiosities in evolutionary history , he goes on to propose that these could be the very mechanisms behind adaptive radiations where new types of organisms evolve rapidly to fill empty niches .
In his model , loss-of-function mutations occur more readily @ @ @ @ @ @ @ allow “ hopeful monsters ” to arise , potentially allowing those organisms to occupy a new niche .
Normally these mutants get outcompeted by other organisms that already fill the niche .
However , if the niche is empty then the organism might persist and undergo further mutations to specialize within the niche .
Murray admits that it ’ s not yet known whether the evidence backs up this hypothesis .
But he observes that loss-of-function mutations drove diversification in some African cichlid populations : Even Michael Behe would agree that such lower @ @ @ @ @ @ @ As he writes in Darwin Devolves , “ degradative mutations can help organisms to adapt and in the process can sometimes shift them into new minor categories of genus and species.
” ( p. 160 ) Murray is aware of various objections to his model .
For example , he notes that some fear “ Killing genes might be beneficial in the short term and even visible in natural populations , but should we worry that if evolution keeps doing it there will be no genes left ?
” The objection is reasonable @ @ @ @ @ @ @ ’ t entirely convincing .
He argues that degradative mutations may eventually be reversed , but this would violate Dollo ’ s Law , a very old postulate in evolutionary biology which holds that evolution is not reversible .
In Darwin Devolves , Michael Behe explains that the evidence suggests Dollo ’ s Law is applicable even at the molecular level : In 2009 Joseph Thornton ’ s group set out to explore whether something like Dollo ’ s Law applied to steroid receptors .
Having shown in 2006 that the reconstructed ancestral @ @ @ @ @ @ @ few mutations into a weakened one they considered more similar to the modern GR receptor ( as discussed above ) , Thornton ’ s lab decided to investigate the reverse problem whether , starting from the modern GR receptor ( which binds just one kind of steroid ) , a pathway conducive to Darwinian evolution could be found back to the ancestral one ( which binds several kinds including the one bound by modern GR ) .
As an analogy , if we show that a metal rod can be made into a @ @ @ @ @ @ @ , can a hammer be turned back into a plain rod in the same manner ?
After much impressive technically difficult work , their answer was no .
The modern GR receptor is stuck where it is .
It can ’ t go home again , at least not with any reasonable probability by a Darwinian process .
The reason is that the modern receptor has accumulated a number of other changes from the ancient one , some positively selected to help its function , others seemingly neutral .
6 Reversing them would @ @ @ @ @ @ @ back , but changing them individually , one at a time , as Darwinism requires , either doesn ’ t help or actively hurts , so natural selection would not be expected to favor them .
The authors conclude that “ the probability of all [ necessary mutations occurring ] in combination would be virtually zero.
” Although theirs is the first study with the necessary depth to address the question of the reversibility of protein molecular evolution , they are confident that the results will be quite general-that is , most proteins @ @ @ @ @ @ @ .
In fact , they predict that further work “ will support a molecular version of Dollo ’ s Law.
” That is , “ as evolution proceeds , shifts in protein structure-function relations become increasingly difficult to reverse.
” If this argument is correct , then it ’ s unlikely that inactivated or degraded genes can be restored even if an organism luckily finds an empty niche to thrive in .
Murray then proposes a second workaround .
He cites the standard evolutionary idea that “ genes can be produced as well @ @ @ @ @ @ @ divergence and by the emergence of coding sequences from non-coding DNA.
” Even if this mechanism is viable for generating new genes , it must be guaranteed that newly functional genes can be created at a faster rate than they are destroyed .
But Behe gives us good reasons to understand why gene duplication is not an efficient mechanism for generating new genes : Up until now the lighthearted assumption was that the acquisition of significant new abilities by divergence of gene duplicates through random mutation and natural selection was unproblematic .
Yet @ @ @ @ @ @ @ difficulties with even comparatively simple transformations-at least by a Darwinian mechanism-calls into grave question whether the others , even the most familiar , could have developed that way either .
As just one example , the alpha and beta chains of hemoglobin are universally thought to have arisen in the distant past from myoglobin-like precursor by gene duplication and divergence .
In fact , more than twenty years ago in Darwin ’ s Black Box I myself pointed to them as examples of what Darwinian evolution could likely do .
They certainly derive @ @ @ @ @ @ @ that could have happened by a Darwinian process—whether a comparatively simple oxygen-binding protein could without direction yield the sophisticated oxygen-delivery system that is hemoglobin — is now very much an open question… .
However , whenever multiple amino-acid substitutions or other mutations were needed to confer a substantially different activity on a duplicated protein , it can no longer be blithely assumed that the transition was navigated by Darwinian evolutionary processes .
Despite the fact that Behe discussed and directly critiqued gene duplication in his book , in a review of Darwin Devolves @ @ @ @ @ @ @ falsely claimed that Behe “ ignores ” mechanisms like gene duplication : The accusation that Behe ignored counterarguments is patently false , thought it was a common theme among critics of his book .
In this case Behe specifically mentions the origin of different hemoglobin genes by gene duplication — the very counterexample that Coyne claims Behe “ ignores ” !
Perhaps unintentionally , Murray ’ s article implies a counterargument .
It explains that mere gene duplication by itself does not represent novelty : That is a most curious sentence — curious @ @ @ @ @ @ @ but curious because it is so correct .
There is no reason to believe that Murray supports intelligent design .
In fact , from the rest of the article there ’ s no doubt that he believes blind evolutionary mechanisms alone can do the job .
But Murray ’ s claim here is exactly what ID proponents would say : evolutionary novelty requires explaining how entire systems come into existence , and citing gene duplication alone is not tantamount to explaining evolutionary novelty .
As Evolution News has argued in the past , @ @ @ @ @ @ @ new ; it only gives you more of something you already had .
Murray offers this conclusion : “ I have argued that loss-of-function mutations may have played a major role in the evolution of novelty.
” He doesn ’ t cite Michael Behe , and there ’ s no evidence that he got any ideas from reading Darwin Devolves .
He would likely disagree with Behe about the efficacy of mechanisms such as gene duplication for generating new genes , as well as with Behe ’ s support for intelligent design .
@ @ @ @ @ @ @ the points of agreement — namely the hypothesis that degradative mutations are very common in the evolutionary process and may even predominate among adaptive features .
So this is good news : Mainstream evolutionary biologists are independently arriving at very similar conclusions to Behe ’ s central thesis in Darwin Devolves , the one that drew the most wrath from critics .
In light of Murray ’ s article in Current Biology , Mike Behe appears to be vindicated .
Photo : Michael Behe signs a copy of Darwin Devolves at a Socrates @ @ @ @ @ @ @ .

When Michael Behe’s book Darwin Devolves came out last year, critics were quick to pounce. Skeptic Magazine wrote that “In Darwin Devolves, Michael Behe continues to dig himself further into the hole he opened 20 years ago with Darwin’s Black Box.” Three Quarks Daily stated that Behe’s central thesis in the book, “is clickbait, the book title misleading, and the argument long since rebutted.”
That thesis is what Behe calls the “first rule of adaptive evolution,” namely that Darwinian processes tend to “Break or blunt any functional gene whose loss would increase the number of a species’s offspring.” A review in the journal Science called Behe’s arguments “quixotic” and charged that “[t]here are indeed many examples of loss-of-function mutations that are advantageous, but Behe is selective in his examples” — so much so that Behe “misrepresents theory and avoids evidence that challenges him.”
A response in the journal Evolution had this to say:
Concise, catchy and matter-of-fact, Behe’s First Rule makes for a quality sound bite, but it is overly simplistic and untruthful to the data. Darwin Devolves overemphasizes loss-of-function mutations, and brushes off countervailing examples as nothing more than a “sideshow.”
You can find many responses to the critics here, but it’s still worth revisiting some relevant questions: Did Behe mislead readers in emphasizing the importance of loss-of-function mutations? Did Behe misrepresent evolutionary theory and ignore evidence by claiming that adaptations tend to involve degradative mutations? Did Behe dig himself into a hole by claiming that constructive mutations are less common than those that break or diminish functions? If a new article Current Biology means anything, the critics are not just rude but plain wrong:
In laboratory-based experimental evolution of novel phenotypes and the human domestication of crops, the majority of the mutations that lead to adaptation are loss-of-function mutations that impair or eliminate the function of genes rather than gain-of-function mutations that increase or qualitatively alter the function of proteins. Here, I speculate that easier access to loss-of-function mutations has led them to play a major role in the adaptive radiations that occur when populations have access to many unoccupied ecological niches. Andrew W. Murray, “Can gene-inactivating mutations lead to evolutionary novelty?” Current Biology, 30(10); R465-R471; emphasis added.
The Importance of Loss-of-Function
The author, Andrew Murray, is a professor of molecular genetics at Harvard. He gives every indication that he is a typical evolutionary biologist who believes that unguided material mechanisms can produce all the diversity of life. But like Behe, he recognizes that loss-of-function is very important to the evolutionary process:
My guiding hypothesis is that a significant fraction of evolutionary novelty has been produced by mutations that reduce or eliminate gene function.
Also much like Behe, Murray knows what the data say. He reviews multiple examples where Darwinian evolution proceeded via mutations that caused loss or degradation, rather than gain or improvement, of function. After predicting that when “there are the same number of genes where loss-of-function mutations improve fitness (i.e. are deleterious for the protein product of the gene but beneficial for the organism) as the number of genes that are targets for gain-of-function mutations and both classes of mutations confer similar fitness increases, the loss-of-function mutations will dominate the initial response to selection,” he observes that this hypothesis is supported by empirical data:
Two forms of evolutionary novelty support the inferences from these calculations: laboratory evolution and agricultural domestication. A variety of laboratory experiments have selected for novelty. One of the earliest such experiments exposed a bacterial species, Pseudomonas fluorescens, to unstirred liquid medium, instead of the traditional shaken flask. In response, two new phenotypes appeared, clones that formed mats on the surface of the medium and those that formed aggregates at the bottom of the flask, with both phenotypes caused by loss-of-function mutations. Further experiments led to even more complex phenotypes and these too were dominated by loss-of-function mutations. In budding yeast, two novel phenotypes have been experimentally evolved: multicellularity and a circadian oscillator. In both cases, most of the mutations that combined to produce the novel phenotypes were loss-of-function mutations. For the populations that evolved multicellularity to proliferate successfully on low sucrose concentrations, four different biological functions were altered by loss-of-function mutations: the transcriptional network inducing cleavage of the shared cell wall that holds mothers and daughters together after cytokinesis, catabolite repression — the functional module that represses metabolism of other carbon sources when cells are grown on glucose — the transcriptional mediator complex and a module that represses cell growth and division in response to carbon starvation.
He further observes that genetic analysis of domesticated corn crops often differ greatly from their wild ancestors, but these differences are largely the result of loss-of-function mutations:
Genetic analysis of crosses between agricultural and ancestral isolates have identified many of the mutations that gave rise to today’s [maize] crops. Of those that have been characterized in detail, more than half are loss-of-function mutations; in a list of 60 candidate genes involved in the domestication of 14 different crops, 38 of the genes have alleles that are either annotated as being loss-of-function mutations or have a high-probability of damaging gene function (frameshifts and premature stop codons).
“Drivers” of Human Evolution
But it’s not just artificially selected organisms like corn that have experienced degenerative mutations. Murray finds that loss-of-function mutations have been “drivers” of evolution in humans:
The evolution of humans also offers support for loss-of-function mutations as drivers of evolution. In 1999, a pioneering review argued that in many organisms, loss-of-function mutations were likely to have been drivers of evolution as populations shifted from one environment to another. For example, a human loss-of-function mutation in the promoter of a red blood cell chemoreceptor, DARC, protects against malaria caused by Plasmodium vivax. A second example, also putatively driven by selection imposed by malaria, is the loss of function in CMAH, a gene whose product produces a sialic acid derivative. A comprehensive analysis identified 80 human genes that have inactivating mutations in humans but are intact in chimpanzees and proposed that at least one of these mutations, in the gene CASPASE12, was selected for because it conferred survival after sepsis.
New Niche for a Hopeful Monster
Lest you think that Murray believes that loss-of-function mutations occur but are mere unimportant curiosities in evolutionary history, he goes on to propose that these could be the very mechanisms behind adaptive radiations where new types of organisms evolve rapidly to fill empty niches. In his model, loss-of-function mutations occur more readily than gain-of-function mutations. Thus they may allow “hopeful monsters” to arise, potentially allowing those organisms to occupy a new niche. Normally these mutants get outcompeted by other organisms that already fill the niche. However, if the niche is empty then the organism might persist and undergo further mutations to specialize within the niche.
Murray admits that it’s not yet known whether the evidence backs up this hypothesis. But he observes that loss-of-function mutations drove diversification in some African cichlid populations:
Another well-studied radiation has produced about 1200 species of cichlids in the rift lakes of East Africa, with an extraordinary variety of morphologies, behaviors, and colorations and in this radiation, inter-species crosses are possible. In three lakes, Victoria, Malawi, and Tanganyika, dark horizontal stripes have arisen, and in all three cases this is due to reduced expression of agouti-related peptide 2 (agrp2), which encodes a peptide that controls pigment distribution. Although the mutations responsible for reduced expression differ between the different lakes, in the youngest lake, Victoria, the causative mutation is a loss-of-function mutation in an agrp2 enhancer.
Even Michael Behe would agree that such lower taxa can diversify via degradative mutations. As he writes in Darwin Devolves,“degradative mutations can help organisms to adapt and in the process can sometimes shift them into new minor categories of genus and species.” (p. 160)
Objections to the Model
Murray is aware of various objections to his model. For example, he notes that some fear “Killing genes might be beneficial in the short term and even visible in natural populations, but should we worry that if evolution keeps doing it there will be no genes left?” The objection is reasonable, and Murray’s response isn’t entirely convincing. He argues that degradative mutations may eventually be reversed, but this would violate Dollo’s Law, a very old postulate in evolutionary biology which holds that evolution is not reversible. In Darwin Devolves, Michael Behe explains that the evidence suggests Dollo’s Law is applicable even at the molecular level:
In 2009 Joseph Thornton’s group set out to explore whether something like Dollo’s Law applied to steroid receptors. Having shown in 2006 that the reconstructed ancestral steroid receptor could be changed by a few mutations into a weakened one they considered more similar to the modern GR receptor (as discussed above), Thornton’s lab decided to investigate the reverse problem whether, starting from the modern GR receptor (which binds just one kind of steroid), a pathway conducive to Darwinian evolution could be found back to the ancestral one (which binds several kinds including the one bound by modern GR). As an analogy, if we show that a metal rod can be made into a hammer by a series of beneficial steps, can a hammer be turned back into a plain rod in the same manner? After much impressive technically difficult work, their answer was no. The modern GR receptor is stuck where it is. It can’t go home again, at least not with any reasonable probability by a Darwinian process. The reason is that the modern receptor has accumulated a number of other changes from the ancient one, some positively selected to help its function, others seemingly neutral. 6 Reversing them would be necessary to get the old function back, but changing them individually, one at a time, as Darwinism requires, either doesn’t help or actively hurts, so natural selection would not be expected to favor them. The authors conclude that “the probability of all [necessary mutations occurring] in combination would be virtually zero.” Although theirs is the first study with the necessary depth to address the question of the reversibility of protein molecular evolution, they are confident that the results will be quite general-that is, most proteins will be stuck in their present roles. In fact, they predict that further work “will support a molecular version of Dollo’s Law.” That is, “as evolution proceeds, shifts in protein structure-function relations become increasingly difficult to reverse.” Darwin Devolves, pp. 208-209
If this argument is correct, then it’s unlikely that inactivated or degraded genes can be restored even if an organism luckily finds an empty niche to thrive in.
A Second Workaround
Murray then proposes a second workaround. He cites the standard evolutionary idea that “genes can be produced as well as destroyed, both by duplication and divergence and by the emergence of coding sequences from non-coding DNA.” Even if this mechanism is viable for generating new genes, it must be guaranteed that newly functional genes can be created at a faster rate than they are destroyed. But Behe gives us good reasons to understand why gene duplication is not an efficient mechanism for generating new genes:
Up until now the lighthearted assumption was that the acquisition of significant new abilities by divergence of gene duplicates through random mutation and natural selection was unproblematic. Yet Thornton’s work demonstrating the severe difficulties with even comparatively simple transformations-at least by a Darwinian mechanism-calls into grave question whether the others, even the most familiar, could have developed that way either. As just one example, the alpha and beta chains of hemoglobin are universally thought to have arisen in the distant past from myoglobin-like precursor by gene duplication and divergence. In fact, more than twenty years ago in Darwin’s Black Box I myself pointed to them as examples of what Darwinian evolution could likely do. They certainly derive from a common gene, but whether that could have happened by a Darwinian process—whether a comparatively simple oxygen-binding protein could without direction yield the sophisticated oxygen-delivery system that is hemoglobin — is now very much an open question…. However, whenever multiple amino-acid substitutions or other mutations were needed to confer a substantially different activity on a duplicated protein, it can no longer be blithely assumed that the transition was navigated by Darwinian evolutionary processes. Darwin Devolves, pp. 213-215
Despite the fact that Behe discussed and directly critiqued gene duplication in his book, in a review of Darwin Devolves in the Washington Post, Jerry Coyne falsely claimed that Behe “ignores” mechanisms like gene duplication:
Behe selectively gives a handful of examples in which mutations have produced broken genes that are nevertheless useful, but he simply ignores the large number of adaptive mutations that do not inactivate genes. These include duplications, in which a gene is accidentally copied twice, with the copies diverging in useful ways (this is how primates acquired our three-color vision, as well as different forms of hemoglobin).
The accusation that Behe ignored counterarguments is patently false, thought it was a common theme among critics of his book. In this case Behe specifically mentions the origin of different hemoglobin genes by gene duplication — the very counterexample that Coyne claims Behe “ignores”!
ID Proponents Wouldn’t Disagree
Perhaps unintentionally, Murray’s article implies a counterargument. It explains that mere gene duplication by itself does not represent novelty:
In molecular evolution, the appearance of a rotary motor, whether as an ATP synthase or a flagellar motor, was clearly novel, whereas most would agree the gene duplication and divergence that produced multiple, paralogous mitotic cyclins in fungi and animals was not.
That is a most curious sentence — curious not because it’s largely correct but curious because it is so correct. There is no reason to believe that Murray supports intelligent design. In fact, from the rest of the article there’s no doubt that he believes blind evolutionary mechanisms alone can do the job. But Murray’s claim here is exactly what ID proponents would say: evolutionary novelty requires explaining how entire systems come into existence, and citing gene duplication alone is not tantamount to explaining evolutionary novelty. As Evolution News has argued in the past, gene duplication does not give you anything new; it only gives you more of something you already had.
Murray offers this conclusion: “I have argued that loss-of-function mutations may have played a major role in the evolution of novelty.” He doesn’t cite Michael Behe, and there’s no evidence that he got any ideas from reading Darwin Devolves. He would likely disagree with Behe about the efficacy of mechanisms such as gene duplication for generating new genes, as well as with Behe’s support for intelligent design. What’s most interesting here are the points of agreement — namely the hypothesis that degradative mutations are very common in the evolutionary process and may even predominate among adaptive features.
So this is good news: Mainstream evolutionary biologists are independently arriving at very similar conclusions to Behe’s central thesis in Darwin Devolves, the one that drew the most wrath from critics. In light of Murray’s article in Current Biology, Mike Behe appears to be vindicated.
Photo: Michael Behe signs a copy of Darwin Devolves at a Socrates in the City event with Eric Metaxas.